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Brief communication Familial resemblance in digit ratio (2D 4D).

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AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 140:376–380 (2009)
Brief Communication: Familial Resemblance in
Digit Ratio (2D:4D)
Martin Voracek* and Stefan G. Dressler
Department of Basic Psychological Research, School of Psychology, University of Vienna, Vienna A-1010, Austria
KEY WORDS
digit ratio (2D:4D); heritability; family study; sex differences; prenatal testosterone
ABSTRACT
Familial resemblance in the secondto-fourth digit ratio (2D:4D), a proxy for prenatal androgen action, was studied in 1,260 individuals from 235
Austrian families. In agreement with findings from twin
studies of 2D:4D, heritability estimates based on parent–
child and full-sib dyad similarity indicated substantial
genetic contributions to trait expression (57% for right
hand, 48% for left hand 2D:4D). Because twin studies
have found nonadditive genetic as well as shared environmental effects on 2D:4D to be negligible or nil, these
family-based estimates in all likelihood reflect the
narrow-sense (additive genetic) heritability of the trait.
Directional (right-minus-left) asymmetry in 2D:4D was
only weakly heritable (6%). The pattern of same-sex and
different-sex parent–child and full-sib correlations yielded
no evidence for X-linked inheritance. This is surprising,
considering evidence for associations of male 2D:4D with
sensitivity to testosterone (functional variants of the
X-linked androgen receptor gene). 2D:4D was particularly
strongly heritable through male lines (father–son and
brother–brother correlations), thus raising the possibility
that Y-linked genes (such as the sex-determining region
SRY) might influence 2D:4D expression. Am J Phys
Anthropol 140:376–380, 2009. V 2009 Wiley-Liss, Inc.
Men on average display a lower second-to-fourth digit
ratio (2D:4D) than women (Manning, 2002). This
anatomical sex difference, rediscovered by Manning et
al. (1998), generalizes to the digit ratios of a variety of
vertebrate non-human species (reviews: Voracek, 2006;
Lombardo and Thorpe, 2008). Individual and sex differences in human 2D:4D emerge prenatally (Malas et al.,
2006; Galis et al., in press) and are fairly stable during
postnatal growth (Trivers et al., 2006).
2D:4D studies have recently become increasingly popular in human biology, medicine, psychology, and the
intersections of these fields (McIntyre, 2006; Voracek
and Loibl, in press). Specifically, 2D:4D has been proposed as an indirect marker for prenatal androgen action
and the organizing (permanent) masculinization effects
of this on the brain, behavior, and physique (Manning,
2002). If this prenatal-androgen-marker hypothesis is
correct, studying within-sex associations of 2D:4D with
target variables would enable straightforward (noninvasive and thus easily implemented) tests of the biological
bases of traits and phenotypes conceivably partly influenced by early sex-hormonal effects.
There is now various circumstantial, but persuasive,
evidence in favor of this hypothesis (review: Voracek
et al., 2007a). More direct evidence includes the finding
that the testosterone-to-estradiol ratio in the amniotic
fluid is a negative correlate of children’s 2D:4D (Lutchmaya et al., 2004). In a similar vein, lower (masculinized) 2D:4D in men is associated with higher sensitivity
to testosterone, through the influence of a functional
polymorphism in the androgen receptor gene (Manning
et al., 2003). Because this gene resides on the X chromosome, one expectation is that 2D:4D should show signs
of sex-influenced (X-linked) inheritance.
This has indeed been suggested in a forerunner study
of modern 2D:4D research (Phelps, 1952), which conjectured an X-linked modifying factor (dominant in men,
recessive in women) for a short index finger (2D).
However, another classic family study (Ramesh and
Murty, 1977) found no evidence for X-linked inheritance.
In hindsight, these two early accounts are open to several points of criticism, e.g., both studies did not actually
analyze 2D:4D, but rather distal finger-extent difference,
and the locale of the second study was within an endogamous group, which may well have affected inheritance
patterns. Also, the second study found no evidence for
sex differences in distal finger-extent difference, which is
known to be sexually differentiated, thereby casting
doubt over study conclusions.
More generally, family studies cannot disentangle
genetic from environmental effects. That is, family
resemblance on a trait results from genetic or environmental similarity or a mixture of both. However, there
are now four twin studies of 2D:4D in humans (United
Kingdom: Paul et al., 2006; Austria: Voracek and
Dressler, 2007; USA: Gobrogge et al., 2008; Australia:
Medland and Loehlin, 2008). Despite great differences in
methodology and in size, recruitment, provenance, and
characteristics of samples, their key findings converge
on the following important points: additive genetic factors contribute substantially to 2D:4D variation, i.e., the
trait is highly heritable (across studies: h2 5 50–80%);
nonshared environmental factors are also significant,
but smaller (20–50%); whereas shared environmental
C 2009
V
WILEY-LISS, INC.
C
*Correspondence to: Martin Voracek, Department of Basic
Psychological Research, School of Psychology, University of Vienna,
Liebiggasse 5, Rm 03-46, Vienna A-1010, Austria.
E-mail: martin.voracek@univie.ac.at
Received 17 November 2008; accepted 17 April 2009
DOI 10.1002/ajpa.21105
Published online 15 June 2009 in Wiley InterScience
(www.interscience.wiley.com).
377
DIGIT RATIO (2D:4D) FAMILY STUDY
factors are not significant and much smaller or nil
(0–20%).
Substantial heritability of 2D:4D (h2 5 60%) was also
indicated in an additional small-sample study of monozygotic lesbian twins (Hall and Love, 2003). One study
(Medland and Loehlin, 2008) explicitly tested for nonadditive genetic factors, i.e., dominance and epistasis
effects (allele–allele and gene–gene interactions), and
found these to be nil. Of note, 2D:4D may well be similarly highly heritable in other species, as indicated by
two studies of zebra finches (h2 5 70–80%; Forstmeier,
2005; Forstmeier et al., 2008).
The twin study findings summarized here have two
important consequences that simplify the interpretation
of family studies of 2D:4D. First, because shared environmental effects apparently are negligible or nil, familial resemblance in 2D:4D will reflect genetic similarity
(conversely, familial dissimilarity will reflect nonshared
environmental effects). Second, because nonadditive
genetic effects also are nil, h2 estimates derived from
family data will reflect narrow-sense heritability (additive genetic effects only) rather than broad-sense heritability (additive plus nonadditive genetic effects). Given
these specific knowns, family studies appear a viable,
informative approach to further elucidate inheritance
patterns of 2D:4D.
Family studies can also help to determine whether
2D:4D is a sex-linked trait or not. Twin study findings
have been inconsistent regarding this question: although
the largest study (Medland and Loehlin, 2008) found no
evidence for it, a smaller one (Gobrogge et al., 2008)
observed stronger shared environmental effects for male
than for female twins. Because male relatives share
their Y chromosome, this could reflect Y-linked genetic
contributions to 2D:4D variation (such as via the sexdetermining region SRY), because in the classic twin
study design such effects are falsely attributed to shared
environmental factors among males.
To recap, given the suggestive findings of Phelps
(1952) and associations of 2D:4D with variants of the
X-linked androgen receptor gene, sex-linked inheritance
of 2D:4D is expected, but the findings from twin studies
on this matter are contradictory. Given the other
(specific and convergent) findings of 2D:4D twin studies
discussed earlier, the family study design appears
informative in this context. So far, three studies have
reported family data for 2D:4D, all of them concluding
that family resemblance for 2D:4D is substantial. These
findings were based on 41 father–child and 64 mother–
child dyads (Marshall, 2000), 62 parent–child dyads
(with the children affected by autism-spectrum disorders; Manning et al., 2001), and 88 mother–child dyads
(Manning, 2002, pp. 12–13). A 2D:4D family study utilizing a larger sample from the general population is
unavailable. Therefore, this study set out to look for
signs of X-linked or Y-linked inheritance of 2D:4D in a
larger family sample.
MATERIALS AND METHODS
Participants were from 235 Austrian families (556
males, 704 females). Because there is evidence for significant variation of 2D:4D across macro-ethnic groups
(Manning et al., 2007), White Caucasians were eligible
for study participation. Several research assistants
recruited families from the general population opportunistically, using snowball-sampling techniques (i.e., per-
sonal contacts, referral, and word-of-mouth advertizing).
Study participation was mainly solicited in the capital
city of Vienna, but also covered the surrounding Eastern
Austrian areas. Data were collected outside academia or
specific university settings, so families representing a
variety of urban and rural living backgrounds as well as
diverse educational levels and occupations were
included. Ages in the sample ranged from 2 to 97 years
(M 5 37.8, SD 5 19.8, lower and upper quartiles: 21 and
52 years). Spousal data from this sample have been used
to test for assortative mating on 2D:4D (Voracek et al.,
2007a).
Palmar-view photocopies of subjects’ right and left
hands were presented in random order to three experienced, mutually blind investigators, who measured finger lengths from the flexion crease proximal-most to the
palm to the fingertip with digital vernier calipers accurate to 0.01 mm. Finger-length measurements were
averaged prior to calculating digit ratios. Interobserver
measurement repeatabilities (assessed with intraclass
correlations coefficients, ICC; two-way mixed-effects
model with absolute-agreement definition; Voracek et al.,
2007b) were found to be in good order (all P \ 0.001):
ICCs were 0.996 (right-hand 2D), 0.997 (right-hand 4D),
0.995 (left-hand 2D), 0.997 (left-hand 4D), 0.913 (righthand 2D:4D), 0.905 (left-hand 2D:4D), and 0.769 (righthand minus left-hand 2D:4D or DR-L).
Following standard practice of family studies (Ramesh
and Murty, 1977), heritability estimates were obtained
by doubling the Pearson correlation coefficients (r) calculated to quantify parent–child and full-sib resemblance.
For calculating the correlations, the full dyadic information extractable from the specific family constellation
was utilized, e.g., a five-member family comprised of the
couple, one son, and two daughters contributed six data
points to the parent–child analysis, three data points
each to the father–child, mother–child, and full-sib analyses, two each to the father–daughter, mother–daughter,
and brother–sister analyses, and one each to the father–
son, mother–son, and sister–sister analyses. The resulting heritability estimates are unaffected by potential
measurement-method effects on 2D:4D (such as measuring fingers from photocopies rather than directly; see
Manning et al., 2005), since r is invariant under linear
transformations (e.g., through measurement-specific
bias) of the variables from which it is computed.
RESULTS
Males had lower right-hand digit ratios (R2D:4D) than
females (males: M 5 0.957, SD 5 0.035; females: M 5
0.977, SD 5 0.035; t1258 5 29.75, two-tailed P \ 0.001,
d 5 20.57), lower left-hand digit ratios (L2D:4D; males:
M 5 0.962, SD 5 0.035; females: M 5 0.976, SD 5
0.034; t1258 5 27.09, P \ 0.001, d 5 20.41), and also
lower DR-L (males: M 5 20.0048, SD 5 0.0298; females:
M 5 0.0007, SD 5 0.0297; t1258 5 23.24, P 5 0.001, d 5
20.18). For both sexes, R2D:4D and L2D:4D were comparably strongly positively correlated (r 5 0.646 and
0.629 for males and females; both P \ 0.001). Consistent
with the literature (Manning, 2002), sex differences in
2D:4D were of medium size, the effect was more pronounced for the right hand than for the left, and 2D:4D
of both hands corresponded strongly. Replicating Manning et al. (2007) and in contrast to the null finding of
Putz et al. (2004), a small, but significant sex effect was
also seen for DR-L.
American Journal of Physical Anthropology
378
M. VORACEK AND S.G. DRESSLER
DISCUSSION
TABLE 1. Familial resemblance in 2D:4D
Pearson r
Relationship type
(dyad)
n
(dyads)
R2D:4D
L2D:4D
DR-L
Parent–child
Father–child (Fa-Ch)
Father–son (Fa-So)
Father–daughter
(Fa-Da)
Mother–child
(Mo-Ch)
Mother–son (Mo-So)
Mother–daughter
(Mo-Da)
Full sibs
Brother–brother
(Br-Br)
Sister–sister (Si-Si)
Brother–sister
(Br-Si)
1145
499
224
275
0.292***a
0.312***a
0.363***a
0.276***
0.232***b
0.222***b
0.305***b,c
0.131*b}
0.027
0.042
0.079
0.015
646
0.299***a 0.245***b
a
b
291
355
0.328***
0.293***
549
104
0.245*** 0.267***b
0.408***} 0.543***c
177
268
0.246**
0.148*}
0.194**
0.299***b,c
0.217**b
0.158*b}
0.019
0.035
0.003
0.017
0.195*
20.048
0.014
Same-column comparisons: aR2D:4D column entries significantly different (P \ 0.05) to lowest (brother–sister) correlation.
b
L2D:4D entries different to highest (brother–brother)
correlation.
c
L2D:4D entries different to lowest (father–daughter) correlation; all other differences not significant. Same-row comparisons:
}
Not significantly different from correlation for DR-L.
* P \ 0.05, ** P \ 0.01, *** P \ 0.001 (two-tailed).
For R2D:4D and L2D:4D, familial resemblance was
significant for all investigated types of parent–child and
full-sib dyads (Table 1). Correlations were numerically
(but never significantly) larger for R2D:4D than for
L2D:4D in 7 of 11 comparisons, and significantly
smaller for DR-L than for R2D:4D or L2D:4D in 18 of 22
comparisons. X-linked inheritance would be indicated
through rSi-Si [ rBr-Br [ rBr-Si and rFa-Da 5 rMo-So [ rMo-Da
[ rFa-So, with the theoretically expected values being
0.75 [ 0.50 [ 0.35 and 0.71 5 0.71 [ 0.50 [ 0 under
additive sex-linked genes (Ramesh and Murty, 1977). Of
note, the current data did not at all conform with this
pattern (tested with difference of correlation tests;
Steiger, 1980). For L2D:4D, the succession of correlation
coefficients was rBr-Br [ [rSi-Si rBr-Si], i.e., the latter
two correlations were commensurable, and both of them
significantly smaller than rBr-Br (for R2D:4D, rBr-Br rSi-Si rBr-Si). Further (using the same notation), rFa-So
rMo-So rMo-Da rFa-Da (for R2D:4D), but [rFa-So rMo-Da] [ [rMo-So rFa-Da] for L2D:4D. Among parent–
child dyads, the strongest resemblance was between
fathers and sons, and for full-sib dyads, among brothers. For DR-L, only brother–brother resemblance was
significant. The heritability estimates (weighted average
of doubled correlation coefficients across all types of
dyads) were 57.4%, 47.7%, and 5.8% for R2D:4D,
L2D:4D, and DR-L.
Supplemental analyses (details omitted) indicated the
following: first, controls for age or nonparametric
analysis (rank-order correlation) did not materially alter
these results. And second, controls for maternal (versus
paternal) digit ratio (in analysis of covariance models)
did not differentially (or significantly) alter the magnitude of the sex difference observed in digit ratios across
brother-sister dyads, which might imply that sexchromosomal loci do not substantially contribute to sex
differences in digit ratios.
American Journal of Physical Anthropology
The heritability estimates from this 2D:4D family
study were very similar to the result of a classic account
(Ramesh and Murty, 1977: weighted average h2 5 57%).
They also tallied to h2 values calculated from parent–
child dyads found in the literature (Marshall, 2000: h2 5
41%; Manning et al., 2001: h2 5 58%; Manning, 2002: h2
5 69%). Familial resemblance in 2D:4D was substantial
(concordant with twin study findings), slightly higher for
R2D:4D than for L2D:4D, but largely absent for DR-L.
The slightly higher heritability estimate for R2D:4D, as
compared with L2D:4D, is consistent with evidence that
L2D:4D seems to be more sensitive to environmental
factors than R2D:4D (Flegr et al., 2008).
DR-L, the directional asymmetry in digit ratios, is considered as an additional pointer to prenatal androgen
exposure (Manning, 2002, pp. 21–22) and has especially
proven useful in digit ratio studies about sports performance (reviews: Voracek et al., 2006; Bescós et al., 2009).
Being another complex phenotype, it may well be affected
by additional factors beyond those that influence digit
ratios. Therefore, it is perhaps not surprising that results
for DR-L diverged. Alternatively or additionally, the lower
repeatability of DR-L may have reduced the strength of its
dyad correlations and, as a consequence, its calculated
heritability. This latter argument is deducible as follows
(see Voracek et al., 2007b): higher random measurement
error (i.e., ‘‘noise’’) leads to lower repeatabilities. Random
measurement errors mutually cancel out, when calculating averages of measurements; but they do not cancel out,
when calculating differences; and they multiply, when calculating ratios. Hence measurement repeatabilities for
2D:4D (a ratio) are lower than for finger lengths, and still
lower for DR-L (the difference of two ratios).
On the other side, assortative mating on a trait will
inflate family-based heritability estimates by the factor
1 1 rAM, where rAM is the spousal correlation on that
trait. There still is a paucity of studies on assortative
mating on 2D:4D. The effect seems rather small
(Manning, 2002, p. 50: rAM 5 0.15 or less; Voracek et al.,
2007a: about 0.20 or less), and it is not known whether it
is partly due to social homogamy (i.e., milieu similarity,
leading to geographic ‘‘background correlations’’). Assuming rAM 5 0.15, this decreases the current heritability
estimates (57.4%, 47.7%, and 5.8% for R2D:4D, L2D:4D,
and DR-L, respectively) to 49.9%, 41.5%, and 5.0%
(assuming rAM 5 0.20, to 47.8%, 39.8%, and 4.8%). At any
rate, owing to the lack of strength of the assortative-mating effect, the impact of these downward corrections is
modest and thus largely preserves the substantial levels
of heritability observed for R2D:4D and L2D:4D.
Although the minimum effective sample size for the
types of dyads investigated here (N 5 104 for the
brother–brother correlations; see Table 1) was larger
than the effective sample sizes of the three prior family
studies of 2D:4D (see Introduction), it is also true that
sample sizes available for analysis of the different types
of dyads varied greatly. This is an inherent characteristic of family study designs and could have impacted
results. On the other side, although 2D:4D varies significantly across macro-ethnic groups (Manning et al.,
2007), the existing evidence supports the idea that
genetic differences between populations rather than
environmental factors contribute significantly to
observed population differences in 2D:4D (Loehlin et al.,
2006). Since the present study’s family sample was
DIGIT RATIO (2D:4D) FAMILY STUDY
ethnically homogeneous, population differences in 2D:4D
could not have influenced the findings.
Heritability estimates from combinations of full-sib
dyads were not larger than those from combinations of
parent–child dyads. This implies absence of dominance
deviation effects (i.e., no contributions of recessive
genes), absence of epistasis effects (i.e., no interloci interactions), and absence of shared environmental effects (in
the case of 2D:4D, evidently prenatal ones, i.e., no
maternal or womb environment influences). These conclusions also concur with the twin study findings.
Replicating Ramesh and Murty (1977), evaluation of
the rank order of h2 estimates for same-sex and different-sex parent–child and full–sib dyads yielded no
evidence for X-linked trait inheritance. This suggests
absence of major genes for 2D:4D variation on this sex
chromosome. By implication, effects of variants of the
X-linked androgen receptor gene on 2D:4D presumably
are small, and, in turn, sensitivity to testosterone may
matter less than testosterone exposure levels. However,
familiality patterns of 2D:4D did not match those of circulating testosterone. Although twin studies evidence
that testosterone levels are more heritable among men
than women (h2 5 66% vs. 41%), corresponding parent–
offspring correlations (including those of fathers and
sons) are nil, with the exception of a moderate mother–
daughter resemblance (Harris et al., 1998). Furthermore,
although the within-sex variation in testosterone levels
is several times larger in males than in females, both
prenatally (Finegan et al., 1989) and postnatally
(Vermeersch et al., 2008), there is no such sex difference
in the variance of 2D:4D (see Results).
Intriguingly, the current data suggest particularly
strong heritability of 2D:4D through male lines, as both
R2D:4D and L2D:4D were most similar for male–male
dyads (replicating Marshall, 2000), and the only significant family correlation for DR-L was for brothers. These
findings raise the possibility that Y-linked genes (e.g.,
the sex-determining region SRY, as suggested by
Gobrogge et al., 2008) might also influence digit ratio
expression. 2D:4D comparisons of sex-chromosome aberrations with normal karyotypes (47,XXY and 47,XYY
men with 46,XY men; 45,XO and 47,XXX women with
46,XX women; and corresponding animal models), halfsib designs, whole-genome scans, and studying the
genetics of individual differences in sex-hormone action
will be fitting methodological approaches to investigate
these matters further.
The exact genetics of 2D:4D is not yet known, remains
to be pinpointed, and in all likelihood is complex. Ultimately, it would be of great interest to undertake
genome scans for 2D:4D, as has been recently done to
elucidate the genetics of finger-ridge counts (Medland
et al., 2007). The exact nature of the nonshared environmental factors influencing the expression of 2D:4D also
remains to be elucidated. Because sex and individual differences in 2D:4D emerge prenatally and appear rather
stable postnatally, the nonshared environmental influences must be searched in the prenatal environment. In
addition, 2D:4D research might also benefit from adopting within-family study designs (e.g., comparisons of
related individuals discordant for a target trait; for a
successful application, see Hall and Love, 2003), to control for the apparently substantial genetic effects on
2D:4D which in studies of unrelated individuals could
obfuscate or attenuate real associations of 2D:4D with
target traits (Forstmeier et al., 2008).
379
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