Aging inside the body: Internal Organ Scarring & Natural Nrf2 Protection

Longevity requires the continued optimal functioning of organs in the body, including heart, lungs, liver and pancreas. Injury and inflammation causes damage to organs, and the body attempts repair by laying down fibrotic tissue (scar tissue) to heal the damage. This process of fibrosis results in non-functional scar tissue being applied to a critical organ. In younger people, the scar tissue is eventually replaced with functional tissue. However, with age, this recovery process becomes compromised, and scar tissue remains, disrupting the ability of the organ to function. Over time scar tissue can accumulate and further inhibits the normal function of the organ.

Scar tissue which accumulates in the heart, lungs, kidneys or liver can result in devastating effects and even lead to death. Pulmonary fibrosis, for example, resulting from smoking or environmental factors progressively scar the lung until the person can no longer breath, and the disease is fatal. Aging of the heart is associated with fibrotic scars, which can lead to atrial fibrillation and decreased capacity of the heart to function.Cirrhosis of the liver is scarring of the liver, from chronic inflammation, which leads to liver failure.

• Aging is considered a risk factor for increased fibrosis, in addition to external factors and inflammation (which incurs a systemic increase with age).

• A report from the University of Alabama estimates that human fibrotic disorders contribute to 45 percent of deaths in the United States.

• Nrf2 is a powerful transcription factor which is activated within the body and regulates antioxdant proteins which protects against the oxidative stress incurred by injury and inflammation. Research suggests that dysfunctional nrf2 levels (lower levels) may play a significant role in fibrosis formation. Experiments with mice with deficient levels of Nrf2 experienced more severe fibrosis and scarring. Increasing activation of Nrf2 is considered an important strategy in reducing fibrosis and the scarring of organs within the body.

Natural Nrf2 activators include sulforaphane (derived from glucoraphanin), curcumin, andrographolide, n-acetyl-cysteine, anthocyanins, C3G (anthocyanin), rosemary (carnosic acid), resveratrol, pterostilbene, baicalin, apigenin, luteolin

XGEVITY
AIR VITALITY
PURPLE LONGEVITY
BLUE NATURALLY
CURCUMIN XTRA-MAX / YELLOW LONGEVITY

LONGEVITY NATURALLY

REFERENCES:

(1) Hecker L, et al. Reversal of persistent fibrosis in aging by targeting Nox4-Nrf2 redox imbalance. Sci Transl Med. 2014 Apr.
(2) Zhao YY, et al. Metabolomics analysis reveals the association between lipid abnormalities and oxidative stress, inflammation, fibrosis, and Nrf2 dysfunction in aristolochic acid-induced nephropathy. Sci Rep. 2015 Aug 7
(3) Ni S, et al. Bone marrow mesenchymal stem cells protect against bleomycin-induced pulmonary fibrosis in rat by activating Nrf2 signaling. Int J Clin Exp Pathol. 2015 Jul 1
(4) Zhang Z, et al. Sulforaphane prevents the development of cardiomyopathy in type 2 diabetic mice probably by reversing oxidative stress-induced inhibition of LKB1/AMPK pathway.
(5) Dzeshka MS, et al. Cardiac Fibrosis in Patients With Atrial Fibrillation: Mechanisms and Clinical Implications. J Am Coll Cardiol. 2015 Aug 25
(6) Lee TY, et al. Modulation of thioacetamide-induced hepatic inflammations, angiogenesis and fibrosis by andrographolide in mice. J Ethnopharmacol. 2014 Dec 2
(7) Aboonabi A, et al. Chemopreventive role of anthocyanins in atherosclerosis via activation of Nrf2-ARE as an indicator and modulator of redox. Biomed Pharmacother. 2015 May
(8) Speciale A, et al. Cyanidin-3-O-glucoside (C3G) counters the response to TNF-alpha of endothelial cells by activating Nrf2 pathway. Mol Nutr Food Res. 2013 Nov.
(9) Paredes-Gonzalez X, et al. Induction of NRF2-mediated gene expression by dietary phytochemical flavones apigenin and luteolin. Biopharm Drug Dispos. 2015 Apr 22.