Deficiencies prevent repair: Mutagens and Multivitamins
June 11, 2014 | James Kohl
Not one to shy away from controversy, Bruce Ames has pitted himself against industry groups, environmentalists, and his peers through his work identifying DNA mutagens. And he’s not done yet.
June 1, 2014|
Excerpt: So I started looking to see if you get DNA damage from a vitamin or mineral deficiency.” Beginning at Berkeley and continuing at Children’s Hospital Oakland Research Institute (CHORI), which Ames joined in 2000, he and his lab found many examples of this phenomenon: iron deficiency causes neuron decay and mitochondrial DNA damage, for example, and zinc deficiency damages DNA and disables tumor suppressor p53. But Ames still didn’t know how such deficiencies could directly damage DNA.
My comment: In my model, deficiencies prevent repair
… Nutrient-dependent/pheromone-controlled adaptive evolution: a model led to an invited review of nutritional epigenetics that linked atoms to ecosystems. The invited review was rejected because no one would review it. I think it was too innovative in its refutation of neo-Darwinian mutation-initiated natural selection and the evolution of biodiversity. I focused on Darwin’s ‘conditions of life’ and linked nutrient uptake to pheromone-controlled reproduction via conserved molecular mechanisms that enable amino acid substitutions in species from microbes to man.
The links from the epigenetic landscape to the physical landscape of DNA in the organized genomes of all species are as clear as they are in Patrick and Ames (2014) Vitamin D hormone regulates serotonin synthesis. Part 1: relevance for autism, which was reported as New research indicates causal link between vitamin D, serotonin synthesis and autism. Simply put, you don’t arrive at socio-cognitive niche construction without ecological, social, and neurogenic niche construction, which explains activation of serotonin, oxytocin, and vasopressin by vitamin D.
If those three brain hormones that affect social behavior were not nutritionally activated, there could be no such thing as nutrient-dependent hormone-organized and hormone-activated behaviors like those we detailed in the context of cell type differentiation in From Fertilization to Adult Sexual Behavior. Unfortunately, even after extension of our model to invertebrates and the life cycle transitions of the honeybee, I may not get to publish another article — like Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems, which refutes the population geneticist’s ideas about mutations, natural selection and the evolution of biodiversity.
They would rather have people continue to believe that some mutations must be beneficial, although no experimental evidence ever suggested that perturbed protein folding created new functional proteins that were manifested in the morphological and behavioral phenotypes of any species. Hemoglobin S, for example, appears to involve a vitamin D-dependent amino acid substitution that stabilizes the organized genome in human populations where endemic malaria could otherwise have limited their adaptive radiation.