September 8, 2009 | 5 Comments
I’m still trying to grasp the concept that testosterone and estrogen and their associated hormones are together managing ontological, social and biological evolution by adjusting to changes in the environment by moderating the rate and timing of ontogeny.
We always knew that sex governed our lives. There is now the possibility that we can understand how exactly this is done.
In both sexes, entering puberty is characterized by a surge in testosterone that, among other things, halts most synaptic growth. If fat levels are not high enough, puberty is delayed. Certain levels of estrogen are required for testosterone surges to occur.
Over ten years ago I hypothesized that a mother’s uterine testosterone levels would influence the likelihood of her child exhibiting autism. I estimated that the rate of maturation would be determined by the amount of testosterone. A mother with high testosterone would feature maturationally delayed sons and maturationally accelerated daughters, both vulnerable to autism.
This last season I’ve been applying the pattern of how estrogen controls the timing of testosterone surges at puberty to early childhood when testosterone surges prune the right hemispheres of most normal right-handed individuals. Might estrogen levels in these infants, toddlers and children be determining the timing of these testosterone surges? What if estrogen levels were so low in boys that testosterone surges did not occur? The result would be an unpruned right hemisphere, a larger brain with two cerebral lobes that are the same size. This is a common feature of autism.
If a mother has both high testosterone and high estrogen, what I estimate to be an archetype of one of two forms of matrifocal social structure, then, according to the principles that I’ve been playing with, she would birth a low-testosterone, low-estrogen son; high-testosterone, high-estrogen daughter.
The implication is that we might predict that autism would be relatively common in cases where the rate of maturation and the timing of maturation combine to engender brains, mostly male brains, which are maturing slowly with little variation is hemispheric size.
Regarding female infants and children with high estrogen encouraging pruning still drifting in an autistic direction, click here. That is a little more complicated.
Right now, I’m wondering if breast milk vs. infant formula might be an influence on this process. If a mother’s body is able to modify her embryo’s maturation rate and timing based upon the various environmental influences that impact testosterone and estrogen levels, then does a mother’s milk also adjust to environmental influences in ways that her child’s ontogenetic timing is modified?
Does what a new mother eats, for instance, a high-fat diet, influence her breast milk to increase the estrogen levels in her sons and daughters? Could a high-fat diet increase the chance of an autistic child?
High-fat diets increase testosterone and estrogen levels.
How much influence does what we eat have upon our children?