[extropy-chat] Re: Kurzweil and aging

[Lifespan Pharma/Morris Johnson CTO]

Robert Bradbury wrote:

>
> It is also true that the more fundamental test(s) are not being done.  
> They aren't measuring overall rates of DNA mutation in the nuclei or 
> mitochondria of long-lived somatic cells (brain, heart and many other 
> tissues and organs).  Nor are they measuring  overall mitochondrial 
> efficiency (which has recently been demonstrated to decline 
> significantly with age).
>
> The markers Ray is discussing are at best secondary indicators of 
> biological age.  I haven't gotten to that part of TSIN yet -- but I 
> suspect that Ray may totally avoid whether or not aging has the same 
> characteristics of the exponential growth curves he discusses in so 
> many other areas.  Ray may still be in the relatively "flat" part of 
> the aging acceleration curve while the people he is comparing himself 
> with (the general population) may be in the more exponential part of 
> the curve.
>
> One should remember that I believe Ray is treating diabetes (or 
> tendencies towards diabetes) in a very aggressive fashion if he is 
> following the lifestyle suggested in the books he has published.  If 
> he is keeping his blood glucose levels relatively low then he is 
> keeping his insulin levels relatively constant which is going to 
> minimize the energy resources (and as a secondary effect the free 
> radical production) in most of the tissues in the body.  Many pieces 
> of experimental evidence are now pointing at this approach as being a 
> form of pseudo- caloric restriction.  If that is accurate one would 
> expect him to be aging more slowly than the average population.  But 
> it doesn't extend into 350 year lifespan projections *unless* you have 
> the means to either (a) replace all of the damage which is 
> accumulating in the DNA in the cells of somatic organs; (b) replace 
> the organs entirely; or (c) "patch" the organs with stem cell 
> supplements.  And (c) is an "iffy" proposition as there is cell loss 
> in the brain and replacement stem cells are not going to be able to 
> recover the stored knowledge/thought patterns which are lost when 
> cells die very easily.
>

http://appft1.uspto.gov/netahtml/PTO/srchnum.html

http://appft1.uspto.gov/netacgi/nph-Parser?TERM1=20050226942&Sect1=PTO1&Sect2=HITOFF&d=PG01&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.html&r=0&f=S&l=50

http://appft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PG01&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.html&r=1&f=G&l=50&s1=%2220050226942%22.PGNR.&OS=DN/20050226942&RS=DN/20050226942

United States Patent Application 20050226942
October 13, 2005

Compositions for alleviating inflammation and oxidative stress in a mammal 

"[0164] Aging

[0165] Aging is a remarkably complex process that has managed to remain 
relatively opaque to scientific understanding. There is now evidence 
that aging is a series of processes, i.e., a series of controlled 
mechanisms, and not just the passive accumulation of wear and tear over 
the years. If aging is a series of processes, some of these processes 
are potentially controllable, or at least modifiable. One of the most 
important of these processes is comprised of an accumulation of the 
molecular injuries that are mediated by free radicals and other ROS. 
Recent studies indicate that the therapeutic manipulation of ROS 
metabolism can actually extend the total life span of mice to a 
significant degree. The maintenance/increase of antioxidant potential by 
administering the compositions of the present invention to a subject 
can, therefore, prevent or treat age-mediate injury."

"[0107] In one aspect, the invention provides a method of increasing the 
antioxidant activity level of a mammalian subject in need thereof, by 
increasing the level of enzyme activity of at least one enzyme, e.g., 
superoxide dismutase; catalase; and glutathione peroxidase, by 
administering to the subject an effective amount of an 
antioxidant-promoting composition of the invention, wherein the 
increased enzyme activity decreases the tissue damage caused by 
pathological free radicals. In one embodiment, the tissue damage caused 
by pathological free radicals occurs in a mammalian subject with a 
disease or condition selected from the group which includes, e.g., 
inflammation; infection; atherosclerosis; hypertension; cancer; 
radiation injury; neurological disease; neurodegenerative disease; 
ischemia/reperfusion injury; aging; wound healing; glutathione 
deficiency; acquired immunodeficiency syndrome; sickle cell anemia; and 
diabetes mellitus. In one embodiment of the method, the 
antioxidant-promoting composition is administered as an oral dietary 
supplement. "


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