I am 65yo and have been taking c60 with some regularity for a few years but have not noticed any positive or negative effects. The original studies offered a number of possible benefits, such as increased lifespan, hepato-protection, and less susceptibility to tumors, if the results are translatable from rats to humans.
I recently came across a blog entry in the excellent website “anti-aging firewalls” written by Jim Watson and Vince Giuliano. In it, there is a proposed mechanism as to why we live longer than rats and get less tumors. This may all be related since most rats die from tumors. I have copy/pasted several relevant excerpts from the blog below. But it essentially has to do with the activity of “TEs, ” transposable elements that are linked to cancer and aging. Rats have more active TEs. If c60 could somehow limit the activation of TEs it occurs to me that it would increase their lifespan and reduce tumor formation. However, and this would be KEY, since our genomes ALREADY have this as a feature, the effect on mice might not be applicable to us! I’d like to hear the thoughts of others on this. Because, if so, c60 might not be doing us any good, and any risks might not be worth taking.
“A transposable element is a segment of DNA with inverted terminal repeats at each end that can excise or copy itself and move from one location to another within or between chromosomes, plasmids, or phage. Not only can some TEs copy their own genomes — they can also copy and paste parts or wholes of adjacent human genes.
Most TEs in humans are no longer active although still present in our DNA and making up about half of our genome. The vast majority of these are no longer active as a result of cumulative mutation, truncation, internal rearrangement and silencing. However, it is estimated that approximately 100 of L1s TEs per nuclear genome still retain their replication activity.
Cancer cells and certain other diseased cells have very high levels of TE expression, especially cancer cells that have progressed to late stages of chemotherapy and radiation resistance.
Human endogenous retroviruses (HERVs) are TEs, but though they make up a great deal of our genome they are largely inactive as viruses.
TEs are highly likely to play major roles in aging. There is widespread agreement that genomic instability and DNA damage are key features of aging – and TEs cause both. Although the research on this topic is not completely definitive yet, it may well turn out to be the case that TEs are more important for aging in elderly people than the “usual suspect” pathways like IGF-1 and mTOR.
Global hypo-methylation associated with aging leads to activation of TEs.
As to keeping TEs silent, we humans are much better at this than lower animals, and this might be a big part of explaining why we live longer.
1. There are Over 2 Million Copy Machines in your Genes, but only 80-100 still work (they are all LINE-1s)
2. Short-lived organisms are more permissive to retrotransposition, whereas long-lived organisms are resistant to retrotranspostion.
11. Cancer is manifested by dramatic increases in transposable element expression
21. Retrotransposon activity is likely to be a MAJOR cause of aging
There are 98,000 fragments of leftover “fossil viruses” in our genomes (HERVs) but none are capable of “self-copying” themselves. In rodents, however, there are many mouse endogenous retroviral elements (MERVs) that are “active” and capable of retrotransposition. This is one of the major genetic differences between “mice and men” and may partially explain why TE insertional mutagenesis in rodents is 100-fold higher than in humans. Likewise in mice several MERVs are very similar looking to exogenous, infections mouse retroviruses (This is why many viruses cause tumors in mice and rats). The fact that LTR-retrotransposons cannot copy themselves in humans is surprising, since HERVs make up 8-9% of the human genome (in terms of DNA base pairs). When transposable elements cannot copy themselves, they are referred to as being “non-autonomous”, which HERVs are in humans (but not rodents). This difference between humans and rodents may be a major reason why we live so much longer than rodents.”