[ExI] Product B

The Avantguardian avantguardian2020 at yahoo.com
Wed Apr 11 10:03:04 UTC 2012


----- Original Message -----
> From: Kryonica <kryonica at gmail.com>
> To: The Avantguardian <avantguardian2020 at yahoo.com>; ExI chat list <extropy-chat at lists.extropy.org>
> Cc: 
> Sent: Wednesday, April 11, 2012 12:26 AM
> Subject: Re: [ExI] Product B
> In his video Andrews stresses that tests had shown that telomerase activators 
> (he quoted the 3 products available, T65, Product B and one other) decrease the 
> proportion of short telomeres in only a few months.  The conclusion he draws is 
> that the telomeres are shortened at a slower pace, and therefore that 
> teleomerase "activator is actually doing its job by protecting cells during 
> cell division from shortening their telomeres.  The mechanism is allegedly that 
> telomerase activator activates telomerase and that consequently telomerase adds 
> a telomere to the chromosome during or after cell division to replace the one 
> lost in cell division.  And so the cell can divide without shortening.  If this 
> is true, then one's next question is : does preserving telomere length on 
> chromosome keep one biologically younger?  Most likely is that telomere length 
> is just ONE aspect of ageing.  And actually Andrews says that but he does stress 
> that it is an important one;  so he takes his Product B.

Actually the only product that has been tested is T65. He talked about *plans* to test Product B
 
Alright I finally found the time to look up the paper on T65:
 
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045570/pdf/rej.2010.1085.pdf
 
 
The in vitro data on low to mid passage fetal cells (foreskin keritinocytes and lung fibroblasts) shows significant telomerase activation but those are cells that are coming from very young subjects. The clinical data in fig 3. is less exciting. In fig 3A, the average telomere length seems to have increased in some patients and decreased in others. So I can't draw much of a conclusion with regard to mean telomere length. Now the percentage of short (defined as less than 4kb) telomeres in fig 3B seems to show a more consistent effect, however you need to be careful interpreting this. All you know is that patients taking the supplement seem to have the same average telomere lengths as people who did not but the minimum telomere length in patients that took the supplement is longer.
 
There are two ways to interpret this data. One is that the supplement selectively increases the telomere length only in cells that have short telomeres. The other way of interpreting it is that taking the supplement *kills* cells with telomeres shorter than 4 kb, so all you get from the patient are average-lengthed telomeres. Looking at their methods, I don't see any aspect of their protocol that could have controlled for the "weeding out" of cells with short telomeres. Since I seem to recall that telomerase, which in humans interacts with a staggering array of other proteins, is thought to be involved in apoptotic pathways for "cellular suicide", this second explanation is certainly possible.
 
Too bad Sierra Biosciences said they couldn't afford to hire me when I applied for a job there a couple of years ago, I might have been able to design an experiment to rule out that possibility. But then again, Dr. Andrew's staff wouldn't let me talk to the man personally. Of course negative results don't get grants, attract investors, or sell product. See the "medical research" thread for a good discussion of this phenemenon.
 
Since I am ranting anyway, allow me a further gripe about medical research as it is practiced. In order to have a career in modern molecular biology, you must take one of the most compex systems in existence i.e. the cell, choose a single gene/protein/molecule out of hundreds of thousands and become the worlds foremost expert on that single gene by discovering something about that gene that nobody else knows. The problem this poses to the scientific understanding of the cell or the entire organism on a system level should be clear. You are never going to understand a car by studying a fan-belt for 20 years.
 
What is not so clear is that no matter how mundane the gene you study is, let's say for example mucin, the key ingredient in snot, you are obliged by the system to hype, toot, and spin it as the end-all-be-all of genes.
 
Forget all those other genes! Fund my mucin project because mucin is the most important gene in the human body! Fools, you would all die without mucus!
 
And that sort of puffery makes some people feel dishonest.     
 
 
Stuart LaForge


"The state that separates its scholars from its warriors will have its thinking done by cowards, and its fighting by fools." -Thucydides. 




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