Effect of prenatal testosterone administration on palmar dermatoglyphic intercore ridge counts of rhesus monkeys (Macaca mulatta).код для вставкиСкачать
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be the result of both genetic and prenatal environmental factors (see Schaumann and Alter, 1976, and hesch, 1983, for historical references; as well as Jantz et al., 1992; Arrieta et al., 1991; Kamali and Mavalwala, 1990; Mukherjee, 1990; Livshits and Kobyliansky, 1987, 1991; Chakraborty, 1991).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. 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