Change in Overweight from Childhood to Early Adulthood and Risk of Type 2 Diabetes

Cadwell, Joshua B.; Shukla, Alpana

doi:10.1056/nejmc1805984

Cited by 20 publications

(9 citation statements)

References 10 publications

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“…This suggests that a window of opportunity exists to mitigate the detrimental impact of early life BMI on risk of these disease outcomes 35 36 . This corroborates findings from some previous research suggesting that there is no persistent influence of childhood obesity on risk of type 2 diabetes and cardiovascular disease, unless adiposity is sustained 37 38 . Furthermore, these findings highlight the importance taking into account adult BMI in order to assess whether childhood adiposity has a direct or persistent effect on disease risk over the life course 39 40 .…”

Section: Discussionsupporting

confidence: 91%

Can the impact of childhood adiposity on disease risk be reversed? A Mendelian randomization study

Richardson

Sanderson

Elsworth

et al. 2019

Preprint

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Objective: To evaluate whether early life adiposity has an independent effect on later life disease risk or whether its influence is mediated by adulthood body mass index (BMI). Design: Two-sample univariable and multivariable Mendelian randomization. Setting: The UK Biobank (UKB) prospective cohort study and four large-scale genome-wide association study (GWAS) consortia. Participants: 453,169 participants enrolled in the UKB and a combined total of over 700,000 individuals from different GWAS consortia. Exposures: Measured BMI during adulthood (mean age: 56.5) and self-reported adiposity at age 10. Main outcome measures: Coronary artery disease (CAD), type 2 diabetes (T2D), breast cancer and prostate cancer. Results: Individuals with genetically predicted higher BMI in early life had increased odds of CAD (OR:1.49, 95% CI:1.33-1.68) and T2D (OR:2.32, 95% CI:1.76-3.05) based on univariable MR (UVMR) analyses. However, there was little evidence of a direct effect (i.e. not via adult BMI) based on multivariable MR (MVMR) estimates (CAD OR:1.02, 95% CI:0.86-1.22, T2D OR:1.16, 95% CI:0.74-1.82). In the MVMR analysis of breast cancer risk, there was strong evidence of a protective direct effect for early BMI (OR:0.59, 95% CI:0.50-0.71), although adult BMI did not appear to have a direct effect on this outcome (OR:1.08, 95% CI:0.93-1.27). Adding age of menarche as an additional exposure provided weak evidence of a total causal effect (UVMR OR:0.98, 95% CI:0.91-1.06) but strong evidence of a direct causal effect, independent of early and adult BMI (MVMR OR:0.90, 95% CI:0.85-0.95). Weak evidence of a causal effect was observed in the MVMR analysis of prostate cancer (early life BMI OR:1.06, 95% CI:0.81-1.40, adult BMI OR:0.87, 95% CI:0.70-1.08). Conclusions: Our findings suggest that increased CAD and T2D risk attributed to early life adiposity can be mitigated if individuals reduce their weight in later life. However, having a low BMI during childhood may increase risk of breast cancer regardless of changes to weight in later life, with timing of puberty also putatively playing an important role.

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Section: Discussionsupporting

confidence: 91%

Can the impact of childhood adiposity on disease risk be reversed? A Mendelian randomization study

Richardson

Sanderson

Elsworth

et al. 2019

Preprint

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“…1 This disease affects millions of people and has an incidence of approximately 13% of the adult population worldwide. 28 Obesity is associated with a high risk of some chronic diseases, including type 2 diabetes, 29 hyperlipemia and non-alcoholic fatty liver disease (NAFLD), 30,31 posing a significant threat to human health. Despite the enormous efforts that have been made so far, current pharmacological approaches to morbid obesity are fairly limited.…”

Section: Discussionmentioning

confidence: 99%

Alisol A attenuates high‐fat‐diet‐induced obesity and metabolic disorders via the AMPK/ACC/SREBP‐1c pathway

Gao

Zheng

et al. 2019

J Cellular Molecular Medi

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Obesity and its associated metabolic disorders such as diabetes, hepatic steatosis and chronic heart diseases are affecting billions of individuals. However there is no satisfactory drug to treat such diseases. In this study, we found that alisol A, a major active triterpene isolated from the Chinese traditional medicine Rhizoma Alismatis, could significantly attenuate high‐fat‐diet‐induced obesity. Our biochemical detection demonstrated that alisol A remarkably decreased lipid levels, alleviated glucose metabolism disorders and insulin resistance in high‐fat‐diet‐induced obese mice. We also found that alisol A reduced hepatic steatosis and improved liver function in the obese mice model.In addition, protein expression investigation revealed that alisol A had an active effect on AMPK/ACC/SREBP‐1c pathway. As suggested by the molecular docking study, such bioactivity of alisol A may result from its selective binding to the catalytic region of AMPK.Therefore, we believe that Alisol A could serve as a promising agent for treatment of obesity and its related metabolic diseases.

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“…6,8,10,11 Further, early postnatal factors such as breastfeeding pattern and formula feeding, introduction of solid foods, activity or inactivity level, and also sleeping behaviour and exposure to antibiotics are currently discussed to modify the infant's obesity risk in the short-and long-term. 7,12,13 Due to the potential to reverse health consequences of childhood obesity if weight normalisation is achieved by puberty, 14 identifying effective early-life strategies that tackle modifiable risk factors are urgently needed. Within the last decade, several randomised controlled trials have been initiated primarily with the aim to improve maternal health outcomes during pregnancy and postpartum.…”

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confidence: 99%

Infant growth during the first year of life following a pregnancy lifestyle intervention in routine care—Findings from the cluster‐randomisedGeliStrial

et al. 2020

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SummaryBackgroundLifestyle interventions in pregnancy may influence postpartum development and obesity risk in offspring. The impact of lifestyle interventions as health system‐based approaches is unclear.ObjectiveTo evaluate the effect of an antenatal lifestyle intervention conducted as public health approach on infant development and feeding practices.MethodsWe followed offspring born to women participating in the cluster‐randomised GeliS trial who received usual care (CG) or repeated lifestyle counselling (IG). We collected data on offspring development and complementary feeding until the 12thmonth postpartum.ResultsOf the 1998 mother‐child pairs, 1783 completed the follow‐up. Mean infant weight at 12 months was comparable between groups (IG: 9497.9 ± 1137.0 g; CG: 9433.4 ± 1055.2 g;P= .177). There was no significant evidence of differences in sex‐ and age‐adjusted z‐scores or in the odds of offspring being overweight. More infants in the IG received whole‐grain products compared to the CG (95.6%vs. 90.8%;P= .003). Despite small differences in the timing of introducing solid foods, there were no further significant differences in the pattern of complementary feeding.ConclusionsThe antenatal lifestyle intervention embedded in routine care did not substantially influence infant anthropometrics and is thus unlikely to impact future development.

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Change in Overweight from Childhood to Early Adulthood and Risk of Type 2 Diabetes

Cited by 20 publications

References 10 publications

Can the impact of childhood adiposity on disease risk be reversed? A Mendelian randomization study

Can the impact of childhood adiposity on disease risk be reversed? A Mendelian randomization study

Alisol A attenuates high‐fat‐diet‐induced obesity and metabolic disorders via the AMPK/ACC/SREBP‐1c pathway

Infant growth during the first year of life following a pregnancy lifestyle intervention in routine care—Findings from the cluster‐randomisedGeliStrial

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