There’s about a three-month lag from the time these pieces are written until they post. It is January 16, 2009, today and Simon Baron-Cohen is releasing another study emphasizing that high mother uterine testosterone levels influence the likelihood of autism in her children.

I’m starting to see pieces on the web suggesting that lowering a mother’s testosterone levels might mitigate the chances of autism. A piece by Baron-Cohen suggested that it would be a very bad idea to approach autism as a disease that can be prevented via foeticide. (See Autism Is Not Cancer)
I’ve outlined in essays on this website a number of different ways that testosterone is managed or manipulated by the various circumstances in our life. In 1998, I noted the connection between a mother’s uterine testosterone levels and conditions informed by maturational delay and acceleration that included autism. Then, as now, I maintain a respect and reverence for the humans that experience the world through this condition.

“The fundamental pattern of the brain thus appears to be asymmetrical, with the same pattern of asymmetries found in most adults. There are, however, influences in pregnancy that tend to diminish the extent of left-sided predominance, at least in the regions involved in handedness and language, and thus secondarily to result in larger regions on the right side. As noted earlier, our hypothesis is that some factor related to male sex, perhaps testosterone or some closely related factor, is the most likely candidate. The net effect of these intrauterine influences is to produce a shift from left predominance to symmetry, and in a smaller number of cases to modest right predominance.” (Geschwind & Galaburda 1987: 46, Cerebral Lateralization)
A discussion has not yet begun that addresses how life style changes influence hormone levels that may influence autism. I’m feeling more than a little uncomfortable with the notion that women will seek either to lower testosterone rates or abort potential autistic children. I would expect that the neurodiversity movement will violently oppose foeticide and hormone manipulation interventions. I foresee major struggles regarding these issues.

“To determine whether ethanol per se affects testosterone metabolism, alcohol was administered to normal male volunteers for periods up to four weeks, resulting in an initial dampening of the episodic bursts of testosterone secretion followed by decreases in both the mean plasma concentration and the production rate of testosterone. The volunteers received adequate nutrition and none lost weight during the study, which tended to exclude a nutritional disturbance as the cause of the decreased testosterone levels. The changes in plasma luteinizing hormone suggested both a central (hypothalamus-pituitary) and gonadal effect of alcohol. In addition, alcohol consumption increased the metabolic clearance rate of testosterone in most subjects studied, probably owing to the combined effects of a decreased plasma binding capacity for the androgen and increased hepatic testosterone A-ring reductase activity. These results indicate that alcohol markedly affects testosterone metabolism independently of cirrhosis or nutritional factors.” (Gordon, G. G., Altman, K., Southren, A. L., Rubin, E. and Lieber, C. S. (1976) Effect of alcohol (ethanol) administration on sex-hormone metabolism in normal men. N Engl J Med 295 (15): 793)

I’ve hypothesized that diet, touch and rhythm are the foundation of what is required for a child born of a mother with high testosterone levels. I estimate that the classic pre-agricultural Neolithic diet is right for the male maturational delayed, female maturational accelerated body. Constant touch keeps these unique children in constant contact. Rhythm is the lifeblood of these pattern-compulsive personalities. The rhythm ties them to the others that are engaged in the rhythms in their lives.

The idea is not to make the autistic child normal. We can seek to make it possible for the autistic child to become what they are naturally inclined to be. The evolutionary theory that this website promotes has its foundation in an understanding that the autistic are emerging in a society behaving in deeply inappropriate ways for autistic health. Our society is changing. It is my belief that it is changing in the direction of becoming a healthier environment for the autistic and the rest of us. Still, it is necessary to understand the context of autism, the ways that humans have evolved, to understand the ways the world would best nourish the autistic. The rest of us may profit handsomely from these insights. Understanding health for an autistic child is to understand foundations for human health.

“Theoretical speculation in humans (S. F Witelson, Psychoneuroendocrinology 16 (1991) 131-153) and empirical findings in animals (R. H. Fitch, P. E. Cowell, L. M. Schrott, V. H. Denenberg, Int. J. Dev. Neurosci. 9 (1991) 35-38) suggest that testosterone (T) may play a significant role in the development of the corpus callosum (CC). However, there are currently no empirical studies directly relating T concentrations to callosal morphology in humans. The purpose of the present study was to investigate the relationship between free T concentrations as determined by radioimmunoassay, and the mid-sagittal area of the corpus callosum, as determined by magnetic resonance imaging (MRI). Subjects were 68 young adult (20-35 years), neurologically normal, right-handed males. All subjects underwent MRI and provided two samples of saliva for radioimmunoassay of T and cortisol. Anatomical regions of interest included total brain volume, left and right hemisphere volume and regional areas of the CC. CC regions were defined using two different measurement techniques, each dividing the CC into six sub-sections. Anatomical measurements were performed blind with respect to the hormone levels of subjects. A significant positive correlation between T concentration and cross-sectional area of the posterior body of the CC was found. This finding was consistent across the two measurement techniques and was not attributable to individual differences in total brain volume. All correlations between cortisol and CC sub-regions were non-significant. The results of this study are consistent with the notion that T, at an earlier stage in development, may play a significant role in modulating cortical/callosal architecture in humans.” (Moffat, S. D, Hampson, E., Wickett, J. C., Vernon, P. A., Lee, D. H. (1997) Testosterone is correlated with regional morphology of the human corpus callosum. Brain Res 767 (2):297)

There is a canary in this coal mine, a signal to society as we navigate the passageways of society’s Vast Depression and the toppling of our hierarchical conventions. That singing bird is our autistic. Understanding autism, we understand ourselves. Not only are we notified of dangerous paths by those environments deleterious to our autistic, but maybe we can allow ourselves to be guided forward by what we learn about ourselves learning about our autistic.

As Baron-Cohen noted, autism is not a cancer. Autism is not a disease. Autism is quite possibly an integral part of human illumination. Understanding our origins, we understand ourselves. In autism is an understanding of how we came to be.

Information coming out today that I haven’t seen before include articles mentioning higher rates of autism in other countries among immigrants. The Huffington Post noted, “Higher than normal autism rates among children of immigrants have also been reported in Ireland, the UK and several cities in North America, especially Montreal.”

One article notes a Swedish study concluding autism is higher among Somali immigrants in Sweden.

I see no articles that mention my posted pieces on the subject, or the work of Norman Geschwind that inspired my hypothesis.

It appeared that hidden beneath the just-so story was a theory, which, if brought to light, could help make useful predictions and illuminate unrecognized relationships. From the beginning, the theory drew information from three different disciplines: anthropology, evolutionary biology and neuropsychology; yet, because these three disciplines did not share a common language, it became my goal to show that they were indeed studying an identical process. Evolutionary biology’s heterochronic theory explored the long-term effects of changing maturation rates, while anthropological explorations of human social structure examined the repercussions that one or more generation’s mate choice has on society. Researchers in the field of neuropsychology largely neglected to acknowledge the evolutionary implications of their discoveries, which could elucidate the parallels between the environment’s influence on uterine hormone levels and the distribution of handedness across a society. It became clear to me that all three subdisciplines were describing the dynamic of sexual selection and how sexual selection’s influence on maturation rates impacts human evolution. There seemed limited opportunities for the practitioners of each discipline to feel moved by potential synergies with their academic neighbors. However, in order to further understand human evolution, there seems a need to speak the basic languages of these three subdisciplines.

This work seeks to transcend the academic language barrier by emphasizing common patterns and ideas shared by all three subdisciplines.

This introduction to the Theory of Waves begins with an overview of four hypothetical, yet fundamental, social structures (two matrifocal and two patrifocal) and outlines the hormonal constellation of the individuals who comprise those four basic prototypes. There exists an elegant dynamic that compels and maintains these four balances. This dynamic, as explained below, can be maintained or propelled at three different levels of two overlapping hormonal paradigms.

Below, I discuss the impact this dynamic has on understanding ethnic variation, disease and condition etiology. For example, I reframe female infanticide as a socially engineered form of sexual selection. The hormonal constellations that arise as a result of this selection process produce a low prevalence of female breast cancer in Asian societies.

Having investigated related theories, I offer several reasons why neuropsychological studies have produced such inconsistent results. This theory, the Theory of Waves, ends by making a number of predictions that concentrate on autism. These predictions provide an opportunity for members of the academic community to prove this story wrong. It has been by matching up anomalies across disciplines and by discovering melodies using the black keys on a piano that this theory has come together.

I believe that understanding neoteny (the prolongation of ancestor infant features into the adults of descendants) is integral to understanding the process of becoming human. Central to understanding neoteny is understanding early play behavior. Experiencing this theory as it has come together over the last ten years has felt like deep play, frequently crossing the line to the reverential. Let the following concepts play across your mind like music. Email me if this theory strikes a chord with your own experiences, or if it harmonizes with your own understanding.

…

In this model, or theory, which I’ve been calling the Theory of Waves, there are eight varieties of humans, four male and four female. These eight types of humans feature specific characteristics, or tendencies. Each type of human can be influenced by other types, and each is susceptible to specific features in the environment. Environmental influences can compel the progeny of these types of humans to transform into other types of humans. These environmental influences compel evolutionary currents, which can provoke a significant transformation within a single generation. More often, however, these transformations occur over the course of centuries or longer.

Similar to Watson and Crick’s double helix, a larger body is created from an assembly of component parts. In this case, societies are made up of eight types of human beings, each of whom represents one of the eight potential combinations derived from the hormonal extremes. The hormonal extremes form a structure that serves as a template for a majority of the individuals within a society. The majority of individuals within a society will exhibit some basic features associated with these hormonal extremes, yet they will exhibit these extremes to less of a degree than the eight prototype humans.

Imagine that the eight basic artist colors (purple, red, blue, yellow, orange, green, black and white) are all being blended in specific ways to paint the character of a society. Or, consider that instead of the two planets Mars and Venus, which represent the classic male/female dichotomy, there are eight planets—four female and four male—which together comprise a pantheon of eight gods and goddesses.

Female Constellations
High testosterone, high estrogen (F TE)
High testosterone, low estrogen (F Te)
Low testosterone, high estrogen (F tE)
Low testosterone, low estrogen (F te)

Male Constellations
High testosterone, high estrogen (M TE)
High testosterone, low estrogen (M Te)
Low testosterone, high estrogen (M tE)
Low testosterone, low estrogen (M te)

As in the double helix, there are natural complementary pairings. In this framework, opposite sexes are not only drawn to each other based on sexual attraction, but they are also drawn to each other based on the attraction to their complementary opposite hormonal counterparts.

Female te/Male TE
Female tE/Male Te
Female Te/Male tE
Female TE/Male te

The complementary counterparts naturally ally themselves into patrifocal and matrifocal social structures. There exist two variations within each.

F te/M TE Conventional Patrifocal
F tE/M Te Warrior Patrifocal
F Te/M tE Contemporary Matrifocal
F TE/M te Classic Matrifocal

Conventional Patrifocal: Domineering, caring and discriminating men who choose cooperative women.

Warrior Patrifocal: Domineering men who choose cooperative, caring and discriminating women.

Contemporary Matrifocal: Commanding women who choose creative, cooperative, caring and discriminating men.

Classic Matrifocal: Commanding, caring and discriminating women who choose creative and cooperative men.

These fundamental paradigms are flexile and have an ability to transform from one societal prototype into another over time. The human hormone thresholds can vary over time and can control the speed and direction of evolution. The thresholds can be influenced at three locations within two interlocking cycles, or feedback loops, as described below.

Mother’s testosterone level > progeny maturation rate > social structure proclivity > mother’s testosterone level.

Mother’s estrogen level > progeny ability to exercise aesthetic discrimination and caring behavior > social structure proclivity > mother’s estrogen level.

The environment can intervene at any of the three levels of these two loops by influencing both maturation rates and timing (via testosterone) or by influencing the intensity of mate selection criteria (via estrogen).

Level 1: A mother’s uterine hormonal levels are impacted by environmental influences, which in turn affect the child’s maturation and development. The hormonal levels of the mother influence the overall disposition of the social structure by predisposing certain tendencies of the progeny.
Level 2: The environment, through a variety of specific hormone-influencing prompts, impacts a person in society, thereby shifting social structure proclivities.
Level 3: Shifts in social structure influence mate selection criteria, which alter evolutionary trajectories.

Changes may occur at the level of the womb, individual ontogeny and/or at the level of society. The relationship among these three environmentally susceptible locations creates an interactive system, which directs evolutionary trajectory.

…

Central to this model are the environmental impact points, which compel the transformation of a society and our species. In a woman’s womb, testosterone levels decide her children’s testosterone levels (Geschwind & Galaburda, 1987) and their maturation rates and social structure proclivity. Females (F) with high testosterone (T) give birth to high-testosterone (T) females and low-testosterone (t) males. F T = F T or M t. The reverse is true for low-testosterone females. Low-testosterone females give birth to low-testosterone females and high-testosterone males. F t = F t or M T. This is how societal prototypes are created and maintained and how the complementary opposite foundation of this thesis emerges.

This may be feeling rather dense. Bear with me. I will define some terms.

“Neoteny” refers to the prolonging of infant features over many generations so that eventually they appear in the adults of the descendants. For example, chimpanzee-like progenitor features, such as having a large head relative to body size, small chin, large eyes, upward stature, curiosity and affection, are all characteristics that over time manifest in the physiology and psychology of adults. Acceleration reverses the evolutionary trajectory, whereby processes featured by ancestor adults condense or withdraw over time and appear earlier in development in the characteristics of children as well as in the infants of future descendants.

Heterochronic dynamics (Gould, 1977) of evolution (i.e., neoteny and acceleration) are embedded in social structure and lead to the very specific mating of neotenous males with accelerated females in matrifocal social structures and accelerated males marrying neotenous females in patrifocal social structures. There is a direct connection between womb conditions, maturation rate directions (neoteny and acceleration) and social structure.

The net result is that not only are males and females mating with their hormonal complementary opposites, but also that societies are evolving with males and females trending evolutionarily in opposite directions by continuing selection for opposite proclivities in opposite sexes. It is conceivable that in human beings there exists a dynamic that demands eventual flipping of social structures, perhaps over periods as long as hundreds of thousands of years or as short as 6,000 years (Gimbutas, 1991). This provides an opportunity for the sexes to realign. It is also possible that this “flipping” is constantly occurring within different lineages in a society, which are taking turns performing the role of the hormonal outliers, or eight prototype humans.

Whereas the influence of a mother’s testosterone levels on her progeny has been established (Geschwind & Galaburda, 1987), this model hypothesizes that the mother’s estrogen levels influence her children via an identical dynamic, which encourages and reinforces the sexually selected focus on partner choice and discrimination, as well as caring and care giving. In this case, the estrogen levels within a woman’s womb determine her children’s estrogen levels, their tendencies toward evaluation of nuance and their compulsion to care. A female (F) with high estrogen (E) gives birth to high-estrogen females and low-estrogen (e) males. F E = F E or M e. The reverse is true for low-estrogen females. F e = F e or M E. This is how estrogen-related societal prototypes are created and maintained. This dynamic also contributes to the complementary opposite foundation of this thesis.

Whether a male or female has high or low estrogen levels does not contribute to maturation rates. This makes it possible to have high or low-estrogen males and females in any social structure. Maturation rates inform heterochronic tendencies and social structure proclivities. Nevertheless, estrogen confers discrimination, an attention to detail that can exaggerate the proclivity of a social structure. In addition, estrogen focuses on the features of a child, attracting those with high estrogen toward individuals who exhibit childlike features. Assign high estrogen to a female with high testosterone and you achieve Classic Matrifocal social structure with commanding females prone to choosing cooperative males with neotenous, or child-like, characteristics. Assign high estrogen to a male and you get either a Scandinavian Contemporary Matrifocal paradigm (Eisler, 2007) with both sexes exhibiting neoteny in a matrifocal context, or you get an Asian Conventional Patrifocal paradigm with males who are focused on mating with females displaying highly neotenous features. When pairing high estrogen with high testosterone, you get an exaggerated intensity of sexual selection, not unlike Fisher’s runaway sexual selection (Fisher, 1930), which results in a powerful focus on neoteny. F TE = Matrifocal selection for neotenous males. M TE = Patrifocal selection for neotenous females.

The particular way that testosterone and estrogen align with individuals within a society compels both social structure and particular physical features of individuals. These two hormones, which influence heterochronic trajectories, also influence personality features, disease and condition proclivities, societal characteristics and even such societal mysteries as female infanticide.

…

Another way to view this is by noting that at the extremes, a society displays the highest and lowest hormonal thresholds. These thresholds exist in those with bodies and minds most impacted by the battle between somatic function and behaviors, which are both required for survival. Those at the hormonal extremes are at the front lines of what a body can easily survive. When the environment changes, the extremes are put under more intense distress as the societal balanced polymorphism (the established balance of social structures within a society) is pushed in a specific direction. The majority of society, which exists in the center of this spectrum and which also has a heterozygote advantage (Annett, 2002), are compelled to drift left or right, matrifocal or patrifocal, over the course of several generations. Those at the margins are under the most intense duress.

Even in a society characterized by one of the four foundation social structures, one or more of the other social structures are integrally involved. Assimilated within a society are representative individuals, couples and subcultures, who act as social structure opposites to the established paradigm. In this way, these couples and subcultures also contribute to the balanced polymorphism. Though we in the West have been living in patrifocal social structures, matrifocal elements are integrated within the larger society and occupy the “left” end of the spectrum. American society displays a combination of all four social structures. Together, all four of these form a balance that is changing, particularly now.

There are a number of repercussions, or implications, of this basic model, and details are explored below. The etiologies for a number of physical and mental diseases and conditions are suggested by understanding the eight human prototypes as hormonal outliers that exist on a continuum within social structures and are held in balance so that they create a heterozygote advantage. Those whose hormonal constellations exist at the center are not burdened by hormonal extremes. The engine behind human evolution can be examined in detail so that one may offer a number of predictions. This work will concentrate on conditions characterized by maturational delay and acceleration, and it will focus particularly on autism. The reader will be able to infer by this example how the principles in this Theory of Waves can be applied to a number of diseases and conditions.

Neuroscientists will recognize at the core of this thesis a variation of the Geschwind and Galaburda (1987) hypothesis that connects hormones, handedness, lateralization and debilitations. Evolutionary developmental biologists familiar with nineteenth century principles of heterochrony (the study of the effects of changing maturation and development rates and timing) will find heterochronic processes (Gould, 1977) manifesting in neuropsychological studies of the endocrine system (specifically, testosterone and estrogen). These evolutionary biologists will also recognize how sexual hormones influence maturation rates and timing (Hall, Person & Muller, 2004). Anthropologists will be able to observe the impact of social structure—and the forms of sexual selection that drive social structure (such as female sexual selection and female infanticide)—on how societies transform and our species evolves. Studies of human social structures are integrally tied to both the evolutionary biological principle of heterochrony and neuropsychological processes driven by testosterone and estrogen.

…

For example, I’m hypothesizing that in highly patrifocal hierarchical Asian societies, originally organized in ways that demanded large-scale cooperation in order to manage irrigation works spanning for hundreds of miles, males need to be high in testosterone relative to females, while simultaneously being low testosterone relative to other males. This would be necessary in order to better facilitate cooperation within a highly combative hierarchical and patrifocal society requiring male/male collaboration. In this hypothesis, I shift down both estrogen and testosterone levels to accommodate lower testosterone levels for males in a patrifocal society with cooperative undertones. A relatively high-estrogen Asian male is suggested by the highly aesthetic and visually discriminating Asian culture. Relatively low female estrogen level is implied by ubiquitous female infanticide. To fit this model, Asian females would have to exhibit the lowest recorded female estrogen levels. This would mean the normally low Conventional Patrifocal female estrogen would have to be shifted lower in order to accommodate Asian male patrifocal cooperation. And, indeed, studies support anomalously low female Asian estrogen levels (Diamond, 1986).

Female infanticide may be integrated into an understanding of patrifocal social structure—particularly the Conventional Patrifocal social structure of hierarchical Asian social structures, which exhibit long-term stability. When the number of females in the procreation pool is reduced, far fewer males are able to have children. A heavy emphasis is placed on the ideal male, the non-ideal males procreating far less. The result is a continuing selection of highly patrifocal traits in the male population. Because of this, left spectrum and older genotype features that accompany matrifocal social structure do not easily emerge. This would include left-handedness, an attraction to innovation and spontaneous creativity. Instead, status, hierarchy and tradition would be highly valued, as is the case with traditional Asian culture. Female infanticide is a powerful sexual selection tool providing long-term stability to Conventional Patrifocal societies. Very low incidence of autism would also be expected, as I will explain shortly.

…

With individuals congregating around the eight hormonal paradigms, we’d expect that many diseases, disorders and conditions would be assigned to those located at the extremes, or outlying positions of the balanced polymorphism. For example, Asian females with very low estrogen should have low rates of breast cancer, while matrifocal societies with high estrogen should exhibit high rates of breast cancer. One would expect the same pattern with prostate cancer. We’d expect to see relatively few cases of prostate cancer in Asian patrifocal societies but high rates of prostate cancer in patrifocal societies that exhibit little cooperation. In Contemporary Matrifocal Scandinavia, one would expect very low rates of prostate cancer, yet relatively high rates of male breast cancer. Social structures compel hormonal tendencies, suggesting disease and condition etiology.

For conditions like autism, Asperger’s, stuttering and phonetic dyslexia, we’d expect to see the four matrifocal categories trending toward these conditions, with a possible emphasis on M te and F TE if Classic Matrifocal is how we primarily evolved (see below). Autism, Asperger’s, stuttering and phonetic dyslexia are often accompanied by male maturational delay, which is a marker of matrifocal societies. Matrifocal societies feature low-testosterone males and high-testosterone females.

There is the possibility that certain mental conditions will trend toward these same hormonal extremes. I would estimate that borderline personality disorder, narcissistic personality disorder and obsessive compulsive disorder, based upon their association with families exhibiting left-handers and maturational delay, will fit the same matrifocal profiles, again with a likely Classic Matrifocal emphasis.

Diseases and conditions may have multiple etiologies depending on the particular symptoms they are associated with. For example, Marian Annett and colleagues noted two types of dyslexia. She observed phonetic dyslexia trending toward the extreme left end of the balanced polymorphism and visual dyslexia trending toward the extreme right (Annett, Eglinton & Smythe, 1996).

Schizophrenia may display two radically different etiologies, which would appear in both patrifocal and matrifocal cultures. These two different etiologies would be based upon the hypothesis that hemispheric differentiation and corpus callosum size vary according to two extremes (Coger & Serafetinides, 1990). One etiology is reinforced by facility with language (Crow, 1995; Crow, Done & Sacker, 1996) and is accompanied by a surge in patrifocal social structures, while the other displays a familial and social structure identical to the familial and social structure of autism, characterized by matrifocal origins.

…

I am hypothesizing a five-step evolutionary continuum that begins with natural selection but then moves to sexual selection. In this continuum, animals focus on particular patterns when they choose a mate. Step three begins with crossing a bridge over to human sexual selection, where adept practitioners of novel pattern creation are selected as procreation partners by mates with sensitivity to these nuances (Miller, 2000). The fourth step is taken when novelty itself becomes desirable outside the partner selection process, and society is thus compelled to embrace in its productions countless nuances of the new. In the fifth stage, awareness of the creation process itself becomes a target experience.

1) natural selection
2) sexual selection (selecting for pattern when seeking a mate)
3) human sexual selection (selection for novel pattern when seeking a mate)
4) art and culture (selecting for novel pattern outside of mate selection)
5) awareness of the selection or creative process

Integrated into the sequence established above is the longer-term dynamic of humans, who evolved from random-handed non-speech users (Annett, 2002) with two equally large cerebral hemispheres and a wide corpus callosum (Witelson, 1991).

I hypothesize that step 3 of this sequence is compelled by long-term male maturational delay and reinforced by sexual selection in a matrifocal context, where child-like features attract more focus (Gould, 1977). Classic Matrifocal was likely our social structure at this stage (Knight, 1991). Stage 4 suggests a shift toward patrifocal social structure as well as a decrease in brain size (Wiercinski, 1979), culminating in the Warrior Patrifocal. This sequence suggests that Classic Matrifocal and Warrior Matrifocal preceded Contemporary Matrifocal as well as Conventional Patrifocal, with the possible emergence of Contemporary and Conventional in the last 5,000 years.

Deep societal change can occur quickly when there is a change in hormonal constellations. Sudden shifts can occur from matrifocal to patrifocal, or patrifocal to matrifocal. For example, if a matrifocal society is highly stressed over time by patrifocal incursions, the ideal male mate may shift from one displaying cooperative tendencies to a male who is quick to fight. Formerly highly valued aesthetic-oriented males may then find themselves outside the pool of highly valued potential mates. In mere generations, physiological, hormonal and neuropsychological transformations can occur.

Migrating populations exposed to changes in sunlight (Geschwind and Galburda, 1987) show radical fluctuations in social structure, which impacts evolution over time. Sunlight impacts the pineal gland, which directly influences the testosterone levels within the individuals of a population (Geschwind and Galburda, 1987). A variety of specific diseases and conditions acquired by the eight prototype hormonal outliers will emerge among these migrating peoples, including autism. In addition, changing diet can exaggerate hormonal changes.

A radical change in diet, such as an increase in high quality fats and nutrients, could raise a female’s estrogen and testosterone levels and lower a male’s testosterone levels (Ahluwalia, Jackson, Jones, Williams, Mamidanna & Rajguru, 1981). These changes in hormonal levels would compel a shift in social structure toward the direction of female choice. Females would then seek mates that were cooperators rather than warriors. Sudden dietary changes that drastically reduce access to high fat foods could compel a hormonal shift toward a patrifocal social structure. These hormonal shifts would be further accentuated if combative situations emerged. This is the variation of the Kuzawa (2007) thesis, which proposes that uterine environments can influence adult physiology. My Theory of Waves thesis suggests that the parent’s hormonal shifts can adjust a progeny’s hormonal constellations and shift a society’s hormonal spectrum in a particular direction, depending on environmental pressures. Such hormonal shifts thus result in modifications of social structure.

Eight environmental variables influence testosterone, including light (Geschwind & Galaburda, 1987), diet (Schmidt, Wijga, Von Zur Muhlen, Brabant & Wagner, 1997), body fat (Ross, Bernstein, Judd, Hanisch, Pike & Henderson, 1986; Glass, Swerdloff, Bray, Dahms & Atkinson, 1977), alcohol and drugs (Castilla-Garcia, Santolaria-Fernandez, Gonzalez-Reimers, Bastita-Lopez, Gonzalez-Garcia, Jorge-Hernandez & Hernandez-Nieto, 1987; Ahluwalia, Clark, Westney, Smith, James, & Rajguru, 1992), tobacco (MacMahon, Trichopoulos, Cole & Brown, 1982; Barrett-Connor & Khaw, 1987), touch, physical activity (MacConnie, Barkan, Lampman, Schork, & Beitins, 1986; Morville, Pesquies, Guezennec, Serrurier & Guignard, 1979) and stress (James, 1986). Estrogen has been far less studied, but diet has been repeatedly shown to dramatically influence estrogen levels (Ahluwalia, et al., 1981).

We can view evolution as both a dynamic and static process that is driven by social structure, environmental influences, maturation rate modifications and hormonal changes. The evolutionary developmental biological view, or the heterochronic perspective, offers a dynamic frame. Annett’s (2002) modern UK society is characterized by a balanced polymorphism, which exhibits an evenly balanced static spectrum view of left and right-handed individuals. On the far left side of this spectrum exist the extreme left-handed, as well as the random-handed, and on the far right side of this spectrum exist the extreme right-handed. Most people in a society exist somewhere in the middle. This spectrum of individuals is aligned along a gradated curve and offers a static snapshot of our society in the process of transition. The older anomalously dominant (both cerebral hemispheres close to the same size) matrifocal prototype is stationed at the left side and balances those with cerebral asymmetry designed for speech facility, the patrifocal prototype, on the right. Annett’s Right Shift Theory (Annett, 1985) argues that cerebral asymmetry with language proclivity offers a heterozygote advantage that allows the moderate right-handed to occupy the center of society. This Theory of Waves integrates social structure, maturation rates and a long-term evolutionary arc into Annett’s static snapshot in time.

…

Four major barriers prevent the easy appraisal of the natural hormonal levels that characterize the eight human prototypes.

Assays that fail to measure the variations of handedness with the degree of sensitivity established by Annett’s peg tests obstruct new insight and obscure potentially valuable observation. Annett’s work concluded that humans evolved as a random-handed species, which transitioned to right-handed when brains became lateralized for speech. Her peg tests measure degrees of right and random-handedness and are integral for establishing a locus related to social structure, disease/condition proclivity and maturation rate propensity. It is essential that different studies, particularly studies across cultures, compare apples to apples and use Annett’s protocols when measuring handedness.

It would be useful if Annett’s techniques were required to measure handedness around the world, quickly. Dietary changes within patrifocal societies may be skewing results dramatically. Aboriginal societies with a matrifocal foundation have almost completely disappeared. There are very few tools available to measure variations in societal balanced polymorphisms. Annett’s peg tests seem to measure the effects of testosterone and some indirect effects of estrogen fairly well.

The eight environmental variables noted above profoundly impact the hormone levels of males and females in a variety of contexts. To effectively measure the natural hormonal thresholds in ontogeny at any point, one must have an understanding of how that person’s hormonal levels are being influenced and altered by external variables. Adult hormone levels are dramatically impacted by a variety of factors. Existing studies show wild variation in results because these studies ignore influential variables. One study that measured testosterone levels neglected to take into consideration the time of day that levels were tested. In addition, the effects of stress cannot be underestimated. For example, measuring the testosterone levels of an autistic child in an institutional setting does little to provide an idea of that child’s base hormonal threshold, particularly if that child is on a standard institutional diet. Diet has been shown to have an effect on the symptoms of autism (Hjiej, Doyen, Couprie, Kaye & Contejean, 2008).

Some diseases and conditions appear at both ends of the left/right spectrum and occupy multiple poles of both matrifocal and patrifocal social structure. Annett approached dyslexia etiologies from a new perspective and established a protocol, which discovered that handedness congregated at both the extreme left and right ends of the spectrum. Diseases and conditions with more than one etiology often confound studies and frustrate attempts to discover patterns in social structure, handedness, hormonal constellations and ethnicity. It may seem that a disease such as schizophrenia, or a condition such as obsessive-compulsive disorder, does not always associate with a specific social structure or prototype predilection when more than one etiology is potentially in play.

Lastly, the season in which an individual is born affects the maturational delay and acceleration of that individual. Season of birth can thus help polarize a society’s social structure to either end of the spectrum. The effects of pineal-influenced testosterone levels may not merely be influencing those who live in migrating populations but also those who live in relative climatic extremes. When individuals within a society congregate at the hormonal extremes, vacating the balanced polymorphistic middle where those with the heterozygote advantage reside, it becomes nearly impossible to form conclusions about a society normally based on a seamless arc, or balance. In other words, climate and migration patterns influence the variables we’ve been noting.

These four conditions that inhibit high quality information regarding hormone levels—inconsistent handedness studies, untracked environmental variables, multiple pole disease/condition etiologies and season of birth effects—are primary reasons that the Geschwind/Galaburda hypothesis drew mixed support.

…

Norman Geschwind and his colleagues suggested that a number of diseases and conditions tend to align with specific handedness and cerebral lateralization tendencies. Geschwind believed that the random-handed (often left-handers) and the anomalously dominant, both of whom exhibit cerebral hemispheres near the same size, were evolutionary derivations. I agree with Annett (2002) that the random-handed and anomalously dominant are our evolutionary forebears, but I’ve added that these ancestral genotypes are matrifocal in origin.

Approaching Geschwind and Galaburda’s (1987) thesis with a heterochronic/social structure perspective gives one the ability to hypothesize the etiologies of a host of diseases and conditions as well as suggest a relationship between handedness, hormonal associations, social structure, lateralization, ethnicity and environmental variables.

These are some of the diseases and conditions noted in the literature (mostly from Geschwind and Galaburda, 1987) that offer correlations with some of the variables addressed in this model: alcoholism, Alzheimer’s disease, anxiety, asthma, ataxia telangiectasia, atopic syndrome, attention deficit disorder, attention deficit hyperactivity disorder, autism, benign intracranial hypertension, bi-polar disorder, borderline personality disorder, breast cancer, congenital adrenal hyperplasia (CAH), cluster headaches, celiac disease, conduct disorder, congenital heart disease, dementia, depression, diabetes, Down’s syndrome, dyslexia, dystrophia myotonica, endometriosis, epilepsy, gastrointestinal issues, harelip, heart disease, Huntington’s disease, immune disorders, hyperkinetic syndrome, Kartagener syndrome, Klinefelter syndrome, Klippel-Feil syndrome, lupus erythematosus, migraine headaches, mital valve prolapse, narcissistic personality disorder, obesity, obsessive compulsive disorder, oppositional defiant disorder, osteoporosis, ovarian cysts, Parkinson’s disease, phobias, pilonidal sinus, polycystic ovary syndrome, prostate cancer, schizophrenia, scoliosis, spina bifida, stuttering, temporal lobe epilepsy, thyroid disorders, torticollis, Tourette’s syndrome, Turner syndrome and twinning. Cross reference these variables with handedness, social structure, maturation rates, ethnicity, family of origin, cerebral dominance and hormonal levels. All of these conditions offer opportunities to observe the relationships of these conditions and diseases to the eight human prototypes.

…

The predictions below focus specifically on issues of relative maturation rates with an emphasis on autism and related conditions.

1) Autistic males, from families of left-handers, will have lower testosterone than the norm, and autistic females will have higher testosterone. The mothers will have high testosterone (Baron-Cohen, Lutchmaya & Knickmeyer, 2004) and quite possibly high estrogen. If we evolved primarily from high F TE, M te, then autistic males will have low estrogen, and autistic females will have high estrogen. (In any study of autism, those with familial male maturation delay tendencies, or families of left-handers, need to be evaluated separately from those possibly traumatized by an environmental effect.)

2) Larger penis and testicle size will be associated with autistic, ambidextrous males and the familial left-handed. Left-handed males and autistics will produce more sperm. (This is based on the large testicle matrifocal bonobo sexual egalitarian paradigm vs. the small testicles patrifocal gorilla harem paradigm.) If larger testicles and increased sperm production are associated with low-testosterone, promiscuous social-structure males, then the two variables will be related in the sense that higher-testosterone males will have smaller testicles or lower sperm production.

3) Autistic males will exhibit more neotenous characteristics, while autistic females should show less neoteny than their contemporaries.

4) The children of parents of widely different ethnicities, separated by tens of thousands of years from common ancestry, will reveal characteristics of their last common progenitor and increased incidence of autism and left-handedness. (Maturational delay progenitor feature emergences will be far more common in matrifocal social structure families.)

5) Neoteny has dental correlations, with smaller teeth being characteristic of the neotenous smaller jaw. Learning that teeth have grown smaller over millions of years, researchers will find that they have actually grown larger in males over the last few tens of thousands of years as patrifocal social structure has taken hold. Ontologically, the teeth of males from older mothers should be smaller than the teeth of males of first-born, young mothers. The reverse should be true for females. In a large family, the male’s teeth will erupt later and later, the female’s earlier and earlier.

6) Because a mother’s testosterone level rises with her age and because she has children across the whole arc of her reproductive years, we might observe a display of personality and physiological features in her children that would roughly reproduce human evolution over a span of eons. An older mother should more frequently have male children with maturational delay, female children with accelerated maturation and increased prevalence of autism in both sexes. Autistic children born to young mothers will more likely come with less frequency from families of left-handers, trauma being a likely cause.

7) Obese mothers (overweight women exhibit increased testosterone and estrogen levels), particularly those who are older, should show high incidence of autism in their children, particularly in migrating populations moving from equatorial regions to northern climates. Equatorial peoples transplanted to northern climates will display higher percentages of maturational-delayed male children, and maturational-accelerated females, including autistics, with the births congregating in certain seasons.

8) If the low-testosterone males and high-testosterone females are late born, and high-testosterone males and low-testosterone females are the oldest children in a family or the first born, then first-borns will mate with first-borns and late-borns will mate with late-borns a higher percentage of the time than would occur by chance.

9) Hypothesizing that social structure has political correlates, it would be likely that in a politically conservative family, if liberals were to emerge, it would be among the youngest sons and daughters. One would also expect a higher incidence of divorce or serial monogamy with youngest children (reflecting matrifocal values).

10) Conditions that display maturational delay, such as autism, Asperger’s and stuttering, will appear more often in males with longer limbs and smaller teeth than in others in their family of origin. This would suggest that the youngest males would also be the tallest. (Longer limbs and smaller teeth are neotenous features.)

11) Eating healthfully (the caveman diet) brings puberty later and provides a longer time for the brain to grow. Putting autistic children on such a late-puberty-enhancing diet may enhance their ability to connect. When puberty or progenesis in humans is dropped to a younger age by several years, it has neurological and cognitive repercussions. In addition to a possible increase in depression and bi-polar disorder, there is the potential for a general curtailment of the final stages of cognitive development.

12) Societal periods of innovation will be preceded by periods of romance, revealing changes in the selection criteria by which females pick their mates or by a widening of the selection criteria for the ideal male. Shifts toward increases in the variety of acceptable features in the procreation population will result in increases in cultural and technical variation. For example, if female infanticide is a tool used for patrifocal cultural stability, decreases in female infanticide over time within a culture will correlate with increases in societal and economic variation. These changes will result in matrifocal societal surges, increases in left-handedness and increases in autism.

13) If rhythm and dance were the aesthetics driving human evolution through rituals of sexual selection, then the sound and feeling of nonstop rhythm may be necessary to encourage the development of an autistic child. Rhythmic environmental triggers may be essential to the healthy growth of maturational-delayed children. By implication, comparing congenitally deaf left and right-handers may reveal an unusually high number of autistics in the left-handed group.

…

I am hypothesizing that evolution is driven by this hormonal ebbing and flowing, or waxing and waning. Mother’s testosterone levels > progeny maturation rate > social structure proclivity > evolutionary trajectory. Mother’s estrogen levels > progeny ability to exercise aesthetic discrimination and caring behavior > social structure proclivity > evolutionary trajectory. These two currents are inextricably intertwined, yet they follow established patterns, not unlike the double helix. Changes in hormone levels, influenced by the environment, impact ontogeny while we are in the womb, when we are children and after we’ve become grown-ups.

I call this the Theory of Waves to suggest the surge of features that travel ontogenetically back and forth from conception to adulthood and adulthood to conception over generations, with the direction of features often opposite between the sexes. Darwin proposed three different theories of evolution. This model in some ways integrates his three models (natural selection, sexual selection and Lamarckian selection, or pangenesis) and seeks to show patterns common to evolutionary biology (heterochronic theory), anthropology (social structure) and neuropsychology (sexual hormone endocrinology and Annett’s balanced polymorphism), all three of which describe ways that human beings may have evolved and may still be evolving.

Clearly, an adjustment (Matsuda, 1987) of Watson and Crick’s (1953) Central Dogma is occurring in several places in this thesis. Let me urge the reader to approach this work playfully while still rummaging for something useful in these conjectures. Most of all, perhaps, this thesis is suggesting that neoteny is central to being human. I believe that by playing with evolution we may discover who we are.

References:

Annett, M. (1985). Left, right, hand and brain: The Right Shift Theory. London: Lawrence Erlbaum.

Annett, M., Eglinton, E. & Smythe, P. (1996). Types of dyslexia and the shift to dextrality. Journal of Child Psychology and Psychiatry, and Allied Disciplines, 37(2), 167-80.

Annett, M. (2002). Handedness and brain asymmetry. New York: Taylor & Francis Inc.

Ahluwalia, B. S., Clark, J. F., Westney, L. S., Smith, D. M., James, M. & Rajguru, S. (1992) Amniotic fluid and umbilical artery levels of sex hormones and prostaglandins in human cocaine users. Reproductive Toxicology, 6(1), 57-62.

Ahluwalia, B., Jackson, M. A., Jones ,G. W., Williams, A. O., Mamidanna, S. R. & Rajguru, S. (1981). Blood hormone profiles in prostate cancer patients in high-risk and low-risk populations. Cancer, 48(10), 2267-73.

Baron-Cohen, S., Lutchmaya, S. & Knickmeyer, R. (2004). Prenatal testosterone in mind. Cambridge: The MIT Press.

Barrett-Connor, E. & Khaw, K. T. (1987) Cigarette smoking and increased endogenous estrogen levels in men. American Journal of Epidemiology, 126(2), 187-92.

Brenton, J. N., Devries, S. P., Barton, C., Minnich, H. & Sokol, D. K. (2008). Absolute pitch in a four-year-old boy with autism. Pediatric Neurology, 39(2), 137-8.

Castilla-Garcia, A., Santolaria-Fernandez, F. J., Gonzalez-Reimers, C. E., Bastita-Lopez, N., Gonzalez-Garcia, C., Jorge-Hernandez, J. A. & Hernandez-Nieto, L. (1987). Alcohol-induced hypogonadism: Reversal after ethanol withdrawal. Drug and Alcohol Dependence, 20(3), 255-60.

Coger, R. W. & Serafetinides, E. A. (1990). Schizophrenia, corpus callosum, and interhemispheric communication: A review. Psychiatry Research, 34(2), 163-84.

Crow, T. J. (1995). A Darwinian approach to the origins of psychosis. British Journal of Psychiatry, 167(1), 12-25.

Crow, T. J., Done, D. J. & Sacker, A. (1996). Cerebral lateralization is delayed in children who later develop schizophrenia. Schizophrenia Research, 22(3), 181-5.

Diamond, J. M. (1986). Variation in human testis size. Nature, 320(6062), 488-9.

Eisler, R. (2007) The Real Wealth of Nations. San Francisco: Berrett-Koehler

Fisher, R. A. (1930). The Genetical Theory of Natural Selection. Oxford: Clarendon Press.

Geschwind, N. & Galaburda, A. M. (1987). Cerebral Lateralization. Cambridge: MIT Press.

Gimbutas, M. (1991) The Civilization of the Goddess. San Francisco: Harper Collins

Glass, A. R., Swerdloff, R. S., Bray, G. A., Dahms, W. T. & Atkinson, R. L. (1977). Low serum testosterone and sex-hormone-binding globulin in massively obese men. Journal of Clinical Endocrinology and Metabolism, 45(6), 1211-19.

Gould, S. J. (1977). Ontogeny and Phylogeny. Cambridge: Belknap Press.

Hjiej, H., Doyen, C., Couprie, C., Kaye, K. & Contejean, Y. (2008). Substitutive and dietetic approaches in childhood autistic disorder: Interests and limits [French]. L’Encephale, 34(5), 496-503.

James, W. H. (1986). Hormonal control of the sex ratio. Journal of Theoretical Biology, 118(4), 427-41.

Hall, B., Pearson, R. & Muller, G. (Eds.) (2004). Environment, Development, and Evolution. Cambridge: The MIT Press.

Kuzawa, C. W. (2008). The developmental origins of adult health: Intergenerational inertia in adaptation and disease. In W. Trevathan, E. O. Smith & J. J. McKenna (Eds). Evolution and Health (325-49). Oxford: Oxford University Press.

Knight, C. (1991) Blood Relations. New Haven, CT: Yale University Press.

MacConnie, S. E., Barkan, A., Lampman, R. M., Schork, M. A. & Beitins, I. Z. (1986). Decreased hypothalamic gonadotropin-releasing hormone secretion in male marathon runners. The New England Journal of Medicine, 315(7), 411-7.

MacMahon, B., Trichopoulos, D., Cole, P. & Brown, J. (1982). Cigarette smoking and urinary estrogens. New England Journal of Medicine, 307, 1062-5.

Matsuda, R. (1987). Animal Evolution in Changing Environments, With Special Reference to Abnormal Metamorphosis. New York: Wiley Press.

Miller, G. (2000). The Mating Mind. New York: Random House.

Morville, R., Pesquies, P. C., Guezennec, C. Y., Serrurier, B. D. & Guignard, M. (1979). Plasma variations in testicular and adrenal androgens during prolonged physical exercise in man. Annales d’Endocrinlogie (Paris), 40(5), 501-10.

Ross, R., Bernstein, L., Judd, H., Hanisch, R., Pike, M., & Henderson, B. E. (1986). Serum testosterone levels in healthy young black and white men. Journal of the National Cancer Institute, 76(1), 45-8.

Schmidt, T., Wijga, A., Von Zur Muhlen, A., Brabant, G. & Wagner, T. O. F. (1997). Changes in cardiovascular risk factors and hormones during a comprehensive residential three month kriya yoga training and vetetarian nutrition. Acta Physiologica Scandinavica Supplement, 640, 158-62.

Watson, J. D. & Crick, F. (1953). Molecular structure of nucleic acids: A structure for deoxyribose nucleic acid. Nature, 171, 737-8.

Wiercinski, A. (1979). Has the brain size decreased since the upper paleolithic. Bulletins et Memoirs de la Societe d’Anthropologie de Paris, 6(6-4), 419-27.

Witelson, S. F. (1991). Neural sexual mosaicism: Sexual differentiation of the human temporo-parietal region for functional asymmetry. Psychoneuroendocrinology, 16(1-3), 131-53

…

The introduction to this piece was modified on 3/8/09

For more details regarding this theory, visit http://www.neoteny.org/?cat=28

For more details regarding this theory and autism, visit http://www.neoteny.org/?cat=29

In previous pieces, I’ve noted these effects on Jewish and American Black populations, with a skewing of populations toward the extremes of maturational delay and acceleration evidenced by a number of diseases and disorders characterized by these hormonal extremes. I would predict that both these populations would evidence higher percentages of autism and left-handedness, perhaps higher in places like Milwaukee and Minnesota than Houston and Miami. In just the way the Somalis in Minneapolis and St. Paul are exhibiting higher rates of autism, I would suggest that this Somali population would exhibit higher rates of left-handedness.

Another population influenced by these processes are the Latino immigrants from South and Central America. Studies could be conducted tracing the effects of sunlight on the pineal by noting the country of origins of Latino individuals, their proximity to the equator and how far north those individuals have traveled.

There are several issues.

First, how often do these people return to their country of origin? The more frequent their returns and the longer their stays, the less influenced they will be by the testosterone pineal effect.

Second, conceiving and bearing their children in Seattle vs. San Diego will likely influence the mother’s testosterone levels in different ways. I would predict that Seattle Latinos have higher incidence of left-handedness, autism and other symptoms related to these issues, such as allergies.

Third, there may be father effects. Recent age-of-father studies suggest older males are more likely to sire autistic children. This may be related to a father’s testosterone levels dropping with age. If the father’s testosterone levels at the time of sperm creation influence the testosterone levels and maturation rates of his children, then where the children are conceived (how far north or south) may influence the children’s maturational disposition.

Fourth, not all indigenous South and Central American populations share the same social structure tendencies. Egalitarian communities such as Mayan peoples with matrifocal tendencies exhibit male maturational delay and female maturational acceleration unlike some South American tribes with the opposite disposition. Individuals from matrifocal communities are more vulnerable to testosterone pineal effects than their patrifocal counterparts.

Fifth, if an indigenous American or Latino woman or man mates with a Black, Asian or White, the progeny may reveal features or characteristics of the last common ancestor, a not uncommon effect. This, in combination with testosterone pineal influences, may in combination further thrust children toward male maturational delay, female maturational acceleration and autism.

Sixth, it is possible that there will be multigenerational echo effects. Second-generation Latinos marrying and then conceiving children at the same time of the year as they themselves were conceived may further boost the influence of seasonal testosterone-pineal effects. Whereas the first generation may not have exhibited effects of extreme maturational delay or acceleration, a second or later generation may show those influences, particularly if other environmental testosterone-influencing variables are in play, for example, if the mother smokes.

Seventh, there are many environmental effects influencing testosterone levels in males and females. A Latino mom eating an American high-fat diet, unfamiliar to her before her migration, can dramatically increase testosterone and estrogen levels, influencing her children’s uterine environment.

In the way that we observe Blacks and Jews impacted by changes in geography, we are likely to see the same variables influencing Latino populations. The fact that there is often frequent travel back to the country of origin will mitigate the testosterone-pineal effect. Other influences noted above may exaggerate them. Just as there have been dramatic increases in allergies for Blacks and Jews, watch for such symptoms appearing in Latinos. Other maladies influenced by testosterone levels are also in play, such as prostate cancer. Autism is not the only condition influenced by testosterone levels.

These are the effects that we can observe by tracing the paths of immigrants in the Americas. What of South-to-North immigrant routines in other parts of the world? We’d hypothesize immigrants from India to the U. K. To manifest these effects, there are populations of southern peoples in Scandinavia. What have those communities been experiencing?

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.

This scheme is part of a larger picture of how humans evolve. Changing maturation rates over generations send societies in one of two directions: matrifocal or patrifocal social structures. Low testosterone males mating with high testosterone females form the foundation of matrifocal social structure. High testosterone males pairing with low testosterone females make up patrifocal social structure. When mothers today exhibit matrifocal features, high testosterone, while exposed to environmental influences that elevate their testosterone further, male children with delay tendencies may shift into extreme delay.

This theory predicts that females with autism will not exhibit maturational delay, but maturational acceleration accompanied by elevated testosterone. When a mother’s testosterone level elevates, she not only influences the maturation rates of her children, she sends them on a journey into the past. Maturation rates unfold on two scales, on the scale of the individual unfolding in a lifetime–personal ontogeny–and on the scale of how our species has evolved over the last few thousand generations. We have recently (25,000 years ago to the last couple hundred years) evolved out of matrifocal social structure to patrifocal social structure. We reverse the process by reversing our maturation rates, reproducing that path we took to arrive in the present. Elevating mother’s testosterone, we instill ancient ontogenetic pathways, propelling our children back in time to when language was still new. For males, backwards is lowered testosterone and maturational delay. For females, backwards is raised testosterone and maturational acceleration.

Light influences testosterone levels via the pineal gland, which regulates testosterone production. Testosterone fluctuations of 30% a day can be observed as thresholds follow diurnal–day & night–cycles, influenced by the availability of sunlight. What happens when a people are shifted away from consistent, daily 30% fluctuations into northern climates where the light in winter is almost nonexistent, in summer almost always there?

Jews and Blacks both display anomalous distributions of testosterone in males. Both Black and Jewish males (studies were conducted with only males) showed either very high or very low testosterone levels. Both these cultures were transplanted from equatorial regions to climates with light-fluctuating seasons.

One would predict that both these ethnicities would exhibit a higher percentage of conditions characterized by maturational delay, such as autism.

Somalis immigrating to Minnesota are discovering radical rates of autism among their children. This theory predicts that these autistic children’s birthdays should cluster in certain times of the year. If mother’s light-influenced testosterone rates are particularly high at six weeks before birth, intervention to lower rates (for example, modifying light exposure) would be prudent.

There is also the possibility that the father’s testosterone levels influence the child’s rates of maturation. There are no studies to support this possibility other than studies concluding that older parents are more likely to give birth to autistic children. (Women experience high testosterone with age, males lower testosterone.) It could be estimated at what seasons a fathers testosterone rates are lowest at conception, and compare that to when mother’s testosterone is highest six weeks before birth and look for the impacts of overlap. It may be that both mother and father are having an effect.

There are also possibilities that autumn September through October allergy seasons are influencing testosterone levels impacting embryo’s maturation rates.

Light and testosterone are related. Many things in our environment influence testosterone levels. Understanding autism involves recognizing how testosterone is influenced and realizing how this influence connects to how we evolved.

Tracing the path of societal ideas is compromised by an interpretation protocol that traces only the productions, not the origins, of the mind. We don’t think of biology or genetics as informing a discussion of the evolution of ideas. Exploring the connection between physical and mental when seeking an understanding of culture is not an intuitive choice. It has a lot to do with our not consciously knowing how we evolve biologically and societally. We are left watching the marble, guessing at what might have influenced its path.

No single variable influences our evolution more powerfully than changes in the rate and timing of maturation. Neoteny, or the prolongation of infant features into the adult of descendants by the slowing down of maturation, is the single most influential factor in our divergence from chimpanzee-like progenitors. Variations in a mother’s testosterone levels while her child is in the womb adjust maturation rates, modifying the personality, physical features, strengths and interests of her child. For example, high testosterone levels in combination with other factors can lead to autism. An extremely powerful determinant of testosterone levels is the degree and duration of exposure to light.

Daily testosterone levels are influenced by diurnal light variations. In Africa and the Middle East, equatorial light patterns throughout the year are relatively constant and do not impact daily testosterone levels to variations of more than 30%. Those variations stay within a constant yearly range.

Africans made slaves and carried to America were forced to labor in the American South, a South subject to very different light cycles than their society of origin. With early 20th century migration to Northern cities, additional latitudinal differences came into play. Light varied seasonally and testosterone levels fluctuated wildly relative to the latitude of origin.

The Jewish Diaspora drew Semitic peoples away from regions near the middle of the earth to Europe, where light varies more radically, seasonally, the farther North one goes.

The pineal gland interprets summer as daytime and winter as nighttime, based upon a multimillion-year equatorial calibration in Africa. Africans in America, as well as Semitics in Europe and now in America, find themselves exposed to radically different light levels from their societies of origin. The result is fundamental change in maturation rates in both the directions of neoteny and acceleration because mothers’ testosterone levels are moving either up or down, depending on the season. Also influenced by the season would be when the mother’s parents were born, because they would be subject to the same light impact. Over generations, if relations are born in the same season, you can get multigenerational exaggerations of the pineal-influencing testosterone effects.

In African and Jewish cultures, you get far wider variations of personality, physical features, strengths and interests than you would get in a culture not impacted in this way. I hypothesize you’d also get more cases of conditions characterized by maturational delay (autism, Asperger’s, stuttering, OCD) and maturational acceleration (aggression disorders). Jews have had a huge influence on American culture in the arts and sciences. Blacks have had a huge influence on American culture in the arts and athletics. I would suggest this influence is directly related to both cultures having origins in or near Africa, near the equator, and having moved or been forced to move away. I predict that comparisons of African Americans and equatorial Africans living in their society of origin, and American Jews compared with multigenerational Israeli Jews, will exhibit notable differences in exhibition of conditions characterized by maturational delay.

Recently it was discovered that Somalis relocating to Minnesota are having children with autism a far higher percentage of the time than is normal. The change in light is an explanation. This being the case, the birthdays of these children exhibiting autism should be congregating in certain times of the year. (For other variables that cause autism, click here, here and here.)

Tracing a moving marble through the hallways of our minds is not as easy as noting the effect of a single variable. Still, the history of culture involves a lot more than the tracing of ideas. It also requires following the bouncing ball as it travels from continent to continent, guiding us to note the influence of light. How we evolve socially and biologically is integrally tied to the ideas we have, our creative proclivities and our inhibiting conditions. Noting light’s influence on this process, we might say that no small amount of who and what we are comes from above.

“Disorders” characterized by maturational delay, such as autism and Asperger’s, are encouraged by the choices we make when we fall in love, in addition to what we expose ourselves to as we live our lives. The previous two entries outline the influence of mate selection on the origin of autism in our children. Working in cooperation with sexual selection are environmental influences that compel how children’s social and mental lives unfold.

Since the death of Darwin, little thought has been given to how the environment might influence human evolution in a single lifetime. Politics has informed what we consider to be true as Russian theorists emphasizing Lamarckian evolutionary theories (effects of the environment on single generation change) have been ignored in the West. Marx and Engels were proponents of a matrifocal origin of society, polarizing the West to emphasize a patrifocal hypothesis and ignore the power of sexual selection on societal change. Environmental and mate-selection origins of autism have been obfuscated by a science influenced by politics. Reductionist natural selection focusing on random selection supports a social Darwinist/neo-conservative perspective. A belief that society should reflect a natural world where only the strongest and cleverest should thrive supports a society where resources remain in the hands of very few.

In other words, we are not encouraged to notice how what we are exposed to and how we live our lives affect our children. This perspective is heresy, according to the fundamentalist sociobiologist and Neo-Darwinist. Those scientists would say that Lamarckianism is dead. There is no way that evolution influenced by the environment in a single generation could cause autism. Evolution occurs mostly from mutation and results of random variation! The environment cannot cause autism because evolution does not respond to the environment in one lifetime.

We are discovering that not only are our genes programmed to take into account a parent’s environment when deciding how to assign features to our kids, our genes are designed to take into consideration information from the environment when deciding how to modify themselves.

There is very little about a human that is random.

There are (at least) eight environmental variables influencing changes in our evolution by modifying testosterone levels. This modification is most obvious in the mother, where the child’s maturational speed is determined by the mother’s blood testosterone levels the sixth week before birth. (See http://serpentfd.org/3-neuropsychology.html) There are almost no studies tracking the influence on estrogen in these matters. No surprise there. There are almost no studies tracing changes in the father’s testosterone levels in a single lifetime as it relates to features in the children.

Exposure to light, changes in diet, percentage of body fat, alcohol and drugs, tobacco, amounts of touch, physical activity and stress all vary testosterone levels in humans. They do not necessarily do so in the same way. For example, increased body fat raises female testosterone levels but lowers it for males.

Increasing the testosterone levels in the mother compels an increase in maturational delay in her sons and in increase in maturational acceleration in her daughters when, at six weeks before birth, lifelong maturational trajectories are set based on mother’s testosterone levels.

Do we in our heart of hearts, in our unconscious minds, know the profound effects that we have upon our unborn children as we live our lives? Are we aware of the path we walk and what happens when we cross that line that influences our kids? Are we purposefully going about the business of creating a society populated by the male maturationally delayed: autistics, borderline autistics, artists, abstract thinkers, gifted ambidextrous athletes, dancers, musicians, gays and males inclined to competitively perform as opposed to dominate and subjugate?

By what we eat, breathe and imbibe and who we choose to mate with, are we unconsciously creating a world that is considering peace?

I often know I know something before the answer emerges. Knowing that I know, I trust that the answer will emerge, and so it does. We don’t often consider how long an insight or understanding has already been grasped before the veil lifts. I suspect hidden knowledge can stay hidden a very long time.

Hormone levels in humans fluctuate in response to a number of environmental influences. One of the most powerful and subtle is light. Cradled in equatorial Africa, our ancestors were exposed to the diurnal cycle of day and night. Human sexual hormone levels ran 24-hour cycles, as they do today, peaking and troughing at specific times in the cycle, with evenings about 30% lower than mornings.

Six weeks before a child is born, a crucial environmental trigger tells the child at what speed he or she will mature during his or her lifetime. The trigger is the amount of testosterone in the mother’s blood. High and low levels lead to very different outcomes of maturation speed. Change in the rate and timing of maturation is the single most powerful force that determines the evolution of our species.

The pineal gland can mediate testosterone levels, varying those levels according to the amount of light we are exposed to. It has been hypothesized that as light influences testosterone levels through the pineal gland, maturational trajectories vary over time.

The bun in the oven grows larger in a hormone stew. Studies conclude that the time of year a child is conceived influences the features of that child, specifically the child’s degree of maturational delay and acceleration. Autistic children’s birthdays congregate in specific seasons.

About 50,000 years ago, our ancestors departed Africa. Some anthropologists estimate they hugged the ocean and estuary shorelines, creeping or boating farther and farther from the equator. The farther from Africa’s equator that they traveled, the more light changed.

Seasonal changes in light caused radical changes in hormone levels, warping the short diurnal cycle in a second long wave pattern with overlapping variations. Children emerged with widely varying maturational speeds, creating the clay that would become the form that individuals in the culture would be molded from.

We can still see the results of equatorial societies plunged into the effects of varying light. African-Americans transplanted to the U. S. exhibit swings to the extremes of maturational delay and acceleration. We observe more autism and Asperger’s at the delay-end along with astonishing creativity around musical and physical proclivities. At the same time, faster-maturing, creative-in-a-different-way, more aggressive males congregate at the accelerated end of the spectrum. Jews run a similar pattern of maturational delay and acceleration, congregating at the maturational extremes. These two ethnic societies hold far more maturational variation than cultures that have not recently been upended. With the increased variation come gifts. And, there are the burdens imposed by a society not compelled to seek the assimilation of unconventional characteristics.

Stable cultures have a chance to adjust to the light of their location on the planet.

It is only now becoming evident that light can transform the features of our children, the characteristics of our culture and the direction that our species evolves. Perhaps, unconsciously, we’ve known this all along.