Age at Menarche: Influences of Prenatal and Postnatal Growth

Sloboda, Deborah M.; Hart, Roger; Doherty, Dorota; Pennell, Craig E.; Hickey, Martha

doi:10.1210/jc.2006-1378

Cited by 244 publications

(210 citation statements)

References 28 publications

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“…Strengths of our study include the large sample size and the prospectively collected data on diet in early and midchildhood as well as at 10 years, close to the time of menarche. Most other studies have collected data on diet only close to or after menarche, but the associations between early growth and pubertal development (23,24) suggest that the critical exposures predicting puberty may occur earlier in childhood. In addition, measuring diet close to the time of puberty introduces the possibility of reverse causation, whereby puberty may affect dietary intakes rather than vice versa.…”

Section: Discussionmentioning

confidence: 99%

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Diet throughout childhood and age at menarche in a contemporary cohort of British girls

Rogers

Northstone

Cooper

et al. 2010

Public Health Nutr.

147

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Objective: To investigate associations between dietary intakes throughout childhood and age at menarche, a possible indicator of future risk of disease, in a contemporary cohort of British girls. Design: Diet was assessed by FFQ at 3 and 7 years of age, and by a 3 d unweighed food diary at 10 years. Age at menarche was categorised as before or after 12 years 8 months, a point close to the median age in this cohort. Setting: Bristol, South-West England. Subjects: Girls (n 3298) participating in the Avon Longitudinal Study of Parents and Children. Results: Higher energy intakes at 10 years were positively associated with the early occurrence of menarche, but this association was removed on adjusting for body size. Total and animal protein intakes at 3 and 7 years were positively associated with age at menarche #12 years 8 months (adjusted OR for a 1 SD increase in protein at 7 years: 1?14 (95 % CI 1?04, 1?26)). Higher PUFA intakes at 3 and 7 years were also positively associated with early occurrence of menarche. Meat intake at 3 and 7 years was strongly positively associated with reaching menarche by 12 years 8 months (OR for menarche in the highest v. lowest category of meat consumption at 7 years: 1?75 (95 % CI 1?25, 2?44)). Conclusions: These data suggest that higher intakes of protein and meat in early to mid-childhood may lead to earlier menarche. This may have implications for the lifetime risk of breast cancer and osteoporosis.

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Section: Discussionmentioning

confidence: 99%

“…The critical period for diet to impact on pubertal timing may be many years earlier, as suggested by the recently demonstrated associations between early growth and AAM (23,24) . Many studies lack information on important potential confounding factors.…”

mentioning

confidence: 99%

Diet throughout childhood and age at menarche in a contemporary cohort of British girls

Rogers

Northstone

Cooper

et al. 2010

Public Health Nutr.

147

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“…68 There are also data showing that children who gain weight faster also have earlier puberty; in both humans and rats there is a synergism between impaired early development and pre-pubertal weight gain in accelerating the age of female puberty. 69,70 One interpretation might be that the primary predictive adaptive response to an impaired early environment is to accelerate maturation in an attempt to preserve fitness. However, it can also be interpreted that as pregnancy in a young female without adequate energetic stores is likely to compromise both maternal and offspring health, accelerated maturation must be associated with increased energy stores before first conception.…”

Section: The 'Mismatch' or 'Thrifty' Pathwaymentioning

confidence: 99%

Developmental and epigenetic pathways to obesity: an evolutionary-developmental perspective

2008

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Although variation in individual lifestyle and genotype are important factors in explaining individual variation in the risk of developing obesity in an obesogenic environment, there is growing evidence that developmentally plastic processes also contribute. These effects are mediated at least in part through epigenetic processes. These developmental pathways do not directly cause obesity but rather alter the risk of an individual developing obesity later in life. At least two classes of developmental pathway are involved. The mismatch pathway involves the evolved adaptive responses of the developing organism to anticipated future adverse environments, which have maladaptive consequences if the environment is mismatched to that predicted. This pathway can be cued by prenatal undernutrition or stresses that lead the organism to forecast an adverse future environment and change its developmental trajectory accordingly. As a result, individuals develop with central and peripheral changes that increase their sensitivity to an obesogenic environment. It provides a model for how obesity emerges in populations in rapid transition, but also operates in developed countries. There is growing experimental evidence that this pathway can be manipulated by, for example, postnatal leptin exposure. Secondly, maternal diabetes, maternal obesity and infant overfeeding are associated with a greater risk of later obesity. Early life offers a potential point for preventative intervention.

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“…This level of parental investment can be conceptualized as an early-life factor that influences a woman's subsequent reproductive scheduling [77] or a consequence of her reproductive strategy that has implications for survival and reproduction in subsequent generations [35]. For example, a woman's birth weight predicts her age at menarche [100,101], and in turn, a woman's menarcheal age is associated with her offspring's birth weight [102,103]. Moreover, as all the primordial follicles a woman will ever have are present in her fetal ovaries, it is likely the fetal environment will directly influence subsequent fertility, as it does in other animals [104].…”

Section: (A) Birth Weight and Fertilitymentioning

confidence: 99%

Developmental influences on fertility decisions by women: an evolutionary perspective

Coall

Tickner

McAllister

et al. 2016

Phil. Trans. R. Soc. B

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Developmental environments are crucial for shaping our life course. Elements of the early social and biological environments have been consistently associated with reproduction in humans. To date, a strong focus has been on the relationship between early stress, earlier menarche and first child birth in women. These associations, found predominately in high-income countries, have been usefully interpreted within life-history theory frameworks. Fertility, on the other hand—a missing link between an individual's early environment, reproductive strategy and fitness—has received little attention. Here, we synthesize this literature by examining the associations between early adversity, age at menarche and fertility and fecundity in women. We examine the evidence that potential mechanisms such as birth weight, childhood body composition, risky health behaviours and developmental influences on attractiveness link the early environment and fecundity and fertility. The evidence that menarche is associated with fertility and fecundity is good. Currently, owing to the small number of correlational studies and mixed methodologies, the evidence that early adversity predicts fecundity and fertility is not conclusive. This area of research is in its infancy; studies examining early adversity and adult fertility decisions that can also examine likely biological, social and psychological pathways present opportunities for future fertility research.

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Age at Menarche: Influences of Prenatal and Postnatal Growth

Cited by 244 publications

References 28 publications

Diet throughout childhood and age at menarche in a contemporary cohort of British girls

Diet throughout childhood and age at menarche in a contemporary cohort of British girls

Developmental and epigenetic pathways to obesity: an evolutionary-developmental perspective

Developmental influences on fertility decisions by women: an evolutionary perspective

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