Behavioral Medicine

Abstract

Behavioral medicine is a form of the behavioral sciences applied to physical health: the interdisciplinary field that integrates behavioral, psychological, and social knowledge with biomedicine to understand, prevent, and treat disease. It grew from the recognition that much of what makes people sick or well runs through behavior and its biological correlates, from smoking and diet to chronic stress and treatment adherence. This article organizes the field around a few problems: the biopsychosocial model that frames it, the pathways by which stress and appraisal reach the body, the psychoneuroimmunology that made those pathways concrete, the change and maintenance of health behavior, the adherence on which treatment depends, and the mind-body interventions used to manage pain. Three interactive demonstrations let the reader combine biopsychosocial inputs, appraise a stressor against coping resources, and turn adherence into outcome odds.

Keywords: behavioral medicine, biopsychosocial model, health behavior

Behavioral medicine is the interdisciplinary field that brings the science of behavior to bear on physical health and illness, integrating what psychology, the behavioral sciences, and the biomedical sciences separately know into a single account of how people become sick, stay well, and recover. Its founding premise is that the leading causes of death and disability in developed societies are no longer simple infections but chronic diseases whose onset, course, and management are shaped by what people do: whether they smoke, how they eat and move, how they cope with adversity, and whether they follow the treatments prescribed for them. The field was named and defined at a 1977 conference at Yale and refined shortly afterward as the interdisciplinary field concerned with the development and integration of behavioral and biomedical knowledge relevant to health and disease (Schwartz & Weiss, 1978). What distinguishes it from folk ideas about mind and body is the same thing that distinguishes any science: it insists on measurement, controlled comparison, and cumulative evidence, and it has repeatedly shown that the boundary between the psychological and the physical, long treated as a wall, is in fact a busy two-way street.

What Behavioral Medicine Is

Behavioral medicine is the scientific study of the reciprocal relations between behavior and physical health, and the application of that science to the prevention, diagnosis, treatment, and rehabilitation of disease. It is deliberately interdisciplinary: its practitioners are drawn from psychology, medicine, epidemiology, nursing, physiology, and public health, and its defining commitment is to integrate their knowledge rather than to keep the psychological and the biological in separate compartments. The field crystallized in the late 1970s, when a series of meetings gave it a name, a definition, and a journal, settling on a characterization of behavioral medicine as the field concerned with integrating behavioral and biomedical science for health and illness (Schwartz & Weiss, 1978). It is useful to distinguish behavioral medicine from two neighbors with which it overlaps. Psychosomatic medicine, its older ancestor, was concerned chiefly with how emotional conflict produces bodily symptoms; behavioral medicine broadened the scope to all of behavior, healthy and unhealthy, and grounded it in the experimental methods of learning theory and psychophysiology rather than in psychodynamic interpretation. Health psychology, its close sibling, is the psychological discipline that studies the same phenomena; behavioral medicine is the broader interdisciplinary umbrella under which health psychology, behavioral cardiology, behavioral pediatrics, and similar specialties meet the biomedical fields. What unites the enterprise is a rejection of the mind-body dualism inherited from the seventeenth century, and an insistence that psychological and physiological events are levels of description of one organism, causally connected and measurable at both levels.

Because the field spans several problems that are studied with different methods, it is useful to see its principal domains side by side before taking them in turn. Table 1 lays out the organizing framework and the four mechanisms this article treats, the central question each asks, and the kind of evidence on which each rests.

Note. The domains are levels of one enterprise, not separate compartments; stress, behavior, and adherence are causally intertwined, and the biopsychosocial model frames them all.

The Biopsychosocial Model

The intellectual charter of behavioral medicine is the biopsychosocial model, proposed by the internist and psychiatrist George Engel as a corrective to what he called the biomedical model, the assumption that disease is fully accounted for by deviations in biological variables and that psychological and social factors are, at best, incidental (Engel, 1977). Engel argued that this reductive model, however successful for acute infectious disease, was inadequate to the realities of clinical medicine, where the same pathology produces different illness in different people, where whether a person becomes a patient depends on psychological and social circumstances as much as on biology, and where the outcome of treatment turns on the relationship between clinician and patient. In its place he offered a model, drawn from general systems theory, in which the person is understood at several nested levels at once, from the molecular and cellular through the level of the whole organism to the interpersonal, familial, and social. Health and disease emerge from the interaction of these levels, so that a full account of a heart attack includes not only the occluded artery but the years of behavior, stress, and social circumstance that produced it and the psychological and social factors that will govern recovery. The model is not a claim that biology matters less; it is a claim that biology alone is an incomplete explanation, and that the psychological and the social are causes in their own right rather than mere epiphenomena. The demonstration below makes the model's central feature concrete: because the three classes of factor combine, the same health outcome can be reached by many different mixtures of biological burden, psychological resource, and social support, and no single input determines the result on its own.

Stress, Appraisal, and Health

If the biopsychosocial model is the field's framework, stress is its most studied mechanism, the principal route by which the psychological reaches the physical. The modern understanding of stress is not that events are inherently stressful but that stress arises from a transaction between a person and a demand, mediated by appraisal. In the influential account of Richard Lazarus and Susan Folkman, a person first appraises whether an event is threatening (primary appraisal) and then whether they have the resources to cope with it (secondary appraisal); the same event is experienced as a manageable challenge when resources seem adequate and as a threat when they fall short, and it is this appraisal, not the event alone, that sets the physiological and emotional response in motion (Lazarus & Folkman, 1984). The interactive demonstration further below builds exactly this transaction, letting the reader vary perceived demands and coping resources and watch the appraisal tip between challenge and threat.

Stress reaches the body along two broad pathways, sketched in Figure 1. The first is direct and physiological: appraisal of threat activates the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis, raising catecholamines and cortisol, altering cardiovascular and immune function, and, if chronic, exacting a cumulative toll. That toll has a name: allostatic load, the wear on the body that accumulates when the same stress mediators that protect in the short run are switched on too often, too long, or fail to switch off, so that the very systems mobilized to adapt become, over years, a cause of disease (McEwen, 1998). The second is behavioral: people under chronic stress sleep less, eat and drink differently, smoke more, exercise less, and adhere less well to treatment, and these behavioral changes are themselves potent causes of disease. The evidence that stress reaches physical illness through these routes is now substantial. In a landmark study, healthy volunteers were assessed for psychological stress and then experimentally exposed to a common-cold virus; the rate of clinical colds rose in a dose-response fashion with the degree of stress, a demonstration under controlled inoculation that stress raises susceptibility to infection rather than merely tracking it (Cohen et al., 1991). A meta-analysis of three decades of research confirmed and specified the immune side of the story, showing that acute stressors can transiently up-regulate some immune parameters while chronic stressors broadly down-regulate immune function, with the magnitude and direction depending on the duration of the stressor (Segerstrom & Miller, 2004). The behavioral cardiology literature added an early and famous piece: the observation that a driven, hostile, time-pressured Type A behavior pattern was associated with coronary disease (Friedman & Rosenman, 1959), a claim later refined so that hostility rather than hurry emerged as the toxic component, but which established behavior as a cardiac risk factor. Because so much rides on how stress is measured, the field has worked to unify its many partial measures, self-report, physiological, and life-event, into a coherent framework for population science (Epel et al., 2018).

Psychoneuroimmunology and Biofeedback

The claim that psychological states reach the immune system was once dismissed as biologically implausible, on the grounds that the immune system was autonomous and self-regulating. That objection was overturned by a single striking experiment. Robert Ader and Nicholas Cohen paired a saccharin solution with a drug that suppresses immune function; later, the taste of saccharin alone suppressed the immune response, a conditioned effect that showed the immune system could learn, and so must be in communication with the brain (Ader & Cohen, 1975). The finding launched the field of psychoneuroimmunology, which traced the anatomical and chemical pathways, nervous, endocrine, and immune, that carry signals between the brain and the body's defenses, and gave the stress-illness link a concrete mechanism. The demonstration that involuntary physiology could be shaped by learning had in fact been prepared a few years earlier by Neal Miller, whose experiments argued that visceral and glandular responses long thought purely automatic, such as heart rate and blood pressure, could be modified by instrumental conditioning (Miller, 1969). Whatever the eventual status of Miller's specific animal results, the idea seeded a durable clinical technology: biofeedback, in which a patient is shown a continuous signal of an ordinarily unconscious bodily process, such as muscle tension or skin temperature, and learns to bring it under voluntary control, a technique now used for tension headache, hypertension, and rehabilitation. Together these lines of work dismantled the assumption that the border between voluntary behavior and involuntary physiology was fixed, and they supplied behavioral medicine with the biological credibility it needed.

Changing Health Behavior

If behavior causes much of chronic disease, then changing behavior is the field's central intervention, and it turns out to be a science of its own, harder than it looks. A first insight is that change is not a single event but a process with stages. The transtheoretical model of James Prochaska and Carlo DiClemente, developed from the study of how smokers quit, describes people as moving through precontemplation, contemplation, preparation, action, and maintenance, and it holds that interventions succeed when they are matched to the stage a person actually occupies, so that pushing action on someone who is not yet contemplating change simply fails (Prochaska & DiClemente, 1983). A second insight concerns the engine of change within a person. Albert Bandura argued that whether people attempt and persist at a difficult change depends on their self-efficacy, their belief in their capacity to execute the behavior, and that self-efficacy, distinct from the outcome one expects, is itself alterable through mastery experiences, modeling, and persuasion (Bandura, 1977). Self-efficacy became one of the most reliable predictors in the health-behavior literature, forecasting who will start exercising, stop smoking, or manage a chronic disease. The hardest problem, however, is not starting but sustaining: most people who change a health behavior relapse, and a systematic review of the theories that attempt to explain why found that maintenance depends on a partly different set of mechanisms from initiation, including sustained self-regulation, habit formation, and a supportive environment, so that keeping a change is not merely more of what began it (Kwasnicka et al., 2016). The practical upshot is that effective behavior-change programs are staged, build self-efficacy, and plan explicitly for maintenance rather than treating the first success as the finish line.

Adherence and Clinical Outcomes

A distinctively behavioral determinant of medical outcome is adherence: whether patients actually take the medicines, keep the appointments, and follow the regimens prescribed for them. Non-adherence is pervasive, and it is not a marginal nuisance but a major cause of treatment failure, because a correct prescription that is not followed cannot work. The scale of the effect was established by meta-analysis: pooling decades of studies, patients who adhered to treatment had markedly better outcomes than those who did not, corresponding to an odds ratio of roughly 2.9 in favor of good outcomes for adherent patients across a wide range of conditions and treatments (DiMatteo et al., 2002). The finding reframes adherence as a therapeutic target in its own right, on the same footing as the choice of drug, and it explains why interventions that improve adherence, through simplification, reminders, education, and the quality of the clinician-patient relationship, can improve outcomes without any change to the underlying medicine. The demonstration below turns the meta-analytic odds ratio into a calculator, letting the reader set a baseline recovery rate and an adherence level and read off the resulting probability of a good outcome; the Worked Example that follows traces one such calculation by hand.

Mind-Body Interventions and Pain

Behavioral medicine has produced a family of interventions that treat physical symptoms by way of the mind, and nowhere are they better developed than in the management of pain. The scientific groundwork was the gate control theory of Ronald Melzack and Patrick Wall, which proposed that a neural gate in the spinal cord modulates the pain signals reaching the brain, and that this gate is influenced from above by attention, emotion, and expectation as well as from below by injury (Melzack & Wall, 1965). The theory transformed the understanding of pain from a simple readout of tissue damage into a modulated experience open to psychological influence, and it made psychological pain management scientifically respectable. Among the most studied of the resulting interventions is mindfulness training, the systematic cultivation of nonjudgmental present-moment attention, adapted for clinical use as mindfulness-based stress reduction and related programs (Kabat-Zinn, 2003). A modern research program has subjected these interventions to controlled trial and mechanistic study, finding reliable if moderate benefits for chronic pain, anxiety, and depression, and beginning to specify the attentional and stress-regulatory pathways through which they act (Creswell, 2017). These interventions are not a return to mind-over-matter mysticism; they are behavioral techniques whose effects are measured against controls and whose mechanisms are traced in the same physiological terms as any other treatment, which is precisely what makes them part of behavioral medicine rather than its fringe.

Worked Example

The meta-analytic finding that adherence is associated with an odds ratio of about 2.88 for a good outcome (DiMatteo et al., 2002) can be made exact, and doing so shows why an odds ratio is not the same as a change in probability. Suppose that among patients who do not adhere to a treatment, the probability of a good outcome is 50 percent. The odds of a good outcome are then the probability of success divided by the probability of failure, or 0.50 divided by 0.50, which is 1.0 (even odds). The odds ratio tells us that adherence multiplies these odds by 2.88, giving new odds of 1.0 times 2.88, or 2.88. To convert odds back to a probability, we divide the odds by one plus the odds: 2.88 divided by 3.88, which is 0.742. So adherence raises the probability of a good outcome from 50 percent to 74.2 percent, a gain of 24.2 percentage points. The size of that gain depends on where the baseline sits, because the odds ratio acts on the odds, not the probability. Repeat the calculation from a baseline of 90 percent: the non-adherent odds are 0.90 divided by 0.10, or 9.0; adherence raises them to 9.0 times 2.88, or 25.9; and the adherent probability is 25.9 divided by 26.9, or 96.3 percent, a gain of only 6.3 points. The same odds ratio thus delivers its largest absolute benefit near a baseline of even odds and a shrinking benefit as the baseline approaches certainty, which is why the interactive calculator above moves the two bars closer together as the baseline rises. The lesson is one behavioral medicine teaches repeatedly: a behavioral factor with a fixed effect on the odds can matter a great deal or a little for a given patient, depending on their starting risk.

Discussion

Behavioral medicine occupies a strategic position in contemporary health care, because the diseases that now dominate mortality and cost, cardiovascular disease, diabetes, cancer, chronic pain, are precisely those in which behavior and its physiological correlates are central to onset, course, and management. The field's enduring contribution has been to dismantle the dualism that treated mind and body as separate domains, and to replace it with a measured, mechanistic account of their traffic: appraisal that sets physiology in motion, immune systems that can be conditioned, involuntary responses that can be trained, behaviors that are as much causes of disease as germs once were, and adherence that determines whether treatment works at all. These findings share a methodological character with the rest of scientific psychology. They are quantitative, expressed as dose-response curves, effect sizes, and odds ratios; they are cumulative, resting on meta-analysis as much as on single studies; and they are experimental where they can be, as in the conditioned immunosuppression and viral-challenge studies that turned plausible correlations into demonstrated causes. The open problems are substantial. Measuring stress in a way that is comparable across studies remains difficult; the mechanisms linking chronic adversity to specific diseases are only partly mapped; and the maintenance of behavior change, the point at which most interventions fail, is imperfectly understood. But the central claim of the field, that health and illness are biopsychosocial phenomena rather than purely biological ones, is now less a manifesto than a working assumption of medicine.

Current Directions

The most active work in behavioral medicine is pushing the stress-and-health program toward both deeper theory and broader application. On the theoretical side, integrative frameworks are trying to explain why social adversity in particular, exclusion, isolation, low status, is so reliably toxic to health; social safety theory proposes that the human stress-immune system is calibrated by cues of social threat and safety, offering a unified account of how social experience becomes biology and disease (Slavich, 2020). On the measurement side, the field is working to unify its fragmented stress metrics, self-report, cortisol, life-event, and physiological reactivity, into a common framework so that findings from different studies can be compared and combined, a prerequisite for population-scale science (Epel et al., 2018). Infectious disease returned to the field's center with the COVID-19 pandemic, which sharpened long-standing questions about how psychosocial vulnerability shapes susceptibility to respiratory infection and its severity, extending a research line that began with the common-cold studies (Cohen, 2021). And the mind-body interventions are being dissected mechanistically rather than merely validated as packages, with mindfulness research increasingly asking which components act on which attentional and stress-regulatory pathways, and for whom (Creswell, 2017). Running through these directions is a move from establishing that psychosocial factors matter, which is now settled, toward specifying how, how much, and by what pathway, and toward building interventions that are targeted, mechanistic, and deliverable at scale.

Common Misconceptions

Behavioral medicine is alternative medicine or mind-over-matter healing.

It is a mainstream, evidence-based, interdisciplinary science that integrates behavioral and biomedical knowledge and tests its interventions against controls (Schwartz & Weiss, 1978). Its treatments, from biofeedback to mindfulness-based stress reduction, are evaluated by the same trial methods as any medical therapy (Creswell, 2017).

Stress is just an unpleasant feeling, not a real cause of disease.

Under controlled viral inoculation, psychological stress raised the rate of clinical colds in a dose-response fashion (Cohen et al., 1991), and chronic stress broadly down-regulates immune function (Segerstrom & Miller, 2004). Stress reaches the body through measurable physiological and behavioral pathways.

If a doctor prescribes the right treatment, the outcome is settled.

Only if the patient follows it. Adherence is a large, behavioral determinant of outcome, worth an odds ratio near 2.9 for a good result, so a correct prescription that is not taken cannot work (DiMatteo et al., 2002).

The immune system is autonomous and cannot be influenced by the mind.

A conditioning experiment showed the immune response could be suppressed by a neutral taste previously paired with an immunosuppressant, proving the immune system communicates with the brain and can be learned upon (Ader & Cohen, 1975).

Glossary

Adherence.

The extent to which a patient's behavior, in taking medication or following a regimen, matches the treatment agreed with the clinician; a major behavioral determinant of outcome.

Allostatic load.

The cumulative wear on the body from repeated or prolonged activation of the stress-response systems; the physiological toll by which chronic stress becomes disease.

Appraisal.

The cognitive evaluation of whether an event is threatening (primary) and whether one can cope with it (secondary); the mediator that turns an event into stress.

Biofeedback.

A technique in which a continuous display of an ordinarily unconscious physiological process lets a person learn to bring it under voluntary control.

Biopsychosocial model.

Engel's framework in which health and disease arise from interacting biological, psychological, and social levels rather than from biological factors alone.

Gate control theory.

Melzack and Wall's account of pain as modulated by a spinal gate that is influenced by attention, emotion, and expectation as well as by injury.

Health behavior.

Any action bearing on physical health, such as smoking, diet, exercise, sleep, or treatment adherence; a principal target of behavioral-medicine intervention.

HPA axis.

The hypothalamic-pituitary-adrenal axis, the neuroendocrine system whose activation releases cortisol and mediates much of the physiological stress response.

Mindfulness-based stress reduction.

A structured program that trains nonjudgmental present-moment attention as a clinical intervention for pain, anxiety, and stress-related conditions.

Odds ratio.

The factor by which an exposure multiplies the odds of an outcome; unlike a probability change, its absolute effect depends on the baseline risk.

Psychoneuroimmunology.

The field studying the signaling pathways among the nervous, endocrine, and immune systems, and how psychological states reach immune function.

Psychosomatic medicine.

The older discipline concerned with how emotional and mental factors produce or influence bodily disease; a historical ancestor of behavioral medicine.

Self-efficacy.

A person's belief in their capacity to execute a specific behavior; a strong and modifiable predictor of whether health behavior change is attempted and sustained.

Social safety theory.

Slavich's framework proposing that the human stress-immune system is calibrated by cues of social threat and safety, linking social adversity to disease.

Transtheoretical model.

Prochaska and DiClemente's stage model of behavior change, running from precontemplation through contemplation, preparation, action, and maintenance.

Type A behavior pattern.

A driven, competitive, hostile, time-pressured behavioral style historically linked to coronary disease, later refined so that hostility is the toxic component.

Key Researchers

Robert Ader (1932-2011). Psychologist at the University of Rochester Medical Center; with Nicholas Cohen he demonstrated behaviorally conditioned immunosuppression, founding the field of psychoneuroimmunology and proving that the immune system communicates with the brain. Wikipedia - Memorial

Sheldon Cohen. Robert E. Doherty University Professor of Psychology at Carnegie Mellon University; his controlled viral-challenge studies established that psychological stress raises susceptibility to infectious illness, and he continues to map the psychosocial determinants of health. Faculty Page - ORCID - Google Scholar - Wikipedia

J. David Creswell. Professor of psychology and neuroscience at Carnegie Mellon University; he studies the mechanisms of mindfulness interventions and how they act on stress and health, bringing controlled-trial rigor to mind-body treatment. Faculty Page - Google Scholar - Wikipedia

George L. Engel (1913-1999). Internist and psychiatrist at the University of Rochester; his 1977 proposal of the biopsychosocial model gave behavioral medicine its intellectual charter and challenged the reductive biomedical model of disease. Wikipedia - Wikidata

Richard S. Lazarus (1922-2002). Psychologist at the University of California, Berkeley; with Susan Folkman he built the transactional theory of stress and coping, establishing appraisal as the mediator between an event and its physiological toll. Wikipedia - In Memoriam

Ronald Melzack (1929-2019). Psychologist at McGill University; with Patrick Wall he proposed the gate control theory of pain and developed the McGill Pain Questionnaire, making the psychological modulation of pain scientifically respectable. Wikipedia - Memorial

James O. Prochaska (1942-2023). Psychologist at the University of Rhode Island; he originated the transtheoretical (stages of change) model of health behavior change, one of the most widely applied frameworks in the field. Wikipedia - Faculty Page

George M. Slavich. Clinical psychologist at the University of California, Los Angeles, and director of the UCLA Laboratory for Stress Assessment and Research; he developed social safety theory and works to unify how life stress is measured and linked to health. ORCID - Google Scholar - Faculty Page

Frequently Asked Questions

What is behavioral medicine? Behavioral medicine is the interdisciplinary field that integrates behavioral, psychological, and social science with biomedicine to understand, prevent, and treat physical disease. It grew from the recognition that behavior and its physiological correlates shape the chronic diseases that now dominate illness, and it was formally defined at the end of the 1970s (Schwartz & Weiss, 1978).

How is behavioral medicine different from health psychology? Health psychology is the psychological discipline that studies the links between behavior and health; behavioral medicine is the broader interdisciplinary umbrella under which health psychology meets medicine, epidemiology, and physiology. In practice the two overlap heavily, but behavioral medicine explicitly integrates biomedical as well as psychological knowledge.

What is the biopsychosocial model? It is the framework, proposed by George Engel, in which health and disease result from interacting biological, psychological, and social factors rather than from biology alone. It corrected the reductive biomedical model without denying biology, treating psychological and social factors as genuine causes (Engel, 1977).

Can psychological stress really cause physical illness? Yes. In controlled experiments, volunteers exposed to a cold virus developed clinical colds at rates that rose with their level of psychological stress (Cohen et al., 1991), and chronic stress broadly suppresses immune function (Segerstrom & Miller, 2004). Stress reaches the body through both physiological and behavioral pathways.

What is psychoneuroimmunology? It is the field that studies communication among the nervous, endocrine, and immune systems. It began when a conditioning experiment showed the immune response could be suppressed by a taste previously paired with an immunosuppressant, proving the immune system is not autonomous of the brain (Ader & Cohen, 1975).

Why do people fail to change health behaviors? Change is a staged process, and interventions fail when they are mismatched to a person's readiness (Prochaska & DiClemente, 1983) or when self-efficacy is low (Bandura, 1977). Even successful change often relapses, because maintaining a behavior depends on partly different mechanisms from starting it (Kwasnicka et al., 2016).

How much does following treatment actually matter? A great deal. A meta-analysis found that adherent patients had substantially better outcomes than non-adherent ones, an odds ratio near 2.9, so that adherence is a therapeutic target on a par with the choice of treatment itself (DiMatteo et al., 2002).

Do mind-body interventions like mindfulness have real effects? Controlled research finds reliable if moderate benefits of mindfulness training for chronic pain, anxiety, and depression, with mechanisms traced to attentional and stress-regulatory pathways (Creswell, 2017). Their scientific basis includes the gate control theory of pain, which showed pain to be open to psychological modulation (Melzack & Wall, 1965).

References

Ader, R., & Cohen, N. (1975). Behaviorally conditioned immunosuppression. Psychosomatic Medicine, 37(4), 333-340. https://doi.org/10.1097/00006842-197507000-00007

Bandura, A. (1977). Self-efficacy: Toward a unifying theory of behavioral change. Psychological Review, 84(2), 191-215. https://doi.org/10.1037/0033-295X.84.2.191

Cohen, S., Tyrrell, D. A. J., & Smith, A. P. (1991). Psychological stress and susceptibility to the common cold. New England Journal of Medicine, 325(9), 606-612. https://doi.org/10.1056/NEJM199108293250903

Cohen, S. (2021). Psychosocial vulnerabilities to upper respiratory infectious illness: Implications for susceptibility to coronavirus disease 2019 (COVID-19). Perspectives on Psychological Science, 16(1), 161-174. https://doi.org/10.1177/1745691620942516

Creswell, J. D. (2017). Mindfulness interventions. Annual Review of Psychology, 68, 491-516. https://doi.org/10.1146/annurev-psych-042716-051139

DiMatteo, M. R., Giordani, P. J., Lepper, H. S., & Croghan, T. W. (2002). Patient adherence and medical treatment outcomes: A meta-analysis. Medical Care, 40(9), 794-811. https://doi.org/10.1097/00005650-200209000-00009

Engel, G. L. (1977). The need for a new medical model: A challenge for biomedicine. Science, 196(4286), 129-136. https://doi.org/10.1126/science.847460

Epel, E. S., Crosswell, A. D., Mayer, S. E., Prather, A. A., Slavich, G. M., Puterman, E., & Mendes, W. B. (2018). More than a feeling: A unified view of stress measurement for population science. Frontiers in Neuroendocrinology, 49, 146-169. https://doi.org/10.1016/j.yfrne.2018.03.001

Friedman, M., & Rosenman, R. H. (1959). Association of specific overt behavior pattern with blood and cardiovascular findings. Journal of the American Medical Association, 169(12), 1286-1296. https://doi.org/10.1001/jama.1959.03000290012005

Kabat-Zinn, J. (2003). Mindfulness-based interventions in context: Past, present, and future. Clinical Psychology: Science and Practice, 10(2), 144-156. https://doi.org/10.1093/clipsy.bpg016

Kwasnicka, D., Dombrowski, S. U., White, M., & Sniehotta, F. (2016). Theoretical explanations for maintenance of behaviour change: A systematic review of behaviour theories. Health Psychology Review, 10(3), 277-296. https://doi.org/10.1080/17437199.2016.1151372

Lazarus, R. S., & Folkman, S. (1984). Stress, appraisal, and coping. Springer Publishing Company.

McEwen, B. S. (1998). Protective and damaging effects of stress mediators. New England Journal of Medicine, 338(3), 171-179. https://doi.org/10.1056/NEJM199801153380307

Melzack, R., & Wall, P. D. (1965). Pain mechanisms: A new theory. Science, 150(3699), 971-979. https://doi.org/10.1126/science.150.3699.971

Miller, N. E. (1969). Learning of visceral and glandular responses. Science, 163(3866), 434-445. https://doi.org/10.1126/science.163.3866.434

Prochaska, J. O., & DiClemente, C. C. (1983). Stages and processes of self-change of smoking: Toward an integrative model of change. Journal of Consulting and Clinical Psychology, 51(3), 390-395. https://doi.org/10.1037/0022-006X.51.3.390

Schwartz, G. E., & Weiss, S. M. (1978). Behavioral medicine revisited: An amended definition. Journal of Behavioral Medicine, 1(3), 249-251. https://doi.org/10.1007/BF00846677

Segerstrom, S. C., & Miller, G. E. (2004). Psychological stress and the human immune system: A meta-analytic study of 30 years of inquiry. Psychological Bulletin, 130(4), 601-630. https://doi.org/10.1037/0033-2909.130.4.601

Slavich, G. M. (2020). Social safety theory: A biologically based evolutionary perspective on life stress, health, and behavior. Annual Review of Clinical Psychology, 16, 265-295. https://doi.org/10.1146/annurev-clinpsy-032816-045159