16.4: Syndemics and the Ecological Model

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, 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, 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. 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 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).

Definition: syndemic

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 behavioral 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 non-communicable diseases, mental health problems, behavioral conditions, toxic exposure, and malnutrition.

Definition: ecological model

Ecological models of health and disease emphasize environmental and policy contexts of behavior, while incorporating social and psychological influences, rather than focusing on individual behaviors. These models encompass multiple levels of influence and can lend themselves to more comprehensive health interventions.

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.

When Columbus “discovered” 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,

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

accompanied by the arrival of Genghis Khan’s hordes, miraculously plague-proof,

the story would have been very different. It might have been similar to what

happened when European settlers followed on the heels of smallpox and other

infections previously unknown to American Indians. [Crosby 2003:xxii]

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 Table \(\PageIndex{1}\)).

Table \(\PageIndex{1}\): Top ten causes of death in the U.S. and worldwide.

United States	Worldwide
1. Heart disease	1. Heart disease
2. Cancer	2. Stroke
3. Accidents	3. Chronic Obstructive Pulmonary Disease
4. Chronic lower respiratory diseases	4. Lower respiratory infections
5. Stroke	5. Alzheimer disease and dementia
6. Alzheimer’s disease	6. Lung cancer
7. Diabetes	7. Diabetes mellitus
8. Influenza and pneumonia	8. Road injury
9. Kidney disease	9. Diarrheal diseases
10. Suicide	10. Tuberculosis

 

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).

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).

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’s 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’s asthma (Findley et al. 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.

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. 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: “Public 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.” 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.

REFERENCES

Akinbami, Lara J., Alan E. Simon, and Lauren M. Rossen. 2016. “Changing Trends in Asthma Prevalence among Children.” Pediatrics 137 (1). doi:10.1542/peds.2015-2354.

Beasley, Richard, Alex Semprini, and Edwin A. Mitchell. 2015. “Risk Factors for Asthma: Is Prevention Possible?” The Lancet 386 (9998): 1075–1085.

Centers for Disease Control and Prevention (CDC). 2017. “Human Papillomavirus.” Genital HPV Infection—Fact Sheet. Atlanta, GA: Centers for Disease Control and Prevention.

Centers for Disease Control and Prevention (CDC). 2017. “Asthma.” National Center for Health Statistics. https://www.cdc.gov/nchs/fastats/asthma.htm.

Chen, Yang, Yi-Lun Lee, and Guang-Hui Dong. 2012. “Gender Difference of Childhood Overweight and Obesity in Predicting the Risk of Incident Asthma: A Systematic Review and Meta-Analysis.” Obesity Reviews 14 (3): 222–231. doi:10.1111/j.1467-789X.2012.01055.x

Crosby, Alfred W., Jr. 2003. The Columbian Exchange: Biological and Cultural Consequences of 1492. 30th Anniversary Edition. Westport, CT: Praeger Publishers.

Diamond, Jared 1997. Guns, Germs, and Steel: The Fates of Human Societies. New York: W. W. Norton.

Dunn, Robb. 2018. Never Home Alone: From Microbes to Millipedes, Camel Crickets, and Honeybees, the Natural History of Where We Live. New York: Basic Books.

Fall, Tove, Cecilia Lundholm, Anne K. Orkqvist, Katja Fall et al. 2015. Early Exposure to Dogs and Farm Animals and the Risk of Childhood Asthma. JAMA Pediatrics 169 (11). doi: 10.1001/jamapediatrics.2015.3219.

Findley, Sally, Katherine Lawler, Monisha Bindra, Linda Maggio, Madeline M. Penachio, and Christopher Maylahn. 2003. “Elevated Asthma and Indoor Environmental Exposures among Puerto Rican Children of East Harlem.” Journal of Asthma 40 (5): 557–569.

Joseph, Christine L. M., Betsy Foxman, Frederick E. Leickly, Edward Peterson, and Dennis Ownby. 1996. “Prevalence of Possible Undiagnosed Asthma and Associated Morbidity among Urban Schoolchildren.” Journal of Pediatrics 129 (5): 735–742.

Omran, Abdel R. 2005. “The Epidemiological Transition: A Theory of the Epidemiology of Population Change.” The Milbank Quarterly 83 (4): 731–757.

Ortega, Alexander Neil, Peter J. Gergen, A. David Paltiel, Howard Bauchner, Kathleen D. Belanger, and Brian P. Leaderer. 2002. “Impact of Site of Care, Race, and Hispanic Ethnicity on Medication Use for Childhood Asthma.” Pediatrics 109 (1): E1.

Pearl, Robert. 2015. “Why Health Care Is Different if You’re Black, Latino, or Poor.” Forbes, March 5. https://www.forbes.com/sites/robertp.../#1ab6e3807869.

Sallis, James F., Neville Owen, and Edwin B. Fisher. 2008. “Chapter 20: Ecological Models of Health Behavior.” In Health Behavior and Health Education: Theory, Research, and Practice, edited by Karen Glanz, Barbara K. Rimer, and K. Viswanath, 465–485. Fourth Edition. San Francisco, CA: Jossey-Bass.

Singer, Merrill, and Hans Baer. 2012. “Health Disparity, Health Inequality.” In Introducing Medical Anthropology: A Discipline in Action, Second edition, edited by Merrill Singer and Hans Baer, 175–205. Lanham, MD: AltaMira.

Singer, Merrill, and Scott Clair. 2003. “Syndemics and Public Health: Reconceptualizing Disease in Bio-Social Context.” Medical Anthropology Quarterly 17 (4): 423–441.

Singer, Merrill, Nicola Bulled, Bayla Ostrach, and Emily Mendenhall. 2017. “Syndemics and the Biosocial Conception of Health.” Lancet 389 (10072): 941–950.

Washington, Jesse. 2010. “Blacks Struggle with 72% Unwed Mothers Rate.” NBCNEWS.com, November 7. http://www.nbcnews.com/id/39993685/n.../#.XEETH89KjBJ.

TABLE ATTRIBUTION

Table \(\PageIndex{1}\):  Top ten causes of death in the U.S. and worldwide original to Explorations: An Open Invitation to Biological Anthropology by Joylin Namie is under a CC BY-NC 4.0 License. Based on data from Centers for Disease Control and Prevention (2016) and World Health Organization (2018).