Heritability Estimates of Body Size in Fetal Life and Early Childhood

Mook‐Kanamori, Dennis O.; Beijsterveldt, Catharina E. M. van; Steegers, Eric A.P.; Aulchenko, Yurii S.; Raat, Hein; Hofman, Albert; Eilers, Paul H.C.; Boomsma, Dorret I.; Jaddoe, Vincent W. V.

doi:10.1371/journal.pone.0039901

Cited by 48 publications

(42 citation statements)

References 40 publications

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“…Documented associations between parental and offspring height are stronger in adulthood than at birth, with heritability estimates of around 80% in adulthood for relatively wealthy populations (Silventoinen et al, 2003). Heritability estimates of various measurements including head circumference, height and weight also increase from approximately 6 months of age compared with at birth when they are typically 25–30% (Levine et al, 1987; Demerath et al, 2007; Johnson et al, 2011; Silventoinen et al, 2011; Mook-Kanamori et al, 2012). Thus fetal growth may be generally more sensitive to the environment than postnatal growth, accounting for closer relationships between parental and offspring anthropometry in adulthood.…”

Section: Discussionmentioning

confidence: 99%

Relationships of maternal and paternal anthropometry with neonatal body size, proportions and adiposity in an Australian cohort

Pomeroy

Wells²,

Cole³

et al. 2014

American J Phys Anthropol

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The patterns of association between maternal or paternal and neonatal phenotype may offer insight into how neonatal characteristics are shaped by evolutionary processes, such as conflicting parental interests in fetal investment and obstetric constraints. Paternal interests are theoretically served by maximizing fetal growth, and maternal interests by managing investment in current and future offspring, but whether paternal and maternal influences act on different components of overall size is unknown. We tested whether parents' prepregnancy height and body mass index (BMI) were related to neonatal anthropometry (birthweight, head circumference, absolute and proportional limb segment and trunk lengths, subcutaneous fat) among 1,041 Australian neonates using stepwise linear regression. Maternal and paternal height and maternal BMI were associated with birthweight. Paternal height related to offspring forearm and lower leg lengths, maternal height and BMI to neonatal head circumference, and maternal BMI to offspring adiposity. Principal components analysis identified three components of variability reflecting neonatal “head and trunk skeletal size,” “adiposity,” and “limb lengths.” Regression analyses of the component scores supported the associations of head and trunk size or adiposity with maternal anthropometry, and limb lengths with paternal anthropometry. Our results suggest that while neonatal fatness reflects environmental conditions (maternal physiology), head circumference and limb and trunk lengths show differing associations with parental anthropometry. These patterns may reflect genetics, parental imprinting and environmental influences in a manner consistent with parental conflicts of interest. Paternal height may relate to neonatal limb length as a means of increasing fetal growth without exacerbating the risk of obstetric complications. Am J Phys Anthropol 156:625–636, 2015.

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Section: Discussionmentioning

confidence: 99%

Relationships of maternal and paternal anthropometry with neonatal body size, proportions and adiposity in an Australian cohort

Pomeroy

Wells²,

Cole³

et al. 2014

American J Phys Anthropol

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show abstract

“…Data from Mook-Kanamori et al (2012) and Gielen et al (2008). Data from Mook-Kanamori et al (2012) and Gielen et al (2008).…”

Section: R E V I S I T I N G H E R I T a B I L I T Ymentioning

confidence: 98%

Worldwide variability in growth and its association with health: Incorporating body composition, developmental plasticity, and intergenerational effects

Wells

2017

American J Hum Biol

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In their seminal book "Worldwide variation in human growth," published in 1976, Eveleth and Tanner highlighted substantial variability within and between populations in the magnitude and schedule of human growth. In the four decades since then, research has clarified why growth variability is so closely associated with human health. First, growth patterns are strongly associated with body composition, both in the short- and long-term. Poor growth in early life constrains the acquisition of lean tissue, while compensatory "catch-up" growth may elevate body fatness. Second, these data are examples of the fundamental link between growth and developmental plasticity. Growth is highly sensitive to ecological stresses and stimuli during early "critical windows," but loses much of this sensitivity as it undergoes canalization during early childhood. Crucially, the primary source of stimuli during early "critical windows" is not the external environment itself, but rather maternal phenotype, which transduces the impact of ecological conditions. Maternal phenotype, representing many dimensions of "capital," thus generates a powerful impact on the developmental trajectory of the offspring. There is increasing evidence that low levels of maternal capital impact the offspring's size at birth, schedule of maturation, and body composition and physiological function in adulthood. While evidence has accrued of substantial heritability in adult height, it is clear that the pathway through which it is attained has major implications for metabolic phenotype. Integrating these perspectives is important for understanding how developmental plasticity may on the one hand contribute to adaptation, while on the other shape susceptibility to non-communicable disease.

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“…Birth weight is a complex multifactorial trait itself with heritability around 20–30 % [46–49]. The importance of genetic factors on birth weight acting independently of the intrauterine environment has also been illustrated by correlations between paternal height or weight and offspring birth weight [50, 51].…”

Section: Influence Of Other Family Risk Factors On Familial Aggregatimentioning

confidence: 99%

Familial Aggregation and Childhood Blood Pressure

Wang

et al. 2014

Curr Hypertens Rep

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There is growing concern about elevated blood pressure (BP) in children. The evidence for familial aggregation of childhood BP is substantial. Twin studies have shown that a large part of the familial aggregation of childhood BP is due to genes. The first part of this review provides the latest progress in gene finding for childhood BP, focusing on the combined effects of multiple loci identified from the genome-wide association studies on adult BP. We further review the evidence on the contribution of the genetic components of other family risk factors to the familial aggregation of childhood BP including obesity, birth weight, sleep quality, sodium intake, parental smoking, and socioeconomic status. At the end, we emphasize the promise of using genomic-relatedness-matrix restricted maximum likelihood (GREML) analysis, a method that uses genome-wide data from unrelated individuals, in answering a number of unsolved questions in the familial aggregation of childhood BP.

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Heritability Estimates of Body Size in Fetal Life and Early Childhood

Cited by 48 publications

References 40 publications

Relationships of maternal and paternal anthropometry with neonatal body size, proportions and adiposity in an Australian cohort

Relationships of maternal and paternal anthropometry with neonatal body size, proportions and adiposity in an Australian cohort

Worldwide variability in growth and its association with health: Incorporating body composition, developmental plasticity, and intergenerational effects

Familial Aggregation and Childhood Blood Pressure

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