revised book is a continuing extension of a lecture I presented at the University of Montreal on a cold, grey, slushy, wet Canadian afternoon long ago in January 2006. This presentation was part of the university’s “Alexis de Tocqueville: Questions on American Society” lecture series. Arnaud Sales of the Sociology Department and Andrée Demers of Groupe de recherche sur les aspects sociaux de la santé et de la prevention (GRASP) were wonderful hosts. In preparing for this lecture, I wanted to look forward in discussing medical sociology and focus on the future rather than the present or past. It seemed clear that the current state of theory and developments in statistics for multilevel and longitudinal analyses allows medical sociologists to better assess the effects of different layers of social structure on the health of individuals. This not only forecasts a greater concern with structure in our future work, but will also permit us as a community of scholars to further uncover the social mechanisms that cause health and disease. This book represents a continuing step in that direction.
I would like to acknowledge the assistance of Jonathan Skerrett, the sociology editor for Polity in Cambridge, England, for his continued high level of professionalism and insightful strategies for revisions concerning this manuscript. Also, I would like to acknowledge the contributions of Karina Jákupsdóttir, the assistant sociology editor in the production of the manuscript.
Mike Bury, Emeritus Professor of Sociology at Royal Holloway University London, was a stalwart critic as a reviewer for Polity on the first edition. His detailed comments helped sharpen the book’s thesis, and he went beyond reviewing to make many cogent and lasting suggestions that proved to be extraordinarily helpful. I would like additionally to acknowledge former University of Alabama at Birmingham doctoral students Brian Hinote, Jason Wasserman, Carrie Betcher, and Katie McIntyre, who provided important assistance for various editions of this book. Anonymous reviewers for Polity likewise provided very helpful comments. I would also like to acknowledge the library resources and support of the sociology departments at UAB and more recently at the College of William & Mary which proved significant in supporting this work. Finally, I would like to thank my wife, Cynthia, for her continued support. Time and time again, as noted previously, she has proven herself to be an intelligent, insightful, and wry observer of the human social condition.
William C. Cockerham
Williamsburg, Virginia
1 The Social Causation of Health and Disease
The capability of social factors to make people ill seems to be widely recognized by the general public. Ask people if they think society can make them sick, and the probabilities are high they will answer in the affirmative. Stress, poverty, low socioeconomic status, unhealthy lifestyles, and unpleasant living and work conditions are among the many inherently social variables typically regarded by lay persons as causes of ill health. However, with the exception of stress, this view is not expressed in much of the research literature. Studies in public health, epidemiology, behavioral medicine, and other sciences in the health field typically minimize the relevance of social factors in their investigations. Usually social variables are characterized as distant or secondary influences on health and illness, not as direct causes (Link and Phelan 1995, 2000; Phelan and Link 2013). Being poor, for example, is held to produce greater exposure to something that will make a person sick, rather than bring on sickness itself. However, social variables have been found to be more powerful in inducing adversity or enrichment in health outcomes than formerly assumed. Society may indeed make you sick or, conversely, promote your health.
It is the intent of this book to assess the evidence indicating that this is so. It is clear that most diseases have social connections. That is, the social context can shape the risk of exposure, the susceptibility of the host, and the disease’s course and outcome – regardless of whether the disease is infectious, genetic, metabolic, malignant, or degenerative (Holtz et al. 2006). This includes major afflictions like heart disease, Type 2 diabetes, stroke, cancers like lung and cervical neoplasms, HIV/ AIDS and other sexually-transmitted infections, pulmonary diseases, kidney disease, and many other ailments. Even rheumatoid arthritis, which might at first consideration seem to be exclusively physiological, is grounded in socioeconomic status, with lower-status persons having a significantly greater risk of becoming arthritic than individuals higher up the social scale (Bengtsson et al. 2005; Pederson et al. 2006). Consequently, the basic thesis of this book is that social factors do more than influence health for large populations and the lived experience of illness for individuals; rather, such factors have a direct causal effect on physical health and illness.
How can this be? Just because most diseases have a social connection of some type does not necessarily mean that such links can actually cause a disease to occur – or does it? Social factors such as living conditions, lifestyles, stressors, norms, social values, and attitudes are obviously not pathogens like germs or viruses, nor are they cancer cells or coagulated clots of blood that clog arteries. Yet, quarantined in a laboratory, viruses, cancers, and the like do not make a person sick. They need to be exposed to a human host and assault the body’s physiological defenses in order to be causal. However, assigning causation solely to biological entities does not account for all of the relevant factors in a disease’s pathogenesis, especially in relation to the social behaviors and conditions that bind the person to the disease in the first place. Social factors can initiate the onset of the pathology and, in this way, serve as a direct cause for several diseases. Two of many examples are the coronavirus and smoking tobacco.
Coronavirus
Coronavirus (COVID-19) unleashed itself on the world in the fall of 2019 in Wuhan, China, a city of 11 million. It subsequently spread across the globe as the most widely contagious pandemic yet to come since the Spanish flu of 1918. By the summer of 2020, over 10 million people were confirmed to have been infected, more than 500,000 were thought to have died, and trade and travel were severely disrupted on a global basis. Final tallies on the disease’s deadly and varied effects are not available as the pandemic is ongoing as this book goes to press. However, it was nevertheless clear at the time that COVID-19 ranks as an event of historic proportions. Nearly every country in the world was affected, air travel and cruise ships were shut down, public gatherings cancelled, businesses and schools closed, stay-at-home orders issued, unemployment soared, and the 2020 Olympics postponed for a year.
Does the “social” have a causation role with respect to COVID-19? The answer is clearly “yes,” as seen in the stringent requirement for “social distancing” (keeping away from other people) and the likely causal trail. Early information indicated that the coronavirus originated in bats in China that likely infected an anteater-like creature known as a pangolin. The evidence comes from testing the genome sequence of the coronavirus in bats and pangolins, which was found to be almost identical with the virus’s genome in infected humans (Andersen et al. 2020; Zhou et al. 2020). If the coronavirus had stayed isolated among bats and pangolins in the wild, it would have remained a biological anomaly. But it didn’t. As a result of urbanization, globalization, and climate change in recent decades, wildlife habitats have been affected and exposed various species to greater contact with humans (Armelagos and Harper 2016; Cockerham and Cockerham 2010).
At the point pangolins became infected, the “social” began to take over as a cause of the pandemic. Pangolins are a desired food delicacy in China and sold in Wuhan’s Huanan Seafood Wholesale Market where live wild animals can be purchased for human consumption. Just as the SARS (severe acute respiratory syndrome) pandemic of 2002–3 began in China’s live wild animal “wet” markets, coronavirus apparently took a similar transmission path from bats through animals (pangolins instead of civets and raccoon dogs) to reach humans in a crowded marketplace. Lax health and safety regulations, combined with ineffective local government inspections in such markets, likely made transmission easier. Regardless of where it originated, a human became sick. The first case (the so-called patient “zero”?) was allegedly a 55-year-old Chinese man in Hubei Province
