In the Journals

Obesity may advance pubertal timing among boys

A cohort of Danish boys with obesity had an earlier mean onset of testicular enlargement when compared with a population-based, normal-weight reference cohort; however, the timing of other pubertal milestones did not differ between groups, according to findings published in The Journal of Clinical Endocrinology & Metabolism.

Alexander Siegfried Busch

“In normal-weight boys, BMI is negatively associated with pubertal timing,” Alexander Siegfried Busch, MD, PhD, a pediatrician in the department of growth and reproduction at the University of Copenhagen, Denmark, told Healio. “Researchers have discussed whether obesity delays or further accelerates pubertal onset. In the present large clinical study, obesity was associated with early testicular growth.”

Busch and colleagues analyzed data from 218 boys with obesity (BMI z score at least 2 standard deviations greater than normal) recruited as part of a prospective, outpatient childhood obesity intervention program in Denmark between 2009 and 2017 (mean baseline age, 11 years), as well as from 660 healthy boys participating in a population-based puberty study between 2006 and 2014 (controls; BMI z score no more than 2 standard deviations less than or greater than normal; mean age at baseline, 11 years). Researchers assessed pubertal development by Tanner staging, including testis volume. Primary outcome was timing of testicular volume of at least 4 mL, genital stage 2 or greater, and pubarche.

For boys with obesity, the mean onset of testicular volume of at least 4 mL was age 11.3 years; mean age to reach genital stage 2 or greater was age 11.6 years, and mean age of pubarche was age 11.9 years.

The researchers did not observe between-group differences in the timing of pubarche or genital stage; however, boys with obesity had an earlier mean onset of testicular volume of 4 mL or greater when compared with controls (P = .01).

In an analysis comparing boys with obesity and control boys with overweight (BMI z score no more than 1 standard deviation less or 2 standard deviations greater than normal), the researchers observed no between-group differences in mean onset of testicular enlargement, genital stage 2 or greater or pubarche. Researchers also noted that boys with severe obesity, defined as a BMI z score 3 standard deviations greater than normal, had an earlier onset of puberty compared with boys with obesity (P = .002).

“Obesity as well as early puberty are associated with later life health,” Busch said. “Early intervention could help to prevent this health burden.”

Busch said genetic studies indicate a causal effect of higher BMI on earlier pubertal onset, and further research on the mechanisms linking metabolism and pubertal reactivation of the hypothalamic-pituitary-gonadal axis is needed. – by Regina Schaffer

For more information:

Alexander Siegfried Busch, MD, PhD, can be reached at the Department of Growth and Reproduction, Rigshospitalet, Section 5064, University of Copenhagen, Blegdamsvej 9, DK-2100, Copenhagen, Denmark; email: alexander.siegfried.busch@regionh.dk.

Disclosures: The authors report no relevant financial disclosures.

A cohort of Danish boys with obesity had an earlier mean onset of testicular enlargement when compared with a population-based, normal-weight reference cohort; however, the timing of other pubertal milestones did not differ between groups, according to findings published in The Journal of Clinical Endocrinology & Metabolism.

Alexander Siegfried Busch

“In normal-weight boys, BMI is negatively associated with pubertal timing,” Alexander Siegfried Busch, MD, PhD, a pediatrician in the department of growth and reproduction at the University of Copenhagen, Denmark, told Healio. “Researchers have discussed whether obesity delays or further accelerates pubertal onset. In the present large clinical study, obesity was associated with early testicular growth.”

Busch and colleagues analyzed data from 218 boys with obesity (BMI z score at least 2 standard deviations greater than normal) recruited as part of a prospective, outpatient childhood obesity intervention program in Denmark between 2009 and 2017 (mean baseline age, 11 years), as well as from 660 healthy boys participating in a population-based puberty study between 2006 and 2014 (controls; BMI z score no more than 2 standard deviations less than or greater than normal; mean age at baseline, 11 years). Researchers assessed pubertal development by Tanner staging, including testis volume. Primary outcome was timing of testicular volume of at least 4 mL, genital stage 2 or greater, and pubarche.

For boys with obesity, the mean onset of testicular volume of at least 4 mL was age 11.3 years; mean age to reach genital stage 2 or greater was age 11.6 years, and mean age of pubarche was age 11.9 years.

The researchers did not observe between-group differences in the timing of pubarche or genital stage; however, boys with obesity had an earlier mean onset of testicular volume of 4 mL or greater when compared with controls (P = .01).

In an analysis comparing boys with obesity and control boys with overweight (BMI z score no more than 1 standard deviation less or 2 standard deviations greater than normal), the researchers observed no between-group differences in mean onset of testicular enlargement, genital stage 2 or greater or pubarche. Researchers also noted that boys with severe obesity, defined as a BMI z score 3 standard deviations greater than normal, had an earlier onset of puberty compared with boys with obesity (P = .002).

“Obesity as well as early puberty are associated with later life health,” Busch said. “Early intervention could help to prevent this health burden.”

Busch said genetic studies indicate a causal effect of higher BMI on earlier pubertal onset, and further research on the mechanisms linking metabolism and pubertal reactivation of the hypothalamic-pituitary-gonadal axis is needed. – by Regina Schaffer

For more information:

Alexander Siegfried Busch, MD, PhD, can be reached at the Department of Growth and Reproduction, Rigshospitalet, Section 5064, University of Copenhagen, Blegdamsvej 9, DK-2100, Copenhagen, Denmark; email: alexander.siegfried.busch@regionh.dk.

Disclosures: The authors report no relevant financial disclosures.