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Birth weight modifies the association between central nervous system gene variation and adult body mass index.

ABSTRACT: Genome wide association studies have identified ~100 loci associated with body mass index (BMI). Persons with low birth weight have an increased risk of metabolic disorders. We postulate that normal mechanisms of body weight regulation are disrupted in subjects with low birth weight. The present analyses included 2215 African American women from the Black Women's Health Study, and were based on genotype data on 20 BMI-associated loci and self-reported data on birth weight, weight at age 18 and adult weight. We used general linear models to assess the association of individual single-nucleotide polymorphisms (SNPs) with BMI at age 18 and later in adulthood within strata of birth weight (above and below the median, 3200 g). Three SNPs (rs1320330 near TMEM18, rs261967 near PCSK1 and rs17817964 in FTO), and a genetic score combining these three variants, showed significant interactions with birth weight in relation to BMI. Among women with birth weight <3200 g, there was an inverse association between genetic score and BMI; beta-coefficient=-0.045 (95% confidence intervals (CI) -0.104, 0.013) for BMI at age 18, and -0.055 (95% CI -0.112, 0.002) for adult BMI. Among women with birth weight ?3200 g, genetic score was positively associated with BMI: beta-coefficient=0.110 (95% CI 0.051, 0.169) for BMI at age 18 (P for interaction=0.0002), and 0.112 (95% CI 0.054, 0.170) for adult BMI (P for interaction<0.0001). Because TMEM18, PCSK1 and FTO are highly expressed in the central nervous system (CNS), our results suggest that low-birth weight may disrupt mechanisms of CNS body weight regulation.

SUBMITTER: Ruiz-Narvaez EA

PROVIDER: S-EPMC4808432 | biostudies-literature | 2016 Mar

REPOSITORIES: biostudies-literature

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Birth weight modifies the association between central nervous system gene variation and adult body mass index.

Ruiz-Narváez Edward A EA Haddad Stephen A SA Rosenberg Lynn L Palmer Julie R JR

Journal of human genetics 20151119 3

Genome wide association studies have identified ~100 loci associated with body mass index (BMI). Persons with low birth weight have an increased risk of metabolic disorders. We postulate that normal mechanisms of body weight regulation are disrupted in subjects with low birth weight. The present analyses included 2215 African American women from the Black Women's Health Study, and were based on genotype data on 20 BMI-associated loci and self-reported data on birth weight, weight at age 18 and a ...[more]

PMID: 26582267

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Project description:BackgroundLow birth weight (LBW) is one of the most common adverse pregnancy outcomes. Previous studies have consistently shown that maternal body mass index (BMI) status before and during pregnancy is associated with LBW. However, previous studies lacked an association between paternal BMI and the conjunction effect of a couple's BMI and LBW in the offspring. Therefore, we established a cohort of pre-pregnancy couples to prospectively assess the relationship between maternal and paternal pre-pregnancy BMI and offspring LBW, very low birth weight (VLBW), and extremely low birth weight (ELBW).MethodsA prospective cohort study was established in Central China. A total of 34,104 pregnant women with singleton pregnancies at 8-14 gestational weeks and their husbands were finally enrolled and followed to 3 months postpartum. The multivariate logistic regression and restrictive cubic spline model were used to explore the relationship between parental pre-pregnancy BMI and the risk of LBW, VLBW, and ELBW in offspring.ResultsOf the 34,104 participants, maternal pre-pregnancy overweight and obesity were associated with a higher risk of LBW (overweight: OR = 1.720, 95% CI = 1.533 ~ 1.930; obesity: OR = 1.710, 95% CI = 1.360 ~ 2.151), VLBW (overweight: OR = 2.283, 95% CI = 1.839 ~ 2.834; obesity: OR = 4.023, 95% CI = 2.855 ~ 5.670), and ELBW (overweight: OR = 3.292, 95% CI = 2.151 ~ 5.036; obesity: OR = 3.467, 95% CI = 1.481 ~ 8.115), while underweight was associated with a higher risk of LBW (OR = 1.438, 95% CI = 1.294 ~ 1.599) and a lower risk of ELBW (OR = 0.473, 95% CI = 0.236 ~ 0.946). Paternal pre-pregnancy overweight and obesity were associated with a higher risk of LBW (overweight: OR = 1.637, 95% CI = 1.501 ~ 1.784; obesity: OR = 1.454, 95% CI = 1.289 ~ 1.641) and VLBW (overweight: OR = 1.310, 95% CI = 1.097 ~ 1.564; obesity: OR = 1.320, 95% CI = 1.037 ~ 1.681), while underweight was associated with a lower risk of LBW (OR = 0.660, 95% CI = 0.519 ~ 0.839). Parents who were both excessive-weights in pre-pregnancy BMI, as well as overweight mothers and normal-weight fathers before pre-pregnancy, were more likely to have offspring with LBW, VLBW, and ELBW. Dose-response relationship existed between parental pre-pregnancy and LBW, VLBW, and ELBW, except for paternal BMI and ELBW.ConclusionsParental pre-pregnancy BMI was associated with the risk of LBW in offspring. Management of weight before pregnancy for couples might help reduce their adverse pregnancy outcomes in future intervention studies.

Project description:ImportanceMaternal obesity, pregestational type 1 diabetes, and gestational diabetes have been reported to increase the risks for large birth weight and preterm birth in offspring. However, the associations for insulin-treated diabetes and non-insulin-treated type 2 diabetes, as well as the associations for joint diabetes disorders and maternal body mass index, with these outcomes are less well documented.ObjectiveTo examine associations of maternal diabetes disorders, separately and together with maternal underweight or obesity, with the offspring being large for gestational age and/or preterm at birth.Design, setting, and participantsThis population-based cohort study used nationwide registries to examine all live births (n = 649 043) between January 1, 2004, and December 31, 2014, in Finland. The study and data analysis were conducted from April 1, 2018, to October 10, 2018.ExposuresMaternal prepregnancy body mass index, pregestational diabetes with insulin treatment, pregestational type 2 diabetes without insulin treatment, and gestational diabetes.Main outcomes and measuresOffspring large for gestational age (LGA) at birth and preterm delivery. Logistic regression models were adjusted for offspring birth year; parity; and maternal age, country of birth, and smoking status.ResultsOf the 649 043 births, 4000 (0.62%) were delivered by mothers who had insulin-treated diabetes, 3740 (0.57%) by mothers who had type 2 diabetes, and 98 568 (15.2%) by mothers who had gestational diabetes. The mean (SD) age of mothers was 30.15 (5.37) years, and 588 100 mothers (90.6%) were born in Finland. Statistically significant interactions existed between maternal body mass index and diabetes on offspring LGA and prematurity (insulin-treated diabetes: LGA F = 3489.0 and prematurity F = 1316.4 [P < .001]; type 2 diabetes: LGA F = 147.3 and prematurity F = 21.9 [P < .001]; gestational diabetes: LGA F = 1374.6 and prematurity F = 434.3 [P < .001]). Maternal moderate obesity, compared with normal-weight mothers with no diabetes, was associated with a mildly increased risk of having an offspring LGA (1069 [3.5%] vs 5151 [1.5%]; adjusted odds ratio [aOR], 2.45; 95% CI, 2.29-2.62), and mothers with insulin-treated diabetes had markedly elevated risks of having an offspring LGA (1585 [39.6%] vs 5151 [1.5%]; aOR, 43.80; 95% CI, 40.88-46.93) and a preterm birth (1483 [37.1%] vs 17 481 [5.0%]; aOR, 11.17; 95% CI, 10.46-11.93). Mothers who were moderately obese with type 2 diabetes were at increased risks of LGA (132 [16.4%] vs 5151 [1.5%]; aOR, 12.44; 95% CI, 10.29-15.03) and prematurity (83 [10.3%] vs 17 481 [5.0%]; aOR, 2.14; 95% CI, 1.70-2.69). Mothers who were moderately obese with gestational diabetes had a milder risk of LGA (1195 [6.7%] vs 5151 [1.5%]; aOR, 4.72; 95% CI, 4.42-5.04). Among spontaneous deliveries, the risks were strongest for moderately preterm births, but insulin-treated diabetes was associated with an increased risk also for very and extremely preterm births.Conclusions and relevanceMaternal insulin-treated diabetes appeared to be associated with markedly increased risks for LGA and preterm births, whereas obesity in mothers with type 2 diabetes had mild to moderately increased risks; these findings may have implications for counseling and managing pregnancies.

Project description:ImportanceThere is a lack of evidence on the association of birth weight, childhood body mass index (BMI), change in BMI during childhood, and childhood height with subsequent risks of hidradenitis suppurativa (HS) in adulthood.ObjectiveTo investigate the association of birth weight, childhood BMI, change in BMI during childhood, and childhood height with subsequent risks of HS in adulthood in a large Danish population-based cohort.Design, setting, and participantsThis cohort study included 347 200 schoolchildren from the Copenhagen School Health Records Register born from 1930 to 1996 who were linked to the Danish National Patient Register of hospital discharge diagnoses to identify cases of HS. Birth weight was reported by parents or guardians, whereas childhood weight and height were measured by school physicians or nurses at ages 7 through 13 years. Cox proportional hazards regressions were used to estimate hazard ratios (HRs) and 95% CIs. Statistical analysis was performed from February 20, 2019, to May 15, 2019.Main outcomes and measuresA diagnosis of HS as recorded in the Danish National Patient Register.ResultsAmong the 347 200 children included in the study (175 750 boys) during the follow-up period from 1977 to 2017, 1037 individuals (677 females; median age at diagnosis, 39 years [range, 15-73 years]) received a diagnosis of HS. A nonlinear (U-shaped) association was found between birth weight and HS, such that both the lightest (2.00-2.75 kg; HR, 1.36 [95% CI, 1.10-1.68]) and the heaviest babies (4.26-5.50 kg; HR, 1.39 [95% CI, 1.01-1.93]) had increased risks of HS compared with normal-weight babies (3.26-3.75 kg; P = .04 for deviation from linearity). The risk of HS increased significantly with increasing BMI z score at each age from 7 to 13 years, from an HR of 1.32 (95% CI, 1.24-1.40) per BMI z score at 7 years of age to an HR of 1.50 (95% CI, 1.40-1.61) per BMI z score at 13 years of age. Compared with children with a normal weight at 7 and 13 years of age, those with a normal weight at 7 years of age and overweight at 13 years of age had a significantly increased risk of HS (HR, 2.11 [95% CI, 1.63-2.74]) and children with persistent overweight at both ages also had an increased risk of HS (HR, 2.61 [95% CI, 2.02-3.38]). Children with overweight at 7 years of age but with normal weight at 13 years of age did not have a significantly increased risk of HS (HR, 1.05 [95% CI, 0.67-1.67]). Childhood height at all ages was not associated with risk of HS (children at 7 years had an HR of 1.00 [95% CI, 0.94-1.07], and those 13 years had an HR of 1.06 [95% CI, 0.99-1.13], per z score).Conclusions and relevanceThis cohort study found that both the lightest and heaviest babies had increased risks of HS. Childhood BMI was positively and significantly associated with risk of HS development in adulthood. These findings suggest that returning to normal weight before puberty reduces risks of HS to levels observed in children who were never overweight. Childhood height was not associated with risk of HS.

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Birth weight modifies the association between central nervous system gene variation and adult body mass index.

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Birth weight modifies the association between central nervous system gene variation and adult body mass index.

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