Excerpt: A number of studies have hinted that we can extend our healthy lifespans by boosting our ability to repair defective proteins.
My comment: Once again, the problem here is belief in mutation-driven evolution, since the defective proteins are associated with mutations. I may stop contributing comments to the National Geographic site unless Carl Zimmer responds. His arguments for genetic engineering seem too far afield of what is already known about the adaptive evolution that supposedly occurred in vertebrates during the past 400 million years. There is a perfect molecule involved that did not require a mutation, which can be compared to the naked mole rat’s mutation to the gene for 28S RNA in the context of age-related systems degeneration.
The perfect protein is gonadotropin releasing hormone (GnRH). Did I say perfect? Yes, but Kochman (2012) said it first: “The discovery of the fact that one decapeptide molecule, among the GnRHs, was constructed perfectly at the beginning of 400 million years evolution and that it is not possible to improve its physiological potency using any natural amino acid is, in my opinion, important, fascinating and beautiful.“
The GnRH molecule is probably very important in the context of mutations theory. This perfect protein was constructed via a single nutrient-dependent amino acid substitution. Achiral glycine was substituted for alanine, which allows a more constrained conformation for receptor binding. Predictably, the more tightly controlled receptor binding contributed positively to the thermodynamics of nutrient-dependent intercellular signaling, intermolecular interactions, stochastic gene expression and organism-level thermoregulation. That explains why the thermodynamics of cellular metabolism in organisms from microbes to man are perturbed by nutrient stress and why organism-level thermoregulation is perturbed by social stress. Presumably, nutrient stress and social stress alter GnRH-dependent receptor-mediated gene transcription with downstream effects on every cell of every vertebrate’s body.
What does that have to do with the mutation and long life in the naked mole rat? Nutrient stress and social stress epigenetically effect GnRH. The naked mole rat shows us that it is best not to mutate anything downsteam from GnRH by over-eating, under-eating, or by social stress. In humans, the avoidance of nutrient stress is associated with balanced intake of glucose and amino acids that epigentically effect hypothalamic GnRH pulse frequency in all mammals. Social stress is associated with the metabolism of nutrients to species-specific pheromones that control nutrient-dependent reproduction in species from microbes to man. Thus, if we want to be more like naked mole rats, and who doesn’t (except for the fact they are so ugly), we should simply eat right and avoid whatever social stress we can avoid.
We are then less likely to have mutated genes that contribute to our ugly demise, but cannot contribute to any species-wide benefits in any species. The idea that a mutation was beneficial to the naked mole rat is the problem I have with Carl Zimmer’s misrepresentation of cause and effect in the context of adaptive evolution. He appears to think that the naked mole rat’s mutation contributes to its longevity.