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

The statistical frequency of myocardial infarct in women aged 30-39 and 40-44 is presented, comparing the occurrences of those women who are users of oral hormonal contraceptives. The relative risk of myocardial infarct in women using steroid contraceptives as compared with nonusers was estimated at 4.5:1. When combined with the presence of another risk factor, such as hypertension, obesity, heavy smoking, diabetes, or high cholesterol, this relative risk increases to 10.5:1. With 3 or more risk factors, this ratio is 78:1. It appears that the risk of steroid contraceptives tends more toward arterial coronary thrombosis than toward the formation of clots. The action of oral steroid contraceptives is considered to be more synergistic with other risk factors than additive.
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PMID:[Myocardial infarct in young women and steroid contraception]. 126 74

The late Surgeon Captain T.L. Cleave (1906-1983) completed his life-long RN professional service by promotion to the post of Director of Medical Research to the Royal Navy. His voyaging as a medical officer gave him unique understanding of patterns of disease throughout the world. He concluded that many of the degenerative illnesses which during this century have become so common in advanced countries have a simple basic dietary cause--the consumption of ever increasing quantities of refined carbohydrates; human beings were not, in Cleave's opinion, adapted to the use of these artificially concentrated foods. He suggested the term "Saccharine Disease" to denote many diverse manifestations, including dental decay, obesity, diabetes and coronary thrombosis, of one master disease having one simple cause. The neglect of this concept by most authorities today repeats the attitudes of the 'medical establishment' towards one of Cleave's distinguished eighteenth century naval predecessors, James Lind, whose advocacy of citrus fruit juice for the prevention of scurvy was greeted with derision.
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PMID:Tribute to Cleave--forgotten prophet. 176 11

A male to female ration of coronary disease of 2:1 has been a consistent finding. This differential persists event when the classic risk factors for coronary disease--hypertension, smoking, obesity, diabetes, and hyperlipidemia--are controlled for gender. The most likely ultimate cause of this phenomenon is male-female differences in sex hormone patterns. Clinical studies in this area have either compared the sex hormone profiles of men and women with and without coronary disease or computed the relative prevalence of disease in populations that differ in their sex hormone patterns. In general, research findings have disputed the hypothesis that persons with coronary disease have low levels of a protective factor such as estrogen or progesterone and high levels of testosterone. Coronary disease patients actually have elevated estrogen levels and low testosterone levels; endogenous progesterone levels are normal before infarction but show a stress-mediated increase in the immediate postinfarction period. Findings of a low prevalence of coronary disease in premenopausal women, a loss of protection after menopause, and a low prevalence of coronary disease in men with cirrhosis-related hyperestrogenemia suggest that natural estrogens are antiatherogenic. The protective effect of pregnancy against myocardial infarction, despite concomitant potentially thrombogenic levels of estrogen at the time, seems to indicate that progesterone, whose levels are also extremely high during pregnancy, plays a major anti-infarction protective effect distinct from that of estrogen. Studies of women oral contraceptive (OC) users and men taking estrogens for brief periods have found that these exogenous hormones produce coronary thrombosis but not atherosclerosis. Finally, the finding of increased coronary disease risk in long-term OC users indicates that synthetic estrogens favor coronary atherosclerosis by suppressing natural estrogen and progesterone production.
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PMID:Sex hormones and coronary disease: a review of the clinical studies. 223 42

This review has discussed some metabolic and endocrine changes that can be associated with a stress type of metabolism, diabetes, obesity, hypertension, smoking and the consumption of diets rich in fat and refined sugar, or poor in ascorbate. These are some of the risk factors associated with premature atherosclerosis, coronary thrombosis and stroke. It has been proposed that an increased control of metabolism by the 'stress' or counter-regulatory hormones, relative to insulin, is a common feature of these risk factors. Particular emphasis was placed upon the action of the glucocorticoids which can produce insulin insensitivity, leading to hyperglycaemia, hypertriglyceridaemia, hypercholesterolaemia and hyperinsulinaemia. Furthermore, glucocorticoids can decrease energy expenditure and, together with insulin, promote energy deposition. These observations provide a partial explanation for the metabolic changes that can accompany the risk factors and clarify why they interact in promoting atherosclerosis.
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PMID:Possible connections between stress, diabetes, obesity, hypertension and altered lipoprotein metabolism that may result in atherosclerosis. 268 77

There are 2 striking differences in the practice of medicine in the US and in the UK: 1) in the former, there is a great emphasis on private medicine, and 2) in the US there is a much higher incidence of litigation, whereas in the UK, family planning services are free, and litigation in this area is almost unknown. British medical opinion agrees with the US on the following oral contraceptive contraindications: 1) cancer of the breast, ovary, uterus, vagina, or cervix; 2) coronary thrombosis, pulmonary embolism, deep vein thrombosis, angina pectoris, or stroke; and 3) unusual or unexplained vaginal bleeding. Both countries agree that it is inadvisable to give the combined pill over the age of 45, and over the age of 35 in smokers. The UK agrees with 75% of the routines adopted by US doctors on a patient's 1st visit for oral contraceptives. However, a patient who becomes amenorrheic while taking the pill is not regarded as lightly in the UK as she would be in the US; she is closely monitored. If 1 of 4 risk factors (age 35 or over, hypertension, obesity, or smoking) is evident, a patient in the UK is closely supervised while taking the pill. If more than 2 risk factors are present, a UK doctor may advise against the pill. Since the 1960s the media have both praisd and condemned the pill. There is no doubt that, in the field of contraceptive advice, the US and the UK lead the way, and a closer liaison between the 2 medical professions is essential to reassure patients.
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PMID:Contraceptive advice: how the English differ from the Americans. 309 Feb 54

Infarction in the adult aged less than 35 is almost always accompanied by risk factors, the most common of which are tobacco abuse, lipid disturbances, obesity, a strong family history of cardiovascular disease and, in the woman, the use of contraceptives. The coronary arteries are sometimes normal (10-15 p. cent) but coronary lesions are most often single vessel, proximal and affect the anterior interventricular branch. Actual coronary thrombosis probably plays a more important role than in the older adult. Ventricular function is often markedly impaired. The infarct is most often anterior, transmural and large in size, with ventricular arrhythmias more frequent and a higher risk of sudden death. Post-hospital complications are the same as in the older adult, with possibly less good results of aorto-coronary venous bypasses. Long term mortality depends directly upon the number of vessels affected, but is markedly better than in the older adult.
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PMID:[Myocardial infarction in the adult under 35 years of age]. 630 67

The risks of cardiovascular disease associated with dyslipidemia differ in women and men, being more strongly associated with triglyceride/high-density lipoprotein in middle-aged women than in men. Although the incidence of heart disease is lower in women because they live longer, over a lifetime, cardiovascular disease in women is equal to that in men, with the greatest incidence after age 65 years. Major coronary events are rare among reproductive-age women who use oral contraceptives and are related to the concomitant effects of age, smoking, diabetes, hypertension, and obesity. Low estrogen-progestin dose oral contraceptives appear not to promote cardiovascular disease and can be used in women with controlled cholesterol elevations. Alternative contraceptive measures should be considered for patients with severe uncontrolled hypercholesterolemia or a lipid disorder that carries a high risk of coronary heart disease. In these conditions, thrombotic propensity associated with supraphysiologic doses of estrogen in oral contraceptives might accelerate coronary thrombosis should an arteriosclerotic plaque rupture. Treatment of hypercholesterolemia should follow the guidelines of the National Cholesterol Education Program and emphasize hygienic measures. Contraceptive selection in hyperlipidemic patients should reflect a balance between the risks--and their management--of developing cardiovascular disease versus the risks of pregnancy.
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PMID:Contraception and dyslipidemia. 851 44

Acute coronary syndromes (ACS) such as unstable angina, myocardial infarction, or sudden ischemic death evolve from coronary thrombosis consequence of atherosclerotic plaque disruption. Plaque stabilization is an important therapeutic strategy in the prevention of ACS. Coronary risk factors include age, male sex, cigarette smoking, hypertension, dislipidemia, diabetes mellitus, insulin resistance and/or hyper insulinemia, obesity, sedentary lifestyle, stress, and the morning surge of sympathetic activity. New risk factors are emerging such as high homocystein, inflammation, and some kinds of infection. Control of blood pressure and cholesterol clearly reduce the risk of coronary events and mortality although the effects of antihypertensive therapy have been less than expected. The benefits of smoking cessation, moderate alcohol consumption, low-dose aspirin prophylaxis, estrogen-replacement therapy in postmenoposal women have also been shown.
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PMID:[Risk factors and prevention of acute coronary syndrome]. 979 37

Plasminogen activator inhibitor-1 (PAI-1) is the major inhibitor of plasminogen activation and likely plays important roles in coronary thrombosis and arteriosclerosis. Tumor necrosis factor-alpha (TNFalpha) is one of many recognized physiological regulators of PAI-1 expression and may contribute to elevated plasma PAI-1 levels in sepsis and obesity. Although TNFalpha is a potent inducer of PAI-1 expression in vitro and in vivo, the precise location of the TNFalpha response site in the PAI-1 promoter has yet to be determined. Transient transfection studies using luciferase reporter constructs containing PAI-1 promoter sequence up to 6.4 kb failed to detect a response to TNFalpha. Moreover, TNFalpha failed to induce expression of enhanced green fluorescent protein under the control of a 2.9-kb human PAI-1 promoter in transgenic mice, although endogenous murine PAI-1 was strongly induced. These data suggested that the TNFalpha response element in the PAI-1 gene is remote from the proximal promoter region. In this study, seven candidate regulatory regions were identified using cross-species sequence homology analysis as well as DNase I-hypersensitive site analysis. We identified a 5' distal TNFalpha-responsive enhancer of the PAI-1 gene located 15 kb upstream of the transcription start site containing a conserved NFkappaB-binding site that mediates the response to TNFalpha. This newly recognized site is fully capable of binding NFkappaB subunits p50 and p65, whereas overexpression of the NFkappaB inhibitor IkappaB prevents TNFalpha-induced activation of this enhancer element.
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PMID:Tumor necrosis factor alpha activates the human plasminogen activator inhibitor-1 gene through a distal nuclear factor kappaB site. 1496 43

Diabetes mellitus is increasing worldwide, resulting from the interaction of obesity, inflammation, and hyperglycemia. Activated immunity and cytokine production lead to insulin resistance and other components of the metabolic syndrome, establishing the link between diabetes and atherosclerosis. Hyperglycemia-induced endothelial dysfunction is mediated by increased oxidative stress, a promoter of adventitial inflammation and vasa vasorum neovascularization in experimental models of diabetic atherosclerosis. Recent studies have documented increased inflammation, neovascularization, and intraplaque hemorrhage in human diabetic atherosclerosis. This inflammatory microangiopathic process is independently associated with plaque rupture, leading to coronary thrombosis. Tissue factor, the most potent trigger of the coagulation cascade, is increased in diabetic patients with poor glycemic control. Circulating tissue factor microparticles are also associated with apoptosis of plaque macrophages, closing the link among inflammation, plaque rupture, and blood thrombogenicity. High-density lipoproteins, responsible for free cholesterol removal, are reduced in patients with insulin resistance and diabetes. High-density lipoprotein therapy leads to a significant decrease in plaque macrophages and increase in smooth-muscle cells. These beneficial effects may be responsible for coronary plaque stabilization in patients treated with recombinant Apolipoprotein A-I Milano/phospholipid complex. Finally, peroxisomal proliferator-activated receptors (PPARs) are now considered the nuclear transcriptional regulators of atherosclerosis. Three subfamilies, including PPAR-alpha, -delta, and -gamma, have been identified with crucial roles in lipid metabolism, plaque inflammation, expression of adhesion molecules and cytokines, and regulation of matrix metalloproteinases. Multiple experimental studies have documented plaque stabilization with PPAR-gamma agonists, a group of medications holding great promise in the treatment of diabetes atherosclerosis.
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PMID:New aspects in the pathogenesis of diabetic atherothrombosis. 1560 89


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