Notes

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Each SD increase in BMI, truncal-to-leg fat ratio, and android-to-gynoid fat ratio was significantly associated with increased risks of elevated HbA
, hypertension, and elevated LDL cholesterol.

Subcutaneous fat in the lower body was associated with a more favorable glycemic profile, but not blood pressure or lipid profile, whereas central adiposity was associated with poor control of cardiovascular risk factors among patients with type 2 diabetes mellitus.
Subcutaneous fat in the lower body was associated with a more favorable glycemic profile, but not blood pressure or lipid profile, whereas central adiposity was associated with poor control of cardiovascular risk factors among patients with type 2 diabetes mellitus.
The objective of this study was to develop a simple and practical guide for discussing and managing obesity in primary care settings.

This study convened representatives from 12 primary care and obesity specialty organizations for a series of roundtable meetings to discuss the key components of obesity treatment in primary care. Attendees identified the need for a guide for primary care providers that outlined the key steps for discussing obesity with patients and managing their care while recognizing the significant time constraints on such provider/patient encounters.

Prevailing themes from the roundtable sessions suggested that the key components of addressing obesity in primary care settings are obtaining patient permission, addressing weight bias, providing a diagnosis, and emphasizing shared decision-making. A modified "6A" framework with the steps "Ask," "Assess," "Advise," "Agree," "Assist," and "Arrange" was deemed appropriate to organize the process of weight management in primary care. An algorithm was developed to provide a script for the patient/provider encounter.

The expert panel developed a short, accessible, practical, and informative guide for obesity management by primary care clinicians. Efforts are under way to disseminate the guide to primary care providers through the 11 participating organizations that have endorsed it.
The expert panel developed a short, accessible, practical, and informative guide for obesity management by primary care clinicians. Efforts are under way to disseminate the guide to primary care providers through the 11 participating organizations that have endorsed it.There is a genetic component to human obesity that accounts for 40% to 50% of the variability in body weight status but that is lower among normal weight individuals (about 30%) and substantially higher in the subpopulation of individuals with obesity and severe obesity (about 60%-80%). The appreciation that heritability varies across classes of BMI represents an important advance. After controlling for BMI, ectopic fat and fat distribution traits are characterized by heritability levels ranging from 30% to 55%. Defects in at least 15 genes are the cause of monogenic obesity cases, resulting mostly from deficiencies in the leptin-melanocortin signaling pathway. Approximately two-thirds of the BMI heritability can be imputed to common DNA variants, whereas low-frequency and rare variants explain the remaining fraction. Diminishing allele effect size is observed as the number of obesity-associated variants expands, with most BMI-increasing or -decreasing alleles contributing only a few grams or less to body weight. Obesity-promoting alleles exert minimal effects in normal weight individuals but have larger effects in individuals with a proneness to obesity, suggesting a higher penetrance; however, it is not known whether these larger effect sizes precede obesity or are caused by an obese state. The obesity genetic risk is conditioned by thousands of DNA variants that make genetically based obesity prevention and treatment a major challenge.Chronic inflammation is considered a precipitating factor and possibly an underlying cause of many noncommunicable diseases, including cardiovascular disease, metabolic diseases, and some cancers. Obesity, which manifests in more than 650 million people worldwide, is the most common chronic inflammatory condition, with visceral adiposity thought to be the major inflammatory hub that links obesity and chronic disease. read more Adipose tissue (AT) inflammation is triggered or heightened in large part by (1) accelerated immune cell recruitment, (2) reshaping of the AT stromal-immuno landscape (e.g., immune cells, endothelial cells, fibroblasts, adipocyte progenitors), and (3) perturbed AT immune cell function. Exercise, along with diet management, is a cornerstone in promoting weight loss and preventing weight regain. This review focuses on evidence that increased physical activity reduces AT inflammation caused by hypercaloric diets or genetic obesity. The precise cell types and mechanisms responsible for the therapeutic effects of exercise on AT inflammation remain poorly understood. This review summarizes what is known about obesity-induced AT inflammation and immunomodulation and highlights mechanisms by which aerobic exercise combats inflammation by remodeling the AT immune landscape. Furthermore, key areas are highlighted that require future exploration and novel discoveries into the burgeoning field of how the biology of exercise affects AT immunity.
This study examined the association between longitudinal trajectories of lifestyle patterns (LPs) and BMI z score in early childhood.

Data of children (n = 439) who participated in the 18-, 42-, and 60-month follow-ups of the Melbourne InFANT Program were used. Multitrajectory modeling identified groups of children following similar LPs and BMI z score trajectories, and multinomial logistic regression assessed the determinants of the trajectory groups.

Three trajectory groups of child LPs and BMI z scores were identified "Unhealthy LP, Low BMIz" (30%), "Healthy LP, Mid BMIz" (53%), and "Unhealthy LP, High BMIz" (17%). Relative to the "Unhealthy LP, Low BMIz" group, the maternal "Fruit and vegetables" dietary pattern was associated with higher odds (odds ratio [OR] 1.22, 95% CI 1.01-1.47) of children following the "Healthy LP, Mid BMIz" group. Maternal prepregnancy BMI (≥25 kg/m
) (OR 2.50, 95% CI 1.31-4.75) and maternal TV-viewing time ≥130 min/d (OR 2.55, 95% CI 1.13, 5.72) increased the odds of children following the "Unhealthy LP, High BMIz" group.
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