John Hemming's Web Log

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/...

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 ...

As I biohacker I do quite a bit of self-experimentation. There is an interesting ethical question about self-experimentation. Obviously people have the right to make their own decisions. Self Experimentation has a long history in Medicine and at least five Nobel Prize winners have won a prize following self experimentation. However, it is potentially dangerous and people have died. The ethical question is whether researchers should be penalised by being unwilling to self-experiment. To that extent some US ethics committee argue against the academic publishing system accepting the results of self-experimentation. I personally, unsurprisingly, think that is wrong. There should not be a condition of employment that people self-experiment, but it cannot be right to exclude the results. We also need to recognise that there are serious problems with animal experiments. Everything Wrong with Mouse Studies (Kinda) subtitled: Odors, magnetic fields, and even a mouse's siblin...

Professor Thomas Seyfried and the Question: Is Cancer Primarily Nuclear DNA or Mitochondrial DNA? Professor Thomas Seyfried argues that cancer is mainly mitochondrial rather than purely nuclear/genetic. Below are the key experiments supporting the view that cytoplasmic/mitochondrial factors, rather than nuclear mutations alone, drive the malignant phenotype. Nuclear Transfer Experiments (Cancer Nuclei → Normal Cytoplasm) McKinnell, R.G., Deggins, B.A., Labat, D.D. (1969) Transplantation of pluripotential nuclei from triploid frog tumors Science, 165(3891):394-6 Summary: Nuclei from frog renal tumor cells transplanted into enucleated eggs developed into normal swimming tadpoles, demonstrating that cancer nuclei retained developmental pluripotency when placed in normal cytoplasm. McKinnell, R.G. (1979) The pluripotential genome of the frog renal tumor cell as revealed by nuclear transplantation International Review of Cytology Supplemen...