Human evolution theory utilizing concepts of neoteny & female sexual selection
An etiology of neuropsychological disorders such as autism and dyslexia, and the origin of left handedness.
Up to this point in our exploration of the history of evolutionary theory, we have summarized the work of theorists who have contributed to a path shared by our point of view, and sought to offer representative arguments for those who would not agree with our hypothesis. In this chapter we revisit the primary composers of evolutionary theory from our four different perspectives: environmental influences, selective processes, hormonal intermediaries, and heterochronic processes; weaving the concepts covered historically in the last three chapters into these four different themes. Once these traditional concepts are remodelled and recomposed into a form we are calling shift theory, we will show their effectiveness when we address cultural and medical anomalies in sections II, III, IV and V.
In the next chapter we will examine other multi-disciplinary evolutionary theories. Then we will describe how the selective processes affecting progeny -- sexual selection, zygote selection, and uterine selection -- are spawned by the original or parental selective process of parents -- natural selection. Last we will return to Charles Darwin as a man 150 years ahead of his time with the conceptual tools but not the data or studies to bring it all together.
An important point, a subtle point, but one that needs to be said: before this theory came together in the form you will shortly visit, the concepts that the theories represent were only patterns in the mind of a theorist. A non-verbal awareness of patterns, anomalies, and relationships between anomalies accompanied by a feeling of "yes", preceded the theory forms to which you are about to be introduced. As the theories themselves began to emerge, along with them emerged an awareness that the theories themselves are not what they represent. The map is not the territory. The theories are a form of mental shorthand representing living breathing multi-leveled extremely subtle life processes unrepresentable by words. We welcome any additions, deletions, or revisions to our work that will make more useful the concepts we are trying to impart. The applications of shift theory, in the form of transitional model 1.0, is prepared for upgrades to transitional model 1.1. Contact us with anything you think or feel might fit, or any "ah ha's" you might experience. If you are interested in a list of anomalies that suggest where shift theory falls short of explaining the data, useful if you are interested in increasing the predictive power of this model, or replacing it with one more effective, E-mail us and we will tell you where that list is posted on this web site. It is our firm belief that what doesn't fit the data is a clue to where closure waits.
If asked to describe 'dance' to a deaf man, most of us would be speechless. The concept is vague without being able to imitate or describe what exactly music is. Describing environmental influences without specifying what is being influenced presents the same problems as in the metaphor we are using. The effect of light, whether it be: an experiment by Waddington on fruit fly embryos, an influence on the pineal gland of an adult human male preceding sperm creation, or response of the retinas of arctic hares beneath an ozone hole; means totally different things depending on which selective process is mediating the effect; uterine selection, zygote selection, or natural selection respectively.
Starting with Buffon (Bowler, 1984), theorists have been focussing on the environment as a source of species variation. Lamarck (Corsi, 1988) suggested that temperature had profound effects upon the transformation of species, and began to explore other variables that might generate species change. St-Hiliare rejected environmentally compelled use and disuse as the engine behind evolution, suggesting the environment could act directly upon individuals. Darwin wrote that the environment was affecting individuals though several doorways, natural selection, sexual selection and progenesis. Mivart (Gottlieb, 1992) was the first to suggest that early in ontogeny, at the embryonic stage, environmental influences might compel physiological change. Cope believed that the environment compelled variation in individuals by increasing or decreasing their rates of development. De Beer (Gottlieb, 1992) codified the variety of ways that the environment might cause an individual to vary the rate and timing of maturation and development. Gould (1977) simplified the system and made a powerful case for their evidence in humans.
Almost without exception, the theorists covered in the previous three chapters, professed a specific mechanism to describe how the environment could be compelling evolutionary change. We postulate that environmental variables influences evolution at the level of the individual at four specific intersections.
Natural selection deletes individuals unfit to survive to procreate. The clearest evidence of this is after an individual is born. His or her physiological and behavioral repertoire can be observed to fail or succeed at creating progeny. 20th century theorists have suggested that individuals may be hereditarily predisposed to register changes in the uterine environment. Uterine environmental changes reflecting extro-somatic environmental changes which result in phylotic or behavioral change that will increase the likelihood that this individual survives to adulthood. No Lamarckian implications need be assumed. Long term naturally selected trial and error at an embryonic level, with the most embryonically flexible individuals surviving, is all that is implied.
The list of environmental variables that support natural selection's primary position as a most powerful selective process is long and fascinating. The literature of the adaptive school of evolutionary theorists concludes that any feature that gives an individual a leg up in reaching procreation age and procreating is a feature worth noting. It is not the goal of this work to add to their list. We take no exception to the diligence and creativity expended exploring the repercussions of the environment on the physiology and behavior of individuals through natural selection. The perspective we are promoting in shift theory is pluralistic. It describes a synthesis of natural selection and other selective processes. For those of you for whom the elegance of the mid-century synthesis of natural selection holds a deep allure, let us say, we too find it beautiful. Consider that there might be a sister theory, not as elegant, yet useful in specific ways.
Sexual selection generally operates at the level of the adult individual as does natural selection, deleting individuals unfit (in combat) or unattractive (to potential mates) making it unlikely that they procreate. The limited environment of specific social structures within which adult individuals operate, combined with an attraction to varying idiosyncrasies creates a context for sexual selection.
Larger environmental influences can have additional effects on sexual selection. If an animal's social structure revolves around females picking males for qualities making them more likely to help with providing for the young, which could be females picking males for seemingly unrelated behavioral or physiological traits that would be consistent with this quality, then a shift in the environment such as a drop in temperature making the environment more hostile could reinforce females choosing cooperative males. The progeny of those cooperative males would be more likely survive to procreation age (Miller, 1994, 2000).
Sexual selection has been hypothesized to have helped guide early flightless bird ancestors into full fledged flyers. This selective process has been believed to be responsible for exotic bird plumage and extravagant fish tails. Frog calls have been connected to female choice. Extreme dinosaur head constructions have been hypothesized to be mating call generators. The list is just about endless. Darwin's (1871) The Descent of Man goes into fascinating detail.
The circumstance that compels species change in sexual selection, more specifically female sexual selection, is an environment which dictates that individuals make choices. Females either pick a handsome male, by the criteria in fashion, or they do not. Males either have the feature and display it confidently, or they do not. Genes contribute to look, sound, and behavior, and some intangibles like perseverance, creativity, and determination. And, as any pet owner will testify, many animals have personalities. They evidence in their behavior the experiences of their lives, in addition to the idiosyncrasies of their genetics. If a male displays to a female without a seeming confidence of success, his efforts may be in vain. The feature and how the male chooses to present it, is assessed by the female; one of the more subtle aspects to female sexual selection. The environment impacts the process in more than just the obvious ways.
Uterine selection occurs when environmental influences effect the mother's hormonal physiology in ways that result in changes in the embryo's physiology or behavior. The difference between these embryonic changes and the changes that occur in the embryo under natural selection is that the changes result in genetic revisions passed on to the following generation. Obviously, this is controversial. There are no theories as elegant as Watson and Crick's central dogma or the Weismann/Mendel synthesis. Yet, when faced with the medical and neuropsychological evidence of uterine selection (see section IV), the pictures are clear and the patterns compelling. Evolution unfolds partly through the response of embryos to their mother's bodies, responses that result in changes that are passed on to following generations.
Geschwind and Galaburda (1987) outline in detail a number of environmental variables evidencing semi-permanent and permanent effects on the descendants of the individual exposed. In rats, stress and handling change the hormonal balances of mothers affecting the gestating embyros. As adults, these embryos evidence hormonal variations based on the mother's experiences, affecting the next generation. Gottlieb, below, describes effects from ionizing radiation.
"How different is Mayr's view, stated elsewhere in the same book, 'that the DNA of the genotype does not itself 'enter into the developmental pathway but simply serves as a set of instructions' (Mayr, 1982, p. 824) from Sewall Wright's physiological view of DNA ...and the view advocated here. That there seems to be some kind of physiological pathway back to the genes is suggested by the observation that genetic mutations can be induced by environmental causes such as extreme temperature or exposure to ionizing radiation. Also, the currently held notion that during individual development genes are "turned on and off" in their activity suggests again some mechanism of feedback from the products that genes produce back to the genes themselves. For example, DNA-binding proteins are known to regulate gene expression (protein to DNA). In sum, there has to be some means for the activity of genes to be regulated by events and processes occurring at other levels of the developmental pathway, otherwise it would not be possible to cause gene mutations by environmental agents, nor to "turn genes on and off" during normal individual development (i.e. as occurs in the construction of a normal individual of the species as opposed to a mutant)." (Gottlieb, G (1992) Individual Development & Evolution. Oxford Univ. Press: New York p. 140)
Aboitiz (1992) describes features changed early in ontogeny by environmental influences that become a part of that individual's genetic inheritance. Temperature, pressure, PH, light, and chemical exposure (Geschwind & Galaburda, 1987) are all variables that effect human ontogeny, effects that can get carried to the next generation.
"One implication of our hypothesis is that even if the genetic endowment of any particular fetus were known precisely, it would not be possible to make predictions concerning the distribution in a population basis. One of the reasons for this relative freedom from genetic determination is that if hormones do play a role in determining laterality, then the effects of testosterone or related substances on the developing brain will be modified by factors not under the control of the fetal genes. Androgens are produced not only by fetal testes and the placenta but also by the maternal ovaries, adrenals, and nonglandular tissues. The fetus can be influenced by the actions of many of the unshared maternal genes. It is reasonable to expect that if a fertilized ovum were transplanted into the uterus of an unrelated female, the final pattern of the brain would be quite different, because the brain would develop in an environment of hormones and other substances that would certainly differ in many respects. It might therefore be reasonable to take a different approach than usual to the genetics of many conditions. One should perhaps consider, not the genes carried by the offspring alone, but rather the genes of that organism existing or active only for the nine months of pregnancy; in other words, one should consider the mother and the fetus as a unit. This unit contains three groups of different genes: one paternal set present in the fetus, one maternal set present in the mother, and another maternal set present both in the mother and in the fetus. The situation is even more complex when dizygotic twins are involved, since the maternal-fetal unit will contain another group of paternal genes." (Geschwind & Galaburda (1987) Cerebral Lateralization. pp.133-134)
Geschwind and Galaburda (1987) suggest that water temperature and food supply help determine cerebral lateralization in flounders. A primary focus of their work is finding the cause of cerebral lateralization in human beings. Light, they (1987) write, may have profound effects on human cerebral lateralization and disorders associated with anomalous dominance or brains without highly lateralized left hemispheres. Aboitiz (1992) notes the evidence that environmental changes do affect the embryo with signs that the created trait becomes hereditary. Geschwind and Galaburda (1987) have noted that an unusually high percentage of autistic children's parents have been exposed to industrial chemicals.
"There will also be nongenetic effects. Thus, when the mother is anomalously dominant, she will often be hormonally anomalous in such a way as to favor the production of children with similar dominance patterns. The anomalous hormonal pattern of the mother may reflect her own genetic pattern, but when the responsible genes are not shared with the fetus, then the effects on the fetus will be independent to a great extent of its own genetic endowment. There will be other cases in which the mother was herself exposed to an anomalous hormonal environment, as a result of her own genetic endowment or as a result of nongenetic effects, for example, hormones controlled by maternal genes that she did not share or exogenous stimuli that altered the hormonal atmosphere, such as sex steroids, other drugs, and even the season of birth." (Geschwind & Galaburda 1987: 177, Cerebral Lateralization)
Pollard (1984) describes Steele's (1979) description of one way that uterine selection might operate. Behe (1998) concurs with a likelihood that DNA can evidently be altered to reflect environmental influences. Ho (1984), Goodwin, (1984) and Gottlieb (1992) cite cell cytoplasm or levels just above the gene (Gottlieb,1992) as a likely source for the information making it possible for environmental influences to modify the genes. Gregory Bateson (1979) suggests that the DNA has little or nothing to do with context, only content: data from outside the gene is required for growth. It is possible that the gene might even be the wrong place to look to discover how an acquired trait might become inheritable. The dances of mitosis and miosis might harbor the secret for how an acquired feature gets perceived and adopted.
Last, as referred to in the last chapter, a number of theorists, such as Cope (1896), suggested that somehow heredity was able to add on to each generation a memory for the experiences of adaptive change experienced by the individual. Haeckel, Hyatt and Butler shared this belief. There is no theory that explains in detail how this might transpire. The concept has seemed unnecessary in light of the effectiveness of established theories. Yet a number of details and anomalies appearing in the studies of unexplained human neurological disorders, gonadal cancers, and psychological disease suggest such a memory exists. The messengers in this system of behavioral and physiological adaptations are the sexual hormones, testosterone, estrogen and related hormones.
To sum up, Ryuichi Matsuda states...
"It has now become clear that neo-Lamarckism has always been a reasonable theory, and it has stood the test of time for more than a century. Once some misunderstandings and inhibitions are removed, the theory can be regarded as a more complete theory (than neo-Darwinism) in that it analyses the evolutionary process in terms of both the proximate and ultimate mechanisms, and in that it is especially suited for analyzing the origin of macroevolutionary change. Through the analysis of the proximate process we come to know the cause of variation and the presumed initial stage of evolution of the structures upon which natural selection has worked. In traditional neo-Darwinism natural selection is considered to be involved throughout the whole evolutionary process (of structures), which is indeed untrue, as Mivart (1871) already knew. In practice obvious cases of over-extension of the theory of natural selection, which actually results from neglect of the proximate process, have often been criticized in terms of their falsifiability. Yet the critics have never offered a solution for this dilemma. Indeed, evolutionary biology has been in a state of constipation caused by the neo-Darwinian constraint that inhibits exploration of the proximate process of evolution. It should now be realized that such a worry will be over once we accept the neo-Lamarckian approach."
"The application of the neo-Lamarkian analysis appears to resolve some outstanding problems and riddles in evolutionary biology. For instance, the problem of "inheritance of acquired characters" is now understood as the result of accumulation of genocopies. The age-old riddle of "Which came first, the chicken or the egg?" can now be answered from the evolutionary viewpoint (Sect. 3B2). "Adaptive response" now must be restored as a fundamental evolutionary concept, though it has been neglected. All phenomena of abnormal metamorphosis (halmatomorphosis, neoteny, caenogenesis) resulting in macroevolutionary structural changes are now attributed primarily to environmentally induced alteration in the response of the genotype (alteration in gene regulation) during the proximate process. The study of the Badwin effect as special cases of genetic assimulation must be encouraged."
"It should be realized that all the above problems can be more clearly understood by inquiring into the hormonal mediation that becomes involved. Indeed, the environmentally induced hormonal intervention controlling gene action was the mechanism that was unknown to the nineteenth century neo-Lamarckists, and the lack of knowledge of such a mechanism might have hindered the acceptance of neo-Lamarckism." (Matsuda, Ryuichi (1987) Animal Evolution in Changing Environments, with Special Reference to Abnormal Metamorphosis. N.Y.: Wiley Press pp.53)
The environment can influence the character of the zygote by generating changes in the physiology of the parent at the time of zygote creation. We are calling this zygote selection, perhaps the most controversial level at which the environment affects an individual. Processes hypothesized to explain how the DNA can change in response to environmental changes are not simple or proven. Yet we are compelled to focus on this issue, supporting our conjectures with the evidence of permanent genetic change in the progeny of human parents who have experienced any number of environmental effects. These environmental effects change the levels of the sexual hormones in the body of the parent reflected by zygotes with either a propensity for maturational delay or maturational acceleration. Section IV will detail the evidence and effects of eight environmental variables which generate the appearance of specific features in the child which carry forward into adulthood.
When we speak of testosterone, estrogen and related hormones, we are speaking of subtle and mysterious forces. Our focus has been on testosterone because, like the story of the man looking for his dropped front door key only in the places that the porch light shines, there are few studies that track estrogen levels in the study of physical and mental diseases and disorders. The established patriarchal conceit has largely resulted in the use of males (particularly medical students) as test subjects with the belief that findings can be generalized to the rest of the population even though there are obvious striking differences.
"The structures most immediately involved in regulating hormone levels in both sexes are the hypothalamus, the pituitary gland, and the gonads (ovaries and testes). The hypothalamus is believed to act as a "relay station," integrating hormonal stimuli which travel through the bloodstream, and neural stimuli from many other parts of the brain. The hypothalamus is also involved in the production of "neurohormones," or releasing factors, which pass through the pituitary portal vessels into the anterior pituitary, stimulating the synthesis and release of pituitary gonadotrophic hormones, including luteinizing hormone (LH), and follicle stimulating hormone (FSH). These pituitary hormones are carried in the blood to the gonads, where they regulate the production and secretion of gonadal or steroid hormones; primarily testosterone in males, primarily estrogen and progesterone in females. In turn, these steroid hormones are released into the blood and registered in the hypothalamus as part of the complex feedback mechanism contributing to hormonal regulation." (Dan AJ (1979) The menstrual cycle and sex-related differences in cognitive variability in Sex-Related Differences in Cognitive Functioning: Developmental Issues. Wittig MA, Petersen AC (eds.) Academic Press, New York p. 241-260)
In humans, the hypothalamus, pituitary, pineal, adrenals, and the gonads are all involved in the manufacture and regulation of these hormones, measured in a variety of ways (Hassler, 1991). These hormones commonly transform into one another, which can profoundly confound the tracking of cause and effect relations (Hassler, 1992). They vary in concentrations depending on numerous factors both within the body and outside. To run testosterone measurements for comparative studies without taking into consideration time of day, time of season, menstrual timing, and geographic location is irresponsible. Changes in rate and timing of maturation are controlled by this extremely intricate, elegant and subtle system. The elegance may seem elusive among so much complexity, but we are hoping that in the couse of this work, the salient patterns will soon become apparent to you.
Environmental factors such as food, temperature, light, population density, and diet (Matsuda, 1987) through the selective forces of natural selection, sexual selection, uterine selection, or zygote selection change developmental trajectories.
"But it does seem likely that normal development is controlled by gradually decreasing concentration of a hormone acting primarily at high levels of the regulatory system. This is also an ideal mechanism for the simple and rapid production of heterochronic effects. Any acceleration of adult characters by reduction in the titer of juvenile hormone, or extension of juvenile traits by maintenance of a high titer, represents heterochrony. Since minor alterations in the concentration of a hormone can lead to substantial changes in morphology, heterochrony may play an important role in geographic variation (secretion of juvenile hormone is influenced by temperature and photoperiod, for example), polymorphism (including sex, caste, and phase) and speciation itself." (Gould, S.J. (1977) Ontogeny and Phylogeny. Cambridge: Belknap Press. p. 295-6)
The absence of a satisfactory intermediary process connecting the environment to changes in maturation rates and timing has hindered the synthesis of the varying evolutionary theories jostling about for the last 150 years. As examples:
Over one hundred years ago French physiologist C. E. Brown-Sequard created epilepsy through brain trauma to guinea pigs (Bowler, 1984). The effect was inherited. Yet, other conjectures seemed more explanatory because there was no identifiable process able to clearly delineate the mechanics of the event. Richard Goldschmidt, starting in 1918 (Gould, 1977), wrote of the ability of enzymes to control rates making possible unforeseen forms of evolutionary change. In 1928, Smirnov (Blatcher, 1982) suggested that hormones were acting as the intermediary force between organs and sex cells eventually generating species transformations. In 1949, Dechambre (Blatcher, 1982) published a paper describing his solution to why it seemed that cows milked by milking machines seems to create daughters that produced more milk. He suggested that the increased milking was raising sexual hormonal levels that could breach the germ line and lead to neoteny in progeny.
A vast literature now exists describing the effects of the environment upon embyronic stages of animals which result in changed rates and timing of maturation. Gould (1977), Matsuda (1987), McKinney & McNamara (1990), and Gottlieb (1992) provide cogent details of the process. If you have been clicking on the linked dates in the citations in this work, you have been reading the excerpts from these and other texts. (Most of the text on this web site are in the form of excerpts navigable through linked citations.)
Steroids (testosterone is a steroid) are extremely ancient compounds with origins going back several hundred million years (Matsuda, 1987). The higher level of testosterone in human males vs females increases male metabolic rates by 5% (Badcock, 1991) and shortens males lifespans by several years (Badcock, 1991), while making males more vulnerable to infection. Increasing and decreasing testosterone in human males and females has dramatic effects on human maturation levels with a staggering number of direct and indirect effects on physiology and behavior (Halpern, 1994), especially in the brain (Geschwind & Galaburda, 1987).
Herein we will list some of the environmental causes influencing maturation through hormones via uterine selection. Then we will list some maturational effects resulting from changes in these hormonal levels.
Worthman et al (1987) note that physical and psychological stress lowers testosterone (T) while dominance encounters raise or lower T depending on whether you are on the winning or losing side. Geschwind & Galaburda (1987) follow the connections between the amount of light and its effect on the pineal gland that regulates the sex hormones. They conclude that there are strong connections between season of birth and handedness. Higher uterine T levels caused by pineal regulation result in maturational delay of progeny manifesting in higher percentages of left-handed children. Hamalainen, et el (1983)correlate diet with T levels. Low fat, high fiber diets lower T in middle aged men. Hypoglycemic stress lowers T levels in men (Cumming, et al; 1983). Alcoholic consumption lowers T levels in men and women. (Gordon, et al, 1976; Castilla-Garcia, et al, 1987). Obese and heavy adults vary in T levels according to sex. Overweight females have raised T (Pasqualli, et al, 1991). Overweight males have lowered T (Glass, et al, 1977). Smoking raises T (Kahw, et al, 1988) and lowers estrogen (MacMahon, et al, 1982) in woman. Smoking raises T in men (Wu, et al, 1995).
The sexual hormones are the device through which the selective processes work to drive human evolution. Evidence of these processes not only exists in animals -- they exists in human beings.
In the summation of his great work, Ontogeny and Phylogeny, Gould writes the following words...
"Human evolution has emphasized one feature of this common primate heritage -- delayed development, particularly as expressed in late maturation and extended childhood. This retardation has reacted synergistically with other hallmarks of hominization -- with intelligence (by enlarging the brain through prolongation of fetal growth tendencies and by providing a longer period of childhood learning) and with socialization (by cementing family units through increased parental care of slowly developing offspring). It is hard to imagine how the distinctive suite of human characters could have emerged outside the context of delayed development. This is what Morris Cohrn, the distinguished philosopher and historian, had in mind when he wrote that prolonged infancy was "more important, perhaps, than any of the anatomical facts which distinguish homo sapiens [sic] from the rest of the animal kingdom" (1947, p. 174). (Gould, S.J. (1977) Ontogeny and Phylogeny. Cambridge: Belknap Press. p. 400)
How specifically do human beings manifest the heterochronic changes? Gould (1977) quotes Schneiderman, "Maturation in man and other higher vertebrates is promoted by the secretion of maturation hormones, the gonadotropins of the pituitary. The juvenile condition in man hinges upon the absence of these maturing hormones."
How does the absence and presence of testosterone (and estrogen) evidence itself in changes in human maturation? The answer to this question and its ramifications in health and disease form the body of the remainder of this work. Section II describes how changes in these hormonal levels drove hominid evolution. Section III describes how changes in these hormonal levels created the physiological and behavioral anomalies that lead to spoken abstract language and culture, and explains the dynamic behind cultural differentiation. Section IV of this work describes the physiological and behavioral repercussions of maturational delay and acceleration along with changes in the onset of puberty: a dynamic driven by variations in gonadol hormone levels.
At this early point in the process of introducing this realignment of patterns, we will briefly list some humans features associated with maturational delay, features influenced by changes in sexual hormone levels in the uterine environment, features that once changed become inheritable by the next generation. Left handedness and ambidextrousness is strongly associated with maturational delay in human males (Bishop, 1990) (anomalous handedness is associated with maturational acceleration in human females) and is one of the many characters that are effected by changes in the uterine hormonal environment (Geschwind and Galaburda, 1987). For example, smoking mothers with high T give birth to a higher percentage of left handed children (Bakan, 1991). Mothers with uterine high T not only produce more left handed progeny (Gotestam, et al, 1992), Left handedness is a powerful marker for maturational delay, and those progeny also display a higher percentage of the following features and propensities..
1) Conditions characterized by maturational delay such as autism, dyslexia and stuttering.
2) Talent in music composition (Hassler, 1991,1992)
3) Homosexuality (McCormick, et al, 1992)
4) Asthma and allergies (Smith, 1987)
5) Alcoholism (Corin, et el, 1991)
6) Females with high testosterone and males with low testosterone.
7) Professions utilizing visual rotation in three dimensions such as architecture.
8) Deftness in endeavors requiring full-body finely tuned responses such as professional tennis players, dancers, and athletes.
9) Facility with language as metaphor (as opposed to language use for goal planning).
10) Thicker corpus callosum.
11) Cerebral anomalous dominance which is either hemispheric symmetry or a more highly lateralized right (instead of the left) hemisphere. (Geschwind & Galaburda, 1987)
Perhaps the most striking single 'effect' that the varying levels of testosterone 'cause', are the changes exhibited by the brain -- corpus callosum (Forget & Cohen, 1994), planum temporel, and cerebral hemispheres (Geschwind & Galaburda, 1987; Small & Hoffman, 1994). These brain structures are associated with maturational delay and maturational acceleration exhibiting physiological and behavioral correlates with the final stage of hominid development: language and culture acquisition. The cluster of characteristics listed above reveal the maturationally delayed (for males) end of the human polymorphic spectrum (maturationally accelerated for females). The male maturationally accelerated (female maturationally delayed) end of the spectrum is characterised by a different set of physiological and behavioral features: features characteristic of most members of contemporary western patriarchal society.
As this hypothesis unfolds into section III, it will become evident how female sexual selection (female choice) and female infanticide have been and are the two most powerful forces determining the hormonal evolution (maturational delay and acceleration) of humans.