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Revisiting the critical weight hypothesis for regulation of pubertal timing in boys

BACKGROUND: Recent findings indicate that there is a body weight–sensing homeostatic regulation of body weight in postpubertal rodents and humans. It is possible that body weight sensing also might be involved in the regulation of pubertal timing. Although an early small study suggested that there i...

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Autores principales: Bygdell, Maria, Kindblom, Jenny M, Jansson, John-Olov, Ohlsson, Claes
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7779230/
https://www.ncbi.nlm.nih.gov/pubmed/33184646
http://dx.doi.org/10.1093/ajcn/nqaa304
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author Bygdell, Maria
Kindblom, Jenny M
Jansson, John-Olov
Ohlsson, Claes
author_facet Bygdell, Maria
Kindblom, Jenny M
Jansson, John-Olov
Ohlsson, Claes
author_sort Bygdell, Maria
collection PubMed
description BACKGROUND: Recent findings indicate that there is a body weight–sensing homeostatic regulation of body weight in postpubertal rodents and humans. It is possible that body weight sensing also might be involved in the regulation of pubertal timing. Although an early small study suggested that there is a critical body weight for pubertal timing in girls, most studies have focused on BMI and reported an inverse association between BMI and pubertal timing. OBJECTIVES: In the present longitudinal well-powered cohort study, we revisited the critical weight hypothesis and tested if prepubertal body weight is a more robust inverse predictor of pubertal timing than prepubertal BMI in boys. METHOD: We included men born during 1945–1961 (old cohort; n = 31,971) and men born during 1981–1996 (recent cohort; n = 1465) in the large BMI Epidemiology Study (BEST) Gothenburg (combined BEST cohort n = 33,436). Men with information on prepubertal body weight and BMI at 8 y of age and age at peak height velocity (PHV; an objective measure of pubertal timing) were included. RESULTS: Body weight explained more of the variance in age at PHV than BMI in both the old cohort and the recent cohort (combined cohort, body weight 6.3%, BMI 3.6%). Both body weight (β: −0.24 SD/SD increase in weight; 95% CI: −0.25, −0.23) and BMI (β: −0.18 SD/SD increase in BMI, 95% CI: −0.19, −0.17) were inversely associated with age at PHV but the association for body weight was significantly more pronounced than the association for BMI (P < 0.001). CONCLUSIONS: In conclusion, prepubertal body weight is a more robust inverse predictor of pubertal timing than prepubertal BMI in boys. We propose that body weight sensing constitutes a feedback mechanism to regulate pubertal timing.
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spelling pubmed-77792302021-01-07 Revisiting the critical weight hypothesis for regulation of pubertal timing in boys Bygdell, Maria Kindblom, Jenny M Jansson, John-Olov Ohlsson, Claes Am J Clin Nutr Original Research Communications BACKGROUND: Recent findings indicate that there is a body weight–sensing homeostatic regulation of body weight in postpubertal rodents and humans. It is possible that body weight sensing also might be involved in the regulation of pubertal timing. Although an early small study suggested that there is a critical body weight for pubertal timing in girls, most studies have focused on BMI and reported an inverse association between BMI and pubertal timing. OBJECTIVES: In the present longitudinal well-powered cohort study, we revisited the critical weight hypothesis and tested if prepubertal body weight is a more robust inverse predictor of pubertal timing than prepubertal BMI in boys. METHOD: We included men born during 1945–1961 (old cohort; n = 31,971) and men born during 1981–1996 (recent cohort; n = 1465) in the large BMI Epidemiology Study (BEST) Gothenburg (combined BEST cohort n = 33,436). Men with information on prepubertal body weight and BMI at 8 y of age and age at peak height velocity (PHV; an objective measure of pubertal timing) were included. RESULTS: Body weight explained more of the variance in age at PHV than BMI in both the old cohort and the recent cohort (combined cohort, body weight 6.3%, BMI 3.6%). Both body weight (β: −0.24 SD/SD increase in weight; 95% CI: −0.25, −0.23) and BMI (β: −0.18 SD/SD increase in BMI, 95% CI: −0.19, −0.17) were inversely associated with age at PHV but the association for body weight was significantly more pronounced than the association for BMI (P < 0.001). CONCLUSIONS: In conclusion, prepubertal body weight is a more robust inverse predictor of pubertal timing than prepubertal BMI in boys. We propose that body weight sensing constitutes a feedback mechanism to regulate pubertal timing. Oxford University Press 2020-11-12 /pmc/articles/PMC7779230/ /pubmed/33184646 http://dx.doi.org/10.1093/ajcn/nqaa304 Text en © The Author(s) 2020. Published by Oxford University Press on behalf of the American Society for Nutrition. http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research Communications
Bygdell, Maria
Kindblom, Jenny M
Jansson, John-Olov
Ohlsson, Claes
Revisiting the critical weight hypothesis for regulation of pubertal timing in boys
title Revisiting the critical weight hypothesis for regulation of pubertal timing in boys
title_full Revisiting the critical weight hypothesis for regulation of pubertal timing in boys
title_fullStr Revisiting the critical weight hypothesis for regulation of pubertal timing in boys
title_full_unstemmed Revisiting the critical weight hypothesis for regulation of pubertal timing in boys
title_short Revisiting the critical weight hypothesis for regulation of pubertal timing in boys
title_sort revisiting the critical weight hypothesis for regulation of pubertal timing in boys
topic Original Research Communications
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7779230/
https://www.ncbi.nlm.nih.gov/pubmed/33184646
http://dx.doi.org/10.1093/ajcn/nqaa304
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