over the life course (Schmeer and Tarrence 2018). Also, being married and integrated into social groups have been found to predict reduced risk of nicotine dependence in men with a genetic susceptibility to intense nicotine cravings when stressed (Perry 2016), while strong family social support prevented genetic predispositions toward alcoholism (Pescosolido et al. 2008). In these studies, social adversity, inequality, childhood stress, marital status, group membership, and family support are all collective social variables acting on individuals as causal entities.
There is additional evidence showing that chronic strain from disadvantaged social circumstances initiates differences in cell aging much earlier among low socioeconomic status (SES) children, thereby triggering premature aging long before the onset of old age (Needham et al. 2012). Other research has found that lower SES persons carry a significantly greater allostatic load in late life than higher SES individuals and their adverse life experiences in the lower class have a cumulative negative effect on their health (Das 2013; Gruenewald et al. 2012; Seeman et al. 2008). Allostatic loads refer to cumulative wear and tear on the body’s organic systems as it repeatedly adapts to chronic stressors. High allostatic loads producing signs of premature aging have been described as “weathering” by Arline Geronimus. She and her colleagues (Geronimus et al. 2006, 2015) found support for the weathering hypothesis among a sample of disadvantaged African Americans subjected to racial discrimination and also in a multiracial sample of distressed neighborhoods in Detroit experiencing poverty. In the latter study, the length of telomeres in the body were shorter for the poor than the nonpoor, indicating greater stress-related biological aging. Telomeres are protein caps at the end of each strand of DNA that function to protect chromosomes. They naturally become shorter over time causing cells to age. Telomeres can be shortened prematurely, however, by chronic stress bringing on early aging or weathering.
Social situations are not just causal in relation to genetics, allostatic loads, and other biological phenomena, but also with respect to class differences and living conditions that either harm or promote health. Adam Lippert (2016) found, for instance, that neighborhoods were significant in determining obesity. Adolescents consistently living in poor neighborhoods were more likely than adolescents in more affluent neighborhoods to become obese as adults. Leaving severe poverty neighborhoods curtailed the risk of obesity, while entering or remaining in such neighborhoods increased the risk. Again, we find social dissimilarities having a causal role.
The relevance of social factors in causation is also apparent from the different roles these factors perform in the traditional epidemiological agent–host–environment triad. Agents are the immediate or proximal cause of a particular disease and can be biological, nutritional, chemical, physical, or social. Hosts are the people susceptible to the agent, and the environment consists of factors external to the person, including agents, which either cause or influence health. Agents can be social, as seen in the health effects generated by class position, occupations, neighborhoods, and lifestyles; human hosts reflect traits that are both social (habits, customs, norms, and lifestyles) and biological (age, sex, degree of immunity, or other physical attributes that promote resistance or susceptibility); while features of the environment are not only physical but social with respect to poverty and unhealthy living conditions, as well as the social relationships, norms, values, and forms of interaction in a particular social context.
Health-related lifestyles are of particular relevance as a social mechanism producing positive or negative health outcomes. As Anthony Giddens (1991: 81) points out, lifestyles can be defined as a more or less integrated set of practices that fulfill utilitarian needs and give material form to particular narratives or expressions of self-identity, such as class position. Everyone has a lifestyle, including the poor. When it comes to health, lifestyles have multiple roles in that they function as a collective or shared pattern of behavior (agent) that is normative in particular settings (environment) for the individual (host). As will be discussed in chapter 3, health lifestyles can be decisive in determining an individual’s health and longevity as that person moves from childhood into old age (Burdette et al. 2017; Cockerham 2013b; Mollborn and Lawrence 2018). Consequently, health outcomes cannot all be blamed on biology. What is decisive in many cases are social factors, as seen in the further examples of diabetes and HIV/AIDS.
Diabetes
Diabetes is of growing importance in the United States and it is clear that race is a key variable in this development, despite claims that race is simply a social label that by itself should not have any effect on health. What makes race most important with respect to health in American society is its close association with being affluent or poor. Even though members of all races are in each socioeconomic category and many whites are poor, blacks and Hispanics are overrepresented among lower-income groups (Cosby et al. 2019). As for diabetes, both the Type 1 and Type 2 versions are diseases in which excess amounts of sugar (glucose) in the blood damage the body’s organs – promoting kidney failure, heart disease, stroke, blindness, amputations of limbs, and other problems. Type 1 typically appears in childhood when the pancreas quits producing insulin that controls blood sugar levels because the body’s immune system has destroyed the cells that make it. Type 2 or adult onset diabetes is the most common form of the disease and usually develops in people after the age of 40. Some 90 percent of all diabetics are Type 2. This type features the ability to make insulin but the inability of the cells to use it to control blood sugar levels. Type 2 diabetes is often controlled through diet and exercise, but if this fails then oral medications and/or insulin injections are required.
Centers for Disease Control and Prevention (CDC) figures for 2017 indicate that 30.3 million Americans nationwide had diabetes and 84.1 million more were in a prediabetic stage (CDC 2017). One in three children could expect to become diabetic; for Hispanics, it may be as high as one in every two children – thereby suggesting a future explosion in the numbers of diabetics in the United States.
Genetics plays a critical role in that diabetes is more prevalent in certain families and groups than others. A variant gene (TCF7L2) has been discovered that increases the risk of Type 2 diabetes and is carried by more than a third of the American population (Grant et al. 2005). Since people carry two copies of each gene, one inherited from each parent, the extent of the risk depends on whether one or two copies of it have been inherited. The estimated 38 percent of Americans with only one copy are 45 percent more likely than the unaffected population to come down with the disease, while the 7 percent who have inherited two copies are 141 percent more likely than those without the gene to develop diabetes. This gene has existed in the American gene pool for generations and its presence in the body does not guarantee its activation; rather, it enhances the risk. However, the rapid acceleration of new cases in recent years cannot be explained by genetics alone since the human gene pool does not change that fast.
Instead, the culprit appears to be social behavior and is inextricably linked to socioeconomic status and race. Low SES is significant because of what the combination of low income, education, and occupational status signify with respect to the greater likelihood of smoking, obesity, sugar and high-fat diets, and lack of exercise – all pointing toward a greater prevalence of unhealthy lifestyles more common in this population group. Race is important because blacks and Hispanics are twice as likely as whites to become diabetic. The overall prevalence of diabetes, according to the Centers for Disease Control and Prevention (2017), is higher among American Indians/ Alaska Natives (15.1 percent), non-Hispanic blacks (12.7 percent), and Hispanics (12.1 percent) than among Asians (8.0 percent) and non-Hispanic whites (7.4 percent). The relationship between SES and race with respect to diabetes is documented in research by Mario Sims and his colleagues (2011), who found diabetes among African Americans to be patterned along socioeconomic lines. Lower SES blacks had both a significantly higher prevalence and greater incidence of new cases of diabetes than blacks higher up the social scale. The lower the SES, the greater the diabetes; the higher the SES, the less the diabetes.
HIV/AIDS
HIV/AIDS
