|Apologies, the webpage I indicated has now (over the past few days) been replaced with the page that is there currently, but had a completely different content before. The intro, and summary (their words, not mine) is as follows below. The next line then said to go the link mentioned in my previous post. It is an elaboration on this subject but is no longer linkable. I have the whole article as a word doc if anyone wants to read it.|
"AOR was the first organization in the world to introduce R-lipoic acid, the superior form of this anti-aging, mitochondrial energy molecule, as a pharmaceutical-grade supplement for the life extension community. In the ensuing years, numerous companies followed our lead. But now some companies are promoting the use of R-dihydro-lipoic acid (R-DHLA) pills. These companies point out that R-dihydrolipoic acid is the more powerful antioxidant, and suggest that most of R-lipoic acid’s benefits come from being converted into R-dihydrolipoic acid in the body, and so they claim that it makes more sense to take R-dihydrolipoic acid directly, which would make it immediately useable.
After a careful review of the evidence, the team at AOR has concluded that these arguments do not hold up to scientific scrutiny. R-lipoic acid is by far the more evidence-backed supplement, and many of its key benefits – on cellular homeostasis, mitochondrial function, and perhaps aging itself – cannot be gained from substituting preformed R-dihydrolipoic acid in its place."
- (From the Moderator) Here is the reply from LEF's supplier of R-dihydrolipoic acid:
I know the owner of AOR and AOR is a very reputable company that likes to
go by what the scientific research says, as we do. AOR was the first to come out with RLA and they showed how it was better than ALA. Their letter is basically an attempt to protect their turf. The Questioner is right, all of RLA's and ALA's good affects come from the liver reducing the R isomer to RDHLA with NADH and other reducing agents. You do not see AOR argue with that. Yes, there is more research done with ALA and RLA because RDHLA has only become available in reasonable quantities recently. Others think highly of RDHLA, check out Geronova's site on RDHLA:http://www.geronova.com/dhla.htm
AOR pushes Packer's and Ames's research, yet they have nothing against RDHLA, as I heard it, and they are going to start using it in research. AOR's reasoning does not make sense, because if there is a problem with using RDHLA directly, once it is oxidized, it becomes RLA and then there is no difference. AOR's joke about
"mainlining" supplements is not logical because in that study the RDHLA would act long term also and they imply it does not and they do imply that it might not work orally, which is false. The statement (that they do not reference) about
RLA being the only form to rejuvenate mitochondria does not make sense. RLA and RDHLA are a redox pair, they are always working together, their term PRE-formed makes no sense as there is always some RLA and RDHLA in a biological system. And since the free radicals are the problem and there are always plenty of them around I think it is more efficient to take reduced supplements. With RLA
this has just not been possible until now. Would you take oxidized C, E, CoQ? But say they are correct about
this NADH/mitochondria excess electrons and no other system can help, then the RDHLA will reduce any excess of NADH after it's first redox cycle, as then it will be RLA.
They seem to contradict themselves in the paragraph that states that
RLA is "upgraded" to RDHLA, for then how can it be so bad? They give no
doses for what they say are excesses, immediate needs, metabolic balance, etc.
Also, it sounds like all this happens in a closed environment with no other antioxidants or influencing biochemical pathways involved. This imbalance may only be significant in very old or very sick people, who have many problems, that may be better helped by the reduced form, RDHLA.
I have heard how RLA is very unstable and will polymerize into a sticky mess
if it is not packaged right. AOR has tried to get around this with a timed release
additive and others have converted RLA to a K salt and added other stabilizers.
How do we know their supplements are absorbed with the time release additives, have they done studies? It is not fair for AOR to state, with no studies to back it up, especially when it is counterintuitive, that "none of these benefits (RLA's) accrue from taking preformed RDHLA". RLA is not an antioxidant until it is reduced to RDHLA. AOR has ended their article with a number of unsubstantiated
statements and then they say, "We just don't know", which is probably the truth.
They even go so far as to say, "It's even possible that RDHLA may exert a negative influence, by exerting prooxidant activities because of interactions with cellular iron." If it does, it is when it is oxidized as RLA. The paper attached below says as much (Note: They use LA/DHLA instead of RLA/RDHLA).
But instead of any more speculation, I think we should let this rest and see what
the researchers come up with in the future. We have nothing against RLA, as
we use it in some of our products, and our RDHLA turns into RLA in the body.
- Protection against amyloid beta peptide and iron/hydrogen peroxide toxicity by alpha lipoic acid.
Lovell MA, Xie C, Xiong S, Markesbery WR.
Sanders-Brown Center on Aging, University of Kentucky, 800 S. Limestone St., Lexington, KY 40536-0230, USA. email@example.com
Current evidence supports the role of oxidative stress in the pathogenesis of neuron degeneration in Alzheimer's disease (AD). alpha-Lipoic acid (LA), an essential cofactor in mitochondrial dehydrogenase reactions, functions as an antioxidant and reduces oxidative stress in aged animals. Here, we describe the effects of LA and its reduced form, dihydrolipoic acid (DHLA), in neuron cultures treated with amyloid beta-peptide (Abeta 25-35) and iron/hydrogen peroxide (Fe/H2O2) . . . Overall, these data suggest that the oxidation state of LA is critical to its function and that in the absence of studies of LA/DHLA equilibria in human brain the use of LA as an antioxidant in disorders where there is increased Fe such as AD is of questionable efficacy.
PMID: 12897407 [PubMed - indexed for MEDLINE]
Post Edited By Moderator (DDye) : 2/17/2005 3:01:02 PM (GMT-5)