The Age of Menarche: The Effect of Endocrine-Disrupting Compounds and other Environmental Factors

 In Education, Endocrinology, Fertility, Pediatrics, Women's Health

Kristina Conner, ND

The rise of endocrine disorders is particularly significant to naturopathic practice, given the strong correlation of endocrine function to the determinants of health. We expect that due to lifestyle in contemporary Western lifestyle, normal patterns of endocrine function have changed. One striking example is the age at onset of menses, or menarche. How much has menarche changed over time? And what are the effects of environmental factors on the age of menarche? For an investigation of this topic, I will review some of the recent research on environmental influences on menarche and female sexual development. Then I will discuss how naturopathic physicians, by addressing the determinants of health, can make an impact on this area.

Recent data indicates a notable movement toward earlier menarche, and other stages of sexual development such as breast development. From 1963-1970, the National Health Examination Survey (NHES) found that the median age at menarche was 12.80 years for Caucasian girls, 12.52 years for African American girls, and 12.76 for all races, which includes data for “other races” which were not tracked separately (MacMahon, 1974). Just 25 years later, the Third National Health and Nutrition Examination Survey (NHANES III), conducted from 1988-1994, found the mean age was 12.6 years for Caucasian girls, and 12.2 years for African American girls (Wu et al, 2002). We find the trend toward an earlier onset of menarche holds in other countries also. A South Korean study found the mean menarcheal age decreased from 16.8 to 12.7 years comparing girls in 1920 to those in 1986 (Hwang et al, 2003). A review of retrospective data on Danish women showed a continuous decline in the mean age at menarche for women born between 1964 and 1973, which was lower by one year than similar data from women born in the years 1939-1968 (Olesen et al, 2000). A Brazilian study found a decline in mean age from 13.07 to 12.40 years comparing women born in the 1920s to those born in the 1970s (Kac et al, 2000).

There are several hypotheses for the change in menarche timing, including better nutrition, increase in height, increase in weight, and the higher incidence of insulin resistance/diabetes; there is some obvious overlap in these hypotheses, which supports the idea of a multifactorial approach to eliminating causes. From the mid-nineteenth to mid-twentieth century, the average age at menarche decreased by three years, presumably due to improved nutritional status. Certainly, we do not want to decrease nutritional status; but we know that being well fed is not the same as being well nourished; being well nourished may decrease the average age slightly, but amongst well-fed yet under-nourished girls, the decrease in age at menarche points to other factors that are well-addressed in naturopathic nutrition.

A main suspected reason for the change in menarche timing is the rise in endocrine-disrupting compounds (EDCs), now ubiquitous in our world. EDCs affect normal functioning in areas of reproduction, metabolism, neurology and other yet unknown effects. Since these compounds are novel in both exposure and effect, and current lifestyle habits provide an untold number of exposures, their entire impact still remains to be seen. Yet there is a growing body of evidence that pubertal timing is particularly sensitive to in utero and early childhood exposure to EDCs (Euling et al, 2008). For example:

  1. High exposure in utero to dichlorodiphenyldichloroethene (DDE), was strongly correlated with a one-year decrease in the age at menarche in one study on women who lived in a shoreline county of Lake Michigan (Vasiliu et al., 2004). DDE is a metabolite of DDT, which is now banned for agricultural use but is still used in some countries to control vectors that transmit malaria and other insect-borne diseases (WHO website). One study found a correlation between an earlier age of menarche and high serum levels of DDT as an adult (Ouyang et al., 2005). However a study from the University at Albany, State University of New York, found no relationship between attainment of menarche and DDE levels (Denham et al., 2005).
  2. Although dioxins have demonstrated anti-estrogenic activity, in at least two separate studies there has been no link found between dioxin exposure and age of menarche (Staessen et al, 2001; Warner et al, 2004).
  3. Polychlorinated biphenyls (PCBs) have also shown anti-estrogenic effects, but so far no strong association has been made between high PCB exposure and pubertal development in girls, although some evidence shows it may delay puberty in boys (Schoeters et al., 2008).
  4. In a study of girls whose mothers were exposed to high levels of polybrominated biphenyls (PBBs) through accidental contamination, an earlier age at menarche was observed. The 327 females assessed were exposed to PBBs in utero and, in many cases, through breastfeeding (Blanck et al., 2000).
  5. In one study, significantly high levels of phthalate esters were found in 68% of girls with premature thelarche, while only one of the control serum samples had these elevated levels (Colon et al., 2000).
  6. High lead exposure appears to delay pubertal development rather than accelerate it (Wu et al, 2003). Other heavy metals such as mercury have also been explored.

Despite inconclusive evidence of the effects of individual chemicals, the research continues to investigate these compounds. Several factors have been identified that may explain the trend of earlier puberty. Most importantly, studies cannot adequately represent the typical experience: chronic exposure with multiple chemicals over a lifetime. Further, we cannot establish any safe level, since these exogenous biological mimickers will unnaturally affect the system in any amount (Crews et al., 2000). While the organism exposed can adapt, more significant effects, including changes in sexual development and eventually infertility, will affect the next generation. We as NDs need to stay vigilant in addressing these concerns.

Using the Determinants of Health

Decreasing outright exposure to these chemicals is an obvious step, but we should also consider exposures with yet unknown effects. I propose that by addressing many of the determinants of health, we are already decreasing exposure to EDCs, providing a genuinely preventative approach.

  1. Air. Heavy metals and other pollutants in our environment are likely to only get worse. But by supporting lifestyles and political action to improve air quality, we can impact this area. Additionally, supporting clean air in environments we do have control over (such as indoor air) provides a healthier foundation.
  2. Nutrition. It is estimated that 90% of the DDT exposure is from food (WHO report). By promotion of an organic whole foods diet, we help decrease exposure and increase elimination of toxic metabolites.
  3. Hydration. Since DDE and other chemicals are found in household water (usually in amounts deemed safe enough, but still present), it makes sense to continue recommendations to filter water for personal use. Also, it is important to support political measures to maintain clean water for longer term results.
  4. Weight. For girls, being overweight tends to lower the age at menarche. In the time interval from the NHES to NHANES III studies, the percentage of girls who were at risk for overweight —BMI above the 85th percentile of growth– increased from 16% to 27% (Anderson, 2003). A Danish study also found that overweight girls had both a younger average age at menarche and a younger age at thelarche (Juul et al, 2006). This trend may be predicted well before adolescence, in fact. In a study of girls followed from ages 5 to 9, those who had a higher percent body fat at age 5, and those with higher BMI percentile, larger waist circumference, or higher percent body fat at age 7 were more likely to show signs of early pubertal development at age 9. In addition, extra weight gain during these ages was shown to accelerate pubertal development. This finding compels us to address the potential concern even sooner, well before delayed or early puberty may even be an issue (Davison et al, 2003).
  5. Congenital/inborn determinants. Much evidence shows that the real effects of EDCs do not present until future generations become sexually mature, or even later. This means that in order to address this subject adequately, we need to address toxicity in every person, not just girls or women who present with symptoms. That is the only way to halt or reverse the trend towards abnormal.

In many instances we do have more specific concerns or exposures, which require addressing more than the determinants alone. But with each patient, if we use these and the other determinants to guide us, we are providing the key to true prevention. We will find improvement in other outcomes for gynecological conditions and beyond. For instance, earlier menarche puts a woman at greater risk for estrogen-related cancers such as breast and endometrial. By increasing the average age of menarche by even 6 months in a large group of women, we may be able to decrease risk in a great number. This serves as an excellent reminder that staying true to naturopathic goals allows us, even with such a complicated and overwhelming health problem as this, to still make a lasting impact.

connernewKristina Conner, ND graduated from Bastyr University in 2001. She completed her residency at the University of Bridgeport, College of Naturopathic Medicine. Dr. Conner is zealous about making classical naturopathic medicine pertinent to current practice. She is currently an assistant professor at the National University of Health Sciences where she teaches in the subject areas of nutrition, women’s health, hydrotherapy, and naturopathic medicine.



Anderson SE et al. Relative weight and race influence average age at menarche: results from two nationally representative surveys of US girls studied 25 years apart. Pediatrics. 2003;111(4 Pt 1):844-850.

Blanck HM et al. Age at menarche and tanner stage in girls exposed in utero and postnatally to polybrominated biphenyl. Epidemiology. 2000;11(6):641-647.

Colon I et al. Identification of phthalate esters in the serum of young Puerto Rican girls with premature breast development. Environ Health Perspect. 2000;108(9):895-900.

Crews D et al. Endocrine disruptors: present issues, future directions. Q Rev Biol. 2000;75(3):243-260.

Davison KK et al. Percent body fat at age 5 predicts earlier pubertal development among girls at age 9. Pediatrics. 2003;111(4 Pt 1):815-821.

Denham M et al. Relationship of lead, mercury, mirex, dichlorodiphenyldichloroethylene, hexachlorobenzene, and polychlorinated biphenyls to timing of menarche among Akewesasne Mohawk girls. Pediatrics. 2005;115(2):e127-e134.

Euling SY et al. Role of environmental factors in the timing of puberty. Pediatrics. 2008;121 Suppl 3:S167-171.

Hwang JY et al. Secular trend in age at menarche for South Korean women

born between 1920 and 1986: the Ansan Study. Ann Hum Biol. 2003;30(4):434-442.

Juul A et al. Pubertal development in Danish children: comparison of recent European and US data. Int J Androl. 2006;29(1):247-255.

Kac G et al. Secular trend in age at menarche for women born between 1920 and 1979 in Rio de Janeiro, Brazil. Ann Hum Biol. 2000;27(4):423-428.

MacMahon B. Age at Menarche: United States, 1973, National Center for Health Statistics: 74–1615, 1974.

Olesen AW et al. A continuous decline in menarcheal age in Denmark. Ann Hum Biol. 2000;27(4):377-386.

Ouyang F et al. Serum DDT, age at menarche, and abnormal menstrual cycle length. Occup Environ Med. 2005;62(12):878-884.

Schoeters G et al. Endocrine disruptors and abnormalities of pubertal development. Basic Clin Pharmacol Toxicol. 2008;102(2):168-175.

Staessen JA et al. Renal function, cytogenetic measurements, and sexual development in adolescents in relation to environmental pollutants: a feasibility study of biomarkers. Lancet. 2001;357(9269):1660-1669.

Vasiliu O et al. In utero exposure to organochlorines and age at menarche. Hum Reprod. 2004;19(7):1506-1512.

Warner M et al. Serum dioxin concentrations and age at menarche. Environ Health Perspect. 2004;112(13):1289-1292.

World Health Organization. DDT and its derivatives in drinking-water – background document for development of WHO Guidelines for Drinking-water Quality. World Health Organization Web site. Published 2004. Accessed June 2, 2009.

Wu T et al. Ethnic differences in the presence of secondary sex characteristics and menarche among US girls: the Third National Health and Nutrition Examination Survey, 1988-1994. Pediatrics. 2002;110(4), 752–757.

Wu T et al. Blood lead levels and sexual maturation in U.S. girls: the Third National Health and Nutrition Examination Survey, 1988-1994. Environ Health Perspect. 2003;111(5):737-741.

Wyshak G, Frisch RE. Evidence for a secular trend in age of menarche. N Engl J Med. 1982;306(17):1033–1035.

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