The diminishing returns of reactive medicine

In an article for Slate, Jay Olshansky argues in favor of a position that one would expect to be common sense at this point:

While we can extend life in aging bodies through behavioral improvements and medical treatments, the time has arrived to acknowledge that our current model of reactive medicine, of trying to treat each separate disease of old age as it occurs, is reaching a point of diminishing returns.

So what is the reason why vast amounts of money are spent on research to treat age-associated diseases but so little on eliminating or mitigating aging as such? Why is this “one-disease-at-a-time model” so dominant? One reason might be that most people believe that overcoming one specific manifestation of aging is easier to do than overcoming aging itself. Not surprisingly, most academic and commercial research is shaped by short term ambitions or short-term financial interests.

Many people who deal with serious age-associated diseases hope that a cure can be found within their lifetime.  This is not so strange if you consider that many people who do advocate meaningful rejuvenation research are technological optimists who think the same thing about overcoming aging. In that sense, people show little interest in supporting research that has little personal benefit to them or close relatives. This is further evidenced by the fact that people are more inclined to contribute to anti-aging efforts that promise benefits in their lifetime. This in turn provokes criticism from mainstream scientists of not being realistic, which further discredits the field.

But as Olshansky indicates, the diminishing returns of the approach to just fight the symptoms of aging should force people to change perspective. Olshansky also observes  that “manufacturing survival time in the absence of decelerated aging” can produce a lot of hardship and suffering in old age:

It’s important to acknowledge the fundamental differences between disease and aging. Although age-associated changes in the body produce an increased risk of disease, the reverse is not true. That is, reducing the risk of disease has no influence on biological aging. Thus, if a population is preserved with increasing efficiency by advances in technology that reduce the risk of disease, those saved will live into increasingly later sections of the lifespan where aging takes a greater toll on body and mind. Life extension achieved in this way could extend old age by exposing survivors to the high-risk conditions of frailty that are common, and largely immutable, near the end of life—the very outcome that medicine and public health practitioners are trying to avoid.

For people who have made cryonics arrangements, there is another danger; the possibility of life extension at the price of increased vulnerability to identity-destroying diseases.  There is no shortage of cryonics patients with Alzheimer’s or impaired brain function. As much as we would like to deny it, there could be a disturbing trade-off between life extension and true personal survival as long as treatments for neurodegenerative diseases are not available.

"Scientific Justification of Cryonics Practice" in Russian

Danila Medvedev has translated Ben Best’s  article “Scientific Justification of Cryonics Practice” into Russian. The translation is available on the KrioRus website. The original Engish article was published in Rejuvenation Research and is available as a PDF file at the Cryonics Institute website.


Very low temperatures create conditions that can preserve tissue for centuries, possibly including the neurological basis of the human mind. Through a process called vitrification, brain tissue can be cooled to cryogenic temperatures without ice formation. Damage associated with this process is theoretically reversible in the same sense that rejuvenation is theoretically possible by specific foreseeable technology. Injury to the brain due to stopped blood flow is now known to result from a complex series of processes that take much longer to run to completion than the 6 min limit of ordinary resuscitation technology. Reperfusion beyond the 6 min limit primarily damages blood vessels rather than brain tissue. Apoptosis of neurons takes many hours. This creates a window of opportunity between legal death and irretrievable loss of life for human and animal subjects for cryopreservation with possibility of future resuscitation. Under ideal conditions, the time interval between onset of clinical death and beginning of cryonics procedures can be reduced to less than 1 min, but much longer delays could also be compatible with ultimate survival. Although the evidence that cryonics may work is indirect, the application of indirect evidence is essential in many areas of science. If complex changes due to aging are reversible at some future date, then similarly complex changes due to stopped blood flow and cryopreservation may also be reversible, with life-saving results for anyone with medical needs that exceed current capabilities.

Ben Best on nuclear DNA damage and aging

The June 2009 issue of Rejuvenation Research features an article by Cryonics Insitute President Ben Best about the involvement of nuclear DNA damage in the aging process:


This paper presents evidence that damage to nuclear DNA (nDNA) is a direct cause of aging in addition to the effects of nDNA damage on cancer, apoptosis, and cellular senescence. Many studies show significant nDNA damage with age, associated with declining nDNA repair, and this evidence for the decline of nDNA repair with age is also reviewed. Mammalian lifespans correlate with the effectiveness of nDNA repair. The most severe forms of accelerated aging disease in humans are due to nDNA repair defects, and many of these diseases do not exhibit increased cancer incidence. High rates of cellular senescence and apoptosis due to high rates of nDNA damage are apparently the main cause of the elderly phenotype in these diseases. Transgenic mice with high rates of cellular senescence and apoptosis exhibit an elderly phenotype, whereas some strains with low rates of cellular senescence and apoptosis show extended lifespan. Age-associated increases of nDNA damage in the brain may be problematic for rejuvenation because neurons may be difficult to replace and artificial nDNA repair could be difficult.

HT Longevity Meme