PART ONE
Biological, Behavioral, and Social Factors Affecting Health

In the early years of scientific medicine, most clinicians and researchers thought only in terms of single causes: specific agents that cause specific disease. For example, an infection was considered to result only from the proliferation of bacteria, while other kinds of ill health might result from viruses, toxins, accidents, or flaws in a person’s genetic makeup. More recent research highlights the relationships between health and behavioral, psychological, and social variables.

Acceptance of the fact that stress is linked to cardiovascular disease or to other health problems has become commonplace. However, research also reveals many reciprocal links among the central nervous system, which recognizes and records experiences; the endocrine system, which produces hormones that govern many body functions; and the immune system, which organizes responses to infections and other challenges.

Similarly, it has long been recognized that specific behaviors are associated with increased risk of specific diseases and related conditions. For example, tobacco use, alcohol consumption, inadequate physical activity, some sexual practices, and high-fat or low-fiber diets have all been recognized as unhealthful. Less widely recognized, however, is the association between socioeconomic status and health, or the influence of social networks, current or anticipated employment status, and personal beliefs. Recent research not only documents the importance of these factors, but also describes some of the mechanisms involved,



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Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences PART ONE Biological, Behavioral, and Social Factors Affecting Health In the early years of scientific medicine, most clinicians and researchers thought only in terms of single causes: specific agents that cause specific disease. For example, an infection was considered to result only from the proliferation of bacteria, while other kinds of ill health might result from viruses, toxins, accidents, or flaws in a person’s genetic makeup. More recent research highlights the relationships between health and behavioral, psychological, and social variables. Acceptance of the fact that stress is linked to cardiovascular disease or to other health problems has become commonplace. However, research also reveals many reciprocal links among the central nervous system, which recognizes and records experiences; the endocrine system, which produces hormones that govern many body functions; and the immune system, which organizes responses to infections and other challenges. Similarly, it has long been recognized that specific behaviors are associated with increased risk of specific diseases and related conditions. For example, tobacco use, alcohol consumption, inadequate physical activity, some sexual practices, and high-fat or low-fiber diets have all been recognized as unhealthful. Less widely recognized, however, is the association between socioeconomic status and health, or the influence of social networks, current or anticipated employment status, and personal beliefs. Recent research not only documents the importance of these factors, but also describes some of the mechanisms involved,

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Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences Part One reviews some of the most important developments on these topics. Chapter 2 addresses the interactions of biobehavioral factors in health, Chapter 3 reviews behavioral risk factors, and Chapter 4 describes the role of social risk factors.

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Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences 2 Biobehavioral Factors in Health and Disease Research into the bidirectional and multilevel relationships between behavior and health has been aided by technology and by conceptual advances in the behavioral, biological, and medical sciences. Our understanding of the interactions between brain function and behavior has been enriched by advances in behavioral neurobiology, neuroscience, and neuroendocrinology from molecular mechanisms to psychological systems. Real-time imaging of the living human brain during different behavioral states has promoted our understanding of the links between human behavior and basic neurochemical processes or specific neuroanatomic pathways. Common availability of monoclonal antibodies, routine production of genetically altered animals, and new understanding of the genetic code have contributed to exploration of how genetics interacts with development and early experiences to influence both vulnerability to disease and resistance to age-related decline. Yet much of the research knowledge is highly compartmentalized, and there is a need to integrate isolated pockets of information. This chapter addresses the interplay among biological, behavioral, and social factors in health and disease, with an emphasis on biologic factors. Subsequent chapters address behavioral and social factors in greater detail.

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Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences STRESS, HEALTH, AND DISEASE The Stress Response Over the past 60 years or so, the study of stress has provided a major link in explaining the behavioral variables and the biological factors that influence physical health. Stress both causes and modulates a diversity of physiological effects that can enhance resistance to disease or cause damage and thereby promote disease. For example, stress-related hormones, such as cortisol and epinephrine, have protective and adaptive functions as well as damaging effects. This idea, first introduced by Hans Selye (1956), is reemerging in contemporary biobehavioral research (McEwen, 1998). A characteristic set of physiological effects—the “stress response” —has been identified and investigated in humans and animals (Chrousos, 1998). The primary and secondary effects of the stress response constitute the biologic pathways along which a person’s experiences, living and working conditions, interpersonal relations, lifestyle, diet, personality traits, and general socioeconomic status can affect the body. Individual behavior is important because it increases or decreases the pathophysiological cost of stress through diet, exercise, and other activities. The stress response is an important component of the body’s regulatory systems. The maintenance of constant and appropriate internal conditions and functioning in the face of changing environmental demands is called homeostasis, an idea first developed by Walter Cannon (1936). The stress response, however, primarily involves reaction in an emergency. This function evolved over millions of years and is critical to the survival of most animals, including humans, when external threats and dangers, such as predation, are encountered. The stress response consists of many coadapted and simultaneous shifts in the physiological functioning of the cardiovascular, respiratory, muscular, metabolic, immune, and central nervous systems. Physiological changes can be accompanied by altered emotional responses, enhanced vigilance, heightened appraisal of risk, enhanced memory storage and retrieval, and changes in motivation. The stress response is a rapid and pervasive adjustment of internal states to prepare an organism to adapt to a threat—to respond to the rigors of “fight or flight” (Chrousos, 1998). Many aspects of the stress response, however, are inappropriate or maladaptive in the context of modern postindustrial societies. The threats posed here are different from those our evolutionary ancestors faced. We

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Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences do not commonly confront acute, life-threatening assault. Instead, contemporary humans face ill-defined, diffuse, often chronic threats that cannot be resolved by fight or flight. Nevertheless, the ancient physiologic stress response is triggered when one experiences, for example, a threat to social position, damage to important interpersonal relationships, loss of possessions, or barriers to the achievement of goals. Because many difficulties of contemporary life and their accompanying stress cannot be rapidly resolved—as could many physical stressors—the stress response persists, homeostasis is not restored, and the response becomes dysfunctional rather than adaptive. An increasing body of evidence indicates that stress is a potent contributor to illness (Cohen and Herbert, 1996; Cohen et al., 1991; Hermann et al., 1995; Kiecolt-Glaser et al., 1996; McEwen, 1998). The continued and unproductive activation of the stress response, including the failure to shut off this response when it is not needed, called allostatic load, is discussed below. The stress response is one aspect of an array of biologic and behavioral processes that either protect or cause damage. For example, secretion of stress-related hormones, such as cortisol and the catecholamines (epinephrine and norepinephrine), typically varies in a daily rhythm that is entrained by the light/dark cycle and by sleep/waking patterns that are part of normal daily life. But chronic increase in cortisol throughout the diurnal cycle is associated with negative consequences, such as accelerated bone mineral loss and hyperglycemia. Because the subjective experience of stress does not always correlate with physiological response (Kirschbaum et al., 1999), long-term measurement of hormone concentrations and of the processes that they regulate (for example, blood cholesterol concentration, fat accumulation, immune function, atrophy of brain structures, blood pressure), constitute an important way to connect life experience and the risk of disease. Allostasis and Allostatic Load An important new attempt to understand the relationships between environmental and behavioral challenges and stressors, the physiological responses to these events, and disease uses the terms allostasis and allostatic load. Allostasis is the maintenance of overall stability (homeostasis) through the constant adjustment and balancing of various components in the process of adapting to challenge. Sterling and Eyer (1988) first used the term to describe cardiovascular system adjustments in response to rest

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Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences and activity states. Later, the idea was generalized to other physiologic mediators, such as adrenal cortisol and the catecholamines. Allostatic load is the wear and tear the body experiences as a result of repeated allostatic response (McEwen, 1998; McEwen and Stellar, 1993). Allostasis and allostatic load operate in all systems of the body and focus attention on the protective, as well as the damaging, property of the primary mediators of the stress response: cortisol and the catecholamines. The major aspects are summarized in Figure 2-1. First, the brain integrates and coordinates behavioral and physiologic responses (hormonal and autonomic) to challenge. Some challenges can be perceived as stressful; others are related to circadian rhythms and to coordination of the functions of sleep and waking with the environment. Second, individual differences in the capacity to cope with challenges are based on multilevel relationships between genetic, developmental, and experiential influences. Third, intrinsic to the autonomic, neuroendocrine, and behavioral responses to challenge is the capacity to adapt (allostasis); indeed, neuroendocrine responses, such as the release of cortisol, are by nature protective and acute. Problems arise only when they persist, so efficient initiation and cessation of these responses is vital. Negative effects result when allostatic responses to challenge or stress occur inappropriately or are terminated inefficiently. Fourth, allostasis has a price that is related to the degree of inefficiency in the response and to the number of challenges and stressors a person experiences. Allostatic load is more than chronic stress. It can also reflect a genetically or developmentally induced failure to cope efficiently with the daily challenges related to the sleep/waking cycle and other experiences. And it also includes contributions of lifestyle factors, such as diet, alcohol and tobacco use, physical activity, and sleep, through their influences on the production of stress hormones. Protective and Damaging Effects of Stress Mediators A behavioral response to challenge or stress can be protective or damaging. The risk of harm or disease can be increased by such patterns of behavior as hostility or aggression, and it can be reduced by cooperation and conciliation. Cigarette-smoking, excessive alcohol consumption, high fat consumption, and exposure to physical hazards increase the risk, as does insufficient physical activity. The link of allostasis and allostatic load can be applied to various behavioral responses: Such behaviors as smoking, high alcohol consumption, and consumption of high-fat foods all have

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Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences FIGURE 2-1 The Stress Response and Development of Allostatic Load. Individuals experience objective psychological and environmental conditions that are conducive to stress, referred to as stressors. The perception of stress is influenced by social, psychological, biophysical factors, genetics, and behavior. When the brain perceives an experience as stressful, physiologic and behavioral responses are initiated, leading to allostasis and adaptation. Over time, allostatic load can accumulate, and the overexposure to mediators of neural, endocrine, and immune stress can have adverse effects on various organ systems, leading to enduring negative health outcomes (physiological, e.g., cardiovascular disease; psychological, e.g., depression; behavioral, e.g., alcoholism). Adapted from McEwen, 1998; Israel and Schurman, 1990. Reprinted with permission from Massachusetts Medical Society. Copyright 1998. All rights reserved. Reprinted by permission of Jossey-Bass, Inc., a subsidiary of John Wiley & Sons, Inc.

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Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences some perceived adaptive effects in the short-term but damaging effects if they persist. Behavior can attenuate some of the damaging effects of physiologic responses. For example, even a brief period of exercise can enhance glucose uptake by reducing the insulin resistance of muscle tissue (Perseghin et al.,1996). The mediators of protective and damaging effects of allostatic responses are mainly adrenal steroids and catecholamines. Other hormones—such as dehydroepiandrosterone, prolactin, growth hormones, and the cytokines—also mediate adaptive or maladaptive effects, but their consequences are often specific to an organ or a system. Once the mediators are released, they produce their effects by acting on cellular receptors. The effects can be classified as primary effects; secondary outcomes, which are risk factors for disease; and tertiary outcomes, which are diseases themselves (McEwen and Seeman, 1999). The actions of the mediators adrenal glucocorticoids and catecholamines are shown in Figure 2-2. These substances act via receptors that trigger changes throughout the target cell (including changes in gene expression) that have long-lasting consequences for cell function. It is important to consider the short- and long-term consequences of hormone release for cell function. There are many examples of beneficial and adverse effects of the mediators of allostatic responses. These factors are introduced here and discussed in more detail later. In the central nervous system, catecholamines and adrenal steroids promote the storage and retrieval of memories of events, pleasant and unpleasant, associated with arousal. However, adrenal steroids acting with excitatory amino acid neurotransmitters are associated with cognitive dysfunction involving various mechanisms that promote atrophy and, in some extreme cases, the death of neurons, particularly in the hippocampal region. In the cardiovascular system, autonomic responses, in part because of catecholamines, promote allostasis (adaptation) by adjusting heart rate and blood pressure according to the changing demands of sleeping, waking, and physical exertion. Damaging allostatic load occurs as a result of a failure to terminate blood pressure surges efficiently. This accelerates atherosclerosis and synergizes with metabolic hormones to accelerate non-insulin-dependent diabetes. The immune system is particularly responsive to the mediators of allostatic response. Adrenal steroids and catecholamines promote the movement of immune cells to organs or tissues where they are needed to

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Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences FIGURE 2-2 Allostasis in the Autonomic Nervous System and HPA Axis. Allostatic systems respond to stress (upper panel) by initiating the adaptive response, sustaining it until the stress ceases, and then shutting it off (recovery). Allostatic responses are initiated (lower panel) by an increase in circulating catecholamines from the autonomic nervous system and glucocorticoids from the adrenal cortex. This sets into motion adaptive processes that alter the structure and function of a variety of cellls and tissues. These processes are initiated through intracellular receptors for steroid hormones, plasma-membrane receptors, and second-messenger systems for catecholamines. Cross-talk between catecholamines and glucocorticoid-receptor signaling systems can occur. From McEwen, 1998, by permission of the Massachusetts Medical Society. All rights reserved.

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Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences resist infection or other challenge, thereby enhancing the effectiveness of immune responses. But adrenal steroids also can increase allostatic load and suppress immune system response when they are secreted chronically or when their release from the adrenal cortex is not terminated properly. Allostatic load is associated with at least four patterns of long-term harm to the body. The first is a perception of excessive stress. This can take the form of repeated events of various types that cause recurring increases in the release of stress mediators. For example, the amount and frequency of economic hardship are good predictors of decline in physical and mental functioning and even death (Lynch et al., 1997b). The second pattern involves a failure to adapt to recurrence of the same stressor. This leads to overexposure to stress mediators because of the failure to dampen response to a repeated event. Most people, for example, adapt to repeated public-speaking challenges, but some continue to show elevated cortisol concentrations, which indicate a failure to adapt (Kirschbaum et al., 1995). The third pattern entails the failure to terminate the hormonal stress response or the lack of appearance of the normal trough in the daily cortisol release pattern. Examples are increased blood pressure caused by work-related stress (Gerin and Pickering, 1995), increased evening cortisol and hyperglycemia caused by sleep deprivation (Van Cauter et al., 1997), and the chronically elevated cortisol that often accompanies depressive illness (Michelson et al., 1996). The fourth pattern involves inadequate release of hormones, thus allowing other systems, such as inflammatory cytokines, to become overactive. In the Lewis rats, for example, inadequate release of cortisol is associated with increased susceptibility to inflammatory and autoimmune disturbances (Sternberg, 1997; Sternberg et al., 1996). Early Development Influences Long-Term Effects of Stress Developmental influences are implicated in susceptibility to stress-related disorders. Classic work by Levine et al. (1967), Denenberg and Haltmeyer (1967), and Ader (1968), shows that the handling of neonatal rats by experimenters leads to reduced emotionality and stress hormone reactivity throughout life. In contrast, prenatal stress increases emotionality and stress hormone reactivity throughout the life of the animal. Post-natal handling reverses the effects of prenatal stress (Fride et al., 1986; Wakschlak and Weinstock, 1990). Handling is believed to increase maternal licking and grooming of pups, which are associated with reduced

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Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences reactivity of the hypothalamic/pituitary/adrenal (HPA) axis (Liu et al., 1997). Use of animal models has revealed that age-related brain deterioration is increased by high-stress reactivity and reduced by low-stress reactivity (Dellu et al., 1996; Liu et al., 1997; Meaney et al., 1988). Animals that show high-stress reactivity also show a high propensity for substance abuse (Dellu et al., 1994). Studies in nonhuman primates show that early maternal deprivation alters brain serotonin functioning, increases alcohol preference, increases aggressive behavior, and decreases affiliate behaviors (Higley et al., 1996a, b; Kraemer et al., 1997). In marmosets, altered HPA axis function was found in offspring that experienced negative parenting (Johnson et al., 1996a). Individual differences in human brain aging are correlated with plasma cortisol concentration (see Lupien et al., 1994, 1998; Seeman et al., 1997), although it is not known whether there are connections to early life events. Some data suggest that extremely low birth weight (Barker, 1997; Wadhwa, 1998) and trauma in early life are risk factors that influence later health in humans (Bremner et al., 1997; Felitti et al., 1998). Studies that link life experience, especially early experience, with stress, allostatic load, and later health risks (Felitti et al., 1998; Bremner et al., 1997; De Bellis et al., 1999a, 1999b) signal the importance of research on the effects of early life experiences on later stress reactivity and health. Some evidence suggests that even prenatal experiences can have long-term health consequences. In laboratory animals, prenatal stress has been linked to alterations in adrenocortical and central serotonergic and dopaminergic circuits (Nelson and Bloom, 1997). These observations led to the hypothesis (Barker and Sultan, 1995) that disease vulnerabilities in childhood and adult life result from “fetal programming” of homeostatic response set points. This is supported by Eriksson et al, (1999), who report that death from coronary heart disease (CHD) among Finnish men was associated with low birth weight and low ponderal index at birth. In addition, prematurity and low birth weight resulting from maternal behaviors has been seen to increase the life-long risk of CHD (Wadhwa, 1998) and diabetes mellitus (Rich-Edwards et al., 1999). THE BRAIN AS INTERPRETER, REGULATOR, AND TARGET The brain is influenced by experiences, including stress, and it is a target of allostatic load, or long-term wear and tear. Since the IOM (1982)

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