How much do we know about the heritability of BMI?

Feng, Rui

doi:10.3945/ajcn.116.139451

Cited by 9 publications

(5 citation statements)

References 9 publications

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“…Obesity may specifically promote leukemogenesis via several mechanisms, including altered adipokine secretion ( 68 ), decreased circulating adiponectin ( 72 ), and increased leptin bioavailability ( 73 , 74 ). Additionally, as obesity heritability is estimated to be 0.85-0.9 ( 75 , 76 ), obese mothers are more likely to have obese children, thus increasing leukemogenesis risk; however, with our data, there was no way to determine leukemia risk attributable to obesity genomics. These mechanisms may not just apply to obese persons individually, but may confer obesity-associated risk to infants during gestation.…”

Section: Discussionmentioning

confidence: 56%

Maternal Body Mass Index, Diabetes, and Gestational Weight Gain and Risk for Pediatric Cancer in Offspring: A Systematic Review and Meta-Analysis

Marley

Domingues

Ghosh

et al. 2022

JNCI Cancer Spectrum

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Background Pediatric cancer incidence has steadily increased concurrent with rising adult obesity, but associations between maternal obesity and associated comorbidities and pediatric cancer risk remain understudied. We aimed to quantitatively characterize associations of pediatric cancer risk with maternal pre-pregnancy BMI, gestational weight gain, and maternal diabetes. Methods We performed a comprehensive and systematic literature search in Ovid and EMBASE from their inception to March 15th, 2021. Eligible studies reported risk estimates, sample sizes, and provided sufficient description of outcome and exposure ascertainment. Random-effects models were used to estimate pooled effects. Results Thirty-four studies were included in the analysis. Pre-pregnancy BMI was positively associated with leukemia risk in offspring (OR per 5-unit BMI increase =1.07 [95% CI = 1.04–1.11] I2 = 0.0%). Any maternal diabetes was positively associated with acute lymphoblastic leukemia (ALL) risk (OR = 1.46 [95% CI = 1.28–1.67] I2 = 0.0%), even after restricting to birthweight-adjusted analyses (OR = 1.74 [95% CI 1.29–2.34] I2 = 0.0%), and inversely associated with risk of central nervous system tumors (OR = 0.73 [95% CI = 0.55–0.97] I2 = 0.0%). Pre-gestational diabetes (OR = 1.57 [95% CI = 1.11–2.24] I2 = 26.8%) and gestational diabetes (OR = 1.40 [95% CI = 1.12–1.75] I2 = 0.0%) were also positively associated with ALL risk. No statistically significant associations were observed for gestational weight gain. Conclusions Maternal obesity and diabetes may be etiologically linked to pediatric cancer, particularly leukemia and central nervous system tumors. Our findings support weight management and glycemic control as important components of maternal and offspring health. Further validation is warranted.

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Section: Discussionmentioning

confidence: 56%

Maternal Body Mass Index, Diabetes, and Gestational Weight Gain and Risk for Pediatric Cancer in Offspring: A Systematic Review and Meta-Analysis

Marley

Domingues

Ghosh

et al. 2022

JNCI Cancer Spectrum

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“…When studying disease etiology, using genetic risk scores as a proxy for disease susceptibility in a healthy population is one way to overcome the effect of confounding factors common in clinical cohorts (Palmos et al, 2018). Genetic factors play a significant role in determining risk for MDD and adulthood BMI, with studies reporting heritability estimates of around 40-50% and 41-85% respectively (Feng, 2016;Lohoff, 2010). MDD and BMI are both considered to be highly polygenic, meaning that many risk variants of small effect size confer genetic risk.…”

Section: Introductionmentioning

confidence: 99%

Reconsidering the reasons for heightened inflammation in major depressive disorder

Palmos

Chung

Frissa

et al. 2021

Journal of Affective Disorders

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“…However, these loci only account for a few percent of variation in BMI [ 4 ]. The explained heritability is thought to be low due to a strong effect of environment and lifestyle on BMI [ 5 ]. This strong environmental effect is thought to be the “obesogenic” environment, i.e.…”

Section: Introductionmentioning

confidence: 99%

An epigenome-wide association study in whole blood of measures of adiposity among Ghanaians: the RODAM study

et al. 2017

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BackgroundEpigenome-wide association studies (EWAS) have identified DNA methylation loci involved in adiposity. However, EWAS on adiposity in sub-Saharan Africans are lacking despite the high burden of adiposity among African populations. We undertook an EWAS for anthropometric indices of adiposity among Ghanaians aiming to identify DNA methylation loci that are significantly associated.MethodsThe Illumina 450k DNA methylation array was used to profile DNA methylation in whole blood samples of 547 Ghanaians from the Research on Obesity and Diabetes among African Migrants (RODAM) study. Differentially methylated positions (DMPs) and differentially methylation regions (DMRs) were identified for BMI and obesity (BMI ≥ 30 kg/m2), as well as for waist circumference (WC) and abdominal obesity (WC ≥ 102 cm in men, ≥88 cm in women). All analyses were adjusted for age, sex, blood cell distribution estimates, technical covariates, recruitment site and population stratification. We also did a replication study of previously reported EWAS loci for anthropometric indices in other populations.ResultsWe identified 18 DMPs for BMI and 23 for WC. For obesity and abdominal obesity, we identified three and one DMP, respectively. Fourteen DMPs overlapped between BMI and WC. DMP cg00574958 annotated to gene CPT1A was the only DMP associated with all outcomes analysed, attributing to 6.1 and 5.6% of variance in obesity and abdominal obesity, respectively. DMP cg07839457 (NLRC5) and cg20399616 (BCAT1) were significantly associated with BMI, obesity and with WC and had not been reported by previous EWAS on adiposity.ConclusionsThis first EWAS for adiposity in Africans identified three epigenome-wide significant loci (CPT1A, NLRC5 and BCAT1) for both general adiposity and abdominal adiposity. The findings are a first step in understanding the role of DNA methylation in adiposity among sub-Saharan Africans. Studies on other sub-Saharan African populations as well as translational studies are needed to determine the role of these DNA methylation variants in the high burden of adiposity among sub-Saharan Africans.Electronic supplementary materialThe online version of this article (10.1186/s13148-017-0403-x) contains supplementary material, which is available to authorized users.

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How much do we know about the heritability of BMI?

Cited by 9 publications

References 9 publications

Maternal Body Mass Index, Diabetes, and Gestational Weight Gain and Risk for Pediatric Cancer in Offspring: A Systematic Review and Meta-Analysis

Maternal Body Mass Index, Diabetes, and Gestational Weight Gain and Risk for Pediatric Cancer in Offspring: A Systematic Review and Meta-Analysis

Reconsidering the reasons for heightened inflammation in major depressive disorder

An epigenome-wide association study in whole blood of measures of adiposity among Ghanaians: the RODAM study

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