The latest link

Understanding e5 development and excitement

 

            E5 has been tested in a joint paper of many authors including Dr. Katcher and Dr. Horvath as this link.

 

https://www.biorxiv.org/content/10.1101/2020.05.07.082917v1.full.pdf/

 

            Dr. Horvath in the list implies data is correct, references good, as per [me]. Every claim in proper science must be tied to experiments, distinct from all religions where a book is believed.

            The paper data raises a related and equally interesting question, which is why does plasma fraction treatment not reduce brain epigenetic age by the same magnitude as it does the other organs? 

The paper does read

(a) epigenetic aging is distinct from the process of cellular senescence and telomere attrition [me], 

(b) several types of tissue stem cells are epigenetically younger than 

non-stem cells of the same tissue [me], 

(c) a considerable number of age-related methylation sites, including some clock CpGs, are proximal to genes whose proteins are involved in the process of development me], 

(d) epigenetic clocks are associated with developmental timing [me], and 

(e) relate to an epigenomic maintenance system [me].

 

Some process in all trillion cells is leaving behind a methyl group every time a C sugar has a phosphate bond to G sugar (called CpG islands) on the DNA. It happens in all cells but the brain and stem cells. Now Katcher believes that all communication in the body is by signal proteins. So clearly the mechanism is not damaged accumulation but programmed death. Trying to extend life is anti-evolution for our size – whales are the top predator in their food chain and live 300 to 500 years, or see elephants.

This data suggests that homeostatic maintenance of the body post-maturity is tied to an epigenomic clock process! As such, if plasma fraction treatment’s rejuvenating effect is mediated through the process of development and involves tissue stem cells, then its effect on the epigenetic age of the brain would appear to be modest, which indeed it does. It is to be noted, however, that improving brain function does not depend on neurogenesis as much as it does on synapse formation and factors such as NMDA receptors which decline in density with age.

Clinical suggestions are there for brain, heart, lung, and liver in that inflammation markers (IL-6 and TNF-α) went down and stayed down, and Nrf2 went up and stayed up. The rats became young and had the chemistry of the young, not just improved age markers! It is this that excites me so much!