The authors are among many, who seem to have missed a likely epigenetic link from maternal and/or acquired ferritin deficiency to thyroxine transport, brain development, and behavior.
Just as the influence of diet and pheromones can be in the larval stages or in other developmental stages of insects, it can also be in the pre- and postconception stages of mammals, including humans.
That interdisciplinary approach has already been adopted by most neuroscientists who currently are not even involving themselves in discussion of theories about behavioral development…
A diet-reponsive neurogenic niche links nutrient chemical intake to receptor-mediated brain development in mammals. Glucose regulates the hormone secreting nerve cells in this niche, which links it and other nutrient chemicals to levels of luteinizing hormone (LH) and brain development.
Any study that indicates no olfactory bulb neurogenesis occurs in adult humans argues against the design in biology that ensures the plasticity of our brain-directed behavioral response to novel stimuli in our environment…
The idea that ecological niches and social niches are the determinants of neurogenic niches, like those that develop with exposure to food odors and social odors, is one that is important to consider whether we intend to look at pharmacogenomics or to better understand the development of human behavior in the context of epigenetic effects of odors on brain development.
…model organisms make clear the extension of the concept to nutrient chemical and pheromone-dependent neurogenic niches, human brain development, and individual differences in behavior.
the epigenetic effects of chemicals from our sensory environment on GnRH are probably essential to the development of an evolved brain and behavior involved in seeking out proper nutrition and reproductively “fit” mates.