3 replies to this topic

[Crepulance]

From Longevin site.

http://www.longevine.....20Upon Dosage

[geddarkstorm]

From Longevin site.

http://www.longevine.....20Upon Dosage

"Later it was shown the lifespan of laboratory mice on this dose (1565 mg) was shortened when placed on a standard calorie diet. [Cell Metabolism 2008 Aug; 8(2):157-68]"

I so want to strangle them with that very paper they are saying says that when it doesn't. Man these people tick me off at times, such BS.

As for the rest of the article, it's about a paper that was published a few months ago: PMID: 18789672. The study is interesting. Rats have a heart rate around 300 bpm, they are fed resveratrol, dissected, and their hearts are used isolated from the body for the study (might have been cut out). The hearts were then left without adequate blood supply for 30 minutes (ischemia). That's about 9000 heartbeats, and for a person that would equal ~128 minutes. I don't know if heart attacks last 128 minutes, all the medical stuff I've seen says the actual attack lasts only a few minutes at most.

But, considering mice given 400 mg/kg of resveratrol, rather than the lower 50 mg/kg in this study, are completely fine heart wise and show markably increased health of arteries.. probably don't have to worry about having a heart attack in the first place. And if your heart stopped long enough to simulate an ischemia equal to the rats, then, well, your brain would be quite dead, so the effects of a high dose of resveratrol hurting your heart a little bit would become moot.

That's just how it seems to me, and I won't pass it off as anything but my opinion. But boy, those longevinex people sure love to ham it up.

[Anthony_Loera]

geddarkstorm

I was looking at it from the ethanol dissolved resveratrol they appear to use, which you can't compare to res in supplements...

but your post throws a new light on this.


A

[maxwatt]

Here's the abstract from another one of the studies BS cited in his Longevinex press release. Resveratrol is not mentioned. They studied up-regulation of Sirt1 by using transgenic mice with heart-specific over-expression of Sirt1 which they stimulated by "pressure overload and oxidative stress". This has nothing to do with humans taking resveratrol; it is highly unlikely to get such an increase -- 12 fold,-- a mere 7.5 fold was still beneficial -- with resveratrol, which restores youthful levels if we are lucky. The entire paper is available free here: http://circres.ahajo...ull/100/10/1512 (I also think the damage, akin to congestive heart failure, may have been caused by the formation of rigid microtubels in heart muscle cells when enlarged by stress, as found in studies at the Gazes Cardiac Research Institute.) To increase Sirt1 expression, they increased stress on the rats' hearts, which eventually caused the hearts to enlarge to the point of failure from the acquired rigidity of the enlarged cells. Had they had another way to increase Sirt1 expression, they likely would have had quite different results.

The press release is polemic, not reliable science.

Circ Res. 2007 May 25;100(10):1512-21. Epub 2007 Apr 19.
Comment in:
Circ Res. 2007 May 25;100(10):1396-8.

Sirt1 regulates aging and resistance to oxidative stress in the heart.
Alcendor RR, Gao S, Zhai P, Zablocki D, Holle E, Yu X, Tian B, Wagner T, Vatner SF, Sadoshima J.

Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, University of Medicine & Dentistry of New Jersey, New Jersey Medical School, Newark, NJ 07103, USA.

Silent information regulator (Sir)2, a class III histone deacetylase, mediates lifespan extension in model organisms and prevents apoptosis in mammalian cells. However, beneficial functions of Sir2 remain to be shown in mammals in vivo at the organ level, such as in the heart. We addressed this issue by using transgenic mice with heart-specific overexpression of Sirt1, a mammalian homolog of Sir2. Sirt1 was significantly upregulated (4- to 8-fold) in response to pressure overload and oxidative stress in nontransgenic adult mouse hearts. Low (2.5-fold) to moderate (7.5-fold) overexpression of Sirt1 in transgenic mouse hearts attenuated age-dependent increases in cardiac hypertrophy, apoptosis/fibrosis, cardiac dysfunction, and expression of senescence markers. In contrast, a high level (12.5-fold) of Sirt1 increased apoptosis and hypertrophy and decreased cardiac function, thereby stimulating the development of cardiomyopathy. Moderate overexpression of Sirt1 protected the heart from oxidative stress induced by paraquat, with increased expression of antioxidants, such as catalase, through forkhead box O (FoxO)-dependent mechanisms, whereas high levels of Sirt1 increased oxidative stress in the heart at baseline. Thus, mild to moderate expression of Sirt1 retards aging of the heart, whereas a high dose of Sirt1 induces cardiomyopathy. Furthermore, although high levels of Sirt1 increase oxidative stress, moderate expression of Sirt1 induces resistance to oxidative stress and apoptosis. These results suggest that Sirt1 could retard aging and confer stress resistance to the heart in vivo, but these beneficial effects can be observed only at low to moderate doses (up to 7.5-fold) of Sirt1.

Edited by maxwatt, 21 December 2008 - 05:04 AM.