The Longevity Medical
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Recommended reading:
A newly-published call-to-arms and technical exposition on the SENS approach to age-related disease
An early study of one of the seven targets of SENS research
What to do in the meantime:
Full of diet and lifestyle tips based on current science, to preserve your health until better technology is developed

Only 7 Pathogenic Age-related Precursors: Chromosomal Mutations


Two of the seven early precursors of age-related pathology are chromosomal and mitochondrial mutations.

In the former, a single cell needs only a few mutations to kill us, because of the exponential growth of cancer cells. The latter however is usually benign, but also can reach a threshold which leads to a cascade of damage.

Chromosomal mutations can be divided into those that lead to cancer and those that don't.


Cancerous Chromosomal Mutations


LMRF won't be providing financial support for research targeting cancer, despite its being the #2 leading killer in the country. The early promises from a decade ago of antisense RNA (aRNA) therapy are now being realized in the clinical setting and approaching approval for a wide array of malignant cancers. Unlike the preventative nature of SENS strategies in general, aRNA therapy treats the pathology after it arises. While SENS does have a strategy for cancer, it relies on gene therapy not yet developed and will take over a decade to bring to clinical trials, where aRNA therapy is also achieving great (and effectively equivalent) success.

(This is not to say that a SENS strategy for cancer shouldn't eventually be developed. After all, even the best post-symptomatic treatment of cancer would still have to be applied with increasing frequency as one gets older and an increasing number of one's cells accumulate pre-cancerous mutations. A preventative cancer strategy as outlined in SENS may become preferable beyond a certain age.)


Non-cancerous Chromosomal Mutations


Most mutations inside a single cell nucleus won't kill us. Cancer is particularly deadly because of the relevant mutation's exponential rate of growth. But it always starts with just one cell, and that cell has to have the right (or wrong) set of mutations and to divide before they are corrected. Therefore, our cells have developed several mechanisms for very effectively repairing mutations to prevent this from happening. As a result, mutations that don't enjoy unrestrained growth don't have anywhere near the opportunity to wreak lethal havoc in a normal lifespan (thus the premise of SENS that the ill effects of aging are mostly of extra-nuclear origin, affording accessibility for therapeutic intervention).

It may be learned around year 2100 that the first 150-year-olds (assuming they're 50 years old today) are strongly affected by non-cancerous chromosomal mutations. Probably by then, some approach to enhance mutation correction would be developed. We have a century to work on it after all.