<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Robertson OC</submitter><funding>U.S. PHS; National Institutes of Health; National Institute of Mental Health</funding><funding>Eunice Kennedy Shriver National Institute of Child Health and Human Development</funding><funding>NICHD NIH HHS</funding><funding>NIDA NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>U.S. Public Health Service</funding><funding>National Institutes of Health</funding><funding>National Institutes of Health; National Institute on Drug Abuse</funding><funding>U.S. PHS</funding><funding>U.S. Public Health Service (PHS)</funding><funding>NIDDK NIH HHS</funding><funding>U.S. PHS; National Institutes of Health; National Institute of Diabetes and Digestive and Kidney Diseases</funding><funding>National Institute of Mental Health</funding><funding>U.S. PHS; National Institutes of Health; Eunice Kennedy Shriver National Institute of Child Health and Human Development</funding><funding>U.S. PHS; National Institutes of Health; Office of Behavioral and Social Sciences Research</funding><funding>National Institute on Drug Abuse</funding><pagination>1817-1831</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9593554</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>58(10)</volume><pubmed_abstract>The thrifty phenotype and fetal overnutrition hypotheses are two developmental hypotheses that originated from the &lt;i>developmental origins of health and disease&lt;/i> (DOHaD) perspective. The DOHaD posits that exposures experienced prenatally and early in life may influence health outcomes through altering form and function of internal organs related to metabolic processes. Obesity risk and early pubertal timing might be influenced by similar mechanisms. The thrifty phenotype hypothesis is primarily characterized by experiencing a deprivation of nutrients during gestation paired with an energy rich postnatal environment. The fetal overnutrition hypothesis says that obesity experienced prenatally will be associated with increased lifetime risk of obesity in the offspring. Both hypotheses were tested by examining developmental pathways from genetic and prenatal risk through early growth trajectories (birth to 7 years) to pubertal timing at age 11 years. Participants included 361 children adopted at birth (57% male; 57% non-Hispanic White, 11% Black, 9% Hispanic; adoptive family income &lt;i>Mdn&lt;/i> = $70,000-$100,000, birth family income &lt;i>Mdn&lt;/i> = &lt; $15,000). Associations between boys' childhood body mass index (BMI) and pubertal timing were confounded by genetics, prenatal risk, and early growth. The thrifty phenotype hypothesis was partially supported for boys' childhood BMI (at ages 4 to 7 years). Both hypotheses were partially supported for girls' childhood BMI but not pubertal timing. A novel Gene × Prenatal Risk interaction showed that genetic risk predicted girls' childhood BMI most strongly at adequate compared with at excessive levels of gestational weight gain. (PsycInfo Database Record (c) 2022 APA, all rights reserved).</pubmed_abstract><journal>Developmental psychology</journal><pubmed_title>Prenatal programming of developmental trajectories for obesity risk and early pubertal timing.</pubmed_title><pmcid>PMC9593554</pmcid><funding_grant_id>R01 MH092118</funding_grant_id><funding_grant_id>R01 HD042608</funding_grant_id><funding_grant_id>R01 DK090264</funding_grant_id><funding_grant_id>R01 DA020585</funding_grant_id><funding_grant_id>R01 DA045108</funding_grant_id><funding_grant_id>R56 HD042608</funding_grant_id><funding_grant_id>K01 DA039288</funding_grant_id><pubmed_authors>Leve LD</pubmed_authors><pubmed_authors>Marceau K</pubmed_authors><pubmed_authors>Robertson OC</pubmed_authors><pubmed_authors>Neiderhiser JM</pubmed_authors><pubmed_authors>Duncan RJ</pubmed_authors><pubmed_authors>Ganiban JM</pubmed_authors><pubmed_authors>Shirtcliff EA</pubmed_authors><pubmed_authors>Natsuaki M</pubmed_authors><pubmed_authors>Shaw DS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Prenatal programming of developmental trajectories for obesity risk and early pubertal timing.</name><description>The thrifty phenotype and fetal overnutrition hypotheses are two developmental hypotheses that originated from the &lt;i>developmental origins of health and disease&lt;/i> (DOHaD) perspective. The DOHaD posits that exposures experienced prenatally and early in life may influence health outcomes through altering form and function of internal organs related to metabolic processes. Obesity risk and early pubertal timing might be influenced by similar mechanisms. The thrifty phenotype hypothesis is primarily characterized by experiencing a deprivation of nutrients during gestation paired with an energy rich postnatal environment. The fetal overnutrition hypothesis says that obesity experienced prenatally will be associated with increased lifetime risk of obesity in the offspring. Both hypotheses were tested by examining developmental pathways from genetic and prenatal risk through early growth trajectories (birth to 7 years) to pubertal timing at age 11 years. Participants included 361 children adopted at birth (57% male; 57% non-Hispanic White, 11% Black, 9% Hispanic; adoptive family income &lt;i>Mdn&lt;/i> = $70,000-$100,000, birth family income &lt;i>Mdn&lt;/i> = &lt; $15,000). Associations between boys' childhood body mass index (BMI) and pubertal timing were confounded by genetics, prenatal risk, and early growth. The thrifty phenotype hypothesis was partially supported for boys' childhood BMI (at ages 4 to 7 years). Both hypotheses were partially supported for girls' childhood BMI but not pubertal timing. A novel Gene × Prenatal Risk interaction showed that genetic risk predicted girls' childhood BMI most strongly at adequate compared with at excessive levels of gestational weight gain. (PsycInfo Database Record (c) 2022 APA, all rights reserved).</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Oct</publication><modification>2025-04-26T19:41:12.726Z</modification><creation>2025-04-06T16:09:50.397Z</creation></dates><accession>S-EPMC9593554</accession><cross_references><pubmed>35727305</pubmed><doi>10.1037/dev0001405</doi></cross_references></HashMap>