Hermaphroditism as a starting state for humans

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About 95% of the known species are sexual.  The other 5% reproduce without sex. Sexual reproduction is biologically advantageous because it introduces a greater diversity of the gene pool, a faster rate of evolution and consequently of adaptiveness of life forms.  However,  these advantages of sexual reproduction can be offset by the simplicity of asexual reproduction, in a minority of species,  especially when the reproductive mechanism and cycle are very rapid.  Among sexual species,  a minority are hermaphroditic and a majority are segregated into males and females.  There are several degress of hermaphroditism.   Full fledged hermaphrodites among some animal species can be equipped with both the male-type and female-type of sexual organ,  and each can mate with any other member of its species.   This form of sexuality is more common among mollusks.   Other “virtual” hermaphrodites let the environment decide which sex they will  “consolidate”.   Many reptiles and some amphibians lack sex chromosomes, relying instead on the temperature of incubation to determine sex.  In the leopard gecko (Eublepharis macularius), an incubation temperature of 26 degrees (centigrade) produces all females, whereas 32.5 degrees results in mostly males.  Alligators and sea turtles also develop fully sexualized body-types as a function of ambient temperature.    Certain worms consolidate their sexual option as a function of population density.  One species of sea worm has its sex determined as a function of whether the free-moving egg makes contact with an adult female or not.  If it does,  it becomes male !   I find that the most telling story of animal hermaphroditism is to be found in a species of fish which lives in the Pacific coral reefs.  These fish live in a harem of several females with one male which heavily dominates them.  When he dies,  the most dominant female of the group soon turns into a male and replaces him. 

In fact, in several respects it is the hermaphrodite (part male - part female) rather than the female which ought to be considered the basic prototype of the human species.  Take the reproductive organs for example.  Whether we are conceived a genetic female or a genetic male,  each zygote actually develops rudimentary gonads of each sex: Wolff's canal for males and Müller's canal for females.  It is only later that one of the two will actually shrink and rapidly disappear.  There is another trait which argues for hermaphroditism as the basic prototype of our species.  It is not only normal men who produce the male hormone testosterone.  Normal women do too.  Men do so primarily with their sex organs (testicles) and secondarily with another endocrine gland called the adrenal gland, an endocrine gland which sits on the kidneys. Endocrine glands secrete hormones into the blood stream. Women also produce a bit of testosterone with their sex-gland (the ovary) but they do so more with their adrenal gland (like men).  This testosterone secreted by a pregnant woman reaches her fetus and slightly masculinizes it.   However, when this adrenal gland is overproductive in a pregnant woman, as in Cushing's disease,  even a genetically female fetus can be made to look relatively masculine -by her own mother !   There is a third argument for hermaphroditism as the basic starting condition for humans:  sex-specific (steroid) hormones are all synthesized, whether they are male or female,  from a common source, namely cholesterol.   The development of full femininity or full masculinity depend on both female and male hormones.    For example,  the structure and function of the erogenous zones of a woman’s body depend on male hormones (androgens):  in the condition known as Androgen Insensitivity Syndrome  (Testicular feminisation) there is an absence or greatly reduced  receptor for androgens in androgen- dependent tissues , these thus  hardly develop.  The clitoris being such a tissue, it is atrophic (abnormally small)  and said to be erotically insensitive.  The nipples are also of the "immature" type  and pale in colour.

Even the Y chromosome is not entirely devoted to controlling the development of the zygote's gender.  Geneticists have actually pinned down the gender-determining action of the Y chromosome to a single gene,  located on the long arm,  called testis-determining gene or SrY (for sex reversal).  This gene expresses itself at a specific moment (between 6 and 8 weeks post-conception) and in a specific place,  the genital ridge.  This minor effect starts a cascade which will gradually put in place all of the basic sex-specific traits,  including synthesis of a müllerian-inhibiting hormone which  is specialized in “getting rid” of the female reproductive organ of the fetus,  Müller’s canal !  Think of it. A single microscopic gene is responsible for whether you are to become a man or a woman ! The rest of the Y chromosome serves more general functions like triggering the synthesis of molecules by various tissues of the body. Very few of these functions are known and they do not seem to be vital.  Indeed,  life is compatible with presence of a single X chromosome (without the Y),  but not with presence of a single Y chromosome (without the X).  So in fact, maleness and femaleness are the outcome of a near-fortuitous early bifurcation engendering a very complex and prolonged cascade of events,  including cultural-biological interactions occurring bi-directionally.   Well actually,  I have over enthusiastically simplified what is known of genetic determination of gender.   Apparently,  there are other determinants very early on in the genetic causal chain.   Firstly,  certain men have no SrY gene and certain women (very few) do have one.   Molecular biologists are therefore now on the lookout for an autosomal (chromosomes 8, 9, 10, 11 and 17 are hot candidates) or X locus gene (the 21rst locus of the short arm is a hot candidate),  prenamed testis determining autosomal (TDA) and testis determining X-linked (TDX), which would also function like the SrY gene.  And several teams have been searching for a gene prenamed Z  which would be inhibited by SrY and which would otherwise command a female phenotype.   What has just recently been found,  by an Italian research team in 1997,  is a femininity gene named DSS (dosage sensitive sex reversal),  located on the X chromosome. This gene programs the development of the ovaries and,  analogously to its counterpart SrY,  “gets rid” of the male reproductive organ,  Wolff’s canal.    However,  when DSS confronts SrY,  SrY wins,  and inactivates DSS.   The SrY is dominant. Another team led by a researcher named Vainio has just recently discovered another such gene, Wnt-4.  This gene also specifically signals the embryos to become female.