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een paar studies, er zijn er echt massas!! lees ook mn vorige post, resveratrol is eigenlijk het enige supplement dat het echt waard is te nemen
Follow-Up Resveratrol Mouse Study Confirms Red Wine Molecule Exerts Profound Positive Effects Upon Health, But Also Produces A Surprise Finding
In a follow-up study to the widely publicized 2006 mouse/resveratrol study published in Nature Magazine (November 1, 2006), researchers now provide more complete long-term analysis of the biological effects of resveratrol as a molecular mimic of calorie restriction in animals.
The results, published in the journal Cell Metabolism, are jaw-dropping, but they also come with a surprise. Resveratrol-fed elderly mice show a marked reduction in signs of aging, including:
• Reduced albumin (a blood protein; elevated albumin often occurs with heart failure)
• Decreased inflammation
• Superior blood-vessel health
• Increased elasticity of the aorta (the first blood vessel outside the heart)
• Greater balance and coordination (motor function)
• Strikingly reduced cataract formation (even better than a reduced-calorie diet)
• Preserved bone mineral density.
But surprisingly, while supplemental resveratrol did, as previously reported, prolong the lifespan of mice who were engorged with a very-high fat diet (60% fat calories, which no human could tolerate), resveratrol did not prolong life in mice fed a standard calorie diet.
Two doses of resveratrol were employed in the mouse study, lower-dose resveratrol (100 mg/kilogram of food (or ~364 milligrams for a 160-pound/70 kilogram adult), or 400 mg/kilogram of food (~1565 milligrams for the 160-pound/70 kilogram adult). While there were no long-term detrimental effects noticed at modest doses, the lower-dose resveratrol group appeared to consistently live a bit longer in all groups than the higher-dose resveratrol groups (see chart). The authors of the paper cite another animal study which showed that 18,000 mg/kilogram of body weight (likely to be difficult for humans to even intentionally achieve) did increase mortality due to heart failure in a mouse study. So there may be decreasing health benefits with increasing dosage.
The effects of a calorie-restricted diet on longevity are diminished when the regimen is initiated at increasing ages. This drawback may be overcome by resveratrol.
Of great interest is the effect resveratrol exerted over the Sirtuin1 gene, the gene that is activated when calorie restricted diets are employed. However, “microarray data on the effects of SIRT1 over-expression in these tissues are not available, making it currently difficult to assess whether SIRT1 is a mediator of these effects,” said researchers.
Matt Kaeberlein, a noted Sirtuin gene researcher at the University of Washington in Seattle, offered his commentary, entitled “The Ongoing Saga of Sirtuins and Aging,” in an accompanying article in Cell Metabolism. Dr. Kaeberlein said:
Unfortunately, what has often been lost in reviews of the sirtuin literature and reports in the popular media are the many complexities and inconsistencies in our understanding of sirtuin biology as it relates to aging. For example, in yeast, Sir2 over-expression increases replicative life span (the span of time when a mother yeast cell produces daughter cells, but shortens chronological life span, which is a measure of the length of time a yeast cell can survive in a non-dividing state.
Multiple labs have reported that sirtuins are not always required for life-span extension from dietary restriction in either yeast or worms. What makes the study by Li et al. particularly interesting is the observation that Sirtuin1 gene inhibition causes some phenotypes (groups with inherited genetic mutations) more consistent with a slower rate of aging. For example, they show that Siruin1 inhibition leads to increased IRS-2 acetylation, decreased Insulin Growth Factor-1 signaling, and decreased Ras/ERK signaling. Decreased Ras gene signaling increases life span in yeast, and reduced insulin/Insulin Growth Factor-1-like signaling is associated with increased life span in worms, flies, and mice. Supporting the idea that inhibition of Sirtuin1 may slow aspects of aging in mice, studies show enhanced resistance to oxidative stress in neuronal cells after Sirtuin1 knockdown and reduced oxidation of proteins and lipids in brains of Sirtuin1 knockout animals.
Taken together, these data may indicate that inhibition of Sirtuin1 can be nerve-protective in aging animals and that some features of aging are slowed rather than accelerated in animals whose Sirtuin1 gene has been eliminated.
The one thing that seems clear is that sirtuin activators are unlikely to be a ‘‘magic bullet’’ for aging. A more realistic hope is that, as we continue to unravel the complexities of sirtuin biology, targeted activation or inhibition of Sirtuin1—and perhaps other sirtuins as well—will prove therapeutically useful toward a subset of age-associated diseases. Such an achievement would be a huge step forward in the transition of aging-related science from the laboratory to the clinic, and we eagerly await the next chapter in the unfolding saga that is sirtuin biology. --Matt Kaeberlein. (Cell Metabolism July 2008)
The next chapter will be written by Longevinex®, which will unveil its mouse study which measures the global-gene array effects of a calorie-restricted diet, a resveratrol-fortified diet and a Longevinex®-fortified diet. Of considerable interest, this upcoming study, to be published in Experimental Gerontology, does not show that resveratrol increases Sirtuin1 gene activity, as measured by messenger RNA. –Copyright 2008 Resveratrol Partners LLC
Cell Metabolism July 2008 early online doi:10.1016/j.cmet.2008.06.011
Resveratrol Delays Age-Related Deterioration and Mimics Transcriptional Aspects of Dietary Restriction without Extending Life Span
Abstract: A small molecule that safely mimics the ability of dietary restriction (DR) to delay age-related diseases in laboratory animals is greatly sought after. We and others have shown that resveratrol mimics effects of DR in lower organisms. In mice, we find that resveratrol induces gene expression patterns in multiple tissues that parallel those induced by DR and every-other-day feeding. Moreover, resveratrol-fed elderly mice show a marked reduction in signs of aging, including reduced albuminuria, decreased inflammation, and apoptosis in the vascular endothelium, increased aortic elasticity, greater motor coordination, reduced cataract formation, and preserved bone mineral density. However, mice fed a standard diet did not live longer when treated with resveratrol beginning at 12 months of age. Our findings indicate that resveratrol treatment has a range of beneficial effects in mice but does not increase the longevity of ad libitum-fed animals when started midlife.
Figure 4. Effects of Resveratrol Treatment on Longevity(A) Mean body weights over the entire life span. EOD feeding lowered body weight, and HC diet increased it (p < 0.001). Resveratrol did not affect body weight in mice fed the SD or EOD diets. The HCLR group was significantly heavier than the HC control group (p < 0.01), while the HCR group showed a slight trend toward decreased body weight that did not reach statistical significance. Error bars indicate SEM.(B) Kaplan-Meier Survival Analyses were performed on the SD, SDLR, and SDR groups, and the curves were not significantly different by the logrank or Wilcoxon tests; n = 60 (SD), 55 (SDLR), and 54 (SDR) at the beginning of the experiment.(C) Kaplan-Meier Survival Analyses were performed on the SD, EOD, EODLR, and EODR groups. There were no significant differences between the three EOD diet groups; however, the EODLR had increased survival compared to the SD control group as determined by both logrank (χ2 = 7.46, p = 0.006) and Wilcoxon (p = 0.0016) tests; n = 60 (SD) and 55 (EOD, EODLR, and EODR) at the beginning of the experiment.(D) Kaplan-Meier survival analyses were performed on the SD, HC, HCLR, and HCR groups. The HC control group had decreased survival compared to the SD control group (logrank: χ2 = 11.65, p = 0.0006, Wilcoxon: p = 0.0003), whereas, survival in the HCLR and HCR groups did not differ significantly from that of SD controls. When compared to HC controls, survival was significantly increased in both the HCLR group (logrank: χ2 = 8.31, p = 0.004, Wilcoxon: p = 0.005) and the HCR group (logrank: χ2 = 4.83, p = 0.03, Wilcoxon: p = 0.001); n = 60 (SD) and 55 (HC, HCLR, and HCR) at the beginning of the experiment.(E) Maximum life span was calculated as the mean of the final 20% of mice in each group as determined by Kaplan-Meier Analysis. Compared to the SD control group, the maximum life span was significantly increased in the EODLR (p = 0.03) and significantly decreased in the HC control (p = 0.003) groups. In addition, HCLR had significantly increased maximum life span compared to the HC control group (p = 0.04), and there was a trend toward increased life span in HCR mice compared to HC controls. *, p < 0.05 versus SD control; #, p < 0.05 versus HC control. Error bars indicate SEM.(F) Kaplan-Meier Survival Analyses were performed on the SD and SDHR groups, and the curves were not significantly different. The earlier SD survival curve (broken line) is shown for reference; n = 48 (SD, SDHR), and 60 (previous SD control) at the beginning of the experiment.
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For the first time researchers show reversal of an aging marker in the human retina correlated with visual improvement using a nutriceutical matrix (Longevinex®)
Seattle (June 27, 2008)- Using a high-output camera to film the back of the human eye, for the first time researchers have shown that a nutraceutical matrix can effectively remove cellular debris from the human eye that accumulates with advancing age and correlated this with significant improvement in visual acuity and night vision in an 80-year old man.
The accumulation of cellular debris in the retina is believed to be the first sign of age-related macular degeneration, an eye disease that robs senior adults of their central vision used for reading or driving, for which there is no cure.
Please Read the Entire Press Release Here.