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Psychosocial and biobehavioral factors and their interplay in coronary heart disease.

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Annual review of clinical psychology

Annual Reviews

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      Abstract

      Recent epidemiological research has confirmed that psychosocial factors are associated with increased risk of developing coronary heart disease (CHD), a major cause of death and disability worldwide. This association is probably mediated by changes in health risk behaviors and neuroendocrine and autonomic functions that affect metabolic, hemostatic, inflammatory, and cardiovascular functions that are the proximal agents in CHD pathogenesis over time as well as the precipitation of acute disease events. Recent developments in genomics have now made it possible to begin the process of identifying specific genetic variants that act either independently or via moderation of the impact of exposures to stressful environmental situations to increase the expression of these health-damaging psychosocial factors and the accompanying behavioral and physiological changes that lead to disease. It will be possible ultimately to use the knowledge emerging from research on gene x environment interactions that affect expression of psychosocial risk factors, health risk behaviors, and biological changes inside the body to speed the development of a new field of prospective medicine-a field where instead of spending the majority of health care resources on the treatment of chronic diseases at the end of life, it will be possible to allocate more resources to develop, test, and implement earlier in the disease process cost-effective, proactive interventions that target persons at high risk.

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      Most cited references 71

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      Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study.

      Although more than 80% of the global burden of cardiovascular disease occurs in low-income and middle-income countries, knowledge of the importance of risk factors is largely derived from developed countries. Therefore, the effect of such factors on risk of coronary heart disease in most regions of the world is unknown. We established a standardised case-control study of acute myocardial infarction in 52 countries, representing every inhabited continent. 15152 cases and 14820 controls were enrolled. The relation of smoking, history of hypertension or diabetes, waist/hip ratio, dietary patterns, physical activity, consumption of alcohol, blood apolipoproteins (Apo), and psychosocial factors to myocardial infarction are reported here. Odds ratios and their 99% CIs for the association of risk factors to myocardial infarction and their population attributable risks (PAR) were calculated. Smoking (odds ratio 2.87 for current vs never, PAR 35.7% for current and former vs never), raised ApoB/ApoA1 ratio (3.25 for top vs lowest quintile, PAR 49.2% for top four quintiles vs lowest quintile), history of hypertension (1.91, PAR 17.9%), diabetes (2.37, PAR 9.9%), abdominal obesity (1.12 for top vs lowest tertile and 1.62 for middle vs lowest tertile, PAR 20.1% for top two tertiles vs lowest tertile), psychosocial factors (2.67, PAR 32.5%), daily consumption of fruits and vegetables (0.70, PAR 13.7% for lack of daily consumption), regular alcohol consumption (0.91, PAR 6.7%), and regular physical activity (0.86, PAR 12.2%), were all significantly related to acute myocardial infarction (p<0.0001 for all risk factors and p=0.03 for alcohol). These associations were noted in men and women, old and young, and in all regions of the world. Collectively, these nine risk factors accounted for 90% of the PAR in men and 94% in women. Abnormal lipids, smoking, hypertension, diabetes, abdominal obesity, psychosocial factors, consumption of fruits, vegetables, and alcohol, and regular physical activity account for most of the risk of myocardial infarction worldwide in both sexes and at all ages in all regions. This finding suggests that approaches to prevention can be based on similar principles worldwide and have the potential to prevent most premature cases of myocardial infarction.
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        Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene.

        In a prospective-longitudinal study of a representative birth cohort, we tested why stressful experiences lead to depression in some people but not in others. A functional polymorphism in the promoter region of the serotonin transporter (5-HT T) gene was found to moderate the influence of stressful life events on depression. Individuals with one or two copies of the short allele of the 5-HT T promoter polymorphism exhibited more depressive symptoms, diagnosable depression, and suicidality in relation to stressful life events than individuals homozygous for the long allele. This epidemiological study thus provides evidence of a gene-by-environment interaction, in which an individual's response to environmental insults is moderated by his or her genetic makeup.
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          Role of genotype in the cycle of violence in maltreated children.

          We studied a large sample of male children from birth to adulthood to determine why some children who are maltreated grow up to develop antisocial behavior, whereas others do not. A functional polymorphism in the gene encoding the neurotransmitter-metabolizing enzyme monoamine oxidase A (MAOA) was found to moderate the effect of maltreatment. Maltreated children with a genotype conferring high levels of MAOA expression were less likely to develop antisocial problems. These findings may partly explain why not all victims of maltreatment grow up to victimize others, and they provide epidemiological evidence that genotypes can moderate children's sensitivity to environmental insults.
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            Author and article information

            Affiliations
            [1 ] Behavioral Medicine Research Center, Duke University Medical Center, Durham, North Carolina 27710, USA. redfordw@duke.edu
            Journal
            Annu Rev Clin Psychol
            Annual review of clinical psychology
            Annual Reviews
            1548-5943
            1548-5943
            2008
            : 4
            17716037 10.1146/annurev.clinpsy.4.022007.141237

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