Читать книгу The Social Causes of Health and Disease - William C. Cockerham - Страница 11

Assembling evidence about the social determinants of health is a challenge because of difficulties in linking the sociological with the biological. Their effects are often intertwined. This is especially the case in this era of postgenomic research demonstrating flexible boundaries between biology and sociocultural experiences. Since the completion of the Human Genome Project in 2003, the field of epigenetics has grown significantly. Epigenetics is the study of the relationship between genotypes (DNA sequences of a cell) and phenotypes (traits) of that cell. Social epigenetics focuses on social phenotypes (Bliss 2018). According to Italian bio-sociologist Maurizio Meloni (2019: ix), the rise of epigenetics has resulted in “a shift [in current thinking] away from notions of biological fixedness and toward ideas of the impressionability of biological material.” This development recognizes the capability of social factors to act on the body’s biological functioning, and by extension on health, much more so than previously believed.

Meloni and others (Bliss 2018; Freese 2008) find that many of the so-called “truths” about a strict dividing line between biology and social influences have become obsolete. These include notions of “fixed” boundaries between heredity and the environment, genes and behavior, nature and nurture, and race as a social construction lacking a biological reality. Instead there appears to be considerable cross-over between the biological and the social, as they act upon each other and either or both can be causal. As Jeremy Freese (2008: S13) points out: “the causal effects of genes are in the first instance causal effects upon the material body” [emphasis in the original]. Genes thus act as causes of individual physiological and behavioral functioning, but they are also acted upon by the social environment. Environments can either suppress or accentuate genetic influences, depending on a person’s social circumstances and, in doing so, affect many bodily conditions (Horwitz 2017: 131). “Genomic causation,” says Freese (2008: S28), “is not in competition with social conditions, but a product of them.”

Social environments provide the triggers that determine whether or not certain genes will be expressed and what forms that expression will take in particular contexts (Bell and Figert 2015; Horwitz 2017; Shostak and Moinester 2015). The landmark study in this area is that of Avshalom Caspi and colleagues (2003), who found that when the short allele (an alternative variant form of a gene) of the 5-HTTLPR gene is affected by stressful environments, an individual with one or more copies of it is more prone to depression than those who do not have the short allele. Conversely, those persons with two long alleles were generally immune to genetic influences associated with stressful situations.

Subsequent research by medical sociologists has demonstrated the effects of social variables on body physiology in a number of studies. Chioun Lee and her colleagues (Lee, Coe, and Ryff 2017), for example, found that severe and multiple types of childhood abuse produced significant physiological dysregulation in adulthood among those who had experienced it. This conclusion was based on a sample of English-speaking US residents providing data on their social characteristics, measures of childhood maltreatment, and biomarkers obtained in a clinical research center involving urine and blood testing, along with blood pressure, hormonal activity, and other biological indicators. Lee et al. (2017: 374) determined that “individuals who experience extreme or chronic abuse as children are likely to secrete abnormal levels of hormones from the primary stress systems (HPA axis and SNS), which appears to be related to poor biological profiles in other body systems associated with stress physiology (glucose regulation, lipid metabolism, cardiovascular function, immune competence).” The findings indicated that socioeconomically disadvantaged individuals were the most intensely stressed in this sample.

Other studies show early social adversity accelerating the speed of biological aging (Simons et al. 2019), social inequality promoting greater weight gain among black women (Hargrove 2018), and exposure to chronic stress in childhood causing increased risk of greater low-grade inflammation in blacks and Hispanics 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.