Article excerpt (from Thyroid hormone is required for hypothalamic neurons regulating cardiovascular functions): “In this study we show that both thyroid hormone receptors are required for the development of a previously unknown population of parvalbuminergic cells in the anterior hypothalamus. Our data link for the first time to our knowledge defects in thyroid hormone signaling during development to a permanent cellular alteration in the hypothalamus. Moreover, as the cells are associated with the control of cardiovascular function, our study shows that developmental hypothyroidism may represent a previously unknown risk factor for cardiovascular disorders.”
The article addresses, in part, neurogenic niche construction in a manner similar to how ecological, social, and socio-cognitive niche construction are addressed in my model of nutrient-chemical dependent, pheromone-controlled, receptor-mediated adaptive evolution that links microbes to man. For example, it is hard for me to imagine that this previously unknown population of parvalbuminergic cells in the anterior hypothalamus does not interact with the neurosecretory neurons of the medial preoptic area of the anterior hypothalamus that control secretion of gonadotropin releasing hormone (GnRH): THE biological core of ALL behavior (e.g., in vertebrates). But perhaps the problem for me is because I know there’s a model for that!
These authors rightfully claim, however, that they are the first to “…identify a permanent cellular defect in the hypothalamus resulting from developmental hypothyroidism and add hypertension to the list of symptoms potentially arising from maternal hypothyroxinemia and/or congenital hypothyroidism.” They are among many, however, who seem to have missed a likely epigenetic link from maternal and/or acquired ferritin deficiency to thyroxine transport, brain development, and behavior. Perhaps they don’t know there’s a model for that!