This news story is available at: news.sciencemag.org. Today’s news from Science and ScienceInsider Mon, 11 June 2012
Aging Is Recorded in Our Genes
As we grow older, we lose DNA modifications that can protect against cancer and other diseases.
Excerpt: … likens the DNA sequence to the genome’s “hardware” and epigenetic changes to its “software,” … supports earlier research suggesting that “as a function of age and environmental exposure, this software accumulates defects” that can cause “age-related cancer and degenerative diseases.”
My Comment:
This seems to be a clear indicator that the epigentic effect of nutrient chemicals on intracellular signaling and stochastic gene expression is central to what shows up in degrees of methylation. Is there any consensus that this is predicted by the direct effect of nutrient chemicals on receptor-mediated events, like those initiated by glucose in neurosecretory neurons of the mammalian hypothalamus that secrete gonadotropin releasing hormone (GnRH)? These hormone-secreting nerve cells of brain tissue link sensory input from our environment directly to a neurogenic niche that controls the wiring of the brain prenatally and postnatally.
Like other animals our sense of smell links food odors and social odors directly to postnatal GnRH regulation of the hypothalamic-pituitary-gonadal (HPG) axis and the HP-adrenal (HPA) axis. And our sense of smell is the first indicator of several neurodegenerative age-related diseases, as well as a likely indicator of neuroproliferation problems like those now being recognized in autism spectrum disorders (ASDs).
Measures of luteinizing hormone (LH) during the development of the brain and behavior seem to be the best indicator of what happens with aging. Simply put, LH is the link between nutrient chemicals, pheromones, hypothalamic neurogenesis, olfactory bulb neurogenesis, hippocampal neurogenesis, learning, memory, and behavior — as modeled across the ecological, social and neurogenic niche construction that contribute to the adaptive evolution of our cognitive niche.
But our cognitive niche won’t do us much good until we hone our collective pattern-recognition skills. For example, olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans, and the trail includes the epigenetic effects of nutrient chemicals and pheromones on methylation in species from microbes to man. Of course, these effects extend to transgenerational epigenetic inheritance and speciation, but I may have taken this too far, already.
Like other animals our sense of smell links food odors and social odors directly to postnatal GnRH regulation of the hypothalamic-pituitary-gonadal (HPG) axis and the HP-adrenal (HPA) axis. And our sense of smell is the first indicator of several neurodegenerative age-related diseases, as well as a likely indicator of neuroproliferation problems like those now being recognized in autism spectrum disorders (ASDs).
Measures of luteinizing hormone (LH) during the development of the brain and behavior seem to be the best indicator of what happens with aging. Simply put, LH is the link between nutrient chemicals, pheromones, hypothalamic neurogenesis, olfactory bulb neurogenesis, hippocampal neurogenesis, learning, memory, and behavior — as modeled across the ecological, social and neurogenic niche construction that contribute to the adaptive evolution of our cognitive niche.
But our cognitive niche won’t do us much good until we hone our collective pattern-recognition skills. For example, olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans, and the trail includes the epigenetic effects of nutrient chemicals and pheromones on methylation in species from microbes to man. Of course, these effects extend to transgenerational epigenetic inheritance and speciation, but I may have taken this too far, already.