Aubrey de Grey’s Large Mouse Antiaging Study

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Aubrey de Grey had a large mouse study of combinations of antiaging treatments. They did show that combination treatments did have additive benefits. Combination treatments worked together to improve the lengthening of lifespans.

Rapamycin is the strongest main confirmed antiaging treatment.

His group is setting up a second experiment with new combination treatments but will add rapamycin and exercise wheels for all of the mice. The goal is try to double remaining life of the mice instead of adding about 40%.

Damage repair could be the something that could work to add 12 extra months of life to mice. Aubrey is more confident that damage repair that works in mice will also work in humans.

Extending the life of mice has been stuck for 50 years at adding 4 months.

3 thoughts on “Aubrey de Grey’s Large Mouse Antiaging Study”

  1. I have a PhD in molecular biology with a specialization in cancer and aging. The study in mice is well done, scientifically sound, and well documented (rather than some wackos that promise immortality through a secret sauce, this is a documented protocol).

    That being said, mice are not necessarily a good model for human aging.

    Every model system has advantages and disadvantages. Working with cell culture is orders of magnitude cheaper than working with animals, and among animal models, working with mice is cheaper and faster than working with primates (where a study like this one would literally take decades).

    For those interested, mice are not a good model because they are highly prolific with short lifespans. They are preyed upon by many predators, and in the wild, they would never reach an age where their health would fail. As soon as their fitness starts to decrease, they are the slowest, weakest, and least aware of a predator, so they die.
    Evolution did not select longevity in mice and they are not optimized for that, we know that because mice express telomerase in their cells, have long thelomeres, yet still age and die, so if you can fix some metabolic pathways they indeed live longer.
    But humans are not mice.
    Even before the modern demographic decline, humans are a low fertility species, due to lack of nutrition, women reached fertility later and likely could not carry more than 5-10 pregnancies (this sounds a lot but in the animal kingdom, it is not).
    With a smaller progeny, there was an advantage in investing more in the progeny, resorting to long parental care.
    Animals with long parental care (like elephants, whales, and primates) have tight social groups because it is more advantageous for the species to collectively take care of the progeny rather than letting them die if a parent dies.
    Humans were selected for longevity because it was advantageous to have some people around past their reproductive age to take care of those who remained orphans.
    But it was advantageous until a certain point.
    The key is focusing on the “until a certain point” part.
    As I said humans have a small number of children, so genetic diversification is somehow limited. While the taxing cost of childbearing (significant risk of death during pregnancy, infections, and traumas that caused sterility) and the length of the pregnancies ensured that no single female could be in a dominant reproductive position for long, promoting genetic diversity, there was the risk of a dominant alpha male being the only active reproductive element of the group, reducing genetic diversity and promoting inbreeding.
    So there was an evolutionary incentive to have humans live long, but get significantly weaker.
    We see the same in elephants: elephants do not die of old age, but of starvation because after they lose their 6th set of molars, their teeth stop regrowing, so the old elephants are not able to sustain their food intake (that requires grinding massive amounts of vegetation every day), become weaker and lose their dominant position in the group.
    We, as humans, have been built to live longer than a mouse, but we have also been engineered by natural selection to weaken and die.
    It is worth noting that for 99% of our time as a species our living conditions were so harsh that we died of old age at 35-40 years, with a very minor fraction reaching 50-60 (probably comparable to the current percentage of ultra centenarian in our modern population).
    Improving our lives reduced the “wear and tear” of our bodies so they could last longer, but at a cellular level we are programmed to GTFO after a certain amount of time, and we see it because as humans we DO NOT express telomerase, and when we reactivate telomerase the whole cellular program is screwed, and we develop tumors (there is also a 15% of tumors that do not activate telomerase, but maintain telomere length through ALT mechanism, but the final effect is the same: our cells are not meant to divide indefinitely).
    That does not mean that de Grey’s work is useless, but it solves only half of the problem, i.e., allowing life extensions of organisms that could potentially live longer, fixing cellular problems because they were not evolutionary selected for longevity.
    Evolution has already worked on the first part of the problem for us, but there is a whole other problem, which is reprogramming cells that have built-in multiple systems granting an expiration date and changing such program for every cell type in your organism, and in a synchronized way, ensuring that you do not develop tumors.

    So, let’s be optimists, but we should not hold our breaths on this one.

    Regards

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