Journal: International journal of obesity (2005)
Objective:Low-density lipoprotein-related receptor protein 1 (LRP1) is a multi-functional endocytic receptor and signaling molecule that is expressed in adipose and the hypothalamus. Evidence for a role of LRP1 in adiposity is accumulating from animal and in vitro models, but data from human studies are limited. The study objectives were to evaluate (i) relationships between LRP1 genotype and anthropometric traits, and (ii) whether these relationships were modified by dietary fatty acids.Design and methods:We conducted race/ethnic-specific meta-analyses using data from 14 studies of US and European whites and 4 of African Americans to evaluate associations of dietary fatty acids and LRP1 genotypes with body mass index (BMI), waist circumference and hip circumference, as well as interactions between dietary fatty acids and LRP1 genotypes. Seven single-nucleotide polymorphisms (SNPs) of LRP1 were evaluated in whites (N up to 42 000) and twelve SNPs in African Americans (N up to 5800).Results:After adjustment for age, sex and population substructure if relevant, for each one unit greater intake of percentage of energy from saturated fat (SFA), BMI was 0.104 kg m(-2) greater, waist was 0.305 cm larger and hip was 0.168 cm larger (all P<0.0001). Other fatty acids were not associated with outcomes. The association of SFA with outcomes varied by genotype at rs2306692 (genotyped in four studies of whites), where the magnitude of the association of SFA intake with each outcome was greater per additional copy of the T allele: 0.107 kg m(-2) greater for BMI (interaction P=0.0001), 0.267 cm for waist (interaction P=0.001) and 0.21 cm for hip (interaction P=0.001). No other significant interactions were observed.Conclusion:Dietary SFA and LRP1 genotype may interactively influence anthropometric traits. Further exploration of this, and other diet x genotype interactions, may improve understanding of interindividual variability in the relationships of dietary factors with anthropometric traits.International Journal of Obesity advance online publication, 29 January 2013; doi:10.1038/ijo.2012.215.
Little is currently known about how exercise may influence dietary patterns and/or food preferences. The present study aimed to examine the effect of a 15-week exercise training program on overall dietary patterns among young adults.
Background:Concern exists regarding gallstones as an adverse event of very-low-calorie diets (VLCDs; <800 kcal per day).Objective:To assess the risk of symptomatic gallstones requiring hospital care and/or cholecystectomy in a commercial weight loss program using VLCD or low-calorie diet (LCD).Design:A 1-year matched cohort study of consecutively enrolled adults in a commercial weight loss program conducted at 28 Swedish centers between 2006 and 2009. A 3-month weight loss phase of VLCD (500 kcal per day) or LCD (1200-1500 kcal per day) was followed by a 9-month weight maintenance phase. Matching (1:1) was performed by age, sex, body mass index, waist circumference and gallstone history (n=3320:3320). Gallstone and cholecystectomy data were retrieved from the Swedish National Patient Register.Results:One-year weight loss was greater in the VLCD than in the LCD group (-11.1 versus -8.1 kg; adjusted difference, -2.8 kg, 95% CI -3.1 to -2.4; P<0.001). During 6361 person-years, 48 and 14 gallstones requiring hospital care occurred in the VLCD and LCD groups, respectively, (152 versus 44/10 000 person-years; hazard ratio, 3.4, 95% CI 1.8-6.3; P<0.001; number-needed-to-harm, 92, 95% CI 63-168; P<0.001). Of the 62 gallstone events, 38 (61%) resulted in cholecystectomy (29 versus 9; hazard ratio, 3.2, 95% CI 1.5-6.8; P=0.003; number-needed-to-harm, 151, 95% CI 94-377; P<0.001). Adjusting for 3-month weight loss attenuated the hazard ratios, but the risk remained higher with VLCD than LCD for gallstones (2.5, 95% CI 1.3-5.1; P=0.009) and became borderline for cholecystectomy (2.2, 95% CI 0.9-5.2; P=0.08).Conclusion:The risk of symptomatic gallstones requiring hospitalization or cholecystectomy, albeit low, was 3-fold greater with VLCD than LCD during the 1-year commercial weight loss program.
Background/Objectives:Cesarean section (CS) and antibiotic use during pregnancy may alter normal maternal-fetal microbiota exchange, thereby contributing to aberrant microbial colonization of the infant gut and increased susceptibility to obesity later in life. We hypothesized that i) maternal use of antibiotics in the second or third trimester of pregnancy and ii) CS are independently associated with higher risk of childhood obesity in the offspring.Subjects/Methods:Of the 727 mothers enrolled in the Northern Manhattan Mothers and Children Study, we analyzed the 436 mother-child dyads followed until 7 years of age with complete data. We ascertained prenatal antibiotic by a questionnaire administered late in the third trimester, and delivery mode by medical record. We derived age- and sex-specific BMI z scores using the CDC SAS Macro, and defined obesity as BMI z≥95(th) percentile. We used binary regression with robust variance and linear regression models adjusted for maternal age, ethnicity, pre-gravid BMI, maternal receipt of public assistance, birth weight, sex, breast feeding in the first year, and gestational antibiotics or delivery mode.Results:Compared to children not exposed to antibiotics during the second or third trimester, those exposed had 84% (33-154%) higher risk of obesity, after multivariable adjustment. Second or third trimester antibiotic exposure was also positively associated with BMI z scores, waist circumference, and % body fat (all P<0.05). Independent of prenatal antibiotic usage, CS was associated with 46% (8-98%) higher offspring risk of childhood obesity. Associations were similar for elective and non-elective CS.Conclusions:In our cohort, CS and exposure to antibiotics in the second or third trimester were associated with higher offspring risk of childhood obesity. Future studies that address the limitations of our study are warranted to determine if prenatal antibiotic use is associated with offspring obesity. Research is also needed to determine if alterations in neonatal gut microbiota underlie the observed associations.International Journal of Obesity accepted article preview online, 09 October 2014. doi:10.1038/ijo.2014.180.
Background:There is emerging literature demonstrating a relationship between the timing of feeding and weight regulation in animals. However, whether the timing of food intake influences the success of a weight-loss diet in humans is unknown.Objective:To evaluate the role of food timing in weight-loss effectiveness in a sample of 420 individuals who followed a 20-week weight-loss treatment.Methods:Participants (49.5% female subjects; age (mean±s.d.): 42±11 years; BMI: 31.4±5.4 kg m(-2)) were grouped in early eaters and late eaters, according to the timing of the main meal (lunch in this Mediterranean population). 51% of the subjects were early eaters and 49% were late eaters (lunch time before and after 1500 hours, respectively), energy intake and expenditure, appetite hormones, CLOCK genotype, sleep duration and chronotype were studied.Results:Late lunch eaters lost less weight and displayed a slower weight-loss rate during the 20 weeks of treatment than early eaters (P=0.002). Surprisingly, energy intake, dietary composition, estimated energy expenditure, appetite hormones and sleep duration was similar between both groups. Nevertheless, late eaters were more evening types, had less energetic breakfasts and skipped breakfast more frequently that early eaters (all; P<0.05). CLOCK rs4580704 single nucleotide polymorphism (SNP) associated with the timing of the main meal (P=0.015) with a higher frequency of minor allele (C) carriers among the late eaters (P=0.041). Neither sleep duration, nor CLOCK SNPs or morning/evening chronotype was independently associated with weight loss (all; P>0.05).Conclusions:Eating late may influence the success of weight-loss therapy. Novel therapeutic strategies should incorporate not only the caloric intake and macronutrient distribution-as is classically done-but also the timing of food.International Journal of Obesity advance online publication, 29 January 2013; doi:10.1038/ijo.2012.229.
The United States (US) Equal Employment Opportunity Commission has proposed rules allowing employers to penalize employees up to 30% of health insurance costs if they fail to meet ‘health’ criteria such as reaching a specified Body Mass Index (BMI). Our objective was to examine cardiometabolic health misclassifications given standard BMI categories. Participants (N=40 420) were individuals aged 18+ in the nationally representative 2005-2012 National Health and Nutrition Examination Survey (NHANES). Using blood pressure, triglyceride, cholesterol, glucose, insulin resistance, and C-reactive protein data, population frequencies/percentages of metabolically healthy versus unhealthy individuals were stratified by BMI. Nearly half of overweight individuals, 29% of obese individuals, and even 16% of obesity type II/III individuals were metabolically healthy. Moreover, over 30% of normal weight individuals were cardiometabolically unhealthy. There was no significant race x BMI interaction, but there was a significant gender x BMI interaction, F(4,64)=3.812, P=0.008. Using BMI categories as the main indicator of health, an estimated 74 936 678 US adults are misclassified as cardiometabolically unhealthy or cardiometabolically healthy. Policymakers should consider the unintended consequences of relying solely on BMI, and researchers should seek to improve diagnostic tools related to weight and cardiometabolic health.International Journal of Obesity accepted article preview online, 04 February 2016. doi:10.1038/ijo.2016.17.
Overweight and obesity are major risk factors for diabetes, cardiovascular disease, and lung disease. These diseases are the most commonly reported health conditions that predispose individuals with SARS-CoV-2 infection to require hospitalization including intensive care unit admissions. The innate immune response is the host’s first line of defense against a human coronavirus infection. However, most coronaviruses are armed with one strategy or another to overcome host antiviral defense, and the pathogenicity of the virus is related to its capacity to suppress host immunity. The multifaceted nature of obesity including its effects on immunity can fundamentally alter the pathogenesis of acute respiratory distress syndrome and pneumonia, which are the major causes of death due to SARS-CoV-2 infection. Elevated circulating leptin concentrations are a hallmark of obesity, which is associated with a leptin-resistant state. Leptin is secreted by adipocytes in proportion to body fat and regulates appetite and metabolism through signaling in the hypothalamus. However, leptin also signals through the Jak/STAT and Akt pathways, among others, to modulate T cell number and function. Thus, leptin connects metabolism with the immune response. Therefore, it seems appropriate that its dysregulation would have serious consequences during an infection. We propose that leptin may be the link between obesity and its high prevalence as a comorbidity of the SARS-CoV-2 infection. In this article, we present a synthesis of the mechanisms underpinning susceptibility to respiratory viral infections and the contribution of the immunomodulatory effects of obesity to the outcome.
Energy intake (EI) and physical activity energy expenditure (PAEE) are key modifiable determinants of energy balance, traditionally assessed by self-report despite its repeated demonstration of considerable inaccuracies. We argue here that it is time to move from the common view that self-reports of EI and PAEE are imperfect, but nevertheless deserving of use, to a view commensurate with the evidence that self-reports of EI and PAEE are so poor that they are wholly unacceptable for scientific research on EI and PAEE. While new strategies for objectively determining energy balance are in their infancy, it is unacceptable to use decidedly inaccurate instruments, which may misguide health care policies, future research, and clinical judgment. The scientific and medical communities should discontinue reliance on self-reported EI and PAEE. Researchers and sponsors should develop objective measures of energy balance.International Journal of Obesity accepted article preview online, 13 November 2014. doi:10.1038/ijo.2014.199.
Circadian physiology has been linked to body weight regulation and obesity. To date, few studies have assessed the association between exercise timing and weight related outcomes. The aim of this secondary analysis was to explore the impact of exercise timing (i.e., 24 h clock time of exercise session) on weight loss and components of energy balance.
To assess longitudinal associations between screen based media use (television and computer hours, having a TV in the bedroom) and body fatness among UK children.