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PURPLE LONGEVITY® - Rich purple Anthocyanins, Activating Longevity Genes Autophagy and Increasing Glutathione

Boosting longevity is a function of many different attributes. Key among these are activating longevity genes (SIRT1 and FOXO) and decreasing levels of oxidative stress. 

PURPLE LONGEVITY

ACTIVATING LONGEVITY GENES -

  • Resveratrol and Pterostilbene  - Act as antiaging gene activators, including SIRT1 gene activator.(1)
  • Resveratrol and Pterostilbene are correlated with longevity.
  • Lingonberry (Lowbush Cranberry) contains powerful anthocyanins which activate FOXO longevity genes. (2)
  • Lingonberry may have beneficial effects on obesity health issues, including high fat diet cholesterol, glucose and inflammation.(3)

BILBERRY ANTHOCYANINS (Blue Color)

  • Significant increases antioxidant capacity and induction of autophagy (4)
  • AUTOPHAGY promotes health and longevity.
  • AUTOPHAGY - invoked through increased AMPK and reduced mTOR
  • AUTOPHAGY further enhanced intestinal epithelial barrier

 GRAPE SEED EXTRACT (GSE) (5-8)

  • GSE grape seeds are anti-oxidative, anti-inflammatory and anti-tumor
  • Vascular protective. Including blood pressure-lowering effect in hypertensive research animals. 
  • Cardio protective properties, especially against cardiac dysfunction after myocardial infarction.
  • Offers protection against ischemic stroke, by reducing oxidative stress levels.
  • Is a natural aromatase inhibitor, an enzyme involved with converting androgens (testosterone) to estrogen. 

 

N-ACETYLCYSTEINE (GLUTATHIONE BOOSTER) (9-11)

  • Is a precursor to glutathione. Decreases in glutathione are correlated with aging. Levels of cellular glutathione are predictive of longevity. 
  • Improved experimental organisms health and longevity. Increased longevity corresponds to Increased levels of antioxidant enzymes (Catalase and Glutathione)
  • Supports restoration of intestinal barrier.
  • May be effective against cardiovascular events by increasing intracellular glutathione levels. Glutathione reduces  inflammatory IL-1β, which can can promote atherogenesis

 

 PURPLE LONGEVITY®  

=> (RESVERATROL | PTEROSTILBENE | LINGONBERRY)

 

REFERENCES:

(1) Li Y, et al. Effect of resveratrol and pterostilbene on aging and longevity. Biofactors. 2018 Jan.

(2) Scerbak C, et al. Lowbush cranberry acts through DAF-16/FOXO signaling to promote increased lifespan and axon branching in aging posterior touch receptor neurons. Geroscience. 2018 Apr.

(3) Ryyti R, et al. Beneficial effects of lingonberry (Vaccinium vitis-idaea L.) supplementation on metabolic and inflammatory adverse effects induced by high-fat diet in a mouse model of obesity. PLoS One. 2020 May.

(4) Li J, et al. Reduction of Aging-Induced Oxidative Stress and Activation of Autophagy by Bilberry Anthocyanin Supplementation via the AMPK-mTOR Signaling Pathway in Aged Female Rats.  J Agric Food Chem. 2019 Jul.

(5) Mas-Capdevila A, et al. Changes in arterial blood pressure caused by long-term administration of grape seed proanthocyanidins in rats with established hypertension. Food Funct. 2020 Oct.

(6) Ruan Y, et al. Grape Seed Proanthocyanidin Extract Ameliorates Cardiac Remodelling After Myocardial Infarction Through PI3K/AKT Pathway in Mice. Front Pharmacol. 2020 Dec. 

(7) Kadri S, et al. Protective effect of grape seed extract and orlistat co-treatment against stroke: Effect on oxidative stress and energy failure. Biomed Pharmacother. 2021  Apr.

(8) Kijima K, et al. Grape seed extract is an aromatase inhibitor and a suppressor of aromatase expression. Cancer Res. 2006 Jun.

(9) Niraula P, et al. N-Acetylcysteine extends lifespan of Drosophila via modulating ROS scavenger gene expression. Biogerontology. 2019 Aug.

(10) McCarty M, et al. Perspective: Prospects for Nutraceutical Support of Intestinal Barrier Function. Adv Nutr. 2021 Mar.

(11) DiNicolantonio J, et al. Supplemental N-acetylcysteine and other measures that boost intracellular glutathione can downregulate interleukin-1β signalling: a potential strategy for preventing cardiovascular events? Open Heart. 2017 Jul.

Mitophagy - Maintaining Mitochondria & Stem Cell Renewal for Regenerative Longevity

MITOPHAGY AND  LONGEVITY

  • Cellular homeostasis, which significantly includes mitochondria function, is critical for longevity. Mitochondria are the energy powerhouses of the cell and are essential cellular elements for health and longevity. As part of aging, the mitochondria accumulate damage which decreases cellular vitality while increasing dysfunction. Mitophagy is the ability to clean the cell of damaged mitochondria which, if left to accumulate, would cause irreversible loss of cellular energy. Dysfunctional mitochondria can lead to cellular death, degenerative diseases and shorten the lifespan.
  • Mitophagy is essential for longevity. Higher activity levels of  mitophagy in the cell has been linked to significant increases in longevity in research animals. Improved aging and extended longevity is correlated with a proper balance of mitochondria biogenesis and mitophagy.(1) Age-related decreases in mitophagy result in the accumulation of damaged mitochondria and a decrease in mitochondria biogenesis, 
  • Mitophagy and Autophagy. Mitophagy is the selective degradation of the mitochondria by cellular process known as autophagy. Autophagy is the cellular process used to remove damaged cellular organelles and debris. Increased autophagy is known as a critical component in cellular survival and longevity. Enhanced levels of autophagy is considered a major factor in the  increased longevity in long lived animals.(2)
 

NRF2 - THE ROLE IN MITOPHAGY AND LONGEVITY  Nrf2 is a latent protein in the cell, which upon activation, regulates the activation of genes which produce antioxidant proteins for cellular protection, reduction of inflammation and reduction of mitochondrial toxins (via glutathione induction).

  • Nrf2 Increases Mitochondria Biogenesis and Mitophagy. .
  • Stem Cells - The basis for extreme longevity. Extreme lifespans are based on the ability to regenerate new cells to replace damaged cells. This is the function of stem cells. Stem cells are undifferentiated cells which, when needed, can differentiate into replacement cells in the body. Examples where stem cells differentiate into new functional cells include cardiomyoctyes (heart cells) and neurons in the brain. Sources of stem cells include a stem cell pool, whereby stem cells undergo a self-renewal (making new stem cell cells) which supply this pool. Additionally there are specific stem cells such as neural stem cells which can produce new neurons in the brain. Aging, and the dysfucntion of stem cell mitochondria, decrease the functional ability of stem cell self renewal and the regeneration ability of stem cells into cells such as neurons.
  • Nrf2 Protects Stem Cells Capacity for Self-Renewal and Differentiation, When levels of Nrf2 are decreased, stem cells and progenitor cells, lose their function for the self renewal and regeneration of cells.. An example of this is seen in neural stem cells in the brain where the ability to stimulate new neuron growth from stem cells  is inhibited when nrf2 levels are low. Researchers believe that nrf2 promotes healthy mitochondria in the stem cells which in turn reverses age related decline in stem cell ability to self-renew and to regenerate new cells. Therefore, nrf2 activation is significant in stem cell self renewal as well as cellular regeneration, including cardiomyocyte regeneration and preserving the function of neural stem cells.(5,6)  
  • SULFORAPHANE is a natural and potent Nrf2 Activator and helps maintain youthful and healthy mitochondria. (4, 7)
  • SULFORAPHANE - BEYOND Nrf2. In addition to providing Nrf2 activation, sulforaphane helps block damage to the mitochondria through non-Nrf2 mechanisms. Sulforaphane supports mitochondria hyperfusion, which is cytoprotective and prevents the formation of pores in the mitochondria.(8)
 
 XGEVITY (Sulforaphane Precursor Glucoraphanin)
 AIR VITALITY (Sulforaphane Precursor Glucoraphanin)

 

 

REFERENCES:

(1)  Palikaras K, et al. Mitophagy: In sickness and in health. Mol Cell Oncol. 2015 Jun.

(2) Palikaras K, et al. Coupling mitogenesis and mitophagy for longevity. Autophagy. 2015.

(3)  LaPierre L, et al. Transcriptional and epigenetic regulation of autophagy in aging. Autophagy. 2015 Jun

(4) Greco T, et al. Sulforaphane Inhibits Mitochondrial Permeability Transition and Oxidative Stress. Free Radic Biol Med, 2012 Dec

(5) Holstrom Kira, et al. The multifaceted role of Nrf2 in mitochondrial function. Curr Opin Toxicol. 2016 Dec

(6) Wang K, et al. Redox homeostasis: the linchpin in stem cell self-renewal and differentiation. Cell Death Dis. 2013 Mar

(7) Russo M, et al. Nrf2 targeting by sulforaphane: a potential therapy for cancer treatment. Crit Rev Food Sci Nutr. 2016 Dec 

(8) O'Mealey GB, et al. Sulforaphane is a Nrf2-independent inhibitor of mitochondrial fission. Redox Biol. 2016 Nov