How modern diets have shortened childhood

Science by Dr. Ben Bikman

The transition from childhood to adulthood is most obviously marked by the development of secondary sex structures that turn the boy into a man and the girl into a woman. This is a period of rapid growth, requiring tremendous energy. Insofar as hormones dictate energy use within the body, puberty is intimately linked with changes in metabolic function.

There are several identified factors that determine the timing of the onset of puberty, some of which are expected (e.g., family history)[1] and some unexpected (e.g., having two parents)[2]. One of the strongest signals is nutritional status and body fat mass[3]. Perhaps because the female bears the metabolic burden in reproduction, having to carry the fetus and feed the newborn, female puberty appears to be much more sensitive to metabolic and nutrition status than male puberty.

Puberty has a lot to do with the hormone leptin, a prototypical metabolic hormone. Leptin is a hormone secreted from fat tissue—the more fat tissue you have, the more leptin you’ll likely have circulating in your blood. Many recognize leptin as a hormone that sends a satiety signal to the brain, letting the body know when it’s eaten enough, but leptin does much more, including telling the brain there is sufficient body fat to sexually develop. Essentially, leptin increases the production of the hormones from the brain that drive puberty. This effect is so strong that leptin injections alone are sufficient to induce puberty in animals[4].

In recent years a global shift has occurred in nutrition. Whereas we were once concerned with people not having enough food, the number of people who eat too much food is now more common across the world. Importantly, much of the increased food we’re eating globally comes in the form of refined and insulin-spiking carbohydrates, such as sugar[5]. Parallel with this shift in nutrition and lifestyle is an equally dramatic increase in blood insulin levels[6].

At first glance, the topic of puberty has nothing to do with insulin. However, insulin and leptin are highly regulated and influence each other. As insulin rises, it stimulates leptin production from fat cells, which then activates precursor sex hormone production in the brain then the gonads.

The global change in nutrition, specifically having more of it, with its changes in insulin and leptin, has had stark effects on puberty over the decades. Current standards mark a normal period for puberty to be from around eight to 12 years old in girls and nine to 14 years old in boys. However, our current lifestyle is very different than in earlier generations, and perhaps in human history. In a broader perspective, the average onset of puberty in the mid 1800s was around 16 years old for girls. This dropped to around 14 in the early 1900s, then 13 and 12 in the mid and late 1900s, respectively. Now the average age is under 10 years old; a difference in puberty onset of almost seven years! The connection between obesity and precocious puberty is strong enough to quantify; every one unit increase in body mass index between the ages of 2 to 8 is associated with a roughly one month earlier onset of puberty [8]. In other words, if a young girl’s BMI increases 5 points above average (a very possible change) during this age range, she can expect puberty to start a half year earlier than what would be normal for her.

In the end, puberty tends to run on its own clock, but nutrition can drastically change the time zone. By lowering insulin and improving sensitivity, precocious puberty can be delayed, helping restore a balance towards normal development.


  1.  Wehkalampi, K., et al., Patterns of inheritance of constitutional delay of growth and puberty in families of adolescent girls and boys referred to specialist pediatric care. J Clin Endocrinol Metab, 2008. 93(3): p. 723-8.
  2.  Ellis, B.J., et al., Quality of early family relationships and individual differences in the timing of pubertal maturation in girls: a longitudinal test of an evolutionary model. J Pers Soc Psychol, 1999. 77(2): p. 387-401.
  3.  Dunger, D.B., M.L. Ahmed, and K.K. Ong, Effects of obesity on growth and puberty. Best Pract Res Clin Endocrinol Metab, 2005. 19(3): p. 375-90.
  4.  Ahima, R.S., et al., Leptin accelerates the onset of puberty in normal female mice. J Clin Invest, 1997. 99(3): p. 391-5.
  5.  Ismail, A.I., J.M. Tanzer, and J.L. Dingle, Current trends of sugar consumption in developing societies. Community Dent Oral Epidemiol, 1997. 25(6): p. 438-43.
  6.  Seidell, J.C., Obesity, insulin resistance and diabetes–a worldwide epidemic. Br J Nutr, 2000. 83 Suppl 1: p. S5-8.
  7.  Zhao, A.Z., K.E. Bornfeldt, and J.A. Beavo, Leptin inhibits insulin secretion by activation of phosphodiesterase 3B. J Clin Invest, 1998. 102(5): p. 869-73.
  8.  Lee, J.M., et al., Weight status in young girls and the onset of puberty. Pediatrics, 2007. 119(3): p. e624-30.

This article is for informational and educational purposes only. It is not, nor is it intended to be substitute for professional medical advice, diagnosis, or treatment and should never be relied upon for specific medical advice.