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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper aims to review the evidence for long-term effectiveness of weight loss on cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL) and triglycerides in overweight/obese people. Current evidence is mostly based on short-term studies. A systematic review of long-term lipid outcomes of weight loss in studies published between 1966 and 2001, was conducted. Inclusion criteria included all cohort studies and trials carried out on participants with body mass index of greater than or equal to 28 kg m(-2). Studies had at least two weight change measurements and follow-up of more than 2 years. Thirteen long-term studies with a follow-up of more than 2 years were included. Cholesterol has a significant positive linear relationship with weight change (r = 0.89) where change in weight explains about 80% of the cholesterol difference variation (Adj R2 = 0.80). For every 10 kg weight loss a drop of 0.23 mmol L(-1) in cholesterol may be expected for a person suffering from obesity or are grossly overweight. Weight loss has long-term beneficial effects especially on LDL and cholesterol. Weight loss in obese patients should be encouraged and sustained.
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PMID:Effects of weight loss in overweight/obese individuals and long-term lipid outcomes--a systematic review. 1496 6

The low-fat "diet-heart hypothesis" has been controversial for nearly 100 years. The low-fat-high-carbohydrate diet, promulgated vigorously by the National Cholesterol Education Program, National Institutes of Health, and American Heart Association since the Lipid Research Clinics-Primary Prevention Program in 1984, and earlier by the U.S. Department of Agriculture food pyramid, may well have played an unintended role in the current epidemics of obesity, lipid abnormalities, type II diabetes, and metabolic syndromes. This diet can no longer be defended by appeal to the authority of prestigious medical organizations or by rejecting clinical experience and a growing medical literature suggesting that the much-maligned low-carbohydrate-high-protein diet may have a salutary effect on the epidemics in question.
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PMID:The diet-heart hypothesis: a critique. 1551 34

Obesity is a major risk factor for several metabolic diseases, frequently clustering to form the metabolic syndrome, carrying a high risk of cardiovascular mortality. We aimed to assess the prevalence of the metabolic syndrome in treatment-seeking obese subjects and the potential protective effect of physical activity. A cross-sectional analysis of data from a large Italian database of treatment-seeking obese subjects was performed. The metabolic syndrome was defined according to the criteria provisionally set by the National Cholesterol Education Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, based on waist circumference, fasting glucose, triglyceride (TG) and high-density lipoprotein-cholesterol (HDL-C) levels, and arterial pressure. Data were available in 1,889 Caucasian subjects, 78% females, from 25 obesity centers. Minimum criteria for the metabolic syndrome were fulfilled in 53% of cases. The prevalence increased with age and obesity class and was negatively associated with participation in a structured program of physical activity (odds ratio, 0.76; 0.58 to 0.99; P =.041), after correction for age, sex, and body mass. The prevalence of cardiovascular disease was higher in subjects with the metabolic syndrome. A subset of 12.8% of cases had no metabolic abnormalities. They had a lower prevalence of abdominal obesity and cardiovascular disease. Isolated obesity was significantly associated with physical activity (odds ratio, 1.86; 1.33 to 2.60; P =.0003). Multiple metabolic disorders are present in most obese patients, and their prevalence is lower in physically active subjects. It is time to move towards a more integrated approach and to reconsider resource allocation to improve lifestyle changes for large-scale control of obesity.
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PMID:The metabolic syndrome in treatment-seeking obese persons. 1504 88

Cholesterol gallstone disease is a common condition in western populations. The etiology is multifactorial with interaction of genetic and environmental factors. Obesity, aging, estrogen treatment, pregnancy and diabetes are consistently associated to a higher risk. A number of dietary factors have been involved in the pathogenesis of cholelithiasis. In this article we summarize several studies that have evaluated the role of diet as a potential risk factor for gallstone formation, including energy intake, cholesterol, fatty acids, fiber, carbohydrates, vitamins and minerals, and alcohol intake. Consumption of simple sugars and saturated fat has been mostly associated to a higher risk, while fiber intake and moderate consumption of alcohol, consistently reduce the risk. The association between cholesterol intake and gallstone disease has been variable in different studies. The effects of other dietary factors are less conclusive; additional studies are therefore necessary to clarify their relevance in the pathogenesis of gallstone disease. Recent discoveries of the role of orphan nuclear receptors in the regulation of fatty acid and hepatic cholesterol metabolism and excretion open new perspectives for a better understanding of the role of dietary constituents on cholesterol gallstone formation. KEY TEACHING POINTS: The etiology of cholesterol gallstone disease is multifactorial with interaction between genome and environment. It has been postulated that dietary constituents are important determinants for the formation of lithogenic bile. Intake of high energy, simple sugar and saturated fat favors gallstone formation. Fiber and moderate consumption of alcohol reduce the risk. The role of orphan nuclear receptors in the regulation of hepatic cholesterol metabolism and excretion open new leads for understanding the role of dietary constituents on cholesterol gallstone formation.
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PMID:Diet as a risk factor for cholesterol gallstone disease. 1519 42

Despite their inherited nature, familial dyslipidemias show large intra- and interfamilial variability in phenotypic expression, clinical presentations, and levels of abnormalities of serum lipid fractions. Once diagnosed, patients shall be considered at high cardiovascular risk and treated as per secondary prevention National Cholesterol Education Program III guidelines. Comorbidity treatments (ie, obesity, diabetes, and hypertension) are imperative. Lifestyle interventions shall soon be concomitantly followed by lipid-regulating drugs. The major aspects of the above interventions are the following: 1) therapeutic lifestyle change: regular aerobic exercises, conventional low-fat, low-cholesterol, low refined but high complex carbohydrates diet, avoidance of unproven fad diets (ie, Atkins); 2) plant stanols and sterol esters, 3) high-potency statins (eg, rosuvastatin, simvastatin, atorvastatin); 4) addition of nicotinic acid, bile acid binders, fibrates, or ezetimibe pending on the lipid fraction affected; 5) statins are the starting drug of choice with these exceptions: in isolated low-density lipoprotein cholesterol, niacin or fibrates may be preferable; in isolated severe hypertriglyceridemic conditions, fibrates or fish oil may be preferable; in children with isolated elevation of low-density lipoprotein cholesterol, ezetimibe or bile acid binders may be preferable; when serum lipoprotein (a) elevation is the most notable abnormality, niacin may be chosen as the initial drug for its unique effect on this fraction. Plasmapheresis, intestinal shunts, or liver transplantation are to be considered in that order as last resorts if the above fails to accomplish serum lipid level goals.
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PMID:Treatment of Familial Hypercholesterolemia and Other Genetic Dyslipidemias. 1521 22

The constellation of dyslipidemia (hypertriglyceridemia and low levels of high-density lipoprotein cholesterol), elevated blood pressure, impaired glucose tolerance, and central obesity is identified now as metabolic syndrome, also called syndrome X. Soon, metabolic syndrome will overtake cigarette smoking as the number one risk factor for heart disease among the U.S. population. The National Cholesterol Education Program-Adult Treatment Panel III has identified metabolic syndrome as an indication for vigorous lifestyle intervention. Effective interventions include diet, exercise, and judicious use of pharmacologic agents to address specific risk factors. Weight loss significantly improves all aspects of metabolic syndrome. Increasing physical activity and decreasing caloric intake by reducing portion sizes will improve metabolic syndrome abnormalities, even in the absence of weight loss. Specific dietary changes that are appropriate for addressing different aspects of the syndrome include reducing saturated fat intake to lower insulin resistance, reducing sodium intake to lower blood pressure, and reducing high-glycemic-index carbohydrate intake to lower triglyceride levels. A diet that includes more fruits, vegetables, whole grains, monounsaturated fats, and low-fat dairy products will benefit most patients with metabolic syndrome. Family physicians can be more effective in helping patients to change their lifestyle behaviors by assessing each patient for the presence of specific risk factors, clearly communicating these risk factors to patients, identifying appropriate interventions to address specific risks, and assisting patients in identifying barriers to behavior change.
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PMID:Metabolic syndrome: time for action. 1522 52

The Adult Treatment Panel III (ATP III) of the National Cholesterol Education Program issued an evidence-based set of guidelines on cholesterol management in 2001. Since the publication of ATP III, 5 major clinical trials of statin therapy with clinical end points have been published. These trials addressed issues that were not examined in previous clinical trials of cholesterol-lowering therapy. The present document reviews the results of these recent trials and assesses their implications for cholesterol management. Therapeutic lifestyle changes (TLC) remain an essential modality in clinical management. The trials confirm the benefit of cholesterol-lowering therapy in high-risk patients and support the ATP III treatment goal of low-density lipoprotein cholesterol (LDL-C) <100 mg/dL. They support the inclusion of patients with diabetes in the high-risk category and confirm the benefits of LDL-lowering therapy in these patients. They further confirm that older persons benefit from therapeutic lowering of LDL-C. The major recommendations for modifications to footnote the ATP III treatment algorithm are the following. In high-risk persons, the recommended LDL-C goal is <100 mg/dL, but when risk is very high, an LDL-C goal of <70 mg/dL is a therapeutic option, ie, a reasonable clinical strategy, on the basis of available clinical trial evidence. This therapeutic option extends also to patients at very high risk who have a baseline LDL-C <100 mg/dL. Moreover, when a high-risk patient has high triglycerides or low high-density lipoprotein cholesterol (HDL-C), consideration can be given to combining a fibrate or nicotinic acid with an LDL-lowering drug. For moderately high-risk persons (2+ risk factors and 10-year risk 10% to 20%), the recommended LDL-C goal is <130 mg/dL, but an LDL-C goal <100 mg/dL is a therapeutic option on the basis of recent trial evidence. The latter option extends also to moderately high-risk persons with a baseline LDL-C of 100 to 129 mg/dL. When LDL-lowering drug therapy is employed in high-risk or moderately high-risk persons, it is advised that intensity of therapy be sufficient to achieve at least a 30% to 40% reduction in LDL-C levels. Moreover, any person at high risk or moderately high risk who has lifestyle-related risk factors (eg, obesity, physical inactivity, elevated triglycerides, low HDL-C, or metabolic syndrome) is a candidate for TLC to modify these risk factors regardless of LDL-C level. Finally, for people in lower-risk categories, recent clinical trials do not modify the goals and cutpoints of therapy.
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PMID:Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. 1524 16

Non-high-density lipoprotein (non-HDL) cholesterol level is determined by subtracting the high-density lipoprotein cholesterol level from the total cholesterol level and thus encompasses not only low-density lipoprotein cholesterol, but also the cholesterol contained in atherogenic, triglyceride-rich particles like remnants. This review summarizes data extracted from English-language publications accessible through MEDLINE on the population distribution of non-HDL cholesterol, its relationship to cardiovascular disease, and the potential benefits of treatment. Non-HDL cholesterol levels in the population vary by age, sex, and race and are closely linked to measures of obesity, especially visceral obesity. Several studies in populations with and without cardiovascular disease show that non-HDL cholesterol levels relate to atherosclerosis severity and subsequent cardiovascular morbidity and mortality. Preliminary data also suggest that pharmacologically induced changes in non-HDL cholesterol levels relate to prognosis. In the National Cholesterol Education Program Adult Treatment Panel III report, non-HDL cholesterol has been designated a secondary target of therapy among patients with hypertriglyceridemia.
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PMID:Non-high-density lipoprotein cholesterol: an alternate target for lipid-lowering therapy. 1524 64

BACKGROUND: Metabolic syndrome, a constellation of truncal obesity, dyslipidemia, disturbed insulin and glucose metabolism, and hypertension, is associated with the development of diabetes mellitus and coronary heart disease. However, the prevalence of metabolic syndrome in Hispanic patients with schizophrenia and whether they differ from comparable non-Hispanic patients is uncertain. METHOD: This cross-sectional study, conducted from January 2002 to May 2002, included 48 patients with schizophrenia who were recruited from an outpatient psychiatric clinic. Metabolic syndrome was defined using the criteria of the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. RESULTS: The prevalence of metabolic syndrome was 63% in all patients with schizophrenia. The metabolic syndrome was present in 41% of non-Hispanic patients and in 74% of Hispanic patients with schizophrenia. Metabolic syndrome was present in 70% of Cuban Americans and 88% of other Hispanic subgroups with schizophrenia. Metabolic syndrome was associated with waist circumference (p <.05) and high-density lipoprotein cholesterol (p <.05) in logistic regression analysis. CONCLUSIONS: These data suggest that schizophrenic patients have a 3-fold greater risk to develop metabolic syndrome than the general population. Hispanic schizophrenic patients have a significantly greater prevalence of metabolic syndrome than non-Hispanic schizophrenic patients (p <.05). An increased waist circumference is the strongest clinical correlate with metabolic syndrome in schizophrenic patients.
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PMID:Prevalence of Metabolic Syndrome in Hispanic and Non-Hispanic Patients With Schizophrenia. 1525

The underlying pathophysiology of the metabolic syndrome is the subject of debate, with both insulin resistance and obesity considered as important factors. We evaluated the differential effects of insulin resistance and central body fat distribution in determining the metabolic syndrome as defined by the National Cholesterol Education Program (NCEP) Adult Treatment Panel III. In addition, we determined which NCEP criteria were associated with insulin resistance and central adiposity. The subjects, 218 healthy men (n = 89) and women (n = 129) with a broad range of age (26-75 years) and BMI (18.4-46.8 kg/m2), underwent quantification of the insulin sensitivity index (Si) and intra-abdominal fat (IAF) and subcutaneous fat (SCF) areas. The metabolic syndrome was present in 34 (15.6%) of subjects who had a lower Si [median: 3.13 vs. 6.09 x 10(-5) min(-1)/(pmol/l)] and higher IAF (166.3 vs. 79.1 cm2) and SCF (285.1 vs. 179.8 cm2) areas compared with subjects without the syndrome (P < 0.001). Multivariate models including Si, IAF, and SCF demonstrated that each parameter was associated with the syndrome. However, IAF was independently associated with all five of the metabolic syndrome criteria. In multivariable models containing the criteria as covariates, waist circumference and triglyceride levels were independently associated with Si and IAF and SCF areas (P < 0.001). Although insulin resistance and central body fat are both associated with the metabolic syndrome, IAF is independently associated with all of the criteria, suggesting that it may have a pathophysiological role. Of the NCEP criteria, waist circumference and triglycerides may best identify insulin resistance and visceral adiposity in individuals with a fasting plasma glucose <6.4 mmol/l.
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PMID:Intra-abdominal fat is a major determinant of the National Cholesterol Education Program Adult Treatment Panel III criteria for the metabolic syndrome. 1527 90


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