# Childhood Infection and Pubertal Timing

> **NIH NIH K01** · COLUMBIA UNIVERSITY HEALTH SCIENCES · 2020 · $54,000

## Abstract

CHILDHOOD INFECTION AND PUBERTAL TIMING (K01 CA186943)
ABSTRACT FROM K01 CA186943
Earlier age at menarche and breast development is associated with an increased risk of breast cancer. The
average age at menarche has been declining in the U.S. and globally, and national studies show even more
dramatic declines in the age of breast development (as defined by Tanner stage T2 or higher); a greater
proportion of U.S. girls are beginning T2+ at ages 7-8. Early pubertal development results in longer lifelong
exposure to sex steroids (i.e. estrogen and progesterone). Sex-steroids promote mammary cell proliferation,
which increases susceptibility to environmental exposures that could initiate carcinogenesis. Larger childhood
body size is one major explanation for the declines in pubertal development. However, even in cultures with
much lower childhood obesity (e.g., Hong Kong), there is evidence that pubertal timing is also declining
suggesting that other factors are at play. One major ecological change has been the decline in childhood
infections from public health measures that have resulted in reduced exposure and increased resistance to
infectious agents. Emerging lines of evidence, though limited, suggests that early infancy and childhood
infections may be associated with delayed pubertal timing. Infection may not allow the body to spend energy in
pubertal development at the expense of the immune system, down-regulating steroid hormone production and/or
receptors; therefore, resulting in later pubertal timing and a decrease in breast cancer risk. While most of the
literature focuses on childhood obesity, there is an urgent need to understand other factors that may contribute
to pubertal timing, such as childhood infections. There are few cohorts in the world however that are available
to address specific hypotheses about childhood infections and pubertal timing. Using LEGACY (R01CA138822),
a prospective study enriched with girls with a breast cancer family history (recruited ages 6-13 years, N=1,040)
designed to study childhood exposures and pubertal development, I will address the understudied etiological
pathway of infection and puberty. My training in infectious disease epidemiology, behavioral oncology, and
cancer epidemiology make me uniquely qualified to examine the association between puberty (i.e. age of onset
of breast development and menarche) and: 1) childhood serologic infection burden of prevalent infections (EBV,
CMV, HSV1/2 32-68% national seroprevalence) and 2) childhood infection burden (as measured by mother
reported infectious exposures and medical records) across 5 time periods (0-12 months, age (years) 1-5 , 6-10,
11-13, 14-18). Specifically, by building efficiently on one of the largest studies in the world of girls' puberty and
coupling my novel research questions with additional training in molecular epidemiology, family-based studies,
infection and health, pubertal development, and longitudinal modeling, I will be able to als...

## Key facts

- **NIH application ID:** 10127372
- **Project number:** 3K01CA186943-05S1
- **Recipient organization:** COLUMBIA UNIVERSITY HEALTH SCIENCES
- **Principal Investigator:** Jasmine Alise McDonald
- **Activity code:** K01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $54,000
- **Award type:** 3
- **Project period:** 2020-03-16 → 2021-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10127372

## Citation

> US National Institutes of Health, RePORTER application 10127372, Childhood Infection and Pubertal Timing (3K01CA186943-05S1). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10127372. Licensed CC0.

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