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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tracking of dietary and physical activity patterns throughout adolescence into adulthood is low, which indicates that risk patterns for coronary heart disease are not maintained. Biological risk factors for heart disease, particularly obesity and clusters of nutritionally modifiable risk factors (e.g. the metabolic syndrome), display somewhat higher tracking correlations. Tracking gives little guidance as to how to use this information for screening purposes. For behavioral and biological risk factors predictive values and sensitivities and specificities are generally low, suggesting that population-based approaches are likely to be more effective than targeting only the high-risk subset for reducing the risk of coronary heart disease.
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PMID:Adolescence: a critical period for long-term tracking of risk for coronary heart disease? 1680 99

The metabolic syndrome has been referred to as a clustering of cardiovascular risk factors, including abdominal obesity, atherogenic dyslipidemia, increased blood pressure, insulin resistance, proinflammatory state, and a prothrombotic state. The metabolic syndrome has become one of the leading clinical issues discussed by physicians and the media, leading to increased public awareness to this potentially catastrophic multiplex risk factor for cardiovascular disease. With increasing prevalence in the United States, the metabolic syndrome has been equated to cigarette smoking as a contributing factor to premature cardiovascular heart disease and one of the underlying causes of type 2 diabetes. The identification and modification of the root causes, overweight/obesity, physical inactivity, and the closely associated condition, insulin resistance, needs to be one of the initial strategies that are addressed by the clinician.
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PMID:What is the metabolic syndrome? Prediabetes and cardiovascular risk. 1682 82

Only 13% of those 65 years and older engage in vigorous physical activity 3 or more days a week and obesity rates are increasing by 45% in adults over the age of 60. Physical activity helps prevent chronic disease and improves quality of life, yet few adults of any age are active. One exception is master athletes who participate in competitive sports during the middle and later years. The aerobic fitness of master athletes, as measured by maximal oxygen consumption, shows some decline, but not nearly as much as in sedentary controls. Master athletes have lipid profiles similar to those of young adults, which decreases their risk of heart disease. Master athletes also have better glucose tolerance and lower waist-to-hip ratios than sedentary adults, decreasing their risk for metabolic syndrome and type 2 diabetes. In the few dietary studies that have been conducted, master athletes consume more food energy while maintaining lower body weights than sedentary adults. Learning what motivates master athletes to stay highly active may help health professionals develop strategies to encourage exercise in the sedentary population of older adults.
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PMID:What can we learn about diet and physical activity from master athletes? 1682 17

A low concentration of high-density lipoprotein-cholesterol (HDL-C) is an independent risk factor for cardiovascular heart disease (CHD), but little is known about the distribution of HDL-C in France. This study evaluated the prevalence of low HDL-C among a large French population (5232 patients) with other cardiovascular risk factors. Depending on the guidelines used, the prevalence of low HDL-C varied from 8.7% (cutoff value of 35 mg/dl) to 26.9% (National Cholesterol Education Program metabolic syndrome cutoff values). The prevalence of low HDL-C gradually increased with the number of associated risk factors. We identified three independent risk predictors for low HDL-C: hypertriglyceridaemia (HTG), abdominal obesity and gender. Overall, the frequency of HDL-C assessment was very high (>85%) and it was highest in patients with hypercholesterolaemia or a history of CHD. Risk factors more frequently associated with low HDL-C (i.e. HTG, abdominal obesity and type 2 diabetes) were not associated with a more frequent assessment of HDL-C. Our findings indicate that in France, the prevalence of low HDL-C remains relatively high, particularly for patients with obesity and HTG.
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PMID:Prevalence of low HDL-cholesterol in patients with cardiovascular risk factors: The ECHOS (Etude du Cholesterol HDL en Observationnel) French Survey. 1694 88

Metabolic syndrome consists of a cluster of metabolic conditions, such as hypertriglyceridemia, hyper-low-density lipoproteins, hypo-high-density lipoproteins, insulin resistance, abnormal glucose tolerance and hypertension, that-in combination with genetic susceptibility and abdominal obesity-are risk factors for type 2 diabetes, vascular inflammation, atherosclerosis, and renal, liver and heart disease. One of the defects in metabolic syndrome and its associated diseases is excess cellular oxidative stress (mediated by reactive oxygen and nitrogen species, ROS/RNS) and oxidative damage to mitochondrial components, resulting in reduced efficiency of the electron transport chain. Recent evidence indicates that reduced mitochondrial function caused by ROS/RNS membrane oxidation is related to fatigue, a common complaint of MS patients. Lipid replacement therapy (LRT) administered as a nutritional supplement with antioxidants can prevent excess oxidative membrane damage, restore mitochondrial and other cellular membrane functions and reduce fatigue. Recent clinical trials have shown the benefit of LRT plus antioxidants in restoring mitochondrial electron transport function and reducing moderate to severe chronic fatigue. Thus LRT plus antioxidant supplements should be considered for metabolic syndrome patients who suffer to various degrees from fatigue.
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PMID:Metabolic syndrome and mitochondrial function: molecular replacement and antioxidant supplements to prevent membrane peroxidation and restore mitochondrial function. 1724 17

Coffee is a commonly consumed beverage with potential health benefits. This review will focus on cardiovascular disease. There are three preparations of coffee that are commonly consumed and thus worthy of examination; boiled unfiltered coffee, filtered coffee, and decaffeinated coffee. Coffee has over a thousand chemicals, many formed during the roasting process. From a physiological point of view, the potential bioactives are caffeine, the diterpenes cafestol and kahweol found in the oil, and the polyphenols, most notably chlorogenic acid. We will examine coffee and its bioactives and their connection with and effect on the risk factors which are associated with heart disease such as lipids, blood pressure, inflammation, endothelial function, metabolic syndrome and potentially protective in vivo antioxidant activity. These will be critically examined by means of in vitro studies, cell experiments, animal supplementation, epidemiology, and the most definitive evidence, human trials.
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PMID:Coffee and cardiovascular disease: in vitro, cellular, animal, and human studies. 1736 41

The World Health Organization estimates that around one billion people throughout the world are overweight and that over 300 million of these are obese and if current trends continue, the number of overweight persons will increase to 1.5 billion by 2015. The number of obese adults in Australia is estimated to have risen from 2.0 million in 1992/93 to 3.1 million in 2005. The prevalence of obesity has been increasing due to a convergence of factors--the rise of TV viewing, our preference for takeaway and pre-prepared foods, the trend towards more computer-bound sedentary jobs, and fewer opportunities for sport and physical exercise. Obesity is not only linked to lack of self esteem, social and work discrimination, but also to illnesses such as the metabolic syndrome and hyperinsulinaemia (which increases the risk of developing heart disease, diabetes, hypertension, fatty liver), cancer, asthma, dementia, arthritis and kidney disease. It has been estimated that the cost of obesity in Australia in 2005 was $1,721 million. Of this amount, $1,084 million were direct health costs, and $637 million indirect health costs (due to lost work productivity, absenteeism and unemployment). The prevalence cost per year for each obese adult has been estimated at $554 and the value of an obesity cure is about $6,903 per obese person. Government efforts at reducing the burden remain inadequate and a more radical approach is needed. The Australian government, for example, has made changes to Medicare so that GPs can refer people with chronic illness due to obesity to an exercise physiologist and dietitian and receive a Medicare rebate, but so far these measures are having no perceptible effect on obesity levels. There is a growing recognition that both Public Health and Clinical approaches, and Private and Public resources, need to be brought to this growing problem. Australian health economist, Paul Gross, from the Institute of Health Economics and Technology Assessment claims there is too much reliance on health workers to treat the problem, especially doctors, who have not been given additional resources to manage obesity outside a typical doctor's consultation. Gross has recommended that further changes should be made to Medicare, private health insurance, and workplace and tax legislation to give people financial incentives to change their behaviour because obesity should not just be treated by governments as a public health problem but also as a barrier to productivity and a drain on resources. A Special Report of the WMCACA (Weight Management Code Administration Council of Australia) (www.weightcouncil.org) on the "Health Economics of Weight Management" has been published in the Asia Pacific Journal of Clinical Nutrition in September 2006. This report explores the cost benefit analysis of weight management in greater detail.
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PMID:Health economics of weight management: evidence and cost. 1739 29

Abdominal -- and not peripheral -- obesity induces insulin resistance. Morbid obesity is not always accompanied by either diabetes mellitus or metabolic syndrome. Development of morbid obesity can require appropriate insulin secretion and recruitment of small insulin-sensitive adipocytes, able to store fatty acids. These fatty acids are therefore not stored in ectopic sites (muscle, liver, islets of Langerhans), and neither insulin resistance nor glucolipid toxicity develops and causes insulin deficiency. This explains the relative rarity of diabetes in morbid obesity. Patients with morbid obesity are at greater risk of developing mechanical complications (e.g. cardiac, pulmonary, or locomotor system, or sleep apnea) than metabolic complications or cardiovascular heart disease.
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PMID:[Obesity, immune resistance and metabolic complications: what morbid obesity can teach the doctor]. 1745 53

Although it has been known for many years that dietary lipids influence the development of atherosclerosis, in the past this has been attributed to their effects on blood cholesterol levels. Recent work, however, has shown that CMRs (chylomicron remnants), the lipoproteins which carry dietary lipids in the blood, potentially have a direct role in initiating atherogenesis by influencing vascular function. The Diet and Cardiovascular Health: Chylomicron Remnants and Their Emerging Roles in Vascular Dysfunction in Atherosclerosis Meeting focused attention on studies which have shown that CMRs influence vascular function via interactions with cells of the artery wall, including endothelial cells and macrophages, and also highlighted the part played by CMRs in the development of premature atherosclerosis in conditions such as the metabolic syndrome, which are an increasing cause of heart disease in developed countries.
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PMID:Introduction to the Biochemical Society Focused Meeting on Diet and Cardiovascular Health: chylomicron remnants and their emerging roles in vascular dysfunction in atherosclerosis. 1751 21

Chronically elevated glucocorticoid levels cause obesity, diabetes, heart disease, mood disorders and memory impairments. 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) catalyses intracellular regeneration of active glucocorticoids (cortisol, corticosterone) from inert 11-keto forms in liver, adipose and brain, amplifying local action. Obese humans and rodents show increased 11beta-HSD1 in adipose tissue. Transgenic mice overexpressing 11beta-HSD1 selectively in adipose tissue faithfully recapitulate metabolic syndrome. Conversely, 11beta-HSD1 knockout mice have a 'cardioprotective' phenotype, whose effects are also seen with 11beta-HSD1 inhibitors in rodents. However, any major metabolic effects of 11beta-HSD1 inhibition in humans are, as yet, unreported. 11beta-HSD1 null mice also resist cognitive decline with ageing, and this is seen in humans with a prototypic inhibitor. Thus 11beta-HSD1 inhibition is an emerging pleiotropic therapeutic target.
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PMID:Inhibition of 11beta-hydroxysteroid dehydrogenase type 1 as a promising therapeutic target. 1763 Dec 44


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