MTHFR and Glutathione Production

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Question: 

I was wondering about the connection between MTHFR and glutathione you mentioned in your video presentation. It seems to me that if there is a MTHFR defect, resulting in undermethylation, that should result in increased availability of homocysteine to be converted to cysteine, and ultimately to formation of glutathione. Yet you are saying there may be problems with glutathione production in MTHFR mutations. Can you explain why?

Thanks

A fellow ND, LAc

Answer:

Great question.

Short term, you are correct.

Short term, the increase in CBS enzyme activity should lead – and does lead – to increased glutathione production.

The problem is, long term, with MTHFR, and oxidative stress, the glutathione oxidation increases beyond the point of glutathione production.

This is because the traditional transmethylation cycle (Methionine cycle) and BHMT pathway help produce CoQ10, carnitine, phosphatidylcholine, creatine, SAMe – all of which are big players in antioxidant production and mitochondrial function.

As those decline, oxidative stress increases, CBS upregulation is even higher – and in turn, due to decreased CoQ10, carnitine, creatine, etc, ammonia levels climb and potentially so does hydrogen sulfide levels – and the inability for the sulfonation pathway to keep up with the increased sulfite/sulfide production thus leading to sulfur sensitivity and molybdenum deficiency.

I should also add that the likelihood of cysteine, glycine and B6 levels declining are high due to long term oxidative stress. Then – the production of glutathione is also affected. Not to mention the decline of vitamin C, selenium and vitamin E which help prevent oxidized glutathione and help recycle it back into reduced glutathione.

I believe that if we support the levels of CoQ10, carnitine, creatine, magnesium, phospholipids, molybdenum, decreased sulfur foods initially – and decreased sulfur supplements – and possibly increase SAMe right out of the gate – before even supplementing with glutathione, methylfolate or methylcobalamin, the degree of improvement should increase quickly.

As improvement occurs, then supporting phase 2 with glutathione, NAC and glycine should further help.

I think now if we support the MTHFR defects this way – by reducing oxidative stress, improving cell membrane stability and replenishing mitochondrial and antioxidant levels – our patients will improve much faster. Then – once those are in play – then supporting MTHFR for long term natural production and hopefully removing that initial supplementation.

Best

Dr Lynch

 

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