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Endometriosis and acetylation

There has been some press attention to Endometriosis recently. To me it looks like a splicing/acetylation type of disease (which requires that sort of intervention to resolve). I have put some prompts into an AI (chatGPT) to produce a more detailed argument with citations and here is the response: Could Endometriosis Result from Aberrant Splicing Caused by Reduced Nuclear Acetylation? Summary: Endometriosis is usually described as an inflammatory, hormonal and fibrotic disease in which endometrial-like tissue grows outside the uterus. However, a growing body of evidence suggests another layer of explanation: endometriosis may involve abnormal RNA splicing, and that abnormal splicing may in some cases arise from reduced acetylation of nuclear proteins. This article sets out the argument for that hypothesis. The evidence does not yet prove that reduced nuclear acetylation is the root cause of endometriosis, but it does make the hypothesis biologically plausible an...
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mtDNA damage in human oocytes

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

Parasites extending life of hosts (buy Peter Lidsky's book)

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 ...

Different definitions of Programmed Aging

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/...

Aubrey de Grey's COA (Cancelling out Argument) and why I disagree with it.

In Aubrey de Grey's 2015 Paper Do we have genes that exist to hasten aging? New data, new arguments, but the answer is still no he puts forward a number of arguments as to why he believes aging to be other than programmed aging (PA). One of these argument is his "COA Cancelling out argument". I extract from the paper his reasons for this. STRONGER CHALLENGES TO PA A simple but remarkably rarely stated argument against PA, which here I shall term the “cancelling-out argument” (COA), is that it is impossible for a species to maintain two sets of genetic pathways whose selected actions diametri cally oppose each other. Specifically, since we clearly have a large amount of genetic anti-aging machinery (repairing and pre-empting the damaging side-effects of metabolism), we cannot also have pro-aging machinery that accelerates the accumulation of such damage, unless the latter machinery is selected for another purpose. The logic leading to this con clusion is ...