The issue till today was understood and solve conflict between NMN, NR, or direct NAD+ etc. A non-natural predecessor to NAD+ has been reported tb better than NMN.
Reduced Nicotinamide Mono-nucleotide (NMNH) Potently Enhances NAD+ and Suppresses Glycolysis, the TCA Cycle, and Cell Growth.
First read the abstract, Then a check - no bias to grind etc. The answer seems to be NMNH alter long analysis of empirical data on use, particularly data on intravenous route and Dr. Sinclair speeches and use on self and family. The molecule proved to be highly efficient and fast in increasing cellular NAD+, largely surpassing the effect of NMN in every cell line tested. In fact, while NMN was only able to double cellular NAD+ at its maximum concentration (1mM), NMNH led to a 3- fold NAD + increase even at 50µM. The response to NMNH was also faster, as 15minutes were enough for NMNH to almost double basal NAD+, with maximal effects after 6 hours, which remained stable even 24hours after supplementation.
All methods for increasing NAD+ bad?
There are critical voices, particularly this doctor. He believes, as I do, in programmed theories of aging which hold that all chemical processes in the human body had useful purposes before mating and became bad with advancing age as that effect is not evolutionary and hence has no evolution purpose. But not all natural processes are good or inevitable. Some chemicals as CD38 are BAD.
What is behind empirical loss in NAD+ that has been documented? It turns out CD38 concentration increases in step and CD38 and NAD+ are enemies! What is the role of CD38? It is produced by senescent cells and destroys NAD+ in nearby cells. CD38 is a marker that attract immune cells that kill the nearby cells from the fact they marked foreign objects. Sounds good, except that NAD+ was inflaming them and CD38 put off that fire. Explains the empirical finding that NAD+ declines with age and CD38 levels increase.
What happens if NAD+ levels are somehow boosted, NAD+ driven fireworks increase, so more CD38 is needed and that worsens the aging. Instead of improving aging, the NAD+ increase increases aging.
I happen to disagree but publicize a well argued other side and point out that I will add anti-CD38 agents to my TPE. I do not think that NAD+ becomes bad as one ages, hence growing CD38 is a curse, not a heroic act by senescent cells.
No age fix in my time?
Most
people are certain
that there is no singularity in their lifetime, even if they live
past 2030. This is not
the conclusion of those who read the stuff related to this issue
but of all the others! And I think that till
2040, people will be bombarded with information on how to benefit
from possibilities of cure,
including reconstitute
of new inspector-raj
in India
and no sane way of distinguishing between sane and insane sellers!
This is the calm before the storm. Already in the USA, emfubar marketeers draw 95% of people to useless brands by
glowing anecdotal
reports. Slow or not, only FDA can shield from free markets! But
that slowness is wrong for aging. What is more, advertiser
goons have discovered ways of politicians and courts to delay and
kill FDA regulators. And all these
shark attacks have some
abused truth! Like all advertising using anecdotes, selective bias is persistent. People using selection bias are not advertising professionals, politicians and other professionals, but severe criminals.
There has also been a lot of excitement over the work of Drs. Irina
and Michael Conboy who have spent over a decade exploring factors in
young and old blood which spur or prevent regeneration respectively.
They have conducted a number of animal studies suggesting that there are
a handful of factors in aged blood which prevent tissue regeneration in
older individuals and most importantly, when these factors are blocked
or removed, tissue regeneration resumes as it did during youth. This
suggests it may be possible to “reset” the signature of aged blood and restore it to a more youthful state. The technology to filter pro-aging factors from our blood already exists too, which means this could reach humans fairly soon.
A second very big reason is the rise of a very important side effect - rejuvenation biotechnology. BEYOND ARRESTING THE EFFECTS OF adverse medical events IN PERSISTENT DISEASES, time is ripe for aging based attack on persistent diseases like diabetes by tools different from usual doctors by chasing doctors conversant with benefits of these, certainly not non-allopathic medicine, but new aging medicine and its rejuvenation biotechnology.
Senolytics
This word was invented by Dr. Aubrey de Grey, used in 2001 to describe one of 7 ways he would attack aging. Cellular senescence is a response to damage or stress in which cells stop dividing and undergo a range of other changes. Senescent cells also secrete a cocktail known as the senescence-associated secretory phenotype (SASP), which includes inflammatory factors such as cytokines as well as growth hormones, protease, and other molecules. The SASP has a variety of local and systemic effects, and it is involved in both wound healing and chronic inflammation. It is known to maintain senescence in senescent cells and to signal for senescent cell clearance by the immune system. The fact that senescent cells become more common with age led researchers to begin developing drugs to target them; these drugs are known as senolytics.
SRF’s Chief Science Officer, Dr. Aubrey de Grey, recently estimated a 50% chance that aging could be brought under medical control in as little as 15 years’ time. In a new interview with NextBigFuture, Dr. de
Grey explains how recent development.
Making senolysis a science?
The concept of senolysis was not based o0n any science existing in 2001. Slowly researchers began to describe their research products as senolytic. Today there exist many senolytic in FDA clinical testing. The Newest problem is that any drug, peripheral to senescence-associated secretory phenotype (SASP) can suggest that insignificant changes are senolytic. Not possible if senolysis can be measured! That makes senolysis a science. This will do it! It has found a lipid whose concentration varies with blood carried senescence cell inflaming markers. Routine lipid profile candidate. Henceforth, senolysis is no more a future science but a science. It is like Horovith clock! I want to know my senolytic age today and after an aging procedure.
Predictions?
Three now predict singularity by 2035
Very big, Dr. kurzweil at google 2029
me 2030
Very big, Dr. de Graey at SENS 2035
No comments:
Post a Comment