John Hemming's Web Log

I have written about DNA Methylation itself on my 2026 poster page here . In short it is an indication of what genes are being transcribed and links to histone acetylation, methylation and many other post translational modifications. It was found that there is a weak link between ageing and DNA methylation and also a weak link between DNA methylation and the pace of biological ageing. A lot of enthusiasm then built up for using this as a tool to measure health in the round. I lost confidence personally in having the tests done a couple of years ago simply because they did not seem to give me any usable information as to what could be done to improve health (unlike blood biomarkers and other biomarkers). More recently there have been some research looking at the technical merits of DNA methylation tests and I will list some here. At the bottom of this page I list four papers. The first finds that the clocks vary as to their reliability. The second finds that the value on a clock...

People who regularly read my blog will know my hypothesis that ageing results primarily from damage to mitochondrial DNA. Details of this can be found here . A question that arises, of course, is given that the laws of chemistry and physics are the same why do different species have different average lifespans. Obviously there are quite a few things that could make a difference. The process of autophagy matters and in which circumstances that happens, but also there are enzymes that are available in the mitochondrion that repair damaged mtDNA. One of these enzymes is OGG1. Interestingly this enzyme is not available for C. Elegans. Nor is MUTYH which gives a second chance to fix errors that OGG1 has failed to fix. More details about this are available here . Unsurprisingly a large amount of unrepaired lesions (where damage is caused to mtDNA) appear in older C. Elegans and it has a relatively short life. Mitochondrial base excision repair positively correlates with longevity in...

Cystatin-C has interested me for some time. It is used as a marker of Kidney function and in theory is a better marker than Creatinine. Creatinine has its problems, but it appears so does Cystatin-C. What I found interesting about Cystatin-C is that it is also a signalling molecule whilst Creatinine is a metabolic by product. Creatinine is produced mainly inside skeletal muscle by the spontaneous, non-enzymatic breakdown of creatine and phosphocreatine. Creatinine is also produced in blood samples between the sample being taken and then tested. As it is excreted by the kidneys a low value is an indicator of good kidney function or low muscle mass. High values can result from exercise and high muscle mass as well as bad kidney function. I have tasked three LLMs to produce some summaries of research and I attach those below. However, there is only one relatively straighforward conclusion I can come to at this point which is that Cystatin-C is a complex molecule and although the...

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...

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 ...