The Scientific Debate That Will Determine How Long We All Live
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Last week, I pointed out an example of researchers who believe engineered longevity must be accomplished by gene engineering and changing the operation of metabolism to slow aging. In that worldview, any significant progress is far in the future, because the task is very complex indeed. Progress in the future is also largely irrelevant to those of us alive today, as slowing aging does next to nothing for people who are already age-damaged to the point of disease and frailty.

I consider it to be unfortunate that the bulk of the pro-longevity aging research camp is focused on an inefficient path forward that will in the end lead to lesser benefits. It is their belief that this is the only practical way ahead: a laborious slog towards complete understanding of aging and metabolism, followed by an even more complex navigation through re-engineering that metabolism to age more slowly. The sheer scale and difficulty of that task is why many scientists feel that meaningful engineered longevity - more healthy years through science - is a long way away indeed.

Fortunately there is a fast boat in addition to the slow boat described above:

It is likely to be easier and less costly to produce rejuvenation therapies than to produce a reliable and significant slowing of aging. A rejuvenation therapy doesn't require a whole new metabolism to be engineered, tested, and understood - it requires that we revert clearly identified changes to return to a metabolic model that we know works, as it's used by a few billion young people already. Those rejuvenation therapies will be far more effective than slowing aging in terms of additional years gained, since you can keep coming back to use them again and again. They will also help the aged, who are not helped at all by a therapy that merely slows aging.

Today, let me point you to another manifestation of the "we can do no better than slow aging by metabolic manipulation" viewpoint:

The extreme arrogance of anti-aging medicine:

The anti-aging medicine movement proposes to alter the human body in order to achieve extreme longevity. To do this it has to reverse or by-pass the multiple causes of human aging. These include a large number of age-associated pathologies, each of which is being studied in great detail in research laboratories around the world. The protagonists of anti-aging medicine claim that it will be far more successful than the combined efforts of the innumerable scientists carrying out this research. Aging has an extremely long evolutionary history, and the anatomical structure and physiology of animals is directly related to their finite lifespan. The anti-aging movement proposes in a few decades to reverse what has been the result of millions of years of evolution.

The above abstract is wrong-headed, to say the least, but it is an output of the sort of worldview described above: a) that aging can only be slowed, b) that doing so requires the day to day operation of human biochemistry to be changed in non-trivial ways, and c) that this is a very tall order indeed for the medical science of the forseeable future.

So, to point out the errors. Firstly, the causes of aging are not the pathologies of aging. Pathologies are end results - if dry rot is a cause, then failing wooden structural beams are the pathology. Today's prospective longevity engineers talk about causes, about the comparatively few types of biochemical damage that build up in our tissues to create many, many different forms of pathology. Dry rot can make a wooden structure fall apart in any one of a hundred distinct ways - but all are still caused by dry rot.

If you want to tackle aging efficiently - and make no mistake, this whole debate is about efficiency - then pathology is the wrong place to start. If you work on patching up pathologies, then you are Canute against the tide. By failing to stem the underlying cause, your efforts are doomed to inefficiency and ultimate failure. Present day gerontological medicine is largely playing the role of Canute because that has historically been the best medical science can do: throw a huge level of resources at treating the consequences of aging and gain little by it. That little was better than nothing for billions, but it was still little in the grand scheme of things.

We stand in the 21st century now, amidst the early years of a revolution in the capabilities of biotechnology. Scientists can move beyond the historical focus of medical technology on patching end results and instead work on prevention and repair of root causes. Taking a different, more efficient path is why new approaches to longevity engineering will succeed in greatly extending the healthy human life span where decades of scientists and vast expenditures have only slightly raised the bar. Holding out the past as an example of the future is a terrible thing to do. You are rarely going to be right, as the future will be accomplished in a different, usually better way.

I predict that the last sentence in the abstact I quoted above - "reverse what has been the result of millions of years of evolution" - will come back to haunt the author for a good many years. No-one wants to be on record as saying something as bone-headed as that. In the past few decades medical science has reversed any number of evolutionary consequences, some of which have billions of years behind them. As if the number of years a feature took to evolve has any bearing upon the development medicine that acts upon it!

The preceeding point on the structure of living beings, however, is very illustrative of the metabolic manipulation viewpoint: hammering home again that biochemistry will be very hard to re-engineer for greater longevity through slower aging. This is absolutely true, and it would be astoundingly hard to follow though that path to developing longevity therapies. Every biochemical component in our metabolism is a part of many different complex evolved systems - evolution loves reuse and interacting, linked feedback systems. You can't change a thing without having to worry about profound side-effects in every connected process, and the processes important to aging are right in the middle of the engines of life.

But the modern longevity engineers, the heretical minority in the aging research community, are not taking that path forward. Rather, they use the metabolism we have when we are young as the ideal reference model, and seek to reverse all changes away from that reference model that occur with age. No re-engineering, no worrying about how change A affects systems B, C, and D - this is a straightforward repair and restoration strategy. The objective is to restore the metabolism we know works, not create some new metabolism that must be extensively tested and understood.

That is efficiency, and the nature of efficiency in longevity research is the most important debate within the life sciences today, for all that most people know nothing of it. The result of this debate will determine how long we all live in good health.

Comments

The goal of research should be Homo Immortalis Omnipoten. The virtues we have given our god's, we will now reach for ourself.

Posted by: Alfred Schickentanz at October 11, 2010 7:57 AM

If we see that the naked mole rat, lives nine times more than similar-sized rats, and that whales can live almost two centuries, the conclusion is that no plans or sizes in this, but a question of genome and metabolism . Now there are 20 ways to extend the life of a mouse, from 10% to 60% and everyone tries to extend longevity, but why do not completely eliminate the damage?. If the only difference between a young body and an old body are: (a) levels of damage and (b) the disruption of biological systems and organs that react to the damage and we only have about 26,000 genes, should not be so difficult to get, from the age of 20 say, a cell replication without error, because the cells spend most of their time doing the same thing over and over again.

Posted by: edward at April 15, 2012 1:38 PM

Is inhibiting (apoptosis) really a good idea?.......Perhaps by inhibiting apoptosis , cancer cells mighr proliferate rather than die.

Posted by: william rice at February 20, 2014 9:44 AM
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