860 resultados para Percent body fat
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Objective: To assess the effectiveness of obesity markers to detect high (>5%) 10- year risk of fatal cardiovascular disease (CVD) as estimated using the SCORE function. Methods: Cross-sectional study including 3,047 women and 2,689 men aged 35-75 years (CoLaus study). Body fat percentage was assessed by tetrapolar bioimpedance. CVD risk was assessed using the SCORE risk function and gender and age-specific cut points for body fat were derived. The diagnostic accuracy of each obesity marker was evaluated through receiver operating characteristics (ROC) analysis. Results: Body fat presented a higher correlation with 10-year CVD risk than waist/hip ratio (WHR), waist or BMI: in men, r=0.31, 0.22, 0.19 and 0.12 and for body fat, WHR, waist and BMI, respectively; the corresponding values in women were 0.18, 0.15, 0.11 and 0.05, respectively (all p<0.05). In both genders, body fat showed the highest area under the ROC curve (AUC): in men, the AUC (and 95% confidence interval) were 76.0 (73.8 - 78.2), 67.3 (64.6 - 69.9), 65.8 (63.1 - 68.5) and 60.6 (57.9 - 63.5) for body fat, WHR, waist and BMI, respectively. In women, the corresponding values were 72.3 (69.2 - 75.3), 66.6 (63.1 - 70.2), 64.1 (60.6 - 67.6) and 58.8 (55.2 - 62.4). The use of body fat percentage criterion enabled to capture three times more subjects with high CVD risk than BMI criterion, and almost twice as much as WHR criterion.. Conclusions: Obesity defined by body fat percentage is more accurate to detect high 10-year risk of fatal CVD than obesity markers based on WHR, waist or BMI.
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OBJECTIVE: Body composition measured by dual-energy X-ray absorptiometry (DXA) is believed to be superior to crude measures such as BMI or waist circumference (WC) to assess health risks associated with adiposity in adults. We compared the ability of BMI, WC, waist-to-height ratio (WHtR), percentage body fat from skinfold thickness, and measures of total and central fat assessed by DXA to identify children with elevated blood pressure (BP). STUDY DESIGN: The QUALITY Study follows 630 Caucasian families (father, mother, and child originally aged 8-10 years). BP, height, weight, WC, and skinfold thickness were measured according to standardized protocols. Elevated BP was defined as systolic or diastolic BP at least 90th age, sex, and height-specific percentile. Total and central fat were determined with DXA. The area under the receiver operating characteristic (ROC) curve (AUC) statistic was computed from logistic models that adjusted for age, sex, height, Tanner stage, and physical activity. RESULTS: All adiposity indicators were highly correlated. WC and WHtR did not show superior ability over BMI to identify children with elevated SBP (P = 0.421 and 0.473). Measures of total and central fat from DXA did not show an improved ability over BMI or WC to identify children with elevated SBP (P = 0.325-0.662). CONCLUSION: Results support the use of BMI in clinical and public health settings, at least in this age group. As all indicators had a limited ability to identify children with elevated BP, results also support measurement of BP in all children of this age independent of a weight status.
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Previously, a single nucleotide polymorphism (SNP), rs9939609, in the FTO gene showed a much stronger association with all-cause mortality than expected from its association with body mass index (BMI), body fat mass index (FMI) and waist circumference (WC). This finding implies that the SNP has strong pleiotropic effects on adiposity and adiposity-independent pathological pathways that leads to increased mortality. To investigate this further, we conducted a meta-analysis of similar data from 34 longitudinal studies including 169,551 adult Caucasians among whom 27,100 died during follow-up. Linear regression showed that the minor allele of the FTO SNP was associated with greater BMI (n = 169,551; 0.32 kg m(-2) ; 95% CI 0.28-0.32, P < 1 × 10(-32) ), WC (n = 152,631; 0.76 cm; 0.68-0.84, P < 1 × 10(-32) ) and FMI (n = 48,192; 0.17 kg m(-2) ; 0.13-0.22, P = 1.0 × 10(-13) ). Cox proportional hazard regression analyses for mortality showed that the hazards ratio (HR) for the minor allele of the FTO SNPs was 1.02 (1.00-1.04, P = 0.097), but the apparent excess risk was eliminated after adjustment for BMI and WC (HR: 1.00; 0.98-1.03, P = 0.662) and for FMI (HR: 1.00; 0.96-1.04, P = 0.932). In conclusion, this study does not support that the FTO SNP is associated with all-cause mortality independently of the adiposity phenotypes.
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Adipose tissue (AT) is distributed as large differentiated masses, and smaller depots covering vessels, and organs, as well as interspersed within them. The differences between types and size of cells makes AT one of the most disperse and complex organs. Lipid storage is partly shared by other tissues such as muscle and liver. We intended to obtain an approximate estimation of the size of lipid reserves stored outside the main fat depots. Both male and female rats were made overweight by 4-weeks feeding of a cafeteria diet. Total lipid content was analyzed in brain, liver, gastrocnemius muscle, four white AT sites: subcutaneous, perigonadal, retroperitoneal and mesenteric, two brown AT sites (interscapular and perirenal) and in a pool of the rest of organs and tissues (after discarding gut contents). Organ lipid content was estimated and tabulated for each individual rat. Food intake was measured daily. There was a surprisingly high proportion of lipid not accounted for by the main macroscopic AT sites, even when brain, liver and BAT main sites were discounted. Muscle contained about 8% of body lipids, liver 1-1.4%, four white AT sites lipid 28-63% of body lipid, and the rest of the body (including muscle) 38-44%. There was a good correlation between AT lipid and body lipid, but lipid in"other organs" was highly correlated too with body lipid. Brain lipid was not. Irrespective of dietary intake, accumulation of body fat was uniform both for the main lipid storage and handling organs: large masses of AT (but also liver, muscle), as well as in the"rest" of tissues. These storage sites, in specialized (adipose) or not-specialized (liver, muscle) tissues reacted in parallel against a hyperlipidic diet challenge. We postulate that body lipid stores are handled and regulated coordinately, with a more centralized and overall mechanisms than usually assumed.
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BACKGROUND: Globally, Africans and African Americans experience a disproportionate burden of type 2 diabetes, compared to other race and ethnic groups. The aim of the study was to examine the association of plasma glucose with indices of glucose metabolism in young adults of African origin from 5 different countries. METHODS: We identified participants from the Modeling the Epidemiologic Transition Study, an international study of weight change and cardiovascular disease (CVD) risk in five populations of African origin: USA (US), Jamaica, Ghana, South Africa, and Seychelles. For the current study, we included 667 participants (34.8 ± 6.3 years), with measures of plasma glucose, insulin, leptin, and adiponectin, as well as moderate and vigorous physical activity (MVPA, minutes/day [min/day]), daily sedentary time (min/day), anthropometrics, and body composition. RESULTS: Among the 282 men, body mass index (BMI) ranged from 22.1 to 29.6 kg/m(2) in men and from 25.8 to 34.8 kg/m(2) in 385 women. MVPA ranged from 26.2 to 47.1 min/day in men, and from 14.3 to 27.3 min/day in women and correlated with adiposity (BMI, waist size, and % body fat) only among US males after controlling for age. Plasma glucose ranged from 4.6 ± 0.8 mmol/L in the South African men to 5.8 mmol/L US men, while the overall prevalence for diabetes was very low, except in the US men and women (6.7 and 12 %, respectively). Using multivariate linear regression, glucose was associated with BMI, age, sex, smoking hypertension, daily sedentary time but not daily MVPA. CONCLUSION: Obesity, metabolic risk, and other potential determinants vary significantly between populations at differing stages of the epidemiologic transition, requiring tailored public health policies to address local population characteristics.
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El propósito de este estudio longitudinal prospectivo es abordar un plan integral de actividad física en niños y niñas entre 6 y 12 años que padezcan sobrepeso y obesidad. El programa se llevará a cabo en el Hospital de San Juan de Dios de Barcelona, donde se utilizarán una serie de variables de medida y tests que serán valorados antes, durante y después de este plan integral. Participarán dos profesionales de la salud, un fisioterapeuta y un nutricionista, quienes intervendrán en 20 niños y niñas con sobrepeso y obesidad. La finalidad de este estudio es disminuir el índice de masa corporal (IMC), así como el porcentaje de grasa corporal total (GCT) en los niños y niñas con sobrepeso y obesidad. También se pretende introducir y fomentar hábitos de vida saludables en relación a la actividad física y la alimentación en los niños y niñas y en su entorno familiar.
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Current obesity prevention strategies recommend increasing daily physical activity, assuming that increased activity will lead to corresponding increases in total energy expenditure and prevent or reverse energy imbalance and weight gain [1-3]. Such Additive total energy expenditure models are supported by exercise intervention and accelerometry studies reporting positive correlations between physical activity and total energy expenditure [4] but are challenged by ecological studies in humans and other species showing that more active populations do not have higher total energy expenditure [5-8]. Here we tested a Constrained total energy expenditure model, in which total energy expenditure increases with physical activity at low activity levels but plateaus at higher activity levels as the body adapts to maintain total energy expenditure within a narrow range. We compared total energy expenditure, measured using doubly labeled water, against physical activity, measured using accelerometry, for a large (n = 332) sample of adults living in five populations [9]. After adjusting for body size and composition, total energy expenditure was positively correlated with physical activity, but the relationship was markedly stronger over the lower range of physical activity. For subjects in the upper range of physical activity, total energy expenditure plateaued, supporting a Constrained total energy expenditure model. Body fat percentage and activity intensity appear to modulate the metabolic response to physical activity. Models of energy balance employed in public health [1-3] should be revised to better reflect the constrained nature of total energy expenditure and the complex effects of physical activity on metabolic physiology.
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This study analyzed the feasibility and efficacy of surgical therapies in patients with sleep-disordered breathing ranging from partial upper airway obstruction during sleep to severe obstructive sleep apnea syndrome. The surgical procedures evaluated were tracheostomy, laser-assisted uvulopalatoplasty (LUPP) and uvulopalatopharyngoplasty (UPPP) with laser or ultrasound scalpel. Obstructive sleep apnea and partial upper airway obstruction during sleep were measured with the static charge-sensitive bed (SCSB) and pulse oximeter. The patients with severe obstructive sleep apnea syndrome were treated with tracheostomy. Palatal surgery was performed only if the upper airway narrowing occurred exclusively at the soft palate level in patients with partial upper airway obstruction during sleep. The ultrasound scalpel technique was compared to laser-assisted UPPP. The efficacy of LUPP to reduce partial upper airway obstruction during sleep was assessed and histology of uvulopalatal specimen was compared to body fat distributional parameters and sleep study findings. Tracheostomy was effective therapy in severe obstructive sleep apnea. Partial upper airway obstruction and arterial oxyhemoglobin desaturation index during sleep decreased significantly after LUPP. The minimal retropalatal airway dimension increased and soft palate collapsibility decreased at the level where the velopharyngeal obstruction had occurred before the surgery. Ultrasound scalpel did not offer any significant benefits over the laser-assisted technique, except fewer postoperative haemorrhage events. The loose connective tissue as a manifestation of edema was the only histological finding showing correlation with partial upper airway obstruction parameters of SCSB. Tracheostomy remains a life-saving therapy and also long-term option when adherence to CPAP fails in patients with obstructive sleep apnea syndrome. LUPP effectively reduces partial upper airway obstruction during sleep provided that obstruction at the other levels than the soft palate and uvula were preoperatively excluded. Technically the ultrasound scalpel or laser surgeries are equal. In patients with partial upper airway obstruction the loose connective tissue is more important than fat accumulation in the soft palate. This supports the hypothesis that edema is a primary trigger for aggravation of upper airway narrowing during sleep at the soft palate level and evolution towards partial or complete upper airway obstruction during sleep.
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It has been commonly thought that standards of beauty are arbitrary cultural conventions that vary between cultures and time. In my thesis I found that it is not so. Instead, I show that attractiveness and preferred traits serve as cues to phenotypic qualities that provide selective benefits for those who choose their mates based on these criteria. In the first study I show that attractive men have a stronger antibody response to the hepatitis b vaccine and higher levels of testosterone than their less attractive peers. Men with low levels of testosterone also tend to have high levels of the stress hormone cortisol, suggesting that their immune responses may have been inhibited by stress hormones. Thus, facial attractiveness may serve as an honest cue of the strength of immune defence in men. In the second study, I show that the attractiveness of the male body is also a cue of better immunity. In addition, I show that adiposity, both in men’s faces and bodies, is a better cue of the strength of immunity and attractiveness than of masculinity. In the third study, I test the preferences of women from 13 countries for facial cues of testosterone and cortisol. I show that there is cross-cultural variation in women’s preference for cues of testosterone and cortisol in male faces. I found a relationship between the health of a nation and women’s preferences for cues of testosterone in the male face and the interaction between preferences for cues of testosterone and cortisol. I show also a relationship between preferences for cues of testosterone and a societal-level measure of parasite stress. Thus, it seems that societal-level ecological factors influence the relative value of traits as revealed by combinations of testosterone and stress hormones. In the fourth study, I show that women’s immune responsiveness (amount of antibodies produced) does not predict facial attractiveness. Instead, plasma cortisol level is negatively associated with attractiveness, indicating that stressed women look less attractive. Fat percentage is curvilinearly associated with facial attractiveness, indicating that being too thin or too fat reduces attractiveness. This study suggests that in contrast to men, facial attractiveness in women does not indicate the strength of immune defence, but is associated with other aspects of long-term health and fertility: circulating levels of the stress hormone cortisol and the percentage of body fat. In the last study I show that the attractiveness of men’s body odor is positively correlated with stress hormone levels, suggesting also that the attractiveness of body odors may signal the phenotypic quality of males to females. However, the attractiveness of men’s body odor was not associated with testosterone levels. My thesis suggests that the standard of beauty is not in the eye of the beholder. Instead, our standard of beauty is hardwired in our brains by genes that are selected by natural selection and also influenced by current environmental conditions.
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The repercussions of secondary hyperparathyroidism on the nutritional status of chronic renal failure patients have not been well established. Therefore, the aim of this study was to compare the nutritional indices of hemodialysis patients with and without secondary hyperparathyroidism. Sixteen hemodialysis patients with serum parathyroid hormone (PTH) levels higher than 420 pg/ml (hyperparathyroidism group) were matched for gender, age and length of dialysis treatment to 16 patients with serum PTH between 64 and 290 pg/ml (control group). The following parameters were assessed: anthropometric indices (body mass index, skinfold thickness, midarm muscle circumference and body fat), 4-day food diaries, protein catabolic rate, biochemical indices (blood urea nitrogen, serum creatinine, albumin, ionized calcium, inorganic phosphorus, serum alkaline phosphatase, PTH, pH and HCO3) and dialysis efficiency. We did not observe differences in the anthropometric indices between the two groups. Only calcium intake was significantly different between groups (307.9 mg/day for the hyperparathyroidism group vs 475.8 mg/day for the control group). Protein catabolic rate tended to be higher in the hyperparathyroidism group compared to the control group (1.3 vs 0.9 g kg-1 day-1; P = 0.08). Except for blood urea nitrogen (86.4 vs 75.7 mg/dl), alkaline phosphatase (175 vs 65 U/l) and PTH (898 vs 155 pg/ml), no other differences were found between groups in the biochemical indices studied. PTH was directly correlated with protein catabolic rate (r = 0.61; P<0.05) and length of dialysis (r = 0.53; P<0.05) only in the hyperparathyroidism group. Considering the indices used, we could not demonstrate the deleterious effect of high PTH levels on the nutritional status of hemodialysis patients. Indirect evidence, however, suggests an action of PTH on protein metabolism.
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To identify early metabolic abnormalities in type 2 diabetes mellitus, we measured insulin secretion, sensitivity to insulin, and hepatic insulin extraction in 48 healthy normal glucose-tolerant Brazilians, first-degree relatives of type 2 diabetic patients (FH+). Each individual was matched for sex, age, weight, and body fat distribution with a person without history of type 2 diabetes (FH-). Both groups were submitted to a hyperglycemic clamp procedure (180 mg/dl). Insulin release was evaluated in its two phases. The first was calculated as the sum of plasma insulin at 2.5, 5.0, 7.5, and 10.0 min after the beginning of glucose infusion, and the second as the mean plasma insulin level in the third hour of the clamp procedure. Insulin sensitivity index (ISI) was the mean glucose infusion rate in the third hour of the clamp experiment divided by the mean plasma insulin concentration during the same period of time. Hepatic insulin extraction was determined under fasting conditions and in the third hour of the clamp procedure as the ratio between C-peptide and plasma insulin levels. FH+ individuals did not differ from FH- individuals in terms of the following parameters [median (range)]: a) first-phase insulin secretion, 174 (116-221) vs 207 (108-277) µU/ml, b) second-phase insulin secretion, 64 (41-86) vs 53 (37-83) µU/ml, and c) ISI, 14.8 (9.0-20.8) vs 16.8 (9.0-27.0) mg kg-1 min-1/µU ml-1. Hepatic insulin extraction in FH+ subjects was similar to that of FH- ones at basal conditions (median, 0.27 vs 0.27 ng/µU) and during glucose infusion (0.15 vs 0.15 ng/µU). Normal glucose-tolerant Brazilian FH+ individuals well-matched with FH- ones did not show defects of insulin secretion, insulin sensitivity, or hepatic insulin extraction as tested by hyperglycemic clamp procedures.
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The introduction of highly active antiretroviral therapy (HAART) for patients infected with HIV has significantly prolonged the life expectancy and to some extent has restored a functional immune response. However, the premature introduction of HAART has led to a significant and alarming increase in cardiovascular complications, including myocardial infarction and the appearance of abnormal distribution of body fat seen as lipodystrophy. One key element in the development of ischemic coronary artery disease is the presence of circulating and tissue-fixed modified low density lipoprotein (mLDL) that contributes to the initiation and progression of arterial lesions and to the formation of foam cells. Even though not completely elucidated, the most likely mechanism involves mLDL in the inflammatory response and the induction of a specific immune response against mLDL. Circulating antibodies against mLDL can serve as an indirect marker of the presence of circulating and vessel-fixed mLDL. In the present study, we measured antibodies to mLDL and correlated them with immune status (i.e., number of CD4+ T cells) in 59 HIV patients and with the clinical manifestation of lipodystrophy in 10 patients. We observed a significant reduction in anti-mLDL antibody levels related both to lipodystrophy and to an immunocompromised state in HIV patients. We speculate that these antibodies may explain in part the rapid development of ischemic coronary artery disease in some patients.
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We evaluated the relationship of leptin with hypertension adjusted for body mass index (BMI) and/or waist circumference in a population of Japanese-Brazilian women aged > or = 30 years with centrally distributed adiposity. After excluding diabetic subjects, the study subjects - who participated in a population-based study on the prevalence of metabolic syndrome - showed prevalence rates of obesity (BMI > or = 25 kg/m²) and central adiposity (waist > or = 80 cm) of 32.0 and 37.8%, respectively. The hypertensive group (N = 162) was older, had higher BMI (24.9 ± 4.2 vs 23.3 ± 3.4 kg/m², P < 0.001), waist circumference (81.1 ± 10.1 vs 76.3 ± 8.2 cm, P < 0.001) and insulin levels (8.0 ± 6.2 vs 7.1 ± 4.9 µU/mL, P < 0.05) than the normotensive group (N = 322) and showed an unfavorable metabolic profile (higher 2-h plasma glucose, C-reactive protein and non-HDL cholesterol levels). Leptin did not differ between groups (8.2 ± 6.8 vs 7.2 ± 6.6 ng/mL, P = 0.09, for hypertensive vs normotensive, respectively) and its levels correlated significantly with anthropometric variables but not with blood pressure. Logistic regression analysis indicated that age and waist were independently associated with hypertension but not with homeostasis model assessment of insulin resistance or leptin levels. The lack of an independent association of hypertension with metabolic parameters (2-h glucose, C-reactive protein and non-HDL cholesterol) after adjustment for central adiposity suggested that visceral fat deposition may be the common mediator of the disturbances of the metabolic syndrome. Our data indicate that age and waist are major determinants of hypertension in this population of centrally obese (waist > or = 80 cm) Japanese-Brazilian women, but do not support a role for leptin in the elevation of blood pressure.
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The purpose of this study was to examine the effects of an exercise intervention on the total caloric intake (TCI) of breast cancer patients undergoing treatment. A secondary purpose was to determine whether or not a relationship existed between changes in TCI, body fat composition (%BF), and fatigue during the study, which lasted 6 months. Twenty females recently diagnosed with breast cancer, scheduled to undergo chemotherapy or radiation, were assigned randomly to an experimental (N = 10) or control group (N = 10). Outcome measures included TCI (3-day food diary), %BF (skinfolds), and fatigue (revised Piper Fatigue Scale). Each exercise session was conducted as follows: initial cardiovascular activity (6-12 min), followed by stretching (5-10 min), resistance training (15-30 min), and a cool-down (approximately 8 min). Significant changes in TCI were observed among groups (F1,18 = 8.582; P = 0.009), at treatments 2 and 3, and at the end of the study [experimental (1973 ± 419), control (1488 ± 418); experimental (1946 ± 437), control (1436 ± 429); experimental (2315 ± 455), control (1474 ± 294), respectively]. A significant negative correlation was found (Spearman rho(18) = -0.759; P < 0.001) between TCI and %BF and between TCI and fatigue levels (Spearman rho(18) = -0.541; P = 0.014) at the end of the study. In conclusion, the results of this study suggest that an exercise intervention administered to breast cancer patients undergoing medical treatment may assist in the mitigation of some treatment side effects, including decreased TCI, increased fatigue, and negative changes in body composition.
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Some studies showed that Asians with obstructive sleep apnea (OSA) are thinner than Caucasians. Because obesity is a major risk factor for OSA, it was concluded that Asians are predisposed to OSA. However, body fat composition varies for a same body mass index (BMI) according to ethnicity. We firstly compared anthropometric characteristics, symptoms and associated disorders in all consecutive male Japanese descendants and white males with OSA referred for polysomnography. In a second analysis, all Japanese descendants were compared to a subgroup of white males, matched for apnea/hypopnea index and age. In the first analysis, age, symptoms, OSA severity and co-morbidities were similar among Japanese descendants (N = 54) and white patients (N = 466). However, Japanese descendants had a lower BMI than white patients: 27.1 (25.5-28.4) vs 29.4 (26.5-33.0) kg/m², respectively (P < 0.001). In the second analysis, Japanese descendants had a lower BMI than white patients (P < 0.001). Multiple linear regression considering the entire group revealed that age, BMI, neck circumference, Epworth sleepiness scale, ethnicity and %REM sleep were independent predictors for apnea/hypopnea index (P < 0.001). Ethnicity was no longer significantly associated with OSA severity when we adopted the World Health Organization criteria for obesity (≥25 and 30 kg/m² among Japanese descendants and white males, respectively). Japanese descendants with OSA have a lower BMI than white subjects of similar severity. However, ethnicity was not associated with OSA severity when an ethnical difference in obesity criteria was respected. Our data suggest that Japanese descendants are not predisposed to OSA.