NADH
Studies (5)
NAD+ homeostasis in human health and disease
In depth review of NAD+, how its made in the human body, how it becomes deficient, and how its deficiency is a causal factor of a wide range of diseases. And how boosting NAD+ via enhancing agents like niacin ( especially niacin since it is the primary, so called Preiss-Handler pathway of manufacture ) can help cure a wide range of diseases.
The COVID-19 Burden or Tryptophan Syndrome: Autoimmunity, Immunoparalysis and Tolerance in a Tumorigenic Environment
Long covid is due to changes in the metabolism of tryptophan and the lack of niacin (NAD/NADH+). Tryptophan has its metabolism altered by the lack of intestinal absorption due to internalization of ACE-2 and hypoxemia and inflammation, diverting its products to the formation of toxic Kynurenine metabolites. The longer time under hypoxemia, the less niacin and the more tryptophan will deviate to Kynurenine in an inflamed environment
Melatonin in Mitochondria: Mitigating Clear and Present Dangers
It's inferred that the majority of melatonin is created inside the mitochondria, independent of the pineal daylight associated melatonin. Melatonin has a 3 billion year history of use inside cells as a highly efficient anti-oxidant. It functions as an anti-oxidant for both plants and animals. It stimulates synthesis of other antioxidants like glutathione. It's the "swiss army knife" of anti-oxidants and uniquely positioned as the "fox in the hen house" inside the mitochondria where many free radicals originate. Melatonin reverses the Warburg effect and aids in arresting cancer cell growth.
Open AccessReview Minireview Exploring the Biological Cycle of Vitamin B3 and Its Influence on Oxidative Stress: Further Molecular and Clinical Aspects
Overview of how niacin and its metabolites like NAD, NADP, NADPH play a key role in cellular signaling, apoptosis, balancing intestinal flora and gene expression. Without external supply of supply of niacin, the genome becomes unstable via the antioxidant system no longer functioning efficiently, which ultimately leads to cell death.
A novel treatment target for Parkinson's disease
The GPR109A receptor and its agonists (niacin and butyrate) have anti-inflammatory actions in the skin, gut and retina. For Parkinson's disease, niacin supplementation may have 3 benefits: lower inflammation via GPR109A-related mechanisms, increase dopamine production in brain by supplying NADPH and boosting mitochondrial functions by increasing the NAD/NADH ratio.