Estrogen, Puberty and Autism | Neurodiversity
To what degree have high and low-fat diets influenced human evolution? If low fat delays puberty and results in more brain growth, might this be because more synapses are useful for finding more fat?
When there is more fat in diets and puberty rates drop, for a woman there is a greater number of children produced over a single lifetime. Less fat in diet, fewer children produced. This seems like an evolutionary process.
Do thin males with less fat have less estrogen, reach puberty later, have bigger brains and exhibit more neotenous features?
Should autistic males be on extremely low-fat diets so that they reach puberty later, thus allowing more time for their brains to mature?
Is the degree of brain synapse pruning that occurs in infancy related to the estrogen levels in the mother or the child? High mother testosterone levels encourage higher rates of autism, which may be directly related to less pervasive synapse pruning. Is it possible that a high mother estrogen level results in low male baby estrogen levels that prolong or diminish the testosterone prunings?
In other words, the Simon Baron-Cohen research regarding mother testosterone levels and autism may be related to mother estrogen levels. If low estrogen at puberty translates to delayed puberty, delayed testosterone surges and increased brain growth, then the same process may be engaged during the first testosterone surges that compel a diminution of the right cerebral hemisphere during infancy. Low estrogen levels as an embryo, infant and toddler may have a direct impact on cerebral lateralization and synapse production.
Another interesting article 'Introduction to Neotenty' Here ............