"Mitochondrial Eve," "Y Chromosome Adam," Testosterone, and Human Evolution

James Michael Howard jmhoward at sprynet.com
Sun Aug 26 11:50:26 EST 2001


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

Abstract. I suggest primate evolution began as a consequence of increased
testosterone in males which increased aggression and sexuality, therefore,
reproduction and success.  With time, negative effects of excessive testosterone
reduced spermatogenesis and started a decline of the group.  Approximately 30-40
million years ago, the gene, DAZ (Deleted in AZoospermia) appeared on the Y
chromosome, increased spermatogenesis, and rescued the early primates from
extinction.  (Note: DAZ is considered by some to specifically, positively affect
spermatogenesis; others suggest it has no effect on spermatogenesis.)  Hominid
evolution continued with increasing testosterone.  The advent of increased
testosterone in females of Homo erectus (or Homo ergaster), increased the
female-to-male body size ratio, and eventually produced another era of excessive
testosterone.  Excessive testosterone caused a reduction in population size
(bottleneck) that produced the "Mitochondrial Eve" (ME) mechanism.  (Only certain
females continued during the bottleneck to transmit their mitochondrial DNA.)
That is, the ME mechanism culminated, again, in excessive testosterone and reduced
spermatogenesis in the hominid line.  Approximately 50,000 to 200,000 years ago, a
"doubling" of the DAZ gene occurred on the Y chromosome in hominid males which
rescued the hominid line with increased spermatogenesis in certain males.  This
produced the "Y Chromosome Adam" event.  The doubling of DAZ allowed further
increases in testosterone in hominids that resulted in the increased size and
development of the brain.  Modern humans periodically fluctuate between the
positive and negative consequences of increased levels of testosterone, currently
identifiable as the secular trend, increased infections, and reduced

"Mitochondrial Eve"

It is my hypothesis that human evolution is primarily a consequence of the effects
of androgens on gene regulation within a relatively stable genome over time
(Howard [2001a]).  That is, our evolution is an extension of ongoing mammalian
evolution (Howard [2001b]), primarily accelerated by testosterone.  Increasing
testosterone probably participated in the formation of primates, and later, the
formation of hominids.  The mechanisms, designated "Mitochondrial Eve" and "Y
Chromosome Adam," represent two aspects of changes that occurred because of
effects of testosterone on hominid reproduction.

"Mitochondrial Eve" resulted from an advantageous increase in testosterone
production by female hominids that positively affected reproduction but
subsequently resulted in decline of the population.  This event produced larger
females which increased the female-to-male ratio in hominids and produced the
large hominid, Homo erectus (or H. ergaster).  This combination of males and
females of high testosterone produced the increase in body and brain size of H.
erectus.  I suggest excessive testosterone may produce negative effects which
eventually, adversely affected reproduction of H. erectus.  As the population
declined, only certain females were able to continue reproduction.  Therefore,
only the mitochondria of this "set" of female hominids would be continued in the

The increase in testosterone of the Mitochondrial Eve (ME) mechanism produced
increased aggressiveness, advantageous to reproduction because of increased
sexuality and dominance in males and females.  This is why H. erectus was so
successful.  ME and her offspring were sexier and drove others away, thereby,
concentrating her genes.  ME is still with us; the mechanism has not changed.  In
modern humans, it produces the "secular trend," the increase in size and height
and earlier puberty currently occurring in children in the U.S.A. (Freedman et al.
[2000]).  I suggest the secular trend is actually an increase in the percentage of
people who produce increased testosterone.  Therefore, they are more aggressive
and sexual; they reproduce faster than those of lesser testosterone.

 I think Homo erectus developed because of increased sexuality in both males and
females. It is my suggestion that populations that include females that exhibit
increased sexuality also have an advantage in reproduction in free-living
primates. This exact situation has been identified in free-living Bonobos.  

 "Differences in social relationships among community members are often explained
by differences in genetic relationships. The current techniques of DNA analysis
allow explicit testing of such a hypothesis. Here, we have analyzed the genetic
relationships for a community of wild Bonobos (Pan paniscus) using nuclear and
mitochondrial DNA markers extracted from faecal samples. Bonobos show an
opportunistic and promiscuous mating behaviour, even with mates from outside the
community. Nonetheless, we find that most infants were sired by resident males and
that two dominant males together attained the highest paternity success.
Intriguingly, the latter males are the sons of high-ranking females, suggesting an
important influence of mothers on the paternity success of their sons." (Gerloff
et al [1999])

"Y Chromosome Adam"

The ME mechanism should occur most rapidly in the most propitious circumstances,
that is, favorable "feed and breed" areas.  This would keep the group together
sufficiently long to produce the ME mechanism and increase testosterone.
Increased aggression occurs coincidentally with increased sexuality, therefore,
high testosterone males and females should concentrate within an area, with lesser
testosterone types at the periphery and beyond.  This is very beneficial for this
type of breeding colony.  However, this situation ultimately produces problems for
hominids.  Excessive testosterone will ultimately produce consequences which
reduce fertility.  The population can expand only so much before negative effects
of testosterone begin to accrue.

Among a number of negative effects of excessive testosterone, reduced immune
response and reduced fertility produce the most adverse effects.  In mammalian
animal models, testosterone reduces resistance to viruses (Holyoak et al. [1993];
McCollum et al. [1994]), bacteria (Yamamoto et al. [1991]), and lowers immune
function following soft-tissue trauma and hemorrhagic shock (Wichmann et al.
[1996]).  Too much testosterone increases the probability of infection.  This
would be especially detrimental to a group of hominids engaged in periodic

Too much testosterone may reduce spermatogenesis.  Testosterone is currently being
considered as a male contraceptive.  Increasing testosterone adversely affects
spermatogenesis in men (Zhengwei et al. [1998]; Ge et al. [1999]).  I suggest
natural, gradual increases in testosterone within a population may gradually
reduce spermatogenesis sufficiently to reduce overall fertility in a hominid

Therefore, increases in the percentage of individuals of higher testosterone may
produce declines in a population because of increasing infections in males and
females and reduced spermatogenesis in males.  Young, aggressive males might not
live to reproduce coincidentally with declines in dominant male reproduction.
This situation could significantly reduce the life span of a population, perhaps
to extinction.

The gene DAZ (Deleted in AZoospermia) is necessary/beneficial for spermatogenesis
(Thielemans et al. [1998]). Since increasing testosterone may have participated in
the formation of original primates, excessive testosterone may have participated
in their potential decline.  DAZ first arose approximately 30-40 million years ago
at the approximate time of the beginning of primates (Xu et al [2001]).  DAZ may
have improved spermatogenesis enough that reproduction increased sufficiently to
overcome the negative effects of testosterone in early primates.

The same mechanism that started, then reduced, then rescued the early primates may
have repeated itself in the evolution of hominids.  Approximately 143,000 years
ago, these groups may have been reaching their viable limits due to excessive
testosterone.  I suggest "a" group, or a very limited number of very similar,
related groups (Mitochondrial Eve), was again altered by DAZ mutations which
affected spermatogenesis sufficiently to continue hominid evolution.  This is
supported.  Approximately 55,000 to 200,000 years ago, DAZ doubled on the Y
chromosome (Agulnik et al. [1998]).  The "Y Chromosome Adam" is dated
approximately to 59,000 years ago.  This doubling of DAZ may have increased
spermatogenesis a second time and allowed hominid survival.  

Homo erectus migrated to various parts of the world but did not survive.  Homo
neandertalensis did not survive.  Both groups survived for lengthy periods in
their environments.  The doubling of the DAZ is thought to have occurred only in
Africa (Agulnik ibid.). Only hominid groups in which the doubling of DAZ occurred
may have survived the negative effects of too much testosterone.


"Mitochondrial Eve" and "Y Chromosome Adam" may represent mechanisms directly tied
to levels of testosterone in hominids.  I suggest ME was the result of the
increase of testosterone in female hominids which increased the ratio of
female-to-male size in Homo erectus.  This increase in testosterone became
excessive and caused negative effects on the fertility of the group, especially
male fertility.  The remaining females of this group are the source of surviving
mitochondria.  DAZ is tied to male fertility; some suggest DAZ positively affects
spermatogenesis.  The mutation of DAZ, which doubled the gene on the Y chromosome,
may have rescued the surviving hominids from decreased fertility.  Hominids
carrying the double DAZ increased brain size as a result of the effects of their
increased testosterone on brain growth and development.

It is my hypothesis that human evolution is driven by increases in testosterone.
Since the mechanism is simply based on the increase in individuals of higher
testosterone, I suggest it occurs today.  The secular trend is its current signal;
it is real and vigorous in the U.S.A. (see Freedman).  We are also seeing an
increase in infections and a decline in spermatogenesis in the U.S.A.  


Agulnik, A.I., A. Zharkikh, H. Boettger-Tong, T. Bourgeron, K. McElreavey, and
C.E. Bishop [1998], Evolution of the DAZ Gene Family Suggests that Y-linked DAZ
Plays Little, or a Limited, Role in Spermatogenesis but Underlines a Recent
African Origin for Human Populations. Hum Mol Genet 7: 1371-7.

Freedman, D.S., L.K. Khan, M.K. Serdula, S.R. Srinivasan, G.S. Berenson [2000],
Secular Trends in Height Among Children During 2 Decades. Arch Pediatr Adolesc Med
154: 155-161.

Ge, Y.F., Y.F. Huang, G.Y. Zhang, X.H. Wang, and J.P. Xu JP [1999], Studies on
Apoptosis of Spermatogenic Cells in Normal Fertile Men Treated with
Supraphysiological Doses of Testosterone Undecanoate. Asian J Androl 1: 155-8.

Gerloff, U., B. Hartung, B. Fruth, G. Hohmann, and D.Tautz [1999] Intracommunity
Relationships, Dispersal Pattern and Paternity Success in a Wild Living Community
of Bonobos (Pan paniscus) Determined from DNA Analysis of Faecal Samples. Proc R
Soc Lond B Biol Sci 266: 1189-95.

Holyoak, G.R., T.V. Little, W.H. McCollam, and P.J. Timoney [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.

Howard, J. [2001a], Androgens in Human Evolution A New Explanation of Human
Evolution. Riv Biol 94: 305-322 (In Press).

Howard, J. [2001b], Hormones in Mammalian Evolution. Riv Biol 94: 177-83.

McCollum, W.H., T.V. Little, P.J. Timoney, and T.W. Swerczek [1994], Resistance of
Castrated Male Horses to Attempted Establishment of the Carrier State with Equine
Arteritis Virus. J Comp Pathol 111: 383-8.

Nagin, D.S. and R.E. Tremblay [2001], Parental and Early Childhood Predictors of
Persistent Physical Aggression in Boys from Kindergarten to High School. Arch Gen
Psychiatry 58: 389-94.

Thielemans, B.F., C. Spiessens, T. D'Hooghe, D. Vanderschueren , and E. Legius
[1998], 25  Genetic Abnormalities and Male Infertility. A Comprehensive Review.
Eur J Obstet Gynecol Reprod Biol 81: 217-25.

Wichmann, M.W., R. Zellweger, C.M. DeMaso, A. Ayala, and L.H. Chaudry [1996],
Mechanism of Immunosuppression in Males Following Trauma-hemorrhage. Critical Role
of Testosterone. Arch Surg 131: 1186-91.

Xu, E.Y., F.L. Moore, and R.A. Pera [2001] A Gene Family Required for Human Germ
Cell Development Evolved from an Ancient Meiotic Gene Conserved in Metazoans. Proc
Natl Acad Sci U S A 98: 7414-9

Yamamoto, Y., H. Saito, T. Setogawa, and H. Tomioka H [1991], Sex Differences in
Host Resistance to Mycobacterium marinum Infection in Mice. Infect Immun 59:

Zhengwei, Y., N.G. Wreford, P. Royce, D.M. de Kretser, and R.I. McLachlan [1998]
Stereological Evaluation of Human Spermatogenesis after Suppression by
Testosterone Treatment: Heterogeneous Pattern of Spermatogenic Impairment. J Clin
Endocrinol Metab 83: 1284-91.

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