CYP21A2 mutations causing defective 21-hydroxylase ::
If one has a mutation which makes defective 21-hydroxylase, cortisol spikes with stress causing an increased demand for 21-hydroxylase. Heme, which is contained in copper - is used to make the enzyme.
Being a carrier of this gene may mean that if you needed 10 units of functional 21-hydroxylase to make the cortisol you need, you also have to make 10 units of the defective version. So, you are using heme at twice the rate of a "normal" person, potentially causing problems related to heme buildup. Such as;
- non-activated copper going into the brain/liver (Wilson's Disease)
- Webbed fingers/toes.
- Poor ability to clear spirochetes
As heme is wasted, copper is depleted and leads to a deficiency of activated copper. We're unable to test for Copper (I) so there is no accurate way to monitor these levels.
Those with deficient 21-hydroxylase mutations won't have these issue.
I think those with mutations for defective (as opposed to low amounts) of 21 hydroxylase may be at risk for bioactive copper deficiency which adds a layer of heme-containing enzyme failure and inappropriate heme deposition in places like the brain (heme has recently been found to be inappropriately deposited in brains of people with MS
21 hydroxylase contains heme moiety. It is possible that heme moieties could rise to high levels if the body was trying unsuccessfully to make 21 hydroxylase in an attempt to raise cortisol to appropriate stress levels
When SOD1 is lacking one of its metal atoms (it has one copper and one zinc atom), it “unfolds” and starts causing damage. Instead of helping to protect motor neurons, it becomes toxic. As described by Dr. Beckman and his colleagues in the The Journal of Neuroscience, CuATSM fed to laboratory animals with ALS actually delivered copper to motor neurons of the spinal cord. Although the animals wound up producing more mutant SOD1, the extra copper allowed SOD1 to stay in its properly folded, protective form
This is not a medical recommendation.
This is a theory which is largely unproven.
Attempting supplementation to correct your copper levels can 'flip' your 21 hydroxylase switch - causing reinjury and making your symptoms worse than before you started with further dosing ineffective. Low copper unravels 21 hydroxylase, spikes cortisol and then may drop off because of the genetic inability to keep up.
Warning :: Increases homocysteine levels. Long term & high dosing can increase risk of heart attack.
The nicotinate ( niacin ) ion and nicotinamide ( niacinamide ) thermodynamically stabilizes Cu(I) ions through complex formation (Activates copper)
Noteably, Copper (I) Niacin is the key ingredient in MitoSynergy products. Part of The Root Cause Protcol, a treatment regime crafted to try and solve this problem (which it does with some success) with expensive patented supplements.
Warning :: Depletes Zinc.
GHK-Cu binds copper from the bloodstream and transports it into cells delivering copper to areas hard to reach.
GHK-Cu binds copper from the bloodstream and transports it into cells, increasing active copper levels in the body, which at high doses can be harmful. Zinc and copper deplete each other, so it is possible negative effects could be from too much copper, as well as not enough zinc. Another possibility is that GHK-CU increases the production of the enzyme SOD1 in the body. SOD1 needs both zinc and copper to function, which would mean that it is further depleting zinc. It has a stimulating effect on the migration of mast cells