Invited Commentary: Socioeconomic Status, Hostility, and Health BehaviorsDoes It Matter Which Comes First?
Redford B. Williams
From the Departments of Psychiatry and Behavioral Sciences, Medicine, and Psychology and the Behavioral Medicine Research Center, Duke University Medical Center, Durham, NC.
Received for publication June 16, 2003; accepted for publication July 10, 2003.
Abbreviations:
Abbreviation: SES, socioeconomic status.
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INTRODUCTION
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Increases in mortality and morbidity as a function of decreasing socioeconomic status (SES) are a well-recognized and growing public health problem (14). Limited public resources, and differences among political leaders about how best to allocate them, make it unlikely that the solution to this problem will be found by simply throwing money at it. If the mechanisms and pathways responsible for the SES gradient of health and disease were known, however, it might be possible to devise and implement less ambitious interventions targeting key elements in the causal chain from low SES to increased disease and death rates. If increased levels of risky health behaviorslike smoking, sedentary exercise habits, and excessive alcohol usecan be shown to account for much of the increased morbidity and mortality among lower SES groups, it might be easier, at least in the short run, to mount programs to change these behaviors than it would be to achieve a substantial reduction in the proportion of the population living below the poverty line.
It is in this context that we should consider the work by Pulkki et al. (5), published in this issue of the Journal. They clearly document, in a population-based sample of healthy young Finnish men and women, that neither participants SES, parents SES, nor intergenerational social mobility is responsible for the observed associations between psychosocial risk factor hostility and the health behaviors, smoking or alcohol use, in men; SES accounts for only a small proportion of the association between hostility and smoking in women. On the basis of these findings, Pulkki et al. believe that they have refuted the "neomaterialisic" view that views associations between psychosocial factors such as hostility and disease risk factors as confounded by low SESthe "true" factor responsible for increased disease risk (5). They also found no evidence that hostility was mediating the associations they found between low SES and increased risky health behaviors.
Perhaps implied in these findings is that reducing socioeconomic inequalities will do little to reduce the impact of hostility on morbidity/mortality; moreover, reducing hostility will also not reduce the SES gradient. To achieve maximum benefit, it may be necessary to reduce both SES inequalities and hostilitya far more daunting task that reintroduces the need to persuade those who control the purse strings to agree to throw money at the problem. I believe that Pulkki et al. and the neomaterialists are both missing the main point in trying to understand and do something about the SES (or the hostility) gradient of health and disease. The key issue is not whether its hostility or low SES (or both) that leads to risky health behaviors that increase disease risk; instead, we need to determine the important processes in the causal chain leading from low SES to death and disease.
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HOW DOES LOW SES GET INSIDE THE SKIN?
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It is important first to note that reduced material resources making it difficult to obtain adequate health care are no more likely than hostility, poor health habits, or other factors to be solely responsible for the SES gradient. In the Whitehall study of British civil servants, for example, there is an increment in mortality for every step down in SES, including the step from top administrators to the professionals in the next level down (6). Access to care is unlikely to account for this effect, because the National Health Service provides basic medical care to all, and there is no reason to believe that the professionals have less access to care than their administrative superiors just one level up.
While there can be no doubting that health behaviors such as smoking, alcohol use, sedentary lifestyle, and dietary habits make important contributions to the risk of morbidity and mortality, it is interesting to note that results from a nationally representative prospective study of US adults found that these health behaviors explained no more than a modest 1213 percent of the excess mortality associated with lower income levels (7). On the other hand, hostility accounted for a more substantial 2434 percent of the educational gradient in perceived general health among 3,494 men and women in the Dutch GLOBE study (8). Only 57 percent of hostilitys effect on the educational gradient in perceived general health could be ascribed to the indirect effects of hostility on risky health behaviors; far more1928 percentwas due to the "direct" effects of hostility on perceived general health. But what are such direct effects and how do they affect health? To answer this question, we must adopt a broader perspective than one that asks whether its hostility or SES, SES or health behaviors.
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A PROPOSED CAUSAL MODEL FOR THE SES GRADIENT OF DISEASE AND DEATH
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To understand how low SES gets inside the skin, we must take into account the entire range of mechanisms that could stand between low SES and increased risk of disease and death. As shown in figure 1, I propose that low SES is associated with increased adversity during childhood, which causesthrough both a reduction in central nervous system serotonergic function and experiential learning mechanismsa clustering of risky health behaviors (smoking, alcohol, poor eating habits), psychosocial risk factors (hostility, depression, anxiety, social isolation), and biologic risk factors (increased sympathetic nervous system and hypothalamic pituitary adrenocortical axis responses to stress, decreased parasympathetic nervous system function) in low SES individuals. The risky health behaviors and biologic characteristics then alter the bodys internal milieu. This causes changes in immune, metabolic, and hemostatic functions. These, in turn, are responsible at the cellular and molecular levels for the developmentoften via potentiation of the effects of physical factors such as environmental toxins, carcinogens, bacteria, and the likeof diseases that result in death. I have reviewed elsewhere the evidence that supports this model (911).

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FIGURE 1. Theoretical model whereby low socioeconomic status leads, over time, to increased risk of disease and death. CNS, central nervous system.
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It will be noted that in this model low SES itself and psychosocial risk factors such as hostility and depression do not have any direct effects on pathogenic processes; it is only through their association with the behavioral and biologic characteristics ultimately responsible for the development of disease that low SES and psychosocial factors affect health and disease. People with a hostile personality, for example, exhibit increased sympathetic nervous system and cardiovascular reactivity to stress, especially when anger is induced (1214). Increased cardiovascular reactivity to stress has been found to predict more rapid progression of carotid atherosclerosis, especially in men of lower SES or men in jobs that place high demands on them (1517). Increased cardiovascular reactivity to stress also predicts increased stroke incidence in middle-aged men (18). Among cynomolgus monkeys fed a high-fat diet and subjected to chronic social disorganization stress, those with larger heart rate increases when stressed develop more severe coronary atherosclerosis (19). Hostility is also associated with increased expression of the metabolic syndrome in nondiabetic persons (20).
Another implication of this proposed causal model is that there is no single pathway that is always responsible for the increased rate of any particular disease or cause of death in low SES individuals or groups. Rather, via stochastic processes, there are many alternate pathways whereby low SES increases risk. In one person, for example, it may be a high-fat diet and the increased cardiovascular reactivity to stress associated with his hostility that are playing the major roles, while in another it could be the cigarette smoking, increased inflammatory cytokines, and increased platelet activation associated with her depression that are doing the damage.
Although they are not shown in figure 1, we can be sure that genetic factors are moderating the causal effects denoted by all of the arrows in the model. Given the importance of the serotonergic system in regulating so many of the behavioral, psychosocial, and biologic characteristics that cluster in low SES groups, much of the early research on genes has focused on variants in genes encoding for proteins involved in the regulation of serotonergic function. A functional polymorphism of the serotonin transporter gene has been shown to be associated with several high risk phenotypes: personality domains related to hostility and depression (21); increased cardiovascular reactivity to stress (22); increased risk of myocardial infarction (23, 24); and altered central nervous system serotonin turnover, though in a way that is moderated by childhood experience as indexed by parents educational levels (25). Further illustrating how early environment and genes interact to influence adult characteristics is a study that found increased rates of violent offenses in men who were abused as children, but only among those with the less active alleles of a polymorphism of the monoamine oxidase A gene (26).
Even though considerable evidence can be adduced supporting the various proposed causal pathways represented by the arrows in the proposed model, my point here is not to document the validity of the model. Ultimately that will require all the proposed elements in the causal chain, including genetic factors, to be measured in the same, very large group of individuals who would then be followed over timea major undertaking that will probably require not only considerable financial resources but also the development of innovative statistical techniques to test the causal pathways.
I am using this model here to make the heuristic point that it is not constructive to engage in debates such as the one between Pulkki et al. and the neomaterialists over whether it is hostility that mediates the effect of low SES on risk factors for coronary heart disease or coronary heart disease incidence, or whether it is low SES that mediates the effects of hostility on disease risk. In my opinion, such debates are not constructive, because they deflect attention away from the important task of characterizing the stochastic processes whereby factors such as low SES and hostility can play varying roles in the development of disease in the real, complicated world we live in.
It will ultimately be essential to understand how the processes making up this modelor a more valid one that improves upon itwork to produce more disease in certain individuals and groups (e.g., low SES) for one very important reason: This understanding will enable us to develop and implement preventive and treatment interventions that will reduce the risk of developing disease in the first place or that will improve its prognosis once present. There are behavioral interventions, for example, that have been shown to decrease hostility in patients with coronary heart disease (27, 28). It remains to be seen, but it is likely that such interventions will reduce mortality and coronary heart disease recurrences in some, but not all, patients who receive them, most likely because of differences in the impact of the intervention on the associated behavioral and biologic characteristics that are responsible for the impact of hostility on coronary heart disease risk and prognosis. It is encouraging in this regard that these behavioral interventions were found to decrease both resting blood pressure (27) and blood pressure and heart rate reactivity to stress (28). If altered central nervous system serotonergic function is ultimately shown to be playing as important a role in the causal chain from low SES to disease and death as the model in figure 1 postulates, it would suggest that treatment with drugs that enhance serotonergic neurotransmission, such as selective serotonin reuptake inhibitors, could reduce the risk associated with low SES. There is already some evidence from both observational studies and randomized clinical trials suggesting that treatment with selective serotonin reuptake inhibitors is associated with reduced coronary heart disease risk (29) and improved prognosis in coronary heart disease patients (30). As with behavioral interventions targeting psychosocial risk factors, it will be important to assess in trials of pharmacologic agents that target psychosocial factors, such as depression, to assess the behavioral and biologic characteristics that mediate the effects of depression on coronary heart disease risk and prognosis.
So does it matter which comes first, low SES or hostility or risky health behaviors? Probably not, as long as we remember that all three are participants in stochastic processes leading to the same outcomeincreased risk of disease and death. By understanding how these processes work, it should be possible to design and implement more effective means of prevention and treatment, which is, after all, why we do research on these matters.
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ACKNOWLEDGMENTS
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Supported by National Heart, Lung, and Blood Institute grant P01HL36587, National Institute of Mental Health grant K05MH79482, Clinical Research Unit grant M01RR30, and the Duke University Behavioral Medicine Research Center.
Dr. Williams is a major stockholder in Williams LifeSkills, Inc. Neither the results described in this commentary nor their interpretation has been influenced by this potential conflict of interest.
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NOTES
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Reprint requests to Dr. Redford B. Williams, Department of Psychiatry and Behavioral Sciences, Box 3926, Duke University Medical Center, Durham, NC 27710 (e-mail: redfordw{at}duke.edu). 
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Related articles in Am. J. Epidemiol.:
- Contribution of Socioeconomic Status to the Association between Hostility and Cardiovascular Risk Behaviors: A Prospective Cohort Study
- Laura Pulkki, Mika Kivimäki, Marko Elovainio, Jorma Viikari, and Liisa Keltikangas-Järvinen
Am. J. Epidemiol. 2003 158: 736-742.
[Abstract]
[FREE Full Text]