This study aimed to investigate the associations of body roundness index (BRI) with cardiometabolic disease (CMD), cardiometabolic multimorbidity (CMM), and all-cause mortality, while evaluating its impact across different stages of CMM progression.
In this prospective cohort study, 87,902 participants from the Kailuan cohort were categorized into BRI quartiles. Cox models estimated hazard ratios (HRs) and 95% CIs for the first occurrence of cardiometabolic disease (FCMD), CMM, and mortality. Multistate models assessed BRI's role across CMM progression.
Over a median follow-up of 13.68 years, 21,636 participants developed FCMD, 2114 developed CMM, and 14,782 died. Elevated BRI increased risks of FCMD, CMM, and mortality in Cox models. Multistate analysis revealed differential BRI effects across CMM progression: participants in the highest versus lowest BRI quartile showed HRs of 2.08 (1.99–2.17) for healthy-to-FCMD transition, 1.61 (1.38–1.88) for FCMD-to-CMM transition, and 1.09 (1.03–1.16), 0.99 (0.89–1.10), and 0.73 (0.54–0.99) for mortality from the healthy state, FCMD, and CMM, respectively. BRI's impact varied by disease type (diabetes mellitus, myocardial infarction, stroke) and sex, with stronger associations in females.
Our findings emphasize dynamic BRI monitoring as a biomarker for early CMM risk identification and prognostic assessment, necessitating disease- and sex-specific prevention strategies.
Access to only high-fat diet (HFD) during the light versus dark cycle promotes different metabolic outcomes. We assessed changes in body weight/composition, feeding behavior, and metabolic parameters in mice fed HFD during the light or dark cycle with concomitant ad libitum access to chow.
Male C57BL/6J mice were housed in metabolic chambers with two hoppers containing chow. HFD was then provided in one hopper, with access restricted to the light or dark cycle. The other hopper provided ad libitum access to chow. Food intake, meal patterns, energy expenditure, activity, and substrate oxidation were measured for ~4 weeks. Body weight/composition was measured before and after ~4-week HFD access.
Light cycle HFD access promoted greater weight and fat mass gain. Although daily caloric intake was equivalent between groups, light cycle HFD access increased preference for HFD and intake of larger, more frequent HFD meals during the daytime. Dark cycle HFD access promoted preference for chow and consumption of larger, more frequent chow meals.
Light cycle HFD access parallels detrimental metabolic outcomes of ad libitum HFD access. Dark cycle HFD access reduces weight gain and adiposity; this is associated with enhanced chow preference.
Incretin-based obesity medication maintains weight loss by mimicking the appetite-inhibiting hormone GLP-1. Interestingly, chronic exercise may improve postprandial appetite control by increasing late postprandial secretion of endogenous GLP-1. Therefore, we investigated whether an exercise program after weight loss could increase late-phase postprandial GLP-1 secretion.
This study is an exploratory analysis of adults with obesity (n = 195) who lost 13.1 kg on a low-calorie diet and were randomized to 52 weeks of either usual activity, moderate-to-vigorous intensity exercise, the GLP-1 receptor agonist liraglutide (3.0 mg/day), or the combination. The primary endpoint was change in late-phase GLP-1 response to a 3-h liquid mixed meal test before and after diet-induced weight loss and after 1 year of intervention.
Diet-induced weight loss did not change late-phase GLP-1 response (3%; 95% CI, −4%–10%). One year of exercise increased late-phase postprandial GLP-1 response within the group by 37% (95% CI, 20%–57%), and this increase was 25% greater (95% CI, 3%–51%, p = 0.02) compared to the usual activity group. Late-phase postprandial GLP-1 response was unchanged in both groups treated with GLP-1 receptor agonist compared to placebo.
One year of exercise increased late-phase postprandial GLP-1 response, which may prevent increased appetite after weight loss and thereby weight regain.
EudraCT number: 2015–005585-32; ClinicalTrials.gov identifier: NCT04122716
This study aimed to evaluate associations of maternal prepregnancy BMI with offspring BMI and blood pressure in childhood, specifically for infants born preterm.
In this observational cohort study of children in the Environmental Influences on Child Health Outcomes (ECHO) Cohort, we utilized four levels of maternal prepregnancy BMI and child BMI. Children were categorized as being born extremely, very, or moderately preterm; late preterm; or term.
In total, 13,810 children from 44 ECHO cohorts were included in these analyses. After adjusting for maternal education, maternal age at delivery, and singleton birth, a monotonic dose relationship was noted between child BMI z-scores and maternal prepregnancy BMI level. For child blood pressure outcomes, only extremely preterm children born to mothers with healthy weight and obesity and very/moderately preterm children born to mothers with healthy weight had higher odds of elevated blood pressure/hypertension compared with their term counterparts.
High maternal prepregnancy BMI was associated with a stepwise increase in offspring BMI in childhood. Preterm children had a higher probability of elevated blood pressure/hypertension than term children. These findings highlight a possible window of opportunity to modify lifestyles and behavior of at-risk children prior to adolescence to positively impact adolescent cardiometabolic health.
This study aimed to evaluate the early effects of a comprehensive redevelopment of a low-income, minority community on adult obesity.
We analyzed longitudinal data on a cohort of public housing residents from Jordan Downs (JD), the community undergoing redevelopment, and a comparison group in Watts, Los Angeles, California. Difference-in-difference models with individual fixed effects were estimated on a sample of 421 adults comparing changes in BMI and waist circumference for JD versus comparison group residents between baseline (2018–2019) and follow-up (2021–2022). Quasi-experimental variation in redevelopment exposure was used to assess dose–response relationships. Secondary outcomes included diet and physical activity barriers and behaviors.
There were no significant differences in BMI or waist circumference changes between JD residents (n = 279) and the comparison group (n = 149) overall. Within JD, those who moved to redeveloped areas (n = 75) experienced a 2.2% larger reduction in waist circumference (95% CI: −0.05 to −0.003) and a 10.6 percentage point (95% CI: −0.20 to −0.02) greater decline in abdominal obesity, relative to the comparison group. They reported greater declines in barriers to healthy eating and exercise, along with reduced added sugar intake, but no differential changes in BMI, obesity, physical activity, or diet quality.
Redeveloping low-income communities can reduce abdominal obesity.
This study aimed to optimize weight loss outcomes in an online behavioral obesity treatment program by evaluating the effects of five novel intervention components using a factorial experiment informed by the multiphase optimization strategy framework.
A randomized factorial experiment tested 12-month weight loss resulting from an established online obesity treatment program with randomization to zero to five novel intervention components (interactive video feedback, tailored intervention to promote physical activity, skills for dysregulated eating, virtual reality skills training, and social support with friendly competition).
Adults (N = 384; 83% female, 12% male, 5% another sex/gender or did not disclose; 23% racial and/or ethnic minority) with (mean ± SD) age of 53.5 ± 11.7 years and BMI of 35.0 ± 6.1 kg/m2 were randomized. No intervention component independently improved weight loss (p values > 0.199). Interaction terms (p values < 0.01) suggest the combination of interactive video feedback, skills for dysregulated eating, and social support with friendly competition improved weight loss. Mediation analysis indicated that social support and dysregulated eating interventions influenced weight loss outcomes through improvements in social support for physical activity and dietary quality.
This study identified a combination of intervention components that may improve weight loss outcomes compared to the established online treatment program.
Trial Registration: ClinicalTrials.gov identifier NCT04520256.
This study aimed to evaluate the weight loss efficacy of semaglutide initiated 6 months after laparoscopic sleeve gastrectomy (LSG).
This retrospective study included patients undergoing primary LSG. Patients receiving semaglutide (1.0 mg weekly) at 6 months post LSG for 6 months were matched 1:3 with controls not receiving semaglutide, balancing demographics, preoperative BMI, waist–hip ratio, comorbidities, and total weight loss (TWL) at 6 months post surgery. Primary outcomes were absolute and percentage weight loss from 6 to 12 months post LSG.
Both the treatment (n = 34) and control (n = 102) groups achieved substantial TWL (23.16% ± 6.50% vs. 23.53% ± 4.87%) at 6 months post LSG. From 6 to 12 months, the treatment group experienced significantly greater absolute (14.03 ± 5.26 kg vs. 5.63 ± 6.25 kg; p < 0.0001) and percentage (12.61% ± 4.11% vs. 4.84% ± 5.18%; p < 0.0001) weight loss than controls. At 12 months, TWL was also higher in the treatment group (35.77% ± 8.35% vs. 28.37% ± 7.41%; p < 0.0001).
Semaglutide initiated 6 months post LSG significantly enhances short-term postoperative weight loss, even among patients who have already achieved substantial initial weight loss. These findings suggest its potential as an effective adjunct therapy for optimizing weight management in early postoperative care.
We investigated the associations of grandmaternal early pregnancy BMI with grand-offspring risks of birth asphyxia-related complications.
In a nationwide three-generation Swedish cohort, we estimated adjusted relative risks (RRs) of Apgar score 0–3 at 5 min and neonatal seizures for categories of grandmaternal BMI among 315,461 maternal and 203,522 paternal singleton live-born grand-offspring. To address unmeasured confounding by shared familial factors, we used the parental full sisters' BMI as a negative control exposure. In the maternal line, we assessed whether associations with grandmaternal obesity were mediated through maternal obesity.
Compared with normal maternal grandmaternal BMI, RRs (95% CI) of low Apgar score were, respectively, 1.29 (1.06, 1.57) and 1.53 (1.03, 2.28) for overweight (BMI 25.0 to 29.9) and obesity (BMI ≥ 30.0). For neonatal seizures, the corresponding RRs (95% CI) were 1.32 (1.05, 1.66) and 1.81 (1.17, 2.79). Maternal sisters' BMI was unrelated to both outcomes. Maternal obesity mediated < 25% of the associations with maternal grandmaternal obesity. Paternal grandmaternal obesity was related to an increased risk of neonatal seizures; paternal sisters' BMI was unrelated to this outcome.
Grandmaternal overweight and obesity are related to increased risks of severe birth asphyxia-related complications in grand-offspring, independent of unmeasured shared familial factors.
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