Low resting metabolic rate is associated with greater lifespan because of a confounding effect of body fatness.
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ABSTRACT:
SUBMITTER: Duarte LC
PROVIDER: S-EPMC4262579 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundDihydrocapsiate is a capsinoid found in chili peppers. Dihydrocapsiate is similar to capsaicin, which is known for its thermogenic properties.ObjectiveThe objective was to determine the acute and chronic effect of dihydrocapsiate on resting metabolic rate (RMR).DesignSeventy-eight healthy subjects in a double-blind, parallel-arm trial were randomly assigned to 3 groups receiving 0 (placebo), 3, or 9 mg dihydrocapsiate/d for 28 d. After a 10-h overnight fast, RMR was measured by indirect calorimetry for 30 min before and 120 min after ingestion of dihydrocapsiate.ResultsRMR was similar in the 3 groups before dosing on day 1 [1714 ± 41 kcal/d (0 mg), 1760 ± 41 kcal/d (3 mg), and 1694 ± 38 kcal/d (9 mg)] and after acute dosing (41 ± 17, 55 ± 17, and 3 ± 24 kcal/d for 3-mg, 9-mg, and placebo groups, respectively). When the chronic effect of dihydrocapsiate on RMR was calculated from the average 2-h RMR on day 28 minus the 30-min preingestion RMR at baseline, a borderline effect in subjects receiving 3 mg dihydrocapsiate/d compared with placebo was observed (61 ± 24 kcal/d compared with -1 ± 12 kcal/d, P = 0.054), whereas no significant increase in RMR in comparison with placebo was noted for the 9-mg/d dose (48 ± 23 kcal/d compared with -1 ± 12 kcal/d, P = 0.12). When data from both groups were combined, the thermic effect of dihydrocapsiate reached significance (53 ± 9 kcal/d compared with -1 ± 12 kcal/d in the placebo group, P = 0.04). Fat oxidation was unaffected by dihydrocapsiate.ConclusionAfter 1 mo of supplementation, dihydrocapsiate had a small thermogenic effect of ≈50 kcal/d, which is in the range of day-to-day RMR variability. This trial was registered at clinicaltrials.gov as NCT00999297.
| S-EPMC2954444 | biostudies-literature
Project description:Background:The resting metabolic rate (RMR) decrease, observed after an obesity reduction therapy is a determinant of a short-time weight regain. Thus, the objective of this study was to evaluate changes in RMR, and the associated hormonal alterations in obese patients with a very low-calorie ketogenic (VLCK)-diet induced severe body weight (BW) loss. Method:From 20 obese patients who lost 20.2 kg of BW after a 4-months VLCK-diet, blood samples and body composition analysis, determined by DXA and MF-Bioimpedance, and RMR by indirect calorimetry, were obtained on four subsequent visits: visit C-1, basal, initial fat mass (FM) and free fat mass (FFM); visit C-2, -?7.2 kg in FM, -?4.3 kg in FFM, maximal ketosis; visit C-3, -?14.4 kg FM, -?4.5 kg FFM, low ketosis; visit C-4, -?16.5 kg FM, -?3.8 kg FFM, no ketosis. Each subject acted as his own control. Results:Despite the large BW reduction, measured RMR varied from basal visit C-1 to visit C-2, -?1.0%; visit C-3, -?2.4% and visit C-4, -?8.0%, without statistical significance. No metabolic adaptation was observed. The absent reduction in RMR was not due to increased sympathetic tone, as thyroid hormones, catecholamines, and leptin were reduced at any visit from baseline. Under regression analysis FFM, adjusted by levels of ketonic bodies, was the only predictor of the RMR changes (R2?=?0.36; p?<?0.001). Conclusion:The rapid and sustained weight and FM loss induced by VLCK-diet in obese subjects did not induce the expected reduction in RMR, probably due to the preservation of lean mass. Trial registration:This is a follow up study on a published clinical trial.
| S-EPMC5816424 | biostudies-literature
Project description:Heritability estimates of human body fatness vary widely and the contribution of body composition methodology to this variability is unknown. The effect of body composition methodology on estimations of genetic and environmental contributions to body fatness variation was examined in 78 adult male and female monozygotic twin pairs reared apart or together. Body composition was assessed by six methods - body mass index (BMI), dual energy x-ray absorptiometry (DXA), underwater weighing (UWW), total body water (TBW), bioelectric impedance (BIA), and skinfold thickness. Body fatness was expressed as percent body fat, fat mass, and fat mass/height2 to assess the effect of body fatness expression on heritability estimates. Model-fitting multivariate analyses were used to assess the genetic and environmental components of variance. Mean BMI was 24.5 kg/m2 (range of 17.8-43.4 kg/m2). There was a significant effect of body composition methodology (p<0.001) on heritability estimates, with UWW giving the highest estimate (69%) and BIA giving the lowest estimate (47%) for fat mass/height2. Expression of body fatness as percent body fat resulted in significantly higher heritability estimates (on average 10.3% higher) compared to expression as fat mass/height2 (p=0.015). DXA and TBW methods expressing body fatness as fat mass/height2 gave the least biased heritability assessments, based on the small contribution of specific genetic factors to their genetic variance. A model combining DXA and TBW methods resulted in a relatively low FM/ht2 heritability estimate of 60%, and significant contributions of common and unique environmental factors (22% and 18%, respectively). The body fatness heritability estimate of 60% indicates a smaller contribution of genetic variance to total variance than many previous studies using less powerful research designs have indicated. The results also highlight the importance of environmental factors and possibly genotype by environmental interactions in the etiology of weight gain and the obesity epidemic.
| S-EPMC4110980 | biostudies-literature
Project description:Underestimating/overestimating resting metabolic rate (RMR) affects energy prescription. The objective was to compare RMR by indirect calorimetry (RMR IC) and RMR estimated by predictive equations in women with excess body fat. This was an analytical cross-sectional study with 41 women aged 18-28 with overnutrition according to body composition. The RMR IC was measured and RMR estimated using the FAO/WHO/UNU (1985), FAO/WHO/UNU (2004), Harris-Benedict, and Mifflin-St Jeor equations. The percentage of adequacy (90-110%), overestimation (>110%), and underestimation (<90%) were evaluated for RMR IC. Data were described by percentiles because of non-normal distribution according to the Shapiro-Wilk test. The Kruskal-Wallis test and Bland-Altman analysis were applied at a significance level of α < 0.05. The RMR IC was 1192 and 1183 calories/day (p = 0.429) in women with obesity and overweight, respectively. The FAO/WHO/UNU (1985), FAO/WHO/UNU (2004), Harris-Benedict, and Mifflin-St Jeor equations overestimated the RMR IC by 283.2, 311.2, 292.7, and 203.0 calories/day and by 296.7, 413.8, 280.0, and 176.6 calories/day for women with overweight and obesity (p < 0.001), respectively. The Harris-Benedict adjusted weight (0.5) equation underestimated RMR IC by 254.7 calories/day. The predictive equations overestimated RMR IC in women with excess body fat. The Mifflin-St Jeor equation showed less overestimation and better adequacy, but was not exempt from inaccuracy.
| S-EPMC9964988 | biostudies-literature
Project description:Observationally, the association of basal metabolic rate (BMR) with mortality is mixed, although some ageing theories suggest that higher BMR should reduce lifespan. It remains unclear whether a causal association exists. In this one-sample Mendelian randomization study, we aimed to estimate the casual effect of BMR on parental attained age, a proxy for lifespan, using two-sample Mendelian randomization methods. We obtained genetic variants strongly (p-value < 5 × 10-8) and independently (r2 < 0.001) predicting BMR from the UK Biobank and applied them to a genome-wide association study of parental attained age based on the UK Biobank. We meta-analyzed genetic variant-specific Wald ratios using inverse-variance weighting with multiplicative random effects by sex, supplemented by sensitivity analysis. A total of 178 and 180 genetic variants predicting BMR in men and women were available for father's and mother's attained age, respectively. Genetically predicted BMR was inversely associated with father's and mother's attained age (years of life lost per unit increase in effect size of genetically predicted BMR, 0.46 and 1.36; 95% confidence interval 0.07-0.85 and 0.89-1.82), with a stronger association in women than men. In conclusion, higher BMR might reduce lifespan. The underlying pathways linking to major causes of death and relevant interventions warrant further investigation.
| S-EPMC10182013 | biostudies-literature
Project description:BackgroundBirth weight is determined by the interplay between infant genetics and the intrauterine environment and is associated with several health outcomes in later life. Many studies have reported an association between birth weight and DNA methylation in infants and suggest that altered epigenetics may underlie birthweight-associated health outcomes. However, birth weight is a relatively nonspecific measure of fetal growth and consists of fat mass and fat-free mass which may have different effects on health outcomes which motivates studies of infant body composition and DNA methylation. Here, we combined genome-wide DNA methylation profiling of buccal cells from 47 full-term one-week old infants with accurate measurements of infant fat mass and fat-free mass using air-displacement plethysmography.ResultsNo significant association was found between DNA methylation in infant buccal cells and infant body composition. Moreover, no association between infant DNA methylation and parental body composition or indicators of maternal glucose metabolism were found.ConclusionsDespite accurate measures of body composition, we did not identify any associations between infant body fatness and DNA methylation. These results are consistent with recent studies that generally have identified only weak associations between DNA methylation and birthweight. Although our results should be confirmed by additional larger studies, our findings may suggest that differences in DNA methylation between individuals with low and high body fatness may be established later in childhood.
| S-EPMC7654595 | biostudies-literature
Project description:The melanocortin system regulates metabolic homeostasis and inflammation. Melanocortin agonists have contradictorily been reported to both increase and decrease metabolic rate and body temperature. We find two distinct physiologic responses occurring at similar doses. Intraperitoneal administration of the nonselective melanocortin agonist MTII causes a melanocortin-4 receptor (Mc4r)-mediated hypermetabolism/hyperthermia. This is preceded by a profound, transient hypometabolism/hypothermia that is preserved in mice lacking any one of Mc1r, Mc3r, Mc4r, or Mc5r. Three other melanocortin agonists also caused hypothermia, which is actively achieved via seeking a cool environment, vasodilation, and inhibition of brown adipose tissue thermogenesis. These results suggest that the hypometabolic/hypothermic effect of MTII is not due to a failure of thermoregulation. The hypometabolism/hypothermia was prevented by dopamine antagonists, and MTII selectively activated arcuate nucleus dopaminergic neurons, suggesting that these neurons may contribute to the hypometabolism/hypothermia. We propose that the hypometabolism/hypothermia is a regulated response, potentially beneficial during extreme physiologic stress.
| S-EPMC4126889 | biostudies-literature
Project description:Current prediction equations for resting metabolic rate (RMR) were validated in a relatively small sample with high-individual variance. This study determined the accuracy of five common RMR equations and proposed a novel prediction equation, including body composition. A total of 3001 participants (41 ± 13 years; BMI 28.5 ± 5.5 kg/m2; 48% males) from nutrition clinics in Israel were measured by indirect calorimetry to assess RMR. Dual-energy X-ray absorptiometry were used to evaluate fat mass (FM) and free-fat mass (FFM). Accuracy and mean bias were compared between the measured RMR and the prediction equations. A random training set (75%, n = 2251) and a validation set (25%, n = 750) were used to develop a new prediction model. All the prediction equations underestimated RMR. The Cunningham equation obtained the largest mean deviation [-16.6%; 95% level of agreement (LOA) 1.9, -35.1], followed by the Owen (-15.4%; 95% LOA 4.2, -22.6), Mifflin-St. Jeor (-12.6; 95% LOA 5.8, -26.5), Harris-Benedict (-8.2; 95% LOA 11.1, -27.7), and the WHO/FAO/UAU (-2.1; 95% LOA 22.3, -26.5) equations. Our new proposed model includes sex, age, FM, and FFM and successfully predicted 73.5% of the explained variation, with a bias of 0.7% (95% LOA -18.6, 19.7). This study demonstrates a large discrepancy between the common prediction equations and measured RMR and suggests a new accurate equation that includes both FM and FFM.
| S-EPMC9960966 | biostudies-literature
Project description:A common single nucleotide polymorphism (SNP) of FTO (rs9939609, T/A) is associated with total body fatness. We investigated the association of this SNP with abdominal and peripheral fatness and obesity-related metabolic traits in middle-aged men through a broad range of fatness present already in adolescence.Obese young Danish men (n = 753, BMI > or = 31.0 kg/m(2)) and a randomly selected group (n = 879) from the same population were examined in three surveys (mean age 35, 46 and 49 years, respectively). The traits included anthropometrics, body composition, oral glucose tolerance test, blood lipids, blood pressure, fibrinogen and aspartate aminotransferase. Logistic regression analysis was used to assess the age-adjusted association between the phenotypes and the odds ratios for the FTO rs9939609 (TT and TA genotype versus the AA genotype), for anthropometrics and body composition estimated per unit z-score. BMI was strongly associated with the AA genotype in all three surveys: OR = 1.17, p = 1.1*10(-6), OR = 1.20, p = 1.7*10(-7), OR = 1.17, p = 3.4*10(-3), respectively. Fat body mass index was also associated with the AA genotype (OR = 1.21, p = 4.6*10(-7) and OR = 1.21, p = 1.0*10(-3)). Increased abdominal fatness was associated with the AA genotype when measured as waist circumference (OR = 1.21, p = 2.2*10(-6) and OR = 1.19, p = 5.9*10(-3)), sagittal abdominal diameter (OR = 1.17, p = 1.3*10(-4) and OR = 1.18, p = 0.011) and intra-abdominal adipose tissue (OR = 1.21, p = 0.005). Increased peripheral fatness measured as hip circumference (OR = 1.19, p = 1.3*10(-5) and OR = 1.18, p = 0.004) and lower body fat mass (OR = 1.26, p = 0.002) was associated with the AA genotype. The AA genotype was significantly associated with decreased Stumvoll insulin sensitivity index (OR = 0.93, p = 0.02) and with decreased non-fasting plasma HDL-cholesterol (OR = 0.57, p = 0.037), but not with any other of the metabolic traits. However, all significant results for both body fat distribution and metabolic traits were explained by a mediating effect of total fat mass.The association of the examined FTO SNP to general fatness throughout the range of fatness was confirmed, and this association explains the relation between the SNP and body fat distribution and decreased insulin sensitivity and HDL-cholesterol. The SNP was not significantly associated with other metabolic traits suggesting that they are not derived from the general accumulation of body fat.
| S-EPMC2493033 | biostudies-literature
Project description:Background and objectivesLower total energy expenditure (TEE) and resting metabolic rate (RMR) are associated with greater weight gain in Native American adults. Whether these effects exist in childhood is unclear. We hypothesized that lower energy expenditure measured in childhood would predict greater relative change in body mass index (BMI) during adolescence.MethodsMeasurements of height, weight, body composition, RMR and TEE were completed in 181 Native American children at exams done at age 5 and 10years, with 126 children having biennial follow-up assessments of weight and height after age 10years until age 20years. TEE and RMR were adjusted for age, sex, height, fat mass and fat free mass. BMI-change was assessed using population specific and Center for Disease Control (CDC) BMI z-scores and change in the relative difference to the 95th BMI-centile.ResultsLower adjusted RMR at age 10years was associated with greater increase in population-specific and CDC BMI z-scores, greater increase in the relative difference to the 95th BMI-centile and greater weight gain (all r≤-0.22, p≤0.01). However, no association was found with adjusted RMR at age 5years and with adjusted TEE and physical activity level assessed at age 5 or 10years.ConclusionsLower adjusted RMR at age 10years predicted greater change in adolescent BMI z-score indicating that the effects of relatively low metabolic rate on future weight gain in this population may begin in late childhood.
| S-EPMC6407417 | biostudies-literature