According to the hygiene hypothesis, growing up in a home cleaned to contemporary standards can increase a child’s risk for developing allergies. Using Lysol and other disinfectants kills microorganisms that play a role in the development of an immune system that won’t overreact when confronted with say pollen or peanut butter.

Taking the hypothesis a step further, Jasmine McDonald, assistant professor of Epidemiology, is studying whether a similar phenomenon is responsible for the increasing number of girls who are experiencing an earlier age of puberty.

Over the last 50 years, the median age of puberty for girls in the United States and other wealthy countries has dropped where breast development is up to a year earlier, and some girls show signs of breast development as early as age 5. Not only is experiencing these changes at a young age socially awkward, it’s also linked to risk for breast cancer, cardiovascular disease, and type 2 diabetes.

Explanations for earlier puberty in girls are varied: some suggest obesity and endocrine–disrupting chemicals could be causal factors. There is also growing evidence that the immune system may play a role. In a 2016 review article in the Journal of Developmental Origins of Health and Disease, McDonald reported an association between childhood infections and later age of breast development.

An evolutionary lens is helpful to understand the link. Over millennia our immune systems have developed to fight life–threatening infections so we can survive to reproductive age. This process helps set the clock for puberty.

When a young girl got an infection, she expended energy to fight off pathogens, from inflammatory respiratory viruses to anti–inflammatory illnesses like schistosomiasis, an infection from a parasitic worm. According to this theory, these infections activate a child’s immune system. Once a girl’s immune system becomes adapted to the pathogenic challenges in her environment, resources can now be directed to the energy–intensive process of puberty. On the other hand, in more sterile environments, energy that would otherwise be fighting infections may be directed to puberty sooner rather than later.

In her new study, funded through a Columbia University Junior Faculty Diversity Grant, McDonald is looking behind the curtain at the biological underpinnings of this process using the New York site of the LEGACY Girls Cohort. The study is the first to look at multiple pubertal outcomes – breast development, pubic hair, and menarche – as well as prospective measures of molecular markers for immune and hormone signaling in a cohort of 37 girls ages 8 to 14 years. The Provost award allows McDonald to scale up her study to over 150 girls with assessments at several time points, where half of these girls are at increased risk of breast cancer due to a family history of the disease.

“We know the immune system communicates with the endocrine system,” she says. “When your immune system is kicking in, you don’t have the same kind of hormonal response.”

While the immune systems of the girls in the study cohort haven’t been challenged to the extent they would in a developing nation, they still likely would have encountered pathogens like herpes simplex virus 1, the bug behind cold sores. Some may have been hospitalized with severe respiratory virus or even gotten a worm infection. McDonald expects to find that girls who were exposed to more infections during childhood experienced puberty later than their counterparts with fewer infections.