Has anyone here tried Longevinex?  (i was told by someone long ago that Dr Myers recommends it, but cannot recall context.)

 

-Shel

Subject: Dose determines whether resveratrol
produces longevity or kills cancer
All followers of resveratrol science take note! In
the study abstract below, researchers describe how
resveratrol affects the cell cycle, that is,
cellular events leading to its division and
duplication (replication) . The S-phase (synthesis
phase) of the cell cycle is when DNA synthesis or
replication occurs.

In modest doses, resveratrol causes the S-phase cell
cycle to proceed in slow gear, giving more time for
DNA to be repaired, producing longevity. In mega-
doses, resveratrol accelerates the S-phase cell
cycle and increases cellular death, thus inducing
mutated tumor cells to die (apoptosis).

Advice to consume mega-dose resveratrol (more than
300 mg) appears to be ill advised. Other studies
confirm that mega-dose resveratrol (as little as 360
milligrams for a 160 lb human) shortened the lives
of laboratory animals on a standard calorie diet.

The widespread false notion that the equivalent of
1000 glasses of red wine is needed to produce the
same effect as pure resveratrol in the laboratory
should be dismissed. It has been shown that 3-5
glasses of red wine, providing 180-300 mg of daily
polyphenolic molecules (resveratrol, quercetin,
ferulic acid, malvidin, catechin, kaempferol, gallic
acid) produces unusual health and longevity in
French wine-drinking populations. Copyright 2009
Bill Sardi, Resveratrol Partners LLC

For the full text of this report, email Bill Sardi at
bsardi@...


British Journal Pharmacology 2009 Jun 25. [Epub
ahead of print]



Induction of a reversible, non-cytotoxic S-phase
delay by resveratrol: implications for a mechanism
of lifespan prolongation and cancer protection.
Zhou R, Fukui M, Choi HJ Zhu BT.
Department of Pharmacology, Toxicology and
Therapeutics, School of Medicine, University of
Kansas Medical Center, Kansas City, KS, USA.

Background and purpose: Resveratrol (RES) has been
shown to prolong lifespan and prevent cancer
formation. At present, the precise cellular
mechanisms of RES actions are still not clearly
understood, and this is the focus of this study.
Experimental approach: Using human hepatocellular
carcinoma-derived HepG2 cells as a model, we studied
RES-induced changes in cell growth, cell cycle
progression and apoptosis (death). Key results:

RES at lower concentrations induced a strong but
reversible S-phase delay and mild DNA synthesis
inhibition, yet without causing apoptotic or
necrotic cell death.
At high concentrations, RES induced apoptosis (cell
death), which is mainly mediated by the
mitochondrial pathway.
Overall, RES was a relatively weak apoptotic agent.
Mechanistically, MEK inhibition was identified as an
important early signalling event for RES-induced
apoptosis. In comparison, activation of CDK2 and
checkpoint kinase 2, and inhibition of
phosphatidylinosito l 3'-kinase/Akt signalling
pathway contributed to the induction by RES of a
reversible, non-cytotoxic S-phase delay. Conclusion
and implications: It is hypothesized that the
induction of a non-cytotoxic S-phase delay may
represent a useful mechanistic strategy for lifespan
prolongation and cancer prevention. When cell cycles
are selectively slowed down in the S phase, it would
cumulatively increase the total lifespan of an
organism if the total numbers of cell divisions of a
given organism are assumed to remain basically
constant. Likewise, when cells proceed through the
cell cycles at a reduced pace during DNA
replication, it may allow cells more time to repair
the damaged DNA, and thereby reduce the chances for
mutagenesis and tumor initiation.



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