Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary heart disease (CHD) is a major cause of mortality in the western world, and is known to be modified by both genetic and environmental factors. This suggests that at the molecular level there is interaction between the gene product(s) and/or the by-products of the environmental insult, and from a statistical viewpoint this implies a deviation from the expected multiplicative effect on risk. In other words genetic risk is modifiable in an environment-specific manner. This Review focuses on recently reported effects of smoking and alcohol (environmental factors) on the impact of variation in the genes for apoE (APOE) and alcohol dehydrogenase (ADHC1) on heart disease risk. Considering gene-environment interaction has the potential not only for improving our understanding of the pathophysiology of the disease, but also in the development and targeting of specific therapies.
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PMID:Gene-environment interaction and its impact on coronary heart disease risk. 1730 34

Alcohol dependence and alcohol abuse or harmful use cause substantial morbidity and mortality. Alcohol-use disorders are associated with depressive episodes, severe anxiety, insomnia, suicide, and abuse of other drugs. Continued heavy alcohol use also shortens the onset of heart disease, stroke, cancers, and liver cirrhosis, by affecting the cardiovascular, gastrointestinal, and immune systems. Heavy drinking can also cause mild anterograde amnesias, temporary cognitive deficits, sleep problems, and peripheral neuropathy; cause gastrointestinal problems; decrease bone density and production of blood cells; and cause fetal alcohol syndrome. Alcohol-use disorders complicate assessment and treatment of other medical and psychiatric problems. Standard criteria for alcohol dependence-the more severe disorder-can be used to reliably identify people for whom drinking causes major physiological consequences and persistent impairment of quality of life and ability to function. Clinicians should routinely screen for alcohol disorders, using clinical interviews, questionnaires, blood tests, or a combination of these methods. Causes include environmental factors and specific genes that affect the risk of alcohol-use disorders, including genes for enzymes that metabolise alcohol, such as alcohol dehydrogenase and aldehyde dehydrogenase; those associated with disinhibition; and those that confer a low sensitivity to alcohol. Treatment can include motivational interviewing to help people to evaluate their situations, brief interventions to facilitate more healthy behaviours, detoxification to address withdrawal symptoms, cognitive-behavioural therapies to avoid relapses, and judicious use of drugs to diminish cravings or discourage relapses.
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PMID:Alcohol-use disorders. 1941 Jul 5