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Effect of prenatal testosterone administration on palmar dermatoglyphic intercore ridge counts of rhesus monkeys (Macaca mulatta).

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AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 94:409-419 (1994)
Effect of Prenatal Testosterone Administration on Palmar
Dermatoglyphic lntercore Ridge Counts of Rhesus Monkeys
(Macaca mulatta)
CHERYL SORENSON JAMISON, PAUL L. JAMISON,AND
ROBERT J. MEIER
Department of Anthropology, Indiana University, Bloomington,
Zndiana 47405
KEY WORDS
Androgen, Hand prints, Finger prints, Steroids,
Hormones, Prenatal development, Geschwind Hypothesis, Wisconsin
Regional Primate Center
ABSTMCT
Dermatoglyphic ridge counts of the prints of 59 rhesus monkeys (Macaca mulatta) whose mothers had been treated with injections of
testosterone during their pregnancies were studied to determine the effect of
the day the hormone began to be administered, the amount of hormone administered, and the number of days of hormone administration upon the
dermatoglyphic variation of the offspring. Of the three hormone variables,
only the day of beginning administration (STARTDAY) was significantly associated with dermatoglyphic variation, and its positive significance was
demonstrated with the ridge counts of Area I on both the left and right hand,
Area I1 of the left hand, and the total ridge counts of both hands. These results
are discussed within the context of the timing of the dermatoglyphic window,
and the differences in the findings between the monkey and earlier human
studies are addressed. o 1994 Wiley-Liss, Inc.
Dermatoglyphic variation has been convincingly demonstrated to be the result of
both genetic and prenatal environmental
factors (see Schaumann and Alter, 1976,
and hesch, 1983, for historical references;
as well as Jantz et al., 1992; Arrieta et al.,
1991; Kamali and Mavalwala, 1990;
Mukherjee, 1990; Livshits and Kobyliansky,
1987, 1991; Chakraborty, 1991). Human
populations may differ significantly in their
dermatoglyphic traits, and these differences
have been used to reconstruct population
history (Froehlich, 1987). There is familial
variation in dermatoglyphic traits with parents and their offspring, siblings, and even
twins showing both similarities and differences (Arrieta et al., 1991; Loesch, 1979;
Reed et al., 1977).
Both the external (Blangero, 1988; Rosa,
1985) and prenatal environment can exert a
powerful effect on dermatoglyphic traits.
Prenatal developmental disruptions can af0 1994 WILEY-LISS. INC.
fect ridge traits if they occur before the 19th
gestational week (Cummins, 1929; Hale,
1949, 1952; Mulvihill and Smith, 1969;
Babler, 1987, 1991), by which time the
ridges are set. Examples of prenatal disruption having a demonstrated dermatoglyphic
effect include rubella (Hook et al., 1971; Purvis-Smith and Menser, 19731, alcohol (Qazi
et al., 19801, and cytomegalovirus infection
(Wright et al., 1972). A summary of studies
investigating prenatal environmental effects upon dermatoglyphics can be found in
Ahuja and Plato (1990). The recent dermatoglyphic research of Bracha and his colleagues (Bracha et al., 1991) on identical
twins discordant for schizophrenia offers
Received November 13,1992; accepted February 3,1994.
Address reprint requests to Cheryl Sorenson Jamison, PhD,
Anthropology Department, Indiana University, Bloomington, IN
47405.
410
C. SORENSON JAMISON ET AL.
support for the importance of the environment (including prenatal environment) in
the development of both schizophrenia and
dermatoglyphics, since the observed differences cannot be genetic in origin.
Our investigations into the causes of dermatoglyphic differences have focused upon
the effect of testosterone, a variable that has
both genetic and prenatal environmental
components (Sorenson Jamison, 1988,1990;
Meier, 1990; Sorenson Jamison et al., 1993).
The prenatal testosterone to which a developing fetus is exposed arises both from the
mother and that which the fetus (male or
female) itself produces (Geschwind and Galaburda, 1985). The latter is essentially genetic in origin, while the former can be
viewed as an environmental effect.
The Geschwind Hypothesis (Geschwind
and Behan, 1982; Geschwind and Galaburda, 1985) provides the theoretical underpinning for our continuing investigation.
This hypothesis, also known as the Testosterone Hypothesis, states that an excess of
prenatal testosterone results in the retarded
development of the left hemisphere of the
brain (and an often associated enhancement
of the right hemisphere). These disruptions
in neural development, according to the
hypothesis, are then associated with conditions such as dyslexia, stuttering, left-handedness, autoimmune disease, and mathematical and artistic giftedness. Prenatal
testosterone is circulating within the fetus
during the time of dermatoglyphic formation (Zaaijer and Price, 1971). The relationships between prenatal testosterone, nerve
growth factor, and epidermal growth factor (Levi-Montalcini and Angeletti, 1963;
Korsching and Thoenen, 1983; Bynny et al.,
1972) in addition to Dell and Munger’s
(1986) illustration of the relationship of
nerve fibers to dermatoglyphic ridge development, convincingly suggest a mechanism
by which prenatal testosterone might influence dermatoglyphic variation.
Previously we found that a sample of dyslexics (who, according to the Geschwind
Hypothesis, were subjected to an excess of
prenatal testosterone) differed dermatoglyphically from controls (Sorenson Jamison, 1988, 1990; Meier, 1990). Also, in a
sample of normal adult males, salivary tes-
tosterone levels were significantly related
to dermatoglyphic asymmetry (Sorenson
Jamison et al., 1993). The latter study was
an investigation of the relationship of secondary testosterone, rather than prenatal
testosterone, to dermatoglyphics. We believe that secondary testosterone can be
viewed as a proxy for prenatal testosterone
(an admittedly imperfect one, but one that
we regard as being empirically useful).
The ongoing Wisconsin Rhesus Monkey
Study is a long-term investigation of the effects of prenatal androgen administration
on anatomy and behavior. It includes a randomly selected sample of animals whose
mothers had been treated with testosterone
during pregnancy, providing us with an opportunity to assess the effects of prenatal
testosterone on dermatoglyphics more directly than previously possible. In general,
the published reports from this study have
found significant results of prenatal androgens on both behavior and anatomy, particularly in females (Goy, 1981; Goy and Resko,
1972; Pomerantz et al., 1988; Goy et al.,
1988; Thornton and Goy, 1986; Kemnitz et
al., 1988; Goy and Kemnitz, 1983). For instance, androgenized females were found to
engage in significantly more mounting and
rough play behaviors than untreated females (but fewer than untreated males), and
they also exhibited varying degrees of genital masculinization. The age of menarche of
treated females was significantly later than
untreated females, but once begun, the menstrual cycles of treated females were normal. Extended discussion of the additional
findings of these studies would require unwarranted space in the present paper, and
the interested reader is referred to the references listed above.
In the first report of the findings from our
dermatoglyphic investigation of the Wisconsin monkeys (Meier et al., 19931, using a
matched-pair design (matched on the basis
of sex and age), we compared the palmar
intercore ridge counts of the experimental
sample against a control sample. For that
investigation, the experimental sample (N
= 45, sexes combined) was limited to those
animals with mothers whose treatment occurred during the “dermatoglyphic window,”
that is, the established time period of der-
PRENATAL TESTOSTERONE EFFECT ON RHESUS DERMATOGLYPHICS
matoglyphic formation (55-70 days: Okajima and Newell-Morris, 1988). We found
that the experimentals had significantly
lower total ridge counts than controls and
also significantly lower ridge counts on both
left and right palms for Areas I and 11, although not in Area 111.
The present study focuses upon the experimental group only, in which all treated animals are included (N = 59), those whose hormone administration we believed to have
occurred outside the window of dermatoglyphic formation (N = 14), as well as those
whose treatment occurred during (N = 45)
the critical time period. The reason for this
change in protocol was that we were interested in investigating the variation in the
treatment variables, and since the control
animals had not been treated, they could not
be included (all values = 0). However, the
experimental animals whose treatment fell
before or after the dermatoglyphic window
was open could be included in the investigation (since they did have real values for the
variables of interest), and their inclusion
might then be viewed as reinforcing our earlier finding if their dermatoglyphic values
mimicked those of the controls (Meier et al.,
1993).
Our hypotheses were that (1) the greater
the number of days of testosterone administration, (2) the earlier the hormone began to
be administered, and (3) the greater the
amount of hormone administered, the more
pronounced would be the dermatoglyphic effect (that is, the lower would be the ridge
counts, since in the study comparing the two
groups, the experimentals had lower ridge
counts than controls).
MATERIALS AND METHODS
The sample for this study included 59
rhesus monkeys from the Wisconsin Regional Primate Center, ranging in age from
4 to 16 years. Forty-seven subjects were females and 12 were males. The mothers of
the animals had been injected with either
testosterone propionate (TP)or dihydrotestosterone propionate (DHTP) at a dosage
level of 5-15 mglday for between 15 and 109
days, beginning on the 26th to the 115th day
of gestation. Independent variables include
STARTDAY-the gestational day on which
411
treatment was begun; AMOUNT-the
amount of testosterone administered at
each treatment; and DAYS-the number of
days the treatment continued. Molds of the
monkeys’ hands were made using the Dow
Corning silicone method (Reed and Meier,
1990). Details of the epidermal ridge systems were enhanced by brushing the molds
with a blue-colored felt pen, after which the
patterns could be studied under a low-power
magnifier. The dermatoglyphic analyses
were carried out by RJM using the methodology followed by Newell-Morris et al. (1989)
and Newell-Morris et al. (1982).
Statistical analyses were carried out using SPSS/PC+ (Version 4.01). T-tests examined sex differences to determine whether or
not males and females needed to be analyzed separately. Multiple regressions investigated the effect of the number of days of
testosterone administration (DAYS), the
amount of hormone administered (AMOUNT),
and the day of gestation that the hormone
began to be administered (STARTDAY) on
the dermatoglyphic variables. The method
of variable entry used was forced entry, with
all variables allowed to enter a t once.
To take into account the possibility that
body size might also have a dermatoglyphic
effect, either separately or in conjunction
with the testosterone variables, the regression analyses were run with the inclusion of
the variables WEIGHT and RULLG (right
upper limb length; the only linear measure
we had).
Dermatoglyphic variables used in the
analyses included the intercore ridge counts
for the left and right hands in three different
palmar areas (I, 11, and 111, described in
Newell-Morris et al., 1989), and the total
ridge counts computed by adding the counts
of the three areas; again, €or the left and
right hand separately. Each of the dermatoglyphic variables was determined to be normally distributed according to the Kolmogorov-Smirnov test (P values varied from a
low of .171 to a high of 582).
RESULTS
Descriptive statistics, by sex, of the intercore ridge count variables for the androgentreated animals are listed in Table 1 along
with the results of t-tests. The latter show
C. SORENSON JAMISON ET AL.
412
TABLE 1 . Descriptiue statistics and t-test results for dermatoglyphic ridge count and body size variables for male and
female androeen-treated animals
Variable'
LICRCI
RICRCI
LICRCII
RICRCII
LICRCIII
RICRCIII
TLICRC
TRICRC
WEIGHT
RULLG
Males (N = 12)
Mean
S.D.
Females (N = 47)
Mean
S.D.
33.92
35.25
28.92
29.42
32.00
32.58
94.83
97.25
10.21
15.63
35.94
36.13
29.70
30.13
30.89
31.22
96.53
97.48
7.42
13.58
4.70
5.59
3.63
4.66
3.19
3.68
10.10
10.64
1.72
0.94
5.38
5.06
3.28
3.17
3.29
2.91
8.86
7.62
1.79
0.78
~
t
-1.19
-0.53
-0.72
-0.63
1.05
1.37
-0.58
-0.08
..
4.86
8.49
D
,240
,601
,472
,534
,300
.177
.567
.933
.om
.OOO
Key to variable names: L = 1 4 R = right; ICRC = intercom ridge aunt; T = total; I, 11, 111 = palmar areas I, 11, and 111.
Weight is measured in kilos.
RULU: = Right Upper Limb Length. measured in centimeters.
significant sex differences for any of the
ridge count variables, although both weight
and right upper arm length (RULLG) were
significantly larger in males. Although not
reported in Table 1, the null hypothesis of
equal variances was not rejected for any of
these variables. In subsequent analyses of
the dermatoglyphic ridge counts, the sexes
were combined (N= 59).
Results from the multiple regression analyses of the dermatoglyphic and size variables with the three testosterone variables
can be seen in Table 2.Of the three hormone
variables, only STARTDAY was significantly related (P< .05) to ridge counts, and
its relationship is significant for five of the
eight dermatoglyphic variables tested: left
and right Area I ridge counts, left count for
Area 11, and left and right total palm counts.
The body size variables, WEIGHT and
RULLG, were not significantly related to
any of the dermatoglyphicvariables.
The effect of STARTDAY was interpreted
as having a significant effect on the five dermatoglyphic variables while holding the effects of AMOUNT and DAYS constant
(Dometrius, 1992). The equation F was significant for three of the five regressions in
which STARTDAY had a significant t (the
equation F was of borderline significancefor
the total count on the left hand [P = .0761,
but it did not approach significance for the
left Area I1 count). Regression analyses testing for interactions among the treatment
variables indicated no significant effects for
any combination of the three variables.
120
To further illustrate the situation, scattergrams presenting the bivariate relationship of both the left and right Area I ridge
counts with STARTDAY can be seen in Figure 1, a and b, respectively. It is immediately apparent from examination of these
figures that the later during gestation the
androgen began to be administered, the
higher is the resulting ridge count for these
animals. Closer scrutiny of the scattergrams
led to the question of whether the dermatoglyphic ridge counts differed significantly
between those animals whose hormone
treatments fell beyond the dermatuglyphic
window and those whose treatment occurred before this window "closed." Furthermore, the scattergram suggests that the period of dermatoglyphic effect ends earlier
than the window of ridge formation (70
days), perhaps even earlier than day 60.
Again, t-tests were run (Table 31, this time
with the groups divided according to their
STARTDAY value. If the STARTDAY value
was less than 60 days, they were assigned to
one group (N= 44), and those whose value
was 60 days or greater were assigned to the
second group (N = 15). Table 3 demonstrates that for all dermatoglyphicvariables
except the ridge counts in Area 111 of both
hands, the values of the animals in Group 2
(STARTDAY 360)were significantlyhigher
than those from Group 1.The groups did not
differ significantlyfor either of the body size
variables. Again, with the exception of one
variable (RICRCI),the variances were equal
between the groups. In the case of RICRCI,
PRENATAL TESTOSTERONE EFFECT ON RHESUS DERMATOGLYPHICS
413
TABLE 2. Regression results of the effects of testosterone a n d body size variables on dermatoglyphic ridge counts
Dependent
variable
LICRCI
Amount
Days
Startday
Weight
RULLG
RICRCI
Amount
Days
Startday
Weight
RULLG
LICRCII
Amount
Days
Startday
Weight
RULLG
RICRCII
Amount
Days
Startday
Weight
RULLG
LICRCIII
Amount
Days
Startday
Weight
RULLG
RICRCIII
Amount
Days
Startday
Weight
RULLG
TLICRC
Amount
Days
Startday
Weight
RULLG
TRICRC
Amount
Days
Startday
Weight
RULLG
Beta
Independent
variable statistics
t
Equation statistics
-
D
R2
F
D
Constant
0.09
-0.18
0.38
-0.26
0.07
0.72
-1.39
3.05
-1.72
0.45
,476
.172
,004
.091
,653
.52
3.93
,004
31.59
0.07
-0.12
0.39
-0.27
0.09
0.54
-0.94
3.10
-1.80
0.58
,591
,349
,003
,078
,566
.50
3.57
,008
30.90
-0.00
0.10
0.30
-0.17
0.27
0.02
0.75
2.21
-1.04
1.68
,982
,459
.031
,304
,100
.35
1.48
,213
17.67
0.14
0.07
0.25
-0.26
0.21
1.05
0.49
1.77
-1.54
1.27
,300
.624
,083
,131
.211
.32
1.15
,348
19.71
-0.09
0.02
-0.01
-0.01
0.25
-0.68
0.14
-0.07
-0.07
1.50
,502
385
.941
,946
,140
.26
0.76
,582
22.25
0.06
-0.03
-0.01
-0.00
0.26
0.48
-0.24
-0.09
-0.00
1.54
.637
.814
,930
,997
.129
.27
0.85
.524
20.61
0.02
-0.06
0.33
-0.22
0.23
0.14
-0.42
2.47
-1.36
1.46
288
.41
2.13
,076
71.51
0.13
-0.06
0.35
-0.28
0.24
0.99
-0.44
2.62
-1.77
1.54
.329
,661
,012
.083
,130
.44
2.49
.042
71.22
'Beta refers to the standardizedregressioncoefficient.N
,678
,017
.181
,151
=
59.
the t-test results are based upon separate
variance estimates for the groups. T-tests
for sex differences within the groups (data
not reported in the tables) were run on those
variables found above to be significant, and
they revealed no significant differences between males and females (P < .05)within
either group (group 1 included 9 males and
35 females; group 2 included 3 males and 12
females).
DISCUSSION
Interpretation of these results leads to
some interesting conclusions. Of our three
original hypotheses, only that concerning
STARTDAY is supported: The earlier the
C. SORENSON JAMISON ET AL.
414
a. SCATTERGRAM OF LlCRCl WITH STARTDAY
(N 59)
LEFT INTERCORE RIDGE COUNT I
-
50
35
:.
30
+
+ +
25
+ +
20
20
40
60
120
100
80
ANDROGEN STARTDAY
i
'
MALE
+
+r
FEMALE
- .43; - .0006 1
p
Note: Three males have identical scores
b. SCATTERGRAM OF RlCRCl WITH STARTDAY
(N 59)
RIGHT INTERCORE RIDGE COUNT I
50
40
35
-
-
+
T
ki-
+
=+/-----i
t
t
-3
t
t
//
/
~
/
-
+
+
c .
f
+
+
25
20
40
60
80
100
120
ANDROGEN STARTDAY
Note: Two males have identical scores
Fig. 1. Scattergrams showing the relationshipof left (a) and right (b)intercore ridge counts in Area 1
to STARTDAY.
treatment was begun, the lower are the resulting ridge counts, while neither the number of days the treatment lasted nor the
amount of hormone administered had a significant dermatoglyphic effect.
Our finding regarding the timing of the
period of dermatoglyphic effect in relation to
the dermatoglyphic window is also of significance. In our previous study, we had assumed that those animals whose treatment
had started and ended before the dermatoglyphic window had "opened" (by day 55)
had received treatment too early for a dermatoglyphic effect to have occurred, and
PRENATAL TESTOSTERONE EFFECT ON RHESUS DERMATOGLYPHICS
415
TABLE 3. Descriptive statistics and t-test results for dermatoglyphic ridge count and body size variables in
androgen-treated animals whose treatment occurred before and after the develoDmenta1 oeriod for ridpe formatwn ended
Variable
Hormonal treatment
Before (N= 44)
ARer (N = 15)
Mean
S.D.
Mean
S.D.
LICRCI
RICRCI
LICRCII
RICRCII
LICRCIII
RICRCIII
TLICRC
TRICRC
WEIGHT’
RULLG’
34.11
34.58
28.86
29.40
30.98
31.37
93.95
95.35
8.06
13.99
5.01
5.05
3.19
3.59
3.23
2.90
8.29
7.42
2.17
1.04
39.67
39.87
31.53
31.67
31.53
31.87
102.73
103.40
7.78
14.05
3.37
2.92
3.04
2.64
3.48
3.72
8.18
7.67
1.92
1.35
t
I,
-3.94
-3.82
-2.83
-2.24
-0.56
-0.53
-3.55
-3.59
0.43
-0.18
,000
.ooo
.006
.029
575
,599
,001
,001
,668
,858
‘Measured in kilos.
‘Measured in centimeters.
that those whose treatment had begun as
late as day 60 would still be able to demonstrate at least some significant effect (as indicated earlier, the window of ridge formation is from day 55 to day 70; Okajima and
Newell-Morris, 1988). However, the results
of the current investigation and examination of the scattergrams (Fig. 1) indicate
that the period of dermatoglyphic effect does
not coincide exactly with the window of dermatoglyphic formation.
If the data on the three animals whose
treatment began on day 26 and stopped 15
days later can be relied upon, they apparently received a significant residual effect of
the hormone. This implies that the period of
dermatoglyphic effect begins prior to day 55
(26 + 15 = 45 days). In contrast, those animals whose treatment did not begin until
day 60 received very minimal, if any, effect.
In fact, the ridge counts of the animals in the
group treated on or after STARTDAY 60
were surprisingly comparable to those of the
controls in our earlier study (Meier et al.,
1993).T-tests run to examine differences between this group of experimentals (N = 15)
and the controls (N = 60) found none of the
dermatoglyphic variables to be significantly
different between the groups (data not presented in the tables). In sum, what this
means is that the ridge counts for those individuals who received the androgen after the
period of dermatoglyphic effect has ended
are indistinguishable from the ridge counts
of control animals, even though the treatment (in some cases) overlapped the final
portion of the dermatoglyphic formation
window. Thus it appears that the period of
dermatoglyphic effect begins and ends considerably earlier than the period of actual
ridge formation (the “dermatoglyphic window”).
The results of our two studies with monkeys, while demonstrating the effect of prenatal testosterone administration upon dermatoglyphic traits to be significant, are
different in direction from our studies with
humans. The research with dyslexics found
dyslexics to have significantly higher ridge
counts than controls.
The critical question to which a response
must be made is, how is it possible for prenatal testosterone to increase dermatoglyphic
ridge counts in humans, and then decrease
these variables in monkeys? In both species,
the effect of the hormone is significant, but
the direction of the effect is opposite.
Three possible explanations to the directional differences in results between the human and monkey and studies present themselves, each of which may provide a partial
answer. The first potential explanation lies
in the fact that for the humans that we studied, testosterone is a naturally occurring
substance, one that has both a genetic and a
prenatal environmental origin (and admittedly, its effect is theoretical not experimental; we know it is present during the dermatoglyphic window, and we do know that
there were significant differences between
the groups investigated, but we cannot state
with certainty that the differences were due
416
C. SORENSON JAMISON ET AL.
to the presence of testosterone). For the
rhesus study, however, the presence of testosterone was experimentally manipulated
and was totally of external environmental
origin.
It may well be that for humans (and normal monkey development as well), the critical dermatoglyphic factor is not the presence
of the testosterone per se, but rather a genetic element that affects both normally
present testosterone and that coincidentally
also affects dermatoglyphic traits. It should
be pointed out that even maternal sources of
testosterone probably have a genetic element, which, unless the mother is a surrogate, the fetus shares to some extent. This
difference between naturally occurring vs.
externally derived sources of testosterone
would explain the great range in the ridge
counts of the monkeys whose treatment began before 60 days (see Fig. 1): The genetic
effect upon ridge development might be pulling in one direction, while the externally administered testosterone might be exerting
an opposing effect. One way in which this
possibility might be investigated would be to
look at the dermatoglyphics of untreated
monkeys whose normal prenatal testosterone levels were monitored.
The second explanation for the differences
between the human and monkey investigations might be that the timing of normal
testosterone secretion in the two species
may differ in relation to the period of dermatoglyphic formation. Human fetal males
are secreting testosterone by 10 weeks, and
females by 13 weeks (Zaaijer and Price,
1971), overlapping the critical dermatoglyphic developmental period of 11-19
weeks. However, the research of Resko and
his coworkers (Resko, 1970; Resko et al.,
1973; Goy and Resko, 1972) has indicated
that measurable testosterone levels cannot
be detected in the male rhesus fetus until
gestational day 45, and then only in very
minute amounts: It is not until day 59 that
large concentrations have been detected. In
female rhesus monkeys, testosterone was
not detected until day 79.
According to our study (as well as that of
Okajima and Newell-Morris, 1988), then,
large amounts of normal fetal testosterone
secretion would be secreted either after the
dermatoglyphic development window, or at
least at the very end of the critical time period. Resko et al. (1973) also investigated
maternal concentrations of testosterone,
and they found that the amount differed significantly by the sex of the fetus, but the
study did not investigate maternal circulation of the hormone until gestational day 80,
so this fails to tell us anything about testosterone circulation during the time of dermatoglyphic formation.
The findings concerning the timing of normal rhesus fetal testosterone circulation
combined with the fact that our study investigated only the effect of an external source
of the hormone would appear to establish a
basis for the differences between our human
and rhesus findings. However, these differences do not resolve the issue of directional
differences in results, and while they do provide some sort of a n answer, it is not a very
elegant one. If there is indeed a causal relationship between testosterone levels and
dermatoglyphics, it should be possible to arrive at a more theoretically satisfactory explanation of the contrasting results from the
two studies.
The third area of explanation for the contrast in the human and rhesus findings is
related to the differences in dermatoglyphic
traits between humans and monkeys. Monkeys retain elevated volar pads throughout
their lifetimes, and the palmar patterns are
usually whorls. In comparison, the volar
pads in human hands recede during the period of ridge development, and when there
are palmar patterns present, they are most
typically loops; often there is only one pattern per palm (or none).
These dermatoglyphic trait differences
may well be due to developmental rate differences between monkeys and humans.
The relationship of this point to testosterone
is that one of the demonstrated effects of
prenatal testosterone upon development is
to retard development (see Geschwind and
Galaburda, 1985, for a summary of the literature). As previously mentioned, the experimental females from the Wisconsin study
were slow to reach sexual maturation, in
comparison to normal females (Goy and
Resko, 1972; Kemnitz et al., 1988).
It may well be that without the presence
of circulating testosterone during the period
of dermatoglyphic formation, ridge develop-
PRENATAL TESTOSTERONE EFFECT ON RHESUS DERMATOGLYPHICS
ment in the rhesus is typically rapid (in comparison to humans) and the ridges are established without the pads receding, as they do
in humans. The results of our study do support this delaying role for testosterone in
that the experimental animals had fewer
ridges than controls-their dermatoglyphic
development may well have been slowed by
the presence of the hormone. The speciestypical whorls were still present, but they
were of lesser complexity (Meier et al.,
1993); the relevance of this point is that
greater pattern complexity is often associated with higher ridge count, a t least in areas where volar pad breadth is believed to
have been great (Babler, 1978,1987).
Human dermatoglyphic development, in
contrast, may be naturally retarded by the
presence of testosterone for a relatively long
period of time, and one effect of this retardation time is that the pads can recede before
the ridge formation is finalized. For humans, then, the effect of prenatal testosterone is to extend the period of dermatoglyphic
development, allowing the volar pads to decrease in size, in turn, leading to the decreasing pattern complexity, while also permitting more time for ridge development to
occur in areas that are now relatively flat. It
may even be that in humans ridge development does not begin until after the pads
have receded (Babler, 1978,1987).
This reasoning would appear at first
glance to be circular-but the key is in the
relative timing of and length of the period of
dermatoglyphic effect. For rhesus monkeys,
this period is earlier and of a shorter duration than for humans; the patterns and
ridges complete development rapidly, while
the volar pads are large before normal testosterone secretion reaches a high level. We
are suggesting that experimental testosterone administration in monkeys may have
the effect of slightly retarding dermatoglyphic development, resulting in patterns
of decreased complexity, which in turn are
associated with a reduction in ridge count.
This effect occurred within an already dermatoglyphically competent genetic background. However, we believe that the experimental effect of testosterone was not strong
enough to delay the completion of dermatoglyphic development-and this is the critical difference between the effects of tes-
417
tosterone on monkey and human dermatoglyphics in our studies.
ACKNOWLEDGMENTS
We thank R.H. Osborne for alerting us to
the opportunity of making this investigation, and we are very much appreciative of
the personnel at the Wisconsin Regional Primate Center, who facilitated this research.
We would especially like to thank W.E. Bridson, W.D. Houser, and R.W. Goy. The project
was supported in part by a Bio-Medical Sciences grant from Indiana University. We
also thank three anonymous reviewers for
their extremely helpful criticisms and suggestions, particularly the one who caused us
to clarify our thinking in regard to the dermatoglyphic window.
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