Yellow Longevity® 60 VCapsules

Extra-Strength Gold and Yellow Colors from Nature. Discount Qty Pricing!

LABEL INFORMATION

QTY Pricing:

QTY 1:   $26.95 each

QTY 3:   $25.95 each

 

YELLOW LONGEVITY® contains the most potent of the natural flavonoid pigments that research indicates may have many positive effects on aging. Curcugen™ is an enhanced bioavailable form of Curcumin.

  • In addition to curcumin, this powerful complex also contains Berberine, Schisandra Saffron and Andrographolide extracts. Also contains high EGCG Green Tea Extract, a potent Ginger Extract, and a full 65mg  of apigenin.

Apigenin is important in mitigating inflammation in the body, with special significance in the brain and cardiovascular system. Inflammation is an age accelerator and is destructive to all parts of the body. In the context of longevity, apigenin directly affects the ability of SIRT1 longevity gene activation by elevating levels of NAD+ - which is a limiting factor for SIRT1 activity. When NAD+ is low then SIRT1 is unable to produce anti-aging effects. Low NAD+ levels in the brain, which occur with aging, are believed to contribute to brain degeneration and senescence,(2)

YELLOW LONGEVITY® also supports muscle maintenance in aging. YELLOW LONGEVITY® is rich in Toll-like receptor 4 (TLR-4) and P38 MAPK inhibitors, which are involved in the inflammatory process. Aging is a factor in increased inflammation. Furthermore, research indicates that TLR-4 is the master switch for muscle catabolism induced by inflammation (3) including the activation of P38 MAPK. In aging active adults, elevation of P38 MAPK is linked to the inability of muscle stem cells to repair injured muscle and ultimately the loss of muscle mass with age. (4-5)  

 

REFERENCES:

1. Escande C, et al. Flavonoid Apigenin Is an Inhibitor of the NAD+ase CD38. Diabetes. 2013 Apr

2. Braidy N, et al. Mapping NAD(+) metabolism in the brain of ageing Wistar rats: potential targets for influencing brain senescence. Biogerontology. 2014 Apr;15

3. Doyle A, et al. Toll-like receptor 4 mediates lipopolysaccharide-induced muscle catabolism via coordinate activation of ubiquitin-proteasome and autophagy-lysosome pathways. FASEB J. 2011 Jan

4. Bernet JD, et al. p38 MAPK signaling underlies a cell-autonomous loss of stem cell self-renewal in skeletal muscle of aged mice. Nat Med. 2014 Mar

5. Cosgrove BD, et al. Rejuvenation of the muscle stem cell population restores strength to injured aged muscles.Nat Med. 2014 Mar

 



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