Any thoughts or opinions on this Jarrow product?
http://www.iherb.com...spx?c=1&pid=143
updated topic description to reflect direction of thread -Funk
Edited by FunkOdyssey, 12 June 2008 - 07:22 PM.
Posted 10 June 2008 - 12:09 PM
Edited by FunkOdyssey, 12 June 2008 - 07:22 PM.
Posted 10 June 2008 - 02:49 PM
Edited by FunkOdyssey, 10 June 2008 - 02:51 PM.
Posted 10 June 2008 - 06:03 PM
Posted 10 June 2008 - 06:35 PM
does this mean that ALA is not useful to balance the effects of Acetyl-L-Carnitine?
Posted 10 June 2008 - 06:39 PM
LA induces a beneficial stress response: Evidence indicates the in vivo mechanisms of action
of LA involve activation of the natural environmental stress response systems which up-regulate the so-
called ‘early response genes’, thus activating Phase II detoxification enzymes via Nr-f2 and the
antioxidant response element (ARE) (63). Activation of these genetic systems is nature’s way of making
the body more adaptable to stress and environmental insults. One physiological result of Nr-f2 and ARE
activation is a significant increase of endogenous antioxidants (vitamin C, vitamin E, GSH, etc.) and
antioxidant enzyme systems (64, 86) Despite its abbreviated half-life, this is how LA is able to affect the
redox status of the cell, not by acting as a direct scavenger of free radicals. The theory that LA acts as a
direct scavenger of free radicals, or that it acts directly as an ‘antioxidant’ in the cell has been
disregarded as a valid theory by most LA experts several years ago (6) and yet is still being advanced by
the advocates of CRLA. To date there is lack of evidence that LA acts this way in vivo and a large body
of research demonstrating the ‘stress-response’ theory of action for therapeutic LA. Thus, the misguided
or ill-conceived basis for suggesting increased efficacy of CRLA products due to their increased “free-
radical scavenging” or “antioxidant properties” due to an increased MRT forms an erroneous rationale.
LA up-regulates the early response genes by inducing a mild “hormetic” or “redox stress” which
paradoxically confers protection against oxidative stress but requires a threshold concentration to initiate
the therapeutic response. The activation of PI3-K & MAP kinases (65, 66) and up-regulation of Nr-f2 (63)
heme oxygenase [HO-1] (66-68) and heat shock proteins [HSPs] (69-70) indicate the mechanism of
action of LA involves induction of a stress response that resets the cell’s homeostatic mechanisms that
become disrupted; for example, during age-related diseases and diabetes. The typical range of
concentrations required to induce the hormetic, Phase II (therapeutic) response is 10-20 µg/mL (~50-100
µM) and can be achieved with multiple oral doses of typical or QRLA preparations (e.g. Na-RLA) (2, 60,
71). Like the name “early response” implies, activation requires only short time periods of 15 minutes-1
hr, which coincides closely with the plasma time course of both IVLA & QRLA products (68). If this theory
is correct, and all of the existing evidence indicates it is, then high concentrations, rapid plasma
clearance and metabolism of LA are essential for both the safety and the efficacy in vivo (1, 2). It further
suggests that CRLA preparations require more toxicity data due to their increased plasma MRT before
being considered safe. Furthermore, it is not valid to utilize QRLA safety or efficacy data to claim CRLA
is safe and effective (88).
Posted 11 June 2008 - 09:43 AM
Posted 11 June 2008 - 12:18 PM
Posted 11 June 2008 - 02:51 PM
Published online on February 19, 2008, 10.1073/pnas.0712162105
PNAS | February 19, 2008 | vol. 105 | no. 7 | 2325-2330
OPEN ACCESS ARTICLE
BIOLOGICAL SCIENCES / BIOCHEMISTRY
Nrf2 mediates cancer protection but not prolongevity induced by caloric restriction
Kevin J. Pearson*, Kaitlyn N. Lewis*, Nathan L. Price*, Joy W. Chang*, Evelyn Perez*, Maria Victoria Cascajo{dagger}, Kellie L. Tamashiro{ddagger}, Suresh Poosala§, Anna Csiszar¶, Zoltan Ungvari¶, Thomas W. Kensler||, Masayuki Yamamoto**, Josephine M. Egan{dagger}{dagger}, Dan L. Longo{ddagger}{ddagger}, Donald K. Ingram*,§§, Placido Navas{dagger}, and Rafael de Cabo*,¶¶
Caloric restriction (CR) is the most potent intervention known to both protect against carcinogenesis and extend lifespan in laboratory animals. A variety of anticarcinogens and CR mimetics induce and activate the NF-E2-related factor 2 (Nrf2) pathway. Nrf2, in turn, induces a number of antioxidative and carcinogen-detoxifying enzymes. Thus, Nrf2 offers a promising target for anticarcinogenesis and antiaging interventions. We used Nrf2-disrupted (KO) mice to examine its role on the biological effects of CR. Here, we show that Nrf2 is responsible for most of the anticarcinogenic effects of CR, but is dispensable for increased insulin sensitivity and lifespan extension. Nrf2-deficient mice developed tumors more readily in response to carcinogen exposure than did WT mice, and CR was ineffective in suppressing tumors in the KO mice. However, CR extended lifespan and increased insulin sensitivity similarly in KO and WT mice. These findings identify a molecular pathway that dissociates the prolongevity and anticarcinogenic effects of CR.
Posted 12 June 2008 - 07:20 PM
IUBMB Life. 2008 Jun;60(6):362-7.
Is alpha-lipoic acid a scavenger of reactive oxygen species in vivo? Evidence for its initiation of stress signaling pathways that promote endogenous antioxidant capacity.
Petersen Shay K, Moreau RF, Smith EJ, Hagen TM.
Linus Pauling Institute, Oregon State University, Corvallis, OR, USA.
The chemical reduction and oxidation (redox) properties of alpha-lipoic acid (LA) suggest that it may have potent antioxidant potential. A significant number of studies now show that LA and its reduced form, dihydrolipoic acid (DHLA), directly scavenge reactive oxygen species (ROS) and reactive nitrogen species (RNS) species and protect cells against a host of insults where oxidative stress is part of the underlying etiology. However, owing to its limited and transient accumulation in tissues following oral intake, the efficacy of nonprotein-bound LA to function as a physiological antioxidant has been questioned. Herein, we review the evidence that the micronutrient functions of LA may be more as an effector of important cellular stress response pathways that ultimately influence endogenous cellular antioxidant levels and reduce proinflammatory mechanisms. This would promote a sustained improvement in cellular resistance to pathologies where oxidative stress is involved, which would not be forthcoming if LA solely acted as a transient ROS scavenger. © 2008 IUBMB IUBMB Life, 60(6): 362-367, 2008.
Posted 09 May 2010 - 10:07 AM
Posted 09 May 2010 - 10:24 AM
Posted 09 May 2010 - 11:02 PM
18069903 suggests that Na-R-ALA has superior absorption characteristics in several respects. The GeroNova shop on nexternals has it for like $83/100g, IIRC.Does anyone have any recommendations on the best form to take, and should I go with a non-sustained release form based on that data/study?
Posted 09 May 2010 - 11:56 PM
Edited by ken_akiba, 10 May 2010 - 12:23 AM.
Posted 10 May 2010 - 12:39 AM
It's hard to say, really. The use of ALA as a chelator is based on a couple of very old Russian papers which Andy Cutler connected the dots on. Here's a quote from his mailing list:The great amalgam debate. I too have a couple of ugly amalgam fillings in my mouth. Does ALA distribute amalgam's mercury into other parts of body? If so, sustained release accelerate or decelerate the distribution?
I feel it necessary to point out that his "protocol" is based almost entirely on theoretical mechanism and the anecdotes of people on his mailing list. I went through the list archives last year and copied out all of the actual research concerning ALA; let me know if you want me to post it. IIRC his protocol calls for ALA round-the-clock every 3 hours, so I assume CRALA would be more effective for that purpose. However, he also recommends not to do this until your fillings are out, so it could be more problematic if they're not.I agree with Ruth that ALA can redistribute mercury to the brain. Any chelator effective for clearing mercury out of the brain can do that. All the chelator does is make the blood-brain barrier permeable to mercury - if the amount in the brain is lower than the amount that should be in equilibrium with the current blood level, then the net movement of mercury will be from the blood to the brain. This is why people who recently ended exposure should wait several months to use ALA, and why things like DMPS and DMSA that do not cross the blood-brain barrier are useful and appropriate for the treatment of acute intoxication where most of the mercury is still in the blood and hasn't made it into the brain.
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