Question: Do supplements such as ASEA increase intracellular glutathione? —T
This is my first posting to FACT.
Asea contains bleach (hypochlorite), even though salt and water are the only ingredients listed on the label. The salt water is processed in some proprietary way, probably through an electrolytic process similar to that used in alkaline-water devices, to convert the chloride into hypochlorite, and possibly higher-oxidation-state chlorine compounds. Hypochlorite is naturally produced in the human body, so drinking bleach is not necessarily as strange as it might sound. If they put bleach on the label, not only might consumers think twice about the product, but the FDA might have something to say as well.
Just like exercise produces free radicals, oxidation stress and induction of antioxidant defenses, Asea seems to do the same thing. In my opinion, this is somewhat analogous to drinking dilute hydrogen peroxide, but it probably lasts longer in the body. Medical equivalents would be hyperbaric oxygen, IV hydrogen peroxide, ozone therapy and ultraviolet blood irradiation. OTC products that might be similar might include MMS, chlorine dioxide, hypericin concentrate and negative ion generators. There’s undoubtedly more.
The primary oxidative effect is likely mediated by glutathione and ascorbate. These are primary cellular antioxidants, relatively plentiful and active reducing agents. Glutathione recycles ascorbate, and is recycled by NADPH, so the oxidative stress is metabolically transferred into energy-production systems (NADH from the Krebs cycle couples to NADPH by a transhydrogenase enzyme). And since hypochlorite (and peroxide, ozone, superoxide, oxygen, etc.) is an aerobic agent, it is probably augmenting cellular energy-production flux at the same time it is tapping energy into the antioxidant defense system. This would seem to explain the immense popularity of Asea in our modern substantially hypometabolic population. The orthodox-medical standard of care is to not treat hypothyroid symptoms and not recognize hypometabolism as a pathology. This is a perfect market opportunity for Asea.
The effect of Asea, MaxGXL and liposomal glutathione (just to mention three) on glutathione needs closer examination. There has been an unfortunate tendency for researchers and companies to use superficial data to infer deeper mechanisms of action. Use of L-cysteine, for example, clearly increases glutathione levels in a day or two, but the issue of whether it is sustainable over longer time courses remains unquantified. The problem is that glutathione biosynthesis is negative-feedback regulated. When glutathione increases, biosynthesis of glutathione decreases. This stabilizes glutathione levels.
Interestingly, the feedback loop appears not to measure actual glutathione. In children with Down’s syndrome, cysteine levels are the highest of any known human subpopulation due to overexpression of CBS (cystathionine beta synthase, if I remember correctly, which is located on the 21st chromosome). Interestingly, children with Down’s syndrome also have extremely low glutathione levels. It appears that cysteine suppresses glutathione comparably to glutathione itself. This makes complete sense if the glutathione feedback loop involves the chemistry of sulfhydryl groups (SH groups), which are the antioxidant-active part of glutathione and cysteine (and NAC).
I have concerns that the “testing” of glutathione levels in blood cells as a measure of glutathione-precursor efficacy is seriously misleading. Blood-cell glutathione is determined in red blood cells and white blood cells, both of which are unique cell populations. Red blood cells are anuclear and have no mitochondria, therefore their glutathione-recycling mechanism is anaerobically (glycolytically) driven, not oxidatively driven like it is in most cells. And white blood cells are wired oppositely to other body cells on an energetic level; when inflammation increases, the metabolic activity of white blood cells increases dramatically, while the metabolic rate of cells in surrounding tissues decreases. White blood cells also preferentially absorb vitamin C in its oxidized state. And white blood cells are also “activated” by chemical exposures that are not necessarily directly immunogenic (antigens) but can be considered systemic toxins (plant phytotoxins, for example). Therefore, increasing blood-cell glutathione can be entirely an artifact of activating white blood cells by inflammatory and toxic mechanisms, which might or might not correlate with corresponding increases in glutathione in liver, brain, heart or kidney cells (where you reall want it), and might actually correlate with decreases if the glutathione response is directly connected to cellular energy flux. When the immune system goes into overdrive, genetic expression, protein synthesis and healing are all specifically inhibited. Therefore, blood-cell glutathione-change data should be backed up with animal data on liver, brain, kidney and muscle glutathione levels.
There is also a potential secondary problem with both glutathione and cysteine in transporting mercury from the gut, bloodstream and tissues into the deeper tissue and cellular compartments. It would seem that liposomal glutathione has the least potential for this mode of action, being protected from mercury exposure by the lipid membranes on its way into the body. Has anybody seen any data on this?
I hope this helps. —Steve