Evolution and Human Behavior 23 (2002) 365 – 372

On genetic variation in menarche and age

at first sexual intercourse
A critique of the Belsky–Draper hypothesis
David C. Rowe
School of Family and Consumer Sciences, Campus Box 210033, University of Arizona,
Tucson, AZ 85721, USA
Received 25 February 2002; accepted 15 April 2002

Abstract

The association of age of menarche, nonvirginity status, and age of first sexual intercourse was
investigated in teenage, female twins (mean age, 17 years) in the National Longitudinal Study of
Adolescent Health (Add Health). The sample sizes were all relatively small, so complex biometric
models were not fit to twin covariance matrices; rather, rough estimators of genetic effects were used.
Accordingly, all three characteristics were influenced by genetic variation, with higher heritabilities on
nonvirginity status and age of menarche than on age of first sex. In MZ twins, the phenotypic (i.e., on
individuals) correlation between menarcheal age and age of first sexual intercourse was .27. The
association of menarcheal age in identical (MZ) Twin 1 and sexual onset age in MZ Twin 2, and vice
versa, was .25. The genetic correlation between them, rg, was roughly estimated to be .72. These
findings weaken a conditional adaptation interpretation of this association as proposed by Belsky and
Draper, suggesting instead that heritable individual differences may give rise to this association.
D 2002 Elsevier Science Inc. All rights reserved.

Keywords: Add Health; Menarche; Sexual intercourse; Conditional adaptation

1. Introduction

A debate exists between certain developmental theorists and behavioral geneticists

over the relative role of conditional adaptations vs. heritable variation in life history

E-mail address: dcr091@ag.arizona.edu (D.C. Rowe).

1090-5138/02/$ – see front matter D 2002 Elsevier Science Inc. All rights reserved.
PII: S 1 0 9 0 - 5 1 3 8 ( 0 2 ) 0 0 1 0 2 - 2
366 D.C. Rowe / Evolution and Human Behavior 23 (2002) 365–372

traits (Rowe, 2000b; Rowe, Vaszonyi, & Figueredo, 1997). The former theorists have
made the counterintuitive prediction that early menarche is due to father absence (Draper
& Harpending, 1982), or to less sensitive and less nurturing experiences in the family
(Belsky, 2000; Belsky, Steinberg, & Draper, 1991). Belsky et al. (1991) regarded family
treatments as answering how father absence might promote an earlier pubertal maturation
in females. Families without fathers, or with stepfathers, are often poor, and discipline
more harshly and physically than other families do. According to these theorists, girls
from such families are also sexually precocious and promiscuous. The family effects
imply a correlation between menarcheal age and the age of first sexual intercourse.
On the other hand, both sides in this debate recognize possible genetic confounds.
One is that the age of menarche is heritable (Belsky, 2000; Rowe, 2000a). Less widely
appreciated is that parenting behaviors are heritable (Losoya, Callor, Rowe, & Gold-
smith, 1997; Rowe, 1981), as are the onset of sexual intercourse and other aspects of
sexual behavior (Dunne et al., 1997; Martin, Eaves, & Eysenck, 1977; Rodgers &
Doughty, 2000; Segal, 1993). In light of this evidence of heritability, Belsky (2000)
modified his position to suggest that only some children may be susceptible to
environmental influences, whereas other children are genetically ‘‘fixed’’ in their
behavioral repertoire. This compromise, however, is empirically supported neither for
age of menarche nor for precocious sex.
In this article, I estimate the heritability of age of menarche, nonvirginity status, and
age of first sexual intercourse using the twins in the National Longitudinal Study of
Adolescent Health (Add Health). Twins were used to control for age differences within
sibling pairs. Because of small sample sizes, biometrical models were not fit to the twin
covariances; rather, rough and simple estimators were used. In any case, larger studies
than this one have established the heritability of menarcheal age and age of onset of
sexual intercourse; these findings are not in doubt.
The unique contribution of this study is to examine genetic and environmental
components of the correlation of menarcheal age and age of first sexual intercourse.
Phenotypic correlations are ordinarily calculated on individuals. Thus, on all the Twin 1s
in the sample, some correlation may exist between menarcheal age and age of sexual
intercourse. Imagine that this correlation was .30. It could represent either effects of
genes in common to menarche and sex, or environmental influences shared by the two
characteristics. To discover which is true, a second correlation is computed, called a
cross-trait, cross-twin correlation. In one case, the correlation is between age of
menarche for Twin 1 and the age of first sex for Twin 2. A second cross-correlation
exists with the roles of Twins 1 and 2 reversed. How are these correlations to be
interpreted? Consider a case in which the MZ twin cross-trait, cross-twin correlation
equals the phenotypic correlation, i.e., rMZ phenotypic =.30, rMZ cross =.30. This is an
example of a genetic effect. Because of their shared genes, a correlation computed on
two MZ twins has the same value as one computed on one MZ twin. In this example,
the values of the DZ twin correlations would be phenotypic, .30, and cross-trait, cross-
twin, .15. The cross-correlation is less because DZ twins share 50% of their genes, not
the 100% that MZ twins share.
 D.C. Rowe / Evolution and Human Behavior 23 (2002) 365–372 367

2. Method

2.1. Sample

These data came from Waves 1–2 of the Add Health. The Add Health Wave 1 was
collected in 1994 and, except for specific subgroups, it was a nationally representative
survey of US adolescents (see details in Udry & Bearman, 1998); the data set is
publicly available. Black children of highly educated parents were oversampled. Wave 2
was collected in 1995, with an interval of about 1 year between Waves 1 and 2. Within
each wave, the twins were often interviewed on different days, and interviewers may
have changed between waves. In Wave 2, the average age of the adolescents was
17 years.
African–American respondents were excluded because their ages of menarche were
the least accurate. Their reports were badly telescoped such that older respondents gave
an older age of menarche than did younger respondents (r
.30). Ideally, chronological
age should correlate zero with age of menarche.
Twins were identified through self-report on an in-school questionnaire completed by
about 90,000 adolescents that preceded Wave 1, and by investigating school rosters. The
majority of same-sex twins were diagnosed as either monozygotic (MZ, N = 247 pairs) or
dizygotic (DZ, N = 200) on the basis of their self-reports of confusability of appearance.
The confusability scale developed for the Add Health study had four items: (1) ‘‘When
you were young children, did you and NAME look very much alike, like two peas in a
pod, or did you just look like members of the same family?’’; (2) ‘‘Are strangers
confused about which of you is which?’’; (3) ‘‘Are your teachers ever confused?’’; and
(4) ‘‘Are family members ever confused?’’. Each item had a 1 or 0 score, with 1
indicating greater confusability of appearance. A score was computed, which is the
average of Twin 1’s and Twin 2’s response to the four items, times 100. Inspection of the
histogram distribution indicated that a score of 60 was the best threshold on which to
separate MZ and DZ twins. The majority of twins were assigned using this confusability
score. Confusability of appearance scales have been found to have greater than .90
agreement with zygosity determination on the basis of DNA evidence (Spitz et al., 1996).
Eighty-nine twin pairs of uncertain diagnosis were classified by their match on DNA
genetic markers (47 DZ, 42 MZ). Twins were diagnosed as MZ if they were the same
for five or more genetic makers, and as DZ if they were different at one or more
markers. Zygosity determination could not be ascertained for an additional 43 twin pairs.
For the present analyses, these undecided (UD) twin pairs were omitted. In the sample
of female twin pairs, 106 pairs were diagnosed as MZ and 76 pairs as DZ.

2.2. Measures

2.2.1. Age of menarche

In Waves 1–2, the female respondents reported their age of menarche to the nearest year.
In the arbitrarily chosen Twin 1, the Waves 1–2 retest correlation was .75 ( P < .0001);
368 D.C. Rowe / Evolution and Human Behavior 23 (2002) 365–372

comparably, in arbitrarily chosen Twin 2, it was .77 ( P < .0001). In both Twins 1 and 2, the
mean menarcheal age in Wave 2 (12.40 and 12.43 years, respectively) was greater than in
Wave 1 (12.15 and 12.18 years), though neither change was statistically significant
(t =  1.14, P =.25; t =  1.18, P =.24). Thus, the mean changed about 3 months between
waves. Ninety percent of the changes was 0 or 1 year. Given the moderate retest correlations
and small absolute changes, the menarcheal age was taken as the average of the Waves 1 and
2 values.

2.2.2. Sexual intercourse

In Wave 2, virgins were scored as 0; respondents reporting one or more acts of sexual
intercourse were scored as 1. Thirty-seven percent of female respondents was a nonvirgin.

2.2.3. Age of first sexual intercourse

In Wave 2, respondents reported retrospectively on their age of first sexual intercourse.
Although there is no ideal way to treat virgins in these data, virgins were given as a score their
current age, which avoids creating a lump score that extremely biases the shape of the
distribution (i.e., if all virgins were to be assigned a single score). The earliest age of first
intercourse was 10.2 years.

3. Results

Table 1 presents the twin correlations. All three outcomes, menarcheal age, nonvirginity
status, and age of first sexual intercourse, had greater MZ twin than DZ twin correlations, as
expected under a hypothesis of genetic variation. A Z score test of the difference of two
correlations was conducted to evaluate the statistical significance of this difference.
Menarcheal age and nonvirginity status MZ twin correlations statistically exceeded the DZ
twin correlations, whereas there was a trend in the same direction for age of first intercourse
(P = .08). Thus, the conditions for an association between variables to be genetically
influenced were established.
Virginity status was uncorrelated with age of menarche. Table 2 shows the correlations
that are critical to an analysis of the origin of the association between menarcheal age and
age of first sexual intercourse. The correlations on MZ twins supported a genetic hypothesis

Table 1
Twin correlations for age of menarche, ever had sex, and age at first sexual intercourse
Variable rMZ N/Pairs rDZ N/Pairs Z P
Age of menarche .57 106 .32 75 2.06 < .05
Ever had sex .63 105 .35 75 2.44 < .05
Age at sex .67 106 .53 75 1.43 < .08a
All correlations, P < .01. Confidence intervals not given because calculating proper intervals require biometric
model fitting.
a
One-tailed test.
 D.C. Rowe / Evolution and Human Behavior 23 (2002) 365–372 369

Table 2
Genetic mediation of the association between age of sexual intercourse and age of menarche
Full sample At least one nonvirgin twin
Association rMZ rDZ rMZ rDZ
Phenotypic Twin 1 .28* (98) .02 (76) .26 (56) .16 (36)
Phenotypic Twin 2 .25* (106) .06 (76) .25 (52) .16 (37)
Twin 1 age of sex with Twin 2 age of menarche .23* (103)  .10 (74) .20 (49)  .22 (35)
Twin 2 age of sex with Twin 1 age of menarche .26* (99) .04 (76) .23 (49) .13 (36)
N values in parentheses.
* P < .02.

in that the phenotypic correlation was of about the same magnitude as the cross-twin, cross-
trait one. In the full sample, the average MZ twin phenotypic correlation was .27; the
average cross-trait, cross-twin correlation was .25. The confidence interval for the former
was .21–.33; for the latter cross-correlation, it was .20–.30. In a worst case scenario, the
phenotypic correlation could equal .33 and the cross-correlation .20, allowing for consid-
erable nongenetic influences on the association between menarcheal age and age of sex. In
the smaller sample of MZ twin pairs, at least one of whom is a nonvirgin twin, there is
even more sampling variation. Nonetheless, the phenotypic and cross-correlations were of
similar magnitudes.
The results were less clear for the DZ twin pairs. In the full sample, all the DZ twin
correlations were close to zero. As one would expect at least for a phenotypic correlation
between ‘‘age of sex’’ and ‘‘age of menarche,’’ this result is challenging. Inspection of
scatterplots reveals no obvious outliers. The findings were better patterned for those DZ twins
at least one of whom was a nonvirgin. Their phenotypic correlation was .16. The cross-
correlations were ambiguous because one was negative and the other positive. Because of the
small sample size, none of these DZ twin correlations attained statistical significance.

4. Discussion

In this study, a comparison of MZ and DZ twin correlations revealed that genetic effects
contributed to the variance (i.e., individual differences) in menarcheal age, nonvirginity
status, and age of first sexual intercourse among teenagers with a mean age of 17 years. A
rough estimate of heritability is twice the difference of the MZ and DZ twin correlations (i.e.,
h2 = 2[rMZ  rDZ]; Rowe, 1994). Using this estimator, the heritabilities in this sample were:
age of menarche, .50; nonvirginity status, .56; age of first sexual intercourse, .28. The age of
menarche heritability estimate is close to that obtained by Doughty and Rodgers (2000) using
a comparison of full and half-siblings, as h2 = 0.54. Given the small sample sizes, my
heritability estimates would have large confidence intervals.
The main question was whether the phenotypic correlation of menarcheal age and age of
first sexual intercourse had a genetic basis. In MZ twins, there was a phenotypic correlation of
.27 between menarcheal age and age of first sexual intercourse such that females who had an
370 D.C. Rowe / Evolution and Human Behavior 23 (2002) 365–372

earlier menarche also tended to have an earlier age of first sex. The interpretation of the
phenotypic correlation depended on the value of the cross-trait, cross-twin correlation, e.g.,
menarcheal age in Twin 1 correlated with age of first sex in Twin 2. The MZ twin cross-trait,
cross-twin correlation of .25 about equaled the phenotypic correlation on individuals, .27.
The mathematical expectation for the phenotypic correlation (rp) and for the MZ twin cross-
trait, cross twin correlation (rc) is (Eq. (1)):
rp ¼ rc ¼ hm hsex rg ð1Þ
where hm is the square root of the heritability of menarcheal age, hsex is the square root of the
heritability of age of first sexual intercourse, and rg is the correlation of the genes influencing
the two characteristics. Solving the equation for rg yields the following result, with a wide
confidence interval (Eq. (2)):
rg ¼ :72 ¼ :27=ð:53  :71Þ: ð2Þ
Thus, the origin of the phenotypic correlation may be a .72 genetic correlation between
menarcheal age and age of first sexual intercourse. Other genes, which influence just one of
the characteristics, would cause rg to be less than 1.0.
There are several possible interpretations for this genetic correlation: (1) physiological,
(2) assortative mating, and (3) reactive heritability. The most straightforward interpretation
is that age of first sex and menarcheal development share some common physiological
pathways that are genetically determined. Comings, Muhleman, Johnson, and MacMurray
(2002) advanced this hypothesis for a polymorphism in the X-linked androgen receptor
gene. They found that fathers carrying the AR risk alleles were more likely to abandon a
marriage. Those same alleles, when passed onto a daughter, were associated with her
having an earlier age of menarche and behavioral problems. A second explanation, which
is not inconsistent with the first, is that the genetic correlation arises from assortative
mating. In this case, the physiological pathways to precocious sex and early menarche
would be distinct, but the genes become correlated because early maturing girls tend to
mate at a young age with impulsive, sensation-seeking men, i.e., Mealey’s (1995) primary
psychopaths. Over generations, a correlation would build up between genes affecting the
two characteristics such that a girl who carried risk alleles for early menarcheal age would
also inherit risk alleles for a younger first sexual intercourse. Finally, a third hypothesis is
that boys are attracted to girls showing secondary sexual characteristics; but while this is
certainly true, it seems unlikely that this reactive heritability would create equal
phenotypic and cross-correlations. After all, nearly all girls in the sample were post-
menarcheal and had their secondary sexual traits in full display; yet about two thirds of
them was still a virgin. I know of no evidence that girls who have early sex are physically
distinct from other girls, and even if so, whether the effect would be strong enough to
explain much variance.
Several limitations reduce the confidence that can be placed in the findings of this study.
First, about two thirds of the adolescent girls was a virgin. No method exists that can account
for missing data on nonvirginity adequately. The solution used here, scoring virgins as their
ages, guarantees that twins are alike when both twins are virgins. It may exaggerate twins’
 D.C. Rowe / Evolution and Human Behavior 23 (2002) 365–372 371

resemblance to one another. Second, the sample sizes were small. Therefore, the correlation
coefficient had wide confidence intervals. The MZ twin phenotypic and cross-trait, cross-twin
correlations appear to be alike, but this could be coincidental. It would take a larger sample to
know what these values are more precisely. Third, the findings for DZ twins were inconsistent
because in the full sample, the DZ correlations were about zero. Their low correlations might
be interpreted as showing epistasis, i.e., gene  gene interactions shared only by MZ twins.
However, there is no reason to expect that all the genetic variations are nonadditive; this
puzzle can be resolved only through a replication study.

Acknowledgments

The Add Health was designed by J. Richard Udry and Peter Bearman and funded by grant
P01-HD31921 from the National Institute of Child Health and Human Development. Data
sets can be obtained by contacting the Carolina Population Center, 123 West Franklin Street,
Chapel Hill, NC 27516-3997, USA, or by e-mailing addhealth@unc.edu.

References

Belsky, J. (2000). Conditional and alternative reproductive strategies: individual differences in susceptibility to
rearing experiences. In: J. L. Rodgers, D. C. Rowe, & W. B. Miller (Eds.), Genetic influences on human
fertility and sexuality: Theoretical and empirical contributions from the biological and behavioral sciences
( pp. 127 – 146). Boston: Kluwer Academic Publishing.
Belsky, J., Steinberg, L., & Draper, P. (1991). Childhood experience, interpersonal development, and reproductive
strategy: An evolutionary theory of socialization. Child Development, 62, 647 – 670.
Comings, D. E., Muhleman, D., Johnson, J. P., & MacMurray, J. P. (2002). Parent – daughter transmission of the
androgen receptor (AR) gene as an explanation of the effect of father absence on age of menarche. Submitted
for publication.
Doughty, D., & Rodgers, J. L. (2000). Behavior genetic modeling of menarche in US females. In: J. L. Rodgers, D. C.
Rodgers, & W. B. Miller (Eds.), Genetic influences on human fertility and sexuality: Theoretical and empirical
contributions from the biological and behavioral sciences ( pp. 169 – 181). Boston: Kluwer Academic Publishing.
Draper, P., & Harpending, H. (1982). Father absence and reproductive strategy: An evolutionary perspective.
Journal of Anthropological Research, 38, 255 – 273.
Dunne, M. P., Martin, N. G., Statham, D. J., Slutske, W. S., Dinwiddie, S. H., Bucholz, K. K., Madden, P. A., &
Heath, A. C. (1997). Genetic and environmental contributions to variance in age at first sexual intercourse.
Psychological Science, 8, 1 – 6.
Losoya, S. H., Callor, S., Rowe, D. C., & Goldsmith, H. H. (1997). The origins of familial similarity in parenting:
A study of twins and adoptive siblings. Developmental Psychology, 33, 1012 – 1024.
Martin, N. G., Eaves, L. J., & Eysenck, H. J. (1977). Genetical, environmental, and personality factors influencing
the age of first sexual intercourse in twins. Journal of Biosocial Science, 9, 91 – 97.
Mealey, L. (1995). The sociobiology of sociopathy: An integrated evolutionary model. Behavioral and Brain
Sciences, 18, 523 – 599.
Rodgers, J. L., & Doughty, D. (2000). Genetic and environmental influences on fertility expectations and out-
comes using NLSY kinship data. In: J. L. Rodgers, D. C. Rowe, & W. B. Miller (Eds.), Genetic influences on
human fertility and sexuality: Theoretical and empirical contributions from the biological and behavioral
sciences ( pp. 85 – 105). Boston: Kluwer Academic Publishing.
372 D.C. Rowe / Evolution and Human Behavior 23 (2002) 365–372

Rowe, D. C. (1981). Environmental and genetic influences on dimensions of perceived parenting: A twin study.
Developmental Psychology, 17, 203 – 208.
Rowe, D. C. (1994). The limits of family influence: Genes, experience, and behavior. New York: Guilford Press.
Rowe, D. C. (2000a). Environmental and genetic influences on pubertal development: evolutionary life history
traits? In: J. L. Rodgers, D. C. Rowe, & W. B. Miller (Eds.), Genetic influences on human fertility and sexuality:
Theoretical and empirical contributions from the biological and behavioral sciences ( pp. 147 – 168). Boston:
Kluwer Academic Publishing.
Rowe, D. C. (2000b). Death hope and sex: steps to an evolutionary ecology of mind and morality by J.S.
Chisholm. Evolution and Human Behavior, 21, 352 – 364.
Rowe, D. C., Vazsonyi, A. T., & Figueredo, A. J. (1997). Mating-effort in adolescence: Conditional or alternative
strategy. Personality and Individual Differences, 23, 105 – 115.
Segal, N. (1993). Heritable and environmental variables affect reproduction-related behaviors, but not ultimate
reproductive success. Personality and Individual Differences, 14, 783 – 794.
Spitz, E., Moutier, R., Reed, T., Busnel, M. C., Marchaland, C., Roubertoux, P. L., & Carlier, M. (1996).
Comparative diagnoses of twin zygosity by SSLP variant analysis, questionnaire, and dermatoglyphic analysis.
Behavior Genetics, 26, 55 – 63.
Udry, J. R., & Bearman, P. S. (1998). New methods for new research on adolescent sexual behavior. In: R. Jessor
(Ed.), New perspectives on adolescent risk behavior ( pp. 241 – 269). New York: Cambridge University Press.