The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) has increased. MASLD notably increases after menopause in women owing to the drastic reduction in estrogen, which regulates lipid metabolism. While prenatal undernutrition leads to hepatic steatosis after birth, whether prenatal undernutrition affects the onset of postmenopausal MASLD remains unknown. Therefore, we examined the impact of early prenatal undernutrition on the predisposition to postmenopausal MASLD in a rat model of menopause. Pregnant female rats were assigned to the control (CNTL) group, while the undernourished (UN) group was fed 40% of the diet of the control group. Furthermore, both groups were assigned to the ovariectomized (CNTL-OVX/UN-OVX) and sham-operated (CNTL-Sham/UN-Sham) groups at 12 weeks of age. Two-way analysis of variance revealed significant main effects of ovariectomy and prenatal undernutrition on body weight and hepatic triglyceride content. Triglycerides accumulated in the liver at 12 and 24 weeks after ovariectomy, while hepatic steatosis was histologically observed at 24 weeks after ovariectomy in UN-OVX rats. Hepatic gene expression analyses showed an interaction effect between prenatal undernutrition × ovariectomy in ESR1 expression; however, PPARα, RXRα, RARα, Raldh1, and Raldh3 expression was not affected by prenatal undernutrition and ovariectomy. These results suggest that early prenatal undernutrition predisposes postmenopausal women to MASLD by uncovering aberrant estrogen signaling, which may be influenced by estrogen reduction.

We examined how BMI, BMI trajectories, and BMI fluctuation around these trajectories in adolescence were correlated with BMI trajectories and BMI fluctuation in early adulthood, as well as the genetic basis of these associations. BMI data from Finnish twins (N = 1379, 48% males) were collected at ages 11.5, 14, 17.5, 24, and 37 years. BMI trajectories in adolescence (11.5–17.5 years) and early adulthood (17.5–37 years) were estimated using linear mixed-effect models. BMI fluctuation was calculated as the average squared differences between observed and expected BMI around these trajectories. Genetic twin models and a polygenic risk score for BMI (PRSBMI) were used to assess genetic contributions to BMI fluctuation and its associations with BMI and BMI trajectories. Adolescent BMI fluctuation was positively correlated with early adulthood BMI trajectories in females, while in males, adolescent BMI trajectories were positively associated with BMI fluctuation in early adulthood. Genetic factors affected BMI fluctuation in both adolescence and early adulthood when estimated using twin modelling and PRSBMI. Adolescent BMI was positively associated with early adulthood fluctuation in both sexes, with genetic factors playing a role (genetic correlations .08–.29). It was concluded that genetic factors play a significant role in BMI fluctuations in adolescence and early adulthood, with some overlap with the genetics of BMI.

Regular physical activity for adults is associated with optimal appetite regulation, though little work has been performed in adolescents. To address this gap in the literature, we conducted a study examining appetite across a range of physical activity and adiposity levels in adolescent males. Healthy males (N=46, 14-18 years old) were recruited across four body weight and activity categories: normal weight/high active (n=11), normal weight/low active (n=13), overweight, obese/high active (n=14), overweight, obese/low active (n=8). Participants from each group completed a six-hour appetite assessment session on Day 0, followed immediately by a 14-day free-living physical activity and dietary assessment period on Days 1-14, and a fitness test session occurring between Days 15-18. Subjective and objective assessment of appetite, resting energy expenditure, body composition using dual energy absorptiometry‘, and thermic effect of feeding was conducted on Day 0. Physiological variables in the normal weight low active group that were different than their peers included lower fat-free mass, cardiorespiratory fitness, glucose/fullness response to a standardized meal, thermic effect of feeding in response to a standardized meal, lower self-rated fullness and satiety, and higher self-rated hunger to a standardized meal. Conversely, the overweight, obese high active group displayed better subjective appetite responses, but higher insulin responses to a standardized meal. Taken together, these results suggest that physical inactivity during adolescence has a negative impact on metabolic health and appetite control which may contribute to future weight gain.

An integrative approach addressing diet and other lifestyle factors is warranted in studying obesity and its related diseases. The objective of this study is to examine the associations of lifestyle patterns with overweight/obesity among children in the United Arab Emirates. Data were derived from a cross-sectional survey of children aged 4–9 years living in Dubai, Sharjah and Abu Dhabi (n 426). Dietary intake was collected using a 24-h dietary recall and evaluated with the Healthy Eating Index. The Youth Physical Activity Questionnaire assessed physical activity, while other lifestyle factors included the presence of a live-in household helper, number of electronic devices in the child’s bedroom, eating while watching TV, family dinner frequency, fast-food and breakfast consumption and hours of sleep. Factor analysis was used to identify the lifestyle patterns. Two lifestyle patterns emerged: an unhealthy pattern marked by higher fast-food intake, eating while watching TV, having a live-in household helper and lower family dinners and a healthy pattern with higher physical activity, better Healthy Eating Index, more sleep, micronutrient supplements and breakfast consumption. The healthy lifestyle pattern was linked to a 30 % reduction in overweight/obesity odds (OR = 0·7, 95 % CI: 0·53, 0·93). A healthy lifestyle pattern, characterised by higher physical activity, better dietary quality, adequate sleep and breakfast consumption, is associated with lower odds of overweight/obesity among children in the United Arab Emirates. These findings highlight the importance of promoting comprehensive lifestyle interventions to effectively address childhood obesity in this population.

High BMI is an important risk factor for female colon and rectal, ovarian and uterine cancers. Current comprehensive studies on its effects on these cancers are limited. This paper aims to explore regional and age differences in the impact of high BMI on these cancers and the commonalities among the three by using the Global Burden of Disease 2021. Deaths, disability-adjusted life years and their age-standardised rates for these cancers were retrieved from 1990 to 2021, and burden trends were assessed using the estimated annual percentage change and percentage changes. The study also analysed the correlation between age-standardised rate and socio-demographic index across twenty-one regions and projected future disease burden trends using the Bayesian Age-Period-Cohort model. Results showed that the global burden of female colon and rectal cancer declined since 1990 but remained at the highest level among the three cancers in 2021. At the same time, these three cancers had high burdens in high-income areas. Since 1990, ovarian and uterine cancer burdens attributable to high BMI increased, and all three burdens grew fastest in low-middle-income regions and among younger people. The burden of all three is projected to continue increasing through 2050. This study confirms that high BMI’s impact on these cancers is regional and age-specific, with long-term effects. Therefore, subsequent public health interventions should adopt more targeted obesity prevention and control strategies based on national and regional situations to effectively mitigate the adverse effects of high BMI on these cancers.

In Aotearoa New Zealand, approximately 1 in 3 adults and 1 in 8 children are classified as obese, with Māori and Pacific communities disproportionately affected(1). While maternal nutrition has been extensively studied, paternal impacts and the combined effect of both parents’ obesogenic environments on offspring health remain underexplored(2). The primary objective of this study is to characterise the metabolic phenotype of parent rats fed a High Fat High Sugar (HFHS) diet and investigate the birth characteristics of their offspring, from a factorial mating design.Eighty female and 40 male Sprague-Dawley rats were randomised to a standard chow diet (SD) (24% protein, 18% fat, 58% carbohydrates) or HFHS diet (Specialty Feeds SF23-120: 16% protein, 41% fat, 43% carbohydrates) for five weeks prior to mating. Females were then continued on their respective diets throughout pregnancy and lactation. Four mating combinations were established: SDmum-SDdad, SDmum-HFHSdad, HFHSmum-SDdad, and HFHSmum-HFHSdad. A subset of parents (n=38) underwent body composition assessments using dual-energy X-ray absorptiometry (DEXA). Additionally, a subgroup (n=23) was evaluated for metabolic profiles using Prometheon metabolic cages. Offspring birth weights and body lengths were recorded. The HFHS diet’s efficacy was confirmed in both male and female rats, with HFHS groups showing higher body weight (females: 327.1 g ± 19.7 vs. 288.2 g ± 20.1; males: 575.8 g ± 39.8 vs. 532.6 g ± 50.3; p < 0.05), greater fat percentage (females: 46.8% ± 5.6 vs. 29.2% ± 5.6; males: 40.5% ± 7.2 vs. 28.7% ± 6.8; p < 0.001), and a lower respiratory exchange ratio (RER) (females: 0.8108 ± 0.0275 vs. 0.8679 ± 0.0288; males: 0.8257 ± 0.0304 vs. 0.8759 ± 0.0266; p < 0.05) compared to the SD group. In male offspring, birth weights in HFHSmum-SDdad (6.3 g ± 0.9) and HFHSmum-HFHSdad (6.0 g ± 0.9) groups were significantly lower (p < 0.0001) than in SDmum-SDdad (6.980 g ± 0.7753) and SDmum-HFHSdad (7.0 g ± 0.7) groups. Birth weights were further reduced in HFHSmum-HFHSdad versus HFHSmum-SDdad (Mean Diff. = 0.3g; p < 0.05).Body lengths in HFHSmum-HFHSdad males were shorter (43.1 mm ± 3.2; p < 0.0001) compared to other groups (≥ 45.3 mm). Female offspring birth weights were lower in the HFHSmum-SDdad (5.8g ± 0.8) and HFHSmum-HFHSdad groups (5.8 g ± 0.9; p<0.0001) compared to the other groups (means ≥ 6.4g) but paternal HFHS diet had no additional effect on birth weight. As with males, body lengths in the HFHSmum-HFHSdad female offspring were significantly shorter (4 mm ± 3; p<0.0001) compared to all other groups (≥44mm). Parental HFHS diets synergistically reduce offspring birth length and weight, with stronger effects in males. These findings underscore the importance of inclusive dietary guidelines for both parents to reduce intergenerational obesity risk and support long-term health.

A Rank Forum was convened to discuss the evidence around food insecurity (FIS), its impact on health, and interventions which could make a difference both at individual and societal level, with a focus on the UK. This paper summarises the proceedings and recommendations. Speakers highlighted the growing issue of FIS due to current economic and social pressures. The health implications of FIS vary geographically since food insecure women in higher income regions tend to be living with overweight or obesity, in contrast to those living in low-to-middle-income countries. This paradox could be due to stress and/or metabolic or behavioural responses to an unpredictable food supply. The gut microbiota may play a role given the negative effects of low fibre diets on bacterial diversity. Solutions to FIS involve individual behavioural change, targeted services and societal/policy change. Obesity-related services are currently difficult to access. Whilst poverty is the root cause of FIS, it cannot be solved solely by making healthy food cheaper due to ingrained beliefs, attitudes and behaviours in target groups. Person-centred models, such as Capability-Opportunity-Motivation Behavioural Change Techniques and Elicit-Provide-Elicit communication techniques, are recommended. Societal change or improved resilience through psychological support may be more equitable ways to address FIS. They can combine with fiscal or food environment policies to shift purchasing towards healthier foods. Policy implementation can be slow to enact due to the need for strong evidence, consultation and political will. Eradicating FIS must involve co-creation of interventions and policies to ensure a consensus on solutions.

Kombucha is a fermented beverage rich in bioactive compounds. This beverage has demonstrated high antioxidant capacity in vitro and experimental animal studies. In this sense, this study aimed to evaluate the effect of daily consumption of green tea kombucha on oxidative stress and endothelial health in individuals with excess body weight. This is a randomized controlled clinical trial, lasting 10 weeks, during which the control group followed a healthy −500 kcal/d energy-restricted diet. In contrast, the kombucha group, in addition to the energy-restricted diet, consumed 200 ml of kombucha green tea daily. This study included men and women aged 18–45 years without chronic diseases. At the beginning and end of the study, fasting blood was collected, and colorimetric assays and immunoassay protocols evaluated markers of oxidative stress and endothelial health. Compared to the control group, kombucha consumption significantly reduced hydrogen peroxide (H2O2) levels (P = 0·007). Initial and final values were as follows: Control group (16·5 v. 15·09 µmol/ml; n 29) and Kombucha group (18·14 v. 14·67 µmol/ml; n 30). The other markers that were evaluated did not change after the kombucha consumption. In conclusion, daily consumption of 200 ml of green tea kombucha for 10 weeks reduces one pro-oxidant marker, without altering other markers of oxidative stress and endothelial health in individuals with excess body weight. Reducing a pro-oxidant marker suggests that kombucha is an antioxidant beverage with promising implications for human health. However, further studies are needed to elucidate other possible beneficial effects on health.

Food insecurity (FIS) is a critical public health issue, particularly among older adults. This study investigates the association between FIS with diet quality and anthropometric indices in the US older adults. A cross-sectional analysis was conducted using NHANES data from 2017 to 2020, involving 2592 participants aged ≥ 60 years. FIS was assessed using the USDA Household Food Security Survey Module. Diet quality was assessed using the Healthy Eating Index (HEI)-2020 and adherence to Mediterranean diet (MedDiet) score. Anthropometric measures were calculated following standardised protocols. Multivariable logistic regression models, adjusted for demographic, socio-economic and behavioural factors examined the association between FIS and the higher quartile and tertile of anthropometric and diet quality indices, respectively. Of the participants, 27·4 % experienced FIS. FIS participants were younger and had lower education and income levels compared with FS individuals (P < 0·05). In the adjusted model, FIS was associated with lower adherence to both the Mediterranean Diet (OR: 0·48, 95 % CI: 0·31, 0·67) and HEI-2020 (OR: 0·61, 95 % CI: 0·37, 0·84), indicating poorer diet quality in older adults. In adjusted analyses, FIS was significantly associated with higher A Body Shape Index quartiles (Q3: OR: 1·44, 95 % CI: 1·06, 1·95; Q4: OR: 1·46, 95 % CI: 1·07, 2·01), the waist-to-hip ratio (Q4: OR: 1·44, 95 % CI: 1·01, 2·06) and the Conicity index (Q4: OR: 1·36, 95 % CI: 1·02, 1·81). FIS in older adults is associated with unfavourable diet quality and body composition patterns, particularly central obesity measures. Addressing FIS may mitigate health risks related to obesity and its complications.

Metabolic syndrome (MetS) is associated with deteriorated mental health and health-related quality of life (HRQOL). Curcumin and probiotics improved MetS, mental health and HRQOL. The present study aimed to investigate the effect of curcumin-probiotic (CurPro) co-supplementation in the form of drink powder on mental health and HRQOL in adults with overweight/obesity and MetS. A four-arm, randomised, double-blinded, placebo-controlled clinical trial with factorial design was conducted for adults with overweight/obesity and MetS (n 128). Participants were randomly allocated into four groups to receive one drink powder sachet containing 1 g curcumin, 109 colony-forming unit (CFU) probiotic (Lactobacillus acidophilus and Lactobacillus rhamnosus strains), CurPro (1 g curcumin and 109 CFU probiotic) or placebo along with a low-calorie diet. Participants were assessed for dietary intake, physical activity, mental health and HRQOL before and after the study. After 8 weeks of intervention, 104 participants finished the study. The CurPro intervention reduced stress (P = 0·001) and anxiety (P = 0·019) and improved general health (P = 0·024) and overall HRQOL (P = 0·011) scores of participants in comparison with the Placebo group. Results were NS for depression and HRQOL subdomains such as physical functioning, role limitations due to physical problems, bodily pain, vitality, social functioning and role limitations due to emotional problems. Curcumin-probiotics co-supplementation could improve the mental health and HRQOL of adults with overweight/obesity and MetS. Further investigations in various populations or with different dosages or durations are recommended.

Curcumin, a natural bioactive compound, is known to exert therapeutic effects on cancer and dysplasia. However, less is known about its effects on DNA damage and repair in obesity. Therefore, this study was to examine the novel role of curcumin in regulating DNA repair signalling using a high-fat diet (HFD)-induced obesity in mice. Male C57BL/6 mice were fed either a 60 % HFD or standard chow with curcumin (2·5 g/kg diet) for 8 weeks. We observed that curcumin alleviated weight gain, preserved glucose balance and enhanced liver fat accumulation and lipid profile in mice with obesity induced by an HFD. Curcumin enhanced the adipocyte-derived mesenchymal stem cell (ADMSC) population (Sca-1 + CD45-) and expression of phosphorylated checkpoint kinase1 (pCHK1), a DNA repair gene, in adipocytes isolated from adipose tissues of HFD-induced obesity in mice. Moreover, in human preadipocytes, treatment with 10 μM curcumin effectively reduced the mRNA levels of IL6 and CCL2 in a dose-dependent manner, while treatment with 100 μM H2O2 together with curcumin upregulated the levels of pCHK2 and total CHK2 protein and reduced level of γH2AX, a biomarker of DNA damage. In addition, curcumin inhibits preadipocyte-to-adipocyte differentiation. In conclusion, our data demonstrated that curcumin reduced the pro-inflammatory response and DNA damage in adipocytes, controlling weight gain in mice with HFD-induced obesity.