The tempo of human childhood: a maternal foot on the accelerator, a paternal foot on the brake

Kotler, Jennifer; Haig, David

doi:10.1002/evan.21579

Cited by 21 publications

(34 citation statements)

References 120 publications

(213 reference statements)

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“…This proposal is testable by studying the psychology of people with atypical inheritance or expression of typically imprinted genes, referred to as genomic imprinting disorders. Many phenotypes resulting from these disorders are consistent with atypical resource demands, making them a model for examining traits related to parent-offspring conflict in humans (Kotler et al, 2016;Kotler & Haig, 2018;Úbeda, 2008). Consistent with proposal, musical responses of individuals with Prader-Willi syndrome are altered, relative to typical development .…”

Section: Response To Music In Angelman Syndromesupporting

confidence: 56%

“…The kinship theory of genomic imprinting has been applied to a variety of human phenomena, from nursing to the pace of human maturation (Haig, 2014;Kotler & Haig, 2018;Úbeda, 2008), but few empirical tests of its psychological predictions have been attempted (see Oliver et al, 2007). The results presented here, in conjunction with our prior work , demonstrate that the effect of listening to vocal music on physiological relaxation depends in part on the relative contribution of genes expressed in the q11-13 region of chromosome 15.…”

Section: Discussionmentioning

confidence: 64%

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Response to vocal music in Angelman syndrome contrasts with Prader-Willi syndrome

Kotler

Mehr

Egner

et al. 2019

Evolution and Human Behavior

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Parent-offspring conflict-conflict over resource distribution within families due to differences in genetic relatedness-is the biological foundation for many psychological phenomena. In genomic imprinting disorders, parent-specific genetic expression is altered causing imbalances in behaviors influenced by parental investment. We use this natural experiment to test the theory that parent-offspring conflict contributed to the evolution of vocal music by moderating infant demands for parental attention. Individuals with Prader-Willi syndrome, a genomic imprinting disorder resulting from increased relative maternal genetic contribution, show enhanced relaxation responses to song, consistent with reduced demand for parental investment (Mehr et al., 2017, Psychological Science). We report the necessary complementary pattern here: individuals with Angelman syndrome, a genomic imprinting disorder resulting from increased relative paternal genetic contribution, demonstrate a relatively reduced relaxation response to song, suggesting increased demand for parental attention. These results support the extension of genetic conflict theories to psychological resources like parental attention.

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Section: Response To Music In Angelman Syndromesupporting

confidence: 56%

Section: Discussionmentioning

confidence: 64%

Response to vocal music in Angelman syndrome contrasts with Prader-Willi syndrome

Kotler

Mehr

Egner

et al. 2019

Evolution and Human Behavior

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“…Two of the four described monogenic causes of CPP are imprinted genes, raising the possibility that imprinting plays an important role in the regulation of puberty and that other imprinted genes might also be involved in pubertal timing (87). There are several hundred genes predicted to be imprinted in the human genome and approximately 50 human imprinted genes have been described to date (88).…”

Section: Role Of Imprinted Genes In Pubertymentioning

confidence: 99%

GENETICS IN ENDOCRINOLOGY: Genetic etiologies of central precocious puberty and the role of imprinted genes

Roberts

Kaiser

2020

European Journal of Endocrinology

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Pubertal timing is regulated by the complex interplay of genetic, environmental, nutritional and epigenetic factors. Criteria for determining normal pubertal timing, and thus the definition of precocious puberty, have evolved based on published population studies. The significance of the genetic influence on pubertal timing is supported by familial pubertal timing and twin studies. In contrast to the many monogenic causes associated with hypogonadotropic hypogonadism, only four monogenic causes of central precocious puberty (CPP) have been described. Loss-of-function mutations in Makorin Ring Finger Protein 3 (MKRN3), a maternally imprinted gene on chromosome 15 within the Prader-Willi syndrome locus, are the most common identified genetic cause of CPP. More recently, several mutations in a second maternally imprinted gene, Delta-like noncanonical Notch ligand 1 (DLK1), have also been associated with CPP. Polymorphisms in both genes have also been associated with age of menarche in genome-wide association studies. Mutations in the genes encoding kisspeptin (KISS1) and its receptor (KISS1R), potent activators of GnRH secretion, have also been described in association with CPP, but remain rare monogenic causes. CPP has both short- and long-term health implications for children, highlighting the importance of understanding the mechanisms contributing to early puberty. Additionally, given the role of mutations in the imprinted genes MKRN3 and DLK1 in pubertal timing, other imprinted candidate genes should be considered for a role in puberty initiation.

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“…Optimal post-natal development for paternal genes engenders vigorous and frequent sucking and rapid early growth (when growth is food-limited rather than hormone-regulated, and involves growth in lean mass as well as fat), delayed weaning, enhanced solicitation of both complementary foods and later, other-provided "family" foods (in comparison to self-feeding), and delayed puberty that lengthens the overall period of dependence (11,14,21,22).…”

Section: Adaptive and Conflictual Human Developmentmentioning

confidence: 99%

“…Finally, theory and evidence indicate that maternally expressed imprinted genes favor fast childhood development and early menarche, which reduce demands on the mother (21). In turn, early menarche is associated with higher risk of metabolic syndrome later in life [e.g., (73)].…”

Section: Trajectories Of Post-natal Feeding Growth and Developmentmentioning

confidence: 99%

Why and How Imprinted Genes Drive Fetal Programming

Crespi

2020

Front. Endocrinol.

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Imprinted genes mediate fetal and childhood growth and development, and early growth patterns drive fetal programming effects. However, predictions and evidence from the kinship theory of imprinting have yet to be directly integrated with data on fetal programming and risks of metabolic disease. I first define paternal-gene and maternal-gene optima with regard to early human growth and development. Next, I review salient evidence with regard to imprinted gene effects on birth weight, body composition, trajectories of feeding and growth, and timing of developmental stages, to evaluate why and how imprinted gene expression influences risks of metabolic disease in later life. I find that metabolic disease risks derive primarily from maternal gene biases that lead to reduced placental efficacy, low birth weight, low relative muscle mass, high relative white fat, increased abdominal adiposity, reduced pancreatic β-cell mass that promotes insulin resistance, reduced appetite and infant sucking efficacy, catch-up fat deposition from family foods after weaning, and early puberty. Paternal gene biases, by contrast, may contribute to metabolic disease via lower rates of brown fat thermiogenesis, and through favoring more rapid postnatal catch-up growth after intrauterine growth restriction from environmental causes. These disease risks can be alleviated through dietary and pharmacological alterations that selectively target imprinted gene expression and relevant metabolic pathways. The kinship theory of imprinting, and mother-offspring conflict more generally, provide a clear predictive framework for guiding future research on fetal programming and metabolic disease.

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The tempo of human childhood: a maternal foot on the accelerator, a paternal foot on the brake

Cited by 21 publications

References 120 publications

Response to vocal music in Angelman syndrome contrasts with Prader-Willi syndrome

Response to vocal music in Angelman syndrome contrasts with Prader-Willi syndrome

GENETICS IN ENDOCRINOLOGY: Genetic etiologies of central precocious puberty and the role of imprinted genes

Why and How Imprinted Genes Drive Fetal Programming

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