Androgens in Human Evolution (brain evolution)

jamesmichaelhoward at jamesmichaelhoward at
Tue Apr 25 16:06:45 EST 2000

Androgens in Human Evolution
A New Explanation of Human Evolution

James Michael Howard
Fayetteville, Arkansas, U.S.A.


Human evolution consists of chronological changes in gene regulation of
a continuous and relatively stable genome, activated by hormones, the
production of which are intermittently affected by endogenous and
exogenous forces. Periodic variations in the gonadal androgen,
testosterone, and the adrenal androgen, dehydroepiandrosterone (DHEA),
significantly participated in all hominid transformations. The hominid
characteristics of early Australopithecines are primarily a result of
increased testosterone. The first significant cold of the early
Pleistocene resulted in an increase in DHEA that simultaneously
produced Homo and the robust Australopithecines. Subsequent Pleistocene
climatic changes and differential reproduction produced changes in DHEA
and testosterone ratios that caused extinction of the robust
Australopithecines and further changes in “Homo.” Changes in
testosterone and DHEA produce allometric and behavioral changes that
are identifiable and vigorous in modern populations.

Humans and chimpanzees differ in hormones that produce significant
effects on anatomy, physiology, and behavior. Human males and females
produce more testosterone than chimpanzee males and females,
respectively (Winter et al., 1980). Chimpanzee and human females
produce similar levels of estradiol (Winter et al., 1980) and
progesterone (Hobson et al., 1976). I suggest early differences in
testosterone levels started species divergence and promoted hominid

Estradiol and testosterone support different functions in females.
Estradiol stimulates genital displays that advertise ovulation in
monkeys (Wilson, 1977), gibbons (Nadler et al., 1993), chimpanzees
(Ozasa & Gould, 1982) and gorillas (Nadler, 1980), but not women.
Estradiol and testosterone both peak near ovulation in female
orangutans, gorillas, chimpanzees and humans. Estradiol and
testosterone act synergistically to maximize reproduction. Estradiol
prepares the sexual apparatus for coitus and impregnation; testosterone
stimulates sexual activity.

While it “is a general trend in Western societies to blame psychosocial
factors for diminished sexuality in women,” diminished sexual drive and
other aspects of sexual dysfunction, in androgen-deficit women, are
primarily improved by testosterone therapy (Davis, 1996; Kaplan &
Owett, 1993). In postmenopausal women, combined estrogen-androgen
therapy significantly improves “sexual desire, satisfaction and
frequency,” whereas estrogen alone, or estrogen-progestin therapies do
not, leading to the conclusions that “androgens play a pivotal role in
sexual function” and “estrogens are not a significant factor
determining levels of sexual drive and enjoyment” (Sarrel et al.,
1998). Because estrogens prepare female genitalia for coitus, it is
best to treat sexual dysfunction in women with testosterone and
estradiol (Davis et al., 1995). Nevertheless, libido is primarily an
effect of testosterone. In sexually functional women, testosterone
treatment produces a “statistically significant increase in genital
responsiveness” and “subjective reports of ‘genital sensations’
and ‘sexual lust’” (Tuiten et al., 2000). Supplementary testosterone
not only corrects deficiencies in sexual desire, it intensifies normal
sex drive.

Estradiol levels in women and chimpanzees are optimal. Therefore,
increasing testosterone to estradiol ratios in hominids increases
sexuality proportionately. As testosterone increases, so does the
sexual activity of the female. This increases male attendance and
reproduction. These females have an advantage in representation in
future generations.

Increasing the testosterone to estradiol ratio reduces the effects of
estradiol. Human female fetal external genitalia contain AR (androgen
receptors) and ER (estrogen receptors), while male external genitalia
lack ER (Kalloo et al., 1993). The AR in the female external
genitalia “were strikingly similar to that in the male.” In women,
increased testosterone competes with the effects of estradiol on
external genitalia. As the testosterone to estradiol ratio increases,
the labial display decreases. This is why humans do not produce a
labial display. (Adrenal androgens stimulate male and female pubic hair
just prior to puberty and probably act through the common AR in both
sexes.) The primary sexual signal of female chimpanzees is the labial
display. In women the primary display of sexual maturity is the breast.
Chimpanzee mothers and small breasted women produce ample nutrition for
nursing offspring. I suggest the increased size of the human breast is
a sexual signal. Breasts are estradiol-dependent structures. Breast
enlargement is a signal of maturing estradiol levels, and may also be a
signal of maturing testosterone levels and, therefore, of increased
sexual arousal.

Fat tissues capture steroid hormones, including testosterone.
Testosterone is aromatized to estradiol in fat tissues. While breast
fat is not as active as axillary fat in converting testosterone into
estradiol, “results indicate a possible role of adipose tissue as a
significant extra-gonadal source of estrogens" (Nimrod & Ryan, 1975).
This increased level of estradiol in the breast could increase breast
size. Aromatization of testosterone occurs in normal female breast
tissue and in gynecomastia in men. Breast tissue from five out of six
men with gynecomastia aromatized testosterone into estradiol (Perel et
al., 1981). (Gynecomastia is true breast development in men, vis-à-vis
pseudogynecomastia caused by fat deposits.) Conversion of testosterone
into estradiol in human breast fat augments breast development and
size. Testosterone and estrogen both inhibit human hair production, in
vitro (Kondo et al., 1990). Increasing testosterone levels in hominids
reduced hair production in both sexes. The combined effects of
testosterone and estradiol further reduce hair growth in women. This
increases the prominence of the breast. The female human breast is a
signal of mature estrogen and testosterone production. The female human
breast is largest among primates due to increased testosterone.

The pubic bones of male mice are shorter and thicker than those of
female mice. Neonatal testosterone treatment of female mice
produces “pubic bones shorter and thicker than those of age-matched
females” and “Pubes in male mice castrated at the day of birth were
thinner than those of intact males.” (Iguchi et al., 1989). Androgens
directly affect bone growth in women (Gasperino, 1995). Testosterone is
involved in bone growth and produces changes in the female pelvis.
Increasing testosterone in hominid females would change growth and
development of the pelvis with time. Essentially all tissues produce
androgen receptors, therefore growth and development of all tissues in
emerging hominids were affected by testosterone. The muscles that
control upright walking increased in strength as a result of increased
testosterone. The large size of the gluteus maximus “is one of the most
characteristic features of the muscular system in man, connected as it
is with the power he has of maintaining the trunk in the erect
posture.” (Gray, 1966).

The brain also enlarged as a response to the effects of increasing
testosterone. The brain produces androgen receptors throughout.
Testosterone exposure of the male human brain, in utero, results in
increased head circumference of male brains at birth (Liebermen L.S.,
1982). Androgen treatment of female monkeys increased performance to
male levels, on an “object discrimination task.” Both male and female
performance levels were adversely affected by lesions in the orbital
prefrontal cortex, indicating that “gonadal hormones may play an
inductive role in the differentiation of higher cortical function in
nonhuman primates.” (Clark & Goldman-Rakic, 1989).

The single phenomenon of increasing testosterone produced the hominid
characteristics of Australopithecus. The single phenomenon of increased
testosterone production participated in every hominid characteristic,
simultaneously. Testosterone increased female sexual activity, reduced
female genital display, reduced hair growth, increased breast size,
changed pelvic growth, and produced increases in brain size. These
combined changes accelerated the advent of upright, bipedal locomotion
and larger brains. (Male and female pubic hair is visually different.
It may be that pubic hair was the first appreciable change in sexual
display as body hair and the labial display digressed in
The canine teeth of Australopithecus were smaller, and
less “projecting” than contemporary primates. However, in living
monkeys, testosterone increases large canine teeth. The canines are
larger in males and prenatal exposure of females to testosterone
increases the size of their canines (Zingeser & Phoenix, 1978). This
appears to present a quandary for this explanation of human evolution.
Humans produce more testosterone, yet the canine teeth are small.


In hominids the effects of testosterone, on brain size, teeth, and
other tissues, are due to changes in availability of DHEA. I suggest
DHEA is involved in growth and maintenance of all tissues, especially
the brain, and is paramount in the formation of the robust
Australopithecines and Homo. DHEA is proven to positively affect growth
and function of many tissues, including the
brain. “Dehydroepiandrosterone and its sulphate ester are neuroactive
and are both imported into the brain from the circulation and produced
in the nervous system. These neurosteroids have neurotrophic and
excitatory effects.” (Baulieu, 1999). (The enlargement of neural tissue
during primitive evolution may be due to increased absorption and
production of DHEA.) Testosterone evolved after DHEA; testosterone is a
conversion product of androstenedione, which is a direct conversion
product of DHEA. Therefore growth before testosterone relied on DHEA.
Testosterone evolved because its molecular structure affected DNA in an
advantageous manner. My principal hypothesis is DHEA optimizes
transcription and replication of DNA. Therefore, a subordinate
hypothesis suggests the advantage of testosterone is that it directs
DHEA use for genes that are targets of testosterone action.
Testosterone increases the rate of DHEA use. (Males produce more
testosterone, therefore, in males, testosterone-target-tissues are
larger, e.g., muscle, bone, etc., or grow at different rates, producing
different structures from the same beginning tissues, e.g., genitalia,
or differences in final brain function, e.g. male-female differences in
the brain. Testosterone is not the male hormone, males simply produce

That testosterone affects levels of DHEA is supported by reductions of
DHEA during increased levels of testosterone in some nonhuman primates.
The following references support a pattern of decline of DHEA levels
when testosterone levels increase. In the crab-eating monkey, “DHA
[DHEA] levels were high during the first months, decreased at about 1
year, remained stable during infancy and prepuberty and then declined
again during puberty. At about 5 years, the values were 28% of those in
neonates.” (Meusy-Dessolle & Dang, 1985). “By contrast the serum
prolactin and dehydroepiandrosterone levels showed an inverse pattern
achieving their highest levels in spring, during the period of reduced
testicular function.” (Wickings & Nieschlag, 1980). “Serum testosterone
levels rose during male development; however, there was a progressive
decrease in dehydroepiandrosterone sulfate levels indicating the
absence of adrenarche.” (Crawford et al., 1997). The decline in DHEA
when testosterone is increased in these examples could indicate that
DHEA is being utilized in tissues, therefore reducing measurable levels
in blood.

In the Australopithecines, as in the primates above, a limited amount
of DHEA was directed toward one tissue at the expense of another. As
testosterone increased in Australopithecus, the brain increased use of
DHEA. When testosterone increased use of DHEA for the brain, the
available DHEA for growth and development of canine teeth was reduced.
(The brain may be the paramount tissue in vertebrate evolution because
it is able to capture DHEA better than other tissues.) The brain
increased slightly and the canines decreased slightly. Brain tissue
simply takes more of the supply of DHEA; canines do not grow as large
in response. (Measurable levels of DHEA are very high in monkeys, much
lower in humans, with chimpanzees levels very similar to humans. I
suggest this is an indication of relative use of DHEA by the respective

The cold periods of the Pleistocene epoch directly caused changes in
hominid evolution. Homo and the robust Australopithecines are the
results of the first, large cold increase around 2.5 mya. A common
phenomenon occurred in both.  This particular cold selected for
individuals that produced more DHEA. Increased DHEA is an advantage
during cold. DHEA treatment in rats “affected body weight, body
composition and utilization of dietary energy by both impairing fat
synthesis and promoting fat-free tissue deposition and resting heat
production.” (Tagliaferro et al., 1986). This effect of DHEA is due to
increased thermogenesis (Bobyleva et al., 1993). Individuals who
produce more DHEA derive more heat from the same nutrition. As cold
decreased available nutrition, individuals that could derive more
benefit from sparse nutrition had a survival advantage. The ratio of
DHEA to testosterone in hominids started to change at this time.
(Increased DHEA may have been involved in early mammalian evolution.
That is, increased ability to make DHEA may have been the reason
mammals survived events that caused extinction of the dinosaurs.)

The Australopithecines remained relatively unchanged during the upper
Pliocene. The change from A. afarensis to A. africanus was probably due
to increasing testosterone. A noticeable change occurred in the
Australopithecines during the first cold of the early Pleistocene. The
robust Australopithecines appeared, i.e., robustus and boisei. Robustus
and boisei differed from afarensis and africanus mainly in teeth size
and facial size, little in body size. Pronounced sexual dimorphism
continued in the Australopithecines, including the robust types. That
is, the survival strategy of these groups continued to mainly depend on
increased testosterone in males. The levels of testosterone did not
increase much, so brain size did not increase much. The cold selected
for individuals of higher DHEA in this group. Therefore, increased
availability of DHEA increased effects on testosterone-target-tissues.
Teeth and facial structures are testosterone-target-tissues. The
available DHEA, not used in thermogenesis, caused increased size in the
teeth and facial structures. The testosterone levels of the males did
not change significantly, so their brain size did not change

Homo differs from Australopithecus mainly in a small increase in brain
size at the time of separation of the two. I suggest separation of Homo
from Australopithecus occurred as a result of increased testosterone in
Homo females. It is in Homo that the true effects of increased
testosterone began to increase rapidly. The breast would increase in
Homo and increase selection pressure for those changes that produce
more efficient bipedal locomotion. As testosterone increased in Homo
females, brain size continued to increase over that of
Australopithecus. When this increase in testosterone first began in
Homo, there should be transitional forms with larger brains, but which
continued to exhibit small bodies and sexual dimorphism, such as Homo
rudolfensis and Homo habilis. H. rudolfensis and habilis developed
contemporaneously with A. robustus and boisei.

As testosterone and DHEA increased during this time period, increases
in growth continued in the brain and began to affect growth of the
body. Homo began to increase in overall size. The effects of these two
hormones increased as the climate began to warm. (There is no selection
pressure to reduce testosterone and DHEA levels by relative warmth.)
Reduced use of DHEA for thermogenesis increased availability for body
and brain growth. Homo ergaster and H. erectus emerged at this time. It
is the increase in females of higher testosterone that produced Homo.
It is first identifiable in Homo erectus/ergaster. Sexual dimorphism
declined in Homo erectus as a result of increased female size, not a
decline in male size. This increase in testosterone in both sexes, and
the increase in DHEA, would increase bone growth and length.

Treatment of rats with DHEA increases bone mineral density. “Treatment
with DHEA caused a 4-fold stimulation of serum alkaline phosphatase, a
marker of bone formation, while the urinary excretion of
hydroxyproline, a marker of bone resorption, was decreased by DHEA
treatment.” (Martel et al., 1998). DHEA treatment of postmenopausal
women stimulates increases in serum osteocalcin, another marker of bone
formation (Labrie, 1997). Adrenarche is the beginning of the measurable
increase of DHEA in humans that begins around five- or six-years-of-age
and increases rapidly until about age twenty. Adrenarche continues for
years prior to puberty. A significant amount of bone growth occurs
prior to the growth spurt of puberty. “Premature adrenarche” produces
an acceleration of bone age that was greater in males, and the
appearance of premature pubic hair in 93.8% of both sexes (Likitmaskul
et al., 1995). The testosterone conversion product, dihydrotestosterone
(DHT), produces no qualitative differences in bone growth, only a more
rapid increase in bone growth in vitro. DHEA and DHT both
stimulated “cell proliferation and differentiated functions, but the
gonadal androgen DHT was significantly more potent than DHEA.” (Kasperk
et al., 1997). Years of bone growth due to DHEA occurs prior to
puberty; testosterone rapidly increases and finalizes body growth at
puberty during the growth spurt. Testosterone and estradiol rapidly
increase the final development of bone. A direct connection of
increased bone formation in individuals of higher testosterone exists.
Serum testosterone, estradiol and bone density are higher in black
women than white women (Perry et al., 1996). Testosterone is
significantly higher in black college students than white college
students (Ross et al., 1986). Black males and females consistently
exhibit greater mean levels of “areal and volumetric bone mineral
density” “at all skeletal sites” than Asians, Hispanics, and whites
(Bachrach et al., 1999). Increased testosterone increases bone growth.
As testosterone and DHEA increased in Homo, growth in size and length
of bones increased.

Homo erectus existed during a time of relative warmth. This climate
change means that its DHEA could be used for purposes other than
thermogenesis. The brain of H. erectus doubled that of
Australopithecus. There was less sexual dimorphism in H. erectus than
in the Australopithecines, but still more than that of later hominids.
Musculoskeletal development was very robust, another consequence of
additional DHEA for growth, not used by the brain or for thermogenesis.
The anterior teeth were larger and the molar teeth smaller than those
of Australopithecus. The decrease in posterior teeth results from an
increase in development of anterior parts of the brain. Brain forming
later, during the time of formation of posterior teeth, reduces
available DHEA for those teeth, therefore, they are smaller. Again, the
brain takes DHEA at the expense of other tissues.

The return of cold later in the Pleistocene returned selection for
increased DHEA. Neandertal habitat was characterized by relative
containment. The cold and containment increased DHEA and testosterone
in Neandertal. Neandertal continued to increase in brain size. The
teeth and facial structures and brain development of Neandertal are
exaggerated due to increased testosterone and DHEA. The large teeth and
brains indicate there was plenty of DHEA for sharing between various
tissues. However, this large brain was increased in posterior regions,
not in anterior areas. This would be consistent with early puberty.

High testosterone and high DHEA could cause early puberty. Increased
androgen receptors in the brains of individuals of higher testosterone
increase use of DHEA for brain growth during childhood. This
accelerates the onset of puberty, because the brain structures that
control puberty mature early. This shortens the time to hypothalamic
stimulation of testosterone production by the gonads. As testosterone-
target-tissues grow and begin to increase use of DHEA, competition for
available DHEA increases. Therefore, early puberty reduces available
DHEA for growth of anterior parts of the cerebrum. Large bodies and
early puberty reduce final (anterior) brain development. That is, early
puberty reduces the time of basic growth and development of the brain
that occurs under the influence of DHEA.
Effects of low testosterone on craniofacial growth and statural height
have been demonstrated in boys with delayed puberty. “These results
show that statural height and craniofacial dimensions are low in boys
with delayed puberty. Low doses of testosterone accelerate statural and
craniofacial growth, particularly in the delayed components, thus
leading towards a normalization of facial dimensions.” (Verdonck et
al., 1999). Osteoporosis in vertebrae, the diaphysis of the radius, and
neck of the femur in male leprosy patients were “significantly
correlated with [reduced] FT [free testosterone] in all three regions
of the skeleton.” (Ishikama et al., 1999). Assuming sufficient DHEA is
available, too much testosterone increases bone size and prognathism;
too little has the opposite effect.

Continued cycling of cold during the upper Pleistocene and changes in
containment areas selected for hominids with different ratios of DHEA
and testosterone. Some combination of testosterone and DHEA occurred
that favored increased use of DHEA for brain growth.  A change in the
ratio of DHEA and testosterone can slow the onset of puberty and
increase anterior brain size. Producing less DHEA reduces the effects
of testosterone. Reduced containment (testosterone) or reduced
nutrition will slow the pace of puberty. (Increased nutrition should
favor those with early puberty.) The percentage of high testosterone
individuals would decrease and average size of the forebrain would
increase. This began in H. antecessor and H. heidelbergensis. Delayed
puberty and increased brain size produced Homo sapiens. Increased brain
growth in H. sapiens occurred in the anterior portion of the brain, the
prefrontal lobes. This produces the high forehead.

Another shift downward in testosterone levels in a population could
occur rapidly. Testosterone compromises the immune system. The effects
are especially dangerous when trauma is involved. “Male gender is
associated with a dramatically increased risk of major infections
following trauma . This effect is most significant following injuries
of moderate severity and persists in all age groups.” (Offner et al.,
1999). “Castration before soft-tissue trauma and hemorrhagic shock
maintains normal immune function in male mice, but sham-castrated male
mice show significant immunodepression. The maintenance of immune
function by androgen deficiency does not seem to be related to changes
in the release of corticosterone. We conclude that male sex steroids
are involved in the immunodepression observed in after trauma-
hemorrhage. Thus, the use of testosterone-blocking agents following
trauma-hemorrhage should prevent the depression of immune functions and
decrease the susceptibility to sepsis under those conditions.”
(Wiehmann et al., 1996). These negative effects of testosterone on
immunity could increase the probability of infectious epidemics that
could radically change the percentage of individuals of higher
testosterone in a population. This is very possibly the mechanism
involved in extinctions of the robust Australopithecines and various
Homo populations.

Once a population is reduced in high testosterone individuals, a stable
population could exist for some time. However, due to the influence of
testosterone on reproduction, most populations will regain their high
levels of testosterone in time. Every positive increase in nutrition
would increase the probability of increasing the percentage of high
testosterone individuals. Therefore, a “cycling” of high testosterone
populations should occur. This may have occurred at the end of the
Upper Paleolithic, through the Neolithic, when body size in males and
females clearly declined (Frayer, 1984). A reduction in body size
indicates that individuals of high testosterone levels in the
population died. Body size then increased into the Middle Ages during
which epidemics occurred with some frequency. Increased availability of
food increases the rate of these cycles, but does not cause them.
People of high testosterone simply reproduce faster when more food is

Homo sapiens exhibit a constellation of characteristics that separate
sapiens from other hominids. Postcranial skeleton, teeth, and
craniofacial size are all reduced coincidentally with changes in brain
growth, that is, increases in size in the frontal areas. Earlier, I
suggested that canines are reduced in size in Australopithecus because
the brain is using DHEA for growth at the expense of these teeth. The
part of the brain that increased in Australopithecus reduced growth of
front teeth. These are increases mainly in the posterior parts of the
brain. Posterior growth of the brain retards growth of anterior teeth
because they occur concurrently. Many hominids exhibit increased
posterior brain size and reduced anterior teeth. The increase in brain
growth of Homo sapiens includes the posterior and the anterior parts of
the cerebrum. Therefore, in Homo sapiens, both the anterior and
posterior teeth compete for DHEA during times of brain growth.  This is
why the entire dentition is reduced in Homo sapiens.

There are two dentitions in humans. DHEA levels are very high at birth,
then decline to very low levels within a year and remain low for some
time. Around age five to six, DHEA levels increase rapidly (adrenarche)
and peak around age twenty, at levels about half as much as that of the
levels at birth. The brain is using so much DHEA for growth and
development during early childhood that measurable levels of DHEA are
very low. From age twenty, DHEA levels begin to decline, reaching very
low levels in old age. The high levels of DHEA at birth stimulate
growth of deciduous teeth. This period of high levels of DHEA declines
rapidly to very low levels in the first year. This decline of DHEA of
early childhood is so low that it does not support continued
maintenance of the deciduous teeth, and they are lost. The permanent
dentition occurs as a result of increasing DHEA beginning at
adrenarche. Adrenarche begins as the brain begins to finalize growth.
These teeth are supported until DHEA begins to decline in old age,
unless something interferes with DHEA. This explains human dentition.
This implies that teeth are very sensitive to DHEA levels. With the
simple assumption that the bone of the mandible is less sensitive to
reduced DHEA, the reduction of the size of the anterior teeth produces
the chin.


Australopithecus and Homo evolved as consequence of differential gene
regulation, in continuous, relatively comparable genomes, resulting
mainly from chronological differences in production of the androgenic
hormones, testosterone and dehydroepiandrosterone (DHEA). The cold
periods of the Pleistocene epoch selected for individuals of higher
DHEA, which interacted with levels of testosterone that varied
according to behavioral advantages. The two principal events of hominid
evolution are 1) increased testosterone in females, that stimulated
increased testosterone in males, and 2) the amplification of
testosterone-directed characteristics by increased DHEA. The effects of
these events resulted in bipedal, upright locomotion, breasts as sexual
displays, larger brains, and the effects of increased use of DHEA by
larger brains throughout the body.

Individuals who produce large amounts of testosterone are vulnerable to
infections. Moreover, high testosterone individuals may act as carriers
of infectious agents. Testosterone and puberty are directly connected
to “establishment and maintenance of the carrier state” of an
infectious virus in horses (McCollum et al., 1994; Holyoak et al.,
1993). This may have caused past epidemics, when populations were
composed of high percentages of high testosterone individuals in dense
populations. The end result would be a new population reduced in the
testosterone to DHEA ratio. This may have produced the first population
of Homo sapiens and, thereafter, periodically reduced the percentages
of individuals of high testosterone in later populations.

Increased amounts of DHEA for relatively lengthy, slower development of
the brain results in larger brains in the remaining population. These
types of events increase during times of higher population density due
to increased nutrition. This phenomenon is identifiable as the decline
in body size that occurred from the upper Paleolithic through the
Neolithic periods. That is, increased food increases reproduction rates
and concentrates high testosterone individuals into population centers.
When testosterone reaches supra-optimal levels, infection rates
increase. Body size increased in the Middle Ages, which frequently
included epidemics. Learning disabilities are “significantly
associated” with high testosterone levels (Kirkpatrick et al., 1993).
The Renaissance followed the Middle Ages. Populations will periodically
cycle through times of increased and reduced percentages of high
testosterone individuals. Civilizations evolve in this manner. I
suggest the increase in percentage of individuals of higher
testosterone produces the “secular trend,” in populations. The secular
trend is real, identifiable, and vigorous in the U.S.A., at this time
(Freedman et al., 2000).

This is a new explanation of human evolution. It accounts for all
aspects of human evolution, including the formation and declines of
Australopithecus and Homo, formation and declines of civilization, and
is identifiable in current populations.


Bachrach, L.K., Hastie, T., Wang, M.C., Narasimhan, B., & Marcus, R.
(1999). Bone mineral acquisition in healthy Asian, Hispanic, black, and
Caucasian youth: a longitudinal study. J. Clin. Endocrinol. Metab. 84,
Baulieu, E.E. (1999). Neuroactive neurosteroids: dehydroepiandrosterone
(DHEA) and DHEA sulphate. Acta. Paediatr. Suppl. 88, 78-80.
Bobyleva, V., Kneer, N., Bellei, M., & Lardy, H.A. (1993).  Concerning
the mechanism of increased thermogenesis in rats treated with
dehydroepiandrosterone. J. Bioenerg. Biomembr. 25, 313-21.
Clark, A.S. & Goldman-Rakic, P.S. (1989). Gonadal hormones influence
the emergence of cortical function in nonhuman primates. Behav.
Neurosci. 103, 1287-95.
Crawford, B.A., Harewood, W.J. & Handelsman, D.J. (1997). Growth and
hormone characteristics of pubertal development in the hamadryas
baboon. J. Med. Primatol. 26, 153-63.
Davis S.R., McCloud, P., Strauss, B.J. & Burger, H. (1995).
Testosterone enhances estradiol’s effects on postmenopausal bone
density and sexuality. Maturitas 21, 227-36.
Davis, S.R. (1998). The clinical use of androgens in female sexual
disorders. J. Sex. Marital Ther. 24, 153-63.
Frayer, D.W. (1984). Biological and cultural change in the european
late pleistocene and early holocene. In (Smith, F. H. & Spencer, F.,
Eds.) The Origins of Modern Humans. A World Survey of the Fossil
Evidence, New York, Alan R. Liss, Inc., pages 211-50.
Freedman, D.S., Khan, L.K., Serdula, M.K., Srinivasan, S.R., &
Berenson, G.S. (2000). Secular Trends in Height Among Children During 2
Decades. The Bogalusa Heart Study. Arch. Pediatr. Adolesc. Med. 154,
Gasperino, J. (1995). Androgenic regulation of bone mass in women. A
review. Clin. Orthop. 311, 278-86.
Gray, H. (1966). Anatomy of the Human Body, (Goss, C.M., Ed.).
Philadelphia, Lea & Fegiber, page 500.
	Hobson, W., Coulston, F., Faiman, C., Winter, J.S. & Reyes, F.
(1976). Reproductive endocrinology of female chimpanzees: a suitable
model of humans. J. Toxicol. Environ. Health 1, 657-68.
Holyoak, G.R., Little, T.V., McCollam, W. H., & Timoney, P.J. (1993).
Relationship between onset of puberty and establishment of persistent
infection with equine arteritis virus in the experimentally infected
colt. J. Comp. Pathol.109, 29-46.
Iguchi, T., Irisawa, S., Fukazawa, Y., Uesugi, Y. & Takasugi, N.
(1989). Morphometric analysis of the development of sexual dimorphism
of the mouse pelvis. Anat. Rec. 224, 490-4.
Ishikawa, S., Ishikawa, A., Yoh, K., Tanaka, H.. & Fujiwara, M. (1999).
Osteoporosis in male and female leprosy patients. Calcif. Tissue Int.
64, 144-7.
Kalloo N.B., Gearhart J.P., & Barrack E.R. (1993). Sexually dimorphic
expression of estrogen receptors, but not of androgen receptors in
human fetal external genitalia. J. Clin. Endocrinol. Metab. 77, 692-8.
Kaplan, H.S. & Owett, T. (1993). The female androgen deficiency
syndrome. J. Sex. Marital Ther. 19, 3-24.
Kasperk, C H., Wakley, G.K., Hierl, T., & Ziegler, R. (1997). Gonadal
and adrenal androgens are potent regulators of human bone cell
metabolism in vitro. J. Bone Miner. Res. 12, 464-71.
Kirkpatrick, S.W., Campbell, P.S., Wharry, R.E. & Robinson, S.L.
(1993). Salivary testosterone in children with and without learning
disabilities. Physiol. Behav. 53, 583-6.
Kondo, S., Hozumi, Y. & Aso, K. (1990). Organ culture of human scalp
hair follicles: effect of testosterone and oestrogen on hair growth.
Arch. Dermatol. Res. 282, 442-5.
Labrie, F., Diamond, P., Cusan, L., Gomez, J.L., Belanger, A., &
Candas, B. (1997). Effect of 12-month dehydroepiandrosterone
replacement therapy on bone, vagina, and endometrium in postmenopausal
women. J. Clin. Endocrinol. Metab. 82, 3498-505.
Lieberman, L.S. (1982). Normal and abnormal sexual dimorphic patterns
of growth and development. In (R.L. Hall, Ed.) Sexual Dimorphism in
Homo Sapiens A Question of Size, New York: Praeger, page 281.
Likitmaskul, S., Cowell, C.T., Donaghue, K., Kreutzmann, D.J., Howard,
N.J., Blades, B., & Silink, M. (1995). ‘Exaggerated adrenarche’ in
children presenting with premature adrenarche. Clin. Endocrinol. (Oxf).
42, 265-72.
Martel, C., Sourla, A., Pelletier, G., Labrie, C., Fournier, M.,
Picard, S., Li, S., Stojanovic, M., & Labrie, F. (1998). Predominant
androgenic component in the stimulatory effect of
dehydroepiandrosterone on bone mineral density in the rat. J.
Endocinol. 157, 433-42.
McCollum, W.H., Little, T.V., Timoney, P.J., & Swerczek, T.W. (1994).
Resistance of castrated male horses to attempted establishment of the
carrier state with equine arteritis virus. J. Comp.Pathol.111, 383-8.
Meusy-Dessolle, N. & Dang, D.C. (1985). Plasma concentrations of
testosterone, dihydrotestosterone, delta 4-androstenedione,
dehydroepiandrosterone and oestradiol-17 beta in the crab-eating monkey
(Macaca fascicularis) from birth to adulthood. J. Reprod. Fertil. 74,
Nadler, R.D. (1980). Reproductive physiology and behaviour of gorillas.
J. Reprod. Fertil. Suppl. 28, 79-89.
Nadler, R.D., Dahl, J.F. & Collins, D.C. (1993). Serum and urinary
concentrations of sex hormones and genital swelling during the
menstrual cycle of the gibbon. J. Endocrinol. 136, 447-55.
Nimrod, A. & Ryan, K.J. (1975). Aromatization of androgens by human
abdominal and breast fat tissue. J. Clin. Endocrinol. Metab. 40, 367-72.
Offner, P.J., Moore, E.E. & Biffl, W.L. (1999). Male gender is a risk
factor for major infections after surgery. Arch. Surg. 134, 935-8.
Ozasa, H. & Gould, K.G. (1982). Demonstration and characterization of
estrogen receptor in chimpanzee sex skin: correlation between nuclear
receptor levels and degree of swelling. Endocrinology 111, 125-31.
Perel, E., Davis, S. & Killinger, D.W. (1981). Androgen metabolism in
male and female breast tissue. Steroids 37, 345-52.
Perry, H.M., 3rd., Horowitz, M., Morley, J.E., Fleming, S., Jensen, J.,
Caccione, P., Miller, D.K., Kaiser, F.E., & Sundarum, M. (1996). Aging
and bone metabolism in African American and Caucasian women. J. Clin.
Endocrinol. Metab. 81, 1108-17.
Ross, R., Bernstein, L., Judd, H., Hanisch, R., Pike, M., & Henderson,
B. (1986). Serum testosterone levels in healthy young black and white
men. J. Natl. Cancer Inst. 76, 45-8.
Sarrel, P., Dobay B.J., & Wiita, B. (1998). Estrogen and estrogen-
androgen replacement in postmenopausal women dissatisfied with estrogen-
only therapy.  Sexual behavior and neuroendocrine responses. Reprod.
Med. 43, 847-56
Tagliaferro, A.R., Davis, J.R., Truchon, S., & Van Hamont, N. (1986).
Effects of dehydroepiandrosterone acetate on metabolism, body weight
and composition of male and female rats. J. Nutr. 116, 1977-83.
Tuiten A., Van Honk J., Koppeschaar, H., Bernaards C., & Verbaten, R.
(2000). Time course of effects of testosterone administration on sexual
arousal in women. Arch. Gen. Psychiatry 57, 149-53.
Verdonck, A. Gaethofs, M., Carels, C., & de Zegher, F. (1999). Effect
of low-dose testosterone treatment on craniofacial growth in boys with
delayed puberty. Eur. J. Orthod. 21, 137-43.
Wickings, E.J. & Nieschlag, E. (1980). Seasonality in endocrine and
exocrine testicular function of the adult rhesus monkey (Macaca
mulatta). Int. J. Androl. 3, 87-104.
Wiehmann, M.W., Zellweger, R., DeMaso, C.M., Ayala, A. & Chaudry, I.H.
(1996). Mechanism of immunosuppression in males following trauma-
hemorrhage. Critical role of testosterone. Arch. Surg. 131, 1186-91.
Wilson, M.I. (1977). A note on the external genitalia of female
squirrel monkeys (Saimiri sciureus). J. Med. Primatol. 6, 181-5.
Winter, J.S.D., Faiman, C., Hobson, W.C. & Reyes, F.I. (1980). The
endocrine basis of sexual development in the chimpanzee. In (R.V. Short
& B.J. Weir, Eds.) The Great Apes of Africa, Text-fig. 2 (testosterone,
males), page 134, Text-fig. 5 (testosterone, females), page 137, and
Text-fig. 3, page 135, (estradiol, females). J. Reprod. Fertil. Suppl.
Zingeser, M.R. & Phoenix, C.H. (1978). Metric characteristics of the
canine dental complex in prenatally androgenized female rhesus monkeys
(Macaca mulatta). Am. J. Phys. Anthropol. 49, 187-92.

James Michael Howard
Fayetteville, Arkansas, U.S.A.

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