The Sex and Race Specific Relationship between Anthropometry and Body Fat Composition Determined from Computed Tomography: Evidence from the Multi-Ethnic Study of Atherosclerosis.

BackgroundFew studies have investigated the relationship of anthropometric measurements with computed tomography (CT) body fat composition, and even fewer determined if these relationships differ by sex and race.MethodsCT scans from 1,851 participants in the population based Multi-Ethnic Study of Atherosclerosis were assessed for visceral and subcutaneous fat areas by semi-automated segmentation of body compartments. Regression models were used to investigate relationships for anthropometry with visceral and subcutaneous fat separately by sex and race/ethnicity.ResultsParticipants were 50% female, 41% Caucasian, 13% Asian, 21% African American, and 25% Hispanic. For visceral fat, the positive relationship with weight (p = 0.028), waist circumference (p<0.001), waist to hip ratio (p<0.001), and waist to height ratio (p = 0.05) differed by sex, with a steeper slope for men. That is, across the range of these anthropometric measures the rise in visceral fat is faster for men than for women. Additionally, there were differences by race/ethnicity in the relationship with height (p<0.001), weight (p<0.001), waist circumference (p<0.001), hip circumference (p = 0.006), and waist to hip ratio (p = 0.001) with the Hispanic group having shallower slopes. For subcutaneous fat, interaction by sex was found for all anthropometric indices at p<0.05, but not for race/ethnicity.ConclusionThe relationship between anthropometry and underlying adiposity differs by sex and race/ethnicity. When anthropometry is used as a proxy for visceral fat in research, sex-specific models should be used

Fatness and fitness: how do they influence health-related quality of life in type 2 diabetes mellitus?

<p>Abstract</p> <p>Objective</p> <p>We examined whether adiposity and fitness explain the decrease in health-related quality of life (HRQOL) associated with type 2 diabetes mellitus.</p> <p>Methods</p> <p>This was a cross-sectional study using baseline data from two exercise training interventions. One study enrolled people with and the other without type 2 diabetes. We assessed aerobic fitness ("fitness") as peak oxygen uptake during treadmill testing, adiposity ("fatness") as percentage of total body fat by dual-energy x-ray absorptiometry, and HRQOL by the Medical Outcomes Study SF-36. Bivariate and multivariate linear regression analyses were used examine determinants of HRQOL were used to examine determinants of HRQOL.</p> <p>Results</p> <p>There were 98 participants with and 119 participants without type 2 diabetes. Participants with type 2 diabetes had a mean hemoglobin A1c of 6.6% and, compared with participants without diabetes had lower HRQOL on the physical component summary score (<it>P </it>= 0.004), role-physical (<it>P </it>= 0.035), vitality (<it>P </it>= 0.062) and general health (<it>P </it>< 0.001) scales after adjusting for age, sex and race. These associations of HRQOL with type 2 diabetes were attenuated by higher fitness, even more than reduced fatness. Only general health remained positively associated with type 2 diabetes after accounting for fatness or fitness (<it>P </it>= 0.003). There were no significant differences between participants with and without diabetes in the mental component score.</p> <p>Conclusion</p> <p>Improved fitness, even more than reduced fatness, attenuated the association of type 2 diabetes with HRQOL. The potential to improve HRQOL may motivate patients with type 2 diabetes to engage in physical activity aimed at increasing fitness. Findings from this cross-sectional analysis will be addressed in the ongoing trial of exercise training in this cohort of participants with type 2 diabetes.</p> <p>Trial registration</p> <p>NCT00212303</p

Late systolic central hypertension as a predictor of incident heart failure : the Multi-Ethnic Study of Atherosclerosis

Background: Experimental studies demonstrate that high aortic pressure in late systole relative to early systole causes greater myocardial remodeling and dysfunction, for any given absolute peak systolic pressure. Methods and Results: We tested the hypothesis that late systolic hypertension, defined as the ratio of late (last one third of systole) to early (first two thirds of systole) pressure-time integrals (PTI) of the aortic pressure waveform, independently predicts incident heart failure (HF) in the general population. Aortic pressure waveforms were derived from a generalized transfer function applied to the radial pressure waveform recorded noninvasively from 6124 adults. The late/early systolic PTI ratio (L/ESPTI) was assessed as a predictor of incident HF during median 8.5 years of follow-up. The L/ESPTI was predictive of incident HF (hazard ratio per 1% increase= 1.22; 95% CI= 1.15 to 1.29; P58.38%) was more predictive of HF than the presence of hypertension. After adjustment for each other and various predictors of HF, the HR associated with hypertension was 1.39 (95% CI= 0.86 to 2.23; P=0.18), whereas the HR associated with a high L/E was 2.31 (95% CI=1.52 to 3.49; P<0.0001). Conclusions: Independently of the absolute level of peak pressure, late systolic hypertension is strongly associated with incident HF in the general population

Ageing, menopause, and ischaemic heart disease mortality in England, Wales, and the United States: modelling study of national mortality data

Objectives To use changes in heart disease mortality rates with age to investigate the plausibility of attributing women’s lower heart disease mortality than men to the protective effects of premenopausal sex hormones

Acute nifedipine withdrawal: Consequences of preoperative and late cessation of therapy in patients with prior unstable angina

Reports of acute ischemic events after withdrawal of calcium antagonist therapy in outpatients and during bypass surgery in patients with prior angina at rest prompted the examination of the effect of nifedipine withdrawal in 81 patients who had completed a prospective, double-blind randomized trial of nifedipine versus placebo for rest angina. Thirty-nine patients underwent bypass surgery for uncontrolled angina or left main coronary artery disease. No significant difference between patients withdrawn from nifedipine or placebo was seen in the incidence of perioperative myocardial infarction, hypotension requiring intraaortic balloon counterpulsation, vasopressor or vasodilator requirements or incidence of significant arrhythmias.An additional 42 patients had completed 2 years on a protocol consisting of nitrates and propranolol in addition to nifedipine or placebo. During a mean of 66 hours of continuous monitoring after withdrawal of nifedipine or placebo, heart rate and blood pressure were unchanged. A worsening of previously present angina at rest occurred in five patients who had continued to experience rest angina before drug withdrawal, four of whom were withdrawn from nifedipine. No patient with class I to III angina experienced new onset of rest angina during drug withdrawal. No patient experienced myocardial infarction. There was no significant difference between patients withdrawn from nifedipine or placebo in the duration or frequency of ischemic ST changes on continuous electrocardiographic monitoring, or in duration or positive results of serial exercise treadmill testing.Thus, no early adverse effects of acute nifedipine withdrawal were found in patients with prior rest angina at the time of bypass surgery or in stable patients receiving long-term medical therapy. Patients with continued symptoms of rest angina, however, may experience adverse ischemic events with nifedipine withdrawal

Mitochondrial uncoupling protein-4 regulates calcium homeostasis and sensitivity to store depletion-induced apoptosis in neural cells

An increase in the cytoplasmic-free Ca2+ concentration mediates cellular responses to environmental signals that influence a range of processes, including gene expression, motility, secretion of hormones and neurotransmitters, changes in energy metabolism, and apoptosis. Mitochondria play important roles in cellular Ca2+ homeostasis and signaling, but the roles of specific mitochondrial proteins in these processes are unknown. Uncoupling proteins (UCPs) are a family of proteins located in the inner mitochondrial membrane that can dissociate oxidative phosphorylation from respiration, thereby promoting heat production and decreasing oxyradical production. Here we show that UCP4, a neuronal UCP, influences store-operated Ca2+ entry, a process in which depletion of endoplasmic reticulum Ca2+ stores triggers Ca2+ influx through plasma membrane store-operated channels. PC12 neural cells expressing human UCP4 exhibit reduced Ca2+ entry in response to thapsigargin-induced endoplasmic reticulum Ca2+ store depletion. The elevations of cytoplasmic and intramitochondrial Ca2+ concentrations and mitochondrial oxidative stress induced by thapsigargin were attenuated in cells expressing UCP4. The stabilization of Ca2+ homeostasis and preservation of mitochondrial function by UCP4 was correlated with reduced mitochondrial reactive oxygen species generation, oxidative stress, and Gadd153 up-regulation and increased resistance of the cells to death. Reduced Ca2+-dependent cytosolic phospholipase A2 activation and oxidative metabolism of arachidonic acid also contributed to the stabilization of mitochondrial function in cells expressing human UCP4. These findings demonstrate that UCP4 can regulate cellular Ca2+ homeostasis, suggesting that UCPs may play roles in modulating Ca2+ signaling in physiological and pathological conditions