Large-scale, international type 1 diabetes registries show that in general, type 1 diabetes incidence increases with age during childhood, and peaks at puberty (Soltesz et al. 2007).
Why? We don't know. Puberty involves not only increased growth but also an increase in hormone levels and increased insulin resistance, which could stress the insulin-producing beta cells. It is understandable then that a "breakdown of the system" could occur during puberty (Ludvigsson 2006). In healthy children, insulin resistance starts to increase a few years before puberty begins, around age 7 (weight gain only explains a small part of this increase) (Jeffery et al. 2012). The onset of puberty may be a time of increased sensitivity to environmental factors (Roy et al. 2009).
One study aimed to determine whether or not increasing insulin resistance before or during puberty may contribute to type 1 diabetes onset. They found that insulin resistance rose continuously in German children from age 5 through the early teens, preceding the onset of puberty. Yet this increase was not related to the onset of islet antibodies in these children, who were at genetic risk of type 1 diabetes (Raab et al. 2013).
With hormones gone wild, blood sugar is hard to control. (While the tendency of teens to rebel may also explain some of the lack of control during puberty, it is also hard to control blood sugar during other times of hormone upheaval, such as pregnancy or even throughout a menstrual cycle). Children who develop type 1 diabetes before puberty are at greater risk for complications than children who develop type 1 after puberty (Cho et al. 2014).
It is not only type 1; German girls who experience early puberty are at higher risk of pre-diabetes and type 2 diabetes as well, no matter what their weight (Stöckl et al. 2012). The same authors found that the earlier that girls experienced puberty, the greater their later risk of high body mass index (BMI), higher waist circumference, higher blood glucose levels, and metabolic syndrome in general (Stöckl et al. 2011). In a large U.K. study of whites, earlier puberty was associated with a higher risk of type 2 diabetes in both men and women (Day et al. 2015).
In the U.S., the large Nurses' Health Study also showed that girls who experienced puberty at younger ages were at increased risk of type 2 diabetes in adulthood. While excess body weight may play a role, the associations remained after controlling for BMI. The association was especially strong in younger women, arguing for a role of sex hormones in the younger type 2 onset (He et al. 2010).
A study from China found that girls with earlier puberty had a higher risk of later gestational diabetes as well (Li et al. 2017).
Puberty is showing up at younger ages, especially in girls. A panel of experts examined the evidence regarding environmental factors and puberty timing. The majority of the panelists concluded that the girls’ data are sufficient to suggest a trend toward earlier puberty from 1940 to 1994 but that the boys’ data are insufficient to suggest a trend during this same period. Their evaluation of human and animal studies suggests that endocrine disrupting chemicals (particularly the estrogenic chemicals and anti-androgens) and body fat are important factors associated in altered puberty timing (Euling et al. 2008).
The decreasing age of puberty has probably contributed to the increased incidence of type 1 diabetes in younger children, by accelerating the disease process. For example, earlier puberty might explain why the peak age of onset of type 1 diabetes in girls has fallen about 4 years in Norway since the 1930s (Gale 2005b). Early puberty also linked to an increased risk of gestational diabetes (Chen et al. 2016).
A large study from Sweden shows that among people diagnosed before age 35, type 1 incidence peaked at age 10-14 (around the time of puberty) in both boys and girls in 1983, the start of the study period. By the end of the study period (2007), type 1 incidence peaked in girls at an earlier age, 5-9 years, while the peak in boys did not change (Dahlquist et al. 2011).
Roy et al. (2009) review the evidence that estrogen-like endocrine disruptors, found in everything from plastics to flame retardants to pesticides, can affect puberty in humans. These chemicals include some persistent organic pollutants (DDT, dioxin, PCBs, PBBs), bisphenol A, phthalates, and some pesticides.
The decreasing age of puberty probably contributes to the ongoing shift of type 1 diabetes incidence toward children of younger ages. Environmental chemical exposures are likely accelerating the appearance of puberty in girls, and thereby may contribute to the acceleration of type 1 diabetes as well as increasing the later risk of type 2 diabetes.
To download or see the references on this page, as well as additional articles on diabetes and puberty, see the collection Puberty and diabetes/obesity in Pubmed.