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Thursday, August 5, 2010

Resveratrol- less pure forms are not active in changing the life extension gene, Sirtuins.

Biotics Research Corp has developed another Resveratrol-containing product called Resverasirt-HP


This was accomplished in conjunction with Mark Houston, M.D. after 3 years of research. Dr Houston is Associate Clinical professor of Medicine at Vanderbilt School of Medicine.

He has written a book called, "What Your Doctor May Not Tell You About Hypertension TM:The Revolutionary Nutrition and Lifestyle Program to Help Fight High Blood Pressure.


Resverasirt-HP

The key is having a 99.9% or higher form of Trans Resveratatrol, because the other forms and less pure forms are not active in changing the life extension gene, Sirtuins.

Resveratrol (Trans not Cis form) is known to stimulate production of a class of enzymes called Sirtuins,
labeled in mammals as SIRT-1 through SIRT-7. Sirtuins are known to affect cellular metabolism via
selective gene expression, including cell survival, fat metabolism, insulin resistance and generalized cell
repair (anti-aging).


A number of beneficial health effects, such as anti-cancer, antiviral, neuroprotective, anti-aging, and
anti-inflammatory effects, have been reported in lab tests using the compound Pure Trans RESVERATROL
found in  Resverasirt . This new product is a very high potency resveratrol product. Specifically, this product is used to support
a healthy vascular system and to promote healthy aging. Most people in this country will suffer from diseases that may greatly benefit from these high quality and researched products in ResveraSIRT-HP.

Resveratrol vs Pterostilbene

Sirtuins (silent information regulator) enzymes are broadly conserved from bacteria to humans and have been shown to be involved with roles in gene silencing, DNA repair, longevity, metabolism and cell physiology. In mammals, seven sirtuin genes have been identified. Sirtuins have been shown to remove acetyl groups from histones allowing DNA to become more tightly coiled. Vulnerable regions of the genome become more protected by the coiling of DNA. Regions of the DNA that are associated with changes caused by cellular divisions (aging) are more conserved or protected by Sirtuin activity.

Sinclair et al. [1] screened over 20,000 molecules to identify 25 molecules that enhanced SIRT 1 activity in vitro. Resveratrol emerged as the most potent stimulator of sirtuin activity. Feeding resveratrol to yeast, worms or flies has been shown to increase their life span by 30 percent. Sirtuin genes have also been shown to increase insulin sensitivity and decrease insulin like growth factor 1 ( IGF-1). Caloric restriction has also been shown to increase Sirutin activity thereby increasing life span. Recent studies conclusively show that resverartol promotes longevity and improves glucose homeostasis in mice by sitmulation of the Sirt mediated deacetylation of nuclear transcription factors [2]. Resveratrol treatment has also prolonged lifespan and delayed the onset of are-related dysfunctions in the annual fish Nothobrachius furzeri.[3] Bauer et al., showed that reseveratrol could increase the survival rate of middle aged mice on a high-calorie diet.[4]

Pterostilbene has not been shown to increase Sirtuin activity.

The roundworm, Caenorhabditis elegans has a short regeneration time of one week. The adult body contains most of the tissues present in higher vertebrates, such as a complete nervous system, striated muscles and an intestine with digestive, detoxification and innate immune function. Wilson compared the bioactivity of resveratrol, pterostilbene and other methoxylated stilbene in vivo using C. elegans. At similar doses resveratrol did not alter the survival of C. elegans and pterostilbene decreased the survival.[5]

Dietary resveratrol at a low daily dose (4.9 mg per kg) has been shown to mimic the effects of caloric restriction (CR) in vivo. Barger [6] showed in mice that CR or low dose resveratrol feeding did not alter Sirt 1 protein or other factors known to impact aging (IGF-1, insulin, Sirt 1, or oxidative stress). The analysis of the individual genes showed that genes expressed by CR or resveratrol were those that played an important role in chromatin remodeling. Chromatin is the combination of DNA and proteins, such as histones that make up the chromosomes. Similar to the activity of Sirt-1 induced by high dose resveratrol, low dose resveratrol or CR may facilitate the pathways that maintain the chromosal architecture and favor the maintenance of genomic stability. Maintaining genomic stability would retard some aspects of the aging process.

Pterostilbene has not been shown mimic the effects of caloric restriction, either at a high or low dose.

Resveratrol and pterostilbene have similar antioxidant activities. Both have an ability to increase plasma
antioxidant activity and to decrease lipid peroxidation. Rimando [7] reported that resveratrol and
pterostilbene are equally effective in scavenging peroxy radicals and reducing singlet-oxygen

Pterostilbene showed moderate inhibition of cycooxygenase (COX)-1 and was weakly active 
against COX-2. Resveratrol was strongly active against both isoforms of the enzymes.

Unlike pterostilbene, which has demonstrated to display only a limited number of health benefits,
has been shown to provide diverse health benefits including cardio protection, inhibition of low density
lipoprotein, activation of nitric oxide production, and hindering of platelet aggregation.[8]
Resveratrol is also a potent inhibitor of NF-kappaB activation in vitro. Based upon Barerjee’s studies with
10 ppm resveratrol diets (1 mg/ kg feed/day), Gescher [9] describes “resveratrol as one of the most potent derived chemo preventive dietary phenols ever described”.


[1] Howitz KT, Nature  2003, 425, 191-196
[2] Koo SH, Montminy M. Cell 2006 Dec 15; 127(6): 1091-3
[3] Valenzano DR, Cellerino A. Cell Cycle 2006 May; 5(10):1027-32. Epub 2006 May15
[4] Baur JA. Nature 2006, Nov 16; 444:337-342.
[5] Wilson, BMC Pharmacology 2008, 8:15, 1-11
[6] Barger, Plos One, June 2008, volume 3, issue 6, e2264
[7] Rimando AM, J. Agriculture and Food Chemistry 2002, 50, 3453-3457
[8] Muckherjee, Dose-Response 2010, prepress University of Massachusetts
[9] Gescher AJ, Cancer Epidemiology, Biomarkers and Prevention, Oct 2003, vol 12, 953-957  

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