The role of diet in the timing of puberty

Anja Kroke’s project identified modifiable growth and dietary factors that may increase or decrease a child’s risk of beginning puberty early

  • Topic: Combination of cancers
  • Institution: University of Bonn
  • Country: Germany
  • Status: Completed
Researcher: Anja Kroke

Grant title

Interactions between growth characteristics and diet in infancy and childhood and their influence on age at puberty-onset, an established cancer risk factor: data from the prospective DONALD study

Scientific abstract

(View plain language abstract)

Background and objectives

Early puberty onset is a risk factor for hormone-related cancers, all-cause mortality, and has been linked to adiposity, insulin resistance, and other hormonal changes associated with cancer risk. The overall objective of this project was to investigate the association of growth characteristics and dietary factors in infancy and childhood with puberty onset.

More specifically, the project aimed to analyse the interplay between childhood growth and puberty onset, investigate the complex interactions between nutritional status and puberty onset and examine the role of dietary factors in the timing of puberty.

Methods

Data came from the prospective DOrtmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study, which collects detailed data on growth, diet and metabolism in healthy children from birth until young adulthood. Puberty onset was defined according to both early and late pubertal markers: the parametric Preece and Baines Model 1 was used to model individual growth curves and to derive the age when the pubertal growth spurt begun (age at take-off, ATO) and age at peak height velocity (APHV).

Additionally, reported age at menarche and voice break in girls/boys, respectively, was available from questionnaires. By the time of the analyses, 376 DONALD participants had already entered puberty and experienced ATO. From this data basis, appropriate sub-samples for each research question were derived (n=112 to n=222).

Results

A birth weight <3,000g, as well as gaining weight rapidly between birth and 24 months, were associated with an earlier ATO and APHV in both sexes, as well as an earlier menarche in girls. These associations were observed independently of prepubertal body composition.

The results suggested that children who experienced an earlier ATO accrued more fat-free mass standard deviation scores (SDS), but not fat mass SDS during the first four years of puberty, as compared to late maturing peers.

While neither dietary energy density nor vitamin D intake in childhood was associated with age or body composition at puberty onset, as defined by ATO, protein intake in childhood was differentially related to pubertal timing. A higher animal protein intake, particularly at the age of 5–6 years, was associated with an earlier ATO, APHV, and menarche/voice break. Conversely, a higher vegetable protein intake at 3–4 and 5–6 years was associated with a delayed puberty.

Additionally, we demonstrated that children with a lower dietary quality 2–3 years prior to ATO, defined according to the nutrient density-based Nutritional Quality Index, entered puberty at an earlier age. This association was independent of prepubertal body composition. In contrast to these two dietary factors in childhood, however, breastfeeding in infancy was not associated with any puberty marker.

Conclusions

Overall, this project identified different growth and dietary factors that may influence risk of beginning puberty early. In view of the long-term health consequences of early puberty onset, these findings have important public health implications. Future studies are warranted that are able to deepen our understanding of the mechanisms by which early growth and childhood dietary factors might operate.

Plain language abstract

Background

Early puberty onset is a risk factor for certain cancers, all-cause mortality, and has also been linked to hormonal changes associated with obesity and cancer risk. The objective of this project therefore was to investigate the association of growth characteristics and dietary factors in infancy and childhood with puberty onset.

Methods

Data came from the DOrtmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study, which collects information on growth, diet and metabolism in healthy children from birth until young adulthood. Puberty onset was defined according to both early and late pubertal markers: the age when the pubertal growth spurt starts (age at take-off, ATO) as well as age at maximal growth (peak height velocity, APHV). In addition, information on age at menarche and voice break in girls/boys, respectively, was reported by the parents and/or the children themselves.

Results

In an analysis of 215 DONALD participants who had already experienced ATO and provided data on growth in early life, it was shown that a relatively low birth weight and gaining weight rapidly between birth and 24 months were associated with an earlier ATO and APHV in both sexes, as well as an earlier menarche in girls.

In 215 children, it was suggested that children who experience an earlier ATO accrue significantly more fat-free, but not fat mass during the first four years of puberty, relative to late maturing peers of the same age. Higher levels of BMI and adiposity observed in adults with early puberty onset may thus develop subsequently in later adolescence.

While neither dietary energy density nor vitamin D intake in childhood was associated with age or body composition at puberty onset, as defined by ATO, protein intake in childhood was differentially related to pubertal timing. A higher animal protein intake, particularly at age 5–6 years, was associated with an earlier ATO, APHV and menarche/voice break independent of prepubertal body composition.

Conversely, a higher vegetable protein intake at 3–4 and 4–5 years might delay pubertal development. Additionally, we demonstrated that children with a higher dietary quality in the years preceding ATO, defined using a nutrient density-based diet index, entered puberty at a later age. Again, this association was independent of prepubertal body composition. In contrast to these dietary factors in childhood, however, breastfeeding in infancy was not associated with any of the puberty markers investigated.

Conclusions

Overall, this project successfully identified modifiable growth and dietary factors that may increase (or decrease) a child’s risk of beginning puberty early. Given the long-term health consequences of early puberty onset, these findings have important public health implications. Future studies are warranted that are able to deepen our understanding of the mechanisms by which early growth and dietary factors might operate.

Grant publications