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SOD2 A16V homozygous mutation - anyone else?


Senior Member
I just found this again, what does it mean if you don't have any SOD1 mutations, but several SOD2 and a SOD3?


Senior Member
what does it mean if you don't have any SOD1 mutations, but several SOD2 and a SOD3
It may mean nothing at all and depends entirely on which variants you have.

A little earlier in this thread there were posts about SOD2, starting here. There's no evidence that the variants identified by Yasko have any consequence.

You would need to research the SOD3 SNPs to determine if they have any effect.
I have the three homozygous "bad" mutations for SOD2 and many symptoms of copper toxcicity, but also of deficiency.

I've read CuZnSOD may compensate when FeMnSOD isn't functioning well.

When copper is needed in excess it will overwhelm ceruloplasmin resulting in it being stored in the body, at which point the majority of bioavailable copper coming into the body will be used in ceruloplasmin and metallothienine production to remove excess unbound copper. If SOD2 continues to be low, the issue will continue to repeat itself.
High serum, RBC and hair copper tests are fairly useless in figuring anything out.

Excess (unbound*) can be the result of too much dietary copper (highly unlikely if you consider the pesticide "Roundup", glyophosphate). Poor forms of copper supplementation (copper sulfate is antagonistic to many functions copper supports). Infection fungal or otherwise, chronic illness (copper is released in times of stress and illness to support the production of white blood cells. High anxiety, epinepherine issues (copper is required for most of the endocrine system). From excess zinc supplementation. Heavy metal poisoning, specifically lead and mercury. Crohns or other digestive issues. And most importantly, paradoxically, copper deficiency.

Ceruloplasmin REQUIRES copper to be manufactured, without it, copper cannot leave the body. If SOD2 is malfunctioning dietary copper will be too split by having to make up for the deficiency and will replace SOD2 with CuZn SOD, which also impairs metallothienine on top of ceruloplasmin which is already impaired.

Why anyone on this entire forum, seeing as we are all very ill, could possibly think they have copper toxcicity without copper deficiency is beyond me. Copper is required for the immune system to function, the endocrine system relies almost entirely on copper, heart function, catecholamine production etc, etc.

I can't count the amount of times I've read about someone spending 5, 10 sometimes 15 years dealing with chronic copper toxcicity, going all this time avoiding copper like the plague. How can you spend more than a year chelating copper, avoiding it's intake the whole while, and really believe you're not deficient by that point? It's an essential mineral, if you're not eating it, or supplementing it, it isn't just going to manifest itself into your body.

What I'm getting at in regards to copper toxcicity is that everything which causes copper toxcicity also causes copper deficiency. Only in extreme and acute cases will copper toxcicity exist independent of copper deficiency, if it took a while to become copper toxic, you can rest assured that you are also deficient in this essential mineral, look at anything that targets or hinders the bodies primary and secondary transport and elimination method of copper (ceruloplasmin) and (metallothienine). These both require copper to function, unless they are or have been impaired to a significant degree at any point, your body will regulate copper on its own.

If you decide to go about it by avoiding copper (essential for ceruloplasmin) for years and years, and chelate heavily with molybdenum and vitamin C. Then what's keeping ceruloplasmin functioning? What's keeping the endocrine system functioning? What's keeping your digestive system functioning? What's regulating catecholamines in the body? The unbound copper you're removing doesn't function in the body as bioavailable copper does in enzymatic functioning. Lacking free ceruloplasmin prevents bioavailable copper from being used in the body.

It's as if people have decided copper is a toxic heavy metal and serves no function in the body and scratch their heads wondering why they're so sick.

This whole copper toxcicity issue stems from a misunderstanding of one report done ages ago, mistaking high copper in the presence of any and all inflammatory conditions or illnesses of any kind (anti-neutrophil antibodies result from copper deficiency) for too much dietary copper. It's mind boggling how people can go to university for a decade and still believe this.

What im curious about is why all these fixes are offered and nothing is really often said about supplementing manganese? If manganese is required for FeMnSOD how would supplementing it help without adequate manganese?

Also how can one safely take manganese when it is a pretty serious neurotoxin?
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Thanx, Alex. It's so tricky with this stuff, cause I have to be careful not to overdo CoQ10 since it's a methyl donor and I'm COMT++, so I'm only taking 100mg. And I've been told not to take NAC because I'm CBS+, and I don't remember why I'm not supposed to take ALA -- maybe it's a sulfur donor, so it's because of the CBS+? Jeez -- trying to navigate through the various mutations, helping certain ones while not exacerbating other ones, is the most unpleasant puzzle I've ever tried to solve.
CBS is the "unlucky" mutation as it forces us to avoid lots of sulfur-containing potent compounds.
I took PQQ on and off over the years and didn't feel it helped at all. Same with Coq10. However, I found something very interesting not just with myself but with some other ppl I've shared this with. Instead of taking the coq10 daily, i did some experimenting with doses and time periods between doses and I found taking a triple dose, every three days it works really great.

I doubled that dose for coq10 but kept it at 3 day intervals and pretty amazing. I did that same experiment with PQQ. Taking 3 doses of 20mg every three days and has same effect. So I settled on taking triple dose of coq10 as well as a triple dose of PQQ and the combined effect has been life changing.

The coq10 took about 24hrs to notice and the PQQ took about a week to really notice. The first 12hrs was a slight dip in energy so i decided to take them with my dinner.

For those out there that haven't had positive effects taking these things daily, i thought this would be worth sharing. I think when it comes to things involving mitochondria, taking daily doses of anything that effects it isn't always going to work. It's a slower process. And before the supplements get a chance to show positive effects, we're stacking on more before it's finished processing whats been sent their way the day before.

I tried 2 days as well and 3 days seems to be the sweet spot. Not just for me but for my gf and a few friends of mine. Hope this helps someone out there. Cheers
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