http://www.iowaaces360.org/uploads/1/0/9/2/10925571/relationship_of_childhood_abuse_and..._1998.pdf

Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. The Adverse Childhood Experiences (ACE) Study

Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis. Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys. Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. When they do so, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia.

Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy.

The self-medication hypothesis of addictive disorders derives primarily from clinical observations of patients with substance use disorders. Individuals discover that the specific actions or effects of each class of drugs relieve or change a range of painful affect states. Self-medication factors occur in a context of self-regulation vulnerabilities--primarily difficulties in regulating affects, self-esteem, relationships, and self-care. Persons with substance use disorders suffer in the extreme with their feelings, either being overwhelmed with painful affects or seeming not to feel their emotions at all. Substances of abuse help such individuals to relieve painful affects or to experience or control emotions when they are absent or confusing. Diagnostic studies provide evidence that variously supports and fails to support a self-medication hypothesis of addictive disorders. The cause-consequence controversy involving psychopathology and substance use/abuse is reviewed and critiqued. In contrast, clinical observations and empirical studies that focus on painful affects and subjective states of distress more consistently suggest that such states of suffering are important psychological determinants in using, becoming dependent upon, and relapsing to addictive substances. Subjective states of distress and suffering involved in motives to self-medicate with substances of abuse are considered with respect to nicotine dependence and to schizophrenia and posttraumatic stress disorder comorbid with a substance use disorder.

The self-medication hypothesis of substance use disorders: a reconsideration and recent applications.

ContextStudies of selected groups of persons with mental illness, such as those
who are institutionalized or seen in mental health clinics, have reported
rates of smoking to be higher than in persons without mental illness. However,
recent population-based, nationally representative data are lacking.ObjectiveTo assess rates of smoking and tobacco cessation in adults, with and
without mental illness.Design, Setting, and ParticipantsAnalysis of data on 4411 respondents aged 15 to 54 years from the National
Comorbidity Survey, a nationally representative multistage probability survey
conducted from 1991 to 1992.Main Outcome MeasuresRates of smoking and tobacco cessation according to the number and type
of psychiatric diagnoses, assessed by a modified version of the Composite
International Diagnostic Interview.ResultsCurrent smoking rates for respondents with no mental illness, lifetime
mental illness, and past-month mental illness were 22.5%, 34.8%, and 41.0%,
respectively. Lifetime smoking rates were 39.1%, 55.3%, and 59.0%, respectively
(P<.001 for all comparisons). Smokers with any
history of mental illness had a self-reported quit rate of 37.1% (P = .04), and smokers with past-month mental illness had a self-reported
quit rate of 30.5% (P<.001) compared with smokers
without mental illness (42.5%). Odds ratios for current and lifetime smoking
in respondents with mental illness in the past month vs respondents without
mental illness, adjusted for age, sex, and region of the country, were 2.7
(95% confidence interval [CI], 2.3-3.1) and 2.7 (95% CI, 2.4-3.2), respectively.
Persons with a mental disorder in the past month consumed approximately 44.3%
of cigarettes smoked by this nationally representative sample.ConclusionsPersons with mental illness are about twice as likely to smoke as other
persons but have substantial quit rates.

https://jamanetwork.com/journals/jama/articlepdf/193305/joc00268.pdf

Smoking and Mental Illness: A Population-Based Prevalence Study

The Self-medication Hypothesis of Substance Use Disorders: A Reconsideration and Recent Applications

A relationship between cigarette smoking and major depressive disorder was suggested in previous work involving nonrandomly selected samples. We conducted a test of this association, employing population-based data (n = 3213) collected between 1980 and 1983 in the St Louis Epidemiologic Catchment Area Survey of the National Institute of Mental Health. A history of regular smoking was observed more frequently among individuals who had experienced major depressive disorder at some time in their lives than among individuals who had never experienced major depression or among individuals with no psychiatric diagnosis. Smokers with major depression were also less successful at their attempts to quit than were either of the comparison groups. Gender differences in rates of smoking and of smoking cessation observed in the larger population were not evident among the depressed group. Furthermore, the association between cigarette smoking and major depression was not ubiquitous across all psychiatric diagnoses. Other data are cited indicating that when individuals with a history of depression stop smoking, depressive symptoms and, in some cases, serious major depression may ensue. ( JAMA . 1990;264:1546-1549)

Smoking, smoking cessation, and major depression.

IntroductionThe proportion of reported AIDS cases is currently low among heterosexuals without any reported risk factors. Further spread of HIV into this population will certainly depend on their sexual contact with drug users [1-4]. The AIDS epidemic has forced investigators to turn their attention to the histories of high risk sexual behaviors and drug-using patterns among their respondents. Primarily studies have been initiated on needle-sharing, homosexual, and other high risk samples, which limits the generalizability of such findings.

Lifetime Patterns of Substance Use among General Population Subjects Engaging in High Risk Sexual Behaviors: Implications for HIV Risk

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Smoking, smoking cessation, and major depression.

Lifetime Patterns of Substance Use among General Population Subjects Engaging in High Risk Sexual Behaviors: Implications for HIV Risk