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.
In these first seven chapters we have sought to establish four unique perspectives, four elements of a larger view, in the context of traditional evolutionary theory. We have presented a history of evolutionary theory tracking the themes or elements common to our new view that, we feel, offer useful additions to the established paradigm. The four unique perspectives are:
a) Evolution can be examined as a four part process; environmental influences, selective processes, hormonal intermediaries, and heterochronic patterns.
b) The selective processes themselves retain an evolutionary orientation: natural selection having created sexual selection, uterine selection and zygote selection. Female sexual selection created culture, or cultural selection (to be examined in Section III).
c) The use of points a) and b) above create opportunities to understand both cultural evolution and differentiation; and physical and mental health and disease, presently outside the Darwinian synthesis, under a single theoretical umbrella increasing the breadth of the mid-century modern synthesis.
d) Charles Darwin's writings can be reapproached as the work of a great synthesizer; natural selection, sexual selection, and pangenesis can be examined as sections of a partially realized and unexamined synthesis 150 years ahead of its time.
Darwin's theory of natural selection conveys that most evolutionary change is derived as a result of organisms producing more progeny than can survive to procreate; that the progeny exhibit a random variety of characteristics; characteristics giving some of them an advantage in reaching a procreative age and reproducing. Darwin (1859) abbreviates a description of this process , "...multiply, vary, let the strongest live and the weakest die."(p. 263). Darwin emphasized the random nature of the variation in characteristics distributed among progeny.
Shift theory asserts that at specific points in evolutionary history shifts away from random variation commenced, and that there have been several such shifts over the course of evolution. Variation became less random because any individual that could evidence an ability to reduce the random nature of the variability in characteristics favorable for survival in their progeny would increase their progeny's survival rate (Wesson, 1991). Natural selection, as defined by Darwin, would select for those individuals that could transcend the random variation barrier by creating progeny with characteristics pre-chosen for an established or a changing environment.
Evidence that species have found ways to reduce the random element in the appearance of characteristics in their young is established in the heterochronic interpretations of evolutionary biological processes. Heterochronic theory (Gould, 1977; McKinney & McNamara, 1990) postulates that by influencing the rates and timing of the development and maturation of individuals, large scale phenotypic change can occur with small genotypic revisions (Wesson, 1991). More specifically, species seem to have been selected for an ability to generate large phenotypic change, through the manipulation of developmental and maturation rates and timing, without evidently changing genotypically. Gregory Bateson (1979) refers to this as manipulating the bias or setting of genetically established propensities. The literature abounds with examples of environmental cues which communicate through hormonal intermediaries to the part of an individual that can adjust its and/or its progeny's developmental trajectories to accommodate to a changing environment, thus transcending the random variation barrier (Matsuda 1987; McKinney & McNamara, 1990). The specifics of this process have been hypothesized (Gottlieb, 1992).
The distinction between genotypic and non-genetic change can be very subtle. Shift theory suggests that our genetic "heritage" is specific sequential genetic memory (Cope, 1896). Our genes are a record of the sequence of changes and variations in our hormonal history (Matsuda, 1987). Ontogeny, growth and maturation from conception, is a hormonal reenactment of the changes that all our ancestors engaged in. Not only are we descendants of surviving individuals with characteristics distributed randomly, but we are descendants of surviving progeny with a genetic memory for the specific revisions in the development and maturation rates and timing that occurred until they reached procreative age. We are able to adjust the characteristics of our children based on messages we receive from the environment (Gottlieb, 1992); We also carry, in our genes, records of the changes that our ancestors made during their lifetimes as they created children while hormonally adjusting to their environment. We are suggesting that a large part of phenotypic change is evidence of evolution caused by environmental messages (Aboitiz, 1992) which cue hormonal changes that create shifts in the rates and timing of development and maturation (heterochrony) which move individuals within species forwards or backwards through their hormonal histories.
An in depth exploration of how other species transcend the random variation barrier can be found in the works of Matsuda (1987), and McKinney and McNamara (1990). For example, diet, light, temperature, humidity, salinity, and population density (pheromones) are environmental cues for hormonal messengers an early developmental stages of specific species, triggering changes in developmental or maturation rates or timing. The net result may be that the species skips later stages of maturation becoming mature at a formerly juvenile stage giving them an edge in the speed that they can generate progeny, a potential boon if the environment has become more competitive, more unpredictable (Miller, 1994), or if there is a sudden increase in resources. Slowing growth can have immediate advantages ( Moriya, 1983; McKinnery and McNamara, 1990), for example increasing the size of the adult stage. Heterochronic theory describes in detail the variety of permutations available as individuals within species respond to environmental cues; permutations which are passed on to the next generation. Matsuda (1987) discusses these issues in his theory of pan-environmentalism (Matsuda, 1987).
Human evolution is approached as a four levelled process in shift theory. The (1) environmental influences via the (2) selective processes change the (3) sexual hormone levels which (4) revise the rates and timing of maturation.
In humans, there are at least eight environmental cues which trigger somatic change through their hormonal intermediaries. Eight cues we have noted and are tracking are light, diet, stress, percentage of body fat, alcohol and drugs, tobacco, physical activity, and touch. We are proposing that there are four impact points that humans use to transcend the random variation barrier; sexual selection, zygote selection, uterine selection and cultural selection. Environmental cues can influence selection at all four levels in the process.
Sexual selection is the selective force primarily responsible for culture. Stephen J. Gould (1993) surmises that sexual selection may have been naturally selected as an effective tool for finding a mate genetically distant enough to avoid the dangers of inbreeding but genetically close enough to avoid an individual selected for an environment too different from the one in which the chooser has found success surviving. Even Wallace (1890), Darwin's co-creator of the theory of natural selection, a foe of sexual selection, composed statements that suggested that sexual selection could support natural selection. Altruism theories (Hamilton, 1964; Trivers, 1971) also hypothesize that there are benefits conferred upon individuals choosing mates genetically close by, but not too close by. Dawkins (1976) concurs with this appraisal. Gould cites P. Bateson's (1982) work with quails to support his suppositions. (Bateson found that female quails choose mates at a first cousin distance avoiding birds closer or more distantly related.) We find this a lucid explanation for the widespread establishment of sexual selection in countless species, an example of how natural selection generates another selective process to transcend the random variation barrier.
The relevance of sexual selection in humans comes with Darwin's (1871) conjectures that females and males in the human species may be choosing different characteristics in each other; using different criteria for their choice in mates. Darwin was not specific on how this dynamic may have unfolded. Tanner (1981), with great insight, notes that patriarchal beliefs and cultural biases blinded Darwin to interpretations of sexual selection based on female choice as the central driving force in human evolution for two million years; a force which effectively guided human evolution and created the foundation for culture until the recent advent of patriarchal social structures.
Uterine selection and zygote selection utilize the human sexual hormones as the message system that carries environmental changes, reflected in the bodies of the parents, to the hereditary mechanisms that transfer those changes to the next generation. Changes in the levels and timing of the sexual hormones change the rates and timing of maturational delay and acceleration in pre-adult human beings.
Uterine selection reflects changes in the embryo in response to the uterine environment. For example, psychological stress in the mother reflected in lowered testosterone levels at the point that maturational rates are established (tentatively week 34) will be reflected in a male child that is maturationally accelerated (see section IV). The environmental variables that raise and lower uterine sexual hormone levels impact an embryo's maturation rates. Rates inheritable by that grown individual's progeny.
Zygote selection reflects changes in the physiology of the father (sperm) or grandmother (egg) at the time of zygote creation reflecting the specific levels of the sexual hormones at that point. For example, a non-smoking, alcoholic father will have lowered his testosterone levels so that at sperm creation the male progeny will have an increased likelihood of lowered testosterone levels evidencing itself as maturational delay.
Cultural selection reflects the features of its lineage as a selective process - female sexual selection being the parent and natural selection the grandparent. The idiosyncrasies of human consciousness, language, and culture are understandable through this model. See sections II and III for details.
Variations in the rate and timing of the sexual hormones and the resulting variations in the rate and timing of maturational delay and acceleration during the growth of individuals has direct and indirect results on the health and disease of human beings. Physical and mental disease is usually not approached from an evolutionary perspective. Attempts to use natural selection alone to determine evolutionary etiologies of disease have been aggravated by inattention to heterochronic theory and a gap in the awareness of the influence of social structures on disease etiology.
A number of neurological diseases characterised by maturational delay can be found in families with a history of male maturational delay accompanied by such features as left-handedness, ambidextrousness and cerebral symmetry. Maturational delay can be genetic or created by environmental factors. We believe that neurological diseases characterised by extreme maturational delay or acceleration are evidencing the same processes responsible for human evolution. These diseases were not understandable when only natural selection was utilized to discern patterns of disease formation. A commitment to the 'central dogma' of Watson and Crick has hindered the alternative view represented in this work. We request that the DNA ---> RNA ---> protein sequence of cause and effect, in reference to the sexual hormones, be abandoned to accommodate the possibility that many medical maladies may be preventable if we countenance an alternative point of view. Details in section IV.
Cancers characterised by elevated levels of the sexual hormones that respond to therapy characterized by lowering sexual hormones, we believe, are directly related to the same processes of human evolution as they evidence themselves in neurological disease. Instead of being impacted primarily by issues of maturational delay or acceleration, these cancers are being caused, at least partly, by the changing hormonal levels that cause the heterochronic variations. Transitional model 1.0 identifies genetic types vulnerable to these cancers, based upon their genetically raised hormonal levels which generates specific heterochronic trajectories. The model suggests preventative interventions and treatments based upon the eight environmental variables and their hormonal intermediaries. Details in section IV.
Immune and auto-immune disorders are directly influenced by the evolutionary processes that we are describing. High testosterone levels inhibit the efficient operation of these systems. The threshold in which testosterone begins these inhibitory actions varies from person to person depending upon their natural rates of maturational ontogeny. Environmental factors can raise a person's testosterone to a point where immune and auto-immune difficulties begin. The model based upon this evolutionary theory approaches immune and auto-immune disorders from an evolutionary perspective. Controlling the eight environmental variables provides intervention alternatives.
The timing of puberty, what is called progenesis in heterochronic theory when puberty occurs earlier in ontogeny than in the previous generation, has a very powerful impact on the origin of species. A sudden increase in nutrients can rock a stable evolutionary ecosystem into an unstable system that eventually generates new varieties and species. And, of course, the same can happen if there is a sudden decrease in resources. When there is an increase in resources, species that can lower the age of procreation will increase the number of progeny created over several generations because the distance between generations has decreased, thereby raising birth rates. Human puberty has dropped 3 1/2 to 4 years worldwide over the last 100 years. Fat, carbohydrate, and protein intake has dramatically increased in the environments where onset of puberty has come earlier. There is an exact relationship. This relationship is reflected in the distribution of mental disease. Correlating with the drop in puberty is a drop in schizophrenia and a skyrocketing of depression and bi-polar disorder. We believe that several mental diseases are a result of changes in pubertal timing in individuals with the genetic propensities of maturational delay and acceleration complicated by the influences of the eight environmental variables. With transitional model 1.0 these conditions can be predicted, prevented and treated. See section IV for details.
In 1859 Charles Darwin published The Origin of Species introducing his arguments in support of natural selection. In that same volume he introduced the concept of sexual selection; also made clear his belief in the use and disuse of organs in response to environmental influences. In 1867 he published his theory of progenesis and in 1871 detailed his arguments for sexual selection guiding the evolution of humans. His last edition of The Origin of Species, published in 1872, discussed all three selective processes. In this revised edition he referred to the works of Mivart and Cope, discussed embryonic ontogenitical change and the influence of developmental delay and acceleration.
Several things were missing that made Darwin's attempted synthesis fall short of this desired goal.
1) Though Darwin had correctly identified natural selection as the most important selective process overall, he had not uncovered the relationship between the selective processes that revealed natural selection to be the parent (or grandparent) of the others. Darwin was not clear on the degrees of randomness in varying contexts. The context of variation randomness or non-randomness, how exactly natural selection reinforces the achievement of non-random variation, suggests the familial relationship of the selective processes.
2) Though Darwin recognized Cope's work on the acceleration and retardation of developmental processes, he did not embrace it. Darwin did not recognize the relevance of maturational delay in the tracking of the change of features in domesticated animals. Darwin's identification of use and disuse of organs did not extend so far as to identify the pattern of neotenic change common to, for example, the pig, sheep and dog.
3) Without the later discoveries made regarding the human hormonal system and its effects on ontogeny, Darwin was bereft of a conceptual system that could bring together unconnected theoretical constructs that were sometimes in conflict in his attempts to form a unified theory. For example, Darwin wrote both that natural selection was random, and that natural selection selected the most fit from non-random progeny influenced by the use and disuse of parental organs. An awareness of hormonal dynamics would have created the opportunity to discern how the environment was generating variation from which natural selection chose the most fit.
4) Darwin postulated the concept of gemmules that could revise heredity so that environmental changes through the use and disuse of organs could be passed on the next generation. This gemmule design did not satisfy his contemporaries or himself. Movable energy concepts put forth by Cope and Haeckel met similar fates. Several other concepts have been written up in the last twenty years but none have managed to gather the attention of the community of theoreticians whose support is necessary for the acceptance of a theory of evolution that would be an adjunct or alternative to natural selection. The lack of a clearly delineated "Lamarckian" mechanism continues to hinder the synthesis that Darwin took giant strides towards achieving.
5) Charles Darwin suggested the possibility that humans were descended from tribal cultures characterised by matrifocal social structures, referencing Morgan's writings, driven by female sexual selection. After suggesting the possibility, he rejected it as being incongruent with his experience of contemporary and primitive society featuring a focus on male hierarchical dominance patterns with a complementary pattern of female compliance. It is not likely that if Darwin had instead embraced what he rejected, that the history of evolutionary theory would have been changed. Female sexual selection was almost ignored for 100 years. And it is only with the work of Geoffrey Miller (2000), that sexual selection theory achieves full acceptance. Yet it is another indication that the vision of Charles Darwin transcended not only his contemporaries, but his culture.
Postulate 1: The process of evolution, the rules of species transformation, evolves. The rules change. Different rules apply to different species, the rules becoming more intricate and subtle with the increase in complexity in hormonal systems.
Postulate 2: At specific points in evolutionary history, shifts away from random variation began, and there have been several such shifts over the course of evolution. Variation became less random because any individual with an ability to reduce the random nature of the variability in the characteristics of their progeny would increase their progeny's survival and procreation rate. Natural selection selects for those individuals who transcend the random variation barrier by creating progeny with characteristics pre-chosen for an established or a changing environment.
Postulate 3: Ontogeny is the manifestation of the sequence of ancestral hormonal evolutionary changes. Ontogeny, growth and maturation from conception, is a hormonal reenactment of the hormonal changes our ancestors engaged in.
(For the rest of the 25 summarizing postulates of shift theory and transitional model 1.0 click here).
This concludes the summary of Section I. Sections II, III, IV and V are, at present, represented by single chapter summaries.