October 16, 2009 | Leave a Comment
“In a 5-year longitudinal study, we examined the effect of disrupting the neonatal activity of the pituitary–testicular axis on the sexual development of male rhesus monkeys. Animals in a social group under natural lighting conditions were treated with a GnRH antagonist (antide), antide and androgen, or both vehicles, from birth until 4 months of age. In antide-treated neonates, serum LH and testosterone were near or below the limits of detection throughout the neonatal period. Antide + androgen-treated neonates had subnormal serum LH, but above normal testosterone concentrations during the treatment period. From 6 to 36 months of age, serum LH and testosterone were near or below the limits of detection. Ten of 12 control animals reached puberty during the breeding season of their 4th year, compared with ﬁve of 10 antide- and three of eight antide + androgen-treated animals. Although matriline rank was balanced across treatment groups at birth, a disruption within the social group during year 2 resulted in a marginally lower social ranking of the two treated groups compared with the controls. More high (78%) than low (22%) ranking animals reached puberty during year 4. During the breeding season of that year, serum LH, testosterone and testicular volume were positively correlated with social rank. Thus the lower social rank of treated animals may have contributed to the subnormal numbers of these animals reaching puberty during year 4. However, of those animals achieving puberty during year 4, the pattern of peripubertal changes in serum testosterone and testicular volume differed between control and antide-treated animals. The results appear to suggest that the disruption of normal activity of the neonatal pituitary–testicular axis retarded sexual development, but that social rank is a key regulatory factor in setting the timing of sexual maturation in male rhesus monkeys. The effect of neonatal treatment with antide and low social rank on sexual development could not be reversed by neo-natal exposure to greater than normal concentrations of androgen.” Abstract from Sexual maturation in male rhesus monkeys: importance of neonatal testosterone exposure and social rank by Mann, Akinbami, Gould, Paul and Wallen.
Today is August 4th. The pieces that appear in this blog are usually written two to three months before. My writing skills demand an editor, hence the delay.
Nithya Krishnan and Elia Lehman are developing aspects of the theory presented on this blog. Nithya is completing a paper on matrifocal social structures and breast cancer. Elia is working on a paper that explores correlations between matrifocal society language structure and primary process (no time, no place, no opposites) in the context of child-rearing practices and autism. Rosanna Schatzki has nearly completed a piece on the influences of testosterone on maturation rates.
Nithya is also writing a paper that details the dynamics of heterochronic theory as it influences human evolution and potentially biological evolution in general. We are running with my hypothesis that testosterone influences the rate of maturation, estrogen the timing, and that environmental influences (in the womb and in all stages of ontogeny) and sexual selection (from within social structure) impact those two hormones, thus influencing evolution.
I feel that this hypothesis, if true, has ramifications in several disciplines. If the principle of heterochrony transcends its hormone dynamics, for example, if physics evidences neoteny and acceleration, then it’s not clear to me what may not be influenced. If the rate and timing of maturation are integral to growth across all scales, then the discovery of this dynamic by Darwin’s contemporaries (Mivart, Cope, Haeckel and others) may rival Darwin’s theory of natural selection. Clearly, the two theories complement each other. I also posit that Darwin’s theory of sexual selection is essential to my interpretation of heterochronic theory. In other posts, I have noted that Darwin’s theory of pangenesis was an early attempt to understand environmental effects on evolution, using what would later be called “endocrinology.”
A sidebar. Darwin’s The Variations of Animals and Plants under Domestication, his second to last great work, was an attempt to integrate observed anomalies that didn’t fit into his theories of natural selection or sexual selection. Thomas Kuhn in his The Structure of Scientific Revolutions noted a particular pattern when a new scientific paradigm becomes embraced by contemporary theorists. Anomalies that had not been integrated into former paradigms, anomalies also not addressed in the most recent paradigm, disappeared from textbooks and were not taught in class.
What Darwin was seeking to understand in this second to last work was how lightning-fast evolution occurred in situations where natural selection or sexual selection was not in play. Darwin observed anomalies all around him. His two-volume work wrestled with what might be necessary to explain these anomalies.
I feel like this has been what I have been wrestling with for the last 12 years. Only in the last few months, with the discovery of the possibility that estrogen controls the timing of maturation, and integrating that with the premise presented in “Introduction to the Theory of Waves,” have I felt that a whole theory has been formed. All three of Darwin’s theories now make sense. Anomalies observed 150 years ago feel integrated.
Nithya discovered the paper quoted at the beginning of this posting. It is significant in that it reveals evidence that testosterone influences maturation rate in rhesus monkeys in the context of hierarchy within social structure. There are other studies that suggest that testosterone influences maturation rates in humans. A question is: How ubiquitous is the influence of testosterone and estrogen on the rate and timing across species? How instrumental are heterochronic processes to evolution?
Studies conducted by Matsuda and his colleagues made clear that there are amphibians that exhibit variations on this theme, maturation rates managed by specific hormones. To my knowledge, no one has done research suggesting that estrogen controls the timing of maturation. Gould’s great Ontogeny and Phylogeny offered little in the way of an explanation of what hormones underlay heterochronic processes.
I hope that Nithya, Elia and Rosanna will continue to help me find ways to make this whole thing make sense and to make ancient anomalies feel relevant today. Their assistance has felt deeply nurturing. I really like working on this with other people. Then again, folks have been working on this stuff for 150 years.