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Objective: The object of this study was to evaluate the evidence linking attachment insecurity to illness. Attachment theory describes lifelong patterns of response to threat that are learned in the interaction between an infant and his or her primary caregiver. Despite its biopsychosocial domain, attachment theory has only recently been applied to psychosomatic medicine., Method: MEDLINE and PsychInfo databases were searched from 1966 to 2000 for English language papers with key words "attachment" and "object relations." Papers and their cited references were reviewed if they were directly related to physical illness, symptoms, or physiology. A hypothetical causal model was developed., Results: Direct and indirect evidence from survey studies supports an association between attachment insecurity and disease. Animal studies and human experiments suggest that attachment contributes to individual differences in physiological stress response. There is also less robust support for insecure attachment leading to symptom reporting and to more frequent health risk behaviors, especially substance use and treatment nonadherence. Evidence supports the prediction from attachment theory that the benefits of social support derive more from attachment relationships than nonattachment relationships., Conclusions: Although the available data are suggestive rather than conclusive, the data can be organized into a model that describe attachment insecurity leading to disease risk through three mechanisms. These are increased susceptibility to stress, increased use of external regulators of affect, and altered help-seeking behavior. This model warrants further prospective investigation.

Objective: The objective of the study was to assess the roles of social stress and social status in susceptibility to upper respiratory infection., Method: Sixty male cynomolgus monkeys were randomly assigned to stable or unstable social conditions for 15 months. Two markers of social status, social rank and percent of behaviors that were submissive, were assessed at independent observation periods. Endocrine, immune, and behavioral responses were each assessed (at 3-month intervals) during the 9th through 14th months of the study. At the beginning of the 15th month, all animals were exposed to a virus (adenovirus) that causes a common-cold-like illness. The primary outcome was whether or not an animal developed an infection (shed virus) after viral exposure., Results: Although the social instability manipulation was associated with increased agonistic behavior as indicated by minor injuries and elevated norepinephrine responses to social reorganizations, the manipulation did not influence the probability of being infected by the virus. However, low social status (as assessed by either marker) was associated with a substantially greater probability of being infected. It was also associated with less body weight, greater elevated cortisol responses to social reorganizations, and less aggressive behavior. However, none of these characteristics could account for the relation between social status and infection., Conclusions: Social stress was not associated with susceptibility to infection. However, animals with lower social status were at higher risk than high social status animals.

Objective: To describe how an animal model system can be used to explore basic questions about the nature of loss and the effects of early loss on later vulnerability to disease., Method: The physiological and behavioral responses of infant rats to separation from their mothers are first described and then analyzed experimentally into component mechanisms., Results: These studies have revealed an extensive layer of processes underlying the psychological constructs generally used to understand the response to loss. Hidden within the observable interactions of parent and offspring, we found a number of discrete sensorimotor, thermal, and nutrient-based events that have unexpected long-term regulatory effects on specific components of infant physiology and behavior. Release from all of these inhibitory and excitatory regulators together during maternal separation constitutes a novel mechanism by which the experience of loss can be translated into a complex patterned response. Evidence for early regulatory processes has also been found in monkey and human mother-infant interactions. Here they may well constitute the building blocks from which attachment and object representations develop. We and others have found long-term effects of loss, and of selective replacement of regulators, on behavioral development and on later vulnerability to disease., Conclusions: The results give us a new understanding of early attachment as a developmental force and of human grief as a risk to health.

Objective: Psychoneuroimmunology, which investigates the bidirectional communication between the central nervous system and the immune system, has been greatly advanced by the use of animal models. The objective of this paper is to describe animal models of disease that can or might be utilized to elucidate neural-immune interactions that alter pathogenesis., Methods: This paper reviews animal studies that have demonstrated a link among the brain, behavior, immunity, and disease, highlighting models in which the potential contribution of CNS-immune interactions has not yet been explored., Results: Animal studies allow for careful control of environmental stimuli, genetic background, and immunological challenge. As such, they are an important component of psychoneuroimmunology research. Models in which one might study the role of psychosocial factors in immunologically mediated disease processes, as in the case of other pathophysiologic processes, profit from an ability to manipulate both stressful events and the magnitude of the challenge to the immune system., Conclusions: Animal studies in psychoneuroimmunology highlight the complexity of the interactions among behavior, the brain, the immune system, and pathogen. The genetic background of the animal (both in terms of central nervous and immune system responses), its previous history, the nature of the stressor, the nature of the pathogen and the type of immune response generated are some of the interacting factors that determine the magnitude and direction of stress-induced changes in disease outcome.

Data from a longitudinal study of women physicians is used to study psychosocial and current implications of good health in midlife. The women comprise the classes 1964 to 1967 of the University of California School of Medicine at San Francisco. The subjects were interviewed and tested using the California Psychological Inventory while they were still in medical school (Time 1, average age 24 years) and at midlife (Time 2, average age 46 years). The women in good health at midlife, in contrast to their peers, were characterized by certain personality traits, including a higher degree of intellectual efficiency and empathy and relatively less hostility. Early antecedents of good health included having better educated parents. Good physical health at Time 2 was also predicted by Time 1 personality traits reflecting planful, logical, and efficacious use of intellectual resources and having optimistic, trusting relationships with others.

In considering new paradigms for the prevention and treatment of disease and disability, we need to incorporate ways to promote social support and develop family and community strengths and abilities into our interventions. There is now a substantial body of evidence that indicates that the extent to which social relationships are strong and supportive is related to the health of individuals who live within such social contexts. A review of population-based research on mortality risk over the last 20 years indicates that people who are isolated are at increased mortality risk from a number of causes. More recent studies indicate that social support is particularly related to survival postmyocardial infarction. The pathways that lead from such socioenvironmental exposures to poor health outcomes are likely to be multiple and include behavioral mechanisms and more direct physiologic pathways related to neuroendocrine or immunologic function. For social support to be health promoting, it must provide both a sense of belonging and intimacy and must help people to be more competent and self-efficacious. Acknowledging that health promotion rests on the shoulders not only of individuals but also of their families and communities means that we must commit resources over the next decade to designing, testing, and implementing interventions in this area.

This article reviews prospective evidence linking certain classes of person variables to multiple disease end points. Included in the review is a consideration of the effects of hostility and anger, emotional suppression, depression, fatalism, and pessimism on coronary heart disease, cancer, and acquired immunodeficiency syndrome. A model is presented that integrates several of these variables into an overall conceptual scheme. In addition, several variables are identified that appear to moderate the strength of the relationships that are found between person variables and health. The article concludes with some suggested directions for future research.

The association of socioeconomic status (SES) with morbidity and mortality is a ubiquitous finding in the health literature. One of the principal challenges for biobehavioral researchers is understanding the mechanisms that link SES with health outcomes. This article highlights possible pathways by which SES may influence health. It also provides a discussion of sociodemographic and geographical modifiers of the SES-health relationship and offers several potentially fruitful directions for future research.

Thoughts, feelings, and moods can have a significant effect on the onset of some diseases, the course of many, and the management of nearly all. Many visits to the doctor are occasioned by psychosocial distress. Even in those patients with organic medical disorders, functional health status is strongly influenced by mood, coping skills, and social support, yet the predominant approach in medicine is to treat people with physical and chemical treatments that neglect the mental, emotional, and behavioral dimensions of illness. This critical mismatch between the psychosocial health needs of people and the usual medical response leads to frustration, ineffectiveness, and wasted health care resources. There is emerging evidence that empowering patients and addressing their psychosocial needs can be health and cost effective. By helping patients manage not just their disease but also common underlying needs for psychosocial support, coping skills, and sense of control, health outcomes can be significantly improved in a cost-effective manner. Rather than targeting specific diseases or behavioral risk factors, these psychosocial interventions may operate by influencing underlying, shared determinants of health such as attitudes, beliefs, and moods that predispose toward health in general. Although the health care system cannot be expected to address all the psychosocial needs of people, clinical interventions can be brought into better alignment with the emerging evidence on shared psychosocial determinants of health by providing services that address psychosocial needs and improve adaptation to illness.

This paper provides a rationale for intervening on shared determinants of health at the community level of analysis, presents strategies for intervening on shared determinant risks at the community-level of analysis, and illustrates through a case study of a youth program how a small-scale community intervention on shared determinants might work in practice. Although there is a long history of community intervention to improve health, high quality research on these interventions has been conducted only recently. In evaluating the usefulness of a community intervention, the distinction between relative risk and population-attributable risk is not always made clear. These two distinct types of risk are reviewed considering their implications for what risk factors are targeted by community interventions and what criteria are reasonable to apply in evaluating the utility of these interventions. A role for linking root cause analysis with attributable risk and interventions to reduce risk is presented.

There is evidence linking psychosocially mediated immunological alterations with cancer, infectious illness, and HIV progression. The data reviewed suggest that immune modulation by psychosocial stressors and/or interventions may importantly influence health status. The research literature also suggests that the impact of chronic stressors and psychosocial factors on sympathetic nervous system and endocrine function influences the immune system, thereby providing shared mechanisms that may impact on disease susceptibility and progression across a broad spectrum of disorders. A better understanding of individual vulnerability, such as occurs with aging, may help to pinpoint those at greatest risk.

A substantial body of research relates socioeconomic, behavioral, social, and psychological factors to the development and progression of a wide variety of diseases. The search for shared pathways that link these factors leads to the investigation of upstream determinants, as opposed to biologic pathways, but these have been little studied by biobehavioral researchers. Available data suggest that socioeconomic factors structure the development and maintenance of behavioral, social, and psychological factors; however, we know little of how this takes place. A consideration of the ways in which socioeconomic position influences the everyday texture of people's lives could advance our understanding of both macroeconomic and microeconomic influences on health, and lead to new, community-centric approaches to intervention. Such a research agenda would help to advance the scientific foundations for reducing the primary origins of disease, which are social and economic.

In critically reviewing the sources of evidence connecting psyche and brain with the immune system, the authors include a brief review of current knowledge of the immune system, its interactions with the neuroendocrine system, and other factors influencing its regulation. These include developmental stages, aging, rhythmicity, and a variety of exogenous influences. The need for developing further information about normal base lines is emphasized. Against that background, many sources of data demonstrating connections between the central nervous system and the immune system are presented: indirect evidence from clinical and experimental illnesses involving the immune system, and direct changes in either humoral or cellular immunity after natural or experimental stress, conditioning, hypnosis, and direct brain stimulation. Possible mechanisms are discussed, as well as some important methodological issues for further research.