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)

Several studies have indicated that moderate drinkers have a lower risk of both nonfatal myocardial infarction and fatal heart disease than do abstainers. To determine whether alcohol truly prevents coronary heart disease or whether other factors may contribute to this observed relationship, researchers conducted a systematic literature review and a combined analysis (i.e., meta-analysis) of 42 published studies. This analysis found that consumption of up to two drinks per day can promote changes in the levels of molecules that reduce the risk of heart disease while also increasing the levels of certain molecules that promote heart disease. Alcohol also may affect the risk of heart disease by acting on other various other molecules involved in a variety of physiological processes related to heart disease. Finally, the relationship between alcohol consumption and heart disease may be modulated by genetic factors.
Alcohol Res Health 2001
PMID:Alcohol's effects on the risk for coronary heart disease. 1191 Jul 2

The effects of ethanol and ethanol-derived acetaldehyde on rat myocardial apoptosis and expression of genes involved in the regulation of apoptosis and cell cycle arrest were studied. Combined ethanol and calcium carbimide treatment for 2, 5 or 8 days (E + CC) markedly increased blood acetaldehyde levels. Cytosolic DNA fragmentation was quantified in the 5-day treatment group. Increased amount of DNA-fragmentation, reflecting increased apoptosis, was evident in the E + CC group (23% increase compared to controls). mRNA levels of genes regulating apoptosis were measured by using quantitative PCR in the 2- and 8-day treatment groups. In the 2-day treatment group, p21 gene expression was increased by 25% and bax/bcl-2 mRNA ratio by 57% in E + CC, compared to the control, group. In the 8-day treatment group, p21 mRNA level was 24% lower, p53 mRNA level was 15% higher (P < 0.005), and bcl-2 mRNA level 36% higher in E + CC-treated, compared to the control, group. Interestingly, both ethanol and calcium carbimide treatments alone increased bax mRNA levels, as compared to the control group at 2 and 8 days. These results indicate that acetaldehyde might regulate the expression of apoptosis-linked genes and that apoptosis of myocardial cells may be involved in the development of alcoholic heart disease.
Alcohol Alcohol
PMID:Combined calcium carbimide and ethanol treatment induces high blood acetaldehyde levels, myocardial apoptosis and altered expression of apoptosis-regulating genes in rat. 1200 8

Alcohol dehydrogenase (ADH) and mitochondrial aldehyde dehydrogenase (ALDH2) are responsible for metabolizing the bulk of ethanol consumed as part of the diet and their activities contribute to the rate of ethanol elimination from the blood. They are expressed at highest levels in liver, but at lower levels in many tissues. This pathway probably evolved as a detoxification mechanism for environmental alcohols. However, with the consumption of large amounts of ethanol, the oxidation of ethanol can become a major energy source and, particularly in the liver, interferes with the metabolism of other nutrients. Polymorphic variants of the genes for these enzymes encode enzymes with altered kinetic properties. The pathophysiological effects of these variants may be mediated by accumulation of acetaldehyde; high-activity ADH variants are predicted to increase the rate of acetaldehyde generation, while the low-activity ALDH2 variant is associated with an inability to metabolize this compound. The effects of acetaldehyde may be expressed either in the cells generating it, or by delivery of acetaldehyde to various tissues by the bloodstream or even saliva. Inheritance of the high-activity ADH beta2, encoded by the ADH2*2 gene, and the inactive ALDH2*2 gene product have been conclusively associated with reduced risk of alcoholism. This association is influenced by gene-environment interactions, such as religion and national origin. The variants have also been studied for association with alcoholic liver disease, cancer, fetal alcohol syndrome, CVD, gout, asthma and clearance of xenobiotics. The strongest correlations found to date have been those between the ALDH2*2 allele and cancers of the oro-pharynx and oesophagus. It will be important to replicate other interesting associations between these variants and other cancers and heart disease, and to determine the biochemical mechanisms underlying the associations.
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PMID:Overview of the role of alcohol dehydrogenase and aldehyde dehydrogenase and their variants in the genesis of alcohol-related pathology. 1509 7

Propolis is a resinous substance collected by honeybees from various plant sources. It is extensively used in food and beverages to improve health and prevent diseases such as heart disease, diabetes, and cancer. To investigate the absorption and metabolism of the components in propolis, in the present study, we administered ethanol extracts of Uruguayan propolis (poplar type propolis) orally to rats and analyzed their plasma and urine by high-performance liquid chromatography with photodiode array and mass spectrometric detection. After deconjugation of the components by beta-glucuronidase/sulfatase treatment of the specimen, pinobanksin 5-methyl ether, pinobanksin, kaempferol, chrysin, pinocembrin, and galangin were detected in plasma of rats orally administered propolis. These compounds were detected also in urine after beta-glucuronidase/sulfatase treatment. Furthermore, pinobanksin 5-methyl ether, pinobanksin, chrysin, pinocembrin, and galangin were present in the urine also in free form. These results suggest that flavonoids in propolis are metabolized and circulate in the body after oral administration of propolis.
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PMID:Identification of metabolites in plasma and urine of Uruguayan propolis-treated rats. 1513 57

Postmenopausal women in Western societies are conscious of breast cancer as a potential cause of death and ill health, which they wish to avoid with the advice of their doctors. Yet many factors that predispose women to the development of cancer will have been laid down before the menopause, in their genetic makeup or during their adolescent years. Even in middle age it is important to take account of the intrinsic level of risk, and to give women advice tailored to their own individual risk level. This results from their family history, previous diseases such as benign breast disease, and previous treatment for breast cancer or Hodgkin's disease. For those at the highest level of risk, strategies will include regular screening, prophylactic mastectomy, and the use of chemoprevention agents, such as tamoxifen. These women should avoid hormone replacement therapy (HRT) and control their menopausal symptoms and osteoporosis through the use of other agents now available - venlafaxine for menopausal symptoms and bisphosphonates for osteoporosis. Raloxifene is an agent under trial that may be valuable for breast cancer control as well as for osteoporosis. Women at standard population risk will require less robust preventive strategies, which will include screening and lifestyle modification. Their decisions regarding HRT should now be modified by recent evidence of associated risks. Recent studies show that tibolone causes less mammographic density and has a lower relative risk of breast cancer than combined estrogen/progestogen preparations. There is limited evidence that controlling obesity, participating in exercise and adopting a diet low in fats and high in fruit and vegetables will alter risk at this age. These precautions will, however, reduce the risk of other diseases common in this age group, such as hypertension, heart disease, stroke, and type 2 diabetes mellitus. Alcohol, even in small amounts, is a risk factor for breast cancer. Given the cardioprotective effect of moderate alcohol intake, advice on alcohol must reflect the individual relative risk of cardiovascular disease and breast cancer. Personal risk assessment is relevant for all women. Screening and a healthy lifestyle are worthwhile approaches for all, with the more aggressive approaches such as chemoprevention and prophylactic surgery reserved for those who have substantially elevated levels of risk. Once the menopause has passed, screening is probably the most effective evidence-based tool for breast cancer control by early diagnosis.
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PMID:Strategies for managing breast cancer risk after the menopause. 1533 Jun 77

Many women take supplemental estrogens after menopause, a practice called hormone replacement therapy (HRT). Moderate alcohol consumption may increase estrogen levels in women receiving HRT, potentially affecting their risk for various adverse health effects. Two recent studies, however, provide no strong evidence for an effect of alcohol on hormones in postmenopausal women. The possible association between alcohol consumption and risk of cancer of the breast does not appear to be mediated by estrogens. Both estrogens and moderate alcohol consumption have been associated with a decreased risk for cardiovascular disease; however, alcohol's beneficial effect on heart disease does not appear to involve hormonal mechanisms. Additional research is needed to define the consequences of moderate drinking on hormone levels after menopause.
Alcohol Health Res World 1998
PMID:Alcohol, hormones, and postmenopausal women. 1570 94

Apoptosis of myocytes is likely to contribute to a variety of heart conditions and could also be important in the development of alcoholic heart disease. A fundamental pathway to apoptosis is through mitochondrial membrane permeabilization and release of proapoptotic factors from the mitochondrial intermembrane space to the cytosol. The authors' results show that prolonged exposure of cultured cardiac cells to ethanol (35 mM for 48 hr) promotes Ca2+-induced activation of the mitochondrial permeability transition pore (PTP). PTP-dependent mitochondrial membrane permeabilization is followed by release of cytochrome c and execution of apoptosis. The authors propose that chronic ethanol exposure, in combination with other stress signals, may allow for activation of the PTP by physiological calcium oscillations, providing a trigger for cardiac apoptosis during chronic alcohol abuse. Coincidence of apoptosis promoting factors occurs in only a small fraction of myocytes, but because of the absence of regeneration, even a modest increase in the rate of cell death may contribute to a decrease in cardiac contractility. Detection of apoptotic changes that are present in only a few myocytes at a certain time in the heart is not feasible with most of the apoptotic assays. Fluorescence imaging is a powerful technology to visualize changes that are confined to a minor fraction of cells in a tissue, and the use of multiphoton excitation permits imaging in situ deep in the wall of the intact heart. This article discusses potential mechanisms of the effect of alcohol on mitochondrial membrane permeabilization and visualization of mitochondria-dependent apoptosis in cardiac muscle.
Alcohol Clin Exp Res 2005 May
PMID:Alcohol and mitochondria in cardiac apoptosis: mechanisms and visualization. 1589 12

Myocardial damage from heavy alcohol intake can cause the heart failure (HF) syndrome, but the relation of lighter alcohol intake to HF has rarely been studied. We examined the risk of HF hospitalization among 126,236 subjects who supplied data about alcohol during health examinations from 1978 to 1985. Among 2,594 subjects who were subsequently hospitalized for HF, record review established an association between coronary artery disease (CAD) and HF (CAD-HF) in 1,559 patients. Among the remaining 1,035 subjects who had HF (non-CAD-HF), we attempted determination of preponderant etiologic and contributory factors. Analyses used Cox models that were controlled for 7 covariates, with usual alcohol intake studied categorically compared with that in subjects who did not drink alcohol. Heavier drinkers (> or =3 drinks/day) but not light to moderate drinkers had increased risk of non-CAD-HF; e.g., relative risk for subjects who reported > or =6 drinks/day was 1.7 (95% confidence interval 1.1 to 2.6). This association of non-CAD-HF with heavy drinking was limited to subsets with cardiomyopathy or of unclear preponderant etiology. Alcohol drinking was inversely related to risk of CAD-HF (e.g., at 1 to 2 drinks/day, relative risk 0.6, 95% confidence interval 0.5 to 0.7), with consistency across subgroups of age, gender, ethnicity, education, smoking status, interval to diagnosis, and presence or absence of baseline heart disease or systemic hypertension. Moderate drinking was inversely related to non-CAD-HF only in subjects who had diabetes mellitus (n = 252). In conclusion, heavy, but not light, alcohol drinking is associated with increased risk of non-CAD-HF and that apparent protection by alcohol drinking against CAD-HF risk provides confirmation of a protective effect of alcohol against CAD.
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PMID:Alcohol drinking and risk of hospitalization for heart failure with and without associated coronary artery disease. 1605 55

Diseases of the heart and blood vessels are a major cause of illness and disability worldwide. The relationship between ethanol consumption and cardiovascular disease are both complex and interconnected. Our aim of this study was to explore the effect of leptin on lipid metabolism in ethanol supplemented mice. Male Swiss mice (Mus musculas) weighing 25+/-2 g were administered ethanol (6.32 g kg(-1) body weight) for the first 30 days. Subsequently, ethanol fed mice were given intraperitoneal injections of exogenous mouse recombinant leptin (230 microg kg(-1) body weight) every alternate day for 15 days. Food and water intake and total body weight were measured every day and at the end of the experimental period of 45 days, plasma and cardiac lipids were analyzed. Exogenous leptin injections to ethanol fed mice significantly (P < 0.05) prevented the accumulation of total cholesterol, phospholipids (PL), triglycerides (TG) and free fatty acids (FFA) in the mouse heart and blood as compared to the untreated ethanol fed mice whereas, the plasma concentration of free cholesterol was significantly increased on leptin administration as compared to normal untreated mice. Moreover leptin administration significantly elevated the activities of cardiac lipoprotein lipase (LPL) and plasma lecithin cholesterol acyl transferase (LCAT) and significantly reduced the activities of cardiac HMG CoA reductase and cholesterol ester synthase (CES) on leptin administration to ethanol fed mice. Thus we could postulate that an increase in systemic leptin level prevents the accumulation of lipids in the plasma and heart of ethanol treated mice.
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PMID:Intraperitoneal leptin regulates lipid metabolism in ethanol supplemented Mus musculas heart. 1613 12

Diabetes mellitus is a major risk factor for heart disease (heart attack, angina, and heart failure), stroke, and hypertension, which shorten the average life expectancy. The main objective of this study was to describe the prevalence of heart disease, hypertension, and stroke among Canadians with diabetes compared to those without diabetes in the Canadian general population aged 12 years and over. It also estimated the strength of association between diabetes, heart disease, hypertension, and other factors such as age, gender, cigarette smoking, alcohol drinking, education status, body mass index (BMI), and other socioeconomic factors. Descriptive statistics were used initially to estimate the prevalence of related comorbidities by age and gender. Logistic regression was then employed to determine the potential strength of association between various effects. Data included 127,610 individuals who participated in the 2.1 cycles of the Canadian Community Health Survey (CCHS) in 2002-2003. The prevalence of self-reported hypertension, heart disease, and stroke among individuals with diabetes were 51.9, 21.7, and 4.8%, respectively. By comparison, prevalence among those without diabetes was 12.7, 4.2, and 0.9%. Adjusted Odds Ratios (OR) were 4.15, 5.04, and 6.75 for males', and 4.10, 5.29, and 4.56 for females' hypertension, heart disease, and stroke, respectively. Lower income (OR from 1.27-1.94) and lower education (OR from 1.23-1.86) were independently associated with a high prevalence of hypertension, heart disease, and stroke among diabetics. Alcohol consumption (OR from 1.06-1.38), high BMI (OR from 1.17-1.40), physical inactivity (OR from 1.21-2.45), ethnicity, and immigration status were also strongly associated with hypertension, heart disease, and stroke. The adjusted prevalence of hypertension, heart disease, and stroke in the CCHS-2003 health survey in Canada was significantly higher among those with diabetes compared to those without. Other factors such as age, gender, BMI, lifestyle, family incomes, physical activity levels, and socioeconomic status also affected the strength of association between diabetes and resulting comorbidities.
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PMID:Prevalence of diabetes and cardiovascular comorbidity in the Canadian Community Health Survey 2002-2003. 1643 38


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