{"id":1699,"date":"2026-08-20T17:18:41","date_gmt":"2026-08-20T21:18:41","guid":{"rendered":"https:\/\/opentextbooks.concordia.ca\/explorations3\/?post_type=chapter&#038;p=1699"},"modified":"2026-10-14T11:53:53","modified_gmt":"2026-10-14T15:53:53","slug":"contemporary-topics-human-biology-and-health-test-wip","status":"publish","type":"chapter","link":"https:\/\/opentextbooks.concordia.ca\/explorations3\/chapter\/contemporary-topics-human-biology-and-health-test-wip\/","title":{"raw":"Contemporary Topics: Human Biology and Health","rendered":"Contemporary Topics: Human Biology and Health"},"content":{"raw":"<div class=\"__UNKNOWN__\">\r\n<div class=\"textbox\">\r\n\r\nLearn more about <a href=\"https:\/\/opentextbooks.concordia.ca\/explorations3\/back-matter\/about-the-authors\/\">authors and editors<\/a>,<a href=\"https:\/\/opentextbooks.concordia.ca\/explorations3\/back-matter\/student-contributors\/\"> Hess' student contributions<\/a>, and <a href=\"https:\/\/opentextbooks.concordia.ca\/explorations3\/back-matter\/versioning-history\/\">versioning history<\/a>.\r\n\r\n<\/div>\r\n\r\n<div class=\"textbox textbox--learning-objectives\"><header class=\"textbox__header\">\r\n<h2 class=\"textbox__title\">Learning Objectives<\/h2>\r\n<\/header>\r\n<div class=\"textbox__content\">\r\n<ul>\r\n \t<li>Describe the major transitions in patterns of disease that have occurred throughout human evolution.<\/li>\r\n \t<li>Describe what is meant by a \u201cmismatch\u201d between our evolved biology and contemporary lifestyles and how this is reflected in modern disease patterns.<\/li>\r\n \t<li>Explain how the human stress response can positively and negatively have an impact on health.<\/li>\r\n \t<li>Explain what a \u201csyndemic\u201d is and why the COVID-19 pandemic represents one.<\/li>\r\n \t<li>Describe the ways institutionalized racism and bias in the medical field contributed to different rates of exposure, differential treatment, morbidity, and mortality from COVID-19 for different ethnic groups in the United States.<\/li>\r\n<\/ul>\r\n<\/div>\r\n<\/div>\r\nWhen was the last time you needed to do research for an upcoming paper? I bet you started by looking for information online. How did you go about your search? Which websites looked promising? Which ones did not entice you to click past the home page? Once you found one you thought might be useful, how much time did you spend searching for information? At what point did you decide to leave that site and move on? I would wager money that you never once thought your behaviour had anything to do with human evolution, but it does.\r\n<p class=\"import-Normal\">Although we may not often stop to think about it, our evolutionary past is reflected in many aspects of modern life. The ways we \u201cforage\u201d for information on the internet mimics the ways we once foraged for food during our several-million-year history as hunter-gatherers (Chin Et al. 2015). Humans are visual hunters (Lieberman 2006). We practice optimal foraging strategy, meaning we make decisions based on energy return for investment (McElroy &amp; Townsend 2009). When we search for information online, we locate a \u201cpatch,\u201d in this case a website or research article, then quickly scan the contents to discern how much of it is useful to us. Like our hominin ancestors, we spend more time in \u201cpatches\u201d with abundant resources and abandon sites quickly once we have exhausted the available goods. As with internet searches, our evolutionary past is also reflected in the kinds of landscapes we find appealing, the foods that taste good to us, why we break a sweat at the gym, and why we have to go to the gym at all (Bogin 1991; Dutton 2009; Lieberman 2015). Many of the health problems facing humans in the 21st century also have their beginnings in the millions of years we roamed the earth as foragers.<\/p>\r\n\r\n<h2 class=\"import-Normal\">Preagricultural Humans<\/h2>\r\n<h3 class=\"import-Normal\"><strong>Diet<\/strong><\/h3>\r\n<p class=\"import-Normal\">Humans may be the species with the longest list of nutritional requirements (Bogin 1991). This is due to the fact that we evolved in environments where there was a high diversity of edible species but low densities of any given species. <em>Homo sapiens sapiens<\/em> require 45\u201350 essential nutrients for growth, maintenance, and repair of cells and tissues. These include protein, carbohydrates, fats, vitamins, minerals, and water. As a species, we are (or were) physically active with high metabolic demands. We are also <strong>[pb_glossary id=\"1912\"]omnivorous[\/pb_glossary]<\/strong> and evolved to choose foods that are dense in essential nutrients. One of the ways we identified high-calorie resources in our evolutionary past was through taste, and it is no accident that humans find sweet, salty, fatty foods appealing.<\/p>\r\n<p class=\"import-Normal\">The human predisposition toward sugar, salt, and fat is innate (Farb &amp; Armelagos 1980). Receptors for sweetness are found in every one of our mouth\u2019s 10,000 taste buds (Moss 2013). Preference for sweet makes sense in an ancestral environment where sweetness signaled high-value resources like ripe fruits. Likewise, \u201cthe long evolutionary path from sea-dwelling creatures to modern humans has given us salty body fluids, the exact salinity of which must be maintained\u201d (Farb &amp; Armelagos 1980), drawing us to salty-tasting things. Cravings for fat are also inborn, with some archaeological evidence suggesting that hominins collected animal bones for their fatty marrow, which contains two essential fatty acids necessary for brain development (Richards 2002), rather than for any meat remaining on the surface (Bogin 1991).<\/p>\r\n<p class=\"import-Normal\">Bioarchaeological studies indicate Paleolithic peoples ate a wider variety of foods than many people eat today (Armelagos Et al. 2005; Bogin 1991; Larsen 2014; Marciniak &amp; Perry 2017). Foragers took in more protein, less fat, much more fibre, and far less sodium than modern humans typically do (Eaton, Konner, &amp; Shostak 1988). Changes in tooth and intestinal morphology illustrate that animal products were an important part of human diets from the time of <em>Homo erectus<\/em> onward (Baltic &amp; Boskovic 2015; Richards 2002; Wrangham 2009). Once cooking became established, it opened up a wider variety of both plant and animal resources to humans. However, the protein, carbohydrates, and fats preagricultural peoples ate were much different from those we eat today. Wild game lacked the antibiotics, growth hormones, and high levels of cholesterol and saturated fat associated with industrialized meat production today (Walker Et al. 2005). Wild game was also protein dense, providing only 50% of energy as fat (Lucock Et al. 2014). The ways meat is prepared and eaten today also have implications for disease.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Meats cooked well done over high heat and\/or over an open flame, including hamburgers and barbecued meats, are highly carcinogenic due to compounds formed during the cooking process (Trafialek &amp; Kolanowski 2014). Processed meats that have been preserved by smoking, curing, salting, or by adding chemical preservatives such as sodium nitrite (e.g., ham, bacon, pastrami, salami, and beef jerky) have been linked to cancers of the colon, lung, and prostate (Abid, Cross, &amp; Sinha 2014; Figure 17.1). Nitrites\/nitrates have additionally been linked to cancers of the ovaries, stomach, esophagus, bladder, pancreas, and thyroid (Abid, Cross &amp; Sinha 2014). In addition, studies analyzing the diets of 103,000 Americans for up to 16 years indicate that those who ate grilled, broiled, or roasted meats more than 15 times per month were 17% more likely to develop high blood pressure than those who ate meat fewer than four times per month, and participants who preferred their meats well done were 15% more likely to suffer from <strong>[pb_glossary id=\"1953\"]hypertension[\/pb_glossary]<\/strong> (high blood pressure) than those who ate their meats rare (Liu 2018). A previous study of the same cohort indicated \u201cindependent of consumption amount, open-flame and\/or high-temperature cooking for both red meat and chicken is associated with an increased risk of type 2 diabetes among adults who consume animal flesh regularly\u201d (Liu Et al. 2018). Although meat has been argued to be crucial to cognitive and physical development among hominins (Wrangham 2009), there has been an evolutionary trade-off between the ability to preserve protein through cooking and the health risks of cooked meat and chemical preservatives.<\/p>\r\n\r\n[caption id=\"\" align=\"alignleft\" width=\"343\"]<img class=\"\" src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/06\/image1-6.png\" alt=\"Consecutive circles outline categories of cancer risk with images of processed meats and red meat.\" width=\"343\" height=\"424\" \/> Figure 17.1: Positive associations have been observed between meat consumption and some types of cancer. The International Agency for Research on Cancer (2018) categorized four groupings of cancer risk. The first group is labeled \"causes cancer\", and the second group \"probably causes cancer\". Group 1 includes processed meats such as bacon, salami and hot dogs. Group 2A includes red meat such as beef, pork and lamb. Credit: <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/chapter\/__unknown__-11\/\">Carcinogenic Meats (Figure 16.1)<\/a> original to <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/\" target=\"_blank\">Explorations: An Open Invitation to Biological Anthropology<\/a> by Katie Nelson is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0 License<\/a>. [Includes <a href=\"https:\/\/pngimg.com\/download\/10217\" target=\"_blank\">Hot dog PNG image<\/a> by unknown, <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0<\/a>; <a href=\"https:\/\/www.publicdomainpictures.net\/en\/view-image.php?image=109418&amp;picture=rasher-of-bacon\" target=\"_blank\">Rasher of Bacon<\/a> by unknown, <a href=\"https:\/\/creativecommons.org\/publicdomain\/zero\/1.0\/\" target=\"_blank\">public domain (CC0)<\/a>; <a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Salami_aka.jpg\" target=\"_blank\">Salami aka<\/a> by Andr\u00e9 Karwath <a href=\"https:\/\/commons.wikimedia.org\/wiki\/User:Aka\" target=\"_blank\">Aka<\/a>, <a href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/2.5\/legalcode\" target=\"_blank\">CC BY-SA 2.5<\/a>; <a href=\"https:\/\/pngimg.com\/download\/2127\" target=\"_blank\">Cow PNG image<\/a> by unknown, <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0<\/a>; <a href=\"https:\/\/pngimg.com\/download\/2184\" target=\"_blank\">sheep PNG image<\/a> by unknown, <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0<\/a>; <a href=\"https:\/\/www.publicdomainpictures.net\/en\/view-image.php?image=55516&amp;picture=pig-on-white-background\" target=\"_blank\">Pig on white background<\/a> by unknown, <a href=\"https:\/\/creativecommons.org\/publicdomain\/zero\/1.0\/\" target=\"_blank\">public domain (CC0)<\/a>.[\/caption]\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Although carbohydrates represent half of the diet on average for both ancient foragers and modern humans, the types of carbohydrates consumed are very different. Ancient foragers ate fresh fruits, vegetables, grasses, legumes, and tubers, rather than the processed carbohydrates common in industrialized economies (Moss 2013). Their diets also lacked the refined white sugar and corn syrup found in many modern foods that contribute to the development of diabetes (Pontzer Et al. 2012).<\/p>\r\n\r\n<h3 class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\"><strong>Physical Activity Patterns<\/strong><\/h3>\r\n<p class=\"import-Normal\">How do we know how active our ancestors were? Hominin morphology and physiology provide us with clues. Adaptations to heat discussed in Chapter 10 evolved in response to the need for physical exertion in the heat of the day in equatorial Africa. Human adaptations for preventing hyperthermia (overheating) suggest an evolutionary history of regular, strenuous physical activity. Research with modern foraging populations also offers clues to ancient activity patterns. Although subject to sampling biases and marginal environments (Marlowe 2005), modern foragers provide the only direct observations of human behaviour in the absence of agriculture (Lee 2013). From such studies, we know foragers cover greater distances in single-day foraging bouts than other living primates, and these treks require high levels of cardiovascular endurance (Raichlen &amp; Alexander 2014). Recent research with the Hadza in Tanzania indicates they walk up to 11 kilometres (6.8 miles) daily while hunting and gathering (Pontzer Et al. 2012), engaging in moderate-to-vigorous physical activity for over two hours each day\u2014meeting the U.S. government\u2019s weekly requirements for physical activity in just two days (Raichlen Et al. 2016; Figure 17.2). The fact that humans were physically active in our evolutionary past is also supported by the fact that regular physical exercise has been shown to be protective against a variety of health conditions found in modern humans, including [pb_glossary id=\"1913\"]<strong>cardiovascular disease<\/strong>[\/pb_glossary] (Raichlen &amp; Alexander 2014) and Alzheimer\u2019s dementia (Mandsager, Harb, &amp; Cremer 2018), even in the presence of brain pathologies indicative of cognitive decline (Buchman Et al. 2019).<\/p>\r\n&nbsp;\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"624\"]<img src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image10-7.png\" alt=\"Two hunters with dogs and bows walk in a savannah. \" width=\"624\" height=\"417\" \/> Figure 17.2: Hadza foragers hunting on foot. Credit: <a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Hadazbe_returning_from_hunt.jpg\" target=\"_blank\">Hadazbe returning from hunt<\/a> by <a href=\"https:\/\/www.flickr.com\/photos\/7177420@N03\" target=\"_blank\">Andreas Lederer<\/a> has been modified (cropped) and is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by\/2.0\/legalcode\" target=\"_blank\">CC BY 2.0 License<\/a>.[\/caption]\r\n<h3 class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\"><strong>Infectious Disease<\/strong><\/h3>\r\n<p class=\"import-Normal\">Population size and density remained low throughout the Paleolithic, by some estimates only 0.4 inhabitants per square kilometre (McClellan &amp; Dorn 2006). This limited <strong>[pb_glossary id=\"1908\"]morbidity[\/pb_glossary]<\/strong> and <strong>[pb_glossary id=\"1907\"]mortality[\/pb_glossary] <\/strong>from infectious diseases, which sometimes require large populations to sustain epidemics. Our earliest ancestors had primarily two types of infections with which to contend (Armelagos 1990). The first were organisms that adapted to our prehominin ancestors and have been problems ever since. Examples include head lice, pinworms, and yaws. A second set of diseases were [pb_glossary id=\"1914\"]<strong>zoonoses<\/strong>[\/pb_glossary], diseases that originate in animals and mutate into a form infectious to humans. One example is the Human Immunodeficiency Virus (HIV) that originated in nonhuman primates and was likely passed to humans through the butchering of hunted primates for food (Sharp &amp; Hahn 2011). Zoonoses that could have infected ancient hunter-gatherers include tetanus and [pb_glossary id=\"1915\"]<strong>vector-borne diseases<\/strong>[\/pb_glossary] transmitted by flies, mosquitoes, fleas, midges, ticks, and the like. Many of these diseases are slow acting, chronic, or latent, meaning they can last for weeks, months, or even decades, causing low levels of sickness and allowing victims to infect others over long periods of time. Survival or cure does not result in lasting immunity, with survivors returning to the pool of potential victims. Such diseases often survive in animal reservoirs, reinfecting humans again and again (Wolfe Et al. 2012). A study of bloodsucking insects preserved in samples of amber dating from 15 to 100 million years ago indicates that they carried microorganisms that today cause diseases such as river blindness, typhus, Lyme disease, and malaria (Poinar 2018). Such diseases may have been infecting humans throughout our history and may have had significant impacts on small foraging communities because they more often infected adults, who provided the food supply (Armelagos Et al. 2005).<\/p>\r\n\r\n<h3 class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\"><strong>Health<\/strong><\/h3>\r\n<p class=\"import-Normal\">Given their diets, levels of physical activity, and low population densities, nomadic preagricultural humans were likely in better health than many modern populations. This assertion is supported by comparative research conducted with modern foraging and industrialized populations. Measures of health taken from 20th-century foraging populations demonstrate excellent aerobic capacity, as measured by oxygen uptake during exertion, and low body-fat percentages, with [pb_glossary id=\"1916\"]<strong>triceps skinfold measurements<\/strong>[\/pb_glossary] half those of white Canadians and Americans. Serum cholesterol levels were also low, and markers for diabetes, hypertension, and cardiovascular disease were missing among them (Eaton, Konner, &amp; Shostak 1988; Raichlen Et al<em>. <\/em>2016).<\/p>\r\n\r\n<h2 class=\"import-Normal\">Health Consequences of the Transition to Agriculture and Animal Domestication<\/h2>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The shift from foraging to food production occurred relatively recently in our evolutionary history (Larsen 2014), and there are indications our biology has not yet caught up (Pritchard 2010). Beginning around 12,000 BCE in several parts of the globe, humans began to move toward a diet based on domesticated plants and animals (Armelagos Et al. 2005). This involved manipulating the natural landscape to facilitate intensive food production, including the clearing of forest and construction of wells, irrigation canals, and ditches, exposing humans to water-borne illnesses and parasites and attracting mosquitos and other vectors of disease to human settlements. The heavy, repetitive physical labour of early agricultural production resulted in negative impacts on articular joints, including [pb_glossary id=\"1917\"]<strong>osteoarthritis<\/strong>[\/pb_glossary] (Larsen 2014). At the same time, nutritional diversity became restricted, focused on major cereal crops that continue to dominate agricultural production today, including corn, wheat, and rice (Jain 2012). This represented a major shift in diet from a wide variety of plant and animal foods to dependence on starchy carbohydrates, leading to increases in dental caries (cavities), reductions in stature and growth rates, and nutritional deficiencies (Larsen 2014). Domesticated animals added new foods to the human diet, including meat that was higher in fat and cholesterol than wild game as well as dairy products (Lucock Et al. 2014). Agriculture provided the means to produce a storable surplus for the first time in human history, leading to the beginnings of economic inequality (see Chapter 13). Social hierarchies led to the unequal distribution of resources, concentrating infectious disease among the poor and malnourished (Zuckerman Et al. 2014), a situation that continues to plague humanity today (Marmot 2005).<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">[pb_glossary id=\"1918\"]<strong>Sedentism<\/strong>[\/pb_glossary] and a rise in population density accompanied the move to agriculture, increasing the risk of infectious disease. Agriculture often provided enough calories, if not enough nutrition, to increase fertility. Although diets were worse and people unhealthier, populations continued to grow, even in the midst of high levels of child and maternal mortality and short life expectancies (Omran 2005). Hygiene became an issue as large settlements increased the problem of removing human waste and providing uncontaminated water (Armelagos Et al. 2005). Domesticated animals provided reservoirs of zoonotic pathogens, which affected farmers more than foragers, as farmers were in closer proximity to their animals on a daily basis (Marciniak &amp; Perry 2017). Many of these diseases became major killers of humankind, including influenza, tuberculosis, malaria, plague, syphilis, and smallpox, functioning as selective pressures in and of themselves (Cooling 2015). As these diseases encountered large human populations, they caused major epidemics that traveled along newly established routes for trade, warfare, and colonization.<\/p>\r\n\r\n<h2 class=\"import-Normal\">Epidemiological Transitions<\/h2>\r\n<p class=\"import-Normal\">Changes in diet and physical-activity patterns, population densities, and exposure to zoonoses associated with agriculture resulted in an epidemiological transition, a shift in the causes of morbidity (sickness) and mortality (death) among humankind (Omran 2005). The first epidemiological transition from foraging to food production resulted in increases in dental caries (see Chapter 13), nutritional deficiencies, infectious disease, and skeletal conditions like osteoarthritis, as well as decreases in growth and height (Larsen 2014). A second epidemiological transition occurred following the Industrial Revolution in Western Europe and the United States when improved standards of living, hygiene, and nutrition minimized the effects of infectious disease, after which people began to experience higher rates of [pb_glossary id=\"1919\"]<strong>noncommunicable diseases<\/strong>[\/pb_glossary], such as <strong>[pb_glossary id=\"1911\"]cancer[\/pb_glossary]<\/strong>, heart disease, and diabetes due to the changes in lifestyle, diet, and activity levels that are the subject of this chapter (Omran 2005). With the addition of immunizations and other public health initiatives, modified forms of this transition remain ongoing in many low- and middle-income countries (Zuckerman Et al. 2014), with several now facing a <strong>[pb_glossary id=\"1920\"]\u201cdouble burden\u201d[\/pb_glossary] <\/strong>of disease, with poor, often rural, populations struggling with infectious diseases due to malnutrition, lack of sanitation, and access to health care, while more affluent citizens are victims of chronic illnesses. A third epidemiological transition is now underway as infectious diseases, including new, re-emergent, and multidrug-resistant diseases, have once again become major health concerns (Harper &amp; Armelagos 2010; Zuckerman Et al. 2014). These include COVID-19, Ebola, HIV\/AIDS, tuberculosis, malaria, dengue, Lyme disease, and West Nile virus\u2014all zoonoses that initially spread to humans through contact with animals.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Patterns of morbidity and mortality continue to shift across the globe. As with the first epidemiological transition resulting from the adoption of large-scale agriculture, such shifts can be the direct, if unintended, result of human interactions with the environment. For example, there has been a rise in chronic inflammatory diseases (CIDs) in developed countries (Versini Et al<em>.<\/em> 2015). This includes increased rates of allergic conditions like asthma and autoimmune diseases like rheumatoid arthritis, multiple sclerosis, Crohn\u2019s disease, and inflammatory bowel disease. This has coincided with the decrease in infectious disease associated with the second epidemiological transition, and the two are related. The \u201chygiene hypothesis\u201d postulates the rise in CIDs is a result of limited exposure to nonlethal environmental pathogens in utero and early childhood (Zuckerman &amp; Armelagos 2014). Modern human societies have become so sanitized that we are no longer exposed to microorganisms that stimulate the development of a healthy immune system (Versini Et al. 2015). \u201cIn effect, the lifestyle changes\u2014sanitary improvements, pasteurization, use of antibiotics, and improved hygiene\u2014that contributed to the second transition may have produced a substantial trade-off, with developed nations exchanging a high burden of infectious disease for a higher burden of CIDs\u201d (Zuckerman Et al. 2014).<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The third epidemiological transition, the re-emergence of infectious disease, reflects the continuing relationship between humans, animals, and pathogens. Over 60% of [pb_glossary id=\"1921\"]<strong>e<\/strong><strong>merging infectious diseases (EIDs)<\/strong>[\/pb_glossary] since 1940 have been of zoonotic origin, with over 70% stemming from human contact with wildlife (Jones Et al. 2008), including COVID-19. The crossover of COVID to humans is believed to have involved transmission from bats to an intermediate species then to humans, with infected humans then passing it to other humans in a wet market in Wuhan, China in late 2019 (Worobey Et al. 2022). Two COVID variants, representing two distinct crossover events from animals to humans, were circulating in the market by February 2020. Similarly, the global bushmeat trade currently devastating Africa\u2019s wildlife is a continuing source of Ebola infection (Asher 2017), as well as the original source of HIV and viruses related to leukaemia and lymphoma among humans (Zuckerman Et al. 2014). New strains of avian (bird) flu, some with mortality rates as high as 60% among humans (WHO n.d.), are transmitted to humans through poultry production and contact with wild birds (Davis 2005). Lastly, the use of antibiotics in commercial meat production is directly related to the rise of drug-resistant strains of previously controlled infectious diseases. An estimated 80% of antibiotics in the U.S. are used to promote growth and prevent infection in livestock, and drug-resistant bacteria from these animals are transmitted to humans through meat consumption (Ventola 2015).<\/p>\r\n\r\n\r\n[caption id=\"\" align=\"alignleft\" width=\"299\"]<img class=\"\" src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image13-7.png\" alt=\"Aerial photograph of a flooded city.\" width=\"299\" height=\"399\" \/> Figure 17.3: Flooding in Sindh, Pakistan, in 2022. Credit: <a href=\"https:\/\/www.flickr.com\/photos\/193804179@N08\/52331043544\/\" target=\"_blank\">Flood in Pakistan<\/a> by <a href=\"https:\/\/www.flickr.com\/photos\/193804179@N08\/\" target=\"_blank\">Ali Hyder Junejo<\/a> is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by\/2.0\/\" target=\"_blank\">CC BY 2.0 License<\/a>.[\/caption]\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">A fourth epidemiological transition is currently underway in which some parts of the globe are suffering from a <strong>[pb_glossary id=\"1922\"]\u201ctriple burden\u201d[\/pb_glossary]<\/strong> of infectious and chronic diseases combined with injuries and diseases related to intensifying globalization, urbanization, deforestation, and climate change (Karn &amp; Sharma 2021). Massive flooding in Pakistan in 2022 (Figure 17.3) will serve to illustrate the concept. Following a severe heat wave in June 2022, Pakistan experienced extremely heavy seasonal monsoon rains, in some provinces 700% above normal. Combined with water flow from melting glaciers, this caused the worst flooding in the country\u2019s history, putting one third of the nation under water (Sheerazi 2022). The heat wave, glacial melt, and extreme rainfall were all attributable to global climate change, inflicting destruction and disease on Pakistan, which produces less than 1% of total global carbon emissions (Government of Pakistan 2021).<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">As a direct result of the flooding, infrastructure, including roads, homes, and bridges, was destroyed, and 1,700 people died, nearly 13,000 were injured, and over 33 million were displaced. In addition to their initial injuries and trauma, displaced people lacked food, health care, safe water, and basic sanitation, leading to starvation and exposure to infectious diseases like malaria and dengue fever, as well as skin conditions like scabies, caused by mites. Pakistan also has a poverty rate of 30\u201340%, contributing to already-high rates of HIV, tuberculosis, and hepatitis. At the same time, the leading causes of death are heart disease, cancer, lower respiratory diseases, and stroke (CDC n.d), all chronic conditions.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">These examples illustrate continuing interaction between humans, our evolved biology, and the physical and cultural environments in which we live. The remainder of this chapter will focus on selected diseases and the social, cultural, and environmental factors that contribute to their <strong>[pb_glossary id=\"2755\"]prevalence[\/pb_glossary]<\/strong> in modern, industrialized economies. We begin with the health condition that affects all of the others\u2014<strong>[pb_glossary id=\"1910\"]obesity[\/pb_glossary]<\/strong>.<\/p>\r\n\r\n<h2 class=\"import-Normal\">Obesity<\/h2>\r\n<p class=\"import-Normal\">According to the World Health Organization (2017), 1.9 billion of the world\u2019s people are overweight and 650 million of these are obese. In the United States, 70% of Americans are overweight, and 40% of these meet the criteria for obesity. For the first time in human history, most of the world's population lives in countries where overweight and obesity kill more people than hunger (Figure 17.4). Improvements in public health and food production have allowed a greater number of people to live past childhood and to have enough to eat. This does not include everyone. Many people still struggle with poverty, hunger, and disease, even in the wealthiest of nations, including the United States. On a global scale, however, many people not only have enough food to survive but also to gain weight\u2014enough extra weight to cause health problems.<\/p>\r\n<img src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image4-5.png\" alt=\"&quot;Bar\" \/>\r\n<p class=\"import-Normal\">Although studies show differences in daily energy expenditure between foraging and farming populations compared with industrialized peoples, the major contributor to obesity in Western populations is energy intake (Pontzer Et al. 2012). Many people not only eat too much but too much of the wrong things. Biological anthropologist Leslie Lieberman (2006) argues that contemporary humans continue to rely on cues from foraging strategies of our evolutionary past that are now counterproductive in the [pb_glossary id=\"1926\"]<strong>obesogenic<\/strong> [\/pb_glossary]environments in which we now live.<\/p>\r\n<p class=\"import-Normal\">Examine your own eating habits in the context of how humans once hunted and gathered. Humans once relied on visual cues to find food, often traveled long distances to obtain it, then transported it back to our home base. There they may have had to process it by hand to render it edible. Think of how much less energy it takes to find food now. If we have the financial resources, we can acquire big energy payoffs by simply sitting at home and using an app on our mobile phone to place an order for delivery. And, voila! High-calorie (if not highly nutritious) food arrives at our door. Should we venture out for food, search time is reduced by signage and advertising directing us toward high-density \u201cpatches\u201d where food is available 24 hours a day. These include vending machines, gas stations, and fast-food outlets. Travel time is minimal and little human energy is used in the process (Lieberman 2006).<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Foods are also prepackaged and prepared in ways that allow us to eat large quantities quickly. Think French fries or chicken nuggets, which we can easily eat with our hands while doing other things, like driving or watching television, rendering eating mindless and allowing us to take in food faster than our <strong>[pb_glossary id=\"2756\"]endocrine systems[\/pb_glossary]<\/strong> can tell us we are getting full. Modern \u201cpatches\u201d offer low-fibre, calorie-dense resources, which allow us to eat larger quantities, a problem already encouraged by larger portion sizes (Lieberman 2006). Processed foods are also engineered to appeal to human preferences for sweet tastes and fatty, creamy textures (Moss 2013). Remember from earlier chapters that natural selection favoured depth perception, colour vision, grasping hands, and coordinated eye-hand movements as general primate traits. Advertising and packaging now use our colour vision against us, attracting us to products that have little nutritional value but that play to our evolutionary predisposition toward variety. Remember those 50 different nutrients we require? That variety is now presented to us in the form of 55 different flavours of Oreo cookies (Cer\u00f3n 2017), which we take out of the package and dip in milk using our hand-eye coordination and depth perception.<\/p>\r\n<p class=\"import-Normal\">Even if we are ostensibly eating the same things our ancestors did, these foods are nothing alike. Take potatoes, for example. One medium-sized, plain, baked potato is a healthy food, especially if we eat the skin too. It contains 110 calories, 0 grams of fat, 26 grams of carbohydrates, and 3 grams of protein, plus 30% of the U.S. Recommended Daily Allowance (RDA) of vitamin C, 10% of vitamin B6, 15% of potassium, and no sodium (<a href=\"https:\/\/potatogoodness.com\/\" target=\"_blank\" rel=\"noopener\">Potato USA<\/a>). In contrast, a medium order of McDonald\u2019s fries, which takes the potato and adds salt and fat, contains 340 calories, 16 grams of fat, 44 grams of carbohydrates, 4 grams of protein, and 230 mg of sodium (<a href=\"https:\/\/www.mcdonalds.com\" target=\"_blank\" rel=\"noopener\">McDonalds<\/a>). Potato chips take food processing to a whole new level, removing even more nutrition and adding a host of additional ingredients, including oils, preservatives, and artificial flavourings and colours (Moss 2013). Take Ruffles Loaded Bacon and Cheddar Potato Skins Potato Chips as an example (St. Pierre 2018). The number of ingredients increases from one to 11 to 35 as we move from the potato to the potato chip, moving further from nature with each step (Figure 17.5). It should be noted that the nutritional information for the potato chips is based on a serving size of 11 chips, an amount likely smaller than many people eat. Many sweet, fatty, salty foods like fries and chips are cheap, which is why many people choose to eat them (Moss 2013). The price of a medium-sized order of McDonald\u2019s fries as of this writing is US$1.79, and the potato chips are $2.98 for an 8.5-ounce bag. A single potato prewrapped for microwaving is available in many supermarkets for US$1.99 but requires access to a microwave and eating utensils, making it less convenient.<\/p>\r\n\r\n\r\n<div style=\"text-align: left\">\r\n<table class=\"grid\" style=\"border-collapse: collapse;width: 100%;height: 197px\" border=\"0\"><caption>Figure 17.5: The potato in three modern forms. Credit: <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/chapter\/__unknown__-11\/\" target=\"_blank\">The potato in three modern forms (Figure 16.4)<\/a> original to <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/\" target=\"_blank\">Explorations: An Open Invitation to Biological Anthropology<\/a> by Joylin Namie and Katie Nelson is a collective work under a <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0 License<\/a>. [Includes <a href=\"https:\/\/www.publicdomainpictures.net\/en\/view-image.php?image=137873&amp;picture=potato\" target=\"_blank\">Potato<\/a> by Charles Rondeau, <a href=\"https:\/\/creativecommons.org\/publicdomain\/zero\/1.0\/\" target=\"_blank\">public domain (CC0)<\/a>; <a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:McDonalds-French-Fries-Plate.jpg\" target=\"_blank\">McDonalds-French-Fries-Plate<\/a> by <a href=\"https:\/\/commons.wikimedia.org\/wiki\/User:Evan-Amos\" target=\"_blank\">Evan-Amos<\/a>, <a href=\"https:\/\/creativecommons.org\/publicdomain\/zero\/1.0\/\" target=\"_blank\">public domain (CC0)<\/a>; <a href=\"https:\/\/pdpics.com\/photo\/2316-potato-chips-bowl\/\" target=\"_blank\">Potato chips bowl<\/a> by pdpics.com, <a href=\"https:\/\/creativecommons.org\/publicdomain\/zero\/1.0\/\" target=\"_blank\">public domain (CC0)<\/a>.]<\/caption>\r\n<thead>\r\n<tr style=\"height: 47px\">\r\n<td style=\"width: 20.0464%;height: 47px\"><\/td>\r\n<td style=\"width: 25.4644%;height: 47px\">\r\n<p style=\"text-align: center\"><strong>Baked Potato<\/strong>\r\n[based, skin on, plain]<\/p>\r\n<\/td>\r\n<td style=\"width: 27.4768%;height: 47px;text-align: center\"><strong>French Fries<\/strong>\r\n[Medium order]<\/td>\r\n<td style=\"width: 27.0124%;height: 47px\"><strong>Potato Chips<\/strong>\r\n[1 oz. serving of 11 chips]<\/td>\r\n<\/tr>\r\n<\/thead>\r\n<tbody>\r\n<tr style=\"height: 15px\">\r\n<td style=\"width: 20.0464%;height: 15px\">Calories<\/td>\r\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">110<\/td>\r\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">340<\/td>\r\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td style=\"width: 20.0464%;height: 15px\">Calories from fat<\/td>\r\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">0<\/td>\r\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">144<\/td>\r\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td style=\"width: 20.0464%;height: 15px\">Fat<\/td>\r\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">0g<\/td>\r\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">16g<\/td>\r\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td style=\"width: 20.0464%;height: 15px\">Carbohydrates<\/td>\r\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">26g<\/td>\r\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">44g<\/td>\r\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td style=\"width: 20.0464%;height: 15px\">Protein<\/td>\r\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">3g<\/td>\r\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">4g<\/td>\r\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td style=\"width: 20.0464%;height: 15px\">Sodium<\/td>\r\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">0g<\/td>\r\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">230mg<\/td>\r\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td style=\"width: 20.0464%;height: 15px\">Dietary fibre<\/td>\r\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">2g<\/td>\r\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">4g<\/td>\r\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td style=\"width: 20.0464%;height: 15px\">Sugars<\/td>\r\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">1g<\/td>\r\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">0g<\/td>\r\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td style=\"width: 20.0464%;height: 15px\">Cholesterol<\/td>\r\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">0g<\/td>\r\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">0g<\/td>\r\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td style=\"width: 20.0464%;height: 15px\">Ingredients<\/td>\r\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">Potato<\/td>\r\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">Potatoes, vegetable oil (canola oil), soybean oil, hydrogenated soybean oil, natural beef flavour (wheat and milk derivatives), citric acid (preservative), dextrose, sodium acid pyrophosphate (main colour), salt.<\/td>\r\n<td style=\"width: 27.0124%;height: 15px\">Potatoes, vegetable oil (sunflower, corn, and\/or canola oil), bacon and cheddar loaded potato skins seasoning (maltodextrin - made from corn) salt, cheddar cheese (milk, cheese cultures, salt enzymes), sour cream (cultured cream, skin milk), whey, dried onion, monosodium.<\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\n<\/div>\r\n<div class=\"__UNKNOWN__\">\r\n<p class=\"import-Normal\">Not only have we transformed the food supply and our eating in ways that are detrimental to our health, but these changes have been accompanied by reductions in physical activity. [pb_glossary id=\"1929\"]<strong>Sedentarism<\/strong>[\/pb_glossary] is built into contemporary lifestyles. Think of how much time you spent sitting down today. Some of it may have been in class or at work, some may have been driving a car or perhaps binge-watching your favourite show, playing a video game, or checking in on social media. An inactive lifestyle is almost dictated by the digital age (Lucock Et al<em>.<\/em> 2014). Levels of physical activity in many countries are now so low that large portions of the population are completely sedentary, including one in five Americans (CDC 2022). For a species whose biology evolved in an environment where walking, lifting, and carrying were part of daily life, this is unhealthy and often leads to weight gain.<\/p>\r\n\r\n<h2 class=\"import-Normal\">Biology and Genetics of Weight<\/h2>\r\n[caption id=\"\" align=\"alignright\" width=\"344\"]<img class=\"\" src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image5-7.png\" alt=\"Four individuals of various ages walk alongside trees.\" width=\"344\" height=\"229\" \/> Figure 17.6: Participants of a walk against diabetes and for general fitness around Nauru airport. Credit: <a href=\"https:\/\/www.flickr.com\/photos\/106853342@N04\/10709038046\" target=\"_blank\">Participants of a walk against Diabetes and for general fitness around Nauru airport<\/a> by Lorrie Graham, <a href=\"https:\/\/www.flickr.com\/photos\/dfataustralianaid\/\" target=\"_blank\">Department of Foreign Affairs and Trade<\/a>, is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by\/2.0\/legalcode\" target=\"_blank\">CC BY 2.0 License<\/a>.[\/caption]\r\n<p class=\"import-Normal\">Research indicates multiple genetic variants influence weight gain, and they are not spread evenly among human populations. Tuomo Rankinen and colleagues (2006) identified 127 genes associated with obesity, of which 22 contributed to weight gain. Claude Bouchard (2007) then identified five categories of obesity-promoting genotypes. These genotypes promote sedentarism, result in low metabolism, and lead to poor regulation of appetite, and a propensity to overeat. An example of the impact such genotypes can have in an environment of plenty is found among the population of the Micronesian island of Nauru. Historically, the island was geographically isolated and the food supply was unpredictable. These conditions favoured genotypes that promoted the ability to rapidly build up and store fat in times of food availability. In Nauruans, there are two genetic variants favouring weight gain and insulin resistance, and both are associated with obesity and type 2 diabetes. One variant is also associated with hypertension. One of these variants is also found in Pima Indians, who live in parts of Arizona and Mexico. In the Pima, this variant is associated with a high [pb_glossary id=\"1930\"]<strong>b<\/strong><strong>ody mass index (BMI) <\/strong>[\/pb_glossary] and type 2 diabetes, although it is not associated with the same outcomes in Japanese and British subjects (de Silva Et al<em>.<\/em> 1999). The other variant was analysed in Finnish and South Indian populations, neither of whom experienced the same outcome as Nauruans. This suggests these alleles may act as modifying genes for type 2 diabetes in some population groups (Baker Et al. 1994). Unfortunately, Nauruans are one of those groups. Eventually, they became wealthy through phosphate mining on the island, gaining access to a calorie-rich Western diet of imported foods and developing a sedentary lifestyle. This resulted in rates of type 2 diabetes as high as 30\u201340% in Nauruans over the age of 15, which became the leading cause of death (Lucock Et al. 2014), something Nauruans are taking seriously (Figure 17.6).<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Factors other than biology influence which populations that carry a genetic predisposition to diabetes actually express it. The Onk Akimel O\u2019odham (Pima) of Arizona, for example, were seriously impacted by U.S. government policies that affected water rights, forcing the population away from subsistence farming to dependence on government handouts and convenience food. This resulted in a significant loss of physical activity, malnutrition, and obesity. The Onk Akimel O\u2019odham continue to experience hardship due to high rates of unemployment, poverty, and depression, sometimes made worse by alcoholism. In the absence of these pressures, the Onk Akimel O\u2019odham were diabetes free for centuries prior, even though they relied on agriculture for subsistence, suggesting genetics alone is not responsible for high rates of obesity and diabetes in current Onk Akimel O\u2019odham populations (Smith-Morris 2004).<\/p>\r\n\r\n\r\n[caption id=\"\" align=\"alignleft\" width=\"372\"]<img src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image3-4-1.jpg\" alt=\"A human body outline with multiple points, each listing related medical complications.\" width=\"372\" height=\"493\" \/> Figure 17.7: Medical complications of obesity include stroke, sleep apnea, lung disease, liver disease, gallstones, cancer, heart disease, diabetes, pancreatitis, abnormal periods and infertility, arthritis, inflamed veins, and gout. Credit: <a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Medical_complications_of_obesity.png\" target=\"_blank\">Medical complications of obesity<\/a> by the <a href=\"https:\/\/www.cdc.gov\/\" target=\"_blank\">Centers for Disease Control and Prevention (CDC)<\/a> has been modified (colour changed and cancer list shortened) and is in the <a href=\"https:\/\/en.wikipedia.org\/wiki\/Public_domain\" target=\"_blank\">public domain<\/a>.[\/caption]\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Obesity also has an epigenetic component. You learned about epigenetics in Chapter 4. With regard to obesity, epigenetics is counterintuitive in that mothers who do not take in enough calories during pregnancy often give birth to babies who grow up to be fat. What takes place is the fetus receives signals during pregnancy from its mother through the placenta and intrauterine environment about environmental conditions outside of the womb, in this case food insecurity. These signals encourage the turning on and off of genes related to metabolism. This alters the phenotype of the fetus so that if the child is born into an environment where food is plentiful, it will put on weight rapidly whenever possible, leading to obesity and related diseases later in life. If the child is a girl, her own eggs are formed in utero with the same genetic changes coded in, meaning she will pass along this same genetic predisposition to gain weight to her children. Hence, a biological propensity toward obesity can continue across generations (Worthman &amp; Kuzara 2005). Epigenetic changes to genes that promote weight gain are argued to be partly responsible for the rapid rise in obesity and diabetes in developing countries gaining access to Western diets (Stearns, Nesse, and Haig 2008).<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Obesity and overweight put a strain on several biological systems of the body, including the [pb_glossary id=\"1931\"]<strong>circulatory<\/strong>[\/pb_glossary], endocrine, and skeletal systems, contributing to hypertension, heart disease, [pb_glossary id=\"1932\"]<strong>stroke<\/strong>[\/pb_glossary], diabetes, and osteoarthritis (Figure 17.7). Obesity also elevates the risk of cancers of the breast, endometrium, kidney, colon, esophagus, stomach, pancreas, and gallbladder (National Institutes of Health 2017; Vucenik &amp; Stains 2012). Diabetes\u2014one of the fastest-growing health conditions around the globe (WHO 2016) and one tightly connected to obesity and overweight\u2014is the focus of the following Special Topics box.<\/p>\r\n\r\n<div class=\"textbox\">\r\n<h2 class=\"import-Normal\">Special Topic: Diabetes<\/h2>\r\n<p class=\"import-Normal\"><strong>[pb_glossary id=\"1936\"]Diabetes mellitus[\/pb_glossary]<\/strong> is an endocrine disorder characterized by excessively high blood glucose levels (Martini Et al<em>.<\/em> 2013). According to a report released by the World Health Organization, the number of people living with diabetes is growing in all regions of the world. Rates of diabetes have nearly doubled in the past three decades, largely due to increases in obesity and sugary diets (WHO 2016). One in 10 people around the world, 537 million people, now have diabetes, and three out of four live in low- and middle-income countries (IDF 2022). In the United States, 37 million people have diabetes (CDC 2020), where the disease is rising fastest among millennials (those ages 20\u201340) (BCBSA 2017), and one in every two adults with diabetes is undiagnosed (IDF 2022). Obesity and diabetes are linked: obesity causes a diet-related disease (diabetes) because of humans\u2019 evolved metabolic homeostasis mechanism, which is poorly suited to contemporary energy environments (Lucock Et al<em>.<\/em> 2014).<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">To function properly, cells need a steady fuel supply. Blood sugar (glucose) is the fuel for most cells in the body, and the body produces the hormone <strong>[pb_glossary id=\"1949\"]insulin[\/pb_glossary]<\/strong> to help move glucose into cells that need it (Figure 17.8). Foods that most readily supply glucose to your bloodstream are carbohydrates, especially starchy foods like potatoes or sweet, sugary foods like candy and soda. The body can also convert other types of foods, including protein-rich foods (e.g., lean meats) and fatty foods (e.g.<em>,<\/em> vegetable oils and butter), into blood sugar in the liver via gluconeogenesis. Insulin\u2019s main job is to tell your cells when to take up glucose. The cell also has to listen to the signal and mobilize the glucose transporters. This not only allows your cells to get the energy they need, but it also keeps blood sugar from building up to dangerously high levels when you are at rest.<\/p>\r\n\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"485\"]<img src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image7-7.png\" alt=\"The cycle of how a body with diabetes processes nutrients from food.\" width=\"485\" height=\"648\" \/> Figure 17.8: Carbohydrates are eaten and broken down into simple sugars (e.g., glucose). Glucose enters the bloodstream from the intestines, and the increase in glucose stimulates the pancreas to release insulin into the bloodstream. Insulin deposits glucose in the muscles and fat cells, where it is stored and used for energy. Credit: <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/chapter\/__unknown__-11\/\" target=\"_blank\">Glucose metabolism (Figure 16.7)<\/a> original to <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/\" target=\"_blank\">Explorations: An Open Invitation to Biological Anthropology<\/a> by Mary Nelson is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0 License<\/a>.[\/caption]\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">This system has limits. Like the rest of our biology, it evolved during several million years when sugar was hard to come by and carbohydrates took the form of fresh foods with a low [pb_glossary id=\"1938\"]<strong>glycemic index (GI)<\/strong>[\/pb_glossary]. Our ancestors were also active throughout the day, taking pressure off of the endocrine system. Now, sedentary lifestyles and processed-food diets cause many of us to take in more calories\u2014and especially more carbohydrates\u2014than our bodies can handle. There is only so much blood sugar your cells can absorb. Many modern populations are taxing those limits. After years of being asked by insulin to take in more glucose than they can use, cells eventually stop responding (McKee &amp; McKee 2015). This is called type 2 diabetes or insulin resistance, which accounts for 90\u201395% of diabetes cases in the United States (Figure 17.9). type 1 diabetes is believed to be caused by an autoimmune response in which your immune system is attacking and destroying the insulin-producing cells in your pancreas (Figure 17.9). type 1 diabetes is a genetic condition that often shows up early in life, while type 2 is more lifestyle-related and develops over time.<\/p>\r\n\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"462\"]<img src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image9-6.png\" alt=\"Type 1 cells and Type 2 cells and their response to insulin.\" width=\"462\" height=\"276\" \/> Figure 17.9: Type 1 and type 2 diabetes. For Type 1 Diabetes, cells do not absorb glucose becuase there is no insulin. For Type 2 Diabetes, although there is insulin available, cells do not respond to it. Credit: <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/chapter\/__unknown__-11\/\" target=\"_blank\">Type 1 and Type 2 Diabetes (Figure 16.8)<\/a> original to <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/\" target=\"_blank\">Explorations: An Open Invitation to Biological Anthropology<\/a> by Mary Nelson has been modified (text) and is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0 License<\/a>.[\/caption]\r\n\r\n<\/div>\r\n<h2 class=\"import-Normal\">Cardiovascular Disease<\/h2>\r\n<p class=\"import-Normal\">Cardiovascular disease (CVD)\u2014which includes coronary heart disease, hypertension (high blood pressure), and stroke\u2014is the leading cause of death globally, and heart disease remains the number one cause of death in the United States (American Heart Association 2018). Risk factors for cardiovascular disease include diet, obesity\/overweight, diabetes, smoking and alcohol consumption, and physical inactivity.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The connections between these factors and heart disease may not seem obvious and will be addressed here beginning with diet. Diets high in saturated fat and cholesterol can lead to atherosclerosis, a condition in which fat and cholesterol form plaque inside the arteries, eventually building up and hardening to the point that blood flow is blocked. Too much salt in the diet leads to fluid retention, which increases blood volume and thereby blood pressure, taxing the heart. Obesity\/overweight contribute to cardiovascular disease directly through increases in total blood volume, cardiac output, and cardiac workload. In other words, the heart has to work much harder if one is overweight (Akil &amp; Ahmad 2011). Obesity also relates to CVD indirectly through elevation of blood pressure (hypertension) and diabetes. High levels of blood glucose from diabetes can damage blood vessels and the nerves that control the heart and blood vessels. Alcohol consumption can raise blood pressure and triglyceride levels, a type of fat found in the blood. Alcohol also adds extra calories, which may cause weight gain, especially around the abdomen, which is directly associated with risk of a heart attack (Akil &amp; Ahmad 2011). Cigarette smoking also increases the risk of coronary heart disease. Nicotine increases blood pressure; in addition, cigarette smoke causes fatty buildup in the main artery in the neck and thickens blood, making it more likely to clot. It also decreases levels of HDL (\u201cgood\u201d) cholesterol (American Heart Association 2018). Even secondhand smoke can have an adverse effect if exposure occurs on a regular basis. Chronic psychological stress also elevates the risk of heart disease (Dimsdale 2008). The repeated release of stress hormones like adrenaline elevates blood pressure and may eventually damage artery walls. The human [pb_glossary id=\"1951\"]<strong>stress response<\/strong>[\/pb_glossary] and its connections to health and disease are discussed in more detail below.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">However, physical activity alters the likelihood of having heart disease, both directly and indirectly. Regular exercise of moderate to vigorous intensity strengthens the heart muscle and allows capillaries, tiny blood vessels in your body, to widen, improving blood flow. Regular exercise can also lower blood pressure and cholesterol levels and manage blood sugar levels, all of which reduce the risk of CVD.<\/p>\r\n\r\n<h2 class=\"import-Normal\">Cancer<\/h2>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Cancer is the second-leading cause of death globally, causing one in every six deaths and killing nearly nine million people in 2015 (WHO 2018). Lifetime cancer risk in developed Western populations is now one in two, or 50% (Greaves 2015). Approximately one-third of deaths from cancer are due to behavioural and dietary factors, including high body mass index (BMI), low fruit and vegetable intake, lack of physical activity, and the use of tobacco and alcohol. Depending on the type of cancer and one\u2019s own genetic inheritance, these factors can increase cancer risk from 2- to 100-fold (Greaves 2015). Cancer is the result of interactions between a person's genes and three categories of external agents: physical carcinogens (e.g., ultraviolet radiation), chemical carcinogens (e.g., tobacco smoke, asbestos), and biological carcinogens, such as infections from certain viruses, bacteria, or parasites (WHO 2018). Obesity is also a risk factor for cancer, including of the breast, endometrium, kidney, colon, esophagus, stomach, pancreas, and gallbladder (National Institutes of Health 2017; Vucenik &amp; Stains 2012).<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Cancer has been regarded as a relatively recent affliction for humans that became a problem after we were exposed to modern carcinogens and lived long enough to express the disease (David &amp; Zimmerman 2010). Given the long history that humans share with many oncogenic (cancer-causing) parasites and viruses (Ewald 2018), and the recent discovery of cancer in the metatarsal bone of a 1.8-million-year-old hominin (Odes Et al. 2016), this view is being challenged (See \u201cSpecial Topic: Life Choices and Reproductive Cancers in Women\u201d). The difficulties of identifying cancer in archaeological populations are many. Most cancer occurs in soft tissue, which rarely preserves, and fast-growing cancers would likely kill victims before leaving evidence in bone. It is also difficult to distinguish cancer from benign growths and inflammatory disease in ancient fossils, and there is often postmortem damage to fossil evidence from scavenging and erosion. However, using 3-D images, South African researchers recently diagnosed a type of cancer called osteosarcoma in a toe bone belonging to a human relative who died in Swartkrans Cave between 1.6 and 1.8 million years ago (Randolph-Quinney Et al. 2016). This study provides the earliest evidence of cancer in hominins.<\/p>\r\n\r\n<div class=\"textbox\">\r\n<h2 class=\"import-Normal\">Special Topic: Life Choices and Reproductive Cancers in Women<\/h2>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Behavioural or \u201clifestyle\u201d choices have an impact on cancer risk. Breast cancer is one example. It is the most common cancer in women worldwide, but <strong>[pb_glossary id=\"1940\"]incidence[\/pb_glossary]<\/strong> of new cases varies from 19.3 per 100,000 women in Eastern Africa to 89.7 per 100,000 women in Western Europe (WHO 2018). These differences are attributable to cultural changes among women in Western, industrialized countries that are a mismatch for our evolved reproductive biology. Age at <strong>[pb_glossary id=\"1941\"]menarche[\/pb_glossary]<\/strong>, the onset of menstrual periods, has dropped over the course of the last century from 16 to 12 years of age in the U.S. and Europe, with some girls getting their periods and developing breasts as young as eight years old (Greenspan &amp; Deardorff 2014, Figure 17.10). A World Health Organization study involving 34 countries in Europe and North America suggests the primary reason for the increase in earlier puberty is obesity, with differences in BMI accounting for 40% of individual- and country-level variance (Currie Et al<em>.<\/em> 2012). Early puberty in girls is associated with increased risk of breast cancer, ovarian cancer, diabetes, and high cholesterol in later life (Pierce &amp; Hardy 2012).<\/p>\r\n\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"554\"]<img src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image12-3.jpg\" alt=\"A graph shows the decrease in age at menarche for five European nations and United States.\" width=\"554\" height=\"434\" \/> Figure 17.10: Decreasing ages at time of first menstruation in selected countries. Credit: <a href=\"https:\/\/en.wikipedia.org\/wiki\/Menarche#\/media\/File:Acceleration1.jpg\" target=\"_blank\">Acceleration1.jpg<\/a> by Yahadzija is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/3.0\/deed.en\" target=\"_blank\">CC BY-SA 3.0 Unported License<\/a>.[\/caption]\r\n\r\n&nbsp;\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">At the same time that age at puberty is dropping for girls in Western nations, age at birth of the first child is later, at 26 years old (Mathews and Hamilton 2016). Women are also having fewer children, two on average (Gao 2015), with 15% of women choosing to remain childless (Livingston 2015). Rates of breastfeeding have risen in recent decades but drop to only 27% of infants once babies reach 12 months of age (CDC 2014). In contrast, data from modern foraging populations (Eaton Et al. 1994) indicate that age at menarche is around 16 years old, age at birth of the first child is 19, breastfeeding on demand continues for three years for each child, and the number of children averages six. These differences relate to elevated risk for reproductive cancers, including breast cancer, among women in developed countries.<\/p>\r\n<p class=\"import-Normal\">Other than an established genetic risk (e.g., BRCA gene), the primary risk factor for breast cancer is exposure to estrogen. For women living in modern, industrialized economies, this exposure now often comes from women\u2019s own ovaries rather than from external environmental sources (Stearns, Nesse, and Haig 2008). Women in cultures without contraception are pregnant or breastfeeding for much of their reproductive lives, resulting in 100 or so menstrual cycles per lifetime. In contrast, Western women typically experience 400 or more (Strassmann 1997). This is partly due to early puberty. From menarche to the birth of a woman\u2019s first child can be 14 years or longer in Western populations, after which breastfeeding, if undertaken at all, lasts for a few weeks or months. Oral contraceptives or other hormonal methods to control reproduction induce monthly periods. Age at menopause (the cessation of menstrual cycles) is 50\u201355 years old across human populations. For Western women, this translates into forty years of menstrual cycling. Each month, the body prepares for a pregnancy that never occurs, experiencing cell divisions that put women at risk for cancers of the breast, endometrium, ovaries, and uterus (Strassmann 1999). Obesity adds to the risk, as adipose (fat) tissues are the primary source of estrogen biosynthesis. Thus, weight gain during the postmenopausal stage means higher exposure to estrogen and a greater risk of cancer (Ali 2014).<\/p>\r\n<p class=\"import-Normal\">Women cannot return to our evolutionary past, and there are significant social and economic reasons for delaying pregnancy and having fewer children. These include achieving educational and career goals, greater earning power, a reduction in the gender pay gap, more enduring marriages, and a decrease in the number of women needing public assistance (Sonfield Et al. 2013). There are also cultural means by which we might reduce the risk of reproductive cancers. These include reformulating hormonal contraceptives with enough estrogen to maintain bone density but reducing the number of menstrual periods over the reproductive lifespan (Stearns, Nesse, &amp; Haig 2008). Reducing fat intake may also lower estrogen levels. High-fat diets contribute to breast tumor development, while high fibre diets are beneficial in decreasing intestinal resorption of estrogenic hormones. Exercise also appears protective. Studies of former college athletes demonstrate risks of breast, uterine, and ovarian cancers later in life, two to five times lower than those of nonathletes (Eaton Et al<em>.<\/em> 1994).<\/p>\r\n\r\n<\/div>\r\n<h2 class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Stress<\/h2>\r\n<p class=\"import-Normal\">Have you ever been \u201cstressed out\u201d in class? Say you\u2019re in a large lecture hall with a hundred other people, or even in a small class where you don\u2019t know anyone. You\u2019re not sure about something the professor just said and you would really like to ask about it, so you start to raise your hand. Does your heart begin to pound and your mouth become dry? Do you get so nervous that you choose to ask a classmate after lecture instead? If so, you are not alone. Fear of speaking in public is one of the most common social phobias (APA 2013). It has been estimated that 75% of all people experience some degree of anxiety or nervousness when it comes to public speaking (Hamilton 2011), and surveys have shown that most people fear public speaking more than they fear death (Croston 2012).<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">We have evolution to thank for this.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Humans, like other primates, are social animals. Being part of a group helped us to survive predation, get enough to eat, and successfully raise our young. When faced with standing up in front of a group, or even speaking up in class, we break into a sweat because we are afraid of rejection. Psychologist Glenn Croston (2012) writes, \u201cThe fear is so great because we are not merely afraid of being embarrassed or judged. We are afraid of being rejected from the social group, ostracized and left to defend ourselves all on our own. We fear ostracism still so much today it seems, fearing it more than death, because not so long ago getting kicked out of the group probably really was a death sentence.\u201d Hence, it is no surprise that public speaking triggers a stress response among much of humankind.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The human nervous system evolved in a context where quick responses to perceived threats presented an evolutionary advantage. The \u201cfight or flight\u201d response was honed during millions of years when threats more often took the form of an approaching lion than an approaching deadline. Our body\u2019s stress response, however, is triggered by a wide variety of stressors that produce the same general pattern of hormonal and physiological adjustments (Martini Et al. 2013). In today\u2019s world, the system is often stuck in the \u201con\u201d position due to the constant pressures of modern life, and this is a significant influence on health and disease.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">It is important to recognize that there are different types of stress and the time in life when adult coping mechanisms are formed is in childhood. In children, some stressors can be positive\u2014for example, stressors that are mild to moderate in magnitude, and accompanied by the support of a caring adult, which help children develop pathways by which stress is dealt with by the body throughout life. In a young child, a positive stress response might be going to the pediatrician to receive a vaccination and receiving encouragement and comfort from both parent and practitioner. A tolerable stress response is more serious, precipitated by something like a divorce or death of a relative. Again, buffered by positive support from surrounding adults, these types of stressors can be successfully managed by children. Toxic stress, however, \u201cresults from strong, frequent or prolonged activation of the stress response in the absence of the buffering protection of a supportive adult relationship\u201d (Shonkoff &amp; Garner 2012). Examples include child abuse or neglect, parental substance abuse, homelessness, and violence. In the absence of adequate psychological and physical support, the biological pathways of a child\u2019s physiological stress response are altered and lead to reduced abilities to cope with life\u2019s challenges as an adult.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The negative effects of sustained, elevated cortisol levels on health are well documented. These include higher levels of infectious disease and slowed growth in childhood (Flinn &amp; England 2003) and increased incidence of heart disease, obesity, and diabetes in adults (Worthman &amp; Kuzara 2005). Contrary to our evolutionary past, many causes of sustained stress in contemporary societies are psychosocial rather than physical threats. These can include an unhappy marriage or frustrations at work (Dimsdale 2008). Stressors can also be more subtle. For example, a review of research into the effects of stress on health indicated that experiencing racism was a significant stressor that was associated with alcohol consumption, psychological distress, overweight, abdominal obesity, and higher fasting-glucose levels among minority groups (Williams &amp; Mohammed 2013). Chronic, everyday racial discrimination is also associated with the hardening of coronary arteries, elevated blood pressure, giving birth to lower-birth-weight infants, cognitive impairment, poor sleep, and visceral fat, which is fat stored deep inside the belly, wrapped around the organs, including the liver and intestines. Visceral fat is a sign of [pb_glossary id=\"1942\"]<strong>m<\/strong><strong>etabolic syndrome<\/strong>[\/pb_glossary], increasing the risk of stroke, heart disease, and type 2 diabetes. These effects have been shown to increase morbidity and mortality among members of affected groups.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Epigenetics can also be a factor in how a person is able to deal with stressful situations. Maternal experiences of stress during pregnancy have the potential to permanently alter the physiology of mothers\u2019 offspring, especially the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis regulates metabolism, blood pressure, and the immune response, and these alterations can predispose prenatally stressed individuals to suffer metabolic, cardiovascular, and mental disorders in adulthood (Palma-Gudiel Et al. 2015). These experiences carry across generations, with children of Holocaust survivors who experienced PTSD demonstrating similar changes in neurochemistry in the absence of a sustained, traumatic event, as did infant offspring of mothers who developed PTSD during pregnancy after witnessing the traumatic events of 9\/11 (Yehuda &amp; LeDoux 2007).<\/p>\r\n\r\n<h2 class=\"import-Normal\" style=\"text-indent: 0pt\">Syndemics and the Ecological Model<\/h2>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">It is important to recognize that disease risk is not spread evenly within or between populations. Diseases combine and interact to create a <strong>[pb_glossary id=\"1943\"]syndemic[\/pb_glossary]<\/strong>, where the coexistence of two or more conditions exacerbates the effects of one or all conditions. A syndemic (versus a pandemic, for example) takes into account social, political, economic, and environmental factors that increase risk for the clustering of two or more diseases (Singer Et al. 2017). One of the first syndemics identified involved substance abuse, violence, and AIDS. In inner cities in the U.S., the health crisis around HIV\/AIDS was related to tuberculosis, sexually transmitted infections, hepatitis, cirrhosis, infant mortality, drug abuse, suicide, and homicide. These were connected to poverty, homelessness, unemployment, poor nutrition, lack of social support, and social and ethnic inequality (Singer Et al. 2017). Together, these factors and others, like health policy and unequal access to health care, form an <strong>[pb_glossary id=\"1944\"]ecological model[\/pb_glossary]<\/strong> of health and disease, one that moves beyond biology and medical intervention (Sallis Et al. 2008).<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The COVID-19 pandemic represents a syndemic in which systemic racism in the healthcare system, differential access to diagnosis and treatment, income, employment, housing, family structure, pre existing conditions, and public health policies combined to result in higher rates of infection and death for African Americans, Native Americans, Asians, and Hispanic populations in the United States (Figure 17.11).<\/p>\r\n\r\n<table class=\"grid\" style=\"border-collapse: collapse;width: 100%\" border=\"0\"><caption>Figure 17.11: Risk for COVID-19 infection, hospitalization, and death by race\/ethnicity. Race and ethnicity are risk markers for other underlying conditions that affect health, including socioeconomic status, access to health care, and exposure to the virus related to occupation, e.g., frontline, essential, and critical infrastructure workers. Credit: <a href=\"https:\/\/www.cdc.gov\/coronavirus\/2019-ncov\/covid-data\/investigations-discovery\/hospitalization-death-by-race-ethnicity.html\" target=\"_blank\">Risk for COVID-19 Infection, Hospitalization, and Death by Race\/Ethnicity<\/a> by the <a href=\"https:\/\/www.cdc.gov\/\" target=\"_blank\">Centers for Disease Control and Prevention<\/a> is in the <a href=\"https:\/\/en.wikipedia.org\/wiki\/Public_domain\" target=\"_blank\">public domain<\/a>.<\/caption>\r\n<thead>\r\n<tr class=\"shaded\">\r\n<td style=\"width: 130.367px\">Rate ratios compared to White, Non-Hispanic persons<\/td>\r\n<td style=\"width: 130.367px\">American Indian or Alaska Native, Non-Hispanic persons<\/td>\r\n<td style=\"width: 130.367px\">Asian, Non-Hispanic persons<\/td>\r\n<td style=\"width: 130.383px\">Black or African American, Non-Hispanic persons<\/td>\r\n<td style=\"width: 130.35px\">Hispanic or Latino persons<\/td>\r\n<\/tr>\r\n<\/thead>\r\n<tbody>\r\n<tr>\r\n<td style=\"width: 130.367px\">Cases<\/td>\r\n<td style=\"width: 130.367px\">1.6x<\/td>\r\n<td style=\"width: 130.367px\">.8x<\/td>\r\n<td style=\"width: 130.383px\">1.1x<\/td>\r\n<td style=\"width: 130.35px\">1.5x<\/td>\r\n<\/tr>\r\n<tr>\r\n<td style=\"width: 130.367px\">Hospitalization<\/td>\r\n<td style=\"width: 130.367px\">2.7x<\/td>\r\n<td style=\"width: 130.367px\">.8x<\/td>\r\n<td style=\"width: 130.383px\">2.3x<\/td>\r\n<td style=\"width: 130.35px\">2.0x<\/td>\r\n<\/tr>\r\n<tr>\r\n<td style=\"width: 130.367px\">Death<\/td>\r\n<td style=\"width: 130.367px\">2.1x<\/td>\r\n<td style=\"width: 130.367px\">.8x<\/td>\r\n<td style=\"width: 130.383px\">1.7x<\/td>\r\n<td style=\"width: 130.35px\">1.8x<\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\n<p class=\"import-Normal\">COVID-19 was the third leading cause of death in the U.S. in 2020 and 2021 (NIH 2022; Figure 17.12), but morbidity and mortality was not equally spread across the population. Working-class people and people of colour in the U.S. are more likely to live in poverty, in areas with high rates of crime and violence, and in close proximity to freeways and environmental threats like petrochemical plants and waste incinerators (Singer and Baer 2012). Many such neighbourhoods are also food \u201cdeserts\u201d without ready access to a healthy, affordable diet, made more challenging by residents not owning a car (Food Empowerment Project n.d.). Low-income people also often lack access to high-quality health care and delay or avoid preventive care and health screenings (Ross Et al. 2007). These factors contributed to higher rates of preexisting conditions, including obesity, diabetes, hypertension, asthma, heart disease, chronic obstructive pulmonary disease (COPD), and smoking behaviour, which then led to more complications and higher death rates from COVID (Ghosh Et al. 2021).<\/p>\r\n<p class=\"import-Normal\">Family structure also affected COVID exposure and severity. Many Americans live in multigenerational households, including 27% of Hispanics, 29% of Asians, 26% of African Americans, and 20% of Whites (Cohn &amp; Passel 2018). Not all multigenerational households are equal, however. Over twice as many African Americans as Whites are in multigenerational families in which at least one family member is unemployed, and over three times as many African Americans are in multigenerational families in which everyone is simultaneously unemployed (Park, Wiemers, and Seltzer 2019). Family members in multigenerational households were at a much higher risk of developing more severe forms of COVID due to decreased personal space and multiple exposures to the virus, as well as higher rates of diabetes, smoking, and residents living below the poverty line (Ghosh Et al. 2021). While aimed at reducing overall infection rates from COVID, public health measures such as mandatory lockdowns only exacerbated the situation in overcrowded and multigenerational housing, resulting in higher rates of infection and death in these communities.<\/p>\r\n\r\n<div style=\"margin: auto\">\r\n<table class=\" aligncenter\" style=\"width: 468pt;height: 195px\"><caption>Figure 17.12: Top five causes of death in the U.S. and worldwide since 2020. Credit: Top five causes of death in the U.S. and worldwide original to Explorations: An Open Invitation to Biological Anthropology (2nd ed.) by Joylin Namie is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0 License<\/a>. Based on data from Shiels Et al. 2022 and Traeger 2022.<\/caption>\r\n<thead>\r\n<tr class=\"shaded\" style=\"height: 30px\">\r\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 164.6px\">\r\n<p class=\"import-Normal\"><strong>United <\/strong><strong>States<\/strong><\/p>\r\n<\/td>\r\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 429.733px\">\r\n<p class=\"import-Normal\"><strong>Worldwide<\/strong><\/p>\r\n<\/td>\r\n<\/tr>\r\n<\/thead>\r\n<tbody>\r\n<tr class=\"Table2-R\" style=\"height: 0\">\r\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 164.6px\">\r\n<p class=\"import-Normal\">1. Heart disease<\/p>\r\n<\/td>\r\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 429.733px\">\r\n<p class=\"import-Normal\">1. Heart disease<\/p>\r\n<\/td>\r\n<\/tr>\r\n<tr class=\"Table2-R\" style=\"height: 0\">\r\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 164.6px\">\r\n<p class=\"import-Normal\">2. Cancer<\/p>\r\n<\/td>\r\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 429.733px\">\r\n<p class=\"import-Normal\">2. Stroke<\/p>\r\n<\/td>\r\n<\/tr>\r\n<tr class=\"Table2-R\" style=\"height: 0\">\r\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 164.6px\">\r\n<p class=\"import-Normal\">3. COVID-19<\/p>\r\n<\/td>\r\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 429.733px\">\r\n<p class=\"import-Normal\">3. COVID-19<\/p>\r\n<\/td>\r\n<\/tr>\r\n<tr class=\"Table2-R\" style=\"height: 0\">\r\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 164.6px\">\r\n<p class=\"import-Normal\">4. Accidents<\/p>\r\n<\/td>\r\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 429.733px\">\r\n<p class=\"import-Normal\">4. Chronic Obstructive Pulmonary Disease<\/p>\r\n<\/td>\r\n<\/tr>\r\n<tr class=\"Table2-R\" style=\"height: 0\">\r\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 164.6px\">\r\n<p class=\"import-Normal\">5. Stroke<\/p>\r\n<\/td>\r\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 429.733px\">\r\n<p class=\"import-Normal\">5. Lower respiratory infections<\/p>\r\n<\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td style=\"height: 15px;width: 165.467px\"><\/td>\r\n<td style=\"height: 15px;width: 430.6px\"><\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\n<\/div>\r\n<p class=\"import-Normal\">There is a long history of systemic racism and discrimination in the medical system in the United States (Washington 2006). African Americans have been subjected to medical testing and experimentation without their consent or knowledge since the time of slavery. They continue to routinely receive care of poorer quality than whites (Williams &amp; Wyatt 2015), less pain medication during treatment and hospitalization (Green Et al. 2003), and differential treatment during pregnancy and childbirth (Washington 2006). Many Americans, including 50% of White medical students and residents in one recent study (Hoffman Et al. 2016), hold at least one false belief about African Americans, including \u201cBlack people\u2019s skin is thicker than white people\u2019s skin,\u201d \u201cBlacks have stronger immune systems than whites,\u201d and \u201cBlacks\u2019 nerve endings are less sensitive than whites\u2019.\u201d Such beliefs affect health care for African Americans in medical emergencies and for chronic conditions.<\/p>\r\n<p class=\"import-Normal\">During the COVID-19 pandemic, patients with darker skin in the United States were negatively affected by the very medical device most commonly used to assess oxygen levels in their blood. The pulse oximeter, a small device that clips onto the tip of your index finger and measures blood oxygen levels, experienced increased use in home, clinical, and hospital settings during the COVID-19 pandemic. Decisions regarding treatment and hospital admission for patients infected with COVID were often based on pulse oximeter readings (Valbuena, Merchant, &amp; Hough 2022). The problem is the device overestimates oxygen saturation in patients with darker skin, an issue which has been recognized for over thirty years (Valbuena, Merchant, &amp; Hough 2022). It would be as if a standard thermometer reported lower body temperatures for patients of colour, making it seem as if they did not have a fever when they actually did. In the case of COVID-19, Asians, Hispanics, and African Americans experienced inaccurately high readings of their oxygen levels (with African Americans and darker-skinned Hispanics having the highest), resulting in delays in treatment, hospital admission, and access to medications to treat COVID and contributing to higher severity of illness and higher death rates among these populations in comparison to whites (Fawzi Et al. 2022).<\/p>\r\n<p class=\"import-Normal\">Employment was also a factor in unequal exposure to and death from COVID-19 (Raifman, Skinner, &amp; Sojourner 2022), with many low-income workers making the choice (which, realistically, may not be a choice at all) to expose themselves to COVID in order to earn the funds necessary to purchase food, housing, and other necessities. Many such workers were then forced to miss work due to COVID infection. With only 35% of low-wage workers (as opposed to 95% of high-wage workers) having paid sick leave, this left many families struggling financially. Three years into the pandemic, low-wage workers continue to have the least access to COVID vaccines and boosters. The U.S. also lacks federal workplace-safety regulations with regard to vaccine and masking mandates that other nations enforce in times of high transmission, and it does not provide high-quality masks to its essential workers. Many occupations deemed essential by the CDC during the height of the pandemic\u2014such as health care, emergency services, meat packing, agricultural work, teaching, and jobs in the hospitality sector\u2014experienced higher rates of morbidity and mortality from COVID. Many of these fields disproportionately employ people of colour (McKinsey &amp; Company 2021). Given this, future policies that address the pandemic at a structural level\u2014for example, providing monetary assistance to people who work in environments with a high risk of infection, such as cleaning, nursing, transportation, retail, restaurant work, and factory work, so that they can remain at home\u2014may function more effectively to prevent transmission and curb future outbreaks (Arnot Et al. 2020).<\/p>\r\n\r\n<h2 class=\"import-Normal\">Food for Thought<\/h2>\r\n<p class=\"import-Normal\">This chapter focused primarily on health conditions prevalent in contemporary, industrialized societies that are due, in part, to the mismatch between our evolved biology and modern environments. These are the built environment and the social environment, which together form the obesogenic environment in which unhealthy behaviours are encouraged. This chapter will close by examining each of these in a college context.<\/p>\r\n\r\n\r\n[caption id=\"\" align=\"alignleft\" width=\"275\"]<img src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image2-3.jpg\" alt=\"Four individuals in a park.\" width=\"275\" height=\"183\" \/> Figure 17.13: Students walking around a campus. Credit: <a href=\"https:\/\/www.maxpixel.net\/Row-Four-Man-Woman-People-Walking-Together-3755342\" target=\"_blank\">Row four man woman people walking together 3755342<\/a> by <a href=\"https:\/\/www.maxpixel.net\/\" target=\"_blank\">MaxPixel<\/a> has been designated to the <a href=\"https:\/\/creativecommons.org\/share-your-work\/public-domain\/cc0\/\" target=\"_blank\">public domain (CC0)<\/a>.[\/caption]\r\n\r\nConsider your campus from an evolutionary perspective. To what degree does the built environment lend itself to physical activity as part of daily life? Is your campus constructed in ways that promote driving at the expense of walking or biking? If driving is necessary, is parking available close to the buildings or do you need to walk a fair distance from the parking lot to your destination? Do the buildings have stairs or ramps or is it necessary to take the elevator? Is it possible to negotiate safely around campus on foot or by bike in all weather? After dark? How about the classrooms and computer labs? Do they have standing or treadmill desks? Does your class schedule encourage walking from building to building between classes, or are most courses in your major scheduled in the same location? Most college majors also lack a physical education requirement, leaving it up to students to incorporate exercise into already-challenging schedules (Figure 17.13).\r\n<p class=\"import-Normal\">Sociocultural factors that contribute to obesity include food advertising, ubiquitous fast-food and junk food options, and social pressure to consume, all of which are present on college campuses. Although nutrition on campuses has improved in recent years, many students find eating healthy in the dining halls and dorms challenging (Plotnikoff Et al. 2015), and students who live off campus fare even worse (Small Et al<em>.<\/em> 2013). There are also parties and other social events, a normal part of college life, that involve unhealthy food and encourage behaviours like alcohol consumption and smoking. Give some thought to the social atmosphere on your campus and the ways it may contribute to obesity. My own freshman orientation involved a succession of pizza parties, ice cream socials, and barbecues, followed by late-night runs to the nearest fast-food outlet. The purpose of these events was to encourage people to make friends and feel comfortable living away from home, but the foods served were unhealthy, and there was social pressure to join in and be part of the group. Such activities set students up for the \u201cfreshman fifteen\u201d and then some. They also reinforce the idea that being social involves eating (and sometimes drinking and\/or smoking).<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Sedentarism and inactivity are also built into the academics of college life. Digital technology is a significant contributor to obesity. Students use laptops and cell phones to take notes, complete their work outside of class, and access social media. There are also video games, virtual reality headsets, and streaming television and movies for entertainment. The built environment of college already necessitates that students sit in class for hours each day, then sit at computers to complete work outside of class. The social environment enabled by digital technology encourages sitting around for entertainment. It is telling that we call it \u201cbinge watching\u201d when we spend hours watching our favourite shows. Doing so often involves eating, as well as multiple exposures to food advertising embedded in the shows themselves. In these ways, college contributes to the development of obesity-causing behaviours that can have negative health ramifications long after college is over (Small Et al. 2013).<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">In the U.S., the greatest increase in obesity is among young adults aged 18\u201329 years, a significant percentage of whom are college students (Plotnikoff Et al. 2015). Analyses of college students\u2019 behaviour across semesters shows consumption of fruits and vegetables drops over time, as does the amount of physical activity, while consumption of sugar-sweetened beverages and fast-food goes up, leading to weight gain at nearly six times the rate of the general public (Small Et al. 2013). In response, many colleges and universities have instituted programs to encourage healthier eating and more physical activity among students (Plotnikoff Et al<em>.<\/em> 2015). It is important to emphasize that neither changes in diet or exercise are effective on their own.. A 2022 study of over 340,000 British participants demonstrated that physical activity and diet quality did not individually have an impact on cardiovascular disease or cancers (Ding Et al. 2022). That is, hitting the gym won\u2019t counteract the consequences of consuming high-calorie, fatty foods, and eating kale all day can\u2019t cancel out sedentary habits.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Just as no one fad diet is going to prove healthier than another, no one type of exercise is better than another. Anything that raises your heart rate and that you enjoy doing for at least an hour each day will work. Take advantage of opportunities to build exercise into everyday life. Take the stairs, park as far away from buildings as possible, ride a bike or walk instead of driving, and take walks between classes instead of sitting down and checking your phone. As far as diets go, eating a few less unhealthy calories each day, one less soda, no sugar in your coffee, or letting that last slice of pizza go to someone else, make a difference in the long run. Little changes add up to bigger ones. We cannot change our biology, but we can certainly change our habits.<\/p>\r\n\r\n<div class=\"textbox shaded\">\r\n<h2>Summary<\/h2>\r\n<p data-start=\"134\" data-end=\"760\">The health problems faced by modern humans can often be understood through the lens of evolution. As early <em>Homo sapiens<\/em> evolved in environments with a wide diversity of edible plants and animals, we developed complex nutritional requirements. However, with dramatic changes in our environments and daily lives, modern humans now encounter a variety of diet-related challenges. These include shifts in dentition and intestinal morphology, changes in food production and preparation, and altered patterns of physical activity. Together, these factors have contributed to changes in the leading causes of morbidity and mortality.<\/p>\r\n<p data-start=\"762\" data-end=\"1565\">These health consequences are often framed through the concept of epidemiological transitions, which are influenced by diet, physical activity, population density, and exposure to zoonotic diseases linked to agriculture. It is proposed that the first transition occurred when humans shifted from foraging to food production, leading to increased exposure to new diseases and dietary changes. The second transition followed the Industrial Revolution, when improvements in lifestyle and living conditions reduced infectious diseases but led to a rise in non-communicable diseases. The third and fourth transitions, still unfolding today, are marked by the spread of drug-resistant pathogens, the re-emergence of infectious diseases, and new health challenges driven by globalization, urbanization, and climate change.<\/p>\r\n<p data-start=\"1567\" data-end=\"1807\">Modern health issues such as obesity, cardiovascular disease, cancer, stress-related conditions, and syndemics illustrate the ongoing interaction between our evolved biology and the cultural and physical environments in which we live.<\/p>\r\n\r\n<h2 class=\"import-Normal\">Review Questions<\/h2>\r\n<ul>\r\n \t<li class=\"import-Normal\">Why do humans like foods that are \u201cbad\u201d for them? Describe the evolutionary underpinnings of our tastes for sugar, salt, and fat.<\/li>\r\n \t<li class=\"import-Normal\">How might understanding contemporary disease from an evolutionary perspective benefit medical practitioners in treating their patients?<\/li>\r\n \t<li class=\"import-Normal\">Several risk factors for conditions like heart disease, diabetes, and cancer are referred to as \u201clifestyle factors,\u201d implying these are behavioural choices people make that put them at risk. These include unhealthy eating, lack of physical activity, smoking, and alcohol consumption. To what degree is unhealthy behaviour structured by the physical and social environment? For example, how does being a college student influence your eating habits, physical activity patterns, smoking, and consumption of alcohol?<\/li>\r\n \t<li class=\"import-Normal\">Who benefits from the global obesity epidemic? Think about how the following industries and institutions might profit from it: The medical establishment? The fitness industry? The diet industry? Fashion? Pharmaceutical companies? Food manufacturers? Advertisers?<\/li>\r\n<\/ul>\r\n<\/div>\r\n<\/div>\r\n<h2 class=\"__UNKNOWN__\">Key Terms<\/h2>\r\n<div class=\"__UNKNOWN__\">\r\n<p class=\"import-Normal\"><strong>Body mass index (BMI)<\/strong>: A person\u2019s weight in kilograms divided by the square of their height in metres. This is the most widely used measure for identifying obesity. The formula using kilograms and metres (or centimetres) is: weight (kg) \/ [height (m)]<sup>2 <\/sup>. The formula using pounds and inches is: 703 x weight (lbs) \/ [height (in)]<sup>2 <\/sup>. Use of the BMI is controversial for several reasons, including that it does not take into account age, bone structure, muscle mass, fat distribution, or ethnic and racial differences in body type.<\/p>\r\n<p class=\"import-Normal\"><strong>Cancer<\/strong>: A collection of related diseases in which some of the body\u2019s cells begin to divide without stopping and spread into surrounding tissues.<\/p>\r\n<p class=\"import-Normal\"><strong>Cardiovascular disease (CVD)<\/strong>: A disease of the heart and blood vessels, often related to atherosclerosis. CVD is a condition in which a substance called plaque builds up in the walls of the arteries, the blood vessels that carry blood away from the heart, which compromises the flow of blood to the heart or brain.<\/p>\r\n<p class=\"import-Normal\"><strong>Central nervous system<\/strong>: The complex of nerve tissues stemming from the brain and spinal cord that controls the activities of the body.<\/p>\r\n<p class=\"import-Normal\"><strong>Circulatory (system)<\/strong>: The biological system that circulates blood around the body via the heart, arteries, and veins, delivering oxygen and nutrients to organs and cells and carrying waste products away.<\/p>\r\n<p class=\"import-Normal\"><strong>Diabetes mellitus<\/strong>: An endocrine disorder in which high glucose (blood sugar) levels occur over a prolonged period of time. Blood glucose is your body\u2019s main source of energy and comes from the food you eat. Insulin, a hormone made by the pancreas, helps glucose from food get into your cells to be used for energy. Sometimes your body does not make enough\u2014or any\u2014insulin (type 1 diabetes) or does not take up insulin well (type 2 diabetes). Glucose then stays in your blood and does not reach your cells.<\/p>\r\n<p class=\"import-Normal\"><strong>\u201cDouble burden\u201d<\/strong>: Refers to parts of the world in which there is a prevalence of chronic disease (e.g., cancer, heart disease) while, at the same time, there are also high rates of infectious disease due to poverty, malnutrition, poor sanitation, and lack of access to health care, often accompanied by high rates of maternal and child mortality.<\/p>\r\n<p class=\"import-Normal\"><strong>Ecological model<\/strong>: Ecological models of health and disease emphasize environmental and policy contexts of behaviour, while incorporating social and psychological influences, rather than focusing on individual behaviours. These models encompass multiple levels of influence and can lend themselves to more comprehensive health interventions.<\/p>\r\n<p class=\"import-Normal\"><strong>Emerging infectious diseases (EIDs)<\/strong>: Infections that have recently appeared within a population or those whose incidence or geographic range is rapidly increasing or threatens to increase in the near future. Examples include Covid-19, Ebola, Zika, SARS, and avian (bird) flu.<\/p>\r\n<p class=\"import-Normal\"><strong>Endocrine system<\/strong>: Those organs in the body whose primary function is the production of hormones.<\/p>\r\n<p class=\"import-Normal\"><strong>Epidemiological transition<\/strong>: A transformation in patterns of disease (morbidity) and death (mortality) among a population.<\/p>\r\n<p class=\"import-Normal\"><strong>Glycemic index (GI)<\/strong>: A system that ranks foods on a scale from 1 to 100 based on their effect on blood-sugar levels. Carbohydrates with a low GI value (55 or less) are more slowly digested and metabolized causing a lower, slower rise in blood glucose and insulin levels.<\/p>\r\n<p class=\"import-Normal\"><strong>Hypertension<\/strong>: High blood pressure. Blood pressure is the force exerted by the blood against the walls of the blood vessels. In a blood pressure reading, the top number (usually higher) refers to the systolic pressure, the amount of pressure in your arteries during the contraction of your heart muscle when your heart beats. The bottom number is the diastolic pressure when your heart muscle is resting between beats. Hypertension can lead to severe health complications and increases the risk of heart attack and stroke.<\/p>\r\n<p class=\"import-Normal\"><strong>Incidence<\/strong>: The rate at which new cases of a disease occur in a population over a given period of time.<\/p>\r\n<p class=\"import-Normal\"><strong>Insulin<\/strong>: A hormone produced in the pancreas that regulates the amount of glucose in the blood. Lack of insulin or the inability to absorb insulin causes diabetes.<\/p>\r\n<p class=\"import-Normal\"><strong>Metabolic syndrome<\/strong>: A cluster of conditions, including increased blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol levels that occur together, increasing the risk of heart disease, stroke, and diabetes. Lifestyle changes like losing weight, exercising regularly, and making dietary changes can help prevent or reverse metabolic syndrome.<\/p>\r\n<p class=\"import-Normal\"><strong>Menarche<\/strong>: The first occurrence of menstruation.<\/p>\r\n<p class=\"import-Normal\"><strong>Morbidity<\/strong>: The number of cases of disease per unit of population occurring over a unit of time.<\/p>\r\n<p class=\"import-Normal\"><strong>Mortality<\/strong>: The number of deaths attributable to a particular cause per unit of population over a unit of time.<\/p>\r\n<p class=\"import-Normal\"><strong>Noncommunicable diseases (NCDs)<\/strong>: Also known as chronic diseases, NCDs tend to be of long duration and are the result of a combination of genetic, physiological, environmental, and behaviour factors. The main types of NCDs are cardiovascular diseases (like heart attacks and stroke<strong>)<\/strong>, cancers, chronic respiratory diseases (such as chronic obstructive pulmonary disease and asthma), and diabetes.<\/p>\r\n<p class=\"import-Normal\"><strong>Obesity<\/strong>: A medical condition in which excess body fat has accumulated to the point that it has adverse effects on health. Although controversial due to its lack of ethnic and racial specificity, the most widely used measure for identifying obesity is the body mass index (BMI), a person\u2019s weight in kilograms divided by the square of their height in metres. A measure of 30 kg\/m<sup>2<\/sup> is considered obese and 25\u201329 kg\/m<sup>2<\/sup> is considered overweight. Distribution of body fat also matters. Fat in the abdominal region has a stronger association with type 2 diabetes and cardiovascular disease, meaning waist-to-hip ratio and waist circumference are also important indicators of obesity-related health risk.<\/p>\r\n<p class=\"import-Normal\"><strong>Obesogenic<\/strong>: Promoting excessive weight gain.<\/p>\r\n<p class=\"import-Normal\"><strong>Omnivorous<\/strong>: Able to eat and digest foods of both plant and animal origins.<\/p>\r\n<p class=\"import-Normal\"><strong>Osteoarthritis<\/strong>: Refers to the degeneration of joint cartilage and underlying bone, causing pain and stiffness. In the absence of previous injury, it is most common in modern populations from middle age onward.<\/p>\r\n<p class=\"import-Normal\"><strong>Prevalence<\/strong>: The proportion of individuals in a population who have a particular disease or condition at a given point in time.<\/p>\r\n<p class=\"import-Normal\"><strong>Sedentarism<\/strong>: A way of life characterized by much sitting and little physical activity.<\/p>\r\n<p class=\"import-Normal\"><strong>Sedentism<\/strong>: Living in groups settled permanently in one place.<\/p>\r\n<p class=\"import-Normal\"><strong>Stress response<\/strong>: A predictable response to any significant threat to homeostasis. The human stress response involves the <strong>Central Nervous System<\/strong> and the endocrine system acting together. Sudden and severe stress incites the \u201cflight or flight\u201d response from the autonomic nervous system in conjunction with hormones secreted by the adrenal and pituitary glands, increasing our heart rate and breathing and releasing glucose from the liver for quick energy.<\/p>\r\n<p class=\"import-Normal\"><strong>Stroke<\/strong>: A stroke occurs when a blood vessel leading to the brain is blocked or bursts, preventing that part of the brain from receiving blood and oxygen, leading to cell death.<\/p>\r\n<p class=\"import-Normal\"><strong>Syndemic<\/strong>: The aggregation (grouping together) of two or more diseases or health conditions in a population in which there is some level of harmful biological or behavioural interface that exacerbates the negative health effects of any or all of the diseases involved. Syndemics involve the adverse interaction of diseases of all types, including infections, chronic noncommunicable diseases, mental health problems, behavioural conditions, toxic exposure, and malnutrition.<\/p>\r\n<p class=\"import-Normal\"><strong>Tricep skinfold measurement<\/strong>: The triceps skinfold site is a common location used for the assessment of body fat using skinfold calipers. A section of skin on the posterior (back) surface of the arm that lays atop the tricep muscle is pinched between calipers. The resulting measurement is matched against a chart standardized for age and gender.<\/p>\r\n<p class=\"import-Normal\"><strong>\u201cTriple burden\u201d<\/strong>: A fourth epidemiological transition currently underway in which some parts of the globe are suffering from the \u201cdouble burden\u201d of infectious and chronic diseases combined with injuries and diseases related to intensifying globalization, urbanization, deforestation, and climate change.<\/p>\r\n<p class=\"import-Normal\"><strong>Vector-borne diseases<\/strong>: Human illnesses caused by parasites, viruses, and bacteria that are transmitted by mosquitoes, flies, ticks, mites, snails, and lice.<\/p>\r\n<p class=\"import-Normal\"><strong>Zoonoses<\/strong>: Diseases that can be transmitted from animals to humans.<\/p>\r\n\r\n<h2 class=\"import-Normal\">For Further Exploration<strong>\r\n<\/strong><\/h2>\r\nLents, Nathan H. 2018. <em>Human Errors: A Panorama of Our Glitches, from Pointless Bones to <\/em><em>Broken Genes<\/em>. Boston: Houghton Mifflin Harcourt.\r\n\r\nStearns, Stephen C., and Jacob C. Koella, eds. 2008. <em>Evolution in Health and Disease<\/em>. 2nd edition. United Kingdom: Oxford University Press.\r\n\r\nZuk, Marlene. 2013. <em>Paleofantasy: What Evolution Really Tells Us about Sex, Diet, and <\/em><em>How We Live<\/em>. New York: W. W. Norton &amp; Company.\r\n<h2 class=\"import-Normal\">References<\/h2>\r\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Abid, Zaynah, Amanda J. Cross, and Rashmi Sinha. 2014. \u201cMeat, Dairy, and Cancer.\u201d <em>The American Journal of Clinical Nutrition<\/em> 100 (S1): 386S\u2013393S.<\/p>\r\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Akil, Luma, and H. Anwar Ahmad. 2011. \u201cRelationships between Obesity and Cardiovascular Diseases in Four Southern States and Colorado.\u201d <em>Journal of Health Care for the Poor and Underserved<\/em> 22 (S4): 61\u201372.<\/p>\r\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Ali, Aus Tariq. 2014. \u201cReproductive Factors and the Risk of Endometrial Cancers.\u201d <em>International Journal of Gynecological Cancer<\/em> 24 (3): 384\u2013393.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">American Heart Association. 2018. \u201cHeart Disease and Stroke Statistics-2018 Update: A Report.\u201d <em>Circulation 137<\/em> (12). Accessed April 7, 2023. https:\/\/www.ahajournals.org\/doi\/10.1161\/cir.0000000000000558.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">American Psychiatric Association (APA). 2013. <em>Diagnostic and Statistical Manual of Mental Disorder<\/em>. 5th Edition: DSM-5. Washington, DC: APA.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Armelagos, George J. 1990. \u201cHealth and Disease in Prehistoric Populations in Transition.\u201d <em>Disease in Populations in Transition: Anthropological and Epidemiological Perspectives,<\/em> edited by George J. Armelagos and Alan C. Swedland, 127\u2013144. New York: Bergin &amp; Garvey.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Armelagos, George J., Peter J. Brown, and Bethany Turner. 2005. \u201cEvolutionary, Historical and Political Economic Perspectives on Health and Disease.\u201d <em>Social Science and Medicine 61<\/em> (4): 755-765.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0.495002746582031pt;margin-right: 0pt;text-indent: 0pt\">Arnot, Megan, Eva Brandl, O. L. K. Campbell, Yuan Chen, Mark Dyble, Emily H. Emmott, et al. 2020. <em>Evolution, Medicine, and Public Health<\/em> 2020 (1): 264\u2013278. https:\/\/doi.org\/10.1093\/emph\/eoaa038.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Asher, Claire. 2017. \u201cIllegal Bushmeat Trade Threatens Human Health and Great Apes.\u201d <em>Mongabay<\/em>, April 6. Accessed April 4, 2023. https:\/\/news.mongabay.com\/2017\/04\/illegal-bushmeat-trade-threatens-human-health-and-great-apes\/.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Baker, W. A., G. A. Hitman, K. Hawrami, M .I. McCarthy, A. Riikonen, E. Tuomilehto-Wolf, A. Nissinen, et al. 1994. \u201cApolipoprotein D Gene Polymorphism: A New Genetic Marker for Type 2 Diabetic Subjects in Nauru and South India.\u201d <em>Diabetic Medicine<\/em> 11 (10): 947\u2013952.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Baltic, Milan Z., and Marija Boskovic. 2015. \u201cWhen Man Met Meat: Meat in Human Nutrition from Ancient Times Till Today.\u201d <em>Procedia Food Science 5<\/em>: 6- 9.<\/p>\r\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Blue Cross Blue Shield Association (BCBSA). 2017. \u201cDiabetes and the Commercially Insured U.S. Population.\u201d <em>The Health of America Report<\/em>, August 1. 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New York: Bergin &amp; Garvey.<\/p>\r\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Bouchard, Claude. 2007. \u201cThe Biological Predisposition to Obesity: Beyond the Thrifty Genotype Scenario.\u201d <em>International Journal of Obesity<\/em> 31 (9): 1337\u20131339.<\/p>\r\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Buchman, Aron S., Lei Yu, Robert S. Wilson, Andrew Lim, Robert J. Dawe, Chris Gaiteri, Sue E. Leurgans, Julie A. Schneider, and David A. Bennett. 2019. \u201cPhysical Activity, Common Brain Pathologies, and Cognition in Community-Dwelling Older Adults.\u201d <em>Neurology<\/em> 98 (2). https:\/\/doi.org\/10.1212\/WNL.0000000000006954.<\/p>\r\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Centers for Disease Control and Prevention (CDC). N.d. \u201cGlobal Health - Pakistan.\u201d Accessed April 4, 2023. https:\/\/www.cdc.gov\/globalhealth\/countries\/pakistan\/default.htm.<\/p>\r\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Centers for Disease Control and Prevention (CDC). 2014. \u201cBreastfeeding Report Card: United States\/2014.\u201d Atlanta, GA: Centers for Disease Control and Prevention.<\/p>\r\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Centers for Disease Control and Prevention (CDC). 2020. <em>National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States<\/em>. Accessed April 7, 2023 from <a class=\"rId83\" href=\"https:\/\/diabetesresearch.org\/wp-content\/uploads\/2022\/05\/national-diabetes-statistics-report-2020.pdf\" target=\"_blank\">https:\/\/diabetesresearch.org\/wp-content\/uploads\/2022\/05\/national-diabetes-statistics-report-2020.pdf<\/a>.<\/p>\r\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Centers for Disease Control and Prevention (CDC). 2022. \u201cCDC Releases Updated Maps of America\u2019s High Levels of Inactivity.\u201d January 20. https:\/\/www.cdc.gov\/media\/releases\/2022\/p0120-inactivity-map.html.<\/p>\r\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Cer\u00f3n, Ella. 2017. \u201cHere\u2019s Every Oreo Flavor Ever Created.\u201d <em>TeenVogue.com<\/em>, June 19. 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Odes, Tanya Augustine, Paul Tafforeau and Lee Berger. 2016. \u201cOsteogenic Tumour in <em>Australopithecus sediba<\/em>: Earliest Hominin Evidence for Neoplastic Disease.\u201d South African Journal of Science 112 (7-8). Accessed April 7, 2023. <a class=\"rId85\" href=\"https:\/\/www.scielo.org.za\/scielo.php?script=sci_arttext&amp;pid=S0038-23532016000400013\" target=\"_blank\">https:\/\/www.scielo.org.za\/scielo.php?script=sci_arttext&amp;pid=S0038-23532016000400013. <\/a>https:\/\/dx.doi.org\/10.17159\/sajs.2016\/20150470<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Rankinen, Tuomo, Aamir Zuberi, Yvon C. Chagnon, S. John Weisnagel, George Argyropoulos, Brandon Walts, Louis P\u00e9russe, and Claude Bouchard. 2006. \u201cThe Human Obesity Gene Map: The 2005 Update.\u201d <em>Obesity<\/em> 14 (4): 529\u2013644.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Richards, M. P. 2002. \u201cA Brief Review of the Archaeological Evidence for Palaeolithic and Neolithic Subsistence.\u201d <em>European Journal of Clinical Nutrition<\/em> 56 (12): 1270\u20131278.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Ross, Joseph S., Susannah M. Bernheim, Elizabeth H. Bradley, Hsun-Mei Teng, and William T. Gallo. 2007. \u201cUse of Preventive Care by the Working Poor in the United States.\u201d <em>Preventive Medicine<\/em> 44 (3): 254\u2013259.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Sallis, James F., Neville Owen, and Edwin B. Fisher. 2008. \u201cChapter 20: Ecological Models of Health Behavior.\u201d In <em>Health Behavior and Health Education: Theory, Research, and Practice<\/em>, edited by Karen Glanz, Barbara K. Rimer, and K. Viswanath, 465\u2013485. 4th edition. San Francisco, CA: Jossey-Bass.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Sharp, Paul M., and Beatrice H. Hahn. 2011. \u201cOrigins of HIV and the AIDS Pandemic.\u201d <em>Cold Springs Harbor Perspectives in Medicine<\/em> 1 (1): a006841.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Sheerazi, Hadia A. 2022. \u201cThe Flood Seen from Space: Pakistan\u2019s Apocalyptic Crisis.\u201d <em>State of the Planet <\/em>(news from the Columbia Climate School), September 12. Accessed April 4, 2023. https:\/\/news.climate.columbia.edu\/2022\/09\/12\/the-flood-seen-from-space-pakistans-apocalyptic-crisis\/.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Shiels, Meredith S., Anika T. Haque, Amy Berrington de Gonz\u00e1lez, and Neal D. 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February 15. Accessed April 8, 2023. https:\/\/www.thinkglobalhealth.org\/article\/just-how-do-deaths-due-covid-19-stack#:~:text=Looking%20at%20official%20statistics%20alone,since%20the%20beginning%20of%202020.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Valbuena, Valeria S.M., Raina M. Merchant, and Catherine L. Hough. 2022. \u201cRacial and Ethnic Bias in Pulse Oximetry and Clinical Outcomes.\u201d Editorial. JAMA Internal Medicine 182 (7): 699\u2013700.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Ventola, C. Lee. 2015. \u201cThe Antibiotic Resistance Crisis: Part I: Causes and Threats.\u201d <em>Pharmacy &amp; Therapeutics<\/em> 40 (4): 277\u2013283.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Versini, Mathilde, Pierre-Yves Jeandel, Tomer Bashi, Giorgia Bizzaro, Miri Blank, and Yahuda Shoenfeld. 2015. \u201cUnraveling the Hygiene Hypothesis of Helminthes and Autoimmunity: Origins, Pathophysiology, and Clinical Applications.\u201d BMC Medicine, 13: 81. https:\/\/doi.org\/10.1186\/s12916-015-0306-7.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Vucenik, Ivana, and Joseph P. Stains. 2012. \u201cObesity and Cancer Risk: Evidence, Mechanisms, and Recommendations.\u201d Special issue, \u201cNutrition and Physical Activity in Aging, Obesity, and Cancer,\u201d <em>Annals of the New York Academy of Sciences<\/em> 1271 (1): 37\u201343.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Walker, Polly, Pamela Rhubart-Berg, Shawn McKenzie, Kristin Kelling, and Robert S. Lawrence. 2005. \u201cPublic Health Implications of Meat Production and Consumption.\u201d <em>Public Health Nutrition<\/em> 8 (4): 348\u2013356.<\/p>\r\n<p class=\"import-Normal\">Washington, Harriet A. 2006. <em>Medical Apartheid: The Dark History of Medical Experimentation on Black Americans from Colonial Times to the Present.<\/em> New York: Anchor Books.<\/p>\r\n<p class=\"import-Normal\">Williams, David R., and Selina A. 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Levy, Lorena Malpica Serrano, Alexander Crits-Christoph, Jonathan E. Pekar, Stephan A. Goldstein, Angela L. Rassmussen, et al. July 26, 2022. \u201cThe Huanan Seafood Wholesale Market in Wuhan was the Early Epicenter of the COVID-19 Pandemic.\u201d <em>SCIENCE <\/em>26 (377): 951\u2013959. <a class=\"rId88\" href=\"https:\/\/doi.org\/10.1126\/science.abp8715\" target=\"_blank\">https:\/\/doi.org\/10.1126\/science.abp8715<\/a>.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Worthman, Carol M., and Jennifer Kuzara. 2005. \u201cLife History and the Early Origins of Health Differentials.\u201d <em>American Journal of Human Biology<\/em> 17 (1): 95\u2013112.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Wrangham, Richard. 2009. <em>Catching Fire: How Cooking Made Us Human<\/em>. New York: Basic Books.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Yehuda, Rachel, and Joseph LeDoux. 2007. \u201cResponse Variation Following Trauma: A Translational Neuroscience Approach to Understanding PTSD.\u201d <em>Neuron<\/em> 56 (1): 19\u201332.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Zuckerman, Molly K., and George J. Armelagos. 2014. \u201cThe Hygiene Hypothesis and the Second Epidemiologic Transition.\u201d In <em>Modern Environments and Human Health: Revisiting the Second Epidemiologic Transition<\/em>, edited by Molly K. Zuckerman, 301\u2013320. Hoboken, NJ: Wiley-Blackwell.<\/p>\r\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Zuckerman, Molly Kathleen, Kristin Nicole Harper, Ronald Barrett, and George John Armelagos. 2014. \u201cThe Evolution of Disease: Anthropological Perspectives on Epidemiologic Transitions.\u201d Special issue, \u201cEpidemiological Transitions: Beyond Omran\u2019s Theory,\u201d <em>Global Health Action<\/em> 7 (1): 23303. https:\/\/doi.org\/10.3402\/gha.v7.23303.<\/p>\r\n\r\n<\/div>\r\n<\/div>","rendered":"<div class=\"__UNKNOWN__\">\n<div class=\"textbox\">\n<p>Learn more about <a href=\"https:\/\/opentextbooks.concordia.ca\/explorations3\/back-matter\/about-the-authors\/\">authors and editors<\/a>,<a href=\"https:\/\/opentextbooks.concordia.ca\/explorations3\/back-matter\/student-contributors\/\"> Hess&#8217; student contributions<\/a>, and <a href=\"https:\/\/opentextbooks.concordia.ca\/explorations3\/back-matter\/versioning-history\/\">versioning history<\/a>.<\/p>\n<\/div>\n<div class=\"textbox textbox--learning-objectives\">\n<header class=\"textbox__header\">\n<h2 class=\"textbox__title\">Learning Objectives<\/h2>\n<\/header>\n<div class=\"textbox__content\">\n<ul>\n<li>Describe the major transitions in patterns of disease that have occurred throughout human evolution.<\/li>\n<li>Describe what is meant by a \u201cmismatch\u201d between our evolved biology and contemporary lifestyles and how this is reflected in modern disease patterns.<\/li>\n<li>Explain how the human stress response can positively and negatively have an impact on health.<\/li>\n<li>Explain what a \u201csyndemic\u201d is and why the COVID-19 pandemic represents one.<\/li>\n<li>Describe the ways institutionalized racism and bias in the medical field contributed to different rates of exposure, differential treatment, morbidity, and mortality from COVID-19 for different ethnic groups in the United States.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<p>When was the last time you needed to do research for an upcoming paper? I bet you started by looking for information online. How did you go about your search? Which websites looked promising? Which ones did not entice you to click past the home page? Once you found one you thought might be useful, how much time did you spend searching for information? At what point did you decide to leave that site and move on? I would wager money that you never once thought your behaviour had anything to do with human evolution, but it does.<\/p>\n<p class=\"import-Normal\">Although we may not often stop to think about it, our evolutionary past is reflected in many aspects of modern life. The ways we \u201cforage\u201d for information on the internet mimics the ways we once foraged for food during our several-million-year history as hunter-gatherers (Chin Et al. 2015). Humans are visual hunters (Lieberman 2006). We practice optimal foraging strategy, meaning we make decisions based on energy return for investment (McElroy &amp; Townsend 2009). When we search for information online, we locate a \u201cpatch,\u201d in this case a website or research article, then quickly scan the contents to discern how much of it is useful to us. Like our hominin ancestors, we spend more time in \u201cpatches\u201d with abundant resources and abandon sites quickly once we have exhausted the available goods. As with internet searches, our evolutionary past is also reflected in the kinds of landscapes we find appealing, the foods that taste good to us, why we break a sweat at the gym, and why we have to go to the gym at all (Bogin 1991; Dutton 2009; Lieberman 2015). Many of the health problems facing humans in the 21st century also have their beginnings in the millions of years we roamed the earth as foragers.<\/p>\n<h2 class=\"import-Normal\">Preagricultural Humans<\/h2>\n<h3 class=\"import-Normal\"><strong>Diet<\/strong><\/h3>\n<p class=\"import-Normal\">Humans may be the species with the longest list of nutritional requirements (Bogin 1991). This is due to the fact that we evolved in environments where there was a high diversity of edible species but low densities of any given species. <em>Homo sapiens sapiens<\/em> require 45\u201350 essential nutrients for growth, maintenance, and repair of cells and tissues. These include protein, carbohydrates, fats, vitamins, minerals, and water. As a species, we are (or were) physically active with high metabolic demands. We are also <strong>omnivorous<\/strong> and evolved to choose foods that are dense in essential nutrients. One of the ways we identified high-calorie resources in our evolutionary past was through taste, and it is no accident that humans find sweet, salty, fatty foods appealing.<\/p>\n<p class=\"import-Normal\">The human predisposition toward sugar, salt, and fat is innate (Farb &amp; Armelagos 1980). Receptors for sweetness are found in every one of our mouth\u2019s 10,000 taste buds (Moss 2013). Preference for sweet makes sense in an ancestral environment where sweetness signaled high-value resources like ripe fruits. Likewise, \u201cthe long evolutionary path from sea-dwelling creatures to modern humans has given us salty body fluids, the exact salinity of which must be maintained\u201d (Farb &amp; Armelagos 1980), drawing us to salty-tasting things. Cravings for fat are also inborn, with some archaeological evidence suggesting that hominins collected animal bones for their fatty marrow, which contains two essential fatty acids necessary for brain development (Richards 2002), rather than for any meat remaining on the surface (Bogin 1991).<\/p>\n<p class=\"import-Normal\">Bioarchaeological studies indicate Paleolithic peoples ate a wider variety of foods than many people eat today (Armelagos Et al. 2005; Bogin 1991; Larsen 2014; Marciniak &amp; Perry 2017). Foragers took in more protein, less fat, much more fibre, and far less sodium than modern humans typically do (Eaton, Konner, &amp; Shostak 1988). Changes in tooth and intestinal morphology illustrate that animal products were an important part of human diets from the time of <em>Homo erectus<\/em> onward (Baltic &amp; Boskovic 2015; Richards 2002; Wrangham 2009). Once cooking became established, it opened up a wider variety of both plant and animal resources to humans. However, the protein, carbohydrates, and fats preagricultural peoples ate were much different from those we eat today. Wild game lacked the antibiotics, growth hormones, and high levels of cholesterol and saturated fat associated with industrialized meat production today (Walker Et al. 2005). Wild game was also protein dense, providing only 50% of energy as fat (Lucock Et al. 2014). The ways meat is prepared and eaten today also have implications for disease.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Meats cooked well done over high heat and\/or over an open flame, including hamburgers and barbecued meats, are highly carcinogenic due to compounds formed during the cooking process (Trafialek &amp; Kolanowski 2014). Processed meats that have been preserved by smoking, curing, salting, or by adding chemical preservatives such as sodium nitrite (e.g., ham, bacon, pastrami, salami, and beef jerky) have been linked to cancers of the colon, lung, and prostate (Abid, Cross, &amp; Sinha 2014; Figure 17.1). Nitrites\/nitrates have additionally been linked to cancers of the ovaries, stomach, esophagus, bladder, pancreas, and thyroid (Abid, Cross &amp; Sinha 2014). In addition, studies analyzing the diets of 103,000 Americans for up to 16 years indicate that those who ate grilled, broiled, or roasted meats more than 15 times per month were 17% more likely to develop high blood pressure than those who ate meat fewer than four times per month, and participants who preferred their meats well done were 15% more likely to suffer from <strong>hypertension<\/strong> (high blood pressure) than those who ate their meats rare (Liu 2018). A previous study of the same cohort indicated \u201cindependent of consumption amount, open-flame and\/or high-temperature cooking for both red meat and chicken is associated with an increased risk of type 2 diabetes among adults who consume animal flesh regularly\u201d (Liu Et al. 2018). Although meat has been argued to be crucial to cognitive and physical development among hominins (Wrangham 2009), there has been an evolutionary trade-off between the ability to preserve protein through cooking and the health risks of cooked meat and chemical preservatives.<\/p>\n<figure style=\"width: 343px\" class=\"wp-caption alignleft\"><img loading=\"lazy\" decoding=\"async\" class=\"\" src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/06\/image1-6.png\" alt=\"Consecutive circles outline categories of cancer risk with images of processed meats and red meat.\" width=\"343\" height=\"424\" \/><figcaption class=\"wp-caption-text\">Figure 17.1: Positive associations have been observed between meat consumption and some types of cancer. The International Agency for Research on Cancer (2018) categorized four groupings of cancer risk. The first group is labeled &#8220;causes cancer&#8221;, and the second group &#8220;probably causes cancer&#8221;. Group 1 includes processed meats such as bacon, salami and hot dogs. Group 2A includes red meat such as beef, pork and lamb. Credit: <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/chapter\/__unknown__-11\/\">Carcinogenic Meats (Figure 16.1)<\/a> original to <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/\" target=\"_blank\">Explorations: An Open Invitation to Biological Anthropology<\/a> by Katie Nelson is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0 License<\/a>. [Includes <a href=\"https:\/\/pngimg.com\/download\/10217\" target=\"_blank\">Hot dog PNG image<\/a> by unknown, <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0<\/a>; <a href=\"https:\/\/www.publicdomainpictures.net\/en\/view-image.php?image=109418&amp;picture=rasher-of-bacon\" target=\"_blank\">Rasher of Bacon<\/a> by unknown, <a href=\"https:\/\/creativecommons.org\/publicdomain\/zero\/1.0\/\" target=\"_blank\">public domain (CC0)<\/a>; <a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Salami_aka.jpg\" target=\"_blank\">Salami aka<\/a> by Andr\u00e9 Karwath <a href=\"https:\/\/commons.wikimedia.org\/wiki\/User:Aka\" target=\"_blank\">Aka<\/a>, <a href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/2.5\/legalcode\" target=\"_blank\">CC BY-SA 2.5<\/a>; <a href=\"https:\/\/pngimg.com\/download\/2127\" target=\"_blank\">Cow PNG image<\/a> by unknown, <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0<\/a>; <a href=\"https:\/\/pngimg.com\/download\/2184\" target=\"_blank\">sheep PNG image<\/a> by unknown, <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0<\/a>; <a href=\"https:\/\/www.publicdomainpictures.net\/en\/view-image.php?image=55516&amp;picture=pig-on-white-background\" target=\"_blank\">Pig on white background<\/a> by unknown, <a href=\"https:\/\/creativecommons.org\/publicdomain\/zero\/1.0\/\" target=\"_blank\">public domain (CC0)<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Although carbohydrates represent half of the diet on average for both ancient foragers and modern humans, the types of carbohydrates consumed are very different. Ancient foragers ate fresh fruits, vegetables, grasses, legumes, and tubers, rather than the processed carbohydrates common in industrialized economies (Moss 2013). Their diets also lacked the refined white sugar and corn syrup found in many modern foods that contribute to the development of diabetes (Pontzer Et al. 2012).<\/p>\n<h3 class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\"><strong>Physical Activity Patterns<\/strong><\/h3>\n<p class=\"import-Normal\">How do we know how active our ancestors were? Hominin morphology and physiology provide us with clues. Adaptations to heat discussed in Chapter 10 evolved in response to the need for physical exertion in the heat of the day in equatorial Africa. Human adaptations for preventing hyperthermia (overheating) suggest an evolutionary history of regular, strenuous physical activity. Research with modern foraging populations also offers clues to ancient activity patterns. Although subject to sampling biases and marginal environments (Marlowe 2005), modern foragers provide the only direct observations of human behaviour in the absence of agriculture (Lee 2013). From such studies, we know foragers cover greater distances in single-day foraging bouts than other living primates, and these treks require high levels of cardiovascular endurance (Raichlen &amp; Alexander 2014). Recent research with the Hadza in Tanzania indicates they walk up to 11 kilometres (6.8 miles) daily while hunting and gathering (Pontzer Et al. 2012), engaging in moderate-to-vigorous physical activity for over two hours each day\u2014meeting the U.S. government\u2019s weekly requirements for physical activity in just two days (Raichlen Et al. 2016; Figure 17.2). The fact that humans were physically active in our evolutionary past is also supported by the fact that regular physical exercise has been shown to be protective against a variety of health conditions found in modern humans, including <strong>cardiovascular disease<\/strong> (Raichlen &amp; Alexander 2014) and Alzheimer\u2019s dementia (Mandsager, Harb, &amp; Cremer 2018), even in the presence of brain pathologies indicative of cognitive decline (Buchman Et al. 2019).<\/p>\n<p>&nbsp;<\/p>\n<figure style=\"width: 624px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image10-7.png\" alt=\"Two hunters with dogs and bows walk in a savannah.\" width=\"624\" height=\"417\" \/><figcaption class=\"wp-caption-text\">Figure 17.2: Hadza foragers hunting on foot. Credit: <a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Hadazbe_returning_from_hunt.jpg\" target=\"_blank\">Hadazbe returning from hunt<\/a> by <a href=\"https:\/\/www.flickr.com\/photos\/7177420@N03\" target=\"_blank\">Andreas Lederer<\/a> has been modified (cropped) and is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by\/2.0\/legalcode\" target=\"_blank\">CC BY 2.0 License<\/a>.<\/figcaption><\/figure>\n<h3 class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\"><strong>Infectious Disease<\/strong><\/h3>\n<p class=\"import-Normal\">Population size and density remained low throughout the Paleolithic, by some estimates only 0.4 inhabitants per square kilometre (McClellan &amp; Dorn 2006). This limited <strong>morbidity<\/strong> and <strong><a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_1699_1907\">mortality<\/a> <\/strong>from infectious diseases, which sometimes require large populations to sustain epidemics. Our earliest ancestors had primarily two types of infections with which to contend (Armelagos 1990). The first were organisms that adapted to our prehominin ancestors and have been problems ever since. Examples include head lice, pinworms, and yaws. A second set of diseases were <strong>zoonoses<\/strong>, diseases that originate in animals and mutate into a form infectious to humans. One example is the Human Immunodeficiency Virus (HIV) that originated in nonhuman primates and was likely passed to humans through the butchering of hunted primates for food (Sharp &amp; Hahn 2011). Zoonoses that could have infected ancient hunter-gatherers include tetanus and <strong>vector-borne diseases<\/strong> transmitted by flies, mosquitoes, fleas, midges, ticks, and the like. Many of these diseases are slow acting, chronic, or latent, meaning they can last for weeks, months, or even decades, causing low levels of sickness and allowing victims to infect others over long periods of time. Survival or cure does not result in lasting immunity, with survivors returning to the pool of potential victims. Such diseases often survive in animal reservoirs, reinfecting humans again and again (Wolfe Et al. 2012). A study of bloodsucking insects preserved in samples of amber dating from 15 to 100 million years ago indicates that they carried microorganisms that today cause diseases such as river blindness, typhus, Lyme disease, and malaria (Poinar 2018). Such diseases may have been infecting humans throughout our history and may have had significant impacts on small foraging communities because they more often infected adults, who provided the food supply (Armelagos Et al. 2005).<\/p>\n<h3 class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\"><strong>Health<\/strong><\/h3>\n<p class=\"import-Normal\">Given their diets, levels of physical activity, and low population densities, nomadic preagricultural humans were likely in better health than many modern populations. This assertion is supported by comparative research conducted with modern foraging and industrialized populations. Measures of health taken from 20th-century foraging populations demonstrate excellent aerobic capacity, as measured by oxygen uptake during exertion, and low body-fat percentages, with <strong>triceps skinfold measurements<\/strong> half those of white Canadians and Americans. Serum cholesterol levels were also low, and markers for diabetes, hypertension, and cardiovascular disease were missing among them (Eaton, Konner, &amp; Shostak 1988; Raichlen Et al<em>. <\/em>2016).<\/p>\n<h2 class=\"import-Normal\">Health Consequences of the Transition to Agriculture and Animal Domestication<\/h2>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The shift from foraging to food production occurred relatively recently in our evolutionary history (Larsen 2014), and there are indications our biology has not yet caught up (Pritchard 2010). Beginning around 12,000 BCE in several parts of the globe, humans began to move toward a diet based on domesticated plants and animals (Armelagos Et al. 2005). This involved manipulating the natural landscape to facilitate intensive food production, including the clearing of forest and construction of wells, irrigation canals, and ditches, exposing humans to water-borne illnesses and parasites and attracting mosquitos and other vectors of disease to human settlements. The heavy, repetitive physical labour of early agricultural production resulted in negative impacts on articular joints, including <strong>osteoarthritis<\/strong> (Larsen 2014). At the same time, nutritional diversity became restricted, focused on major cereal crops that continue to dominate agricultural production today, including corn, wheat, and rice (Jain 2012). This represented a major shift in diet from a wide variety of plant and animal foods to dependence on starchy carbohydrates, leading to increases in dental caries (cavities), reductions in stature and growth rates, and nutritional deficiencies (Larsen 2014). Domesticated animals added new foods to the human diet, including meat that was higher in fat and cholesterol than wild game as well as dairy products (Lucock Et al. 2014). Agriculture provided the means to produce a storable surplus for the first time in human history, leading to the beginnings of economic inequality (see Chapter 13). Social hierarchies led to the unequal distribution of resources, concentrating infectious disease among the poor and malnourished (Zuckerman Et al. 2014), a situation that continues to plague humanity today (Marmot 2005).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\"><strong>Sedentism<\/strong> and a rise in population density accompanied the move to agriculture, increasing the risk of infectious disease. Agriculture often provided enough calories, if not enough nutrition, to increase fertility. Although diets were worse and people unhealthier, populations continued to grow, even in the midst of high levels of child and maternal mortality and short life expectancies (Omran 2005). Hygiene became an issue as large settlements increased the problem of removing human waste and providing uncontaminated water (Armelagos Et al. 2005). Domesticated animals provided reservoirs of zoonotic pathogens, which affected farmers more than foragers, as farmers were in closer proximity to their animals on a daily basis (Marciniak &amp; Perry 2017). Many of these diseases became major killers of humankind, including influenza, tuberculosis, malaria, plague, syphilis, and smallpox, functioning as selective pressures in and of themselves (Cooling 2015). As these diseases encountered large human populations, they caused major epidemics that traveled along newly established routes for trade, warfare, and colonization.<\/p>\n<h2 class=\"import-Normal\">Epidemiological Transitions<\/h2>\n<p class=\"import-Normal\">Changes in diet and physical-activity patterns, population densities, and exposure to zoonoses associated with agriculture resulted in an epidemiological transition, a shift in the causes of morbidity (sickness) and mortality (death) among humankind (Omran 2005). The first epidemiological transition from foraging to food production resulted in increases in dental caries (see Chapter 13), nutritional deficiencies, infectious disease, and skeletal conditions like osteoarthritis, as well as decreases in growth and height (Larsen 2014). A second epidemiological transition occurred following the Industrial Revolution in Western Europe and the United States when improved standards of living, hygiene, and nutrition minimized the effects of infectious disease, after which people began to experience higher rates of <strong>noncommunicable diseases<\/strong>, such as <strong>cancer<\/strong>, heart disease, and diabetes due to the changes in lifestyle, diet, and activity levels that are the subject of this chapter (Omran 2005). With the addition of immunizations and other public health initiatives, modified forms of this transition remain ongoing in many low- and middle-income countries (Zuckerman Et al. 2014), with several now facing a <strong>\u201cdouble burden\u201d <\/strong>of disease, with poor, often rural, populations struggling with infectious diseases due to malnutrition, lack of sanitation, and access to health care, while more affluent citizens are victims of chronic illnesses. A third epidemiological transition is now underway as infectious diseases, including new, re-emergent, and multidrug-resistant diseases, have once again become major health concerns (Harper &amp; Armelagos 2010; Zuckerman Et al. 2014). These include COVID-19, Ebola, HIV\/AIDS, tuberculosis, malaria, dengue, Lyme disease, and West Nile virus\u2014all zoonoses that initially spread to humans through contact with animals.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Patterns of morbidity and mortality continue to shift across the globe. As with the first epidemiological transition resulting from the adoption of large-scale agriculture, such shifts can be the direct, if unintended, result of human interactions with the environment. For example, there has been a rise in chronic inflammatory diseases (CIDs) in developed countries (Versini Et al<em>.<\/em> 2015). This includes increased rates of allergic conditions like asthma and autoimmune diseases like rheumatoid arthritis, multiple sclerosis, Crohn\u2019s disease, and inflammatory bowel disease. This has coincided with the decrease in infectious disease associated with the second epidemiological transition, and the two are related. The \u201chygiene hypothesis\u201d postulates the rise in CIDs is a result of limited exposure to nonlethal environmental pathogens in utero and early childhood (Zuckerman &amp; Armelagos 2014). Modern human societies have become so sanitized that we are no longer exposed to microorganisms that stimulate the development of a healthy immune system (Versini Et al. 2015). \u201cIn effect, the lifestyle changes\u2014sanitary improvements, pasteurization, use of antibiotics, and improved hygiene\u2014that contributed to the second transition may have produced a substantial trade-off, with developed nations exchanging a high burden of infectious disease for a higher burden of CIDs\u201d (Zuckerman Et al. 2014).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The third epidemiological transition, the re-emergence of infectious disease, reflects the continuing relationship between humans, animals, and pathogens. Over 60% of <strong>e<\/strong><strong>merging infectious diseases (EIDs)<\/strong> since 1940 have been of zoonotic origin, with over 70% stemming from human contact with wildlife (Jones Et al. 2008), including COVID-19. The crossover of COVID to humans is believed to have involved transmission from bats to an intermediate species then to humans, with infected humans then passing it to other humans in a wet market in Wuhan, China in late 2019 (Worobey Et al. 2022). Two COVID variants, representing two distinct crossover events from animals to humans, were circulating in the market by February 2020. Similarly, the global bushmeat trade currently devastating Africa\u2019s wildlife is a continuing source of Ebola infection (Asher 2017), as well as the original source of HIV and viruses related to leukaemia and lymphoma among humans (Zuckerman Et al. 2014). New strains of avian (bird) flu, some with mortality rates as high as 60% among humans (WHO n.d.), are transmitted to humans through poultry production and contact with wild birds (Davis 2005). Lastly, the use of antibiotics in commercial meat production is directly related to the rise of drug-resistant strains of previously controlled infectious diseases. An estimated 80% of antibiotics in the U.S. are used to promote growth and prevent infection in livestock, and drug-resistant bacteria from these animals are transmitted to humans through meat consumption (Ventola 2015).<\/p>\n<figure style=\"width: 299px\" class=\"wp-caption alignleft\"><img loading=\"lazy\" decoding=\"async\" class=\"\" src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image13-7.png\" alt=\"Aerial photograph of a flooded city.\" width=\"299\" height=\"399\" \/><figcaption class=\"wp-caption-text\">Figure 17.3: Flooding in Sindh, Pakistan, in 2022. Credit: <a href=\"https:\/\/www.flickr.com\/photos\/193804179@N08\/52331043544\/\" target=\"_blank\">Flood in Pakistan<\/a> by <a href=\"https:\/\/www.flickr.com\/photos\/193804179@N08\/\" target=\"_blank\">Ali Hyder Junejo<\/a> is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by\/2.0\/\" target=\"_blank\">CC BY 2.0 License<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">A fourth epidemiological transition is currently underway in which some parts of the globe are suffering from a <strong>\u201ctriple burden\u201d<\/strong> of infectious and chronic diseases combined with injuries and diseases related to intensifying globalization, urbanization, deforestation, and climate change (Karn &amp; Sharma 2021). Massive flooding in Pakistan in 2022 (Figure 17.3) will serve to illustrate the concept. Following a severe heat wave in June 2022, Pakistan experienced extremely heavy seasonal monsoon rains, in some provinces 700% above normal. Combined with water flow from melting glaciers, this caused the worst flooding in the country\u2019s history, putting one third of the nation under water (Sheerazi 2022). The heat wave, glacial melt, and extreme rainfall were all attributable to global climate change, inflicting destruction and disease on Pakistan, which produces less than 1% of total global carbon emissions (Government of Pakistan 2021).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">As a direct result of the flooding, infrastructure, including roads, homes, and bridges, was destroyed, and 1,700 people died, nearly 13,000 were injured, and over 33 million were displaced. In addition to their initial injuries and trauma, displaced people lacked food, health care, safe water, and basic sanitation, leading to starvation and exposure to infectious diseases like malaria and dengue fever, as well as skin conditions like scabies, caused by mites. Pakistan also has a poverty rate of 30\u201340%, contributing to already-high rates of HIV, tuberculosis, and hepatitis. At the same time, the leading causes of death are heart disease, cancer, lower respiratory diseases, and stroke (CDC n.d), all chronic conditions.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">These examples illustrate continuing interaction between humans, our evolved biology, and the physical and cultural environments in which we live. The remainder of this chapter will focus on selected diseases and the social, cultural, and environmental factors that contribute to their <strong>prevalence<\/strong> in modern, industrialized economies. We begin with the health condition that affects all of the others\u2014<strong>obesity<\/strong>.<\/p>\n<h2 class=\"import-Normal\">Obesity<\/h2>\n<p class=\"import-Normal\">According to the World Health Organization (2017), 1.9 billion of the world\u2019s people are overweight and 650 million of these are obese. In the United States, 70% of Americans are overweight, and 40% of these meet the criteria for obesity. For the first time in human history, most of the world&#8217;s population lives in countries where overweight and obesity kill more people than hunger (Figure 17.4). Improvements in public health and food production have allowed a greater number of people to live past childhood and to have enough to eat. This does not include everyone. Many people still struggle with poverty, hunger, and disease, even in the wealthiest of nations, including the United States. On a global scale, however, many people not only have enough food to survive but also to gain weight\u2014enough extra weight to cause health problems.<\/p>\n<p><img decoding=\"async\" src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image4-5.png\" alt=\"&quot;Bar\" \/><\/p>\n<p class=\"import-Normal\">Although studies show differences in daily energy expenditure between foraging and farming populations compared with industrialized peoples, the major contributor to obesity in Western populations is energy intake (Pontzer Et al. 2012). Many people not only eat too much but too much of the wrong things. Biological anthropologist Leslie Lieberman (2006) argues that contemporary humans continue to rely on cues from foraging strategies of our evolutionary past that are now counterproductive in the <strong>obesogenic<\/strong> environments in which we now live.<\/p>\n<p class=\"import-Normal\">Examine your own eating habits in the context of how humans once hunted and gathered. Humans once relied on visual cues to find food, often traveled long distances to obtain it, then transported it back to our home base. There they may have had to process it by hand to render it edible. Think of how much less energy it takes to find food now. If we have the financial resources, we can acquire big energy payoffs by simply sitting at home and using an app on our mobile phone to place an order for delivery. And, voila! High-calorie (if not highly nutritious) food arrives at our door. Should we venture out for food, search time is reduced by signage and advertising directing us toward high-density \u201cpatches\u201d where food is available 24 hours a day. These include vending machines, gas stations, and fast-food outlets. Travel time is minimal and little human energy is used in the process (Lieberman 2006).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Foods are also prepackaged and prepared in ways that allow us to eat large quantities quickly. Think French fries or chicken nuggets, which we can easily eat with our hands while doing other things, like driving or watching television, rendering eating mindless and allowing us to take in food faster than our <strong>endocrine systems<\/strong> can tell us we are getting full. Modern \u201cpatches\u201d offer low-fibre, calorie-dense resources, which allow us to eat larger quantities, a problem already encouraged by larger portion sizes (Lieberman 2006). Processed foods are also engineered to appeal to human preferences for sweet tastes and fatty, creamy textures (Moss 2013). Remember from earlier chapters that natural selection favoured depth perception, colour vision, grasping hands, and coordinated eye-hand movements as general primate traits. Advertising and packaging now use our colour vision against us, attracting us to products that have little nutritional value but that play to our evolutionary predisposition toward variety. Remember those 50 different nutrients we require? That variety is now presented to us in the form of 55 different flavours of Oreo cookies (Cer\u00f3n 2017), which we take out of the package and dip in milk using our hand-eye coordination and depth perception.<\/p>\n<p class=\"import-Normal\">Even if we are ostensibly eating the same things our ancestors did, these foods are nothing alike. Take potatoes, for example. One medium-sized, plain, baked potato is a healthy food, especially if we eat the skin too. It contains 110 calories, 0 grams of fat, 26 grams of carbohydrates, and 3 grams of protein, plus 30% of the U.S. Recommended Daily Allowance (RDA) of vitamin C, 10% of vitamin B6, 15% of potassium, and no sodium (<a href=\"https:\/\/potatogoodness.com\/\" target=\"_blank\" rel=\"noopener\">Potato USA<\/a>). In contrast, a medium order of McDonald\u2019s fries, which takes the potato and adds salt and fat, contains 340 calories, 16 grams of fat, 44 grams of carbohydrates, 4 grams of protein, and 230 mg of sodium (<a href=\"https:\/\/www.mcdonalds.com\" target=\"_blank\" rel=\"noopener\">McDonalds<\/a>). Potato chips take food processing to a whole new level, removing even more nutrition and adding a host of additional ingredients, including oils, preservatives, and artificial flavourings and colours (Moss 2013). Take Ruffles Loaded Bacon and Cheddar Potato Skins Potato Chips as an example (St. Pierre 2018). The number of ingredients increases from one to 11 to 35 as we move from the potato to the potato chip, moving further from nature with each step (Figure 17.5). It should be noted that the nutritional information for the potato chips is based on a serving size of 11 chips, an amount likely smaller than many people eat. Many sweet, fatty, salty foods like fries and chips are cheap, which is why many people choose to eat them (Moss 2013). The price of a medium-sized order of McDonald\u2019s fries as of this writing is US$1.79, and the potato chips are $2.98 for an 8.5-ounce bag. A single potato prewrapped for microwaving is available in many supermarkets for US$1.99 but requires access to a microwave and eating utensils, making it less convenient.<\/p>\n<div style=\"text-align: left\">\n<table class=\"grid\" style=\"border-collapse: collapse;width: 100%;height: 197px\">\n<caption>Figure 17.5: The potato in three modern forms. Credit: <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/chapter\/__unknown__-11\/\" target=\"_blank\">The potato in three modern forms (Figure 16.4)<\/a> original to <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/\" target=\"_blank\">Explorations: An Open Invitation to Biological Anthropology<\/a> by Joylin Namie and Katie Nelson is a collective work under a <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0 License<\/a>. [Includes <a href=\"https:\/\/www.publicdomainpictures.net\/en\/view-image.php?image=137873&amp;picture=potato\" target=\"_blank\">Potato<\/a> by Charles Rondeau, <a href=\"https:\/\/creativecommons.org\/publicdomain\/zero\/1.0\/\" target=\"_blank\">public domain (CC0)<\/a>; <a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:McDonalds-French-Fries-Plate.jpg\" target=\"_blank\">McDonalds-French-Fries-Plate<\/a> by <a href=\"https:\/\/commons.wikimedia.org\/wiki\/User:Evan-Amos\" target=\"_blank\">Evan-Amos<\/a>, <a href=\"https:\/\/creativecommons.org\/publicdomain\/zero\/1.0\/\" target=\"_blank\">public domain (CC0)<\/a>; <a href=\"https:\/\/pdpics.com\/photo\/2316-potato-chips-bowl\/\" target=\"_blank\">Potato chips bowl<\/a> by pdpics.com, <a href=\"https:\/\/creativecommons.org\/publicdomain\/zero\/1.0\/\" target=\"_blank\">public domain (CC0)<\/a>.]<\/caption>\n<thead>\n<tr style=\"height: 47px\">\n<td style=\"width: 20.0464%;height: 47px\"><\/td>\n<td style=\"width: 25.4644%;height: 47px\">\n<p style=\"text-align: center\"><strong>Baked Potato<\/strong><br \/>\n[based, skin on, plain]<\/p>\n<\/td>\n<td style=\"width: 27.4768%;height: 47px;text-align: center\"><strong>French Fries<\/strong><br \/>\n[Medium order]<\/td>\n<td style=\"width: 27.0124%;height: 47px\"><strong>Potato Chips<\/strong><br \/>\n[1 oz. serving of 11 chips]<\/td>\n<\/tr>\n<\/thead>\n<tbody>\n<tr style=\"height: 15px\">\n<td style=\"width: 20.0464%;height: 15px\">Calories<\/td>\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">110<\/td>\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">340<\/td>\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td style=\"width: 20.0464%;height: 15px\">Calories from fat<\/td>\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">0<\/td>\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">144<\/td>\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td style=\"width: 20.0464%;height: 15px\">Fat<\/td>\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">0g<\/td>\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">16g<\/td>\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td style=\"width: 20.0464%;height: 15px\">Carbohydrates<\/td>\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">26g<\/td>\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">44g<\/td>\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td style=\"width: 20.0464%;height: 15px\">Protein<\/td>\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">3g<\/td>\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">4g<\/td>\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td style=\"width: 20.0464%;height: 15px\">Sodium<\/td>\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">0g<\/td>\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">230mg<\/td>\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td style=\"width: 20.0464%;height: 15px\">Dietary fibre<\/td>\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">2g<\/td>\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">4g<\/td>\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td style=\"width: 20.0464%;height: 15px\">Sugars<\/td>\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">1g<\/td>\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">0g<\/td>\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td style=\"width: 20.0464%;height: 15px\">Cholesterol<\/td>\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">0g<\/td>\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">0g<\/td>\n<td style=\"width: 27.0124%;height: 15px\"><\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td style=\"width: 20.0464%;height: 15px\">Ingredients<\/td>\n<td style=\"width: 25.4644%;height: 15px;text-align: center\">Potato<\/td>\n<td style=\"width: 27.4768%;height: 15px;text-align: center\">Potatoes, vegetable oil (canola oil), soybean oil, hydrogenated soybean oil, natural beef flavour (wheat and milk derivatives), citric acid (preservative), dextrose, sodium acid pyrophosphate (main colour), salt.<\/td>\n<td style=\"width: 27.0124%;height: 15px\">Potatoes, vegetable oil (sunflower, corn, and\/or canola oil), bacon and cheddar loaded potato skins seasoning (maltodextrin &#8211; made from corn) salt, cheddar cheese (milk, cheese cultures, salt enzymes), sour cream (cultured cream, skin milk), whey, dried onion, monosodium.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<\/div>\n<div class=\"__UNKNOWN__\">\n<p class=\"import-Normal\">Not only have we transformed the food supply and our eating in ways that are detrimental to our health, but these changes have been accompanied by reductions in physical activity. <strong>Sedentarism<\/strong> is built into contemporary lifestyles. Think of how much time you spent sitting down today. Some of it may have been in class or at work, some may have been driving a car or perhaps binge-watching your favourite show, playing a video game, or checking in on social media. An inactive lifestyle is almost dictated by the digital age (Lucock Et al<em>.<\/em> 2014). Levels of physical activity in many countries are now so low that large portions of the population are completely sedentary, including one in five Americans (CDC 2022). For a species whose biology evolved in an environment where walking, lifting, and carrying were part of daily life, this is unhealthy and often leads to weight gain.<\/p>\n<h2 class=\"import-Normal\">Biology and Genetics of Weight<\/h2>\n<figure style=\"width: 344px\" class=\"wp-caption alignright\"><img loading=\"lazy\" decoding=\"async\" class=\"\" src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image5-7.png\" alt=\"Four individuals of various ages walk alongside trees.\" width=\"344\" height=\"229\" \/><figcaption class=\"wp-caption-text\">Figure 17.6: Participants of a walk against diabetes and for general fitness around Nauru airport. Credit: <a href=\"https:\/\/www.flickr.com\/photos\/106853342@N04\/10709038046\" target=\"_blank\">Participants of a walk against Diabetes and for general fitness around Nauru airport<\/a> by Lorrie Graham, <a href=\"https:\/\/www.flickr.com\/photos\/dfataustralianaid\/\" target=\"_blank\">Department of Foreign Affairs and Trade<\/a>, is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by\/2.0\/legalcode\" target=\"_blank\">CC BY 2.0 License<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\">Research indicates multiple genetic variants influence weight gain, and they are not spread evenly among human populations. Tuomo Rankinen and colleagues (2006) identified 127 genes associated with obesity, of which 22 contributed to weight gain. Claude Bouchard (2007) then identified five categories of obesity-promoting genotypes. These genotypes promote sedentarism, result in low metabolism, and lead to poor regulation of appetite, and a propensity to overeat. An example of the impact such genotypes can have in an environment of plenty is found among the population of the Micronesian island of Nauru. Historically, the island was geographically isolated and the food supply was unpredictable. These conditions favoured genotypes that promoted the ability to rapidly build up and store fat in times of food availability. In Nauruans, there are two genetic variants favouring weight gain and insulin resistance, and both are associated with obesity and type 2 diabetes. One variant is also associated with hypertension. One of these variants is also found in Pima Indians, who live in parts of Arizona and Mexico. In the Pima, this variant is associated with a high <strong>b<\/strong><strong>ody mass index (BMI) <\/strong> and type 2 diabetes, although it is not associated with the same outcomes in Japanese and British subjects (de Silva Et al<em>.<\/em> 1999). The other variant was analysed in Finnish and South Indian populations, neither of whom experienced the same outcome as Nauruans. This suggests these alleles may act as modifying genes for type 2 diabetes in some population groups (Baker Et al. 1994). Unfortunately, Nauruans are one of those groups. Eventually, they became wealthy through phosphate mining on the island, gaining access to a calorie-rich Western diet of imported foods and developing a sedentary lifestyle. This resulted in rates of type 2 diabetes as high as 30\u201340% in Nauruans over the age of 15, which became the leading cause of death (Lucock Et al. 2014), something Nauruans are taking seriously (Figure 17.6).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Factors other than biology influence which populations that carry a genetic predisposition to diabetes actually express it. The Onk Akimel O\u2019odham (Pima) of Arizona, for example, were seriously impacted by U.S. government policies that affected water rights, forcing the population away from subsistence farming to dependence on government handouts and convenience food. This resulted in a significant loss of physical activity, malnutrition, and obesity. The Onk Akimel O\u2019odham continue to experience hardship due to high rates of unemployment, poverty, and depression, sometimes made worse by alcoholism. In the absence of these pressures, the Onk Akimel O\u2019odham were diabetes free for centuries prior, even though they relied on agriculture for subsistence, suggesting genetics alone is not responsible for high rates of obesity and diabetes in current Onk Akimel O\u2019odham populations (Smith-Morris 2004).<\/p>\n<figure style=\"width: 372px\" class=\"wp-caption alignleft\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image3-4-1.jpg\" alt=\"A human body outline with multiple points, each listing related medical complications.\" width=\"372\" height=\"493\" \/><figcaption class=\"wp-caption-text\">Figure 17.7: Medical complications of obesity include stroke, sleep apnea, lung disease, liver disease, gallstones, cancer, heart disease, diabetes, pancreatitis, abnormal periods and infertility, arthritis, inflamed veins, and gout. Credit: <a href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Medical_complications_of_obesity.png\" target=\"_blank\">Medical complications of obesity<\/a> by the <a href=\"https:\/\/www.cdc.gov\/\" target=\"_blank\">Centers for Disease Control and Prevention (CDC)<\/a> has been modified (colour changed and cancer list shortened) and is in the <a href=\"https:\/\/en.wikipedia.org\/wiki\/Public_domain\" target=\"_blank\">public domain<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Obesity also has an epigenetic component. You learned about epigenetics in Chapter 4. With regard to obesity, epigenetics is counterintuitive in that mothers who do not take in enough calories during pregnancy often give birth to babies who grow up to be fat. What takes place is the fetus receives signals during pregnancy from its mother through the placenta and intrauterine environment about environmental conditions outside of the womb, in this case food insecurity. These signals encourage the turning on and off of genes related to metabolism. This alters the phenotype of the fetus so that if the child is born into an environment where food is plentiful, it will put on weight rapidly whenever possible, leading to obesity and related diseases later in life. If the child is a girl, her own eggs are formed in utero with the same genetic changes coded in, meaning she will pass along this same genetic predisposition to gain weight to her children. Hence, a biological propensity toward obesity can continue across generations (Worthman &amp; Kuzara 2005). Epigenetic changes to genes that promote weight gain are argued to be partly responsible for the rapid rise in obesity and diabetes in developing countries gaining access to Western diets (Stearns, Nesse, and Haig 2008).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Obesity and overweight put a strain on several biological systems of the body, including the <strong>circulatory<\/strong>, endocrine, and skeletal systems, contributing to hypertension, heart disease, <strong>stroke<\/strong>, diabetes, and osteoarthritis (Figure 17.7). Obesity also elevates the risk of cancers of the breast, endometrium, kidney, colon, esophagus, stomach, pancreas, and gallbladder (National Institutes of Health 2017; Vucenik &amp; Stains 2012). Diabetes\u2014one of the fastest-growing health conditions around the globe (WHO 2016) and one tightly connected to obesity and overweight\u2014is the focus of the following Special Topics box.<\/p>\n<div class=\"textbox\">\n<h2 class=\"import-Normal\">Special Topic: Diabetes<\/h2>\n<p class=\"import-Normal\"><strong>Diabetes mellitus<\/strong> is an endocrine disorder characterized by excessively high blood glucose levels (Martini Et al<em>.<\/em> 2013). According to a report released by the World Health Organization, the number of people living with diabetes is growing in all regions of the world. Rates of diabetes have nearly doubled in the past three decades, largely due to increases in obesity and sugary diets (WHO 2016). One in 10 people around the world, 537 million people, now have diabetes, and three out of four live in low- and middle-income countries (IDF 2022). In the United States, 37 million people have diabetes (CDC 2020), where the disease is rising fastest among millennials (those ages 20\u201340) (BCBSA 2017), and one in every two adults with diabetes is undiagnosed (IDF 2022). Obesity and diabetes are linked: obesity causes a diet-related disease (diabetes) because of humans\u2019 evolved metabolic homeostasis mechanism, which is poorly suited to contemporary energy environments (Lucock Et al<em>.<\/em> 2014).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">To function properly, cells need a steady fuel supply. Blood sugar (glucose) is the fuel for most cells in the body, and the body produces the hormone <strong>insulin<\/strong> to help move glucose into cells that need it (Figure 17.8). Foods that most readily supply glucose to your bloodstream are carbohydrates, especially starchy foods like potatoes or sweet, sugary foods like candy and soda. The body can also convert other types of foods, including protein-rich foods (e.g., lean meats) and fatty foods (e.g.<em>,<\/em> vegetable oils and butter), into blood sugar in the liver via gluconeogenesis. Insulin\u2019s main job is to tell your cells when to take up glucose. The cell also has to listen to the signal and mobilize the glucose transporters. This not only allows your cells to get the energy they need, but it also keeps blood sugar from building up to dangerously high levels when you are at rest.<\/p>\n<figure style=\"width: 485px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image7-7.png\" alt=\"The cycle of how a body with diabetes processes nutrients from food.\" width=\"485\" height=\"648\" \/><figcaption class=\"wp-caption-text\">Figure 17.8: Carbohydrates are eaten and broken down into simple sugars (e.g., glucose). Glucose enters the bloodstream from the intestines, and the increase in glucose stimulates the pancreas to release insulin into the bloodstream. Insulin deposits glucose in the muscles and fat cells, where it is stored and used for energy. Credit: <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/chapter\/__unknown__-11\/\" target=\"_blank\">Glucose metabolism (Figure 16.7)<\/a> original to <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/\" target=\"_blank\">Explorations: An Open Invitation to Biological Anthropology<\/a> by Mary Nelson is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0 License<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">This system has limits. Like the rest of our biology, it evolved during several million years when sugar was hard to come by and carbohydrates took the form of fresh foods with a low <strong>glycemic index (GI)<\/strong>. Our ancestors were also active throughout the day, taking pressure off of the endocrine system. Now, sedentary lifestyles and processed-food diets cause many of us to take in more calories\u2014and especially more carbohydrates\u2014than our bodies can handle. There is only so much blood sugar your cells can absorb. Many modern populations are taxing those limits. After years of being asked by insulin to take in more glucose than they can use, cells eventually stop responding (McKee &amp; McKee 2015). This is called type 2 diabetes or insulin resistance, which accounts for 90\u201395% of diabetes cases in the United States (Figure 17.9). type 1 diabetes is believed to be caused by an autoimmune response in which your immune system is attacking and destroying the insulin-producing cells in your pancreas (Figure 17.9). type 1 diabetes is a genetic condition that often shows up early in life, while type 2 is more lifestyle-related and develops over time.<\/p>\n<figure style=\"width: 462px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image9-6.png\" alt=\"Type 1 cells and Type 2 cells and their response to insulin.\" width=\"462\" height=\"276\" \/><figcaption class=\"wp-caption-text\">Figure 17.9: Type 1 and type 2 diabetes. For Type 1 Diabetes, cells do not absorb glucose becuase there is no insulin. For Type 2 Diabetes, although there is insulin available, cells do not respond to it. Credit: <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/chapter\/__unknown__-11\/\" target=\"_blank\">Type 1 and Type 2 Diabetes (Figure 16.8)<\/a> original to <a href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/\" target=\"_blank\">Explorations: An Open Invitation to Biological Anthropology<\/a> by Mary Nelson has been modified (text) and is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0 License<\/a>.<\/figcaption><\/figure>\n<\/div>\n<h2 class=\"import-Normal\">Cardiovascular Disease<\/h2>\n<p class=\"import-Normal\">Cardiovascular disease (CVD)\u2014which includes coronary heart disease, hypertension (high blood pressure), and stroke\u2014is the leading cause of death globally, and heart disease remains the number one cause of death in the United States (American Heart Association 2018). Risk factors for cardiovascular disease include diet, obesity\/overweight, diabetes, smoking and alcohol consumption, and physical inactivity.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The connections between these factors and heart disease may not seem obvious and will be addressed here beginning with diet. Diets high in saturated fat and cholesterol can lead to atherosclerosis, a condition in which fat and cholesterol form plaque inside the arteries, eventually building up and hardening to the point that blood flow is blocked. Too much salt in the diet leads to fluid retention, which increases blood volume and thereby blood pressure, taxing the heart. Obesity\/overweight contribute to cardiovascular disease directly through increases in total blood volume, cardiac output, and cardiac workload. In other words, the heart has to work much harder if one is overweight (Akil &amp; Ahmad 2011). Obesity also relates to CVD indirectly through elevation of blood pressure (hypertension) and diabetes. High levels of blood glucose from diabetes can damage blood vessels and the nerves that control the heart and blood vessels. Alcohol consumption can raise blood pressure and triglyceride levels, a type of fat found in the blood. Alcohol also adds extra calories, which may cause weight gain, especially around the abdomen, which is directly associated with risk of a heart attack (Akil &amp; Ahmad 2011). Cigarette smoking also increases the risk of coronary heart disease. Nicotine increases blood pressure; in addition, cigarette smoke causes fatty buildup in the main artery in the neck and thickens blood, making it more likely to clot. It also decreases levels of HDL (\u201cgood\u201d) cholesterol (American Heart Association 2018). Even secondhand smoke can have an adverse effect if exposure occurs on a regular basis. Chronic psychological stress also elevates the risk of heart disease (Dimsdale 2008). The repeated release of stress hormones like adrenaline elevates blood pressure and may eventually damage artery walls. The human <strong>stress response<\/strong> and its connections to health and disease are discussed in more detail below.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">However, physical activity alters the likelihood of having heart disease, both directly and indirectly. Regular exercise of moderate to vigorous intensity strengthens the heart muscle and allows capillaries, tiny blood vessels in your body, to widen, improving blood flow. Regular exercise can also lower blood pressure and cholesterol levels and manage blood sugar levels, all of which reduce the risk of CVD.<\/p>\n<h2 class=\"import-Normal\">Cancer<\/h2>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Cancer is the second-leading cause of death globally, causing one in every six deaths and killing nearly nine million people in 2015 (WHO 2018). Lifetime cancer risk in developed Western populations is now one in two, or 50% (Greaves 2015). Approximately one-third of deaths from cancer are due to behavioural and dietary factors, including high body mass index (BMI), low fruit and vegetable intake, lack of physical activity, and the use of tobacco and alcohol. Depending on the type of cancer and one\u2019s own genetic inheritance, these factors can increase cancer risk from 2- to 100-fold (Greaves 2015). Cancer is the result of interactions between a person&#8217;s genes and three categories of external agents: physical carcinogens (e.g., ultraviolet radiation), chemical carcinogens (e.g., tobacco smoke, asbestos), and biological carcinogens, such as infections from certain viruses, bacteria, or parasites (WHO 2018). Obesity is also a risk factor for cancer, including of the breast, endometrium, kidney, colon, esophagus, stomach, pancreas, and gallbladder (National Institutes of Health 2017; Vucenik &amp; Stains 2012).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Cancer has been regarded as a relatively recent affliction for humans that became a problem after we were exposed to modern carcinogens and lived long enough to express the disease (David &amp; Zimmerman 2010). Given the long history that humans share with many oncogenic (cancer-causing) parasites and viruses (Ewald 2018), and the recent discovery of cancer in the metatarsal bone of a 1.8-million-year-old hominin (Odes Et al. 2016), this view is being challenged (See \u201cSpecial Topic: Life Choices and Reproductive Cancers in Women\u201d). The difficulties of identifying cancer in archaeological populations are many. Most cancer occurs in soft tissue, which rarely preserves, and fast-growing cancers would likely kill victims before leaving evidence in bone. It is also difficult to distinguish cancer from benign growths and inflammatory disease in ancient fossils, and there is often postmortem damage to fossil evidence from scavenging and erosion. However, using 3-D images, South African researchers recently diagnosed a type of cancer called osteosarcoma in a toe bone belonging to a human relative who died in Swartkrans Cave between 1.6 and 1.8 million years ago (Randolph-Quinney Et al. 2016). This study provides the earliest evidence of cancer in hominins.<\/p>\n<div class=\"textbox\">\n<h2 class=\"import-Normal\">Special Topic: Life Choices and Reproductive Cancers in Women<\/h2>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Behavioural or \u201clifestyle\u201d choices have an impact on cancer risk. Breast cancer is one example. It is the most common cancer in women worldwide, but <strong>incidence<\/strong> of new cases varies from 19.3 per 100,000 women in Eastern Africa to 89.7 per 100,000 women in Western Europe (WHO 2018). These differences are attributable to cultural changes among women in Western, industrialized countries that are a mismatch for our evolved reproductive biology. Age at <strong>menarche<\/strong>, the onset of menstrual periods, has dropped over the course of the last century from 16 to 12 years of age in the U.S. and Europe, with some girls getting their periods and developing breasts as young as eight years old (Greenspan &amp; Deardorff 2014, Figure 17.10). A World Health Organization study involving 34 countries in Europe and North America suggests the primary reason for the increase in earlier puberty is obesity, with differences in BMI accounting for 40% of individual- and country-level variance (Currie Et al<em>.<\/em> 2012). Early puberty in girls is associated with increased risk of breast cancer, ovarian cancer, diabetes, and high cholesterol in later life (Pierce &amp; Hardy 2012).<\/p>\n<figure style=\"width: 554px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image12-3.jpg\" alt=\"A graph shows the decrease in age at menarche for five European nations and United States.\" width=\"554\" height=\"434\" \/><figcaption class=\"wp-caption-text\">Figure 17.10: Decreasing ages at time of first menstruation in selected countries. Credit: <a href=\"https:\/\/en.wikipedia.org\/wiki\/Menarche#\/media\/File:Acceleration1.jpg\" target=\"_blank\">Acceleration1.jpg<\/a> by Yahadzija is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/3.0\/deed.en\" target=\"_blank\">CC BY-SA 3.0 Unported License<\/a>.<\/figcaption><\/figure>\n<p>&nbsp;<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">At the same time that age at puberty is dropping for girls in Western nations, age at birth of the first child is later, at 26 years old (Mathews and Hamilton 2016). Women are also having fewer children, two on average (Gao 2015), with 15% of women choosing to remain childless (Livingston 2015). Rates of breastfeeding have risen in recent decades but drop to only 27% of infants once babies reach 12 months of age (CDC 2014). In contrast, data from modern foraging populations (Eaton Et al. 1994) indicate that age at menarche is around 16 years old, age at birth of the first child is 19, breastfeeding on demand continues for three years for each child, and the number of children averages six. These differences relate to elevated risk for reproductive cancers, including breast cancer, among women in developed countries.<\/p>\n<p class=\"import-Normal\">Other than an established genetic risk (e.g., BRCA gene), the primary risk factor for breast cancer is exposure to estrogen. For women living in modern, industrialized economies, this exposure now often comes from women\u2019s own ovaries rather than from external environmental sources (Stearns, Nesse, and Haig 2008). Women in cultures without contraception are pregnant or breastfeeding for much of their reproductive lives, resulting in 100 or so menstrual cycles per lifetime. In contrast, Western women typically experience 400 or more (Strassmann 1997). This is partly due to early puberty. From menarche to the birth of a woman\u2019s first child can be 14 years or longer in Western populations, after which breastfeeding, if undertaken at all, lasts for a few weeks or months. Oral contraceptives or other hormonal methods to control reproduction induce monthly periods. Age at menopause (the cessation of menstrual cycles) is 50\u201355 years old across human populations. For Western women, this translates into forty years of menstrual cycling. Each month, the body prepares for a pregnancy that never occurs, experiencing cell divisions that put women at risk for cancers of the breast, endometrium, ovaries, and uterus (Strassmann 1999). Obesity adds to the risk, as adipose (fat) tissues are the primary source of estrogen biosynthesis. Thus, weight gain during the postmenopausal stage means higher exposure to estrogen and a greater risk of cancer (Ali 2014).<\/p>\n<p class=\"import-Normal\">Women cannot return to our evolutionary past, and there are significant social and economic reasons for delaying pregnancy and having fewer children. These include achieving educational and career goals, greater earning power, a reduction in the gender pay gap, more enduring marriages, and a decrease in the number of women needing public assistance (Sonfield Et al. 2013). There are also cultural means by which we might reduce the risk of reproductive cancers. These include reformulating hormonal contraceptives with enough estrogen to maintain bone density but reducing the number of menstrual periods over the reproductive lifespan (Stearns, Nesse, &amp; Haig 2008). Reducing fat intake may also lower estrogen levels. High-fat diets contribute to breast tumor development, while high fibre diets are beneficial in decreasing intestinal resorption of estrogenic hormones. Exercise also appears protective. Studies of former college athletes demonstrate risks of breast, uterine, and ovarian cancers later in life, two to five times lower than those of nonathletes (Eaton Et al<em>.<\/em> 1994).<\/p>\n<\/div>\n<h2 class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Stress<\/h2>\n<p class=\"import-Normal\">Have you ever been \u201cstressed out\u201d in class? Say you\u2019re in a large lecture hall with a hundred other people, or even in a small class where you don\u2019t know anyone. You\u2019re not sure about something the professor just said and you would really like to ask about it, so you start to raise your hand. Does your heart begin to pound and your mouth become dry? Do you get so nervous that you choose to ask a classmate after lecture instead? If so, you are not alone. Fear of speaking in public is one of the most common social phobias (APA 2013). It has been estimated that 75% of all people experience some degree of anxiety or nervousness when it comes to public speaking (Hamilton 2011), and surveys have shown that most people fear public speaking more than they fear death (Croston 2012).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">We have evolution to thank for this.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Humans, like other primates, are social animals. Being part of a group helped us to survive predation, get enough to eat, and successfully raise our young. When faced with standing up in front of a group, or even speaking up in class, we break into a sweat because we are afraid of rejection. Psychologist Glenn Croston (2012) writes, \u201cThe fear is so great because we are not merely afraid of being embarrassed or judged. We are afraid of being rejected from the social group, ostracized and left to defend ourselves all on our own. We fear ostracism still so much today it seems, fearing it more than death, because not so long ago getting kicked out of the group probably really was a death sentence.\u201d Hence, it is no surprise that public speaking triggers a stress response among much of humankind.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The human nervous system evolved in a context where quick responses to perceived threats presented an evolutionary advantage. The \u201cfight or flight\u201d response was honed during millions of years when threats more often took the form of an approaching lion than an approaching deadline. Our body\u2019s stress response, however, is triggered by a wide variety of stressors that produce the same general pattern of hormonal and physiological adjustments (Martini Et al. 2013). In today\u2019s world, the system is often stuck in the \u201con\u201d position due to the constant pressures of modern life, and this is a significant influence on health and disease.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">It is important to recognize that there are different types of stress and the time in life when adult coping mechanisms are formed is in childhood. In children, some stressors can be positive\u2014for example, stressors that are mild to moderate in magnitude, and accompanied by the support of a caring adult, which help children develop pathways by which stress is dealt with by the body throughout life. In a young child, a positive stress response might be going to the pediatrician to receive a vaccination and receiving encouragement and comfort from both parent and practitioner. A tolerable stress response is more serious, precipitated by something like a divorce or death of a relative. Again, buffered by positive support from surrounding adults, these types of stressors can be successfully managed by children. Toxic stress, however, \u201cresults from strong, frequent or prolonged activation of the stress response in the absence of the buffering protection of a supportive adult relationship\u201d (Shonkoff &amp; Garner 2012). Examples include child abuse or neglect, parental substance abuse, homelessness, and violence. In the absence of adequate psychological and physical support, the biological pathways of a child\u2019s physiological stress response are altered and lead to reduced abilities to cope with life\u2019s challenges as an adult.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The negative effects of sustained, elevated cortisol levels on health are well documented. These include higher levels of infectious disease and slowed growth in childhood (Flinn &amp; England 2003) and increased incidence of heart disease, obesity, and diabetes in adults (Worthman &amp; Kuzara 2005). Contrary to our evolutionary past, many causes of sustained stress in contemporary societies are psychosocial rather than physical threats. These can include an unhappy marriage or frustrations at work (Dimsdale 2008). Stressors can also be more subtle. For example, a review of research into the effects of stress on health indicated that experiencing racism was a significant stressor that was associated with alcohol consumption, psychological distress, overweight, abdominal obesity, and higher fasting-glucose levels among minority groups (Williams &amp; Mohammed 2013). Chronic, everyday racial discrimination is also associated with the hardening of coronary arteries, elevated blood pressure, giving birth to lower-birth-weight infants, cognitive impairment, poor sleep, and visceral fat, which is fat stored deep inside the belly, wrapped around the organs, including the liver and intestines. Visceral fat is a sign of <strong>m<\/strong><strong>etabolic syndrome<\/strong>, increasing the risk of stroke, heart disease, and type 2 diabetes. These effects have been shown to increase morbidity and mortality among members of affected groups.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Epigenetics can also be a factor in how a person is able to deal with stressful situations. Maternal experiences of stress during pregnancy have the potential to permanently alter the physiology of mothers\u2019 offspring, especially the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis regulates metabolism, blood pressure, and the immune response, and these alterations can predispose prenatally stressed individuals to suffer metabolic, cardiovascular, and mental disorders in adulthood (Palma-Gudiel Et al. 2015). These experiences carry across generations, with children of Holocaust survivors who experienced PTSD demonstrating similar changes in neurochemistry in the absence of a sustained, traumatic event, as did infant offspring of mothers who developed PTSD during pregnancy after witnessing the traumatic events of 9\/11 (Yehuda &amp; LeDoux 2007).<\/p>\n<h2 class=\"import-Normal\" style=\"text-indent: 0pt\">Syndemics and the Ecological Model<\/h2>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">It is important to recognize that disease risk is not spread evenly within or between populations. Diseases combine and interact to create a <strong>syndemic<\/strong>, where the coexistence of two or more conditions exacerbates the effects of one or all conditions. A syndemic (versus a pandemic, for example) takes into account social, political, economic, and environmental factors that increase risk for the clustering of two or more diseases (Singer Et al. 2017). One of the first syndemics identified involved substance abuse, violence, and AIDS. In inner cities in the U.S., the health crisis around HIV\/AIDS was related to tuberculosis, sexually transmitted infections, hepatitis, cirrhosis, infant mortality, drug abuse, suicide, and homicide. These were connected to poverty, homelessness, unemployment, poor nutrition, lack of social support, and social and ethnic inequality (Singer Et al. 2017). Together, these factors and others, like health policy and unequal access to health care, form an <strong>ecological model<\/strong> of health and disease, one that moves beyond biology and medical intervention (Sallis Et al. 2008).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The COVID-19 pandemic represents a syndemic in which systemic racism in the healthcare system, differential access to diagnosis and treatment, income, employment, housing, family structure, pre existing conditions, and public health policies combined to result in higher rates of infection and death for African Americans, Native Americans, Asians, and Hispanic populations in the United States (Figure 17.11).<\/p>\n<table class=\"grid\" style=\"border-collapse: collapse;width: 100%\">\n<caption>Figure 17.11: Risk for COVID-19 infection, hospitalization, and death by race\/ethnicity. Race and ethnicity are risk markers for other underlying conditions that affect health, including socioeconomic status, access to health care, and exposure to the virus related to occupation, e.g., frontline, essential, and critical infrastructure workers. Credit: <a href=\"https:\/\/www.cdc.gov\/coronavirus\/2019-ncov\/covid-data\/investigations-discovery\/hospitalization-death-by-race-ethnicity.html\" target=\"_blank\">Risk for COVID-19 Infection, Hospitalization, and Death by Race\/Ethnicity<\/a> by the <a href=\"https:\/\/www.cdc.gov\/\" target=\"_blank\">Centers for Disease Control and Prevention<\/a> is in the <a href=\"https:\/\/en.wikipedia.org\/wiki\/Public_domain\" target=\"_blank\">public domain<\/a>.<\/caption>\n<thead>\n<tr class=\"shaded\">\n<td style=\"width: 130.367px\">Rate ratios compared to White, Non-Hispanic persons<\/td>\n<td style=\"width: 130.367px\">American Indian or Alaska Native, Non-Hispanic persons<\/td>\n<td style=\"width: 130.367px\">Asian, Non-Hispanic persons<\/td>\n<td style=\"width: 130.383px\">Black or African American, Non-Hispanic persons<\/td>\n<td style=\"width: 130.35px\">Hispanic or Latino persons<\/td>\n<\/tr>\n<\/thead>\n<tbody>\n<tr>\n<td style=\"width: 130.367px\">Cases<\/td>\n<td style=\"width: 130.367px\">1.6x<\/td>\n<td style=\"width: 130.367px\">.8x<\/td>\n<td style=\"width: 130.383px\">1.1x<\/td>\n<td style=\"width: 130.35px\">1.5x<\/td>\n<\/tr>\n<tr>\n<td style=\"width: 130.367px\">Hospitalization<\/td>\n<td style=\"width: 130.367px\">2.7x<\/td>\n<td style=\"width: 130.367px\">.8x<\/td>\n<td style=\"width: 130.383px\">2.3x<\/td>\n<td style=\"width: 130.35px\">2.0x<\/td>\n<\/tr>\n<tr>\n<td style=\"width: 130.367px\">Death<\/td>\n<td style=\"width: 130.367px\">2.1x<\/td>\n<td style=\"width: 130.367px\">.8x<\/td>\n<td style=\"width: 130.383px\">1.7x<\/td>\n<td style=\"width: 130.35px\">1.8x<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p class=\"import-Normal\">COVID-19 was the third leading cause of death in the U.S. in 2020 and 2021 (NIH 2022; Figure 17.12), but morbidity and mortality was not equally spread across the population. Working-class people and people of colour in the U.S. are more likely to live in poverty, in areas with high rates of crime and violence, and in close proximity to freeways and environmental threats like petrochemical plants and waste incinerators (Singer and Baer 2012). Many such neighbourhoods are also food \u201cdeserts\u201d without ready access to a healthy, affordable diet, made more challenging by residents not owning a car (Food Empowerment Project n.d.). Low-income people also often lack access to high-quality health care and delay or avoid preventive care and health screenings (Ross Et al. 2007). These factors contributed to higher rates of preexisting conditions, including obesity, diabetes, hypertension, asthma, heart disease, chronic obstructive pulmonary disease (COPD), and smoking behaviour, which then led to more complications and higher death rates from COVID (Ghosh Et al. 2021).<\/p>\n<p class=\"import-Normal\">Family structure also affected COVID exposure and severity. Many Americans live in multigenerational households, including 27% of Hispanics, 29% of Asians, 26% of African Americans, and 20% of Whites (Cohn &amp; Passel 2018). Not all multigenerational households are equal, however. Over twice as many African Americans as Whites are in multigenerational families in which at least one family member is unemployed, and over three times as many African Americans are in multigenerational families in which everyone is simultaneously unemployed (Park, Wiemers, and Seltzer 2019). Family members in multigenerational households were at a much higher risk of developing more severe forms of COVID due to decreased personal space and multiple exposures to the virus, as well as higher rates of diabetes, smoking, and residents living below the poverty line (Ghosh Et al. 2021). While aimed at reducing overall infection rates from COVID, public health measures such as mandatory lockdowns only exacerbated the situation in overcrowded and multigenerational housing, resulting in higher rates of infection and death in these communities.<\/p>\n<div style=\"margin: auto\">\n<table class=\"aligncenter\" style=\"width: 468pt;height: 195px\">\n<caption>Figure 17.12: Top five causes of death in the U.S. and worldwide since 2020. Credit: Top five causes of death in the U.S. and worldwide original to Explorations: An Open Invitation to Biological Anthropology (2nd ed.) by Joylin Namie is under a <a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\">CC BY-NC 4.0 License<\/a>. Based on data from Shiels Et al. 2022 and Traeger 2022.<\/caption>\n<thead>\n<tr class=\"shaded\" style=\"height: 30px\">\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 164.6px\">\n<p class=\"import-Normal\"><strong>United <\/strong><strong>States<\/strong><\/p>\n<\/td>\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 429.733px\">\n<p class=\"import-Normal\"><strong>Worldwide<\/strong><\/p>\n<\/td>\n<\/tr>\n<\/thead>\n<tbody>\n<tr class=\"Table2-R\" style=\"height: 0\">\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 164.6px\">\n<p class=\"import-Normal\">1. Heart disease<\/p>\n<\/td>\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 429.733px\">\n<p class=\"import-Normal\">1. Heart disease<\/p>\n<\/td>\n<\/tr>\n<tr class=\"Table2-R\" style=\"height: 0\">\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 164.6px\">\n<p class=\"import-Normal\">2. Cancer<\/p>\n<\/td>\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 429.733px\">\n<p class=\"import-Normal\">2. Stroke<\/p>\n<\/td>\n<\/tr>\n<tr class=\"Table2-R\" style=\"height: 0\">\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 164.6px\">\n<p class=\"import-Normal\">3. COVID-19<\/p>\n<\/td>\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 429.733px\">\n<p class=\"import-Normal\">3. COVID-19<\/p>\n<\/td>\n<\/tr>\n<tr class=\"Table2-R\" style=\"height: 0\">\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 164.6px\">\n<p class=\"import-Normal\">4. Accidents<\/p>\n<\/td>\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 429.733px\">\n<p class=\"import-Normal\">4. Chronic Obstructive Pulmonary Disease<\/p>\n<\/td>\n<\/tr>\n<tr class=\"Table2-R\" style=\"height: 0\">\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 164.6px\">\n<p class=\"import-Normal\">5. Stroke<\/p>\n<\/td>\n<td class=\"Table2-C\" style=\"background-color: transparent;padding: 5pt;border: 1pt solid #000000;height: 30px;width: 429.733px\">\n<p class=\"import-Normal\">5. Lower respiratory infections<\/p>\n<\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td style=\"height: 15px;width: 165.467px\"><\/td>\n<td style=\"height: 15px;width: 430.6px\"><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<\/div>\n<p class=\"import-Normal\">There is a long history of systemic racism and discrimination in the medical system in the United States (Washington 2006). African Americans have been subjected to medical testing and experimentation without their consent or knowledge since the time of slavery. They continue to routinely receive care of poorer quality than whites (Williams &amp; Wyatt 2015), less pain medication during treatment and hospitalization (Green Et al. 2003), and differential treatment during pregnancy and childbirth (Washington 2006). Many Americans, including 50% of White medical students and residents in one recent study (Hoffman Et al. 2016), hold at least one false belief about African Americans, including \u201cBlack people\u2019s skin is thicker than white people\u2019s skin,\u201d \u201cBlacks have stronger immune systems than whites,\u201d and \u201cBlacks\u2019 nerve endings are less sensitive than whites\u2019.\u201d Such beliefs affect health care for African Americans in medical emergencies and for chronic conditions.<\/p>\n<p class=\"import-Normal\">During the COVID-19 pandemic, patients with darker skin in the United States were negatively affected by the very medical device most commonly used to assess oxygen levels in their blood. The pulse oximeter, a small device that clips onto the tip of your index finger and measures blood oxygen levels, experienced increased use in home, clinical, and hospital settings during the COVID-19 pandemic. Decisions regarding treatment and hospital admission for patients infected with COVID were often based on pulse oximeter readings (Valbuena, Merchant, &amp; Hough 2022). The problem is the device overestimates oxygen saturation in patients with darker skin, an issue which has been recognized for over thirty years (Valbuena, Merchant, &amp; Hough 2022). It would be as if a standard thermometer reported lower body temperatures for patients of colour, making it seem as if they did not have a fever when they actually did. In the case of COVID-19, Asians, Hispanics, and African Americans experienced inaccurately high readings of their oxygen levels (with African Americans and darker-skinned Hispanics having the highest), resulting in delays in treatment, hospital admission, and access to medications to treat COVID and contributing to higher severity of illness and higher death rates among these populations in comparison to whites (Fawzi Et al. 2022).<\/p>\n<p class=\"import-Normal\">Employment was also a factor in unequal exposure to and death from COVID-19 (Raifman, Skinner, &amp; Sojourner 2022), with many low-income workers making the choice (which, realistically, may not be a choice at all) to expose themselves to COVID in order to earn the funds necessary to purchase food, housing, and other necessities. Many such workers were then forced to miss work due to COVID infection. With only 35% of low-wage workers (as opposed to 95% of high-wage workers) having paid sick leave, this left many families struggling financially. Three years into the pandemic, low-wage workers continue to have the least access to COVID vaccines and boosters. The U.S. also lacks federal workplace-safety regulations with regard to vaccine and masking mandates that other nations enforce in times of high transmission, and it does not provide high-quality masks to its essential workers. Many occupations deemed essential by the CDC during the height of the pandemic\u2014such as health care, emergency services, meat packing, agricultural work, teaching, and jobs in the hospitality sector\u2014experienced higher rates of morbidity and mortality from COVID. Many of these fields disproportionately employ people of colour (McKinsey &amp; Company 2021). Given this, future policies that address the pandemic at a structural level\u2014for example, providing monetary assistance to people who work in environments with a high risk of infection, such as cleaning, nursing, transportation, retail, restaurant work, and factory work, so that they can remain at home\u2014may function more effectively to prevent transmission and curb future outbreaks (Arnot Et al. 2020).<\/p>\n<h2 class=\"import-Normal\">Food for Thought<\/h2>\n<p class=\"import-Normal\">This chapter focused primarily on health conditions prevalent in contemporary, industrialized societies that are due, in part, to the mismatch between our evolved biology and modern environments. These are the built environment and the social environment, which together form the obesogenic environment in which unhealthy behaviours are encouraged. This chapter will close by examining each of these in a college context.<\/p>\n<figure style=\"width: 275px\" class=\"wp-caption alignleft\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/opentextbooks.concordia.ca\/explorations\/wp-content\/uploads\/sites\/57\/2023\/08\/image2-3.jpg\" alt=\"Four individuals in a park.\" width=\"275\" height=\"183\" \/><figcaption class=\"wp-caption-text\">Figure 17.13: Students walking around a campus. Credit: <a href=\"https:\/\/www.maxpixel.net\/Row-Four-Man-Woman-People-Walking-Together-3755342\" target=\"_blank\">Row four man woman people walking together 3755342<\/a> by <a href=\"https:\/\/www.maxpixel.net\/\" target=\"_blank\">MaxPixel<\/a> has been designated to the <a href=\"https:\/\/creativecommons.org\/share-your-work\/public-domain\/cc0\/\" target=\"_blank\">public domain (CC0)<\/a>.<\/figcaption><\/figure>\n<p>Consider your campus from an evolutionary perspective. To what degree does the built environment lend itself to physical activity as part of daily life? Is your campus constructed in ways that promote driving at the expense of walking or biking? If driving is necessary, is parking available close to the buildings or do you need to walk a fair distance from the parking lot to your destination? Do the buildings have stairs or ramps or is it necessary to take the elevator? Is it possible to negotiate safely around campus on foot or by bike in all weather? After dark? How about the classrooms and computer labs? Do they have standing or treadmill desks? Does your class schedule encourage walking from building to building between classes, or are most courses in your major scheduled in the same location? Most college majors also lack a physical education requirement, leaving it up to students to incorporate exercise into already-challenging schedules (Figure 17.13).<\/p>\n<p class=\"import-Normal\">Sociocultural factors that contribute to obesity include food advertising, ubiquitous fast-food and junk food options, and social pressure to consume, all of which are present on college campuses. Although nutrition on campuses has improved in recent years, many students find eating healthy in the dining halls and dorms challenging (Plotnikoff Et al. 2015), and students who live off campus fare even worse (Small Et al<em>.<\/em> 2013). There are also parties and other social events, a normal part of college life, that involve unhealthy food and encourage behaviours like alcohol consumption and smoking. Give some thought to the social atmosphere on your campus and the ways it may contribute to obesity. My own freshman orientation involved a succession of pizza parties, ice cream socials, and barbecues, followed by late-night runs to the nearest fast-food outlet. The purpose of these events was to encourage people to make friends and feel comfortable living away from home, but the foods served were unhealthy, and there was social pressure to join in and be part of the group. Such activities set students up for the \u201cfreshman fifteen\u201d and then some. They also reinforce the idea that being social involves eating (and sometimes drinking and\/or smoking).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Sedentarism and inactivity are also built into the academics of college life. Digital technology is a significant contributor to obesity. Students use laptops and cell phones to take notes, complete their work outside of class, and access social media. There are also video games, virtual reality headsets, and streaming television and movies for entertainment. The built environment of college already necessitates that students sit in class for hours each day, then sit at computers to complete work outside of class. The social environment enabled by digital technology encourages sitting around for entertainment. It is telling that we call it \u201cbinge watching\u201d when we spend hours watching our favourite shows. Doing so often involves eating, as well as multiple exposures to food advertising embedded in the shows themselves. In these ways, college contributes to the development of obesity-causing behaviours that can have negative health ramifications long after college is over (Small Et al. 2013).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">In the U.S., the greatest increase in obesity is among young adults aged 18\u201329 years, a significant percentage of whom are college students (Plotnikoff Et al. 2015). Analyses of college students\u2019 behaviour across semesters shows consumption of fruits and vegetables drops over time, as does the amount of physical activity, while consumption of sugar-sweetened beverages and fast-food goes up, leading to weight gain at nearly six times the rate of the general public (Small Et al. 2013). In response, many colleges and universities have instituted programs to encourage healthier eating and more physical activity among students (Plotnikoff Et al<em>.<\/em> 2015). It is important to emphasize that neither changes in diet or exercise are effective on their own.. A 2022 study of over 340,000 British participants demonstrated that physical activity and diet quality did not individually have an impact on cardiovascular disease or cancers (Ding Et al. 2022). That is, hitting the gym won\u2019t counteract the consequences of consuming high-calorie, fatty foods, and eating kale all day can\u2019t cancel out sedentary habits.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Just as no one fad diet is going to prove healthier than another, no one type of exercise is better than another. Anything that raises your heart rate and that you enjoy doing for at least an hour each day will work. Take advantage of opportunities to build exercise into everyday life. Take the stairs, park as far away from buildings as possible, ride a bike or walk instead of driving, and take walks between classes instead of sitting down and checking your phone. As far as diets go, eating a few less unhealthy calories each day, one less soda, no sugar in your coffee, or letting that last slice of pizza go to someone else, make a difference in the long run. Little changes add up to bigger ones. We cannot change our biology, but we can certainly change our habits.<\/p>\n<div class=\"textbox shaded\">\n<h2>Summary<\/h2>\n<p data-start=\"134\" data-end=\"760\">The health problems faced by modern humans can often be understood through the lens of evolution. As early <em>Homo sapiens<\/em> evolved in environments with a wide diversity of edible plants and animals, we developed complex nutritional requirements. However, with dramatic changes in our environments and daily lives, modern humans now encounter a variety of diet-related challenges. These include shifts in dentition and intestinal morphology, changes in food production and preparation, and altered patterns of physical activity. Together, these factors have contributed to changes in the leading causes of morbidity and mortality.<\/p>\n<p data-start=\"762\" data-end=\"1565\">These health consequences are often framed through the concept of epidemiological transitions, which are influenced by diet, physical activity, population density, and exposure to zoonotic diseases linked to agriculture. It is proposed that the first transition occurred when humans shifted from foraging to food production, leading to increased exposure to new diseases and dietary changes. The second transition followed the Industrial Revolution, when improvements in lifestyle and living conditions reduced infectious diseases but led to a rise in non-communicable diseases. The third and fourth transitions, still unfolding today, are marked by the spread of drug-resistant pathogens, the re-emergence of infectious diseases, and new health challenges driven by globalization, urbanization, and climate change.<\/p>\n<p data-start=\"1567\" data-end=\"1807\">Modern health issues such as obesity, cardiovascular disease, cancer, stress-related conditions, and syndemics illustrate the ongoing interaction between our evolved biology and the cultural and physical environments in which we live.<\/p>\n<h2 class=\"import-Normal\">Review Questions<\/h2>\n<ul>\n<li class=\"import-Normal\">Why do humans like foods that are \u201cbad\u201d for them? Describe the evolutionary underpinnings of our tastes for sugar, salt, and fat.<\/li>\n<li class=\"import-Normal\">How might understanding contemporary disease from an evolutionary perspective benefit medical practitioners in treating their patients?<\/li>\n<li class=\"import-Normal\">Several risk factors for conditions like heart disease, diabetes, and cancer are referred to as \u201clifestyle factors,\u201d implying these are behavioural choices people make that put them at risk. These include unhealthy eating, lack of physical activity, smoking, and alcohol consumption. To what degree is unhealthy behaviour structured by the physical and social environment? For example, how does being a college student influence your eating habits, physical activity patterns, smoking, and consumption of alcohol?<\/li>\n<li class=\"import-Normal\">Who benefits from the global obesity epidemic? Think about how the following industries and institutions might profit from it: The medical establishment? The fitness industry? The diet industry? Fashion? Pharmaceutical companies? Food manufacturers? Advertisers?<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<h2 class=\"__UNKNOWN__\">Key Terms<\/h2>\n<div class=\"__UNKNOWN__\">\n<p class=\"import-Normal\"><strong>Body mass index (BMI)<\/strong>: A person\u2019s weight in kilograms divided by the square of their height in metres. This is the most widely used measure for identifying obesity. The formula using kilograms and metres (or centimetres) is: weight (kg) \/ [height (m)]<sup>2 <\/sup>. The formula using pounds and inches is: 703 x weight (lbs) \/ [height (in)]<sup>2 <\/sup>. Use of the BMI is controversial for several reasons, including that it does not take into account age, bone structure, muscle mass, fat distribution, or ethnic and racial differences in body type.<\/p>\n<p class=\"import-Normal\"><strong>Cancer<\/strong>: A collection of related diseases in which some of the body\u2019s cells begin to divide without stopping and spread into surrounding tissues.<\/p>\n<p class=\"import-Normal\"><strong>Cardiovascular disease (CVD)<\/strong>: A disease of the heart and blood vessels, often related to atherosclerosis. CVD is a condition in which a substance called plaque builds up in the walls of the arteries, the blood vessels that carry blood away from the heart, which compromises the flow of blood to the heart or brain.<\/p>\n<p class=\"import-Normal\"><strong>Central nervous system<\/strong>: The complex of nerve tissues stemming from the brain and spinal cord that controls the activities of the body.<\/p>\n<p class=\"import-Normal\"><strong>Circulatory (system)<\/strong>: The biological system that circulates blood around the body via the heart, arteries, and veins, delivering oxygen and nutrients to organs and cells and carrying waste products away.<\/p>\n<p class=\"import-Normal\"><strong>Diabetes mellitus<\/strong>: An endocrine disorder in which high glucose (blood sugar) levels occur over a prolonged period of time. Blood glucose is your body\u2019s main source of energy and comes from the food you eat. Insulin, a hormone made by the pancreas, helps glucose from food get into your cells to be used for energy. Sometimes your body does not make enough\u2014or any\u2014insulin (type 1 diabetes) or does not take up insulin well (type 2 diabetes). Glucose then stays in your blood and does not reach your cells.<\/p>\n<p class=\"import-Normal\"><strong>\u201cDouble burden\u201d<\/strong>: Refers to parts of the world in which there is a prevalence of chronic disease (e.g., cancer, heart disease) while, at the same time, there are also high rates of infectious disease due to poverty, malnutrition, poor sanitation, and lack of access to health care, often accompanied by high rates of maternal and child mortality.<\/p>\n<p class=\"import-Normal\"><strong>Ecological model<\/strong>: Ecological models of health and disease emphasize environmental and policy contexts of behaviour, while incorporating social and psychological influences, rather than focusing on individual behaviours. These models encompass multiple levels of influence and can lend themselves to more comprehensive health interventions.<\/p>\n<p class=\"import-Normal\"><strong>Emerging infectious diseases (EIDs)<\/strong>: Infections that have recently appeared within a population or those whose incidence or geographic range is rapidly increasing or threatens to increase in the near future. Examples include Covid-19, Ebola, Zika, SARS, and avian (bird) flu.<\/p>\n<p class=\"import-Normal\"><strong>Endocrine system<\/strong>: Those organs in the body whose primary function is the production of hormones.<\/p>\n<p class=\"import-Normal\"><strong>Epidemiological transition<\/strong>: A transformation in patterns of disease (morbidity) and death (mortality) among a population.<\/p>\n<p class=\"import-Normal\"><strong>Glycemic index (GI)<\/strong>: A system that ranks foods on a scale from 1 to 100 based on their effect on blood-sugar levels. Carbohydrates with a low GI value (55 or less) are more slowly digested and metabolized causing a lower, slower rise in blood glucose and insulin levels.<\/p>\n<p class=\"import-Normal\"><strong>Hypertension<\/strong>: High blood pressure. Blood pressure is the force exerted by the blood against the walls of the blood vessels. In a blood pressure reading, the top number (usually higher) refers to the systolic pressure, the amount of pressure in your arteries during the contraction of your heart muscle when your heart beats. The bottom number is the diastolic pressure when your heart muscle is resting between beats. Hypertension can lead to severe health complications and increases the risk of heart attack and stroke.<\/p>\n<p class=\"import-Normal\"><strong>Incidence<\/strong>: The rate at which new cases of a disease occur in a population over a given period of time.<\/p>\n<p class=\"import-Normal\"><strong>Insulin<\/strong>: A hormone produced in the pancreas that regulates the amount of glucose in the blood. Lack of insulin or the inability to absorb insulin causes diabetes.<\/p>\n<p class=\"import-Normal\"><strong>Metabolic syndrome<\/strong>: A cluster of conditions, including increased blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol levels that occur together, increasing the risk of heart disease, stroke, and diabetes. Lifestyle changes like losing weight, exercising regularly, and making dietary changes can help prevent or reverse metabolic syndrome.<\/p>\n<p class=\"import-Normal\"><strong>Menarche<\/strong>: The first occurrence of menstruation.<\/p>\n<p class=\"import-Normal\"><strong>Morbidity<\/strong>: The number of cases of disease per unit of population occurring over a unit of time.<\/p>\n<p class=\"import-Normal\"><strong>Mortality<\/strong>: The number of deaths attributable to a particular cause per unit of population over a unit of time.<\/p>\n<p class=\"import-Normal\"><strong>Noncommunicable diseases (NCDs)<\/strong>: Also known as chronic diseases, NCDs tend to be of long duration and are the result of a combination of genetic, physiological, environmental, and behaviour factors. The main types of NCDs are cardiovascular diseases (like heart attacks and stroke<strong>)<\/strong>, cancers, chronic respiratory diseases (such as chronic obstructive pulmonary disease and asthma), and diabetes.<\/p>\n<p class=\"import-Normal\"><strong>Obesity<\/strong>: A medical condition in which excess body fat has accumulated to the point that it has adverse effects on health. Although controversial due to its lack of ethnic and racial specificity, the most widely used measure for identifying obesity is the body mass index (BMI), a person\u2019s weight in kilograms divided by the square of their height in metres. A measure of 30 kg\/m<sup>2<\/sup> is considered obese and 25\u201329 kg\/m<sup>2<\/sup> is considered overweight. Distribution of body fat also matters. Fat in the abdominal region has a stronger association with type 2 diabetes and cardiovascular disease, meaning waist-to-hip ratio and waist circumference are also important indicators of obesity-related health risk.<\/p>\n<p class=\"import-Normal\"><strong>Obesogenic<\/strong>: Promoting excessive weight gain.<\/p>\n<p class=\"import-Normal\"><strong>Omnivorous<\/strong>: Able to eat and digest foods of both plant and animal origins.<\/p>\n<p class=\"import-Normal\"><strong>Osteoarthritis<\/strong>: Refers to the degeneration of joint cartilage and underlying bone, causing pain and stiffness. In the absence of previous injury, it is most common in modern populations from middle age onward.<\/p>\n<p class=\"import-Normal\"><strong>Prevalence<\/strong>: The proportion of individuals in a population who have a particular disease or condition at a given point in time.<\/p>\n<p class=\"import-Normal\"><strong>Sedentarism<\/strong>: A way of life characterized by much sitting and little physical activity.<\/p>\n<p class=\"import-Normal\"><strong>Sedentism<\/strong>: Living in groups settled permanently in one place.<\/p>\n<p class=\"import-Normal\"><strong>Stress response<\/strong>: A predictable response to any significant threat to homeostasis. The human stress response involves the <strong>Central Nervous System<\/strong> and the endocrine system acting together. Sudden and severe stress incites the \u201cflight or flight\u201d response from the autonomic nervous system in conjunction with hormones secreted by the adrenal and pituitary glands, increasing our heart rate and breathing and releasing glucose from the liver for quick energy.<\/p>\n<p class=\"import-Normal\"><strong>Stroke<\/strong>: A stroke occurs when a blood vessel leading to the brain is blocked or bursts, preventing that part of the brain from receiving blood and oxygen, leading to cell death.<\/p>\n<p class=\"import-Normal\"><strong>Syndemic<\/strong>: The aggregation (grouping together) of two or more diseases or health conditions in a population in which there is some level of harmful biological or behavioural interface that exacerbates the negative health effects of any or all of the diseases involved. Syndemics involve the adverse interaction of diseases of all types, including infections, chronic noncommunicable diseases, mental health problems, behavioural conditions, toxic exposure, and malnutrition.<\/p>\n<p class=\"import-Normal\"><strong>Tricep skinfold measurement<\/strong>: The triceps skinfold site is a common location used for the assessment of body fat using skinfold calipers. A section of skin on the posterior (back) surface of the arm that lays atop the tricep muscle is pinched between calipers. The resulting measurement is matched against a chart standardized for age and gender.<\/p>\n<p class=\"import-Normal\"><strong>\u201cTriple burden\u201d<\/strong>: A fourth epidemiological transition currently underway in which some parts of the globe are suffering from the \u201cdouble burden\u201d of infectious and chronic diseases combined with injuries and diseases related to intensifying globalization, urbanization, deforestation, and climate change.<\/p>\n<p class=\"import-Normal\"><strong>Vector-borne diseases<\/strong>: Human illnesses caused by parasites, viruses, and bacteria that are transmitted by mosquitoes, flies, ticks, mites, snails, and lice.<\/p>\n<p class=\"import-Normal\"><strong>Zoonoses<\/strong>: Diseases that can be transmitted from animals to humans.<\/p>\n<h2 class=\"import-Normal\">For Further Exploration<strong><br \/>\n<\/strong><\/h2>\n<p>Lents, Nathan H. 2018. <em>Human Errors: A Panorama of Our Glitches, from Pointless Bones to <\/em><em>Broken Genes<\/em>. Boston: Houghton Mifflin Harcourt.<\/p>\n<p>Stearns, Stephen C., and Jacob C. Koella, eds. 2008. <em>Evolution in Health and Disease<\/em>. 2nd edition. United Kingdom: Oxford University Press.<\/p>\n<p>Zuk, Marlene. 2013. <em>Paleofantasy: What Evolution Really Tells Us about Sex, Diet, and <\/em><em>How We Live<\/em>. New York: W. W. Norton &amp; Company.<\/p>\n<h2 class=\"import-Normal\">References<\/h2>\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Abid, Zaynah, Amanda J. Cross, and Rashmi Sinha. 2014. \u201cMeat, Dairy, and Cancer.\u201d <em>The American Journal of Clinical Nutrition<\/em> 100 (S1): 386S\u2013393S.<\/p>\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Akil, Luma, and H. Anwar Ahmad. 2011. \u201cRelationships between Obesity and Cardiovascular Diseases in Four Southern States and Colorado.\u201d <em>Journal of Health Care for the Poor and Underserved<\/em> 22 (S4): 61\u201372.<\/p>\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Ali, Aus Tariq. 2014. \u201cReproductive Factors and the Risk of Endometrial Cancers.\u201d <em>International Journal of Gynecological Cancer<\/em> 24 (3): 384\u2013393.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">American Heart Association. 2018. \u201cHeart Disease and Stroke Statistics-2018 Update: A Report.\u201d <em>Circulation 137<\/em> (12). 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N.d. \u201cGlobal Health &#8211; Pakistan.\u201d Accessed April 4, 2023. https:\/\/www.cdc.gov\/globalhealth\/countries\/pakistan\/default.htm.<\/p>\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Centers for Disease Control and Prevention (CDC). 2014. \u201cBreastfeeding Report Card: United States\/2014.\u201d Atlanta, GA: Centers for Disease Control and Prevention.<\/p>\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Centers for Disease Control and Prevention (CDC). 2020. <em>National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States<\/em>. 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Rosalie, and Michael Zimmerman. 2010. \u201cCancer: An Old Disease, A New Disease or Something In Between?\u201d <em>Nature Reviews: Cancer<\/em> 10 (10): 728\u2013733.<\/p>\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Davis, Mike. 2005. <em>The Monster at Our Door: The Global Threat of Avian Flu<\/em>. New York: Owl Books.<\/p>\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">de Silva, A. M., K. R. Walder, T. J. Aitman, T. Gotoda, A. P. Goldstone, A. M. Hodge, M. P. de Courten, P. Z. Zimmet, and G. R. Collier. 1999. \u201cCombination of Polymorphisms in OB-R and the OB <span style=\"color: #333333\">Gene<\/span> Associated with Insulin Resistance in Nauruan Males.\u201d <em>International Journal of Obesity<\/em> 23 (8): 816\u2013822.<\/p>\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Dimsdale, Joel E. 2008. \u201cPsychological Stress and Cardiovascular Disease.\u201d Journal of the American College of Cardiology 51 (13): 1237\u20131246.<\/p>\n<p class=\"import-Normal\" style=\"background-color: #ffffff;color: #ffffff;margin-left: 0pt;margin-right: -12pt;text-indent: 0pt\"><span style=\"color: #333333\">Ding, Ding, Joe Van Buskirk, Binh Nguyen, Emmanuel Stammotakis, Mona Elbarbary, Nicole Veronese, Philip J. 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Boyd, Melvin Konner, and Marjorie Shostak. 1988. \u201cStone Agers in the Fast Lane: Chronic Degenerative Diseases in Evolut<\/span>ionary Perspective.\u201d <em>American Journal of Medicine<\/em> 84 (4): 739\u2013749.<\/p>\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Eaton, S. Boyd, Malcolm C. Pike, Roger V. Short, Nancy C. Lee, James Trussell, Robert A. Hatcher, James W. Wood, et al. 1994. \u201cWomen\u2019s Reproductive Cancers in Evolutionary Context.\u201d <em>The Quarterly Review of Biology<\/em> 69 (3): 353\u2013367.<\/p>\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Ewald, Paul W. 2018. \u201cAncient Cancers and Infection-Induced Oncogenesis.\u201d <em>International Journal of Paleopathology<\/em> 21: 178\u2013185. https:\/\/dx.doi.org\/10.1016\/J.ijpp.2017.08.007.<\/p>\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Farb, Peter, and George Armelagos. 1980. <em>Consuming Passions: The Anthropology of Eating<\/em>. New York: Washington Square Press.<\/p>\n<p class=\"import-Normal\" style=\"background-color: transparent;text-align: left;margin-left: 0pt;margin-right: 0pt;text-indent: 0pt\">Fawzi, Ashraf, Tianshi David Wu, Kunbo Wang, Matthew L. 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Stains. 2012. \u201cObesity and Cancer Risk: Evidence, Mechanisms, and Recommendations.\u201d Special issue, \u201cNutrition and Physical Activity in Aging, Obesity, and Cancer,\u201d <em>Annals of the New York Academy of Sciences<\/em> 1271 (1): 37\u201343.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Walker, Polly, Pamela Rhubart-Berg, Shawn McKenzie, Kristin Kelling, and Robert S. Lawrence. 2005. \u201cPublic Health Implications of Meat Production and Consumption.\u201d <em>Public Health Nutrition<\/em> 8 (4): 348\u2013356.<\/p>\n<p class=\"import-Normal\">Washington, Harriet A. 2006. <em>Medical Apartheid: The Dark History of Medical Experimentation on Black Americans from Colonial Times to the Present.<\/em> New York: Anchor Books.<\/p>\n<p class=\"import-Normal\">Williams, David R., and Selina A. Mohammed. 2013. \u201cRacism and Health I: Pathways and Scientific Evidence.\u201d <em>American Behavioral Scientist<\/em> 57 (8). https:\/\/doi.org\/<a class=\"rId87\" href=\"https:\/\/doi.org\/10.1177%2F0002764213487340\" target=\"_blank\">10.1177\/0002764213487340. <\/a><\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Williams, David R., and Ronald Wyatt. 2015. \u201cRacial Bias in Health Care and Health: Challenges and Opportunities.\u201d <em>JAMA <\/em>314 (6): 555\u2013556. https:\/\/doi.org10.1001\/jama.2015.9260.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Wolfe, Nathan, Claire P. Dunavan, and Jared Diamond. 2012. \u201cOrigins Of Major Human Infectious Diseases.\u201d In <em>Institute of Medicine: Improving Food Safety through a One Health Approach: Workshop Summary<\/em>, A16. Washington, DC: National Academies Press. Accessed April 4, 2023. https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK114494\/.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">World Health Organization (WHO). 2016. <em>Global Report on Diabetes<\/em>. Accessed April 4, 2023. https:\/\/apps.who.int\/iris\/bitstream\/handle\/10665\/204871\/9789241565257_eng.pdf.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">World Health Organization (WHO). 2017. \u201cObesity and Overweight.\u201d Fact Sheet. Last modified June 9, 2021; accessed April 4, 2023. https:\/\/www.who.int\/mediacentre\/factsheets\/fs311\/en\/.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">World Health Organization (WHO). 2018. \u201cCancer.\u201d Fact Sheet. Last modified February 3, 2022; accessed April 5, 2023. https:\/\/www.who.int\/news-room\/fact-sheets\/detail\/cancer.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Worobey, Michael, Joshua I. Levy, Lorena Malpica Serrano, Alexander Crits-Christoph, Jonathan E. Pekar, Stephan A. Goldstein, Angela L. Rassmussen, et al. July 26, 2022. \u201cThe Huanan Seafood Wholesale Market in Wuhan was the Early Epicenter of the COVID-19 Pandemic.\u201d <em>SCIENCE <\/em>26 (377): 951\u2013959. <a class=\"rId88\" href=\"https:\/\/doi.org\/10.1126\/science.abp8715\" target=\"_blank\">https:\/\/doi.org\/10.1126\/science.abp8715<\/a>.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Worthman, Carol M., and Jennifer Kuzara. 2005. \u201cLife History and the Early Origins of Health Differentials.\u201d <em>American Journal of Human Biology<\/em> 17 (1): 95\u2013112.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Wrangham, Richard. 2009. <em>Catching Fire: How Cooking Made Us Human<\/em>. New York: Basic Books.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Yehuda, Rachel, and Joseph LeDoux. 2007. \u201cResponse Variation Following Trauma: A Translational Neuroscience Approach to Understanding PTSD.\u201d <em>Neuron<\/em> 56 (1): 19\u201332.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Zuckerman, Molly K., and George J. Armelagos. 2014. \u201cThe Hygiene Hypothesis and the Second Epidemiologic Transition.\u201d In <em>Modern Environments and Human Health: Revisiting the Second Epidemiologic Transition<\/em>, edited by Molly K. Zuckerman, 301\u2013320. Hoboken, NJ: Wiley-Blackwell.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Zuckerman, Molly Kathleen, Kristin Nicole Harper, Ronald Barrett, and George John Armelagos. 2014. \u201cThe Evolution of Disease: Anthropological Perspectives on Epidemiologic Transitions.\u201d Special issue, \u201cEpidemiological Transitions: Beyond Omran\u2019s Theory,\u201d <em>Global Health Action<\/em> 7 (1): 23303. https:\/\/doi.org\/10.3402\/gha.v7.23303.<\/p>\n<\/div>\n<\/div>\n<div class=\"glossary\"><span class=\"screen-reader-text\" id=\"definition\">definition<\/span><template id=\"term_1699_1912\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_1699_1912\"><div tabindex=\"-1\"><\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_1699_1953\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_1699_1953\"><div tabindex=\"-1\"><\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_1699_1913\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_1699_1913\"><div tabindex=\"-1\"><\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_1699_1908\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_1699_1908\"><div tabindex=\"-1\"><\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_1699_1907\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_1699_1907\"><div tabindex=\"-1\"><div class=\"__UNKNOWN__\">\n<p class=\"import-Normal\">Michael B. C. Rivera, Ph.D., University of Cambridge<\/p>\n<p class=\"import-Normal\"><em>This chapter is a revision from <\/em><em>\"<\/em><a class=\"rId7\" href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/chapter\/__unknown__-12\/\"><em>Chapter 13: Race and Human Variation<\/em><\/a><em>\u201d by Michael B. C. Rivera. In <\/em><a class=\"rId8\" href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/\"><em>Explorations: An Open Invitation to Biological Anthropology, first edition<\/em><\/a><em>, edited by Beth Shook, Katie Nelson, Kelsie Aguilera, and Lara Braff, which is licensed under <\/em><a class=\"rId9\" href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\"><em>CC BY-NC 4.0<\/em><\/a><em>. <\/em><\/p>\n<div class=\"textbox textbox--learning-objectives\">\n<header class=\"textbox__header\">\n<h2 class=\"textbox__title\">Learning Objectives<\/h2>\n<\/header>\n<div class=\"textbox__content\">\n<ul>\n<li>Illustrate the troubling history of \u201crace\u201d concepts.<\/li>\n<li>Explain human variation and evolution as the thematic roots of biological anthropology as a discipline.<\/li>\n<li>Critique earlier \u201crace\u201d concepts based on a contemporary understanding of the apportionment of human genetic variation.<\/li>\n<li>Explain how biological variation in humans is distributed clinally and in accordance with both isolation-by-distance and Out-of-Africa models.<\/li>\n<li>Identify phenotypic traits that reflect selective and neutral evolution.<\/li>\n<li>Extend this more-nuanced view of human variation to today\u2019s research, the implications for biomedical studies, applications in forensic anthropology, and other social\/cultural\/political concerns.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<p>Humans exhibit biological variation. Humans also have a universal desire to categorize other humans in order to make sense of the world around them. Since the birth of the discipline of <strong>biological anthropology, <\/strong>we have been interested in studying how humans vary biologically and what the sources of this variation are. Before we tackle these big problems, first consider this question: Why <em>should<\/em> we study human variation?<\/p>\n<figure style=\"width: 429px\" class=\"wp-caption alignright\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2023\/06\/image26-3.png\" alt=\"Culturally and biologically diverse humans.\" width=\"429\" height=\"429\" \/><figcaption class=\"wp-caption-text\">Figure 14.1: Humans are culturally diverse (in that cultural differences contribute to a great degree of variation between individuals), but those shown are genetically undiverse. (Top left: Hadzabe members in Tanzania; top right: Inuit family; bottom left: Andean man in Peru; bottom right: English woman.) Credit: <a class=\"rId11\" href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/chapter\/__unknown__-12\/\">Humans are diverse (Figure 13.1)<\/a> original to <a class=\"rId12\" href=\"https:\/\/pressbooks-dev.oer.hawaii.edu\/explorationsbioanth\/\">Explorations: An Open Invitation to Biological Anthropology<\/a> by Michael Rivera is a collective work under a <a class=\"rId13\" href=\"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/\">CC BY-NC-SA 4.0<\/a> license. [Includes <a class=\"rId14\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Tanzania_-_Hadzabe_hunter_(14533536392).jpg\">Tanzania - Hadzabe hunter (14533536392)<\/a> by <a class=\"rId15\" href=\"https:\/\/www.flickr.com\/people\/67947877@N06\">A_Peach<\/a>, <a class=\"rId16\" href=\"https:\/\/creativecommons.org\/licenses\/by\/2.0\/legalcode\">CC BY 2.0<\/a>; <a class=\"rId17\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Inuit-Kleidung_1.jpg\">Inuit-Kleidung 1<\/a> by Ansgar Walk, <a class=\"rId18\" href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/3.0\/legalcode\">CC BY-SA 3.0<\/a>; <a class=\"rId19\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Andean_Man.jpg\">Andean Man<\/a> by <a class=\"rId20\" href=\"https:\/\/commons.wikimedia.org\/wiki\/User:Cacophony\">Cacophony<\/a>, <a class=\"rId21\" href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/4.0\/legalcode\">CC BY-SA 4.0<\/a>; <a class=\"rId22\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Jane_Goodall_GM.JPG\">Jane Goodall GM<\/a> by <a class=\"rId23\" href=\"https:\/\/commons.wikimedia.org\/wiki\/User:Floatjon\">Floatjon<\/a>, <a class=\"rId24\" href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/3.0\/legalcode\">CC BY-SA 3.0<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">There are certainly academic reasons for studying human variation. First, it is highly interesting and important to consider the evolution of our species (see Chapters 10-13) and how our biological variation may be similar to (or different from) that of other species (e.g., other primates and apes; see Chapters 6 and 7). Second, anthropologists study modern human variation to understand how different biological traits developed over evolutionary time (see Figure 14.1). Suppose we are able to grasp the evolutionary processes that produce the differences in biology, physiology, body chemistry, behaviour, and culture (<strong><a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_1699_804\">human variation<\/a><\/strong>). In that case, we can make more accurate inferences about evolution and adaptation among our hominin ancestors, complementing our study of fossil evidence and the archaeological record. Third, as will be discussed in more detail later on, it is important to consider that biological variation among humans has biomedical, forensic, and sociopolitical implications. For these reasons, the study of human variation and evolution has formed the basis of anthropological inquiry for centuries and continues to be a major source of intrigue and inspiration for scientific research conducted today.<\/p>\n<p class=\"import-Normal\">An even-more-important role of the biological anthropologist is to improve public understanding of human evolution and variation\u2014outside of academic circles. Terms such as <strong>race<\/strong> and <strong>ethnicity<\/strong> are used in everyday conversations and in formal settings within and outside academia. The division of humankind into smaller, discrete categories is a regular occurrence in day-to-day life. This can be seen regularly when governments acquire census data with a heading like \u201cgeographic origin\u201d or \u201cethnicity.\u201d Furthermore, such checkboxes and drop-down lists are commonly seen as part of the identifying information required for surveys and job applications.<\/p>\n<p class=\"import-Normal\">According to professors of anthropology, ethnic studies, and sociology, race is often understood as rooted in biological differences, ranging from such familiar traits as skin colour or eye shape to variations at the genetic level. However, race can also be studied as an \u201cideological construct\u201d that goes beyond biological and genetic bases (Fuentes Et al. 2019), at different times relating to our ethnicities, languages, religious beliefs, and cultural practices. Sometimes people associate racial identity with the concept of socioeconomic status or position, or they link ideas about race to what passport someone has, how long they have been in a country, or how well they have \u201cintegrated\u201d into a population.<\/p>\n<p class=\"import-Normal\">Some of these ideas about ethnicity have huge social and political impacts, and notions of race have been part of the motivation behind various forms of racism and prejudice today, as well as many wars and genocides throughout history. <strong>Racism<\/strong> manifests in many ways\u2014from instances of bullying between kids on school playgrounds to underpaid minorities in the workforce, and from verbal abuse hurled at people of colour to violent physical behaviours against those of a certain race. <strong>Prejudice<\/strong> can be characterized as negative views toward another group based on some perceived characteristic that makes all members of that group worthy of disdain, disrespect, or exclusion (not solely along racial lines but also according to [dis]ability, gender, sexual orientation, or socioeconomic background, for example). According to Shay-Akil McLean (2014), \u201cRacism is not something particular to the United States and race is not the same everywhere in the world. Racial categories serve particular contextual purposes depending on the society they are used in, but generally follow the base logic of the supremacy of one type of human body over all others (ordering these human bodies in a hierarchical fashion).\u201d Choosing which biological or nonbiological features to use when discussing race is always a social process (Omi and Winant 2014). Race concepts have no validity to them unless people continue to use them in their daily lives\u2014and, in the worst cases, to use them to justify racist behaviours and problematic ideas about racial difference or superiority\/inferiority. Recent work in anthropological genetics has revealed the similarities amongst humans on a molecular level and the relatively few differences that exist between populations (Omi and Winant 2014).<\/p>\n<p class=\"import-Normal\">The role of the biological anthropologist becomes crucial in the public sphere, because we may be able to debunk myths surrounding human variation and shed light, for the nonanthropologists around us, on how human variation is actually distributed worldwide (see Figure 14.1). Rooted in scientific observations, our work can help nonanthropologists recognize how common ideas about \u201crace\u201d often have no biological or genetic basis. Many anthropologists work hard to educate students on the history of where race concepts come from, why and how they last in public consciousness, and how we become more conscious of racial issues and the need to fight against racism in our societies. Throughout this chapter, I will highlight how humans cannot actually be divided into discrete \u201craces,\u201d because most traits vary on a continuous basis and human biology is, in fact, very <strong>homogenous<\/strong> compared to the greater genetic variation we observe in closely related species. Molecular anthropology, or anthropological genetics, continues to add new layers to our understanding of human biological variation and the evolutionary processes that gave rise to the contemporary patterns of human variation. The study of human variation has not always been unbiased, and thinkers and scientists have always worked in their particular sociohistorical context. For this reason, this chapter opens with a brief overview of race concepts throughout history, many of which relied on unethical and unscientific notions about different human groups.<\/p>\n<\/div>\n<div class=\"textbox\">\n<h2 class=\"import-Normal\">Special Topic: My Experiences as an Asian Academic<\/h2>\n<figure style=\"width: 578px\" class=\"wp-caption aligncenter\"><img class=\"\" src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image10-4.jpg\" alt=\"Outdoor photo of this chapter\u2019s author.\" width=\"578\" height=\"433\" \/><figcaption class=\"wp-caption-text\">Figure 14.2: Michael B. C. Rivera in Hong Kong. Credit: Michael B. C. Rivera in Hong Kong original to Explorations: An Open Invitation to Biological Anthropology (2nd ed.) is under a <a class=\"rId26\" href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\">CC BY-NC 4.0 License<\/a>.<\/figcaption><\/figure>\n<p>My name is Michael, and I am a biological anthropologist and archaeologist (Figure 14.2). What strikes me as most interesting to investigate is human biological variation today and the study of past human evolution. For instance, some of my research on ancient coastal populations has revealed positive effects of coastal living on dietary health and many unique adaptations in bones and teeth when living near rivers and beaches. I love talking to students and nonscientists about bioanthropologists\u2019 work, through teaching, science communication events, and writing book chapters like this one. I grew up in Hong Kong, a city in southern China. My father is from the Philippines and my mother is from Hong Kong, which makes me a mixed Filipino-Chinese academic. Growing up, I noticed that people came in all shapes, sizes, and colours. My life is very different now in that I have gained the expertise to explain those differences, and I feel a great responsibility to guide those new to anthropology toward their own understandings of diversity.<\/p>\n<p class=\"import-Normal\">Biological anthropology is not taught extensively in Hong Kong, so I moved to the United Kingdom to earn my bachelor\u2019s, master\u2019s, and doctorate degrees. It was fascinating to me that we could answer important questions about human variation and history using scientific methods. However, I did not have many minority academic role models to look up to while I was at university. My department was made up almost exclusively of white westerner faculty, and it was hard to imagine I could one day get a job at these western institutions. While pursuing my degrees, I also remember several instances of my research contributions being overlooked or dismissed. Sometimes professors and fellow students would make racist comments toward Asian scholars (including me) and other Black, Indigenous and researchers of colour, making us greatly uncomfortable in those spaces. When one of us would work up the courage to tell university leaders our experiences of being stereotyped, dismissed, or insulted, we received little support and were further excluded from research and teaching activities. This is a common experience for Black, Indigenous, and other people of colour who pursue biological anthropology, and we face the difficult choice between leaving the field or bearing with such unsafe spaces.<\/p>\n<p class=\"import-Normal\">It became important to me at that time to find other academics of colour with whom to share experiences and form community. I feel inspired by all my colleagues who advocate for greater representation and diversity in universities (whether they are minority academics or not). I admire many of my fellow researchers who are underrepresented and do a great job of representing minority groups through their cutting-edge research and quality teaching at the undergraduate and graduate levels. Although I no longer work in the West, it has remained my great hope that those in the West and the \u201cGlobal North\u201d will continue to improve university culture, and I support any efforts there to welcome all scholars.<\/p>\n<p class=\"import-Normal\">My current work is based in Hong Kong, where I am deeply dedicated to helping develop biological anthropology in East and Southeast Asia and promoting research from our home regions on the international scene. The study of anthropology really highlights how we share a common humanity and history. Being somebody who is \u201cmixed race\u201d and Asian likely played a key role in steering me toward the study of human variation. As this chapter hopefully shows, there is a lot to discuss about race and ethnicity regarding the discipline\u2019s history and current understandings of <strong>human diversity<\/strong>. Some scientific and technological advancements today are misused for reasons to do with money, politics, or the continuation of antiquated ideas. It is my belief, alongside many of my friends and fellow anthropologists, that science should be more about empathy toward all members of our species and contributing to the intellectual and technological nourishment of society. After speaking to many members of the public, as well as my own undergraduate students, I have received lovely messages from other individuals of colour expressing thanks and appreciation for my presence and understanding as a minority scientist and mentor figure. Anthropology needs much more diversity as well as to make room for those who have traveled different routes into the discipline. All paths taken into anthropology are valid and valuable. I would encourage everyone to study anthropology\u2014it is a field for understanding and celebrating the intricacies of human diversity.<\/p>\n<\/div>\n<div class=\"__UNKNOWN__\">\n<h2 class=\"import-Normal\">The History of \"Race\" Concepts<\/h2>\n<h3 class=\"import-Normal\"><strong>\u201cRace\u201d in the Classical Era<\/strong><\/h3>\n<figure style=\"width: 435px\" class=\"wp-caption alignleft\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image11-8.png\" alt=\"Painting of four individuals with varied skin colors, head hair, facial hair, and clothing styles.\" width=\"435\" height=\"331\" \/><figcaption class=\"wp-caption-text\">Figure 14.3: (From left to right) Depicting a Berber (Libyan), a Nubian, an Asiatic (Levantine), and an Egyptian, copied from a mural on the tomb of Seti I. Credit: Egyptian races drawing by Heinrich von Minutoli (1820) of a mural by an unknown artist from the tomb of Seti I is in the public domain.<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The earliest classification systems used to understand human variation are evidenced by ancient manuscripts, scrolls, and stone tablets recovered through archaeological, historical, and literary research. The Ancient Egyptians had the <em>Book of Gates<\/em>, dated to the New Kingdom between 1550 B.C.E. and 1077 B.C.E (Figure 14.3). In one part of this tome dedicated to depictions of the underworld, scribes used pictures and hieroglyphics to illustrate a division of Egyptian people into the four categories known to them at the time: the Aamu (Asiatics), the Nehesu (Nubians), the Reth (Egyptians), and the Themehu (Libyans). Though not rooted in any scientific basis like our current understandings of human variation today, the Ancient Egyptians believed that each of these groups were made of a distinctive category of people, distinguishable by their skin colour, place of origin, and even behavioural traits.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Another well-known early document is the Bible, where it is written that all humankind descends from one of three sons of Noah: Shem (the ancestor to all olive-skinned Asians), Japheth (the ancestor to pale-skinned Europeans), and Ham (the ancestor to darker-skinned Africans). Similar to the Ancient Egyptians, these distinctions were based on behavioural traits and skin colour. More recent work in historiography and linguistics suggest that the branches of \u201cHamites,\u201d \u201cJaphethites,\u201d and \u201cShemites\u201d may also relate to the formation of three independent language groups some time between 1000 and 3000 B.C.E. With the continued proliferation of Christianity, this concept of approximately three racial groupings lasted until the Middle Ages and spread as far across Eurasia as crusaders and missionaries ventured at the time.<\/p>\n<figure style=\"width: 309px\" class=\"wp-caption alignright\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image9-9.png\" alt=\"Rows of organisms, with plants and animals at the bottom and humans, angels, and God at top.\" width=\"309\" height=\"449\" \/><figcaption class=\"wp-caption-text\">Figure 14.4: The Great Chain of Being from the Rhetorica Christiana by Fray Diego de Valades (1579). Credit: Great Chain of Being 2 by Didacus Valades (Diego Valades 1579) and photographed by Rhetorica Christiana (via Getty Research) is in the public domain.<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">There is also the \u201cGreat Chain of Being,\u201d conceived by ancient Greek philosophers like Plato (427\u2012348 B.C.E.) and Aristotle (384\u2012322 B.C.E.). They played a key role in laying the foundations of empirical science, whereby observations of everything from animals to humans were noted with the aim of creating taxonomic categories. Aristotle describes the Great Chain of Being as a ladder along which all objects, plants, animals, humans, and celestial bodies can be mapped in an overall hierarchy (in the order of existential importance, with humans placed near the top, just beneath divine beings; see Figure 14.4). When he writes about humans, Aristotle expressed the belief that certain people are inherently (or genetically) more instinctive rulers, while others are more natural fits for the life of a worker or enslaved person. Based on research by biological anthropologists, we currently recognize that these early systems of classification and hierarchization are unhelpful in studying human biological variation. Both behavioural traits and physical traits are coded for by multiple genes each, and how we exhibit those traits based on our genetics can vary significantly even between individuals of the same population.<\/p>\n<h3 class=\"import-Normal\"><strong>\u201cRace\u201d during the Scientific Revolution<\/strong><\/h3>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The 1400s to 1600s saw the beginnings of the <strong>Scientific Revolution<\/strong> in Western societies, with thinkers like Nicholas Copernicus, Galileo Galilei, and Leonardo Da Vinci publishing some of their most important findings. While by no means the first or only scholars globally to use observation and experimentation to understand the world around them, early scientists living at the end of the medieval period in Europe increasingly employed more experimentation, quantification, and rational thought in their work. This is the main difference between the work of the ancient Egyptians, Romans, and Greeks and that of later scientists such as Isaac Newton and Carl Linnaeus in the 1600s and 1700s.<\/p>\n<figure style=\"width: 215px\" class=\"wp-caption alignleft\"><img class=\"\" src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image24-2.png\" alt=\"Historic painting of a man in 18th-century wig and garments.\" width=\"215\" height=\"259\" \/><figcaption class=\"wp-caption-text\">Figure 14.5: Carl Linnaeus. Credit: <a class=\"rId35\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Carl_von_Linn%C3%A9.png\">Carl von Linn\u00e9<\/a> by <a class=\"rId36\" href=\"https:\/\/en.wikipedia.org\/wiki\/en:Alexander_Roslin\">Alexander Roslin<\/a> (1718-1793) is in the <a class=\"rId37\" href=\"https:\/\/en.wikipedia.org\/wiki\/Public_domain\">public domain<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Linnaeus is the author of <em>Systema Naturae<\/em> (1758), in which he classified all plants and animals under the formalized naming system known as <strong>binomial nomenclature<\/strong> (Figure 14.5). This system is <strong>typological<\/strong>, in that organisms are placed into groups according to how they are similar or different to others under study. What was most anthropologically notable about Linnaeus\u2019s typological system was that he was one of the first to group humans with apes and monkeys, based on the anatomical similarities between humans and nonhuman primates. However, Linnaeus viewed the world in line with <strong>essentialism<\/strong>, a problematic concept that dictates that there are a unique set of characteristics that organisms of a specific kind <em>must<\/em> have and that would remove organisms from taxonomic categorizations if they lacked any of the required criteria.<\/p>\n<p>Linnaeus subdivided the human species into four varieties, with overtly racist categories based on skin colour and \u201cinherent\u201d behaviours. Some European scientists during this period were not aware of their own biases skewing their interpretations of biological variation, while others deliberately worked to shape public perceptions of human variation in ways that established \u201c<strong>otherness<\/strong>\u201d and enforced European domination and the subordination of non-European people. The conclusions and claims at which they arrived, consciously or subconsciously, often fit the times they were living through\u2014the so-called <strong>Age of Discovery<\/strong>, when the superiority of European cultures over others was a pervasive idea throughout people\u2019s social and political lives. Although much of Eurasia was linked by spice- and silk-trading routes, the European colonial period between the 1400s and 1700s was marked by many new and unfortunately violent encounters overseas (Figure 14.6). When Europeans arrived by ship on the shores of continents that were already inhabited, it was their first meeting with the Indigenous peoples of the Americas and Australasia, who looked, spoke, and behaved differently from peoples with whom they were familiar. Building on the idea of species and \u201csubspecies,\u201d natural historians of this time invented the term <em>race<\/em>, from the French <em>rasse<\/em> meaning \u201clocal strain.\u201d<\/p>\n<figure style=\"width: 421px\" class=\"wp-caption alignright\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image25-4.png\" alt=\"Spanish explorers with their military and religious gear surrounding indigenous people.\" width=\"421\" height=\"273\" \/><figcaption class=\"wp-caption-text\">Figure 14.6: A painting depicting the colonization of the Mississippi River environs by Spaniard Hernando DeSoto in 1541 (painted in 1853 by William H. Powell). Credit: <a class=\"rId39\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Discovery_of_the_Mississippi.jpg\">Discovery of the Mississippi<\/a> by <a class=\"rId40\" href=\"https:\/\/en.wikipedia.org\/wiki\/en:William_Henry_Powell\">William Henry Powell<\/a> (photograph courtesy of <a class=\"rId41\" href=\"https:\/\/en.wikipedia.org\/wiki\/Architect_of_the_Capitol\">Architect of the Capitol<\/a>) is in the <a class=\"rId42\" href=\"https:\/\/en.wikipedia.org\/wiki\/Public_domain\">public domain<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\">Another scientist of the times, Johann Friedrich Blumenbach (1752\u20121840), classified humans into five races based on his observations of cranial form variation as well as skin colour. He thus dubbed the \u201coriginal\u201d form of the human cranium the \u201cCaucasian\u201d form, with the idea that the ideal climate conditions for early humans would have been in the Caucasus region near the Caspian Sea. The key insight Blumenbach presented was that human variation in any particular trait should be more accurately viewed as falling along a gradation (Figure 14.7). While some of his theories were correct according to what we observe today with more knowledge in genetics, they erroneously believed that human \u201csubspecies\u201d were \u201cdegenerated\u201d or \u201ctransformed\u201d varieties of an ancestral Caucasian or European race. According to them, the Caucasian cranial dimensions were the least changed over human evolutionary time, while the other skull forms represented geographic variants of this \u201coriginal.\u201d As will be discussed in greater detail later in this chapter, we have genetic and craniometric evidence for sub-Saharan Africa being the origin of the human species instead (see Chapter 13 on the fossil record that places the origins of modern <em>Homo sapiens<\/em> in north and east Africa). Based on work that shows how most biological characteristics are coded for by nonassociated genes, it is not reasonable to draw links between individuals\u2019 personalities and their skull shapes.<\/p>\n<figure style=\"width: 686px\" class=\"wp-caption aligncenter\"><img class=\"\" src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image7-10.png\" alt=\"Historic drawing of five skulls.\" width=\"686\" height=\"259\" \/><figcaption class=\"wp-caption-text\">Figure 14.7: Five skull drawings representing specimens for Blumenbach\u2019s \u201cMongolian,\u201d \u201cAmerican,\u201d \u201cCaucasian,\u201d \u201cMalayan,\u201d and \u201cAethiopian\u201d races. Credit: <a class=\"rId44\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Blumenbach&apos;s_five_races.JPG\">Blumenbach's five races<\/a> by Johann Friedrich Blumenbach is in the <a class=\"rId45\" href=\"https:\/\/en.wikipedia.org\/wiki\/Public_domain\">public domain<\/a>. Original in the 1795 Treatise on \"De generis humani varietate nativa,\" unnumbered page at the end of the book titled \"Tab II\".<\/figcaption><\/figure>\n<h3 class=\"import-Normal\"><strong>\u201cRace\u201d and the Dawn of Scientific Racism<\/strong><\/h3>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Between the 1800s and mid-1900s, and contrary to what you might expect, an increased use of scientific methods to justify racial schemes developed in scholarship. Differing from earlier views, which saw all humans as environmentally deviated from one \u201coriginal\u201d humankind, classification systems after 1800 became more <strong>polygenetic<\/strong> (viewing all people as having separate origins) rather than <strong>monogenetic<\/strong> (viewing all people as having a single origin). Instead of moving closer to our modern-day understandings of human variation, there was increased support for the notion that each race was created separately and with different attributes (intelligence, temperament, and appearance).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The 1800s were an important precursor to modern biological anthropology as we know it, given that this was when the scientific measurement of human physical features (anthropometry) truly became popularized. However, empirical studies in the 1800s pushed even further the idea that Europeans were culturally and biologically superior to others. While considered one of the pioneers of American \u201cphysical\u201d anthropology, Samuel George Morton (1799\u20121851) was a scholar who had a large role in perpetuating 1800s scientific racism. By measuring cranial size and shape, he calculated that \u201cCaucasians,\u201d on average, have greater cranial volumes than other groups, such as the Indigenous peoples of the Americas and peoples Morton referred to collectively as \u201cNegros.\u201d Today, we know that cranial size variation depends on such factors as Allen\u2019s and Bergmann\u2019s rules, which give a more likely explanation: in colder environments, it is advantageous for those living there to have larger and rounder heads because they conserve heat more effectively than more slender heads (Beals Et al. 1984). The leading figures in craniometry during the 1800s instead were linked heavily with powerful individuals and wealthy sociopolitical institutions and financial bodies. Theories in support of hierarchical racial schemes using \u201cscientific\u201d bases certainly helped continue the exploitative and unethical trafficking and enslavement of Africans between the 1500s and 1800s.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Morton went on to write in his publication <em>Crania Americana<\/em> (1839) a number of views that fit with a concept called <strong>biological determinism<\/strong>. The idea behind biological determinism is that an association exists between people\u2019s physical characteristics and their behaviour, intelligence, ability, values, and morals. If the idea is that some groups of people are essentially superior to others in cognitive ability and temperament, then it is easier to justify the unequal treatment of certain groups based on outward appearances. Another such problematic thinker was Paul Broca (1824\u20121880), after whom a region of the frontal lobe related to language use is named (Broca\u2019s area). Influenced by Morton, Broca likewise claimed that internal skull capacities could be linked with skin colour and cognitive ability. He went on to justify the European colonization of other global territories by purporting it was noble for a biologically more \u201ccivilized\u201d population to improve the \u201chumanity\u201d of more \u201cbarbaric\u201d populations. Today, these theories of Morton, Broca, and others like them are known to have no scientific basis. If we could speak with them today, they would likely try to emphasize that their conclusions were based on empirical evidence and not <em>a priori<\/em> reasoning. However, we now can clearly see that their reasoning was biased and affected by prevailing societal views at the time.<\/p>\n<h3 class=\"import-Normal\"><strong>\u201cRace\u201d and the Beginnings of Physical Anthropology<\/strong><\/h3>\n<p class=\"import-Normal\">In the early 20th century, we saw a number of new figures coming into the science of human variation and shifting the theoretical focus within. Most notably, these included Ale\u0161 Hrdli\u010dka and Franz Boas.<\/p>\n<figure style=\"width: 430px\" class=\"wp-caption alignleft\"><img class=\"\" src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image19-4.jpg\" alt=\"Historic photo of a middle-aged person in suit and bowtie.\" width=\"430\" height=\"558\" \/><figcaption class=\"wp-caption-text\">Figure 14.8: Ale\u0161 Hrdli\u010dka (1869\u00ad\u20121943), a Czech anthropologist who founded the American Journal of Physical Anthropology. Credit: <a class=\"rId47\" href=\"https:\/\/siarchives.si.edu\/collections\/siris_sic_10822?back=%2Fcollections%2Fsearch%3Fquery%3Dczech%26online%3Dtrue%26page%3D1%26perpage%3D10%26sort%3Drelevancy%26view%3Dlist#\">(Ales Hrdlicka) SIA2009-4246<\/a> (1903) by an unknown photographer <a class=\"rId48\" href=\"https:\/\/www.si.edu\/termsofuse\">is used for educational and non-commercial purposes as outlined by the Smithsonian.<\/a>. [<a class=\"rId49\" href=\"https:\/\/www.si.edu\/\">Smithsonian Institution<\/a> Archives, Record Unit 9521, Box 1, T. Dale Stewart Oral History Interview; and Record Unit 9528, Box 1, Henry B. Collins Oral History Interview.]<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Ale\u0161 Hrdli\u010dka (1869\u00ad\u20121943) was a Czech anthropologist who moved to the United States. In 1903, he established the physical anthropology section of the National Museum of Natural History (Figure 14.8). In 1918, he founded the <em>American Journal of Physical Anthropology<\/em>, which remains one of the foremost scientific journals disseminating bioanthropological research. As part of his work and the scope of the journal, he differentiated \u201c<strong>physical anthropology<\/strong>\u201d from other kinds of anthropology: he wrote that physical anthropology is \u201cthe study of racial anatomy, physiology, and pathology\u201d and \u201cthe study of man\u2019s variation\u201d (Hrdli\u010dka 1918). In some ways, although the scope and technological capabilities of biological anthropologists have changed significantly, Hrdli\u010dka established an area of inquiry that has continued and prospered for over a hundred years.<\/p>\n<p class=\"import-Normal\">Franz Boas (1858\u20121942) was a German American anthropologist who established the four-field anthropology system in the United States and founded the American Anthropological Association in 1902. He argued that the scientific method should be used in the study of human cultures and the comparative method for looking at human biology worldwide. One of Boas\u2019s significant contributions to biological anthropology was the study of skull dimensions with respect to race. After a long-term research project, he demonstrated how cranial form was highly dependent on cultural and environmental factors and that human behaviours were influenced primarily not by genes but by social learning. He wrote in one essay for the journal <em>Science<\/em>: \u201cWhile individuals differ, biological differences between races are small. There is no reason to believe that one race is by nature so much more intelligent, endowed with great willpower, or emotionally more stable than another, that the difference would materially influence its culture\u201d (Boas 1931:6). This conclusion directly contrasted with the theories of the past that relied on biological determinism. Biological anthropologists today have found evidence that corroborates Boas\u2019s explanations: societies do not exist on a hierarchy or gradation of \u201ccivilizedness\u201d but instead are shaped by the world around them, their demographic histories, and the interactions they have with other groups.<\/p>\n<figure style=\"width: 358px\" class=\"wp-caption alignleft\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image2-7.png\" alt=\"Black-and-white sketch of tree labeled \u201cEugenics.\u201d \" width=\"358\" height=\"275\" \/><figcaption class=\"wp-caption-text\">Figure 14.9: Logo of the Second International Exhibition of Eugenics, held in 1921. The text of the logo states: \"Eugenics is the self-direction of human evolution. Like a tree, eugenics draws its materials from many sources and organizes them into an harmonious entity.\" Credit: <a class=\"rId51\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Eugenics_congress_logo.png\">Eugenics congress logo<\/a> scanned from <a class=\"rId52\" href=\"https:\/\/en.wikipedia.org\/wiki\/Harry_H._Laughlin\">Harry H. Laughlin<\/a>, The Second International Exhibition of Eugenics held September 22 to October 22, 1921, is in the <a class=\"rId53\" href=\"https:\/\/en.wikipedia.org\/wiki\/Public_domain\">public domain<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The first half of the 1900s still involved some research that was essentialist and focused on proving racial determinism. Anthropologists like Francis Galton (1822\u20121911) and Earnest A. Hooton (1887\u20121954) created the field of <strong>eugenics<\/strong> as an attempt to formalize the social scientific study of \u201cfitness\u201d and \u201csuperiority\u201d among members of 19th-century Europe. As a way of \u201cdealing with\u201d criminals, diseased individuals, and \u201cuncivilized\u201d people, eugenicists recommended prohibiting parts of the population from being married or sterilizing these members of society so they could no longer procreate (Figure 14.9). They instead encouraged \u201creproduction in individual families with sound physiques, good mental endowments, and demonstrable social and economic capability\u201d (Hooton 1936). In the 1930s, Nazi Germany used this false idea of there being \u201cpure races\u201d to highly destructive effect. The need to be protected against admixture from \u201cunfit\u201d groups was their justification for their blatant racism and purging of citizens that fell under their subjective criteria.<\/p>\n<p class=\"import-Normal\">It should be noted that eugenicist ideas were popularly discussed and debated in many non-European contexts, as in the U.S., China, and South Africa, too. The Immigration Restriction Act of 1924 was passed in the United States, with the explicit aim of reducing the country\u2019s \u201cburden\u201d of people considered inferior by restricting immigration of eastern European Jews, Italians, Africans, Arabs, and Asians. In the early 1900s, Chinese scientists and politicians showed great interest in eugenic ideologies, which came to dictate decisions in law-making, family life, and the medical field. Noted American anthropologist Ruth Benedict wrote extensively on Japanese culture and society during and after World War II. Her essentialist portrayals of Japanese people were heavily cited in popular discourse at the time. In 1950s South Africa, interracial marriages and sexual relations were banned by law; antimiscegenation became one of the huge focuses of apartheid resistance activists in later years. We still see the continuation of eugenics-based logic today around the world\u2014in exclusionary immigration laws, cases of incarcerated prison inmates being forcibly sterilized, and the persistence of intelligence testing as a form of measuring people\u2019s \u201cfitness\u201d in a society.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Shortly after World War II and the Nazi Holocaust, the full extent of essentialist, eugenicist thinking became clear. Social constructions of race, and the notion that one can predict psychological or behavioural traits based on external appearance, had become unpopular both within and outside the discipline. It was up to those in the field of physical anthropology at the time to separate physical anthropology from race concepts that supported unscientific and socially damaging agendas. This does not mean that there are no physiological or behavioural differences between different members of the human species. However, going forward, a number of physical anthropologists saw human biological variation as more complicated than simple typologies could describe.<\/p>\n<h3 class=\"import-Normal\"><strong>\u201cThe New Physical Anthropology\u201d<\/strong><\/h3>\n<figure style=\"width: 219px\" class=\"wp-caption alignright\"><img class=\"\" src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image14-6.png\" alt=\"Black-and-white photo of a person with short hair in a white shirt and tie.\" width=\"219\" height=\"291\" \/><figcaption class=\"wp-caption-text\">Figure 14.10: Theodosius Dobzhansky, an important scientist who formulated the 20th-century \u201cmodern synthesis\u201d reconciling Charles Darwin\u2019s theory of evolution and Gregor Mendel\u2019s ideas on heredity. Credit: <a class=\"rId55\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Dobzhansky_no_Brasil_em_1943.jpg\">Dobzhansky no Brasil em 1943<\/a> by unknown photographer via <a class=\"rId56\" href=\"https:\/\/www.flickr.com\/photos\/celycarmo\/\">Flickr user Cely Carmo<\/a> is in the <a class=\"rId57\" href=\"https:\/\/en.wikipedia.org\/wiki\/Public_domain\">public domain<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\">After 1950, focus steered away from the concept of \u201crace\u201d as a unit of variation and toward understanding why variation exists in <strong>population<\/strong><strong>s<\/strong> from an evolutionary perspective. This was outlined by those pioneering the \u201cnew physical anthropology,\u201d such as Sherwood Washburn, Theodosius Dobzhansky (Figure 14.10), and Julian Huxley, who borrowed this approach from contemporary population geneticists. Whether using genetic or phenotypic markers as the units of study, \u201cgroups\u201d or \u201cclusters\u201d of humans differentiated by these became defined as populations that differ in the frequency of some gene or genes. Anthropologists consider what \u201cmakes\u201d a population\u2014a group of individuals potentially capable of or actually interbreeding due to shared geographic proximity, language, ethnicity, culture, and\/or values. Put another way, a population is a local interbreeding group with reduced gene flow between themselves and other groups of humans. Members of the same population may be expected to share many genetic traits (and, as a result, many phenotypic traits that may or may not be visible outwardly).<\/p>\n<figure style=\"width: 240px\" class=\"wp-caption alignleft\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image15-6.png\" alt=\"Black-and-white photo of smiling person in a suit and tie in front of a building.\" width=\"240\" height=\"300\" \/><figcaption class=\"wp-caption-text\">Figure 14.11: Julian Huxley (1942). Credit: <a class=\"rId59\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Julian_Huxley_1-2.jpg\">Julian Huxley 1-2<\/a> by unknown photographer is in the <a class=\"rId60\" href=\"https:\/\/en.wikipedia.org\/wiki\/Public_domain\">public domain<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\">Thinking of humans in terms of populations was part of Julian Huxley\u2019s (1942) \u201cModern Synthesis\u201d\u2014so named because it helped to reconcile two fundamental principles about evolution that had not been made sense of together before (Figure 14.11). As discussed in Chapter 4, Gregor Mendel (1822\u20121884) was able to show that inheritance was mediated by discrete particles (or genes) and not blended in the offspring. However, it was difficult for some 19th-century scientists to accept this model of genetic inheritance at the time because much of biological variation appeared to be continuous and not particulate (take skin colour or height as examples). In the 1930s, it was demonstrated that traits could be polygenic and that multiple alleles could be responsible for any one phenotypic trait, thus producing the continuous variation in traits such as eye colour that we see today. Thus, Huxley\u2019s \u201cModern Synthesis\u201d outlines not only how human populations are capable of exchanging genes at the microevolutionary level but also how multiple alleles for one trait (polygenic exchanges) can cause gradual macroevolutionary changes.<\/p>\n<h2 class=\"import-Normal\">Human Variation in Biological Anthropology Today<\/h2>\n<h3 class=\"import-Normal\"><strong>Many Human Traits Are Nonconcordant<\/strong><\/h3>\n<p class=\"import-Normal\">In our studies of human (genetic) variation today, we understand most human traits to be nonconcordant (Figure 14.12). \u201c<strong>Nonconcordance<\/strong>\u201d is a term used to describe how biological traits vary independent of each other\u2014that is, they do not get inherited in a correlative manner with other genetically controlled traits. For example, if you knew an individual had genes that coded for tall height, you would not be able to predict if they are lighter-skinned or have red hair. This is different from earlier essentialist views of human variation: the idea that skin colour could predict one\u2019s brain function or even \u201ctemperament\u201d and tendencies toward criminal behaviour.<\/p>\n<figure style=\"width: 594px\" class=\"wp-caption aligncenter\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image17-2-1.jpg\" alt=\"World map with human silhouettes scattered across the continents.\" width=\"594\" height=\"304\" \/><figcaption class=\"wp-caption-text\">Figure 14.12: Most human biological traits are non-concordant, meaning traits vary independently and each trait has its own pattern of distribution around the world. In this image, different colours and patterns represent trait varieties. For example, the colour and pattern of the head may represent hair colour (dark to light), but sharing dark hair with another person does not mean you will share other traits (e.g. ability to digest lactose or ABO blood type). Credit: Nonconcordance original to Explorations: An Open Invitation to Biological Anthropology (2nd ed.) by Katie Nelson is under a <a class=\"rId62\" href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\">CC BY-NC 4.0 License<\/a>.<\/figcaption><\/figure>\n<h3 class=\"import-Normal\"><strong>Human Variation Is Clinal\/Continuous (Not Discrete)<\/strong><\/h3>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Frank B. Livingstone (1928\u20122005) wrote: \u201cThere are no races, only clines\u201d (1962: 279). A <strong><a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_1699_1875\">cline<\/a><\/strong> is a gradation in the frequency of an allele\/trait between populations living in different geographic regions. Human variation cannot be broken into discrete \u201craces,\u201d because most physical traits vary on a continuous or \u201cclinal\u201d basis. One obvious example of this is how human height does not only come in three values (\u201cshort,\u201d \u201cmedium,\u201d and \u201ctall\u201d) but instead varies across a spectrum of vertical heights achievable by humans all over the world. On the one hand, we can describe human height as exhibiting <strong>continuous <\/strong><strong>variation<\/strong>, forming a continuous pattern, but height does not vary according to where people live across the globe and does not exhibit a clinal pattern. On the other hand, skin colour variation between populations does show patterning that fits quite well on to how near or far they are from each other on a world map. This makes a trait like skin colour clinally distributed worldwide. When large numbers of genetic loci for large numbers of samples were sampled from human populations distributed worldwide during the 1960s and 1970s, the view that certain facets of human diversity were clinally distributed was further supported by genetic data.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">To study human traits that are clinally distributed, genetic tests must be performed to uncover the true frequencies of an allele or trait across a certain geographic space. One easily visible example of a clinal distribution seen worldwide is the patterning of human variation in skin colour. Whether in southern Asia, sub-Saharan Africa, or Australia, dark brown skin is found. Paler skin tones are found in higher-latitude populations such as those who have lived in areas like Europe, Siberia, and Alaska for millennia. Skin colour is easily observable as a phenotypic trait exhibiting continuous variation.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">A clinal distribution still derives from genetic inheritance; however, clines often correspond to some gradually changing environmental factor. Clinal patterns arise when selective pressures in one geographic area differ from those in another as well as when people procreate and pass on genes together with their most immediate neighbours. There are several mechanisms, selective and neutral, that can lead to the clinal distribution of an allele or a biological trait. <strong>Natural selection<\/strong> is the mechanism that produced a global cline of skin colour, whereby darker skin colour protects equatorial populations from high amounts of UV radiation; there is a transition of lessening pigmentation in individuals that reside further and further away from the tropics (Jablonski 2004; Jablonski and Chaplin 2000; see Figure 14.13). The ability and inability to digest lactose (milk sugar) among different world communities varies according to differential practices and histories of milk and dairy-product consumption (Gerbault Et al. 2011; Ingram Et al. 2009). Where malaria seems to be most prevalent as a disease stressor on human populations, a clinal gradient of increasing sickle cell anemia experience toward these regions has been studied extensively by genetic anthropologists (Luzzatto 2012). Sometimes, culturally defined mate selection based on some observable trait can lead to clinal variation between populations as well.<\/p>\n<figure style=\"width: 676px\" class=\"wp-caption aligncenter\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image22-6.png\" alt=\"A global map shaded representing skin colors. \" width=\"676\" height=\"370\" \/><figcaption class=\"wp-caption-text\">Figure 14.13: A global map of skin colours shows that dark skin pigmentation is more common in areas that receive more UV radiation (near the equator and in high altitude areas). Light skin is more common at northern and southern latitudes. It is worth bearing in mind, though, that these do not tell the full story of how human skin pigmentation varies worldwide. Each region will contain populations that exhibit a range of skin tones. In this way, this map is not perfect as an illustration of skin-colour distribution. Credit: Mercator style projection map showing human skin colour according to Biasutti 1940.png by Dark Tichondrias at English Wikipedia, modified (cropped) by Tuvalkin, is under a CC BY-SA 4.0 License.<\/figcaption><\/figure>\n<p class=\"import-Normal\">Two neutral microevolutionary processes that may produce a cline in a human allele or trait are <strong>gene flow<\/strong> and <strong>genetic drift <\/strong>(see Chapter 5). The ways in which neutral processes can produce clinal distributions is seen clearly when looking at clinal maps for different blood groups in the human ABO blood group system (Figure 14.14). For instance, scientists have identified an East-to-West cline in the distribution of the blood type <em>B<\/em> allele across Eurasia. The frequency of <em>B<\/em> allele carriers decreases gradually westward when we compare the blood groups of East and Southeast Asian populations with those in Europe. This shows how populations residing nearer to one another are more likely to interbreed and share genetic material (i.e., undergo gene flow). We also see 90%\u2012100% of native South American individuals, as well as between 70%\u201290% of Aboriginal Australian groups, carrying the <em>O<\/em> allele (Mourant, \u200b\u200bKope\u0107, and Domaniewska-Sobczak 1976). These high frequencies are likely due to random genetic drift and founder effects, in which population sizes were severely reduced by the earliest <em>O<\/em> allele-carrying individuals migrating into those areas. Over time, the <em>O<\/em> blood type has remained predominant.<\/p>\n<p class=\"import-Normal\"><img class=\"aligncenter\" src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image8.gif\" alt=\"World map showing varying frequencies of blood type A.\" width=\"516\" height=\"284\" \/><\/p>\n<p class=\"import-Normal\"><img class=\"aligncenter\" src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image5.gif\" alt=\"World map shows the highest frequencies of blood type B in parts of Asia.\" width=\"518\" height=\"283\" \/><\/p>\n<figure style=\"width: 516px\" class=\"wp-caption aligncenter\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image13.gif\" alt=\"World map shows the highest frequencies of blood type O.\" width=\"516\" height=\"284\" \/><figcaption class=\"wp-caption-text\">Figure 14.14a\u2013c: a. Global distribution of blood type A. b. Global distribution of blood type B. c. Global distribution of blood type O. <a href=\"https:\/\/docs.google.com\/document\/d\/1VUDKMBJYS_jNONjLxT04jQN0_z9Ua50BRN6auGSHUuU\/edit\" target=\"_blank\" rel=\"noopener\">A text description of this image is available<\/a>. Credit: a. <a class=\"rId69\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Map_of_blood_group_a.gif\">Map of blood group a<\/a> by <a class=\"rId70\" href=\"https:\/\/en.wikipedia.org\/wiki\/User:Muntuwandi\">Muntuwandi<\/a> at <a class=\"rId71\" href=\"https:\/\/en.wikipedia.org\/\">en.wikipedia<\/a> is under a <a class=\"rId72\" href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/3.0\/legalcode\">CC BY-SA 3.0 License<\/a>. b. <a class=\"rId73\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Map_of_blood_group_b.gif\">Map of blood group b<\/a> by <a class=\"rId74\" href=\"https:\/\/en.wikipedia.org\/wiki\/User:Muntuwandi\">Muntuwandi<\/a> at <a class=\"rId75\" href=\"https:\/\/en.wikipedia.org\/\">en.wikipedia<\/a> is under a <a class=\"rId76\" href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/3.0\/legalcode\">CC BY-SA 3.0 License<\/a>. c. <a class=\"rId77\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Map_of_blood_group_o.gif\">Map of blood group o<\/a> is based on diagrams from <a class=\"rId78\" href=\"https:\/\/anthro.palomar.edu\/vary\/vary_3.htm\">https:\/\/anthro.palomar.edu\/vary\/vary_3.htm<\/a>, reproduced from A. E. Mourant Et al. (1976), and is under a <a class=\"rId79\" href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/3.0\/legalcode\">CC BY-SA 3.0 License<\/a>.<\/figcaption><\/figure>\n<h3 class=\"import-Normal\"><strong>Genetic Variation Is Greater Within Group than Between Groups<\/strong><\/h3>\n<figure style=\"width: 295px\" class=\"wp-caption alignleft\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image27-2.jpg\" alt=\"Two medium-sized circles labeled Asian and European largely overlap. A larger circle labeled African surrounds both. \" width=\"295\" height=\"274\" \/><figcaption class=\"wp-caption-text\">Figure 14.15: Circles represent human genetic variation. Most variants are shared among individuals on all continents. There are more variants in Africa, some of which are not found in Europe or Asia. Credit: Human Genetic Variation original to Explorations: An Open Invitation to Biological Anthropology (2nd ed.) by Katie Nelson is under a <a class=\"rId81\" href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\">CC BY-NC 4.0 License<\/a>.<\/figcaption><\/figure>\n<p>One problem with race-based classifications is they relied on an erroneous idea that individuals with particular characteristics would share more similar genes with each other within a particular \u201crace\u201d and share less with individuals of other \u201craces\u201d possessing different traits and genetic makeups. However, since around 50 years ago, scientific studies have shown that the majority of human genetic differences worldwide exist <em>within<\/em> groups (or \u201craces\u201d) individually rather than <em>between<\/em> groups. Indeed, most genetic variation we see occurs in Africa, and many variants are shared among individuals on all continents (Figure 14.15).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">In 2002, a landmark article by Noah Rosenberg and colleagues explored worldwide human genetic variation using an even-greater genetic data set. They used 377 highly variable markers in the human genome and sampled from 1,056 individuals representative of 52 populations. The markers chosen for study were not ones that code for any expressed genes. Because these regions of the human genome were made of unexpressed genes, we may understand these markers as neutrally derived (as opposed to selectively derived) because they do not code for functional advantages or disadvantages. These neutral genetic markers likely reflect an intricate combination of regional founder effects and population histories. Analyses of these neutral markers allowed scientists to identify that 93%\u201295% of global genetic differences, referred to as <strong>variance<\/strong>, can be accounted for by within-population differences, while only a small proportion of genetic variance (3%\u20125%) can be attributed to differences among major groups (Rosenberg Et al. 2002). This research supports the theory that distinct biological races do not exist, even though misguided concepts of race may still have real social and political consequences.<\/p>\n<h3 class=\"import-Normal\"><strong>Biological Data Fit Isolation-By-Distance and Out-of-Africa Models<\/strong><\/h3>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">One further note is that the world\u2019s population may be genetically divided into \u201cgroups,\u201d \u201csubsets,\u201d \u201cclumps,\u201d or \u201cclusters\u201d that reflect some degree of genetic similarity. These identifiable clusters reflect genetic or geographic distances\u2014either with gene flow facilitated by proximity between populations or impeded by obstacles like oceans or environmentally challenging habitats (Rosenberg Et al. 2005). Sometimes, inferred clusters using multiple genetic loci are interpreted by nongeneticists literally as \u201cancestral populations.\u201d However, it would be wrong to assume from these genetic results that highly differentiated and \u201cpure\u201d ancestral groups ever existed. These groupings reflect differences that have arisen over time due to clinal patterning, genetic drift, and\/or restricted or unrestricted gene flow (Weiss and Long 2009). The clusters identified by scientists are arbitrary and the parameters used to split up the global population into groups is subjective and dependent on the particular questions or distinctions being brought into focus (Relethford 2009).<\/p>\n<figure style=\"width: 341px\" class=\"wp-caption alignright\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image6-7.png\" alt=\"Map of the continent of Africa with the lower two-thirds shaded.\" width=\"341\" height=\"341\" \/><figcaption class=\"wp-caption-text\">Figure 14.16: Sub-Saharan Africa (shaded dark\/green). Credit: <a class=\"rId83\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Sub-Saharan-Africa.png\">Sub-Saharan Africa<\/a> by <a class=\"rId84\" href=\"https:\/\/commons.wikimedia.org\/wiki\/User:Ezeu\">Ezeu<\/a> has been designated to the <a class=\"rId85\" href=\"https:\/\/creativecommons.org\/share-your-work\/public-domain\/cc0\/\">public domain (CC0)<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Additionally, research on worldwide genetic variation has shown that human variation decreases with increasing distance from sub-Saharan Africa, where there is evidence for this vast region being the geographical origin of anatomically modern humans (Liu Et al. 2006; Prugnolle, Manica, and Balloux 2005; see Figures 14.16 and 14.17). Genetic differentiation decreases in human groups the further you sample data from relative to sub-Saharan Africa because of serial founder effects (Relethford 2004). Over the course of human colonization of the rest of the world outside Africa, populations broke away in expanding waves across continents into western Asia, then Europe and eastern Asia, followed by Oceania and the Americas. As a result, founder events occurred whereby genetic variation was lost, as the colonization of each new geographical region involved a smaller number of individuals moving from the original larger population to establish a new one (Relethford 2004). The most genetic variation is found across populations residing in different parts of sub-Saharan Africa, while other current populations in places like northern Europe and the southern tip of South America exhibit some of the least genetic differentiation relative to all global populations (Campbell and Tishkoff 2008).<\/p>\n<figure style=\"width: 469px\" class=\"wp-caption aligncenter\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image3-6.png\" alt=\"Two scatterplots.\" width=\"469\" height=\"516\" \/><figcaption class=\"wp-caption-text\">Figure 14.17: Comparison of the genetic distance and geographical distance between populations. In the top graph, the pattern reveals that genetic variation conforms to an Out-of-Africa model, as those populations further away from Addis Ababa in Ethiopia share a smaller number of alleles; in the bottom graph, we see the populations follow an isolation-by-distance model, as pairs of populations further apart geographically seem to have greater genetic distance (Kanitz Et al. 2018). Credit: <a class=\"rId87\" href=\"https:\/\/journals.plos.org\/plosone\/article?id=10.1371\/journal.pone.0192460\">Complex genetic patterns (figure 1)<\/a> by Kanitz Et al. (2018) is under a <a class=\"rId88\" href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\">CC BY 4.0 License<\/a>.<\/figcaption><\/figure>\n<\/div>\n<div class=\"__UNKNOWN__\">\n<figure style=\"width: 377px\" class=\"wp-caption alignleft\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image1-9.png\" alt=\"Two large circles connected by a small area.\" width=\"377\" height=\"309\" \/><figcaption class=\"wp-caption-text\">Figure 14.18: The founder effect is a change in a small population\u2019s gene pool due to a limited number of individuals breaking away from a parent population. Credit: <a class=\"rId90\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Bottleneck_effect.jpg\">Bottleneck effect<\/a> by <a class=\"rId91\" href=\"https:\/\/wikieducator.org\/User:Tsaneda\">Tsaneda<\/a> is under a <a class=\"rId92\" href=\"https:\/\/creativecommons.org\/licenses\/by\/3.0\/legalcode\">CC BY 3.0 License<\/a>.<\/figcaption><\/figure>\n<p>Besides fitting nicely into the <strong>Out-of-Africa model<\/strong>, worldwide human genetic variation conforms to an <strong>isolation-by-distance model<\/strong>, which predicts that genetic similarity between groups will decrease exponentially as the geographic distance between them increases (Kanitz Et al. 2018). This is because of the greater and greater restrictions to gene flow presented by geographic distance, as well as cultural and linguistic differences that occur as a result of certain degrees of isolation. Since genetic data conform to isolation-by-distance and Out-of-Africa models, these findings support the abolishment of \u201crace\u201d groupings. This research demonstrates that human variation is continuous and cannot be differentiated into geographically discrete categories. There are no \u201cinherent\u201d or \u201cinnate\u201d differences between human groups; instead, variation derives from some degree of natural selection, as well as neutral processes like <strong>population bottle-necking<\/strong> (Figure 14.18), random <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_1699_1474\"><strong>mutations<\/strong><\/a> in the DNA, genetic drift, and gene flow through between-mate interbreeding.<\/p>\n<h3 class=\"import-Normal\"><strong>Humans Have Higher Homogeneity Compared to Many Other Species<\/strong><\/h3>\n<p class=\"import-Normal\">An important fact to bear in mind is that humans are 99.9% identical to one another. This means that the apportionments of human variation discussed above only concern that tiny 0.1% of difference that exists between all humans globally. Compared to other mammalian species, including the other great apes, human variation is remarkably lower. This may be surprising given that the worldwide human population has already exceeded seven billion, and, at least on the surface level, we appear to be quite phenotypically diverse. Molecular approaches to human and primate genetics tells us that external differences are merely superficial. For a proper appreciation of human variation, we have to look at our closest relatives in the primate order and mammalian class. Compared to chimpanzees, bonobos, gorillas and other primates, humans have remarkably low average genome-wide <strong>heterogeneity<\/strong> (Osada 2005).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">When we look at chimpanzee genetic variation, it is fascinating that western, central, eastern, and Cameroonian chimpanzee groups have substantially more genetic variation between them than large global samples of human DNA (Bowden Et al. 2012; Figure 14.19). This is surprising given that all of these chimpanzee groups live relatively near one another in Africa, while measurements of human genetic variation have been conducted using samples from entirely different continents. First, geneticists suppose that this could reflect differential experiences of the founder effect between humans and chimpanzees. As it has been argued that all non-African human populations descended from a small number of anatomically modern humans who left Africa, it would be expected that all groups descended from that smaller ancestral group would be similar genetically. Second, our species is really young, given that we have only existed on the planet for around 150,000 to 300,000 years. This gave humans little time for random genetic mutations to occur as genes get passed down through genetic interbreeding and meiosis. Chimpanzees, however, have inhabited different <strong>ecological niches<\/strong>, and less interbreeding has occurred between the four chimpanzee groups over the past six to eight million years compared to the amount of gene flow that occurred between worldwide human populations (Bowden Et al. 2012).<\/p>\n<figure style=\"width: 648px\" class=\"wp-caption aligncenter\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image16-7.png\" alt=\"Map of Africa showing the ranges of chimpanzees from west to east.\" width=\"648\" height=\"339\" \/><figcaption class=\"wp-caption-text\">Figure 14.19: Distribution of the genus Pan, including bonobos and the four subspecies of chimpanzee, across western and central Africa (Clee Et al. 2015). <a href=\"https:\/\/docs.google.com\/document\/d\/1VUDKMBJYS_jNONjLxT04jQN0_z9Ua50BRN6auGSHUuU\/edit\" target=\"_blank\" rel=\"noopener\">A text description of this image is available<\/a>. Credit: <a class=\"rId94\" href=\"https:\/\/bmcecolevol.biomedcentral.com\/articles\/10.1186\/s12862-014-0275-z\">Chimpanzee subspecies ranges (Figure 1)<\/a> by Clee Et al. 2015 is under a <a class=\"rId95\" href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\">CC BY 4.0 License<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Recent advances have now enabled the attainment of genetic samples from the larger family of great apes and the evaluation of genetic variation among bonobos, orangutans, and gorillas alongside that of chimpanzees and humans (Prado-Martinez Et al. 2013). Collecting such data and analyzing primate genetic variation has been important not only to elucidate how different ecological, demographic, and climatic factors have shaped our evolution but also to inform upon conservation efforts and medical research. Genes that may code for genetic susceptibilities to tropical diseases that affect multiple primates can be studied through genome-wide methods. Species differences in the genomes associated with speech, behaviour, and cognition could tell us more about how human individuals may be affected by genetically derived neurological or speech-related disorders and conditions (Prado-Martinez Et al. 2013; Staes Et al. 2017). In 2018, a great ape genomic study also reported genetic differences between chimpanzees and humans related to brain cell divisions (Kronenberg Et al. 2018). From these results, it may be inferred that cognitive or behavioural variation between humans and the great apes might relate to an increased number of cortical neurons being formed during human brain development (Kronenberg Et al. 2018). Comparative studies of human and nonhuman great ape genetic variation highlight the complex interactions of population histories, environmental changes, and natural selection between and within species. When viewed in the context of overall great ape variation, we may reconsider how variable the human species is relatively and how unjustified previous \u201crace\u201d concepts really were.<\/p>\n<h3 class=\"import-Normal\"><strong>Phenotypic Traits That Reflect Neutral Evolution<\/strong><\/h3>\n<p class=\"import-Normal\">Depending on the trait being observed, different patterns of phenotypic variation may be found within and among groups worldwide. In this subsection, some phenotypic traits that reflect the aforementioned patterns of genetic variation will be discussed.<\/p>\n<figure style=\"width: 301px\" class=\"wp-caption alignleft\"><img class=\"\" src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image18-4.jpg\" alt=\"Illustration of one anthropologist studying teeth, and another looking into a microscope.\" width=\"301\" height=\"301\" \/><figcaption class=\"wp-caption-text\">Figure 14.20: Contemporary anthropologists who use many types of skeletal markers have demonstrated that a majority of cranial variation occurs within populations rather than between populations and that there is a decrease in variation with distance from Africa. Credit: <a class=\"rId97\" href=\"https:\/\/img1.wsimg.com\/isteam\/ip\/0f6c1c17-41ea-4caf-b839-73c676d69f01\/DentalHeartNecklace.jpg\/:\/rs=w:1280,h:1280\">Dental Anthropologist Heart Necklace<\/a> by <a class=\"rId98\" href=\"https:\/\/anthroillustrated.com\/\">Anthro Illustrated<\/a> is under a <a class=\"rId99\" href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\">CC BY-NC 4.0 License<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Looking beyond genetic variation briefly, recent studies have revisited biological anthropology\u2019s earlier themes of externally observable traits, such as skull shape. In the last 20 or so years, anthropologists have evaluated the level to which human cranial shape variation reflects the results from genetic markers, such as those used previously to fit against Out-of-Africa models (Relethford 2004) or those used in the apportionment of human variation between and within groups (Lewontin 1972; Rosenberg Et al. 2002). Using larger sample sizes of cranial data collected from thousands of skulls worldwide and a long list of cranial measurements, studies demonstrate a similar decrease in variation with distance from Africa and show that a majority of cranial variation occurs within populations rather than between populations (Betti Et al. 2009; Betti Et al. 2010; Manica Et al. 2007; Relethford 2001; von Cramon-Taubadel and Lycett 2008; see Figure 14.20). The greatest cranial variation is found among skulls of sub-Saharan African origin, while the least variation is found among populations inhabiting places like Tierra del Fuego at the southern tip of Argentina and Chile. While ancient and historical thinkers previously thought \u201crace\u201d categories could reasonably be determined based on skull dimensions, modern-day analyses using more informative sets of cranial traits simply show that migrations out of Africa and the relative distances between populations can explain a majority of worldwide cranial variation (Betti Et al. 2009).<\/p>\n<figure style=\"width: 250px\" class=\"wp-caption alignright\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image21-6.png\" alt=\"Sketch of bone with bony loops at the top and coil at the bottom.\" width=\"250\" height=\"208\" \/><figcaption class=\"wp-caption-text\">Figure 14.21: Diagram of the bony labyrinth in the inner ear. Credit: <a class=\"rId101\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Bony_labyrinth.png\">Bony labyrinth<\/a> by <a class=\"rId102\" href=\"https:\/\/commons.wikimedia.org\/wiki\/User:Selket\">Selket<\/a> has been designated to the <a class=\"rId103\" href=\"https:\/\/creativecommons.org\/share-your-work\/public-domain\/cc0\/\">public domain (CC0)<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\">This same patterning in phenotypic variation has even been found in studies examining shape variation of the pelvis (Betti Et al. 2013; Betti Et al. 2014), the teeth (Rathmann Et al. 2017), and the human <strong>bony labyrinth<\/strong> of the ear (Ponce de Le\u00f3n Et al. 2018;Figure 14.21). The skeletal morphology of these bones still varies worldwide, but a greater proportion of that variation can still be attributed to the ways in which human populations migrated across the world and exchanged genes with those closer to them rather than those further away. Human skeletal variation in these parts of the body is continuous and nondiscrete. Given the important functions of the cranium and these other skeletal parts, we may infer that the genes that underpin their development have been relatively conserved by neutral evolutionary processes such as genetic drift and gene flow. It is also important to note that while some traits such as height, weight, cranial dimensions, and body composition are determined, in part, by genes, the underlying developmental processes behind these traits are underpinned by complex polygenic mechanisms that have led to the continuous spectrum of variation in such variables among modern-day human populations.<\/p>\n<h3 class=\"import-Normal\"><strong>Phenotypic Traits That Reflect Natural Selection<\/strong><\/h3>\n<p class=\"import-Normal\">Even though 99.9% of our DNA is the same across all humans worldwide, and many traits reflect neutral processes, there are parts of that remaining 0.1% of the human genome that code for individual and regional differences. Similarly to craniometric analyses that have been conducted in recent decades, human variation in skin colour has also been reassessed using new methods and in light of greater knowledge of biological evolution.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">New technologies allow scientists to use colour photometry to sample and quantify the visible wavelength of skin colour, in a way 19th- and 20th-century readers could not. In one report, it was found that 87.9% of global skin colour variation can be attributed to genetic differences <em>between<\/em> groups, 3.2% to those among local populations within regions, and 8.9% <em>within<\/em> local populations (Relethford 2002). This apportionment differs significantly and is the reverse situation found in the distribution of genetic differences we see when we examine genetic markers such as blood type\u2013related alleles. However, this pattern of human skin colour worldwide is not surprising, given that we now understand that past selection has occurred for darker skin near the equator and lighter skin at higher latitudes (Jablonski 2004; Jablonski and Chaplin 2000). While most genetic variation reflects neutral variation due to population migrations, geographic isolation, and restricted gene flow dynamics, some human genetic\/phenotypic variation is best explained as local adaptation to environmental conditions (i.e., selection). Given that skin colour variation is atypical compared to other genetic markers and biological traits, this, in fact, goes against earlier \u201crace\u201d typologies. This is because recent studies ironically show how so much of genetic variation relates to neutral processes, while skin colour does not. It follows that skin colour <em>cannot<\/em> be viewed as useful in making inferences about other human traits.<\/p>\n<figure style=\"width: 580px\" class=\"wp-caption aligncenter\"><img class=\"\" src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image23-3.jpg\" alt=\"Person standing at podium in front of a screen with arms partly raised.\" width=\"580\" height=\"384\" \/><figcaption class=\"wp-caption-text\">Figure 14.22: Genomicists and biological anthropologists have dedicated efforts to improving quantitative methods of measuring hair and skin variation over the last twenty years. Dr. Nina Jablonski is one such biological anthropologist specializing in the evolution and variation of human skin pigmentation. Credit: <a class=\"rId105\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Nina_Jablonski_2016_The_Skin_of_Homo_sapiens_01_%28cropped%29.jpg\">Nina Jablonski 2016 The Skin of Homo sapiens 01 (cropped)<\/a> by <a class=\"rId106\" href=\"https:\/\/commons.wikimedia.org\/wiki\/User:Ptolusque\">Ptolusque<\/a> is under a <a class=\"rId107\" href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/4.0\">CC BY-SA 4.0 license<\/a>.<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">It is also true that some populations have not been studied extensively in skin pigmentation genetics (e.g., African, Austronesian, Melanesian, Southeast Asian, Indigenous American, and Pacific Islander populations, according to Lasisi and Shriver 2018). Earlier dispersals of these populations, and their local genetic varition, will have contributed to worldwide genetic variation, inclusive of skin pigmentation variation. Gene loci we did not previously appreciate as being linked to pigmentation are now being recognized thanks to better tools, more diverse genetic samples, and more accessible datasets (Quillen Et al. 2018). Biological anthropologists look forward to further discoveries elucidating the different selective pressures and population dynamics that influence skin pigmentation evolution.<\/p>\n<h2 class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Social Implications<\/h2>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">To finish this chapter, we will consider the social, economic, political, and biological implications of poor understandings of race and the deliberate perpetuation of social and medical racism.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The Black Lives Matter movement (BLM) of 2013 began with the work of racial justice activists and community organizers Alicia Garza, Opal Tometi, and Patrissa Cullors. First incited by the murder of Trayvon Martin, a 17-year-old African American, and the acquittal of the man who shot him, BLM went on to protest against the deaths of numerous Black individuals, most of whom were killed by police officers (for example, Ahmaud Arbery was killed in February of 2020 by two white non-police officers). Some key characteristics of BLM from the start were its decentralized grassroots structure, the role of university students and social media in spreading awareness of the movement, and its embrace of other movements (e.g., climate justice, ending police brutality, feminist campaigns, queer activism, immigration reform, etc.). When George Floyd was murdered by a white police officer on May 25, 2020, the BLM gained new momentum, across 2,000-plus cities in the United States, and among many protesting against historic racism and police brutality in other contexts around the globe. Many in the biological anthropology community have responded to these events with a great dedication to working against systemic racism in society and institutions (American Association of Biological Anthropologists 2020).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">BLM continues to be an important movement, as is evidenced in the degree of community organizing, mutual aid efforts, calls for political reform, progress toward curriculum reform and equality, inclusion and diversity (EDI) work in businesses and universities, the removal of monuments honoring historical figures associated with slavery and racism, and many other important actions. Garza (2016) writes: \u201cThe reality is that race in the United States operates on a spectrum from black to white \u2026 the closer you are to white on that spectrum, the better off you are.\u201d Tometi (2016) has stated: \u201cWe need [a human rights movement that challenges systemic racism] because the global reality is that Black people are subject to all sorts of disparities in most of our challenging issues of our day. I think about climate change, and how six of the ten worst impacted nations by climate change are actually on the continent of Africa.\u201d In the words of Cullors (2016), \u201cBlack Lives Matter is our call to action. It is a tool to reimagine a world where Black people are free to exist, free to live. It is a tool for our allies to show up differently for us.\u201d We gather from their words the importance of learning from the egregious role that anthropologists have played in the past, recognizing the legacies of \u201cscientific\u201d justifications for eugenics and racism in our society today, and proactively working toward environmental and social equity.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Another major industry that engages in the quantification and interpretation of human variation is medical and clinical work (National Research Council [U.S.] Committee on Human Genome Diversity 1997). Large-scale genomic studies sampling from human populations distributed worldwide have produced detailed knowledge on variation in disease resistance or susceptibility between and within populations. Let\u2019s think about drug companies who develop medicines for Black patients particularly. The predispositions to particular diseases are higher among people of African descent than some pharmaceutical businesses have taken into account. Through targeted sampling of various world groups, clinical geneticists may also identify genetic risk factors of certain common disorders such as chronic heart disease, asthma, diabetes, autoimmune diseases, and behavioural disorders. Having an understanding of population-specific biology is crucial in the development of therapies, medicines, and vaccinations, as not all treatments may be suitable for every human, depending on their genotype. During diagnosis and treatment, it is important to have an evolutionary perspective on gene-environment relationships in patients. Typological concepts of \u201crace\u201d are not useful, given that most racial groups (whether self-identified or not) popularly recognized lack homogeneity and are, in fact, variable. <strong>Cystic fibrosis<\/strong>, for instance, occurs in all world populations but can often be underdiagnosed in populations with African ancestry because it is thought of as a \u201cwhite\u201d disease (Yudell Et al. 2016).<\/p>\n<p class=\"import-Normal\">Sociologists, law scholars, and professors of race studies have written extensively on how genetic\/technological\/medical revolutions impact people of colour. In her book, <em>Fatal Invention: How Science, Politics, and Big Business Re-create Race in the Twenty-First Century <\/em>(2013), Professor Dorothy E. Roberts writes about how technological advances have been used in resuscitating race as a biological category for dividing humans in essentialist ways (Figure 14.23). She notes how members of law enforcement have engaged in racial profiling, sometimes with the use of machine-learning and facial-recognition technologies. Ancestry-testing services also purport to tell us \u201cwhat\u201d we are and to insist that this information is \u201cwritten\u201d in our genes. Such advertising campaigns obscure the nuances of genetic variation with the primary motive of tapping into people\u2019s desire to \u201cknow themselves\u201d and driving up profits for their businesses. Commercial genetic testing reinforces the idea that genes map neatly onto race, all while generating massive stores of data in DNA databases. In Roberts\u2019s view, the myth of the biological concept of race being perpetuated in these ways undermines a just society and reproduces racial inequalities.<\/p>\n<figure style=\"width: 593px\" class=\"wp-caption aligncenter\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image12-6.png\" alt=\"Book cover with two DNA strands and next to the smiling portrait of the author.\" width=\"593\" height=\"305\" \/><figcaption class=\"wp-caption-text\">Figure 14.23: Professor Dorothy E. Roberts is a sociologist, legal scholar, and expert on the relationships among technology, medicine, bioethics, policymaking, race, and racism. Credit: <a class=\"rId109\" href=\"https:\/\/kpfa.org\/episode\/talkies-august-23-2016\/\">Dorothy Roberts author of Fatal Invention<\/a> by <a class=\"rId110\" href=\"https:\/\/kpfa.org\/\">https:\/\/kpfa.org\/<\/a> is copyrighted and used with permission.<\/figcaption><\/figure>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">The COVID-19 pandemic has had a significant impact on the world\u2019s population, particularly people living in the economic Global South and many Black, Indigenous and communities of colour residing in the Global North. We have witnessed disproportionately high numbers of COVID-related deaths and infection cases among marginalized groups. Many immigrants and ethnic minorities in various societies have also experienced scapegoating and blame directed at them for being the source of COVID-19 spread.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">To inform us on how to interpret this current worldwide pandemic, historians and anthropologists are looking back at the lessons learned from past instances of racist medicine (discriminatory practices based on broader social discrimination) and medical racism (application of discriminatory practices justified on medical grounds). Historically, who could become doctors and medical professionals was often racialized, gendered, and class specific. This made it difficult for many to overcome prejudices against women, Black people, Indigenous individuals, or other people of colour from becoming doctors and clinical researchers in places such as South Africa and the United States. This, in turn, affects the sorts of information we know about health levels and health outcomes among these very groups. In the past decade, long-overdue attention is finally being paid to how race affects biological outcomes. For instance, researchers have focused on the negative legacies of racial discrimination and racism-induced stress on hormone (im)balances, mental health disorders, cardiovascular disease prevalence, and other health outcomes (Kuzawa and Sweet 2009; Shonkoff, Slopen, and WIlliams 2021; Williams 2018). The technology and standards of protocol in medical testing have been scrutinized (for more on how pulse oximeters were not designed with nonwhite patients in mind, for example, see Sjoding Et al. 2020). Scholars of race and medicine have also written on how illness and disease spread have often been used to perpetuate societal prejudices. This manifests as xenophobic tendencies at a societal level, such as the blaming of \u201coutgroups\u201d and increased \u201cin-group\u201d protectiveness. Overreliance on the idea that people are \u201cinherently\u201d disease carriers due to genetic or biological reasons leads to improper accounting for socioeconomic or infrastructural issues that lead to differential disease prevalence amongst minority communities. (For more on race and COVID, see Tsai 2021 as well as this textbook\u2019s Chapter 16: Contemporary Topics: Human Biology and Health.)<\/p>\n<p>Lastly, consider the changing field of forensic anthropology. In the past, forensic anthropologists ascribed <strong>ancestry<\/strong> or racial categories to sets of skeletons, reliant on the belief that different human groups will exhibit biologically \u201cdiscrete\u201d assortments so as to divide along culturally constructed categories (Sauer 1992). Now, a number of forensic anthropologists have argued that we should abandon these methods, both because it is unscientific and because it further validates and perpetuates this idea that race is biologically meaningful. As scientists, whether we affirm biological race as real has huge influence on the beliefs of members of the public, the judicolegal system, and law enforcement. Not all forensic experts agree with abandoning ancestry estimation. Some prefer to refocus on the neutral or selective <em>causes<\/em> of human biological variation, and assess how <em>probabilistic<\/em> it may be to assign bones of certain dimensions to one of several identified racial categories. These debates continue today as this textbook chapter is being written. More details on population affinity may be found in Chapter 17: Forensic Anthropology.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">It is important to remember that while it is possible to look for clues about one\u2019s ancestry or geographic origin based on skull morphology, again, the amount of distinctiveness in any given sample makes it impossible to distinguish whether a cranium belongs to one group (Relethford 2009). Individuals can vary in their skeletal dimensions by continental origin, country origin, regional origin, sex, age, environmental factors, and the time period in which they lived, making it difficult to assign individuals to particular categories in a completely meaningful way (Ousley, Jantz, and Freid 2009). When forensic reports and scientific journal articles give an estimation of ancestry, it is crucial to keep in mind that responsible assignments of ancestry will be done through robust statistical testing and stated as a probability estimate. Today, we also live in a more globalized world where a skeletal individual may have been born originally to parents of two separate traditional racial categories. In contexts of great heterogeneity within populations, this definitely adds difficulty to the work of forensic scientists and anthropologists preparing results for the courtroom (genetic testing may be comparatively more helpful in such situations).<\/p>\n<\/div>\n<div class=\"textbox\">\n<h2 class=\"import-Normal\">Dig Deeper: Measuring F<sub>ST<\/sub><\/h2>\n<p class=\"import-Normal\">Richard Lewontin (1929\u2012) is a biologist and evolutionary geneticist who authored an article evaluating where the total genetic variation in humans lies. Titled \u201cThe Apportionment of Human Diversity\u201d (Lewontin 1972), the article addressed the following question: On average, how genetically similar are two randomly chosen people from the same group when compared to two randomly chosen people from different groups?<\/p>\n<p class=\"import-Normal\">Lewontin studied this problem by using genetic data. He obtained data for a large number of different human populations worldwide using 17 genetic markers (including alleles that code for various important enzymes and proteins, such as blood-group proteins). The statistical analysis he ran used a measure of human genetic differences in and among populations known as the fixation index (F<sub>ST<\/sub>).<\/p>\n<p class=\"import-Normal\">Technically, F<sub>ST<\/sub> can be defined as the proportion of total genetic variance within a <em>subpopulation<\/em> relative to the total genetic variance from an <em>entire population<\/em>. Therefore, F<sub>ST<\/sub> values range from 0 to 1 (or, sometimes you will see this stated as a percentage between 0% and 100%). The closer the F<sub>ST<\/sub> value of a population (e.g., the world\u2019s population) approaches 1, the higher the degree of genetic differentiation among subpopulations relative to the overall population (see Figure 14.24 for a detailed illustration).<\/p>\n<figure style=\"width: 561px\" class=\"wp-caption aligncenter\"><img src=\"http:\/\/opentextbooks.concordia.ca\/wp-content\/uploads\/sites\/71\/2025\/07\/image4-5.jpg\" alt=\"Three cases each illustrate two populations with a mix of two types of alleles.\" width=\"561\" height=\"473\" \/><figcaption class=\"wp-caption-text\">Figure 14.24: This diagram shows a range of different case studies with which we may understand how FST is calculated in different populations. In Case 1, the gene pools of Populations 1 and 2 are 100% different from each other but possess 0% variation within themselves, so FST has a value of 1. When there is no genetic variation at all between two populations and 100% variation within them, as in Case 2, we see that FST is calculated as 0. When we look at Case 3, where variation between and within are some values between 0% and 100%, we will get a decimal figure for FST dependent upon how much variation there is between and within populations. It is through such comparisons of population genetic data that we may quantify the relative similarities or differences between and within populations, and we may thus speak to the nonexistence of \u201cracial groups\u201d that divide up our species into broad continental or racial categories. Credit: F<sub>ST<\/sub> original to Explorations: An Open Invitation to Biological Anthropology (2nd ed.) by Katie Nelson is under a <a class=\"rId112\" href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\">CC BY-NC 4.0 License<\/a>.<\/figcaption><\/figure>\n<p>&nbsp;<\/p>\n<p>In his article, Lewontin (1972) identified that most of human genetic differences (85.4%) were found within local subpopulations (e.g., the Germans or Easter Islanders), whereas 8.3% were found between populations within continental human groups, and 6.3% were attributable to traditional \u201crace\u201d groups (e.g., \u201cCaucasian\u201d or \u201cAmerind\u201d). These findings have been important for scientifically rejecting the existence of biological races (Long and Kittles 2003).<\/p>\n<\/div>\n<div class=\"__UNKNOWN__\">\n<h2 class=\"import-Normal\">Talking About Human Biological Variation Going Forward<\/h2>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">To conclude, utilizing the term <em>races<\/em> to describe human biological variation is not accurate or productive. Using a select few hundred genetic loci, or perhaps a number of phenotypic traits, it may be possible to assign individuals to a geographic ancestry, but what constitutes a bounded genetic or geographical grouping is both arbitrary and potentially harmful owing to ethical and historical reasons. The discipline of biological anthropology has moved past typological frameworks that shoehorn continuously variable human populations into discrete and socially constructed subsets. Improvements in the number of markers, the genetic technologies used to study variation, and the number of worldwide populations sampled have led to more nuanced understandings of human variation. It is of utmost importance that scientists make the following points clear to the public:<\/p>\n<ul>\n<li class=\"import-Normal\" style=\"text-indent: 0pt\">Today, we refer to different local human groups as \u201cpopulations.\u201d What constitutes a population should be carefully defined in scientific reports based on some geographical, linguistic, or cultural criteria and some degree of relativity to other closely or distantly related human groups.<\/li>\n<li class=\"import-Normal\" style=\"text-indent: 0pt\">Humans have significantly less genetic variation than other primates and mammals, and all human beings on Earth share 99.9% of their overall DNA. Some of the remaining 0.1% of human variation varies on a clinal or continuous basis, such as can be seen when looking at ABO blood-type <strong>polymorphisms<\/strong> worldwide.<\/li>\n<li class=\"import-Normal\" style=\"text-indent: 0pt\">Many biological characteristics in humans are actually determined nonconcordantly and\/or polygenically. Therefore, superiority or inferiority in human behaviour or body form cannot justifiably be linked to fixed and innate differences between groups.<\/li>\n<li class=\"import-Normal\" style=\"text-indent: 0pt\">Genetic distances are correlated with geographic distances among the global human population. This is especially apparent when we consider that genetic variation is highest in sub-Saharan Africa, and average genetic heterogeneity decreases in populations further away from the African continent in accordance with the migratory history of anatomically modern <em>Homo sapiens<\/em>.<\/li>\n<li class=\"import-Normal\" style=\"text-indent: 0pt\">The effects of gene flow, genetic drift, and population bottlenecking are reflected in some phenotypic traits, such as cranial shape.<\/li>\n<li class=\"import-Normal\" style=\"text-indent: 0pt\">We recognize other traits, like skin colour and lactase persistence, to be the products of many millennia of natural selective pressures influencing human biology from the external environment.<\/li>\n<\/ul>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Taken together, genetic analyses of human variation do not support 20th-century (or even-earlier) concepts of race. In discussions about human variation, these genomic results help clarify how biological variation is distributed across the human population today. Taking care to think about and debate the nature of human variation is important, because although the effects and events that produced genetic differences among groups occurred in the ancient past, sociocultural concepts about race and ethnicity continue to have real social, economic, and political consequences.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Beyond talking about variation in the university setting, it is important that teachers, researchers, and students of anthropology recognize and assume the responsibility of influencing public perspectives of human variation. Race-based classification systems were developed during the colonial era, the transatlantic trafficking of kidnapped Africans and the so-called \u201cScientific Revolution\u201d by the first \u201canthropologists\u201d and scholars of humankind\u2019s variation. Unfortunately, some of their early ideas have persisted and evolved into present-day lived realities. Some of today\u2019s politicians and socioeconomic bodies have racially charged agendas that promote racism or certain kinds of economic or racial inequalities. As anthropologists, we must acknowledge that while human \u201craces\u201d are not a biological reality, their status as a (misguided) social construction does have real consequences for many people (Antrosio 2011).<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">In other words, while \u201crace\u201d is a sociocultural invention, the treatment different individuals receive due to their perceived \u201crace\u201d can have significant financial, emotional, sociopolitical, and physiological costs. However\u2014and importantly assuming a \u201ccolour-blind\u201d position when it comes to the topics of \u201crace\u201d and ethnicity (especially in political discussions) is actually counterproductive, because the negative social consequences of modern \u201crace\u201d ideas could be ignored, making it harder to examine and address instances of discrimination properly (Wise 2010). Rather than shy away from these topics, we can use our scientific findings to establish socially relevant and biologically accurate ideas concerning human diversity. Today, research into genetic and phenotypic differentiation among and within various human populations continues to expand in its scope, its technological capabilities, its sample sizes, and its ethical concerns. It is thanks to such scientific work done in the past few decades that we now have a deeper understanding not only of how humans vary but also of how we are biologically a rather homogenous, intermixing world population.<\/p>\n<p>&nbsp;<\/p>\n<div class=\"textbox shaded\">\n<h2>Summary<\/h2>\n<p>Historically, most concepts of race were shaped by religious and early \u2018scientific\u2019 attempts to classify people, many of which justified inequality and racism. Today, biological anthropology emphasizes that human variation is continuous (clinal), polygenic, and shaped by both evolutionary pressures and neutral processes. Misunderstandings of race, however, continue to have serious social and medical consequences; evident in systemic racism and inequities in health care.<\/p>\n<p>Biological anthropologists now play a critical role in discrediting myths about race. By studying\u00a0 human variation, we can begin to understand evolutionary processes, adaptation, and the social implications of differences among human populations. Modern research shows that that humans are far more genetically homogenous than many other species, reinforcing a conclusion that \u2018race\u2019 is not a biological reality but a powerful social construct with real effects. Through evolutionary history and genetics, human diversity can be researched and understood, rather than than through racial categories.<\/p>\n<h2 class=\"import-Normal\">Review Questions<\/h2>\n<ul>\n<li class=\"import-Normal\">How is the genetic variation of the human species distributed worldwide?<\/li>\n<li class=\"import-Normal\">What evolutionary processes are responsible for producing genotypic\/phenotypic variation within and between human populations?<\/li>\n<li class=\"import-Normal\">Should we continue to attribute any value to \u201crace\u201d concepts older than 1950, based on our current understandings of human biological variation?<\/li>\n<li class=\"import-Normal\">How should we communicate scientific findings about human biological variation more accurately and responsibly to those outside the anthropological discipline?<\/li>\n<\/ul>\n<\/div>\n<h2 class=\"import-Normal\">Key Terms<strong><br \/>\n<\/strong><\/h2>\n<p class=\"import-Normal\"><strong>Age of Discovery<\/strong>: A period between the late 1400s and late 1700s when European explorers and ships sailed extensively across the globe in pursuit of new trading routes and territorial conquest.<\/p>\n<p class=\"import-Normal\"><strong>Ancestry<\/strong>: Biogeographical information about an individual, traced either through the study of an individual\u2019s genome, skeletal characteristics, or some other form of forensic\/archaeological evidence. Anthropologists carry out probabilistic estimates of ancestry. They attribute sets of human remains to distinctive \u201cancestral\u201d groups using careful statistical testing and should report ancestry estimations with statistical probability values.<\/p>\n<p class=\"import-Normal\"><strong>Binomial nomenclature<\/strong>: A system of naming living things developed by Linnaeus in the 1700s. It employs a scientific name made up of two italicized Latin or Greek words, with the first word capitalized and representative of an organism\u2019s genus and the second word indicating an organism\u2019s species (e.g., <em>Homo sapiens<\/em>, <em>Australopithecus afarensis<\/em>, <em>Pongo tapanuliensis<\/em>, etc.).<\/p>\n<p class=\"import-Normal\"><strong>Biological anthropology<\/strong>: A branch of study under anthropology (the study of humankind) that focuses on when and where humans and our human ancestors first originated, how we have evolved and adapted globally over time, and the reasons why we see biological variation among humans worldwide today.<\/p>\n<p class=\"import-Normal\"><strong>Biological determinism<\/strong>: The erroneous concept that an individual\u2019s behavioural characteristics are innate and determined by genes, brain size, or other physiological attributes\u2014and, notably, without the influence of social learning or the environment around the individual during development.<\/p>\n<p class=\"import-Normal\"><strong>Bony labyrinth<\/strong>: A system of interconnected canals within the auditory (ear- or hearing-related) apparatus, located in the inner ear and responsible for balance and the reception of sound waves.<\/p>\n<p class=\"import-Normal\"><strong>Cline<\/strong>: A gradient of physiological or morphological change in a single character or allele frequency among a group of species across environmental or geographical lines (e.g., skin colour varies clinally, as, over many generations, human groups living nearer the equator have adapted to have more skin pigmentation).<\/p>\n<p class=\"import-Normal\"><strong>Continuous variation<\/strong>: This term refers to variation that exists between individuals and cannot be measured using distinct categories. Instead, differences between individuals within a population in relation to one particular trait are measurable along a smooth, continuous gradient.<\/p>\n<p class=\"import-Normal\"><strong>Cystic fibrosis<\/strong>: A genetic disorder in which one defective gene causes overproduction and buildup of mucus in the lungs and other bodily organs. It is most common in northern Europeans (but also occurs in other world populations).<\/p>\n<p class=\"import-Normal\"><strong>Ecological niche<\/strong>: The position or status of an organism within its community and\/or ecosystem, resulting from the organism\u2019s structural and functional adaptations (e.g., bipedalism, omnivorous diets, lactose digestion, etc.).<\/p>\n<p class=\"import-Normal\"><strong>Essentialism<\/strong>: A belief or view that an entity, organism, or human grouping has a specific set of characteristics that are fundamentally necessary to its being and classification into definitive categories.<\/p>\n<p class=\"import-Normal\"><strong>Ethnicity<\/strong>: A term used commonly in an interchangeable way with the term <em>race<\/em>, complicated because how different people define this term depends on the qualities and characteristics they use to assign a label or identity to themselves and\/or others (which may include aspects of family background, skin colour, language(s) spoken, religion, physical proportions, behaviour and temperament, etc.).<\/p>\n<p class=\"import-Normal\"><strong>Eugenics<\/strong>: A set of beliefs and practices that involves the controlled selective breeding of human populations with the hope of improving their heritable qualities, especially through surgical procedures like sterilization and legal rulings that affect marriage rights for interracial couples.<\/p>\n<p class=\"import-Normal\"><strong>Gene flow<\/strong>: A neutral (or nonselective) evolutionary process that occurs when genes get shared between populations.<\/p>\n<p class=\"import-Normal\"><strong>Genetic drift<\/strong>: A neutral evolutionary process in which allele frequencies change from generation to generation due to random chance.<\/p>\n<p class=\"import-Normal\"><strong>Heterogeneity<\/strong>: The quality of being diverse genetically.<\/p>\n<p class=\"import-Normal\"><strong>Homog<\/strong><strong>enous<\/strong>: The quality of being uniform genetically.<\/p>\n<p class=\"import-Normal\"><strong>Human diversity<\/strong>: Human diversity is a measure of variation that may describe how many different forms of human there are, separated or clustered into groups according to some genetic, phenotypic, or cultural trait(s). The term can be applied to culture (in which case humans can be described as significantly diverse) or genetics (in which case humans are not diverse because all humans on Earth share a majority of their genes).<\/p>\n<p class=\"import-Normal\"><strong>Human variation<\/strong>: Differences in biology, physiology, body chemistry, behaviour, and culture. By measuring these differences, we understand the degrees of variation between individuals, groups, populations, or species.<\/p>\n<p class=\"import-Normal\"><strong>Isolation-by-distance model<\/strong>: A model that predicts a positive relationship between genetic distances and geographical distances between pairs of populations.<\/p>\n<p class=\"import-Normal\"><strong>Monogenetic<\/strong>: Pertaining to the idea that the origin of a species is situated in one geographic region or time (as opposed to <em>polygenetic<\/em>).<\/p>\n<p class=\"import-Normal\"><strong>Mutation<\/strong>: A gene alteration in the DNA sequence of an organism. As a random, neutral evolutionary process that occurs over the course of meiosis and early cell development, gene mutations are possible sources of variation in any given human gene pool. Genetic mutations that occur in more than 1% of a population are termed <em>polymorphisms<\/em>.<\/p>\n<p class=\"import-Normal\"><strong>Natural selection<\/strong>: An evolutionary process whereby certain traits are perpetuated through successive generations, likely owing to the advantages they give organisms in terms of chances of survival and\/or reproduction.<\/p>\n<p class=\"import-Normal\"><strong>Nonconcordance<\/strong>: The fact of genes or traits not varying with one another and instead being inherited independently.<\/p>\n<p class=\"import-Normal\"><strong>Otherness<\/strong>: In postcolonial anthropology, we now understand \u201cothering\u201d to mean any action by someone or some group that establishes a division between \u201cus\u201d and \u201cthem\u201d in relation to other individuals or populations. This could be based on linguistic or cultural differences, and it has largely been based on external characteristics throughout history.<\/p>\n<p class=\"import-Normal\"><strong>Out-of-Africa model<\/strong>: A model that suggests that all humans originate from one single group of <em>Homo sapiens<\/em> in (sub-Saharan) Africa who lived between 100,000 and 315,000 years ago and who subsequently diverged and migrated to other regions across the globe.<\/p>\n<p class=\"import-Normal\"><strong>Physical anthropology<\/strong>: This used to be the more common name given to the subdiscipline of anthropology centred upon the study of human origins, evolution and variation (also see <em>biological anthropology<\/em> above). This name for the field has gradually become less popular due to two reasons: first, it may not reflect our interests in other aspects of humankind that are not physical (such as those behavioural, cultural and spiritual), and second, using this term popular in the early decades of our field may be viewed by some as harkening back to a time when biological anthropologists conducted their work in unethical ways.<\/p>\n<p class=\"import-Normal\"><strong>Polygenetic<\/strong>: Having many different ancestries, as in older theories about human origins that involved multiple traditional groupings of humans evolving concurrently in different parts of the world before they merged into one species through interbreeding and\/or intergroup warfare. These earlier suggestions have now been overwhelmed by insurmountable evidence for a single origin of the human species in Africa (see the \u201cOut-of-Africa model\u201d).<\/p>\n<p class=\"import-Normal\"><strong>Polymorphism<\/strong>: A genetic variant within a population (caused either by a single gene or multiple genes) that occurs at a rate of over 1% among the population. Polymorphisms are responsible for variation in phenotypic traits such as blood type and skin colour.<\/p>\n<p class=\"import-Normal\"><strong>Population<\/strong>: A group of humans living in a particular geographical area, with more local interbreeding within-group than interbreeding with other groups. A limited or restricted amount of gene flow between populations can occur due to geographical, cultural, linguistic, or environmental factors.<\/p>\n<p class=\"import-Normal\"><strong>Population bottlenecking<\/strong>: An event in which genetic variation is significantly reduced owing to a sharp reduction in population size. This can occur when environmental disaster strikes or as a result of human activities (e.g., genocides or group migrations). An important example of this loss in genetic variation occurred over the first human migrations out of Africa and into other continental regions.<\/p>\n<p class=\"import-Normal\"><strong>Prejudice<\/strong>: An unjustified attitude toward an individual or group that is not based on reason, whether positive (and showing preference for one group of people over another) or negative (and resulting in harm or injury to others).<\/p>\n<p class=\"import-Normal\"><strong>Race<\/strong>: The identification of a group based on a perceived distinctiveness that makes that group more similar to each other than they are to others outside the group. This may be based on cultural differences, genetic parentage, physical characteristics, behavioural attributes, or something arbitrarily and socially constructed. As a social or demographic category, perceptions of \u201crace\u201d can have real and serious consequences for different groups of people. This is despite the fact that biological anthropologists and geneticists have demonstrated that all humans are genetically homogenous and that more differences can be found within populations than between them in the overall apportionment of human biological variation. This term is sometimes used interchangeably with <em>ethnicity<\/em>.<\/p>\n<p class=\"import-Normal\"><strong>Racism<\/strong>: Any action or belief that discriminates against someone based on perceived differences in race or ethnicity.<\/p>\n<p class=\"import-Normal\"><strong>Scientific Revolution<\/strong>: A period between the 1400s and 1600s when substantial shifts occurred in the social, technological, and philosophical sense, when a scientific method based on the collection of empirical evidence through experimentation was emphasized and inductive reasoning was used to test hypotheses and interpret their results.<\/p>\n<p class=\"import-Normal\"><strong>Typolog<\/strong><strong>ical<\/strong>: Of or describing an assortment system that relies on the interpretation of qualitative similarities or differences in the study of variation among objects or people. The categorization of cultures or human groups according to \u201crace\u201d was performed with a typological approach in the earliest practice of anthropology, but this practice has since been discredited and abandoned.<\/p>\n<p class=\"import-Normal\"><strong>Variance<\/strong>: In statistics, variance measures the dispersal of a set of data around the mean or average value.<\/p>\n<h2 class=\"import-Normal\">For Further Exploration<strong><br \/>\n<\/strong><\/h2>\n<h3 class=\"import-Normal\"><strong>Videos<\/strong><\/h3>\n<p>American Medical Association (AMA). 2020. \u201c<a href=\"https:\/\/www.youtube.com\/watch?v=tqA3KvvscYc\" target=\"_blank\" rel=\"noopener\">Examining Race-Based Medicine<\/a>.\u201d YouTube, October 29. Accessed June 4, 2023.<\/p>\n<p>Crenshaw, Kimberl\u00e9. 2016. \u201c<a href=\"https:\/\/www.youtube.com\/watch?v=akOe5-UsQ2o\" target=\"_blank\" rel=\"noopener\">The Urgency of Intersectionality<\/a>.\u201d YouTube, December 7. Accessed June 4, 2023.<\/p>\n<p>Golash-Boza, Tanya. 2018. \u201c<a href=\"https:\/\/www.youtube.com\/watch?v=NQOimokvJXo\" target=\"_blank\" rel=\"noopener\">What Is Race? What Is Ethnicity? Is There a Difference?<\/a>.\u201d YouTube, October 28. Accessed June 4, 2023.<\/p>\n<p>Lasisi, Tina. 2020. \u201c<a href=\"https:\/\/naturalhistory.si.edu\/education\/teaching-resources\/social-studies\/webinar-how-hair-reveals-futility-race-categories\" target=\"_blank\" rel=\"noopener\">How Hair Reveals the Futility of Race Categories<\/a>.\u201d National Museum of Natural History webinar, October 21.<\/p>\n<p>Lasisi, Tina. 2022. \u201c<a href=\"https:\/\/www.youtube.com\/watch?v=_BEJvVFxKV4\" target=\"_blank\" rel=\"noopener\">Where Does My Skin Color Come From?<\/a>.\u201d PBS Terra, August 18. Accessed June 4, 2023.<\/p>\n<p>PBS Origins. 2018. \u201c<a href=\"https:\/\/www.youtube.com\/watch?v=CVxAlmAPHec\" target=\"_blank\" rel=\"noopener\">The Origin of Race in the USA<\/a>.\u201d YouTube, April 3. Accessed June 4, 2023.<\/p>\n<p>Roberts, Dorothy. 2016. \u201c<a href=\"https:\/\/www.youtube.com\/watch?v=KxLMjn4WPBY\" target=\"_blank\" rel=\"noopener\">The Problem with Race-Based Medicine<\/a>.\u201d YouTube, March 4. Accessed June 4, 2023.<\/p>\n<p>Vox. 2015. \u201c<a href=\"https:\/\/www.youtube.com\/watch?v=VnfKgffCZ7U\" target=\"_blank\" rel=\"noopener\">The Myth of Race, Debunked in 3 Minutes<\/a>.\u201d YouTube, January 13. Accessed June 4, 2023.<\/p>\n<h3 class=\"import-Normal\"><strong>Podcast Episodes<\/strong><\/h3>\n<p>Kwong, Emily, and Rebecca Ramirez. 2021. \u201c<a href=\"https:\/\/www.npr.org\/2021\/10\/05\/1043391809\/heres-a-better-way-to-talk-about-hair\" target=\"_blank\" rel=\"noopener\">Here\u2019s a Better Way to Talk about Hair: A 16 Minute Listen with Tina, Lasisi<\/a>\u201d NPR Short Wave, October 6. Accessed June 4, 2023.<\/p>\n<p>Speaking of Race. 2020. \u201c<a href=\"https:\/\/soundcloud.com\/user-88955638\/sets\/race-and-health?fbclid=IwAR2U1jdQL3XYFS5llGvYZ6uSrvPikuakmbxUZb--8voxgAMKrLbu7Ym7LGU\" target=\"_blank\" rel=\"noopener\">Race and Health series<\/a>.\u201d Speaking of Race, April 10. Accessed June 4, 2023.<\/p>\n<h3 class=\"import-Normal\"><strong>Websites<\/strong><\/h3>\n<p>Choices Program. 2023. \u201c<a href=\"https:\/\/www.choices.edu\/teaching-news-lesson\/an-interactive-timeline-black-activism-and-the-long-fight-for-racial-justice\/\" target=\"_blank\" rel=\"noopener\">An Interactive Timeline: Black Activism and the Long Fight for Racial Justice<\/a>.\u201d <em>Choices Program, Brown University<\/em> [Interactive Timeline], Updated February, 2023.<\/p>\n<h2 class=\"import-Normal\">References<\/h2>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">American Association of Biological Anthropologists. 2020. \u201c<a href=\"https:\/\/bioanth.org\/about\/position-statements\/open-letter-our-community-response-police-brutality-against-african-americans-and-call-antiracist-action\/\" target=\"_blank\" rel=\"noopener\">An Open Letter to Our Community in Response to Police Brutality against African-Americans and a Call to Antiracist Action<\/a>\u201d. <em>American Association of Biological Anthropologists<\/em>, June 10, 2020. Accessed June 4, 2023.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Antrosio, Jason. 2011. \u201c\u2018<a href=\"https:\/\/www.livinganthropologically.com\/biological-anthropology\/race-reconciled-debunks-race\/\" target=\"_blank\" rel=\"noopener\">Race Reconciled\u2019: Race Isn\u2019t Skin Color, Biology, or Genetics<\/a>.\u201d <em>Living Anthropologically <\/em>(website), June 5, 2011; updated May 20, 2020. Accessed June 4, 2023.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Beals, Kenneth L., Courtland L. Smith, Stephen M. Dodd, J. Lawrence Angel, Este Armstrong, Bennett Blumenberg, Fakhry G. Girgis, et al. 1984. \u201cBrain Size, Cranial Morphology, Climate, and Time Machines [and Comments and Reply].\u201d <em>Current Anthropology<\/em> 25 (3): 301\u2012330.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Betti, Lia, Fran\u00e7ois Balloux, Tsunehiko Hanihara, and Andrea Manica. 2010. \u201cThe Relative Role of Drift and Selection in Shaping the Human Skull.\u201d <em>American Journal of Physical Anthropology<\/em> 141 (1): 76\u201282. https:\/\/doi.org\/10.1002\/ajpa.21115.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Betti, Lia, Fran\u00e7ois Balloux, William Amos, Tsunehiko Hanihara, and Andrea Manica. 2009. \u201cDistance from Africa, Not Climate, Explains Within-Population Phenotypic Diversity in Humans.\u201d <em>Proceedings: Biological Sciences<\/em> 276 (1658): 809\u2012814. https:\/\/doi.org\/10.1098\/rspb.2008.1563.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Betti, Lia, Noreen von Cramon-Taubadel, Andrea Manica, and Stephen J. Lycett. 2013. \u201cGlobal Geometric Morphometric Analyses of the Human Pelvis Reveal Substantial Neutral Population History Effects, Even across Sexes.\u201d <em>PloS ONE<\/em> 8 (2): e55909. https:\/\/doi.org\/10.1371\/journal.pone.0055909.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Betti, Lia, Noreen von Cramon-Taubadel, Andrea Manica, and Stephen J. Lycett. 2014. \u201cThe Interaction of Neutral Evolutionary Processes with Climatically Driven Adaptive Changes in the 3D Shape of the Human Os Coxae.\u201d <em>Journal of Human Evolution<\/em> 73 (August): 64\u201274. https:\/\/doi.org\/10.1016\/j.jhevol.2014.02.021.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Boas, Franz. 1931. \u201cRace and Progress.\u201d <em>Science<\/em> 74 1905): 1\u20128.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Bowden, Rory, Tammie S. MacFie, Simon Myers, Garrett Hellenthal, Eric Nerrienet, Ronald E. 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Valley. 2020. \u201cRacial Bias in Pulse Oximetry Measurement.\u201d <em>The New England Journal of Medicine<\/em> 383: 2477-2478.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Staes, Nicky, Chet C. Sherwood, Katharine Wright, Marc de Manuel, Elaine E. Guevara, Tomas Marques-Bonet, Michael Kr\u00fctzen, et al. 2017. \u201cFOXP2 Variation in Great Ape Populations Offers Insight into the Evolution of Communication Skills.\u201d <em>Scientific Reports<\/em> 7 (1): 1\u201210. https:\/\/doi.org\/10.1038\/s41598-017-16844-x.<\/p>\n<p class=\"import-Normal\">Tomati, Opal. 2016. \u201cAn Interview with the Founders of Black Lives Matter.\u201d TED Talks 2016, October 26\u201228. 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San Francisco: City Lights.<\/p>\n<p class=\"import-Normal\" style=\"margin-left: 0pt;text-indent: 0pt\">Yudell, Michael, Dorothy Roberts, Rob DeSalle, and Sarah Tishkoff. 2016. \u201cTaking Race out of Human Genetics.\u201d <em>Science<\/em> 351 (6273): 564\u2012565. https:\/\/doi.org\/10.1126\/science.aac4951.<\/p>\n<\/div>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_1699_1914\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_1699_1914\"><div tabindex=\"-1\"><\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_1699_1915\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_1699_1915\"><div tabindex=\"-1\"><\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close 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definition<\/span><\/button><\/div><\/template><\/div>","protected":false},"author":96,"menu_order":34,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["joylin-namie"],"pb_section_license":""},"chapter-type":[],"contributor":[85],"license":[],"class_list":["post-1699","chapter","type-chapter","status-publish","hentry","contributor-joylin-namie"],"part":20,"_links":{"self":[{"href":"https:\/\/opentextbooks.concordia.ca\/explorations3\/wp-json\/pressbooks\/v2\/chapters\/1699","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/opentextbooks.concordia.ca\/explorations3\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/opentextbooks.concordia.ca\/explorations3\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/opentextbooks.concordia.ca\/explorations3\/wp-json\/wp\/v2\/users\/96"}],"version-history":[{"count":5,"href":"https:\/\/opentextbooks.concordia.ca\/explorations3\/wp-json\/pressbooks\/v2\/chapters\/1699\/revisions"}],"predecessor-version":[{"id":1890,"href":"https:\/\/opentextbooks.concordia.ca\/explorations3\/wp-json\/pressbooks\/v2\/chapters\/1699\/revisions\/1890"}],"part":[{"href":"https:\/\/opentextbooks.concordia.ca\/explorations3\/wp-json\/pressbooks\/v2\/parts\/20"}],"metadata":[{"href":"https:\/\/opentextbooks.concordia.ca\/explorations3\/wp-json\/pressbooks\/v2\/chapters\/1699\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/opentextbooks.concordia.ca\/explorations3\/wp-json\/wp\/v2\/media?parent=1699"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/opentextbooks.concordia.ca\/explorations3\/wp-json\/pressbooks\/v2\/chapter-type?post=1699"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/opentextbooks.concordia.ca\/explorations3\/wp-json\/wp\/v2\/contributor?post=1699"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/opentextbooks.concordia.ca\/explorations3\/wp-json\/wp\/v2\/license?post=1699"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}