Girls, and probably boys, are reaching puberty years younger than they did in our great-grandparents' generation. Why? There's no shortage of explanations, but the primary reason is probably quite simple.
In the 1980s, a Duke public health researcher named Marcia Herman-Giddens began to notice something strange. While the textbooks said that most girls should begin showing signs of puberty after age 11, the majority of girls in the pediatric clinic where she worked were hitting this milestone before age 10 (1).
This led her to conduct a study of more than 17,000 girls, confirming that the first signs of puberty were occurring before age 10 both in girls of European and African descent in the US (2). Although the initial research was controversial, several other studies have bolstered the finding that puberty is occurring substantially younger in girls (and probably boys) than it used to.
The further back we look in history, the later puberty begins. Among the Hadza, perhaps the last true hunter-gatherers left in the world, menarche (onset of menstruation) occurs at an average age of 16.5 years (Marlowe. The Hadza. 2010). Historically, among the Ache, hunter-gatherers in Paraguay, the mean age of menarche was 15.3 years (Hill and Hurtado. Ache Life History. 1996). Herman-Giddens found that in the modern US, menarche occurs at an average age of 12.2 years in girls of African descent, and 12.9 years in girls of European descent. The limited data we have suggests that age of menarche in Europe and the US 150 years ago was similar to that of hunter-gatherers (3).
Explanations abound for the decline in the age of puberty in girls and boys. Some contend it's due to the artificial hormones in conventionally produced milk. Others attribute it to estrogen-like endocrine-disrupting chemicals in plastic and agricultural chemicals. But there's a much simpler explanation that also happens to have some very convincing evidence behind it: we're bigger and fatter than we used to be.
As part of the research for my upcoming book The Hungry Brain, I recently interviewed Mark Wilson, a researcher at Emory who studies reproductive health (among other things) using rhesus monkeys.
Wilson pointed me to the research of Ei Terasawa and colleagues at the University of Wisconsin-Madison, who published a paper in 2012 reporting the effects of a high-calorie diet on puberty in female rhesus monkeys (3).
At the age of 12 months, monkeys were randomly assigned to receive either a standard low-fat/normal-calorie diet, or a higher-fat/high-calorie diet. The animals were allowed to eat as much of each diet as they wanted.
As expected, the monkeys eating the high-calorie diet grew faster and fatter. Yet the effects on sexual maturation were even more striking. The high-calorie group reached menarche at 19.8 months, while the normal-calorie group didn't reach menarche until 25 months.
In this study, earlier menarche was associated with hormonal differences. High-calorie-fed monkeys had higher levels of leptin, insulin-like growth factor-1 (IGF-1), follicle-stimulating hormone, and a trend toward higher luteinizing hormone. These hormones are all involved in growth and sexual maturation.
In 2013, Mark Wilson and colleagues published a paper attempting to uncover the mechanism behind these hormonal effects (4). To do this, they randomly assigned two groups of rhesus monkeys to receive either leptin injections, or injections not containing leptin, from ages 12 to 30 months. All monkeys were on a standard, normal-calorie diet. Remember that leptin is a signal that informs the brain of the amount of fat mass we carry. Higher leptin makes the brain think there's more fat around.
Just as Terasawa had observed with a high-calorie diet, leptin caused the monkeys to mature faster. "The girls that were getting leptin grew faster", explains Wilson. "You had increased growth hormone particularly at night, you had increased IGF-1. It all made sense." And, most importantly, they reached menarche earlier.
As Wilson says, it all makes sense. Energy is perhaps the most fundamental requirement for reproduction, and the reproductive system is therefore very sensitive to energy status. As usual, the brain is at the helm of this regulatory system.
Since leptin is the main signal that communicates the amount of energy stored in the body to the brain, it plays a key role in the onset of puberty. We actually know quite a bit about how this works. Puberty results from a hormonal cascade originating in the hypothalamus of the brain and cascading down to the pituitary gland and the gonads. The hypothalamus is also the primary part of the brain that detects and regulates body energy status, and neurons regulating body energy status and reproductive function are intimately connected. So it makes perfect sense that leptin, and ultimately calorie intake and body fatness, regulates the hormonal cascade that determines when puberty happens*.
Simply stated, we're hitting puberty earlier because our food environment and lifestyle are driving us to eat excess calories. This is consistent with our increase in body fatness over the last century, and particularly over the last 35 years. My upcoming book The Hungry Brain will attempt to explain why we often eat too much, despite our best intentions.
* This also explains why women who are very lean or have high physical activity levels often stop menstruating. Their leptin levels are too low, and the brain shuts down ovulation because it doesn't think there's enough energy in the body to support reproduction.