"We are on the verge of a revolution in medicine: understanding, treating, and ultimately preventing the causes of degenerative aging. But medical revolutions only happen if we all stand up in support of funding and research. We did it for cancer. We're doing it for Alzheimer's. We can do it for aging - and create an era of longer, healthier lives!"

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  • Thursday, January 7, 2010

    A Defense of Programmed Aging

    The view that the processes of aging are programmed fits well with the school of gerontology that believes the only viable path forward to increased human longevity is to slow down aging through the manipulation of metabolism. Changing the program, in other words. Programmed aging is one set of theories that can be built atop the evolutionary consideration of aging; that life span in any given species is what it is because of selection pressure, and some combination of biological programs that produce that life span will be selected for. But whether and to what degree aging is programmed is a hotly debated topic, with reputable researchers arguing the points on both sides. There are a good many scientists from the "slow aging" camp who don't support programmed aging theories.

    You might want to head back into the archives for the posts in which I've mentioned the programmed aging viewpoint in the past:

    Over at PubMed Steven Austad provides a good argument for considering aging as unprogrammed decay rather than a programmed process in the body. This sort of high level thinking about processes and purpose - like the reliability theory of aging - is an important part of effectively directing the research community. "Aging, except in exceptional cases such as the rapid decay and death of Pacific salmon, is not design but decay. The decay of senescence is not due to natural selection's designing hand, but to its absence. The empirical difference between programed and nonprogramed senescence becomes evident when comparing the stereotypical steps leading to death in salmon contrasted with the lack of such stereotypy in most organisms such as humans and mice." ...

    On the other side of this debate Valter Longo and Paola Fabrizio have authored a paper suggesting that aspects of aging in mammals may indeed be programmed. "Programmed human aging is just a possibility. We don't know whether it's true yet or not. But if aging is programmed in yeast, and the pathway is very similar, then isn't it possible that humans also die earlier than they have to?" This discussion is still at the level of educated hand-waving - much more work is needed to settle it one way or another. My suspicion is that the genetics and biochemistry will turn out to be more complex than a simple yes or no.

    My attention was recently directed to a website devoted to the background science that supports programmed aging. I think it's worth taking a look:

    There are two main aging concepts as applied to humans and most other mammals. The programmed aging theories, also known as adaptive or active aging theories, propose that mammals purposely deteriorate with age because a limited life span provides evolutionary benefits. Non-programmed theories, also known as passive or non-adaptive theories, contend that a limited life span is entirely adverse and that aging is not genetically programmed for the purpose of causing deterioration or death.

    Programmed theories provide a better match to observations, but are based on newer concepts regarding evolution mechanisms. Non-programmed theories have difficulty explaining many observations but are compatible with older evolutionary mechanics concepts.

    This issue is important because most people in developed countries now die of age-related diseases. Understanding, preventing, and treating these diseases requires that we understand the aging process.

    I agree with the general sentiments on the importance of aging research. However, I don't see that the evidence for programmed aging theories is as good as the author believes it to be, nor that a full understanding of aging is required to prevent and treat age-related diseases. The debate over programmed aging is yet another example of the way in which Aubrey de Grey's SENS approach shines by cutting straight to the desired goal of extending life. The scholarly divisions over theories of aging will continue for the foreseeable future, as thousands of researchers add their individual contributions to our knowledge of aging human biochemistry. But if instead of working on full understanding, we rather aim to identify and reverse all the specific age-associated biochemical changes that are the root cause of degenerative aging, then for this purpose it doesn't matter whether aging is programmed or not.

    As outlined at the SENS Foundation, we can be reasonably certain that all the biochemical causes of aging that are important across the present human life span have been identified for more than 20 years. No new root causes in our biochemistry have been discovered in that time, despite a blossoming of biotechnology. Further, researchers presently know enough to outline ways to reverse all of these changes, and the required research and development programs are in some cases already underway. Advances in our general knowledge of aging and metabolism should generally be helpful - there's no such thing as useless knowledge in the life sciences - but are not required for progress at this point. If a resolution on programmed versus non-programmed aging occurred tomorrow, it would make no difference to the SENS approach to reversing aging.

    Posted by Reason

     
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    Posted by: kurt9 at January 8, 2010 1:20 PM

    I have always thought that the programmed aging theories were bunk. In any case, you are correct that whether aging is programmed or not is irrelevant to the development of SENS.

    [Posted by: kurt9 at January 8, 2010 1:20 PM]

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