Reply To: Lead poisoning- chelation- benefit/risks…?

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Cheesey
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lmm;43837 wrote:

From what I’ve been reading (see Richard van Konynenburg’s work on Glutathione – http://iaomt.media.fnf.nu/2/skovde_2011_me_kroniskt_trotthetssyndrom/$%7Bweburl%7D – and forum discussion: http://forums.phoenixrising.me/index.php?threads/andrew-cutler-and-alpha-lipoic-acid.259/), I would be very careful about going beyond glutathione supplementation/augmentation if you have CFS/ME. Only once the body is detoxing/methylating should you consider ALA, DMPS or (if you have to) DMSA. I’ve think I now get how it “fits” together for CFS/ME sufferers whose illness was caused by emotional/physical stress overload:

– Glutathione levels plummet due to overburdening the body with stress; and then other factors creep in:
– May cause an increase in heavy metals stored in the body
(NOTE: if your test presents normal mercury in the body, you should consider using “counting rules”. This involves looking at certain other markers in the body that, if low, indicate mercury poisoning – useful since mercury rarely shows up as being high in the body);
– Th2 dominance;
– Dybiosis.

In this case, glutathione methylation and supplements that improve Th1 dominance are the first line of attack. You can then approach solving the dysbiosis with more confidence. I think I’ve been going after the tail, thinking it was wagging the dog.

Best,
Len

Yes absolutely. My health is far too poor to do anything drastic right now. It would be wonderful and miraculous if I was one of those people you hear about who had their amalgam removed and then recovered straight away (if only), but I somehow doubt that is going to happen. Accordingly, I will just get the amalgam removed then very slowly add in supportive supplements. I have been stung heavily these past 6 months by jumping from one thing to another and it making me drastically worse.

Since you mention stress, I will note that I am also starting psychotherapy as a means to regain overall health. I think the reasons I feel so bad are physical in origin, but my mental states are either holding them there or at least undermining recovery. I know people sometimes get very angry when you say that CFS pathogenesis has psychological elements, but I think probably nearly all disease states have a psychological element as the mind can wreak such havoc with the body. Of course, however, my CFS was precipitated by a virus and then significantly worsened by die-off, so I’m not sure psychology can paint a full picture for me.

I am a bit concerned, however, as the following study suggested glutathione can actually worsen heavy metal toxicity:

NAC and GSH [glutathione] merit special mention as some physicians recommend them as antidotes to mercury toxicity. At first glance this would seem logical, since GSH is known to be involved in the biliary excretion of methylmercury (Ballatori and Clarkson, 1985) and it is thought that intracellular GSH plays a role in protecting cells (Clarkson, 2002). However, only 1% of the body burden of methylmercury per day is eliminated from the gut by undergoing demethylation by microflora—the remainder is reabsorbed and undergoes entero-hepatic cycling (Clarkson, 2002). Furthermore, it has been found in rats that mercuric conjugates of GSH are in fact part of the uptake mechanism of inorganic mercury by the kidneys (Bridges and Zalups, 2005). The mercury–GSH conjugates appear to be converted to mercuric conjugates of cysteine by the enzymes γ-glutamyltranferase and cysteinylglycinase in the proximal tubules of the kidney, leading to increased uptake by the kidneys of mercury. It has also been shown that the renal uptake of methylmercury is dependent upon GSH (Richardson and Murphy, 1975). Aposhian et al. (2003) demonstrated in rats exposed to elemental mercury that NAC apparently increased brain mercury concentration. In addition, recently published results by Zalups and Ahmad (2005b) have shown that NAC conjugates of methylmercury and inorganic mercury are potentially transportable mercuric species taken up in vivo in proximal tubular epithelial cells. Furthermore, this latest experiment was carried out using canine Madin-Darby Canine kidney Cells (MDCK) cells transfected with the human organic anion transporter1 (hOAT1).

Given the inefficiency of elimination of methylmercury via the bile, the known entero-hepatic cycling of methylmercury and the mercury uptake mechanisms of the kidneys and the brain ( Bridges and Zalups, 2005 and Kerper et al., 1992) (for mercury species complexed with low molecular weight thiols), NAC and GSH would appear to be poor treatment choices for mercury toxicity due to the high risk of redistribution of mercury to those organs.

http://www.sciencedirect.com/science/article/pii/S0300483X07001096
(I copied and pasted the relevant bit, I get these articles free).

However, there are other opinions:

Because mercury has a high affinity for thiol (sulfydryl (SH)) groups, the thiol-containing antioxidant, glutathione (GSH), provides the major intracellular defence against mercury-induced neurotoxicity (James et al., 2005). According to these data, Sarafian suggested that the selective vulnerability of cells in the nervous system arise from a “critical absence of inherent protective mechanisms” (Sarafian et al., 1996). Cellular defences are obviously decisive in determining the toxic outcome and defense mechanism. Thiol compounds play a key role (Miura et al., 1994) and resistant cells were demonstrated to have higher levels of the thiol-containing peptide glutathione (Miura et al., 1994). Glutathione, in fact, plays an important role in the excretion of methyl mercury. Furthermore, the thiol-rich family of proteins, known generically as metallothioneins, plays a protective role for instance in kidney damage from inorganic mercury (Satoh et al., 1997). Accordingly, recently, metallothioneine-null mice showed more severe lung damage than normal mice after exposure to mercury vapor (Yoshida et al., 1999).

http://www.sciencedirect.com/science/article/pii/S0300483X07007561

I have tried to get more but my logins are being very uncooperative. As ever, though, it appears that glutathione supplementation may not be as clear cut as one might have hoped. Interestingly, I came across a lot of articles suggesting that ALA, DMSA and DMSP are also ineffective. Notable amongst these was one article that said ALA was ineffective at chelating mercury from the brain. Either way, I am not going to do anything drastic with any of those 3 supplements.

EDIT:

I also just found this study from Alternative Medicine Review (apologies for the long post):

Glutathione, as both a carrier of mercury and an antioxidant, has three specific roles in pro- tecting the body from mercury toxicity. First, glu- tathione, specifically binding with methylmercury, forms a complex that prevents mercury from bind- ing to cellular proteins and causing damage to both enzymes and tissue.30 Glutathione-mercury com- plexes also reduce intracellular damage by pre- venting mercury from entering tissue cells and becoming an intracellular toxin.

Second, glutathione-mercury complexes have been found in the liver, kidney, and brain, and appear to be the primary form in which mer- cury is transported and eliminated from the body.24 The transport mechanism is unclear, but com- plexes of glutathione and mercury are the predomi- nant form of mercury in both the bile and the urine.31 Glutathione and cysteine, acting as carri- ers of mercury, actually appear to control the rate of mercury efflux into bile; the rate of mercury secretion in bile appears to be independent of ac- tual bile flow. When bile flow rate is increased or decreased, the content of mercury in the bile changes inversely so net mercury efflux from the liver remains unchanged.32 However, increasing bile levels of both glutathione and cysteine in- creases the biliary secretion of methylmercury in rats.13 Other studies have confirmed this data in animal models.33-35 Conversely, glutathione deple- tion inhibits biliary secretion of methylmercury in animal models and blocking glutathione pro- duction appears to shut down biliary release of mercury.35

Cells of the blood-brain barrier (brain cap- illary endothelial cells) release mercury in a gluta- thione complex. Inhibiting glutathione production in these cells inhibits their ability to release mer- cury.23 Mercury accumulates in the central nervous
system primarily in astrocytes, the cells that pro- vide the first line of defense for the central ner- vous system against toxic compounds.36 Astrocytes are the first cells in brain tissue to encounter met- als crossing the blood-brain barrier. They also contain high levels of metallothionein and gluta- thione, both carriers for heavy metals. It is hy- pothesized that astrocytes are the main depot of mercury in the brain.37 In studies with astrocytes, the addition of glutathione, glutathione stimula- tors, or glutathione precursors significantly en- hances the release of mercury from these cells in a complex with glutathione. Fujiyama et al38 also suggest that conjugation with glutathione is the major pathway for mercury efflux from astrocytes. Glutathione also increases mercury elimination from renal tissue. Studies in mammalian renal cells reveal glutathione is 50 percent as effective as the chelating agent DMSA (2,3-dimercaptosuccinic acid) in preventing inorganic mercury accumula- tion in renal cells.39

Third, glutathione increases the antioxi- dant capacity of the cell, providing a defense against hydrogen peroxide, singlet oxygen, hy- droxyl radicals, and lipid peroxides produced by mercury.30 The addition of glutathione to cell cul- tures exposed to methylmercury also prevented the reduction of cellular levels of glutathione per- oxidase, a crucial antioxidant enzyme necessary for protection against the damaging effects of lipid peroxidation.30

As an antioxidant, glutathione appears to protect against renal damage resulting from inor- ganic mercury toxicity. The co-incubation of rat renal cells with glutathione and inorganic mercury was significantly more protective of renal cell in- jury when compared to inorganic mercury expo- sure alone.40 Antioxidant levels – specifically glu- tathione, vitamin E, and ascorbic acid – are de- pleted in renal tissue exposed to mercuric chlo- ride (inorganic mercury), and the addition of glu- tathione increased levels of both vitamin E and ascorbic acid in renal cells exposed to mercuric chloride.24

Mammalian cell lines resistant to mercury toxicity have been cloned.41 They do not readily accumulate mercury and are resistant to the toxic

Patrick, L (2002). Mercury Toxicity and Antioxidants: Part I: Role of Glutathione and alpha-Lipoic Acid in the Treatment of Mercury Toxicity, in: Alternative Medicine Review. 7:6 (456-471)