John Hemming's Web Log

I am collecting links to papers which look at mtDNA damage in human oocytes. Mitochondrial DNA Damage and Its Repair Mechanisms in Aging Oocytes Human ovarian aging is characterized by oxidative damage and mitochondrial dysfunction Mitochondrial deoxyribonucleic acid deletions in oocytes and reproductive aging in women Mitochondrial deoxyribonucleic acid deletions in oocytes and reproductive aging in women Mitochondrial DNA point mutation in human oocytes is associated with maternal age Mitochondrial Dysfunction and Age-related Oocyte Quality Allele frequency selection and no age-related increase in human oocyte mitochondrial mutations

I was interested to read in Peter Lidsky's book of the known behaviour of parasites in extending the life (if not the quality of life) of their hosts from time to time and I thought I would read up on this. I do recommend buying Peter's Book Aging: Why Does Evolution Kill . I have given the link to Amazon. I have, therefore, asked three LLMs to produce a summary of this behaviour and I copy their results below. I will go through this myself, but that will take some time and I thought it would be useful to have the results available. Gemini: Review: Parasite-Induced Host Longevity 1. Introduction Conventionally, parasitism is defined by a fitness cost to the host. However, a specific evolutionary paradox exists where parasites actively extend the host's lifespan ("longevity assurance") to ensure their own transmission, particularly in intermediate hosts waiting for trophic transmission. 2. Key Research ...

A debate has been ensuing on X/Twitter about Programmed aging in which unsurprisingly the question as to what is programmed aging came up. I thought I would ask chatGPT, Claude and Gemini for an answer. These are the answers: The prompt was: "what is the definition of programmed aging?" chatGPT: Programmed aging is the idea that aging is an evolved, genetically regulated process —more like a built-in “life-cycle program” that actively drives the gradual decline in function and increases the risk of death, rather than aging being only the passive accumulation of random damage. In this view: Aging happens because biological pathways are set up to shift the body into a late-life state (reduced repair/maintenance, altered immune/endocrine signaling, etc.), even if that late-life state is harmful to the individual . The “program” can be direct (genes/pathways exist to promote senescence/decline) or indirect/quasi-programmed (genes optimized for growth/...