A recent study that was conducted shows that there may be a correlation between race, weight, and the timing of puberty in males. Get details in full article.
Spurred by mixed and even conflicting results from studies evaluating whether an association exists between weight and timing of puberty in boys, as it is known to exist in girls, a recent article published in Pediatrics reported findings that body weight not only does affect timing of puberty in U.S. boys, but does so in a strikingly nonlinear fashion.
In “Timing of Puberty in Overweight Versus Obese Boys,” study authors led by Joyce Lee, MD, at the University of Michigan in Ann Arbor, found that in certain ethnic groups, obesity contributed to delayed puberty in boys compared to normal-weight boys, whereas overweight contributed to earlier pubertal timing. Using data collected by pediatricians during routine well-child visits from approximately 3,900 boys, in addition to height and weight for age, researchers analyzed the age at which Tanner genital development stages 2 through 5 were reached. Of the participants, 49.9% were white, 25.8% were African American, and 24.3% were Hispanic, with 60% being normal weight, 17% overweight, and 23% obese (body weight categories defined by the Centers for Disease Control and Prevention).
“Prevention of obesity would prevent a slight delay in timing of puberty, but nobody has a handle on prevention of obesity because it is such a complex, multifactorial issue. Moreover, there are far more serious consequences of being obese than what you can say about altering the timing of puberty.”- Paul Kaplowitz, MD, Children’s National Health System, Washington, D.C.
The data showed that overweight white boys entered Tanner stage 2 genital development (Tanner GD2), an early stage of puberty comprising testicular enlargement, at average age 9.3 years, which is about .7 years earlier than their normal-weight peers who entered puberty at an average age of 10 years. This cohort also entered Tanner GD5, the final pubertal stage, earlier, at about age 14.5 years compared with age 15.2 years. Obese white boys, by contrast, entered Tanner GD5 later than average, at around 15.4 years old.
In African-American boys, obese boys entered Tanner GD3 (characterized primarily by penile elongation) about 11 months later than overweight boys and Tanner GD4 12 months later, whereas normal-weight boys entered Tanner GD4 (characterized by overall penile enlargement and other changes) four months later than overweight boys.
In Hispanic boys, significant differences in puberty onset were not found across weight categories.
It’s Complicated
Such findings come from taking the data at face value, explains Paul Kaplowitz, MD, from the Children’s National Health System in Washington, D.C., who is acknowledged as contributing his expert opinion on development of the study manual and who is also an Endocrine Society expert. The actual take-away is considerably more nuanced.
The idea of body weight affecting pubertal timing in boys is still controversial, despite the many attempts to verify a relationship, in part because there are problems with reliably assessing the onset of puberty in males. “The bottom line is that defining the onset of puberty in boys is somewhat more challenging than defining the onset of puberty in girls, in whom breast development is a fairly reliable indicator,” Kaplowitz says. “In boys, the earliest sign of puberty is not genital enlargement but testicular enlargement, which can be very subtle and takes careful measurement. The question is, then, what point of testicular size determines onset of puberty? I believe that the 3-ml and 4-ml markers used in this study might not be reliable indicators of puberty. In my practice, I have seen many boys with 3-4-ml testes who are not going into puberty, but 5 or 6 ml is a different story.”
A related issue is the confounding delay between Tanner GD2 and Tanner GD3 that researchers reported. “If puberty were really starting at stage 2, then stage 3 should have been reached within six to 12 months later, instead of two to three years later,” Kaplowitz says. For example, normal-weight African-American boys were reported to have reached GD2 at an average age of 8.8 years and GD3 at age 11.1 years, or 2.3 years later. Further evidence that 3 ml testicular volume (TV) is not reliable for defining onset of puberty is that progressing from TV 3 ml or greater to TV 4 ml or greater was reported to take 1.6 to 2.0 years to, a very long time for such a small increase. Therefore, staging male puberty at GD3, which is characterized by both penile and testicular enlargement, is more reliable. Focusing on when Tanner GD3 was reached rather than on Tanner GD2 reveals little overall difference among the groups, except in African-American boys — obese African-American boys reached Tanner GD3 about 0.6 years later than normal-weight African-American boys, and this delay continued through Tanner GD4 and GD5. “If there is a relationship between pubertal delay and obesity, it is most clearly seen in African-American boys, although there may be a smaller trend in the same direction in Hispanic boys,” Kaplowitz says.
Another puzzling problem with the data analysis is that it leads to the conclusion that overweight boys start puberty earlier than normal-weight boys, which seems counterintuitive. If obese boys start puberty later, logically, overweight boys would enter puberty either at slightly less of a delay than their obese counterparts or show no difference in timing from their normal-weight counterparts. “Due to the problem with the definition of GD2 used in the study, I think there is reason to be suspicious of claims that overweight induces earlier timing of puberty,” Kaplowitz says. “A fundamental problem with this article is that it looks at the data and says there must be two opposite things going on: There is an overweight puberty effect and there is a separate obesity puberty effect, and that does not make biological sense.”
“If there is a relationship between pubertal delay and obesity, it is most clearly seen in African-American boys, although there may be a smaller trend in the same direction in Hispanic boys.” – Paul Kaplowitz, MD, from the Children’s National Health System in Washington, D.C.
It Gets Even More Complicated!
If no clear relationship exists between obesity and the timing of puberty in males that covers all ethnic groups, why is this association so much more robust in girls, in whom earlier puberty, as indicated by breast development and the appearance of pubic hair, is consistently seen with obesity? “There is quite a sexual dimorphism regarding the impact of obesity on puberty,” Kaplowitz says. His theory as to why the dimorphism arises centers on the reproductive axis, specifically, the leptin produced in adipocytes, which not only regulates appetite and is an essential factor in entering and progressing through puberty, but is also found in higher levels in females and even more so just before puberty.
“It makes a lot of sense to have a mechanism that shuts down reproduction in females when fat stores are low and increases the likelihood of being reproductively mature and capable of supporting a pregnancy when fat stores are good,” Kaplowitz explains. “With males, once they make their contribution, the sperm, there really is no evolutionary reason why body weight would influence reproduction or ability to go through puberty.”
Weight Limits — The Role of Weight and Puberty in Boys
Supposing obesity does cause delayed puberty in males, are there implications for individual patients? “Prevention of obesity would prevent a slight delay in timing of puberty,” Kaplowitz says. “But nobody has a handle on prevention of obesity because it is such a complex, multifactorial issue. Moreover, there are far more serious consequences of being obese than what you can say about altering the timing of puberty.”
Nevertheless, according to the study authors, the inconsistent findings themselves in this study warrant further investigation into the possible role of weight and puberty in boys.
— Horvath is a freelance writer based in Baltimore, Md. She wrote about growth hormone and its effects on osteoporosis outcomes in the May issue.
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