Sex differences in infant psychomotor function

There is huge overlap between the sexes in sexually characteristic behavior in newborns and infants.  In other words,  there are hardly any sex differences at all.  The behavioral domain in which most of the sex differences have been observed, I think,  is the domain of psychomotor function.   Psychomotor function can be conceived in a wide ranging manner.   A French medical doctor and theoretician named Henri Wallon had such a view of psychomotor function.   His numerous publications during the first half of the century led to what is now called the French school of psychomotricity,  whose adepts and practitioners intervene clinically  -inspired by Wallon’s theory of psychomotor development.   This school of thought considers that the infants’ tendency to explore the environment,  its’ general muscle tone,  the strength of its grabbing (prehension),  its’ tendency to stand up early,  its’ general level of activity,  and even its’ character,  are all phenomena within the domain of psychomotricity.    In a recent book,  published in 1997,   Roger Deldime and Sonia Vermeulen presented a table proposing that this whole domain of psychomotricity expresses itself somewhat differently in infants of either sex.   Their main point,  I think,  is that human male infants are somewhat psychomotorically precocious.  See table 2.

Table 2

Summary of differences between hypertonic and hypotonic babies

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Hypertonic babies

Hypotonic babies

Proportion  of boys and girls

more  boys

more girls

Standing position

precocious

tardive

Walking

precocious

tardive

Prehension

tardive

précocious

Mobility

excessive

limited

Character

irascible, less fixed in adulthood

fearful, affectionate, dependent

From Deldime, R., & Vermeulen, S.  (1997).  Le développement psychologique de l’enfant (7ième édition).  Bruxelles:  De Boeck & Belin.

This point of view,  according to which boy infants are psychomotorically precocious, has recently been corroborated by June Reinisch. She collected data from maternal observations of the day of initial attainment for each of 10 developmental milestones for a cohort of 4,653 infants. Three milestones were reached significantly earlier in boys than girls, while none of the milestones appeared earlier in girls than boys. Of the 45 intervals between milestones, 7 were longer in boys and 12 were longer in girls.  Of course,  the very early developnmental milestones mostly consist of psychomotor behaviors.

Sex differences in turning behavior.    A large body of literature has documented the existence of individual preferences in turning direction among rodents which appear to be dependent on striatal dopaminergic mechanisms. The striatum is a group of neuronal aggregates embedded near the center of the brain known to play an important role in primitive aspects of movement.  Recent work has indicated that humans also demonstrate individual turning preferences, and that these preferences may also be related to the nigrostriatal dopamine system.  This system is a particular network whose input starts in a brain nucleus called the substantia nigra and consists primarily of neurons which use dopamine as their neurotransmitter.  One team of researchers recently developed a new method for measuring turning preferences in humans.  They reported a sex difference in the magnitude of the directional preference. While both men and women tended to turn towards the right, this tendency was significantly stronger among women. Analyses of test-retest reliability across two sessions (1-2 weeks apart) indicated that, in general, the rotation task elicited consistent turning biases. However, the turning biases of men and of women using oral contraceptives were significantly more consistent than those of regularly cycling females. These results are compatible with the animal literature and provide indirect evidence that ovarian hormones may modulate the mechanism(s) underlying this motor asymmetry.

Sex differences having to do with aggressiveness and fearfulness.   Though there are several bits of evidence to the effect that the human male is more aggressive from infancy and early childhood on through adulthood -as in most mammals,  I will first review the evidence in adults.

As is the case for all the psychological traits which are relatively sex-specific in humans,  aggressiveness certainly is socially conditioned.  However,  not only is there a biological component to aggressiveness,  but there are several distinct types of aggressiveness in mammals:  predatorial,  self-defense,  territorial, sexual,  protection of offspring, etc.  Though brain circuits are basically the same for all these types of aggression,  there is some specificity of the brain physiology underlying each type of aggressiveness.    The environmental context favoring expression of these types of aggressiveness is also distinct.   The male mammal is usually more territorially aggressive than the female.   The female mammal typically spends more time nurturing the offspring. People’s exposure to frustration is a major cause of violence. Rhawn Joseph has stated that the limbic system (emotional brain) of men is wired in such a manner that aggression produces pleasure.   Indeed there are many examples of male animals going out of their way to accede to a fight.   He states that women’s limbic systems are wired more to derive pleasure from nurturance.    However, neurobiological details of this hypothesized sex difference in “wiring” remain to be discovered,  so that at present,  Joseph’s point of view should be considered speculative.  

It is perhaps not so surprising then that statistics prove that man-to-man violence is much higher than woman-to-woman violence and that infanticide is more frequently mother-to- (male) child,  than father-to-child.   Of course, everybody knows that the human male is generally more aggressive than the human female (Maccoby & Jacklin, 1980).  The vast majority of assaulters causing bodily harm,  and of murderers,  are men.  However,  their victims are far more often other men (who I suppose are themselves relatively aggressive).  In the United States today,  the risk for a black male of being killed is 1 in 30;  for a white male, 1 in 179,  for a black female, 1 in 132,  and for a white female, 1 in 495.   The U.S. Bureau of Census stated in 1989 that 94% of all American prisoners were of the male sex. 

Though there are obvious and outstanding sociocultural factors involved in all kinds of human aggressiveness,  there is also an endocrinological and neurobiological underpinning, as in other species.   Male mammals as a whole are more aggressive than females mammifère en général (Wallen, 1996).  There is an interesting and notable exception:  hyenas.  Female hyenas are larger, more vicious and more dangerous than the males.  But then,  they are stuffed with testosterone...  to such a point that their clitoris looks like a large penis.   A rat fetus which is masculinized by an appropriate single dose of steroid hormone of the opposite sex will undergo a sex-change in level of aggressivity which will be apparent in adulthood. So-feminized males will be less aggressive,  and so-masculinized females will be more aggressive once they reach adulthood. Testosterone injections increase aggressiveness in rodents and primates even when administered in adulthood (see Van de Poll et al, 1981). Castration inhibits aggressiveness in several mammalian species including humans (ww)  Birds,  like many other animals,  have love seasons.  These seasons are the period of the year where they mate and keep territory for nesting.  The circulating testosterone of the males of these species is higher during this season,  and they are more aggressive (Nottebohm, 1970).  Both male and female levels of aggressiveness are increased,  in monkeys,  by injections of androgens.  It seems that humans resemble other mammals in this respect:   a recent study investigated 87 female inmates,  several of whom were quite aggressive.   The aggressive women had significantly higher levels of testosterone in their blood.

The most extreme form of aggressiveness in humans is observed in psychopaths.   Now some of the interesting findings in psychopaths is that they are of the male sex nine times out of ten, that adult psychopathy is usually traceable back to childhood (oppositional disorder) and even infancy (difficult temperament),  and finally that antisocial adults have significantly higher levels of circulating testosterone than normal controls (see chapter 11 for more details).  

Another piece of evidence of prenatal hormonal mediation of the life-long disposition toward aggressivity has been provided by studies of fetally androgenized women.  The two most common forms of fetal masculinization are progeny of women having been prescribed synthetic hormones (ex: diethylstilbestrol or DES) during pregnancy and the androgenital syndrome which results from congenital adrenal hyperplasia (CAH) of the pregnant mother or of the fetus itself,  resulting in overproduction of androgens.

One study (Helledey et al, 1993) investigated personality traits and platelet monoamine oxidase (MAO) activity (a marker of serotonergic neurotransmission) in 22 women (aged 17-34 yrs) with prenatal virilization due to CAH due to 21-hydroxylase deficiency and in 22 healthy controls. The CAH group differed significantly on 2 scales of the Karolinska Scales of Personality which have shown significant gender differences. Both differences were in the masculine direction, with a high, male level, score for Detachment and a lower score for Indirect Aggression. There was no significant difference in platelet MAO activity between the CAH group and the controls. Although an influence of psychosocial factors cannot be excluded, results suggest a possible association between prenatal androgen exposure and the high Detachment score for the CAH group. Gender differences in empathy, affiliation motivation, intimacy, and maternal nurturant behavior may be relevant parallels.  Another study  (Berenbaum & Resnick, 1997) compared very young, less young and adult CAH girls and control groups.  The CAH groups were more aggressive on several measures.  Similar results have been reported by Reinisch and colleagues (1981).  Hines and Kaufman (1994) compared CAH girls to controls to determine whether they prefer « rough and tumble » play.  There were no group differences in that respect,  but the CAH girls prefered boys as playmates.  Of course,  CAH is not the most critical test of hypotheses about hormonal masculinization.  Indeed,  masculinization varies in this syndrome from negligeable to very marked. 

One study investigated boys with androgenital syndrome resulting in excessive fetal exposure to androgens.  Though these boys engaged in rougher and more sports,  these boys were not more aggressive than controls (Reinisch & Sanders, 1992).  Because non effects like this are frequently observed in psychoendocrinology,  it is commonly believed that there are saturation points for various hormonal effects on the brain which are sex specific.   In other words,  nature cannot easily «masculinize» a male fetus or «feminize» a female fetus. However,  it must be recalled that there are many other biological factors of male-typical behavior (genes, neurotransmitters, later occuring hormones, low levels of the sex hormones of the opposite sex,  etc).   Also,  it is always a good idea to reserve judgment on negative findings.

Reinisch and colleagues found that women born of DES-treated mothers (synthetic estrogens were administered in the 50s to prevent miscarriage),  the former of which are known to be somewhat masculinized as a result,   were also significantly more aggressive than their unexposed sisters.  In another study by the same author,  the effect of maternal treatment with a synthetic progestin (19-NET,  or 19-nor-17-alpha-ethnyltestosterone) on offspring’s aggressiveness was studied.  Offspring of both sexes were more aggressive than control same-sex siblings (brothers or sisters). Synthetic progestins are known to masculinize animal and human fetuses.

One study investigated boys of diabetic mothers exposed to high doses of estrogens during pregnancy.   Both the estrogen-exposed girls and boys manifested significantly lower levels of aggressiveness.  In humans,  androgens may not be the only hormone prenatally involved in fixing future levels of aggressiveness.  In fact,  prenatal androgens have been shown to predict the degree of activational effect pubertal sex hormones will have many years later.   The brains of prenatally masculinized animals are less affected (transformed) by pubertal estrogen in several species.  Specifically,  prenatal masculinization results in a gradual reduction of the number of estrogen receptors in the brain.   Not all hormonal influence on aggressiveness is prenatal.  Castration of adult male mammals usually has the effect of reducing their levels of aggressiveness.  Prenatal androgenization of macaque females increases levels of aggressiveness observed in adulthood.  In similar experiments with rats,  the same effect could be obtained by prenatal androgenization or estrogenization.

I have always found it intriguing that the obvious opposite of aggressiveness,  fearfulness,  has not been an object of much neurobiological study or commentary.   It is a very basic mammalian trait that when cornered,  the two options available to an animal are "fight" or "flight".    In other words,  these two behavioral dispositions are linked opposites.   When an animal has a high disposition for one of these traits, it usually has a low one for the other.   Fear can be just as handicapping a state,  in humans,  as aggressivity.   It paralyzes,  it constrains the range of activities,  it makes a person dependent,  it makes a person weak and despondent,  it confines a person to intellectual, emotional and even to financial poverty.   It  imposes on people a boring narrow life.   It must end up being terribly depressing.   Everybody knows that women are more fear prone than men (see Johnsen & Hugdahl, 1990).  One study evaluated Norwegian versions of 4 phobic fear questionnaires in 248 university students in Norway. The scales were (1) the snake questionnaire and the spider questionnaire; (2) the Fear of Flying Scale; and (3) the Fear Survey Schedule. High internal consistency and high test-retest reliability were found for all questionnaires. A low to moderate degree of intercorrelation between the questionnaires appeared, and a clear sex difference emerged in responses to all the questionnaires.  Women consistently reported more fear than men.   Is anything known about the neurobiology of fear ? In a first pass,  I would say that it can all be inferred.  Everything particular about aggressiveness should be negatively correlated with fearfulness.  Though this seems highly likely,  it remains to be proven and deserves much more scientific attention than it has yet received.   The most extreme form of fear in humans is phobia.   The type of phobia which has most been studied neurobiologically,  I think,  is anorexia nervosa,  phobia of fatness.  Nine anorexics out of ten are female.  Now anorexics are known to have a complex set of imbalances of the hypothalamo-hypophysial-adrenal axis.  Testosterone is low compared to controls in human anorexics of both sexes. The abnormality of estrogen metabolism appears to be more complex.  In women anorexics, it has been proposed that the hypothalamus does not respond normally to the negative feedback effects of estrogen affecting luteinizing hormone -thus explaining the amenorhea (loss of menses) as well as dysregulation of appetite.  Rat anorexia is favored by high estrogen and low testosterone,   and administration of testosterone has been reported to significantly help both male and female human anorexics gain weight (see chapter 11 for more details on anorexia nervosa).