Disease became conceptualized after 1900 as a social no less than a biological phenomenon, to be understood statistically, sociologically, and psychologically – even politically. Medicine’s gaze had to incorporate wider questions of income, lifestyle, diet, habit, employment, education, and family structure – in short, the entire psychosocial economy. Only thus could medicine meet the challenge of mass society, supplanting laboratory medicine preoccupied with minute investigation of lesions but indifferent as to how they got there.
Contemporary physicians now treat many health maladies that are aptly described as “problems of living,” dysfunctions that may involve multiple sources of causation, including those that are social in origin and part of everyday life. This includes social structural factors like class, living conditions, and social capital that can cause health or illness. These factors are causal because good or bad health originates from their influence. Consider, for example, the problem of low birth-weights among newborn babies. Such babies are more likely to have health problems than infants with normal birth-weights and less likely to survive the postnatal period. In researching this situation, Dalton Conley, Kate Strully, and Neil Bennett (2003) determined that if there are two groups of couples – one with high incomes and the other with low incomes – and each group has the same 20 percent biological predisposition toward having a low-birth-weight baby – the high-income group has a very high probability of counteracting their biological predisposition with better nutrition and prenatal care. In this instance, social factors – namely, income and how it translates into better education, living situations, jobs, quality medical care, and a good diet and other healthy lifestyle practices – reverse the biological risk. In the low-income group, the biological risk proceeds unimpeded. In both groups, social factors are causal in that biological predispositions are blunted in the high-income group and do not allow the biological risk to be countered in the low-income group. In fact, it could be argued that low income and how it signifies poor education, less healthy living situations, inadequate employment, less quality medical care, and poor diets along with less healthy lifestyle practices like smoking and alcohol abuse, promotes the biological risk into reality.
Social factors not only can determine whether or not a person becomes sick, but also shape the pattern of a population’s health and disease, as well as how people experience illness. These direct effects of social factors on health and disease are depicted in figure 1.1. First, social factors can mold the illness experience, for example, in helping or hindering adaptation, alleviating or exacerbating symptoms by making remedies more or less accessible, providing therapeutic or detrimental environments, or in causing good or poor health care to be available. Second, social factors determine the patterning of health, disease, and mortality at the population level. This is seen in studies of population health displaying patterns and trends occurring at particular times and in specific geographical places (Hummer and Hamilton 2019). Invariably, these patterns illustrate the influence of social variables – such as income, education, race, and gender – in determining their direction and profile.
Third, is the topic of this book: the social causation or determinants of health and disease to be discussed in this and forthcoming chapters. Social factors can have a direct effect on health by acting as a determinant or cause. According to the World Health Organization (2011), the social determinants of health are “the conditions in which people are born, grow, work, live, and age, and the set of forces and systems shaping the conditions of daily life.” As determinants of health, the “social” refers to social practices and circumstances (such as inequality, lifestyles, living and work situations, neighborhood characteristics, poverty, and environmental pollution), socioeconomic status, social stressors, and racial discrimination, along with economic (e.g., unemployment), political (e.g., government policies, programs, and public health insurance benefits), and religious (e.g., piety, proscriptions against smoking and drinking alcohol) factors that affect the health of individuals, families, groups, and communities – either positively or negatively (Cockerham et al. 2017c). Social determinants can have a causal role in fostering illness and disability but, conversely, can promote prospects for preventing disease and maintaining health.
Figure 1.1 The direct effects of social factors on health and disease
For example, all societies have social hierarchies and within those hierarchies health and longevity consistently reflect a gradient in health that is better at the top than at the bottom, while most diseases are also concentrated at earlier ages at the bottom. This outcome is not preordained but arises from the differing lifestyle practices, living conditions, and resources of the diverse social strata comprising the hierarchy.
Elements of Proof
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