No New Neurons for Smell?
Excerpt: The finding may mean that as humans evolved from animals, we lost the ability to produce new neurons in this area because we don’t rely as much on our sense of smell. On the other hand, it may mean that people living in an affluent, Western city like Stockholm aren’t exposed to enough new smells to keep the neurons alive.
My comment:
Evidence for the epigenetic effects of nutrient chemicals and pheromones on mammalian olfactory bulb neurogenesis, hypothalamic neurogenesis and hippocampal neurogenesis attest to design in biology. For example, nutrient chemicals are required for survival of individual organisms in the ecological niche where pheromones control interactions in the social niche of microbes.
In the honeybee model organism, this obvious design, where nutrients and pheromones are both required, extends to brain development. What the queen bee eats determines her pheromone production and everything about the interactions of every other organism in the colony — including the neuroanatomy of the worker bees’ brains.
An extension of this model to vertebrates is found in nutrient-dependent ecological niches of the threespine stickleback that determine their social niches and speciation. Extending this model of transgenerational epigenetic inheritance from yeasts to mammals is done by examining the direct effect of nutrient chemicals, like glucose, and the direct effect of pheromones on the gonadotropin releasing hormone neurons of the hypothalamic neurogenenic niche that is responsible for luteinizing hormone secretion, fertility, steroidogenesis, sex differences in behavior, brain development (among other things), and learning and memory via hippocampal neurogenesis.
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, like the visual and auditory input associated with the development of behavior via correlates with the direct effect of nutrient chemicals and pheromones.
Is there another model for the epigenetic effects of sensory input (like food odors and social odors/pheromones) that directly effect the hormones that affect our behavior via basic principles of biology and neuroscientifically established levels of biological organization? If not, the ‘right’ model of nutrient chemical and pheromone activation of genes in hormone secreting nerve cells of brain tissue (i.e., in the organ of the organ system responsible for our behavior) suggests that the results of this study are misleading. Positing a lesser role for olfaction or for olfactory bulb neurogenesis in humans is inconsistent with the fact that olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.
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