January 10, 2009 | 1 Comment
Category: Causes of Autism, Environmental Effects, Estrogen, Neoteny, Ontogeny, Sexual Selection, Sexual Selection/Social Structure, Social Structure, Society, Somali Autism & Ethnicity, Testosterone & Estrogen
Ten days ago we waded into what little information we have on estrogen to estimate if we know enough to inform an understanding on the influence of estrogen on human evolution and current societal formations. Eight days ago we came up with the following matrix of relationships…
Patri Female low T, low e Male high T, high e Asian
Patri Female low T, low e Male high T, low e
Hybrid Female low T, low e Male low T, high e Scandinavian?
Hybrid Female low T, low e Male low T, low e Scandinavian?
Patri Female low T, high e Male high T, high e
Patri Female low T, high e Male high T, low e
Hybrid Female low T, high e Male low T, high e Scandinavian?
Hybrid Female low T, high e Male low T, low e Scandinavian?
Hybrid Female high T, low e Male high T, high e
Hybrid Female high T, low e Male high T, low e
Matri Female high T, low e Male low T, high e
Matri Female high T, low e Male low T, low e
Hybrid Female high T, high e Male high T, high e
Hybrid Female high T, high e Male high T, low e
Matri Female high T, high e Male low T, high e
Matri Female high T, high e Male low T, low e African/ Polynesian
Let’s amend that chart to reveal what we’ve concluded might be useful in our ruminations of the last few days. Let’s delete, to see what happens, all pairings that are not complementary in that a female/male matching can’t have both high T, high E, low t, or low e. That would set up the following four tentative testosterone and estrogen matrix of relationships, with the addition of the classic patrifocal hormonal constellation, thresholds shifted down, to create the Asian archetype.
Patri Female low t, low e Male high T, high E Asian (shift down)
Patri Female low t, low e Male high T, high E Classic Patrifocal
Patri Female low t, high E Male high T, low e Warrior Patrifocal
Matri Female high T, low e Male low t, high E Scandinavian
Matri Female high T, high E Male low t, low e Classic Matrifocal
I don’t know if this is any more realistic than the 16-node breakdown. It seems reasonable to tentatively hypothesize that estrogen/testosterone across-sex pairings have to be opposites. If the mother’s estrogen and testosterone levels are setting her progeny’s levels, with girls opposite from boys, this would suggest the four-node solution.
The Female tE, male Te pairing seems to patrifocal society what the Scandinavian societies are to matrifocal society, an intensification of the paradigm. This seems to be the classic dominator warrior with no aesthetic sense, no caregiving tendencies and not choosey in the features that he looks for in a mate. The female seems docile, cooperative, caring and caregiving, with an aesthetic orientation. Perhaps over the course of hominid evolution all four of these polarities engage.
What are some of the implications of this paradigm?
Jared Diamond and Marvin Harris have explored hypothetical environmental influences on human social evolution. Juxtaposing those variables with the four-pole matrix proposed here may suggest specific evolutionary trajectories. Ethnic physical features may be predictable, particularly when seen against this hormonal hypothesis. Geoffrey Miller’s work focuses on the power of sexual selection or aesthetic compulsion to create features in physiology and society. Aesthetic choice in combination with hormonal constellation proclivities may go a long way toward informing an understanding of societal evolution since the African Diaspora.
What seems most powerful in the implications of this hypothesis is an enhanced understanding of diseases, disorders and conditions characterized by hormonal markers or tendencies. Studies suggest Asian women get breast cancer far less often than Westerners because they have unusually low estrogen levels, consonant with our hypothesis of the Asian shift down in hormonal thresholds to accommodate a neotenized, patrifocal society. If elevated and diminished hormone levels are markers for specific kinds of social structures, then we would expect to see specific diseases correlate with specific societies. For example, we might expect to see Scandinavian males get breast cancer more often than would be expected.
For another example, I hypothesized that equatorial peoples moving to northern climates will exhibit season-of-birth variations in testosterone levels, resulting in higher rates of autism. Recent news stories supported that prediction by calling attention to Somalis in Minnesota exhibiting exaggerated rates of autism. That would be low-testosterone males, high-testosterone females. I would predict you’d also get a higher percentage of prostate cancer when the exaggerated higher testosterone males reach adulthood, higher rates caused by those same light-influencing, pineal gland-impacting testosterone levels in the uterine environment. (See Minnesota Somali Autism: Geography and Light for an explanation of how radical changes in light compel the extremes of both male and female maturational delay and acceleration, high and low testosterone for both sexes.)
Taking things one step further, if indeed estrogen levels are set for life while a person is in the womb, then those diseases with high or low estrogen level markers may be directly related to impacts of the environment on the mother’s estrogen levels and environmental impacts later in ontogeny. (Chris Kuzawa explores how changes in the fetal environment influence adult disease.) Environmental impacts in combination with the natural high or low estrogen levels of that particular social structure constellation might lead directly to an etiological understanding for numerous diseases.
There is another implication. This work now hypothesizes that human evolution was driven by the female TE, male te constellation. That is a change from the high-testosterone female, low-testosterone male archetype this work has been presenting until the last few days. We now surmise, with the addition of estrogen, that the evolving male was low estrogen. If low-estrogen males were the prototype male during much of our evolution, and we hypothesize autistic males to feature a genotype from this period, then low e would be a feature of the autistic male. This would suggest that the autistic’s mother has elevated E in addition to T, and the elevated E is contributing to autism in contemporary society.
Ten years ago, I wrestled with an impact of estrogen on this theory as a possibility. Testosterone alone seemed not robust enough to form a theory to explain the origin of many cancers, though studies I read suggested hormone patterns. Exploring both testosterone and estrogen in combination with this modified theory of human biological and social evolution, modified to take into consideration estrogen as integral to the thesis, opens up the model to explaining far more than conditions characterized by maturational delay or acceleration.