Childhood and adolescence are critical periods for lifelong bone mineral accrual, but few studies have determined the impact of childhood adiposity on adult bone density.

There are established links between the accumulation of body fat as visceral adipose tissue (VAT) and the risk of developing obesity-associated metabolic disease. Previous studies have suggested that levels of intake of specific foods and nutrients are associated with VAT accumulation after accounting for total energy intake.

Nonalcoholic fatty liver disease (NAFLD) is a risk factor for liver cancer and prevalence varies by ethnicity. Along with genetic and lifestyle factors, the gut microbiome (GM) may contribute to NAFLD and its progression to advanced liver disease. Our cross-sectional analysis assessed the association of the GM with hepatic adiposity among African American, Japanese American, White, Latino, and Native Hawaiian participants in the Multiethnic Cohort. We used MRI to measure liver fat and determine nonalcoholic fatty liver disease (NAFLD) status (n = 511 cases) in 1,544 participants, aged 60-77 years, with 12-53% overall adiposity (BMI of 17.8-46.2 kg/m2). The GM was measured by 16S rRNA gene sequencing and, on a subset, by metagenomic sequencing. Alpha diversity was lower overall with NAFLD and in certain ethnicities (African Americans, Whites, and Latinos). In models regressing genus on NAFLD status, 62 of 149 genera (40%) exhibited a significant interaction between NAFLD and ethnicity stratified analysis found 69 genera significantly associated with NAFLD in at least one ethnic group. No single genus was significantly associated with NAFLD across all ethnicities. In contrast, the same bacterial metabolic pathways were over-represented in participants with NAFLD regardless of ethnicity. Imputed secondary bile acid and carbohydrate pathways were associated with NAFLD, the latter of which was corroborated by metagenomics, although different genera in different ethnicities were associated with these pathways. Overall, we found that NAFLD was associated with altered bacterial composition and metabolism, and that bacterial endotoxin, assessed by plasma lipopolysaccharide binding protein (LBP), may mediate liver fat-associated systemic inflammation in a manner that seems to vary by ethnicity.

Body mass index (BMI) is moderately correlated with %Fat and often used to assess obesity in athletes. Limited research assesses BMI as a surrogate for %Fat in female collegiate athletes. Body Adiposity Index (BAI) is an anthropometric measurement suggested to be superior to BMI at predicting adiposity but has not been well assessed within female athletic populations. This study aimed to determine if BAI is superior to other anthropometric indices to predict %Fat in female collegiate athletes and college-aged female non-athletes. Collegiate female athletes and female non-athletes were invited into the laboratory for anthropometrics and %Fat measurements via BOD POD. BAI was calculated as Hip Circumference/Height1.5 - 18. Eighty-eight female non-athletes and 72 female athletes from soccer (n = 27), softball (n = 28), and basketball (n = 17) completed the study. Using BMI, 19% of non-athletes had a false positive (FP). Sensitivity of BMI in non-athletes was 85.5%, while specificity was 73%. 16% of athletes had a FP. Sensitivity of BMI within athletes was 100%, specificity was 81%. BMI outperformed BAI in athletic (BMI: r = .725, p < .001; BAI: r = .556, p < .001) and nonathletic (BMI: r = .650, p < .001; BAI: r = .499, p < .001) groups. The strongest anthropometric predictor of %Fat within the non-athlete population was BMI (r2 = .42, p < .001). Waist circumference was the strongest predictor in the athletic population (r2 = .62, p < .001). BMI outperformed BAI in its ability to predict %Fat.

Results from genome-wide association studies (GWAS) identified many loci and biological pathways that influence adult body mass index (BMI). We aimed to identify if biological pathways related to adult BMI also affect infant growth and childhood adiposity measures.

Obesity and obesity-related co-morbidities, diabetes mellitus, and hypertension are among the fastest-growing risk factors of heart failure and kidney disease worldwide. Obesity, which is not a unitary concept, or a static process, ranges from alterations in distribution to the amount of adiposity. Visceral adiposity, which includes intraabdominal visceral fat mass and ectopic fat deposition such as hepatic, cardiac, or renal, was robustly associated with a greater risk for cardiorenal morbidity than subcutaneous adiposity. In addition, morbid obesity has also demonstrated a negative effect on cardiac and renal functioning. The mechanisms by which adipose tissue is linked with the cardiorenal syndrome (CRS) are hemodynamic and mechanical changes, as well neurohumoral pathways such as insulin resistance, endothelial dysfunction, nitric oxide bioavailability, renin-angiotensin-aldosterone, oxidative stress, sympathetic nervous systems, natriuretic peptides, adipokines and inflammation. Adiposity and other associated co-morbidities induce adverse cardiac remodeling and interstitial fibrosis. Heart failure with preserved ejection fraction has been associated with obesity-related functional and structural abnormalities. Obesity might also impair kidney function through hyperfiltration, increased glomerular capillary wall tension, and podocyte dysfunction, which leads to tubulointerstitial fibrosis and loss of nephrons and, finally, chronic kidney disease. The development of new treatments with renal and cardiac effects in the context of type 2 diabetes, which improves mortality outcome, has highlighted the importance of CRS and its prevalence. Increased body fat triggers cellular, neuro-humoral and metabolic pathways, which create a phenotype of the CRS with specific cellular and biochemical biomarkers. Obesity has become a single cardiorenal umbrella or type of cardiorenal metabolic syndrome. This review article provides a clinical overview of the available data on the relationship between a range of adiposity and CRS, the support for obesity as a single cardiorenal umbrella, and the most relevant studies on the recent therapeutic approaches.

Lower cord blood leptin levels have been associated with lower and higher adiposity in childhood and associations seem to differ according to the child’s age, methods of adiposity assessment and sex. Our aim was to investigate sex-specific associations of cord blood leptinemia with childhood adiposity at birth, 3 and 5 years of age. We measured cord blood leptin using Luminex immunoassays in 520 offspring from the Gen3G cohort. We tested associations between cord blood leptin and body mass index (BMI) z-score, skinfolds thicknesses (SFT), and body composition using dual-energy X-ray absorptiometry, adjusted for confounders. At birth, girls had almost twice as much leptin in cord blood as boys (15.5 [8.9; 25.6] vs. 8.6 [4.9; 15.0] ng/mL; p < 0.0001) as well as significantly greater adiposity. Lower levels of cord blood leptin were associated with higher sum of SFT (β = −0.05 ± 0.02; p = 0.03) and higher BMI z-score (β= −0.22 ± 0.08; p = 0.01) in 3-year-old boys only. We did not observe these associations at age 5, or in girls. Our results suggest a sexual dimorphism in the programming of leptin sensitivity and childhood adiposity, but further observational and functional studies are needed to better understand the role of leptin in early life.

More research is needed about the association between physical activity (PA), sedentary behaviour (SB), and adiposity in preschoolers, particularly using more direct clinical measures of adiposity. Therefore, the main objective of this study was to investigate the association between objectively measured PA and different clinical adiposity measures in a large sample of preschoolers.

Greater maternal adiposity before or during pregnancy is associated with greater offspring adiposity throughout childhood, but the extent to which this is due to causal intrauterine or periconceptional mechanisms remains unclear. Here, we use Mendelian randomisation (MR) with polygenic risk scores (PRS) to investigate whether associations between maternal pre-/early pregnancy body mass index (BMI) and offspring adiposity from birth to adolescence are causal.

The relationship between facial cues and perceptions of health and attractiveness in others plays an influential role in our social interactions and mating behaviors. Several facial cues have historically been investigated in this regard, with facial adiposity being the newest addition. Evidence is mounting that a robust link exists between facial adiposity and attractiveness, as well as perceived health. Facial adiposity has also been linked to various health outcomes such as cardiovascular disease, respiratory disease, blood pressure, immune function, diabetes, arthritis, oxidative stress, hormones, and mental health. Though recent advances in the analysis of facial morphology has led to significant strides in the description and quantification of facial cues, it is becoming increasingly clear that there is a great deal of nuance in the way that humans use and integrate facial cues to form coherent social or health judgments of others. This paper serves as a review of the current literature on the relationship between facial adiposity, attractiveness, and health. A key component in utilizing facial adiposity as a cue to health and attractiveness perceptions is that people need to be able to estimate body mass from facial cues. To estimate the strength of the relationship between perceived facial adiposity and body mass, a meta-analysis was conducted on studies that quantified the relationship between perceived facial adiposity and BMI/percentage body fat. Summary effect size estimates indicate that participants could reliably estimate BMI from facial cues alone (r = 0.71, n = 458).

This study aims to assess the construct validity of a body composition-defined definition of sarcopenic obesity based on low appendicular lean mass relative to fat mass (ALMIFMI ) and high fat mass index (FMI) and to compare with an alternative definition using appendicular lean mass index (ALMI) and percent body fat (%BF).

There is a well established link between obesity and cancer. Emerging research is characterising this relationship further and delineating the specific role of excess visceral adiposity, as opposed to simple obesity, in promoting tumorigenesis. This review summarises the evidence from an epidemiological and pathophysiological perspective.

Production of Annexin A1 (ANXA1), a protein that mediates the anti-inflammatory action of glucocorticoids, is altered in obesity, but its role in modulation of adiposity has not yet been investigated. The objective of this study was to investigate modulation of ANXA1 in adipose tissue in murine models of obesity and to study the involvement of ANXA1 in diet-induced obesity in mice. Significant induction of ANXA1 mRNA was observed in adipose tissue of both C57BL6 and Balb/c mice with high fat diet (HFD)-induced obesity versus mice on chow diet. Upregulation of ANXA1 mRNA was independent of leptin or IL-6, as demonstrated by use of leptin-deficient ob/ob mice and IL-6 KO mice. Compared to WT mice, female Balb/c ANXA1 KO mice on HFD had increased adiposity, as indicated by significantly elevated body weight, fat mass, leptin levels, and adipocyte size. Whereas Balb/c WT mice upregulated expression of enzymes involved in the lipolytic pathway in response to HFD, this response was absent in ANXA1 KO mice. A significant increase in fasting glucose and insulin levels as well as development of insulin resistance was observed in ANXA1 KO mice on HFD compared to WT mice. Elevated plasma corticosterone levels and blunted downregulation of 11-beta hydroxysteroid dehydrogenase type 1 in adipose tissue was observed in ANXA1 KO mice compared to diet-matched WT mice. However, no differences between WT and KO mice on either chow or HFD were observed in expression of markers of adipose tissue inflammation. These data indicate that ANXA1 is an important modulator of adiposity in mice, with female ANXA1 KO mice on Balb/c background being more susceptible to weight gain and diet-induced insulin resistance compared to WT mice, without significant changes in inflammation.

Obesity/overweight is the most prevalent body composition abnormality in COPD. However, little is known about the impact of fat distribution on cardiometabolic health in COPD.

Evidence suggests that individuals who are more obese may be more responsive to stress. Stress activates the sympathetic nervous system (SNS) and the adipose-tissue cytokine leptin stimulates SNS activity in animals. We examined the relationship between adiposity, leptin and physiological responses to acute laboratory stress in 67 women. We predicted that individuals with greater adiposity and/or higher plasma leptin would be more stress-responsive. Adiposity was unrelated to cardiovascular or neuroendocrine stress reactivity. However, women with larger waists had greater stress-induced increases in plasma leptin and interleukin-1 receptor antagonist (IL-1Ra). Similarly, women with higher basal leptin displayed greater stress-induced increases in heart rate and plasma interleukin-6, and larger decreases in heart rate variability and cardiac pre-ejection period. Heightened cardiovascular and inflammatory stress responses are predictive of future cardiovascular risk. Our findings suggest that the cytokines leptin and IL-1Ra may play a role in the association between obesity, stress and cardiovascular health.

Recent genome-wide association studies have identified multiple loci robustly associated with plasma lipids, which also contribute to extreme lipid phenotypes. However, these common genetic variants explain <12% of variation in lipid traits. Adiposity is also an important determinant of plasma lipoproteins, particularly plasma TGs and HDL cholesterol (HDLc) concentrations. Thus, interactions between genes and clinical phenotypes may contribute to this unexplained heritability. We have applied a weighted genetic risk score (GRS) for both plasma TGs and HDLc in two large cohorts at the extremes of BMI. Both BMI and GRS were strongly associated with these lipid traits. A significant interaction between obese/lean status and GRS was noted for each of TG (P(Interaction) = 2.87 × 10(-4)) and HDLc (P(Interaction) = 1.05 × 10(-3)). These interactions were largely driven by SNPs tagging APOA5, glucokinase receptor (GCKR), and LPL for TG, and cholesteryl ester transfer protein (CETP), GalNAc-transferase (GALNT2), endothelial lipase (LIPG), and phospholipid transfer protein (PLTP) for HDLc. In contrast, the GRSLDL cholesterol × adiposity interaction was not significant. Sexual dimorphism was evident for the GRSHDL on HDLc in obese (P(Interaction) = 0.016) but not lean subjects. SNP by BMI interactions may provide biological insight into specific genetic associations and missing heritability.

Requirements for selenium and other antioxidant nutrients are increased in pro-oxidant and pro-inflammatory conditions such as excess adiposity. Data concerning the association of excess general and central adiposity with circulating selenium concentrations, however, are limited. We examined the cross-sectional associations of body mass index (BMI), percent body fat (%BF), and waist circumference (WC) with serum selenium concentrations in 6440 men and 6849 women aged ≥20 years who participated in the U.S. Third National Health and Nutrition Examination Survey. In multivariable analyses, the average difference (95% confidence interval (CI)) in serum selenium comparing the highest with the lowest quartiles of BMI was -4.0 (-5.5, -1.6) ng/mL in both men and women. These inverse associations were evident after further adjustment for WC. For %BF, the average differences (95% CI) in serum selenium between the highest and the lowest quartiles of %BF were -1.7 (-4.2, 0.7) ng/mL in men and -4.5 (-7.0, -1.9) ng/mL in women. The inverse association in women persisted after adjusting for WC. For WC, the average differences (95% CI) in serum selenium between the highest and the lowest quartiles were -1.9 (-3.8, -0.1) ng/mL in men and -3.9 (-5.8, -2.0) ng/mL in women. After further adjustment for BMI, the inverse association became positive in men and null in women. Our findings suggest that general and central adiposity have different associations with serum selenium levels and that these associations may depend on gender.

Excess adipose tissue increases other cardiovascular risk factors, which may be associated with vascular brain injury and cognitive impairment. However, the extent to which the amount and distribution of adipose tissue may be associated with lower cognitive scores, independent of its association with cardiovascular risk factors, is not well characterized.

Visceral adiposity is an important risk factor for cardiometabolic diseases.

Worldwide obesity has a high prevalence, as well as carries a high risk of several chronic diseases, including hypertension. Studies of the association between obesity and ambulatory blood pressure (BP) are scarce and most use only body mass index (BMI) as indicator of adiposity. Thus, we aimed to examine for associations between total and central adiposity and ambulatory BP parameters (BP means and variability, nocturnal dipping and morning surge) among participants in the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil).