Parent-offspring body mass index associations in the Norwegian Mother and Child Cohort Study: a family-based approach to studying the role of the intrauterine environment in childhood adiposity

In the present study, the authors investigated the role of the intrauterine environment in childhood adiposity by comparing the maternal-offspring body mass index (BMI) association with the paternal-offspring BMI association when the offspring were 3 years of age, using parental prepregnancy BMI (measured as weight in kilograms divided by height in meters squared). The parent-offspring trios (n = 29,216) were recruited during pregnancy from 2001 to 2008 into the Norwegian Mother and Child Cohort Study conducted by The Norwegian Institute of Public Health. Data from self-administered questionnaires were used in linear regression analyses. Crude analyses showed similar parental-offspring BMI associations; the mean difference in offspring BMI was 0.15 (95% confidence interval: 0.13, 0.16) per each 1-standard-deviation increase in maternal BMI and 0.15 (95% confidence interval: 0.13, 0.17) per each 1-standard-deviation increase in paternal BMI. After all adjustments, the mean difference in offspring BMI per each 1-standard-deviation increment of maternal BMI was 0.12, and the mean difference in offspring BMI per each 1-standard-deviation increment of paternal BMI was 0.13. There was no strong support for heterogeneity between the associations (P > 0.6). In conclusion, results from the present large population-based study showed similar parental-offspring BMI associations when the offspring were 3 years of age, which indicates that the maternal-offspring association may be explained by shared familial (environmental and genetic) risk factors rather than by the intrauterine environment.     

Invited commentary: How early in life does the risk of obesity originate?

Mothers and fathers influence the risk of obesity in their children through genetic, environmental, and behavioral factors. Unique to the mother, however, is the intrauterine environment in which the fetus develops, and it is during this time in the uterus that the risk of later obesity in the child may develop. In this issue of the Journal, Fleten et al. (Am J Epidemiol. 2012;176(2):83-92) investigate whether the intrauterine environment plays a role in the development of adiposity by comparing the association between maternal prepregnancy body mass index (BMI; measured as weight in kilograms divided by height in meters squared) and offspring BMI at 3 years of age with the paternal-offspring association at the same age in the Norwegian Mother and Child Cohort Study. In that large study of stable, relatively healthy and well-educated families, significant differences in maternal-offspring and paternal-offspring BMI associations were not identified. These findings are interpreted as indicating that the influence on the child's BMI of the intrauterine environment is less important than that of genetics and shared environment. Results from that study suggest that further consideration should be given to the specificity of the fetal overnutrition hypothesis in terms of which aspects of the intrauterine environment may influence offspring adiposity and when across the life course these effects may manifest themselves.     

Substantial intergenerational increases in body mass index are not explained by the fetal overnutrition hypothesis: the Cardiovascular Risk in Young Finns Study

BACKGROUND: According to the fetal overnutrition hypothesis, intrauterine influences of maternal obesity increased lifelong obesity risk in the offspring. If the hypothesis is true, then the association between maternal body mass index (BMI; in kg/m(2)) and offspring BMI should be stronger than the association between paternal BMI and offspring BMI, because only the mother directly influences the fetal environment. OBJECTIVES: We prospectively examined intergenerational change in BMI and tested the fetal overnutrition hypothesis. DESIGN: Data on offspring weight were obtained from mothers. BMI was assessed from 2980 complete parent-offspring trios when the offspring were 3 to 18 y of age. The assessment of offspring BMI was repeated 21 y later at age 24-39 y. RESULTS: Adult BMI of the offspring was 1.21 units higher than the BMI of their parents at the same age, which indicates an increase in obesity levels across generations (P < 0.0001). Maternal BMI was more strongly associated with offspring birth weight than was paternal BMI (P = 0.0009). However, there were no such differences in parent-offspring associations for BMI at later developmental stages when offspring were aged 3-39 y (P > 0.35). The results did not materially change in a sensitivity analysis for 1% to 15% nonpaternity. CONCLUSIONS: Because offspring share all genes with their parents, the observed substantially higher adult BMI for offspring than for parents is likely explained by environmental influences. No support was found for any specific influence from fetal environment on this intergenerational increase in adult obesity. The findings were consistent with the fetal overnutrition hypothesis only in relation to birth weight.     

Parents' growth in childhood and the birth weight of their offspring

BACKGROUND: A person's birth weight is inversely related to both their own and their parents' cardiovascular disease mortality risk, but mechanisms underlying such transgenerational associations are unclear. We investigated the influence of the childhood growth of the mother or father on the birth weight of their first-born offspring. METHODS: We used data from the long-term follow up (in 1997-1998) of 4999 children from 1352 families who participated in the Boyd Orr Survey of Diet and Health in Pre-War Britain (1937-1939). Complete information on childhood height, potential confounding variables, and the birth weight of first-born offspring was available for 637 subjects. RESULTS: Mother's height in childhood was positively associated with her offspring's birth weight. Leg length, but not trunk length, was the component of maternal height associated with offspring birth weight. For each unit increase in z-score for maternal childhood leg length, there was a 96-g (95% confidence interval = 6-186) increase in offspring birth weight after controlling for childhood socioeconomic variables and adult height. There were weaker positive associations of paternal height and leg length in childhood with offspring birth weight. Associations were not confounded by maternal birth weight or midgrandparental height. CONCLUSIONS: Our findings are consistent with the hypothesis that maternal growth during childhood influences offspring birth weight, independently of maternal birth weight, final attained height, or midgrandparental height. Because leg length is a sensitive marker of adverse nutritional and social exposures during childhood, these results suggest a key role for a mother's early environmental exposures as a determinant of her child's subsequent health.     

Birth size, growth, and blood pressure between the ages of 7 and 26 years: failure to support the fetal origins hypothesis

The "fetal origins hypothesis" asserts that birth weight is inversely related to later blood pressure. Data from a cohort of 891 infants born in Dunedin, New Zealand, in 1972-1973 whose blood pressure was measured at 2-year intervals from age 7 years to age 15 years and at ages 18 and 26 years were used to test this hypothesis. Three regression models based on standardized scores for weight and height were used. The first showed that at any of the ages at which the cohort was assessed, an increase in birth weight of one z score (one standard deviation) was commensurate with a decrease of 0.29 mmHg (95% confidence interval: -0.17, 0.76) in blood pressure. The second model showed that a one-z-score increase in weight between birth and a subsequent age was associated with an increase in systolic blood pressure of 0.96 mmHg (95% confidence interval: 0.53, 1.38). This estimate applied to all ages. The third model showed that the effect of an interaction between birth weight and later weight was not significant; thus, there was no evidence to suggest that children with a low birth weight who became overweight or obese had extra high blood pressure. Similar results were obtained for height. These results fail to support the fetal origins hypothesis.     

Offspring birth weight and parental mortality: prospective observational study and meta-analysis

The authors have investigated associations between offspring size at birth and parental cardiovascular disease mortality among 12,086 mothers and 6,936 fathers of participants in the British 1958 birth cohort. Birth weight was inversely associated with all-cause mortality and cardiovascular mortality in both mothers and fathers. The adjusted hazard ratio of cardiovascular disease mortality for a 1-standard deviation increase in offspring birth weight in mothers was 0.87 (95% confidence interval (CI): 0.82, 0.93) and in fathers was 0.94 (95% CI: 0.89, 0.99). The association was not specific for cardiovascular disease. In fathers, similar weak associations with violent and accidental deaths, stomach cancer, and alcohol- and smoking-related outcomes were found. Weak associations for these outcomes were also found for mothers, but the magnitude of the association with cardiovascular disease was greater than with any other outcomes. In a meta-analysis pooling results from this study with six others, the adjusted hazard ratio of cardiovascular disease mortality among mothers was 0.75 (95% CI: 0.67, 0.84) and that among fathers was 0.93 (95% CI: 0.91, 0.95), with evidence that the difference in effect between mothers and fathers was not due to chance (p < 0.001). The weak association of offspring birth weight with cardiovascular disease in fathers may be due to residual confounding by factors such as socioeconomic position and smoking that they share with the offspring's mother and that would therefore be associated with low offspring birth weight as well as adverse outcomes in the father. The stronger association in mothers is consistent with intergenerational effects on intrauterine growth and with the fetal origins hypothesis.     

Association between leg length and offspring birthweight: partial explanation for the trans-generational association between birthweight and cardiovascular disease: findings from the British Women's Heart and Health Study

Low birthweight individuals not only have increased risk of cardiovascular disease themselves, but cardiovascular disease risk is also increased in their parents. The mechanisms underlying these trans-generational associations are not fully understood. We hypothesise that, in part, they reflect the trans-generational effects of poor maternal environmental circumstances in early childhood. Adverse environmental factors acting early in the mother's life will not only influence her own predisposition to cardiovascular disease but will also result in adverse consequences - low birthweight and increased cardiovascular disease risk in later life - for her offspring. Adult leg length is a valid indicator of early life environmental circumstances, in particular of infant nutrition. If our hypothesis is correct, then adult leg length should be positively associated with offspring birthweight. In this study of 4286 randomly selected women aged 60-79 years from 23 towns across England, Scotland and Wales, the magnitude of the association between leg length and offspring birthweight was greater than the association between trunk length and offspring birthweight. After control for potential confounding factors, offspring birthweight increased by 89.8 g [95% confidence interval 66.1, 113.5 g] for each standard deviation increase in maternal leg length, and by 55.2 g [32.2, 78.1 g] for each standard deviation increase in maternal trunk length. The association between leg length and offspring birthweight was unaffected by adjustment for maternal birthweight, but the association between trunk length and offspring birthweight was attenuated to 38.0 g [1.0, 74.9 g]. These findings support the hypothesis that adverse early childhood environmental circumstances affect not only the vitality and health of the woman in later life but also the birthweight of her offspring, and suggest that the trans-generational association between birthweight and cardiovascular disease is in part explained by early childhood maternal environmental circumstances.     

Maternal protein intake is not associated with infant blood pressure

BACKGROUND: Animal data show that low protein intake in pregnancy programs higher offspring blood pressure, but similar data in humans are limited. We examined the associations of first and second trimester maternal protein intake with offspring blood pressure (BP) at the age of six months. METHODS: In a prospective US cohort study, called Project Viva, pregnant women completed validated semi-quantitative food-frequency questionnaires (FFQ) to measure gestational protein intake. Among 947 mother-offspring pairs with first trimester dietary data and 910 pairs with second trimester data, we measured systolic blood pressure (SBP) up to five times with an automated device in the offspring at the age of six months. Controlling for blood pressure measurement conditions, maternal and infant characteristics, we examined the effect of energy-adjusted maternal protein intake on infant SBP using multivariable mixed effects models. RESULTS: Mean daily second trimester maternal protein intake was 17.6% of energy (mean 2111 kcal/day). First trimester nutrient intakes were similar. Mean SBP at age 6 months was 90.0 mm Hg (SD 12.9). Consistent with prior reports, adjusted SBP was 1.94 mm Hg lower [95% confidence interval (CI) -3.45 to -0.42] for each kg increase in birth weight. However, we did not find an association between maternal protein intake and infant SBP. After adjusting for covariates, the effect estimates were 0.14 mm Hg (95% CI 20.12 to 20.40) for a 1% increase in energy from protein during the second trimester, and 20.01 mm Hg (95% CI 20.24 to -0.23) for a 1% increase in energy from protein in the first trimester. CONCLUSIONS: Variation in maternal total protein intake during pregnancy does not appear to program offspring blood pressure.     

Maternal and paternal smoking during pregnancy and risk of ADHD symptoms in offspring: testing for intrauterine effects

Maternal smoking during pregnancy is associated with attention deficit hyperactivity disorder (ADHD) in offspring. It is assumed by many that this association is causal. Others suggest that observed associations are due to unmeasured genetic factors or other confounding factors. The authors compared risks of maternal smoking during pregnancy with those of paternal smoking during pregnancy. With a causal intrauterine effect, no independent association should be observed between paternal smoking and offspring ADHD. If the association is due to confounding factors, risks of offspring ADHD should be of similar magnitudes regardless of which parent smokes. This hypothesis was tested in 8,324 children from a well-characterized United Kingdom prospective cohort study, the Avon Longitudinal Study of Parents and Children (data from 1991-2000). Associations between offspring ADHD and maternal and paternal smoking during pregnancy were compared using regression analyses. Offspring ADHD symptoms were associated with exposure to both maternal and paternal smoking during pregnancy (mothers: β = 0.25, 95% confidence interval: 0.18, 0.32; fathers: β = 0.21, 95% confidence interval: 0.15, 0.27). When paternal smoking was examined in the absence of maternal smoking, associations remained and did not appear to be due to passive smoking exposure in utero. These findings suggest that associations between maternal smoking during pregnancy and child ADHD may be due to genetic or household-level confounding rather than to causal intrauterine effects.     

Associations of obesity with lower urinary tract symptoms and noncancer prostate surgery in the Third National Health and Nutrition Examination Survey

The authors examined the association between obesity and lower urinary tract symptoms (LUTS) in the Third National Health and Nutrition Examination Survey. This 1988-1994 US cross-sectional study included 2,797 men aged > or = 60 years whose current weight, weight at age 25 years, highest weight ever, height, waist circumference, and body mass index (BMI) were assessed. LUTS cases had at least three of these symptoms: nocturia, incomplete emptying, weak stream, and hesitancy. Controls were men without symptoms or noncancer prostate surgery. Odds ratios adjusted for age and race and weighted for selection probability were estimated by logistic regression. The odds of LUTS were lower for men who were obese at age 25 years compared with men whose BMI was normal (odds ratio = 0.49, 95% confidence interval: 0.27, 0.91). An increase in BMI between age 25 years and the highest BMI ever was positively associated with LUTS (odds ratio = 1.90, 95% confidence interval: 0.89, 4.05). Men with a larger waist circumference (> or = 102 cm) were more likely to have LUTS compared with men with a smaller waist circumference (odds ratio = 1.48, 95% confidence interval: 0.87, 2.54). Results suggest that being overweight in young adulthood may be associated with a lower prevalence of LUTS later in life, whereas weight gain and central adiposity in adulthood are possibly associated with a higher prevalence of LUTS.     

Body mass index and incident ischemic heart disease in South Korean men and women

Asian populations have a higher body fat percentage for a given body mass index (BMI) than Caucasians. However, little information is available on the association of BMI with ischemic heart disease (IHD) incidence in Asians at low BMI levels. The authors prospectively evaluated the association of BMI (weight (kg)/height m2) with IHD incidence over 9 years of follow-up (1993-2001) among 133,740 South Korean adults (89,050 men, 44,690 women) who participated in the 1990 and 1992 examinations of the Korea Medical Insurance Corporation Study. Average BMI at baseline was 23.4 (standard deviation, 2.3) in men and 22.3 (standard deviation, 2.3) in women. After multivariate adjustment, there was a 14% (95% confidence interval: 12, 16) increased risk of incident IHD per unit of increase in BMI. This trend was also observed within the range considered normal by Western standards, and a BMI of 24-<25 was associated with an IHD hazard ratio of 2.01 (95% confidence interval: 1.32, 3.05) in comparison with a BMI of 18-<19. The association of BMI with IHD in this cohort of relatively young South Korean men and women was progressive over the range of BMI values, with no threshold of change in risk and no indication of a U-shaped relation at low BMI levels.     

Maternal smoking during pregnancy in relation to child overweight: follow-up to age 8 years

BACKGROUND: Data from several studies indicate that children of mothers who smoked during pregnancy may be at a risk of overweight compared with children of non-smoking mothers. The size of this relation, however, is unclear, as is the age at which it becomes detectable. METHODS: Prospective data for 34 866 children enrolled in the US Collaborative Perinatal Project were analysed to examine maternal pregnancy smoking in relation to weight, height, and body mass index (BMI) in offspring at ages 1, 3, 4, 7, and 8 years. RESULTS: Compared with offspring of non-smokers, children of smokers had (i) weight that was lower at birth but then quickly equalled or exceeded that of non-smokers, (ii) consistently decreased height, and (iii) increased risk of overweight, particularly in girls. For example, at age 7 years, the adjusted odds ratio of BMI>or=85th percentile in boys of mothers who smoked on an average>or=20 cigarettes per day while pregnant was 1.22 (95% confidence interval 1.03-1.46), and in girls it was 1.30 (1.08-1.56). CONCLUSIONS: In these data, maternal smoking during pregnancy was associated with a modest increase in risk of overweight in children before the age of 8 years.     

Adiposity, its related biologic risk factors, and suicide: a cohort study of 542,088 taiwanese adults

Recent studies in Western nations have shown inverse associations between body mass index (BMI, measured as weight (kg)/height (m)(2)) and suicide. However, it is uncertain whether the association is similar in non-Western settings, and the biologic pathways underlying the association are unclear. The authors investigated these issues in a cohort of 542,088 Taiwanese people 20 years of age or older who participated in a health check-up program (1994-2008); there were 573 suicides over a mean 8.1 years of follow up. There was a J-shaped association between BMI and suicide risk (P for the quadratic term = 0.033) but limited evidence of a linear association (adjusted hazard ratio per 1-standard-deviation increase = 0.95 (95% confidence interval: 0.85, 1.06)); compared with individuals whose BMI was 18.5-22.9, adjusted hazard ratios for those with a BMI <18.5 or ≥35 were 1.56 (95% confidence interval: 1.07, 2.28) and 3.62 (95% confidence interval: 1.59, 8.22), respectively. A high waist-to-hip ratio was associated with an increased risk of suicide. There was some evidence for a reverse J-shaped association of systolic blood pressure and high density lipoprotein cholesterol with suicide and an association of higher triglyceride level with increased suicide risk; these associations did not appear to mediate the associations of BMI and waist-to-hip ratio with suicide.     

Association of body mass index with peripheral arterial disease in older adults: the Cardiovascular Health Study

The authors hypothesized that the absence of cross-sectional associations of body mass index (BMI; weight (kg)/height (m)(2)) with peripheral arterial disease (PAD) in prior studies may reflect lower weight among persons who smoke or have poor health status. They conducted an observational study among 5,419 noninstitutionalized residents of 4 US communities aged ≥ 65 years at baseline (1989-1990 or 1992-1993). Ankle brachial index was measured, and participants reported their history of PAD procedures. Participants were followed longitudinally for adjudicated incident PAD events. At baseline, mean BMI was 26.6 (standard deviation, 4.6), and 776 participants (14%) had prevalent PAD. During 13.2 (median) years of follow-up through June 30, 2007, 276 incident PAD events occurred. In cross-sectional analysis, each 5-unit increase in BMI was inversely associated with PAD (prevalence ratio (PR) = 0.92, 95% confidence interval (CI): 0.85, 1.00). However, among persons in good health who had never smoked, the direction of association was opposite (PR = 1.20, 95% CI: 0.94, 1.52). Similar results were observed between BMI calculated using weight at age 50 years and PAD prevalence (PR = 1.30, 95% CI: 1.11, 1.51) and between BMI at baseline and incident PAD events occurring during follow-up (hazard ratio = 1.32, 95% CI: 1.00, 1.76) among never smokers in good health. Greater BMI is associated with PAD in older persons who remain healthy and have never smoked. Normal weight maintenance may decrease PAD incidence and associated comorbidity in older age.     

Is there a fetal origin of depression? Evidence from the Mater University Study of Pregnancy and its outcomes

It is unclear whether there is a fetal origin of adult depression. In particular, previous studies have been unable to adjust for the potential effect of maternal depression during pregnancy on any association. The association of birth weight with adult symptoms of depression was examined in an Australian prospective birth cohort, the Mater University Study of Pregnancy and its outcomes. Depressive symptoms were assessed with the Center for Epidemiologic Studies Depression Scale among 3,719 participants at the 21-year follow-up in 2002-2005. In multivariable analyses, there were a weak inverse association between birth weight and symptoms of depression in the whole cohort and some evidence of sex differences in this association. Among females, there was a graded inverse association: In the fully adjusted model, the odds ratio for a high level of depressive symptoms for a 1-standard deviation increase in birth weight (gestational age-standardized z score) was 0.82 (95% confidence interval: 0.73, 0.92). Among males, there was no association (with sex in all models: p(interaction) < 0.004). Study results provide some support for a fetal origin of adult depression and suggest that the association is not explained by maternal mental health characteristics during pregnancy. Further research is needed to better understand the mechanisms underlying the association.     

Fetal growth indicators and perfluorinated chemicals: a study in the Danish National Birth Cohort

Perfluorooctanoate (PFOA) and perfluorooctanesulfonate (PFOS) are widespread persistent organic pollutants that have been associated with reduced birth weight at doses expected in many pregnant populations. The authors randomly selected 1,400 pregnant women and their newborns from the Danish National Birth Cohort (1996-2002) to investigate whether these compounds reduce organ growth. PFOS and PFOA were measured in maternal blood samples taken early in pregnancy. Placental weight, birth length, and head and abdominal circumferences were measured shortly after birth by trained midwives or nurses. Maternal PFOA levels in early pregnancy were associated with smaller abdominal circumference and birth length. For each ng/ml increase in PFOA, birth length decreased by 0.069 cm (95% confidence interval: 0.024, 0.113) and abdominal circumference decreased by 0.059 cm (95% confidence interval: 0.012, 0.106). An inverse association was also observed between PFOA and placental weight and head circumference, and a positive association was observed with newborn ponderal index, but none of these associations was statistically significant. Maternal PFOS levels were not associated with any of the five fetal growth indicators. These findings suggest that fetal exposure to PFOA but not PFOS during organ development may affect the growth of organs and the skeleton.     

Blood pressure in different gestational trimesters, fetal growth, and the risk of adverse birth outcomes: the generation R study

Researchers have suggested that maternal hypertensive disorders during pregnancy affect fetal growth. The authors examined the associations between systolic and diastolic blood pressures in different trimesters of pregnancy and both repeatedly measured fetal growth characteristics and the risks of adverse birth outcomes. The present study (2001-2005) was performed in 8,623 women who were participating in a population-based prospective cohort study from fetal life onwards. Blood pressure and fetal growth characteristics were assessed in each trimester of pregnancy. Information on hypertensive complications and adverse birth outcomes was obtained from medical records. The results suggested that higher blood pressure was associated with smaller fetal head circumference and femur length, as well as lower fetal weight from the third trimester onward. An increase in blood pressure from the second trimester to the third trimester was associated with an increased risk of adverse birth outcomes. Compared with women who did not experience hypertension during pregnancy, women with preeclampsia had increased risks of having children who were preterm (odds ratio = 5.89, 95% confidence interval: 2.63, 13.14), had a low birth weight (odds ratio = 8.94, 95% confidence interval: 6.19, 12.90), or were small for their gestational age (odds ratio = 5.03, 95% confidence interval: 3.31, 7.62). The present results suggest that higher maternal blood pressure is associated with impaired fetal growth during the third trimester of pregnancy and increased risks of adverse birth outcomes.     

Relation of height and body mass index to renal cell carcinoma in two million Norwegian men and women

A positive association between body mass index (BMI) and renal cell carcinoma (RCC) has been observed. The association between height and RCC has been less clear. The authors explored these relations in a very large Norwegian cohort. Height and weight were measured in two million Norwegian men and women aged 20-74 years during 1963-2001. During follow-up, 6,453 cases of RCC were registered in the national cancer database. Measurements were also performed in 227,000 adolescents aged 14-19 years, and 154 cases of RCC were registered. Relative risks for RCC were estimated using Cox proportional hazards regression. The risk of RCC increased with increasing BMI among both adults and adolescents. Among adults, the relative risk associated with a one-unit increase in BMI was 1.05 (95% confidence interval (CI): 1.04, 1.06) in both sexes. The relative risk associated with a 10-cm increase in height was 1.19 (95% CI: 1.13, 1.26) in men and 1.17 (95% CI: 1.09, 1.26) in women. In a subgroup analysis, the relation between BMI and RCC was most pronounced in men and women who were never smokers, and the relation between height and RCC was confined to ever smokers. The authors conclude that elevated BMIs are associated with RCC risk in both males and females across a wide age range.     

Parental growth at different life stages and offspring birthweight: an intergenerational cohort study

Using three generations of the 1958 British national birth cohort we investigated ways in which parental size is related to offspring birthweight. By age 41 years, 4566 singleton female and 4050 male cohort members (born 3-9 March, 1958) had become parents and provided information on their singleton offspring. Mother's birthweight (standardised for gestational age and sex) was the strongest determinant of offspring birthweight (effect size [ES] per SDS 112 g [95% CI 97, 128]), which was little affected by adjustment for maternal height or BMI (ES 95 g and 105 g respectively). The intergenerational birthweight association was not observed for mothers born very small or large. Mother's childhood height at age 7 (ES 46 g [24, 67]), but not BMI (ES 3 g [-18, 23]), was associated with offspring birthweight after adjustment for grandparental size, own birthweight, and adult size. Controlling for other growth measures strongly attenuated the association between mother's adult height and offspring birthweight: (ES 90 g, unadjusted, and 25 g, adjusted), while the association between adult BMI and offspring birthweight was little affected (ES 55 g and 51 g respectively). Father's BMI did not affect offspring birthweight, while the associations for height were similar, albeit weaker, than those observed for the mother. Our results suggest that intergenerational associations in birthweights are largely independent of postnatal size. Maternal height in childhood was positively related to offspring birthweight, while the effect of her BMI was restricted to adulthood.