Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up of participants in the Framingham Heart Study.
TL;DR: Intervention in obesity, in addition to the well established risk factors, appears to be an advisable goal in the primary prevention of CVD.
Abstract: The relationship between the degree of obesity and the incidence of cardiovascular disease (CVD) was reexamined in the 5209 men and women of the original Framingham cohort. Recent observations of disease occurrence over 26 years indicate that obesity, measured by Metropolitan Relative Weight, was a significant independent predictor of CVD, particularly among women. Multiple logistic regression analyses showed that Metropolitan Relative Weight, or percentage of desirable weight, on initial examination predicted 26-year incidence of coronary disease (both angina and coronary disease other than angina), coronary death and congestive heart failure in men independent of age, cholesterol, systolic blood pressure, cigarettes, left ventricular hypertrophy and glucose intolerance. Relative weight in women was also positively and independently associated with coronary disease, stroke, congestive failure, and coronary and CVD death. These data further show that weight gain after the young adult years conveyed an increased risk of CVD in both sexes that could not be attributed either to the initial weight or the levels of the risk factors that may have resulted from weight gain. Intervention in obesity, in addition to the well established risk factors, appears to be an advisable goal in the primary prevention of CVD.
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TL;DR: Transcript expression in perigonadal adipose tissue from groups of mice in which adiposity varied due to sex, diet, and the obesity-related mutations agouti (Ay) and obese (Lepob) found that the expression of 1,304 transcripts correlated significantly with body mass.
Abstract: Obesity alters adipose tissue metabolic and endocrine function and leads to an increased release of fatty acids, hormones, and proinflammatory molecules that contribute to obesity associated complications. To further characterize the changes that occur in adipose tissue with increasing adiposity, we profiled transcript expression in perigonadal adipose tissue from groups of mice in which adiposity varied due to sex, diet, and the obesity-related mutations agouti (Ay) and obese (Lepob). We found that the expression of 1,304 transcripts correlated significantly with body mass. Of the 100 most significantly correlated genes, 30% encoded proteins that are characteristic of macrophages and are positively correlated with body mass. Immunohistochemical analysis of perigonadal, perirenal, mesenteric, and subcutaneous adipose tissue revealed that the percentage of cells expressing the macrophage marker F4/80 (F4/80+) was significantly and positively correlated with both adipocyte size and body mass. Similar relationships were found in human subcutaneous adipose tissue stained for the macrophage antigen CD68. Bone marrow transplant studies and quantitation of macrophage number in adipose tissue from macrophage-deficient (Csf1op/op) mice suggest that these F4/80+ cells are CSF-1 dependent, bone marrow-derived adipose tissue macrophages. Expression analysis of macrophage and nonmacrophage cell populations isolated from adipose tissue demonstrates that adipose tissue macrophages are responsible for almost all adipose tissue TNF-alpha expression and significant amounts of iNOS and IL-6 expression. Adipose tissue macrophage numbers increase in obesity and participate in inflammatory pathways that are activated in adipose tissues of obese individuals.
8,902 citations
TL;DR: The global epidemic of obesity results from a combination of genetic susceptibility, increased availability of high-energy foods and decreased requirement for physical activity in modern society, and should be regarded as an epidemic that threatens global well being.
Abstract: Obesity is now so common within the world's population that it is beginning to replace undernutrition and infectious diseases as the most significant contributor to ill health. In particular, obesity is associated with diabetes mellitus, coronary heart disease, certain forms of cancer, and sleep-breathing disorders. Obesity is defined by a body-mass index (weight divided by square of the height) of 30 kg m(-2) or greater, but this does not take into account the morbidity and mortality associated with more modest degrees of overweight, nor the detrimental effect of intra-abdominal fat. The global epidemic of obesity results from a combination of genetic susceptibility, increased availability of high-energy foods and decreased requirement for physical activity in modern society. Obesity should no longer be regarded simply as a cosmetic problem affecting certain individuals, but an epidemic that threatens global well being.
4,697 citations
TL;DR: Since 1980, the American College of Cardiology and American Heart Association have translated scientific evidence into clinical practice guidelines (guidelines) with recommendations to improve cardiovascular health.
Abstract: Since 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines (guidelines) with recommendations to improve cardiovascular health. In 2013, the National Heart, Lung, and Blood Institute (NHLBI) Advisory
4,604 citations
TL;DR: Bariatric surgery for severe obesity is associated with long-term weight loss and decreased overall mortality.
Abstract: Background Obesity is associated with increased mortality. Weight loss improves cardiovascular risk factors, but no prospective interventional studies have reported whether weight loss decreases overall mortality. In fact, many observational studies suggest that weight reduction is associated with increased mortality. Methods The prospective, controlled Swedish Obese Subjects study involved 4047 obese subjects. Of these subjects, 2010 underwent bariatric surgery (surgery group) and 2037 received conventional treatment (matched control group). We report on overall mortality during an average of 10.9 years of follow-up. At the time of the analysis (November 1, 2005), vital status was known for all but three subjects (follow-up rate, 99.9%). Results The average weight change in control subjects was less than ±2% during the period of up to 15 years during which weights were recorded. Maximum weight losses in the surgical subgroups were observed after 1 to 2 years: gastric bypass, 32%; vertical-banded gastropl...
4,297 citations
TL;DR: The next generation of scientists and decision-makers will have a greater understanding of what constitutes a credible threat to public health and how to protect them from that threat.
3,748 citations
References
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TL;DR: Direct evidence indicates that lean 40-49-yr-old men would have a markedly more favorable lipoprotein profile and consequently a much lower risk of CHD, and the impact of obesity as a risk factor for CHD may have been underestimated.
Abstract: This study examines the relationship between obesity and low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and very-low-density lipoprotein (VLDL) cholesterol in 4260 young adult men and women. The strongest association between obesity and LDL cholesterol was found in 20-29 yr-old males, the weakest in 40-49-yr-old males. Conversely, in women the relationship between LDL cholesterol and obesity was modest except in the oldest (40-49 yr) age group. An inverse relationship between obesity and HDL cholesterol was of similar shape and strength in all sex and age-specific groups. When the ratio of total cholesterol (TCHOL) to HDL cholesterol was compared in lean and grossly obese 20-29-yr-old males, substantial differences were found. Since other data show this index of the lipoprotein profile to be the single best indicator of CHD risk, it would appear that the atherogenic potential of obesity is greater than would be suggested by the relatively weak association between obesity and TCHOL or any single lipoprotein cholesterol. These data also suggest that the impact of obesity as a risk factor for CHD may have been underestimated. The paucity of lean males 40-49-yr-old prevents firm conclusions about the CHD risk in such a group. Indirect evidence indicates that lean 40-49-yr-old men would have a markedly more favorable lipoprotein profile and consequently a much lower risk of CHD.
152 citations
TL;DR: This study of adults demonstrates significant genetic influence on change in weight even after maturation as well as consistent evidence of significant genetic variance in Quetelet Index.
Abstract: Longitudinal study of 514 pairs of US white male twin veterans was made possible by compiling data from military records, mailed questionnaires, and physical examinations. Height and weight were used to calculate the Quetelet index for twins at different ages covering induction into the Armed Forces (generally 17-24 years), 25 years, 40-50 years at questionnaire response, and 42-56 at physical examination. Cross-sectional analyses of Quetelet Index at these 4 points in time showed consistent evidence of significant genetic variance. Additional twin analyses of change in Quetelet Index both from induction and from age 25 to approximately age 48 were done. Both analyses showed significant genetic variance for change in Quetelet Index during this time span of 25 or more years for most subjects. Heritability estimates were 0.6 for change in Quetelet Index from induction (mean age 20) to examination (mean age 48) and 0.7 for change in Quetelet Index from age 25 to examination. While studies of younger twins have shown significant genetic influence on growth (height and weight), this study of adults demonstrates significant genetic influence on change in weight even after maturation.
24 citations