by Biologist » Mon Oct 06, 2008 1:10 am
Brian,
I agree Ames has a good site and he has a lot of accomplishments. I will check it out real well. Just getting to it. This is some pretty relevant reading right here from his home page. Looks like we have been doing the right thing regarding Acetyl-L-Carnitine and Alpha Lipoic Acid. There is a recent thread on what we can do about mitochondrial problems. This ranks up at the top as far as I am concerned. ALA was not mentioned in the advice Dr. G. had given as I remember. I think it should be added to the treatment list. When I mentioned to the doctor that had me on Zocor for years that I was taking it to address statin damage he looked shocked for a second and repeated what I had said "Alpha Lipoic Acid?!" The next visit months later, he said at least two times to continue my supplements. It later crossed my mind that he had researched ALA on PubMed or something similar. The research is endless, and its all good. I just finished reading TWO books on ALA. It is pretty remarkable what it can do.
BTW, I spent some time on Jeff's site this weekend and also read a lot of the comments from his World Health Organization petition. He is doing good work! Interesting how doctors are being directly compensated for prescribing statins in England these days. Phama must have a hell of a grip there too.
Here's Ames text that I liked:
"Mitochondrial decay with age due to oxidation of RNA/DNA, proteins, and lipids, is a major contributor to aging and the degenerative diseases of aging. In old rats (vs. young rats) mitochondrial membrane potential, cardiolipin level, respiratory control ratio, and cellular O2 uptake are lower; oxidants/02, neuron RNA oxidation, and mutagenic aldehydes from lipid peroxidation are higher (1-3). Feeding old rats the normal mitochondrial metabolites acetyl carnitine (ALC) and lipoic acid (LA) at high levels for a few weeks reverses much of this decay, the two complementing each other, in some cases synergistically, and restores the lost mitochondrial function to the level of young mitochondria (1-3). Ambulatory activity, cognition, heart, and immune function decline with age and feeding ALC and LA to the old rats also restores a good part of the lost function (1-4). Considerable progress has been made in understanding the mechanism of action of the two metabolites (1-3, 5, 6). LA is a mitochondrial coenzyme and is reduced in the mitochondria to a potent antioxidant, dihydrolipoic acid. LA is also an effective inducer of the phase-2 antioxidant enzymes, about 200 enzymes including those required for glutathione synthesis (5, 6).
Inadequate intakes of vitamins and minerals from food can lead to DNA damage, mitochondrial decay, and other pathologies (7). Intakes below the EAR, i.e. 2 standard deviations <RDA, are widespread (e.g. in the U.S.: 56% for magnesium; 12% for zinc; 16% menstruating women for iron; 16% of women for folate) (7). Intakes <EAR are particularly widespread among the poor, African-Americans, teenagers, the obese, and the elderly (7). Inadequate intake of folate, B12, or B6 leads to uracil incorporation into DNA and chromosome breaks ---a radiation mimic (8, 9). Inadequate zinc in human cells in culture causes release of oxidants, oxidative damage to DNA, and inactivation of p53 and other zinc enzymes involved in DNA damage repair (10, 11). Inadequate iron intake inactivates Complex IV in mitochondria, which causes oxidant release, mitochondrial decay, and DNA damage; in the brain complex IV inactivation mimics the neurodegeneration of aging (12, 13). Biotin inadequacy from food is present in 40% of pregnant women; biotin deficiency in human cells in culture leads to oxidant release, DNA damage, accelerated mitochondrial decay, and premature senescence (14). Magnesium deficiency in human cells in culture causes mtDNA- protein crosslinks, accelerated telemore shortening, and premature senescence (15). I suggest evolutionary allocation of scarce micronutrients by enzyme triage is an explanation of why DNA damage is commonly found on micronutrient deficiency (7). We are developing sensitive assays for measuring DNA damage in human blood (16) so as to determine what level of each micronutrient is optimum for keeping DNA damage to a minimum."
Biologist