Measures Of Obesity Research Articles

The companion dog as a model for inflammaging: a cross-sectional pilot study.

Inflammaging, the chronic, progressive proinflammatory state associated with aging, has been associated with multiple negative health outcomes in humans. The pathophysiology of inflammaging is complex; however, it is often characterized by high serum concentrations of inflammatory mediators such as tumor necrosis factor alpha (TNF-α), interleukin (IL)-6, and C-reactive protein (CRP). Few studies have evaluated the effects of age on inflammatory cytokines in companion dogs, and most of these studies included dogs of a single breed. In this cross-sectional study, we measured multiple circulating inflammatory markers and hematological parameters in banked serum samples from 47 healthy companion dogs of various breeds enrolled in the Dog Aging Project. Using univariate linear models, we investigated the association of each of these markers with age, sex, body weight, and body condition score (BCS), a measure of obesity in the dog. Serum IL-6, IL-8, and TNF-α concentrations were all positively associated with age. Lymphocyte count was negatively associated with age. Platelet count had a negative association with body weight. IL-2, albumin, cholesterol, triglyceride, bilirubin, S100A12, and NMH concentrations were not associated with age, weight, BCS, or sex after adjustment for multiple comparisons. Our findings replicate previous findings in humans, including increases in IL-6 and TNF-α with age, giving more evidence to the strength of the companion dog as a model for human aging.

Normative values for body composition in 22,191 healthy Norwegian adults 20–99 years: The HUNT4 study

BackgroundBody mass, body mass index (BMI), and body composition components are essential for health and longevity. Considering the influence of demographic factors on body composition, there is a need for tailored reference values based on age-, sex-, and geography. We aimed to construct a comprehensive reference material on body composition in healthy Norwegian adults. MethodsIn this cross-sectional study, we estimated age- and sex-specific reference values for body-, fat-, and muscle mass variables using multi-frequency bioelectrial impedance analysis (such as body fat percentage, skeletal muscle mass and visceral fat area) in 22,191 healthy adults aged 20–99 years participating in the Trøndelag Health Study 4 (HUNT4). We calculated the fat mass and skeletal muscle mass index as the total fat and muscle mass relative to height squared and used general linear models to explore the associations between physical activity (PA), BMI, and age. ResultsWith a BMI (kg/m2) of 25.4 (SD 5.1) and 26.0 (4.5) for women and men, respectively, the youngest age group (20–39 yrs) had a lower BMI compared to their counterparts aged 40–59 years (26.3 [4.5] and 27.5 [3.8]) and ≥ 60 years (25.7 [4.1] and 26.5 [3.4]), respectively. Those aged 20–39 years also had the lowest values for the different body fat variables measured. Fat mass index (kg/m2) was 8.41 (4.00) and 5.81 (3.29) for women and men aged 20–39 years, respectively, compared to 9.25 (3.21) and 6.86 (2.46) for those aged ≥60 years. The oldest age group had the lowest values for the various muscle mass variables; women and men aged 60+ years had a skeletal muscle mass index (kg/m2) of 8.91 (0.85) and 10.96 (1.00), respectively. Corresponding values for those aged 20–39 years were 9.33 (0.97) and 11.49 (1.15). For all age groups and both sexes, regular physical activity was associated with lower levels of fat mass, whereas the association between muscle mass and PAwas less conclusive. When using body fat percentage as an obesity measure, we observed a much higher obesity prevalence (41.2%) in the study population compared to BMI (17.3%). ConclusionsOur study offers a comprehensive reference for body composition among healthy adults in Norway, aiding the identification of abnormal fat and muscle mass values across age groups. We also highlight that BMI often misclassifies individuals with adiposity levels in the overweight or obese category as lean. Therefore, incorporating body composition when defining obesity could enable early intervention to prevent cardiometabolic diseases.

Evaluation of body mass index, ponderal index, visceral cross-sectional area, subcutaneous fat cross-sectional area, and liver volume as predictive factors for obesity-related comorbidities: a retrospective cohort study

BackgroundThe body mass index is an imperfect clinical measure of obesity that should be used in conjunction with other valid measures of weight-related risk. We studied whether there is a superior measure of obesity-related comorbidities. MethodsRecords of bariatric clinic patients who had an abdominal computed tomography (CT) within one year of visit were reviewed. The presence of obesity-related comorbidities was determined at the time of the scan. Body mass index (BMI) and ponderal index (PI) were calculated, and CT scans were reviewed to determine the visceral cross-sectional area (VCSA), subcutaneous fat cross-sectional area (SFCSA), and liver volume (LV). Data was analyzed using the Kruskal-Wallis test and Mann-Whitney U test. ResultsA higher number of comorbidities were found to be associated with a larger BMI (p=0.011), VCSA (p=0.014), SFCSA (p=0.007), and LV (p=0.014), but not a larger PI (p=0.11). Of the 16 comorbidities assessed, VCSA and LV were associated with more than BMI and SFCSA. However, each measure could be associated with different comorbidities. A higher BMI was associated with increased insulin use (p=0.034), HTN (p=0.007), and history of OSA (p=0.015), none of which were associated with PI. BMI and PI were the only measures associated with a history of DVT/PE (both p<0.01). Only SFCSA was found to be associated with GERD (p=0.029). VCSA (p=0.038) and LV (p=0.001) were associated with NAFLD. ConclusionNo measure could account for all obesity-related comorbidities, implying the need for targeted measurements. However, the ponderal index was the least effective measure.

Short sleep duration is associated with higher risk of central obesity in adults: A systematic review and meta-analysis of prospective cohort studies.

The relationship between sleep duration and obesity has been the focus of numerous investigations. This systematic review and meta-analysis of prospective cohort studies aimed to assess the relationship between sleep duration, abdominal obesity, and body composition. PubMed, Scopus, and Web of Science were searched until February 2024. Cohort studies that assessed the relationship between sleep duration at night and central obesity measures or body composition indices in adults were included. The quality of studies was assessed using the Newcastle-Ottawa scale. Random-effects meta-analysis was conducted on studies that reported risk ratio (RR) and 95% confidence intervals (CIs). Eighteen studies were eligible to be included. Eleven out of the 18 studies were not included in the analysis as 10 studies did not report RR, and in one study, the definition of short and normal sleep duration was different from others. Theresults of the meta-analysis indicated that short sleep duration was significantly associated with abdominal obesity (RR = 1.08; 95% CI: 1.04-1.12;I 2= 49.1%, n=7), but long sleep duration was not (RR = 1.02; 95% CI: 0.83-1.24;I 2= 98.2%, n= 6). Short sleep duration was associated with a slightly higher risk of central obesity, while long sleep duration was not.

Correlation of cardiometabolic index and sarcopenia with cardiometabolic multimorbidity in middle-aged and older adult: a prospective study.

Research has demonstrated that sarcopenia and visceral obesity are significant risk factors for chronic disease in middle-aged and older adults. However, the relationship between sarcopenia, the cardiac metabolic index (CMI), a novel measure of visceral obesity, and cardiometabolic multimorbidity (CMM) remains unclear. In this study, data from the China Longitudinal Study of Health and Retirement (CHARLS) were analyzed to investigate the association between sarcopenia and CMI with CMM in the middle-aged and older adult population. The study included 4,959 participants aged 45 and over. Sarcopenia was defined using the criteria of the Asian Sarcopenia Working Group 2019. CMM is defined as having two or more of the following conditions: physician-diagnosed heart disease, diabetes, stroke, and/or hypertension. CMI was calculated using the formula: CMI = (TG/HDL-C) × WHtR. To explore the association between CMI and sarcopenia and CMM, cox proportional risk regression models were used. The median age of all participants was 57 years, with 47.1% being male. Over the 8-year follow-up, 1,362 individuals developed CMM. The incidence of CMM was 8.7/1,000 person-years in the group without sarcopenia or high CMI, 17.37/1,000 person-years in those with high CMI, 14.22/1,000 person-years in the sarcopenia group, and 22.34/1,000 person-years in the group with both conditions. After adjusting for covariates, the group with both sarcopenia and high CMI had a significantly increased risk of CMM (HR 2.48, 95% CI 1.12-5.51) and heart disease (HR 2.04, 95% CI 1.05-3.98). Among those over 65 years, sarcopenia was discovered to be associated with an increased risk of CMM [HR (95% CI: 4.83 (1.22, 19.06)]. The risk of CMM was further increased to 7.31-fold (95% CI:1.72, 31.15) when combined with high CMI. The combination of sarcopenia and high CMI is associated with an increased risk of developing CMM. Early identification and intervention of sarcopenia and CMI not only enable the development of targeted therapeutic strategies but also provide potential opportunities to reduce the morbidity and mortality of CMM.

Mediation Mendelian randomisation study on the effects of shift work on coronary heart disease and traditional risk factors via gut microbiota.

Epidemiological evidence suggests that there is an increased risk of coronary heart disease (CHD) related to jobs involving shift work (JSW), but the causality of and mechanism underlying such a relationship remain unclear. Therefore, we aimed to explore the relationship between JSW and CHD, investigating both causality and potential mediating factors. We performed univariate, multivariate, and mediation Mendelian randomisation (MR) analyses using data from large genome-wide association studies focussed on JSW and CHD, as well as data on some CHD risk factors (type 2 diabetes, hypertension, obesity, and lipids measurement) and 196 gut microbiota taxa. Single-nucleotide polymorphisms significantly associated with JSW acted as instrument variables. We used inverse-variance weighting as the primary method of analysis. Bidirectional MR analysis indicated a robust effect of JSW on increased CHD risk; however, the existence of CHD did not affect the choice of JSW. We identified a mediating effects of type 2 diabetes and hypertension in this relationship, accounting for 11.89% and 14.80% of the total effect of JSW on CHD, respectively. JSW were also causally associated with the risk of type 2 diabetes and hypertension and had an effect on nine microbial taxa. The mediating influence of the Eubacterium brachy group at the genus level explained 16.64% of the total effect of JSW on hypertension. We found limited evidence for the causal effect of JSW on obesity and lipids measurements. Our findings suggest a causal effect of JSW on CHD, diabetes, and hypertension. We also found evidence for a significant connection between JSW and alterations in the gut microbiota. Considering that certain microbial taxa mediated the effect of JSW on hypertension risk, targeting gut microbiota through therapeutics could potentially mitigate high risks of hypertension and CHD associated with JSW.

GR.2 Obesity and multiple sclerosis severity: a Mendelian randomization study

Background: Obesity is increasingly implicated in the development of multiple sclerosis (MS), but its effect on disease disability is less well-established. This study aims to investigate the association between obesity and MS severity utilizing Mendelian Randomization (MR). Methods: Employing a two-sample MR setting, we examined the effects of various obesity measures and adiposity distribution metrics on MS severity. Genetic proxies for body mass index (BMI) were selected from a study of 806,834 participants, with MS severity determined from a genetic study of age-related MS severity scores in 12,584 individuals with MS. Results: The main analysis reveals an association between elevated BMI and increased MS severity (P = 0.03). This is supported by a significant effect of whole body fat (P = 0.04), aligning with the hypothesis that obesity exacerbates MS disability. Sensitivity analyses suggest minimal heterogeneity and bias, indicating a potential causal effect. Conclusions: Our findings suggest that obesity adversely influences long-term disability outcomes in MS. The convergence of this genetic evidence with some of the prior observational studies strengthens the argument for a causal relationship between obesity and MS severity. These insights highlight obesity as a potentially modifiable risk factor in managing MS, underscoring the importance of weight management in MS treatment strategies.

Association Between Dietary Intake of Phosphorus and Measures of Obesity in the Jackson Heart Study

BackgroundThe relation between phosphorus (P) intake and obesity is equivocal, with hypotheses in both directions. ObjectivesWe investigated the relationship between P intake, assessed from a current database, and calculated bioavailable P intake and obesity among African-American adults. MethodsWe examined associations between original and bioavailable P (total, added, and natural) and BMI and waist circumference (WC) in a cross-sectional study of 5306 African-American adults (21–84 y) from the Jackson Heart Study. A total of 3300 participants had complete interviews, valid dietary data, and normal kidney function. Diet was assessed by food frequency questionnaire. A novel algorithm was used to estimate P bioavailability. BMI or WC was regressed on each P variable, adjusting for total energy intake and potential confounders. ResultsAfter adjusting for covariates, original P (total and added) and bioavailable P (total and added) intakes (expressed/100 mg) were associated with BMI (β: 0.11, 0.67, 0.31, and 0.71, respectively; all P < 0.0001). Neither original nor bioavailable natural P was significantly associated (β: −0.03 and 0.09, respectively; both P > 0.05). When added and natural P were included in the same model, added P (original and bioavailable) intakes remained strongly associated with BMI (0.70 and 0.73, respectively; both P < 0.0001). Similar results were seen for WC. Intake of original added P tended to be more strongly associated with BMI, in females (β: 0.72; P < 0.0001) than in males (β: 0.56; P = 0.003) (P-interaction = 0.06). ConclusionsWe found that greater intake of added, not natural, which may be a proxy for intake of processed foods was associated with higher BMI and WC. These were somewhat stronger when bioavailability was considered and for women than for men. Further investigation is needed to fully understand the mechanisms driving these associations.

Type 2 diabetes mediates the causal relationship between obesity and osteomyelitis: A Mendelian randomization study.

Mendelian randomization (MR) analysis was used to determine the causal relationship between Type 2 diabetes (T2D) and osteomyelitis (OM). We performed MR analysis using pooled data from different large-scale genome-wide association studies (GWAS). Instrumental variables were selected based on genome-wide significance, instrumental strength was assessed using F-values, and thresholds for the number of exposed phenotypes were further adjusted by Bonferroni correction. univariable and multivariable MR analyses were performed to assess causal effects and proportions mediated by T2D. IVW (inverse variance weighting) showed a significant genetic effect of osteomyelitis on the following: After correction by Bonferroni, univariable analyses showed that childhood body mass index (BMI) was not significantly associated with genetic susceptibility to OM [odds ratio (OR), 1.26; 95% confidence interval (CI), 1.02, 1.55; P = .030], not significantly associated with adulthood BMI (OR, 1.28; 95% CI, 1.02, 1.61; P = .034), significantly associated with waist circumference (OR, 1.84; 95% CI, 1.51, 2.24; P < .001), and significantly associated with hip circumference (OR, 1.52; 95% CI, 1.31, 1.76; P < .001). Meanwhile, multivariable analyses showed no significant effect of childhood BMI on OM (OR, 1.16; 95% CI, 0.84, 1.62; P = .370), no significant effect of adulthood BMI on OM (OR, 0.42; 95% CI, 0.21, 0.84; P = .015), a significant association between waist circumference and OM (OR, 4.30; 95% CI, 1.89, 9.82; P = .001), T2D mediated 10% (95% CI, 0.02, 0.14), and no significant association between hip circumference and OM (OR, 1.01; 95% CI, 0.54, 1.90; P = .968). Our study provides evidence for a genetically predicted causal relationship among obesity, T2D, and OM. We demonstrate that increased waist circumference is positively associated with an increased risk of OM and that T2D mediates this relationship. Clinicians should be more cautious in the perioperative management of osteomyelitis surgery in obese patients with T2D. In addition, waist circumference may be a more important criterion to emphasize and strictly control than other measures of obesity.

Causal effects of BMI, waist circumference, and body fat percentage on the risk of bladder cancer: A Mendelian randomization study.

The causal role of body mass index (BMI) in bladder cancer (BC) by Mendelian randomization (MR) has not yet been reported. We evaluated the causal associations between the measures of obesity (BMI, waist circumference, and body fat percentage) and BC. We conducted a 2-sample MR analysis to assess the genetic effect of measures of obesity on BC. The BMI dataset (GWAS ID: ukb-b-2303) comprised 454,884 Europeans, and we identified 9,851,867 single nucleotide polymorphisms (SNPs). The waist circumference data (GWAS ID: ukb-b-9405) included 462,166 Europeans and 9,851,867 SNPs. The body fat percentage dataset (GWAS ID: ukb-a-264) contained data from 331,117 Europeans and 10,894,596 SNPs. For the outcome data, the GWAS ID was finn-b-C3_BLADDER, consisting of 1115 cases and 217,677 controls, with 16,380,466 SNPs. The inverse-variance weighted (IVW) model was used as the primary MR analysis. Cochran Q-statistic was used to identify heterogeneity between the SNPs. The MR-Egger and MR-PRESSO methods were employed to assess directional pleiotropy and outlier SNPs. We detected a decisive causal link between BMI and BC by the IVW analysis (odds ratio [OR] = 1.41, 95% confidence interval [CI]: 1.08-1.85, P = .011). The IVW analyses revealed a significant correlation between BC and waist circumference (OR = 1.55, 95% CI: 1.08-2.12, P = .016). However, the IVW method (OR = 1.49, 95% CI: 0.99-2.00, P = .05) did not report any statistical significance between body fat percentage and BC. We did not observe heterogeneity and directional pleiotropy in the 3 pairs of MR studies. The 2-sample MR analysis revealed a conceivable causal association between obesity (BMI, waist circumference) and BC.

O11 Investigating the genetic basis of the influence of adiposity on psoriasis

Abstract Introduction and aims Obesity is a chronic inflammatory state that is highly prevalent in people with psoriasis. There is evidence to suggest that increasing levels of adiposity promotes the risk of psoriasis development and worsens disease severity. The degree to which adiposity influences psoriasis varies between individuals, and it is also unclear which key genetic factors underpin this variation. Identifying this could be mechanistically informative in uncovering immunological pathways connecting adiposity and psoriasis. This project explores the hypothesis that the influence of adiposity on psoriasis has a genetic basis. Methods Firstly, we examined the comparative strength of association between a range of measures of adiposity and psoriasis in a population-based study (UK Biobank, n = 336 806). Secondly, we performed a genome-wide by environment interaction study (GWEIS) meta-analysis examining the interaction between key measures of adiposity and psoriasis susceptibility in two large population-based studies [UK Biobank and HUNT (n = 164 753)]. Thirdly, in view of this association between human leucocyte antigen (HLA)-C*06:02 and higher adiposity levels in psoriasis, we wanted to explore whether biological differences existed between HLA-stratified subgroups. To explore this, we performed HLA-C*06:02-stratified Mendelian randomization to establish whether a difference in causal effect of adiposity on psoriasis existed between subgroups. Results We found that measures of central obesity (including impedance and dual-energy x-ray absorptiometry/magnetic resonance imaging measures) were most strongly associated with both psoriasis risk and severity. A sexual dimorphism was observed, with a stronger effect in men compared with women. Through GWEIS meta-analysis, we found a significant interaction between HLA-C*06:02-status and waist circumference on psoriasis risk (P = 3.69e−08). No significant difference in causal effect of body mass index or waist circumference on psoriasis risk were found in HLA-C*06:02-stratified subgroups. Conclusions These findings underscore the significance of central adiposity in influencing psoriasis risk. This study also emphasizes both the value and limitations of HLA-C*06:02 as a potential biomarker for distinguishing metabolically-driven psoriasis.

Vaporized nicotine in utero results in reduced birthweight, increased locomotion, and decreased voluntary exercise, dependent on sex and diet in offspring.

Rationale Clinical research has shown that prenatal exposure to nicotine may result in increased obesity risk later in life. Preclinical research has corroborated this finding, but few studies have investigated inhaled nicotine or the interaction with diet on obesity risk. Objective The aim of this study was to investigate the effects of prenatal nicotine exposure on both direct and indirect obesity measures, with both sex and diet as factors. Methods Pregnant rats were exposed to either vehicle or nicotine vapor (24mg/mL or 59mg/mL) throughout the entire gestational period. Offspring from each treatment group were given either a normal diet or a high fat diet starting at postnatal day 22. Caloric intake, body weight, spontaneous locomotion, sleep/wake activity, and voluntary exercise were measured throughout adolescence. Pregnancy weight gain and pup birthweights were collected to further measure developmental effects of prenatal nicotine exposure. Results Both maternal weight gain during pregnancy and pup weight at birth were decreased with prenatal nicotine exposure. Early adolescent males showed increased spontaneous activity in the open field following prenatal nicotine exposure compared to vehicle counterparts, particularly those given high-fat diet. Additionally, high dose nicotine prenatal treated males ran significantly less distance on the running wheel in late adolescence compared to vehicle counterparts, in the normal diet group only. Conclusion The results presented here show decreased birthweight, hyperactivity, and decreased voluntary exercise in adolescence following prenatal nicotine exposure in dose, sex, and diet dependent manners, which could lead to increased obesity risk in adulthood.

Waist-to-height ratio and body fat percentage as risk factors for ischemic cardiovascular disease: a prospective cohort study from UK Biobank

BackgroundThe independent effect of waist-to-height ratio (WHtR) and body fat percentage (BF%) on ischemic cardiovascular disease (CVD) remains uncertain. ObjectivesThis study aimed to investigate the independent associations of WHtR and BF% with ischemic CVD. MethodsThis prospective cohort study used data from the UK Biobank. BF% was calculated as fat mass divided by body weight, measured by bioimpedance. Cox models estimated hazard ratios (HRs) with 95% confidence intervals (CIs) for overall and sex-specific associations of BF% and WHtR with risks of ischemic CVD and its main subtypes [myocardial infarction (MI) and ischemic stroke (IS)], adjusted for a range of potential confounders, including mutual adjustment for BF% and WHtR. ResultsIn total, 468,333 participants without existing CVD were included in the analysis. During 12 y of follow-up, 20,151 ischemic CVD events, 13,604 MIs, and 6681 ISs were recorded. WHtR was linearly associated with ischemic CVD, MI, and IS, with an HR per 5% increase of 1.23 (95% CI: 1.20, 1.25), 1.24 (95% CI: 1.21, 1.27), and 1.22 (95% CI: 1.18, 1.26), respectively, independent of BF%. A stronger association between WHtR and MI was seen in females than in males. The association of BF% with these outcomes was substantially attenuated in both sexes after adjustment for WHtR. For example, in females, the HR (highest compared with lowest fifth) was reduced from 1.94 (95% CI: 1.76, 2.15) to 1.04 (95% CI: 0.90, 1.01) for ischemic CVD, from 2.04 (95% CI: 1.79, 2.32) to 0.97 (95% CI: 0.81, 1.16) for MI, and from 1.81 (95% CI: 1.54, 2.13) to 1.07 (95% CI: 0.85, 1.33) for IS. ConclusionsWHtR, when used as a proxy measure for central obesity, is linearly associated with ischemic CVD in both sexes, which is independent of BF%. In contrast, the relationship of BF% with these health outcomes is predominantly driven by its correlation with WHtR.

U-SHAPED ASSOCIATION OF WEIGHT-ADJUSTED-WAIST INDEX AND ARTERIAL STIFFNESS AMONG US HYPERTENSIVE PATIENTS: A POPULATION-BASED STUDY

Objective: The weight-adjusted-waist index (WWI) is an innovative measure of obesity that appears to surpass body mass index (BMI) in assessing lean body mass and fat mass. This study aimed to evaluate the relationship between WWI and arterial stiffness in hypertensive adults in the United States. Design and method: This study included 9,753 adults diagnosed with hypertension from the National Health and Nutrition Examination Survey (NHANES) spanning from 2007 to 2016. The WWI was computed by dividing waist circumference (WC) by the square root of body weight, with arterial stiffness (represented by estimated pulse wave velocity, ePWV) as the outcome. Weighted multiple linear regression and smooth curve fitting were used to test for linear and nonlinear associations. Threshold effects were determined using a two-part linear regression model. Additionally, subgroup analyses and interaction tests were conducted. Results: Among the participants included, the mean WWI was 11.32 ± 0.76. After multivariable adjustment, WWI showed a significant nonlinear association with ePWV. A U-shaped association between WWI and ePWV was observed. Specifically, WWI below the threshold (WWI &lt; 10.41) was negatively associated with arterial stiffness [β=-0.50, 95%CI:(-0.57, -0.43)], while WWI above the threshold (WWI &gt; 10.41) was positively associated with arterial stiffness [β=0.09, 95%CI:(0.07-0.11)]. Conclusions: Our study indicates a U-shaped association between WWI and arterial stiffness among hypertensive adults in the United States. However, this needs to be confirmed in large clinical trials.

The predictive ability of ABSI compared to BMI for mortality and frailty among older adults.

To study the utility of A Body Shape Index (ABSI) alongside body mass index (BMI) to predict mortality and frailty in an aging community population. Participants (n = 1,580) were drawn from the first Israeli national health and nutrition survey of older adults ("Mabat Zahav") conducted from 2005 to 2006, constituting adults aged ≥65 years. Socio-demographic, clinical, behavioral, and psychosocial data were collected. Baseline weight, height, and waist circumference (WC) were measured and expressed as the allometric indices BMI (kg/m2) and ABSI, a BMI-independent measure of abdominal obesity [WC/(BMI2/3*m1/2)]. Mortality follow-up lasted through 2019. Frailty was assessed in 2017-2019 by the Fried Biological Phenotype in a sub-cohort of 554 survivors. Cox and logistic regression models assessed associations of BMI and ABSI with mortality and frailty. At baseline, mean [SD] age was 74.5 [6.1] years, and 52.4% were women. The correlation between BMI and WC Z scores was 0.71, reduced to -0.11 for BMI and ABSI. Over a median follow-up of 13 years, 757 deaths occurred. The multivariable-adjusted hazard ratios (95% CIs) for mortality per standard deviation increase in BMI and ABSI were 1.07 (0.99;1.17) and 1.13 (1.05;1.21), respectively. Among participants assessed for frailty, 77 (14%) met the frailty criteria. After multivariable adjustment, the odds ratios (95% CIs) for frailty were 0.83 (0.69-1.01) for BMI and 1.55 (1.34-1.79) for ABSI. In a nationwide cohort of older adults, ABSI was independently associated with mortality risk. Furthermore, ABSI, but not BMI, was a strong predictor of frailty.

Anthropometric measures of obesity in patients with knee joint pathology: Body surface area versus body mass index.

Obesity is quantified using body mass index. Body surface area may provide a superior and more anthropometric method of quantifying obesity in patients with musculoskeletal knee disease. This study compares the effect of weight, height, age and gender on body mass index and body surface area in a population with orthopaedic knee disease. An observational cohort study was conducted of patients presenting with musculoskeletal knee disease. Associations between body mass index, body surface area, age, gender, height, weight and operative versus non-operative management were analysed. A total of 151 patients were included. Body surface area was more strongly correlated to weight than body mass index (r = 0.98, p < 0.001 versus r = 0.84, p < 0.001). Body surface area also reflects height which body mass index under presents (r = 0.65, p < 0.001 versus r = -0.08, p = 0.35). Body mass index and body surface area were correlated with one another (r = 0.70, p < 0.001). Age was inversely correlated with body surface area (r = -0.20, p = 0.013) but not body mass index (r = 0.05, p = 0.585). Body mass index did not differ between males and females (30.1 versus 30.9, p = 0.37); however, BSA scores were significantly higher in males than females (2.11 versus 1.91, p < 0.001). Neither body surface area nor body mass index scores influenced operative versus non-operative treatment. Body surface area could be a useful alternative to body mass index when considering obesity in patients with musculoskeletal knee pathology. Body surface area better reflects the effects of height, weight, age and gender than body mass index.

Abstract SY38-02: Clinical investigations of obesity in cancer: BMI and other confounders

Abstract SY38-02: Clinical investigations of obesity in cancer: BMI and other confounders

Is Waist to Height Ratio Better than Other Indices of Obesity in Determining Cardiovascular Risk?

Background: The indices of obesity (measured by Body Mass Index, waist circumference, and weight-to-height ratio) have been observed to be strongly associated with cardiovascular risk. Body mass index (BMI) is a measure of general obesity while waist circumference (WC) and waist-to-height ratio (WHtR) are used to measure central obesity, with the latter suggested to be the indicator for the prediction of cardiovascular risks. This study aimed to determine the advantage of WHtR for cardiovascular risk over the use of other indices of obesity. Methods: The study was a cross-sectional descriptive design carried out among 441 participants at the Metabolic Research Laboratory LTH Ogbomoso excluding pregnant or breastfeeding mothers, thyroid disease, those diagnosed with hypertension, diabetes, or hyperlipidemia, those on blood-pressure, blood-glucose or lipid-lowering medications; those on weight-control medications or supplements. A structured self-administer questionnaire was distributed to obtain socio-demographic data of participants. Physical examination was done with anthropometry measurements. Fasting blood samples were obtained for blood glucose and lipid profiles. Data analysis was done using SPSS version 21. Results: The study included 441 subjects with male to female ratio of 1:1.47 mean age of 37.92±11.80 and 34.72±12.16 respectively. Blood pressure, pulse rate, height and other obesity indices except waist circumference were all statistically significantly higher in the males than in the females p &lt;0.05. There was a statistically significant difference in the BMI between the sexes for all categories with the majority of female subjects having abnormal BMI and waist circumference. There was a statistically significant relationship between all the obesity indices (BMI, WHtR &amp; WC) and the cardiovascular risk factors excluding TG and HDLC P &lt;0.05. Conclusion: It was observed that all indices of obesity measured in this study were sensitive and significant in determining cardiovascular risk. It could be concluded that WHtR does not have a special or greater advantage over BMI and WC as all indices showed a significant association with cardiovascular risks. Also, the level of statistical significance suggested that either of these obesity indices could be used independently as a predictor of cardiovascular risk.

The synergistic effect of obesity and dyslipidemia on hypertension: results from the STEPS survey

BackgroundObesity and dyslipidemia are important risk factors for hypertension (HTN). When these two conditions coexist, they may interact in a synergistic manner and increase the risk of developing HTN and its associated complications. The aim of this study was to investigate the synergistic effect of general and central obesity with dyslipidemia on the risk of HTN.MethodData from 40,387 individuals aged 25 to 64 years were obtained from a repeated cross-sectional study examining risk factors for non-communicable diseases (STEPS) in 2007, 2011 and 2016. Body mass index (BMI) was calculated as a measure of general obesity and waist circumference (WC) as a measure of central obesity. Dyslipidemia was defined as the presence of at least one of the lipid abnormalities. Hypertension was defined as systolic blood pressure ≥ 140 mmHg or diastolic blood pressure ≥ 90 mmHg or current use of antihypertensive medication. To analyze the synergistic effect between obesity and dyslipidemia and HTN, the relative excess risk due to interaction (RERI), attributable proportion due to interaction (AP), and synergy index (SI) were calculated. A weighted logistic regression model was performed to estimate the odds ratios (ORs) for the risk of HTN.ResultsThe results showed an association between obesity, dyslipidemia and hypertension. The interaction between obesity and dyslipidemia significantly influences the risk of hypertension. In hypertensive patients, the presence of general obesity increased from 14.55% without dyslipidemia to 64.36% with dyslipidemia, while central obesity increased from 13.27 to 58.88%. This interaction is quantified by RERI and AP values of 0.15 and 0.06 for general obesity and 0.24 and 0.09 for central obesity, respectively. The corresponding SI of 1.11 and 1.16 indicate a synergistic effect. The OR also show that the risk of hypertension is increased in the presence of obesity and dyslipidemia.ConclusionObesity and dyslipidemia are risk factors for HTN. In addition, dyslipidemia with central obesity increases the risk of HTN and has a synergistic interaction effect on HTN. Therefore, the coexistence of obesity and lipid abnormalities has many clinical implications and should be appropriately monitored and evaluated in the management of HTN.

Adiponectin as a predictor of mortality and readmission in patients with community-acquired pneumonia: a prospective cohort study.

Adiponectin is secreted by adipocytes and is inversely associated with obesity. Given the association between low body mass index (BMI) and higher mortality risk after community-acquired pneumonia (CAP), we hypothesized that high adiponectin levels are associated with a higher risk of adverse clinical outcomes in patients with CAP. In a prospective cohort study of 502 patients hospitalized with CAP, adiponectin was measured in serum at admission. The associations between adiponectin and clinical outcomes were estimated with logistic regression analyses adjusted for age, sex, and measures of obesity (BMI, waist circumference or body fat percentage). Adiponectin was associated with higher 90-day mortality for each 1 μg/mL increase [OR 1.02, 95% CI (1.00, 1.04), p = 0.048] independent of age and sex. Likewise, adiponectin was associated with a higher risk of 90-day readmission for each 1 μg/mL increase [OR 1.02, 95% CI (1.01, 1.04), p = 0.007] independent of age and sex. The association between adiponectin and 90-day mortality disappeared, while the association with 90-day readmission remained after adjusting for adiposity. Adiponectin was positively associated with mortality and readmission. The association with mortality depended on low body fat, whereas the association with readmission risk was independent of obesity.