{"id":204,"date":"2023-03-30T22:41:58","date_gmt":"2023-03-30T22:41:58","guid":{"rendered":"https:\/\/pressbooks.ccconline.org\/ppscant2550medicalanthropology\/chapter\/4-9-syndemics-and-the-ecological-model\/"},"modified":"2023-04-06T20:03:15","modified_gmt":"2023-04-06T20:03:15","slug":"4-9-syndemics-and-the-ecological-model","status":"publish","type":"chapter","link":"https:\/\/pressbooks.ccconline.org\/ppscant2550medicalanthropology\/chapter\/4-9-syndemics-and-the-ecological-model\/","title":{"raw":"4.9: SYNDEMICS AND THE ECOLOGICAL MODEL","rendered":"4.9: SYNDEMICS AND THE ECOLOGICAL MODEL"},"content":{"raw":"
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It is important to recognize that disease risk is not spread evenly within or between populations. Diseases also combine and interact to create a syndemic<\/strong>, where the coexistence of two or more conditions exacerbates the effects of one or all conditions. One example is coinfection with HIV and Mycobacterium tuberculosis<\/em>, which is associated with more rapid disease progression, worse symptoms, and a higher pathogenic load than during a single infection with either agent (Singer et al. <\/em>2017). Syndemic risk also includes social, political, economic, and environmental factors that increase risk for the clustering of two or more diseases (Singer et al. 2017; Singer and Clair 2003). One of the first syndemics identified involved substance abuse, violence, and AIDS (SAVA), in which the inner-city health crisis around HIV\/AIDS was related to other conditions, including tuberculosis, sexually transmitted infections, hepatitis, cirrhosis, infant mortality, drug abuse, suicide, and homicide. These were, in turn, 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 ecological model<\/strong> of health and disease, a more holistic way of viewing health issues and their solutions than focusing solely on biology and medical intervention (Sallis et al. 2008).<\/p>\r\n

A historical example will serve to illustrate these concepts. You will remember the discussion of the first epidemiological transition from earlier in this chapter. This involved a rise in infectious disease following human adoption of agriculture as a primary subsistence strategy. This transition took place in the Old World and was fueled by zoonotic pathogens that infected humankind following the domestication of cattle, pigs, horses, sheep, goats, chickens, and other species. During the thousands of years following that transition, epidemics repeatedly occurred among Old World populations resulting in periods of crisis mortality, when large numbers of people died. This was followed by population recovery as survivors, who often became immune to reinfection, produced new generations to be infected during the next epidemic (Omran 2005). This same set of interactions did not, however, occur in the New World, where species that might have developed into domesticated animals equivalent to horses and cattle were wiped out at the end of the last Ice Age, when humans are hypothesized to have migrated to the New World across an exposed land bridge in the Arctic (Diamond 1997). These extinctions may have been the result of hunting or climate change or a combination of both. What is important to note is that the land bridge disappeared as sea levels rose at the end of the Ice Age, isolating the Americas until European contact in the 15th century. This isolation was to have severe consequences for Native Americans.<\/p>\r\n

When Columbus \u201cdiscovered\u201d the New World in 1492, he unleashed one of the first waves of infectious disease that decimated Native American populations in the centuries to follow (Crosby 2003), eventually killing 90% of the population, an estimated 20 million people (Diamond 1997). The devastation of native communities was the result of a combination of factors. One was the very different histories of Europe and the Americas. With no history of animal domestication beyond dogs, turkeys, ducks, guinea pigs, llamas, and alpacas, Native Americans did not fall prey to zoonotic pathogens that produced highly contagious infectious diseases, leaving them with no resistance. Also, in spite of their profound differences in culture, language, subsistence, and political and economic systems, Native Americans were genetically very much alike (Crosby 2003). This was due to the small number of individuals who crossed the land bridge, which then closed, leaving them in genetic isolation for 10,000 years or more. This meant there was not a high degree of variation for natural selection to act upon in the midst of the severe evolutionary pressure of smallpox and other infectious diseases introduced by Europeans. Native Americans had also not benefited from the technological developments associated with warfare in the Old World, including steel swords, guns, and fighting on horseback, that had been perfected over centuries of conflict (Diamond 1997). European conquest also toppled existing political and social systems already crippled by epidemics of disease, leading to social disorder and cultural and economic disruption. To compound the situation, European colonization included the enslavement and forced labor of native populations to serve European interests, resulting in injury, starvation, and other mistreatment and leading to further loss of life. This complex of epidemiological, technological, social, political, and economic factors (a syndemic) combined to nearly exterminate Native Americans in the centuries following European contact, but this need not have been the case. Alfred Crosby (2003) points out that although epidemics among immunologically unprepared populations produce high mortality rates, some individuals survive, and the population will recover if left alone. He reminds us that,<\/p>\r\n\r\n

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Europe, for instance, lost one-third of its population to the Black Death in the fourteenth century and recovered in time. If the Black Death had been\u00a0accompanied by the arrival of Genghis Khan\u2019s hordes, miraculously plague-proof, the story would have been very different. It might have been similar to what\u00a0happened when European settlers followed on the heels of smallpox and other infections previously unknown to American Indians. [Crosby 2003:xxii]<\/p>\r\n\r\n<\/div>\r\n

Unfortunately, syndemics did not begin or end with European colonization of the New World. Interactions between disease and income inequality, education, discrimination, warfare, migration, climate change, and a host of other factors continue to affect humans today, causing health disparities that lead to differences in morbidity and mortality within and across nations (Singer and Baer 2012; see Figure 16.9).<\/p>\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n
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United States<\/strong><\/p>\r\n<\/td>\r\n

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Worldwide<\/strong><\/p>\r\n<\/td>\r\n<\/tr>\r\n

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1. Heart disease<\/p>\r\n<\/td>\r\n

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1. Heart disease<\/p>\r\n<\/td>\r\n<\/tr>\r\n

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2. Cancer<\/p>\r\n<\/td>\r\n

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2. Stroke<\/p>\r\n<\/td>\r\n<\/tr>\r\n

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3. Accidents<\/p>\r\n<\/td>\r\n

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3. Chronic Obstructive Pulmonary Disease<\/p>\r\n<\/td>\r\n<\/tr>\r\n

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4. Chronic lower respiratory diseases<\/p>\r\n<\/td>\r\n

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4. Lower respiratory infections<\/p>\r\n<\/td>\r\n<\/tr>\r\n

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5. Stroke<\/p>\r\n<\/td>\r\n

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5. Alzheimer disease and dementia<\/p>\r\n<\/td>\r\n<\/tr>\r\n

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6. Alzheimer\u2019s disease<\/p>\r\n<\/td>\r\n

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6. Lung cancer<\/p>\r\n<\/td>\r\n<\/tr>\r\n

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7. Diabetes<\/p>\r\n<\/td>\r\n

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7. Diabetes mellitus<\/p>\r\n<\/td>\r\n<\/tr>\r\n

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8. Influenza and pneumonia<\/p>\r\n<\/td>\r\n

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8. Road injury<\/p>\r\n<\/td>\r\n<\/tr>\r\n

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9. Kidney disease<\/p>\r\n<\/td>\r\n

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9. Diarrheal diseases<\/p>\r\n<\/td>\r\n<\/tr>\r\n

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10. Suicide<\/p>\r\n<\/td>\r\n

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10. Tuberculosis<\/p>\r\n<\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\n

Figure 4.7<\/strong>\u00a0Top ten causes of death in the U.S. and worldwide.<\/em><\/p>\r\n

Although a full discussion of global health disparities is beyond the scope of this chapter, a brief discussion of asthma in the United States can shed light on several common factors that contribute to inequalities in health today. Nearly 20 million people in the U.S. suffer from asthma, over a third of whom are children under 18 years of age (CDC 2017). Childhood-asthma prevalence doubled from 1980 to 1995, then increased slowly from 2001 to 2010, leveling off in 2013. Rates of asthma are highest among African American and Latino children (Akinbami et al. 2016). Among Latinos, Puerto Ricans have the highest lifetime asthma rate (16.9%), more than three times the rate for Mexican Americans (Singer and Baer 2012). Given that most adult asthma has its origins in early life, discovering the causes of childhood asthma and preventing it has become a major public health focus (Beasley et al. 2015).<\/p>\r\n

A range of factors contribute to the development of asthma in childhood. These include genetics and family history, as well as exposure to stress and being born into a single-parent family. Other factors include being a low-birth-weight baby or being born prematurely. Living in an urban environment, being exposed to indoor and outdoor air pollution, including cigarette smoke, is also a contributor. Certain childhood infections (e.g., pertussis), antibiotics use, and exposure to environmental toxins like mold are also associated with asthma. Diets high in trans-fatty acids and salt, especially fast-food, also contribute to the development of asthma. Sedentarism, high BMI, overweight, and obesity are also factors, with incidence increased by 20% in overweight children and doubled for obese kids (Chen et al. 2012). There are also gender differences associated with the obesity-asthma connection, with boys experiencing higher rates until age 13 and asthma becoming more prevalent in girls post-puberty (Beasley et al. 2015). The mechanisms behind this are unknown but may include anatomical differences in lung capacity, sleep disorders, body fat distribution, and inflammation (Chen et al. 2012). In keeping with the hygiene hypothesis, children exposed to dogs or farm animals in early childhood, including before age one, are less likely to develop asthma (Fall et al. 2015), especially children in urban environments where they may have less frequent contact with the natural environment (Dunn 2018).<\/p>\r\n

Differences in prevalence of childhood asthma between ethnic groups within a population are not mainly because of genetic differences but, rather, because of differences in exposure to environmental and lifestyle factors (Beasley et al. 2015). Given this, let us examine the case of African American and Latino children in light of the risk factors just described. Working-class people and people of color in the U.S. are more likely to live in close proximity to freeways and environmental threats like petrochemical plants and waste incinerators. They are also more likely to live in poverty and in areas with high rates of crime and violence, which elevate stress levels, as does racial discrimination (Singer and Baer 2012). African American children are also far more likely than other groups in the U.S. to grow up in female-headed households, with 72% now being born to single mothers (Washington 2010), many of whom live in poverty and lack access to health care (Pearl 2015). Accurate diagnosis and treatment are key to management of childhood asthma, yet many children of color remain undiagnosed, in part because of lack of regular check-ups. One study conducted among Puerto Ricans in Chicago found prevalence of asthma among Puerto Rican children jumped to 34% when counting cases of possible asthma based on reports of patient symptoms rather than a physician\u2019s diagnosis (Joseph et al. 1996). Another study, conducted in New York City, demonstrated that Puerto Rican children were more likely to miss school because of asthma than other ethnic groups in the same neighborhoods, and that low-income Latino families with children with asthma were less likely to have training, education, and resources to manage their child\u2019s asthma (Findley et al.<\/em> 2003). A 2002 study of over 1,000 American children and their families found that Latino and African American children were less likely to be prescribed the standard treatment for asthma and that Latino children received fewer inhaled steroids than white children (Ortega et al. 2002). Clearly, there are multiple factors contributing to health disparities in asthma for American children of different ethnic backgrounds, suggesting an ecological approach is necessary for addressing the problem.<\/p>\r\n

Currently, there is no cure for asthma and no vaccine against it. Instead, public health efforts have largely focused on diagnosis, treatment, and education in place of prevention (Beasley et al. <\/em>2015). Given the sheer number of risk factors involved, some scholars have begun to question whether prevention is even possible. Richard Beasley and colleagues (2015:1078) explain: \u201cPublic health efforts will need to focus on reducing environmental tobacco exposure, reducing indoor and outdoor air pollution and occupational exposures, reducing childhood obesity and encouraging a diet high in vegetables and fruit, improving fetal and maternal health, encouraging breastfeeding, promoting childhood vaccinations, and reducing social inequalities.\u201d These challenges serve to remind us to take an ecological approach to health and disease. As humans, we all have our biology and genetics with which to contend, but we often do so in the midst of very different life circumstances.<\/p>\r\n\r\n

ARE WE STILL EVOLVING?<\/h2>\r\n

Given the current global burden of non-communicable diseases like heart disease, cancer, and diabetes discussed in this chapter, many students ask why humans have not yet evolved in response. First, the health conditions highlighted here do not typically have repercussions on reproductive success, meaning natural selection cannot act to favor one genotype over another to protect against them. There also may not have been sufficient time for natural selection to act (Stearns et al. 2008). The cultural transformation of our food supply and lifestyle came about quickly. The transition from foraging to farming took place beginning 12,000 years ago, industrial food production came about in the last 200 years, and technologies like television, the internet, and social media that promote sedentarism are less than 75 years old\u2014one human lifetime. Even under the strongest selective pressure, evolution takes many generations. For example, the mutation that led pastoral populations to be able to digest fresh milk likely took 8,000 years, or 325 generations, to reach a frequency of 90% (Crow and Kimura 1970). This does not mean, however, that humans have stopped evolving. As a species, we continue to respond to selective pressures biologically and culturally. This portion of the chapter will focus on contemporary examples of human evolution.<\/p>\r\n

Before beginning, let\u2019s remind ourselves of the modern definition of evolution<\/em>, which is a change in allele frequencies across generations in a given population for a particular trait. We must also review the conditions necessary for natural selection to operate on a trait. First, the trait must be heritable, meaning it is transmitted genetically from generation to generation. Non-inherited traits are learned and include things like cultural preferences for certain types of foods or who we think it is best to marry. Not only must a trait be heritable, there must also be variation of the trait in human populations and the trait must influence reproductive success. Three examples of traits that meet these criteria are immunity to HIV, height, and wisdom teeth (Andrews et al. 2011).<\/p>\r\n

AIDS is a potentially fatal infectious disease caused by the Human Immunodeficiency Virus (HIV), a zoonosis believed to be derived from Simian Immunodeficiency Viruses (SIVs) found in chimpanzees and monkeys, most likely transmitted to humans through the butchering of infected animals (Sharp and Hahn 2011). In total, 35 million people have died from AIDS-related illnesses since the start of the global epidemic in the 1980s. There were 36.7 million people around the world living with AIDS as of 2016, including 1.8 million new cases and 1 million deaths in that year alone (UNAIDS 2018). A disease causing this level of morbidity and mortality represents a major selective pressure, especially given that infection can occur before birth (Goulder et al. 2016), having an affect on future reproductive success.<\/p>\r\n

The majority of people in the world are highly susceptible to HIV infection, but some are not. There are individuals who are homozygous for a rare, recessive allele at the CCR5 locus who are immune. Heterozygotes who inherit a single copy of this allele are more resistant to infection and the disease takes longer to progress in the event they are infected. The mechanism by which the allele prevents infection involves a 32-base pair deletion in the DNA sequence of the CCR5 gene, creating a non-functioning receptor on the surface of the cell that prevents HIV from infecting the cell. The allele is inherited as a simple Mendelian trait, and there is variation in its prevalence, ranging as high as 14% of the population in northern Europe and Russia (Novembre et al. 2005; see Figure 16.8). What is interesting about the allele\u2019s geographic distribution is that it does not map onto parts of the world with the highest rates of HIV infection (UNAIDS 2018), suggesting that AIDS was not the original selective pressure favoring this allele (Figure 16.10 and Figure 16.11).<\/p>\r\n\r\n\r\n[caption id=\"\" align=\"alignleft\" width=\"194\"]\"Map Figure 4.8<\/strong>\u00a0Map of CCR5-delta32 allele distribution.[\/caption]\r\n\r\n[caption id=\"\" align=\"alignleft\" width=\"225\"]\"Map Figure 4.9 <\/strong>Map of global HIV infection.[\/caption]\r\n

Given its current geographic distribution, the bubonic plague, which ravaged Europe repeatedly from the 14th to the 19th centuries (Pamuk 2007), was initially proposed as the selective agent. Subsequent research suggests smallpox, which killed up to 400,000 people annually in 18th-century Europe (Hays 2005), was more likely the selective pressure (Novembre et al. 2005). Given the mortality rates for smallpox and the selective pressure it has exhibited on humanity for centuries (Crosby 2003), an allele that conferred immunity was highly advantageous, as it is for those faced with the threat of HIV infection today. There are efforts to employ the natural immunity this mutation provides in the creation of an AIDS vaccine (Lopalco 2010).<\/p>\r\n

Height is another example of a trait currently experiencing selective pressure. If you have ever toured a historical site, you have likely hit your head on a doorframe or become claustrophobic trying to squeeze down a narrow hallway under a lower-than-average ceiling. It is not your imagination. Humans have gotten taller in recent centuries. In fact, the average height of people in industrialized nations has increased approximately 10 centimeters (about four inches) in the past 150 years. This increase has been attributed to improvements in nutrition, sanitation, and access to medical care (Hatton 2014). But this is only part of the story.<\/p>\r\n

Height is highly heritable. Studies indicate 80% of variation in height within populations is due to genetics, with 697 different genetic variances identified as having an effect on adult stature (Devuyst 2014). Multiple studies also demonstrate a positive relationship between height and reproductive success for men (Andrews et al. 2011). This is primarily due to sexual selection and nonrandom mating, namely women\u2019s preferences for taller men, which may explain why height is one characteristic men often lie about on dating websites (Guadagno et al. 2012). Sexual selection also plays out with regard to economic success in Western cultures, with taller men more likely to be in higher-level positions that pay well. Research demonstrates an inch of height is worth an additional $789 per year in salary, meaning a man who is six feet tall will earn on average $5,525 more per year than an identical man who is five foot five (Gladwell 2007). Over the course of a thirty-year career, this adds up to hundreds of thousands of dollars, likely allowing the taller man to attract more potential mates and increase his reproductive success.<\/p>\r\n

Wisdom teeth are also undergoing evolutionary pressure. Have you or anyone in your family had their wisdom teeth removed? It can be a painful and expensive process, and it is a common experience in Western nations. Conversely, do you know anyone whose wisdom teeth never came in? That is fairly common in other populations, suggesting evolutionary pressure favoring the absence of wisdom teeth has been culturally influenced. According to research by physical anthropologists, the oldest fossil evidence of skulls missing third molars was found in China and is 300,000 to 400,000 years old, suggesting the earliest mutation selecting against the eruption of wisdom teeth arose in Asia (Main 2013). Since that time, jaws have continued to decrease in size to the point they often cannot accommodate third molars, which can become impacted, painful, and even infected, a condition physical anthropologist Alan Main argues might have interfered with the ability to survive and reproduce in ancestral populations (Main 2013). As we have learned, a mutation that positively influences reproductive success\u2014such as being born without the trait to develop wisdom teeth in an environment where food was cooked before eating\u2014would likely be selected for over time. Evidence in modern humans suggests this is the case, with 40% of modern Asians and 45% of Native Alaskans and Greenlanders (populations descended from Asian populations) lacking wisdom teeth. The percentage among those of European descent ranges from 10 to 25% and for African Americans is 11% (Main 2013). Earlier chapters in this text emphasize that directional selection progresses along a particular path until the environment changes and a trait is no longer advantageous. In the case of wisdom teeth, the ability of modern dentistry to preempt impaction through surgery may, in fact, be what is preventing natural selection from doing away with wisdom teeth altogether.<\/p>\r\n\r\n

FOOD FOR THOUGHT<\/h2>\r\n

This chapter focused on health conditions prevalent in contemporary, industrialized societies that are due, in part, to the mismatch between our evolved biology and modern cultural and physical environments. Obesity is at the root of it all. Claude Bouchard (2007) identified factors contributing to the global epidemic of obesity and the diseases associated with it. These are the built environment and the social environment, which together form the obesogenic environment in which unhealthy behaviors 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\"]\"Students Figure 4.10<\/strong>\u00a0Students walking around campus.[\/caption]\r\n

In terms of the built environment, consider your campus or neighborhood from an evolutionary perspective. To what degree does the construction of the space lend itself to physical activity as part of daily life? Is your campus constructed in such a way that it promotes the use of automobiles 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 or the neighborhood on foot or by bike in all weather? After dark? How about the classrooms and computer labs? Do they have standing or treadmill desks as options? Does your class schedule encourage walking from building to building between classes, or are most courses in your major scheduled in the same location? I regularly have students who sit in the same room for hours, not even changing desks, while instructors rush from place to place. Most college majors also lack a physical activity requirement, leaving it up to students to incorporate exercise into already-busy schedules (See Figure 4.10).<\/p>\r\n

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 nutritional options on campuses have 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> 2013). There are also parties and other social events, a normal part of college life, that often involve unhealthy food and encourage behaviors like alcohol consumption and smoking. Give some thought to the social atmosphere on your campus and the ways in which 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 not healthy, 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

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 favorite shows. Doing so often involves eating, as well as multiple exposures to food advertising embedded in the shows themselves. In these many ways, college contributes to the development of obesogenic behaviors that can have negative health ramifications long after college is over (Small et al. 2013).<\/p>\r\n

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 behavior 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). Realizing this, many colleges and universities have instituted programs to encourage healthier eating and more physical activity among students (Plotnikoff et al.<\/em> 2015). Some schools have even done away with collegiate sports, which often serve a small percentage of students, in favor of campus-wide efforts at getting everyone active (Tierney 2013). Investigate the options on your campus and take advantage of opportunities. We cannot change our biology, but we can certainly change our habits.<\/p>\r\n\r\n

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Exercises<\/p>\r\n\r\n<\/header>\r\n

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Review Questions<\/h2>\r\n