Aging and diseases – video blog

Everyone knows that old age can lead to many diseases and problems.  And sooner or later one of those diseases or problems will kill everybody.    But, what exactly is the relationship of aging to diseases?  The question leads to surprisingly interesting answers.

First, please have a look at this video for opinions of some prominent scientists:

Here, I address the points in the video and expand on several key related points. 

Aging increases the probability of multiple diseases and conditions which enhance the probability of death, and the rate of increase accelerates with age. 

Nobody dies of old age per-se but most everybody will die from a disease or problem of old age.  In the video Dr Guarante mentioned several disease susceptibilities that increase radically with aging including the biggies of cancer, heart disease, dementia and diabetes.  And there are many other conditions of aging that also lead to disability and death. For example, loss of eyesight and hearing can lead to automobile accidents.  Age related neurological and muscular changes can affect balance and body control leading to falls that create serious damage, disabilities and more imminent death.  Among trauma patients “Increasing age was associated with higher mortality, an increased proportion of falls and fatal head or spine injuries(ref).”

Increasing lifespans implies increasing healthspans.

Animal experiments with multiple species ranging from roundworms to fruit flys to mice indicate that interventions that radically increase lifespans have a similar effect on healthspans.  See, for example, the blog entry New extraordinary longevity lessons from the nematode which chronicles how researchers over 20 years have managed to discover interventions that multiply both the lifespans and healthspans of nematode worms (C-elegans) by a factor of over seven. 

In humans the ratio of healthspans to lifespans has been historically increasing, not decreasing.     

We are not only evolving to live longer(ref)(ref) but also the proportion of our life spent in a healthy state is increasing.  This is the gist of the message in the 2004 publication CHANGES IN THE DISPARITIES IN CHRONIC DISEASE DURING THE COURSE OF THE TWENTIETH CENTURY by the Nobel-Prize winning economist Robert W. Fogel.  This fact is contrary to the fear that extending lives will lead to longer and longer periods of disability and skyrocketing medical costs. If this tendency were to continue long enough we could approach the state of the “One hoss shay” where most of us live full healthy active lives until one day we simply drop dead.  Personally, I intend to be one of those. 

Interventions that increase our lifespans might be the most direct approach to addressing most diseases of old age

The major diseases of aging occur in the biomolecular architecture or “remodeling” that occurs with advancing age in individuals on the organ, cellular, proteomic and epigenetic levels.  An age-related disease like Alzheimer’s Disease (AD) is not due to a bacterial bug that could be cured with any conceivable antibiotic.  Rather, the disease is associated with multiple and complex changes in gene expression, cells and tissues that go with aging.  So far, despite billions of dollars spent on research on AD, there is still nothing approaching being a cure.  See my May 2010 blog entry Alzheimer’s Disease research update.  (I am, by the way, currently working on an update reflecting the vast recent research efforts being devoted to AD.)

In animal models, an intervention that increases lifespan tends to postpone all of the disease susceptibilities and problems that occur with aging.  They still happen, but happen later.  This has led to a simple but powerful hypothesis:

The best way to get at most intractable diseases of aging is to go first after aging itself.    

Along with some highly respected researchers I very strongly suspect that if in fact a cure for AD is found, it will turn out also to be an anti-aging treatment.  Supportive of this point is the July 2010 publication SIRT1 Suppresses β-Amyloid Production by Activating the α-Secretase Gene ADAM10.  On the one hand “Our findings indicate SIRT1 activation is a viable strategy to combat AD and perhaps other neurodegenerative diseases.”  On the other hand SIRT1 activation is activation of the calorie restriction pathway known to be life-extending for a wide variety of species.  I will say more about this particular research when I write next about AD research.  This research, incidentally, originated in Dr Guarante’s lab at MIT, the Glenn Laboratory for the Science of Aging.

Finding a cure to a single disease of old age may or may not by itself have a big effect on average lifespans. 

If such a cure addresses epigenetic factors related to aging, such a cure might indeed increase average lifespans(ref).  And I believe that for aging-related diseases, any approach to a cure that does not address the epigenetic factors is doomed to fail.  That is why I am optimistic that a good chunk of the $31.2 billion currently being spent by the NIH on medical research may turn out to be research on aging – even if it is now labeled as cancer, dementia or other research(ref). 

Many of the current anti-aging interventions like use of Rapamycin were discovered accidentally, and I expect that pattern to continue.  Rapamycin was discovered from a random soil sample on Easter Island, an island known by locals as “Rapa Nui.”  That is how the drug got its name.  Later the mTOR gene was discovered because it was the gene that most reacted to rapamycin.  mTOR stands for “mammalian target of rapamycin.  And a little later yet it was discovered that inhibiting mTOR via rapamycin was life-extending across many species.  And now, rapamycin and the mTOR pathway are the subjects of intense research mainly addressed at curing diseases(ref).”