Anti Aging Tricks
Many Symptoms One Cause (Aging)

Author: Gianpiero Pescarmona
Date: 27/03/2018


How long will we live in 2069, Medium 2019

The influence of pro-longevity gene Gclc overexpression on the age-dependent changes in Drosophila transcriptome and biological functions. 2016

  • Gclc level demonstrated associations with the expression of genes involved in a variety of cellular processes including Jak-STAT, MAPK, FOXO, Notch, mTOR, TGF-beta signaling pathways, translation, protein processing in endoplasmic reticulum, proteasomal degradation, glycolysis, oxidative phosphorylation, apoptosis, regulation of circadian rhythms, differentiation of neurons, synaptic plasticity and transmission.

Gclc human analog is GCLC (GSH1_HUMAN)

Catalytic activity

ATP + L-glutamate + L-cysteine = ADP + phosphate + gamma-L-glutamyl-L-cysteine.

gsh and endoplasmic reticulum

gsh and longevity

A decrease of free radical production near critical targets as a cause of maximum longevity in animals. 1994

  • A comprehensive study was performed on the brains of various vertebrate species showing different life energy potentials in order to find out if free radicals are important determinants of species-specific maximum life span. Brain superoxide dismutase, catalase, Se-dependent and independent GSH-peroxidases, GSH-reductase, and ascorbic acid showed significant inverse correlations with maximum longevity, whereas GSH, uric acid, GSSG/GSH, in vitro peroxidation (thiobarbituric acid test), and malondialdehyde (measured by HPLC), did not correlate with maximum life span. Superoxide dismutase, catalase, GSH-peroxidase, GSH and ascorbate results agree with those previously reported in various independent works using different animal species. GSSG/GSH, and true malondialdehyde (HPLC) results are reported for the first time in relation to maximum longevity. The results suggest that longevous species simultaneously show low antioxidant concentrations and low levels of in vivo free radical production (a low free radical turnover) in their tissues. The "free radical production hypothesis of aging" is proposed: a decrease in oxygen radical production per unit of O2 consumption near critical DNA targets (mitochondria or nucleus) increases the maximum life span of extraordinarily long-lived species like birds, primates, and man. Free radical production near these DNA sites would be a main factor responsible for aging in all the species, in those following Pearl's (Rubner's) metabolic rule as well as in those not following it.

gsh and Vitamin D

Vitamin D and L-cysteine levels correlate positively with GSH and negatively with insulin resistance levels in the blood of type 2 diabetic patients. 2014

  • Similarly, illustrates that a significant correlation exists between blood levels of LC and those of vitamin D. shows that there was a statistically significant inverse regression dependence of triglyceride levels with blood levels of GSH and LC, but that the inverse relationship between GSH and cholesterol was not statistically significant (r=−0.18, P=0.12, data not given).

An observational approach (not causal)

Find drugs that delay many diseases of old age


  • Common mechanisms seem to underpin several age-related diseases, including diabetes, Parkinson’s disease and Alzheimer’s. A review of more than 400 studies of people and animal models indicates that similar mechanisms underlie six conditions2. These can involve DNA damage, such as that caused by free radicals; cellular senescence (in which cells stop dividing and start secreting inflammatory factors); or inflammation and autophagy (the degradation of organelles, misfolded proteins and so on)-
  • This may explain why people over 65 are at a higher risk than younger people of developing more than one disease at the same time. In the United States, 7 out of 10 people over 65 with diabetes will die of heart disease, for instance.
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