Still copper toxic two years later?

[I] quit chelating around seven months ago to do liver and colon cleansing and just recently did my third annual hair test. When the results arrived, I was very upset to see my copper has gone back up. It went from 560 to 170 to 280 (whereas the reference range is 11 – 30). First I’ll show you the results compared with my previous two hair tests and then show you all the questions I’ve wanted to answer. I’m documenting all this research because my memory is so impaired, it’s likely one of the things that caused me to drop the ball on lowering my copper!

Why should I care about high copper?

• copper antagonizes potassium – low potassium results in tight muscles and other problems.
• copper imbalances are highly associated with most psychological, emotional and often neurological conditions.  These include memory loss, especially in young people, depression, anxiety, bipolar disorder, schizophrenia and others discussed below.
• copper toxicity symptoms are very similar to mercury (Dr. Cutler) – in other words, very serious.
• the places where copper accumulates are the liver first, then the brain and the reproductive organs. because copper targets the liver, it gets in the way of heavy metal chelation using ALA and other chelators that rely on bile secretion.
• copper and vitamin C are direct antagonists.  This means that they oppose each other in the body.  This is one reason many people feel better taking a lot of vitamin C.  Copper tends to oxidize and destroy vitamin C in the body.  Meanwhile, vitamin C chelates or removes copper from the body.  This requires a dose of vitamin C of at least about 500 mg daily, far higher than the minimum daily requirement of about 60 mg. On the other hand, two small studies in healthy, young adult men indicate that the oxidase activity of ceruloplasmin may be impaired by relatively high doses of supplemental vitamin C – I don’t know what that means but I can’t find any suggestion anywhere that vitamin C is harmful in the case of copper toxicity, just the opposite in fact: “Vitamin C can and does do miraculous things for patients afflicted with toxic levels of copper.”

Is hair testing for copper a reliable indicator of body copper?

According to Dr. Cutler, hair testing is “believed to accurately reflect body inventory” either when mineral transport is normal or deranged (when showing high/red). since all three of my hair tests have shown extreme high toxic levels of copper.

What are the possible causes of high copper?

• adrenal weakness – low hair levels of sodium and potassium and a low ratio of sodium to potassium have been found to correlate with adrenal weakness or insufficiency.  This reduces the body’s ability to produce ceruloplasmin, and thus reduces its ability to transport and remove excess copper. Low ceruloplasmin allows unbound copper to build up in the body tissues. Definitely me.
• drinking water – either through copper pipes or spring water that is high in copper. Neither apply to me.
• environmental exposure – I don’t believe this applies to me
• genetic flaws – possibly in metallothionein (MT) genes, molybdenum cofactors GPHN and MOCS1 or MOCS2, or the Wilson’s disease protein ATP7B. Here are livewello reports on my ATP7B SNPs, GPHN SNPs, and MOCS1 & 2  genes (lots of yellow and red in the first two).The ATP7B gene provides instructions for making a protein called copper-transporting ATPase 2. This protein is part of the P-type ATPase family, a group of proteins that transport metals into and out of cells by using energy stored in the molecule adenosine triphosphate (ATP). Copper-transporting ATPase 2 is found primarily in the liver, with smaller amounts in the kidneys and brain. It plays a role in the transport of copper from the liver to other parts of the body. Copper is an important part of certain enzymes that maintain normal cell functions. Copper-transporting ATPase 2 is also important for the removal of excess copper from the body.Within liver cells, copper-transporting ATPase 2 is found in a structure called the Golgi apparatus, which modifies newly produced enzymes and other proteins. Here, copper-transporting ATPase 2 supplies copper to a protein called ceruloplasmin, which transports copper to other parts of the body via the blood. If copper levels in the liver get too high, copper-transporting ATPase 2 leaves the Golgi and transfers copper to small sacs (vesicles) for elimination through bile. Bile is a substance produced by the liver that is important for digestion and the removal of waste products.
  The GPHN gene provides instructions for making a protein called gephyrin, which has two major functions in the body: the protein aids in the formation (biosynthesis) of a molecule called molybdenum cofactor, and it also plays a role in communication between nerve cells (neurons).Gephyrin performs the final two steps in molybdenum cofactor biosynthesis. Molybdenum cofactor, which contains the element molybdenum, is essential to the function of several enzymes called sulfite oxidase, aldehyde oxidase, xanthine dehydrogenase, and mitochondrial amidoxime reducing component (mARC). These enzymes help break down (metabolize) different substances in the body, some of which are toxic if not metabolized.
• liver sluggishness or toxicity – yes, this probably applies to me or did. I’m confident I’m well on my way to fixing this one.
• mercury toxicity – derangement of mineral transport by mercury is closely associated with copper accumulation (Dr. Cutler). I believe I’m one of those cases discussed by Dr. Cutler with hidden mercury, I have the symptoms and patterns but the mercury doesn’t show on the hair test. Also my significant lead increases the toxicity of the Mercury I do have by 18 times.
• plant-based diets – that’s not me!

Can my 23andme results tell me anything about my copper problem?

I loaded my 23andme data into Promethease.com and found out that of 8 SNP’s checked, I have 6 good and 2 not classified. This report cost five dollars and is really really interesting. Here are a few tidbits from my report showing how awesome I will be once I detoxify my body:

• “You are part of the 12% of the population who can lose weight with any type of exercise”
• “Any diet works for you”
• “Better performing muscles. Likely sprinter. This genotype indicates better performing muscles, particularly for sprinting and power sports.“
• “Better odds of living to 100”
• “Optimistic and empathetic; handle stress well The one in four subjects who inherited a variation in this allele called G/G were significantly better at accurately reading the emotions of others by observing their faces than were the remaining three-quarters of subjects, who had inherited either a pair of A’s or an A and a G from their parents at this site. . . . also less likely to startle when blasted by a loud noise, or to become stressed at the prospect of such a noise. And by their own reports, the G/G subjects were mellower and more attuned to other people than were the A/As or A/Gs.”

Now, let’s see what Livewello.com can tell me…

Report notes:

Wilson disease protein is associated with ATP7B gene [1]
Wilson disease protein (WND), also known as ATP7B protein, is a copper-transporting P-type ATPase which is encoded by the ATP7B gene. ATP7B protein locates in trans-Golgi network of liver and brain, balances the copper level in the body by excrete excess copper into bile and plasma.

Genetic disorder of ATP7B gene may cause Wilson’s disease, a disease in which copper accumulates in tissues leading to neurological or psychiatric issues and liver diseases.

Wilson disease happens when accumulation of copper inside the liver causes mitochondrial damage and cell destruction and shows symptoms of hepatic disease. Then, the loss of excretion of copper in bile leads to an increasing concentration of copper level in urine and causes kidney problems. Therefore, symptoms of Wilson disease could be various including kidney disease and neurological disease.[8] The major cause is the malfunction of ATP7B[8] by single base pair mutations, deletions, frame-shifts, splice errors in ATP7B gene.[1]

So, we can see in my case, 51% of the 35 ATP7B genes checked by this report have genetic variations – maybe I should consider copper chelation with pharmaceuticals… And there’s more:

The GPHN gene provides instructions for making a protein called gephyrin, which has two major functions in the body: the protein aids in the formation (biosynthesis) of a molecule called molybdenum cofactor, and it also plays a role in communication between nerve cells (neurons). Gephyrin performs the final two steps in molybdenum cofactor biosynthesis. Molybdenum cofactor, which contains the element molybdenum, is essential to the function of several enzymes called sulfite oxidase, aldehyde oxidase, xanthine dehydrogenase, and mitochondrial amidoxime reducing component (mARC). These enzymes help break down (metabolize) different substances in the body, some of which are toxic if not metabolized. Gephyrin also plays an important role in neurons. Communication between neurons depends on chemicals called neurotransmitters. To relay signals, a neuron releases neurotransmitters, which attach to receptor proteins on neighboring neurons. Gephyrin anchors certain receptor proteins to the correct location in neurons so that the receptors can receive the signals relayed by neurotransmitters.

GPHN gene mutations cause a disorder called molybdenum cofactor deficiency. This disorder is characterized by seizures that begin early in life and brain dysfunction that worsens over time (encephalopathy); the condition is usually fatal by early childhood. At least two mutations in the GPHN gene have been found to cause a form of the disorder designated type C or complementation group C. This is the rarest form of the condition, affecting only a small number of individuals. The GPHN gene mutations involved in molybdenum cofactor deficiency likely reduce or eliminate the function of gephyrin. The known mutations impair gephyrin’s ability to perform one or both of the final two steps of molybdenum cofactor biosynthesis. Without the cofactor, the metabolic enzymes that rely on it cannot function. The resulting loss of enzyme activity leads to buildup of certain chemicals, including sulfite, S-sulfocysteine, xanthine, and hypoxanthine, and low levels of another chemical called uric acid. (Testing for these chemicals can help in the diagnosis of this condition.) Sulfite, which is normally broken down by sulfite oxidase, is toxic, especially to the brain. Researchers suggest that damage caused by the abnormally high levels of sulfite (and possibly other chemicals) leads to encephalopathy, seizures, and the other features of molybdenum cofactor deficiency.

How do people lower copper and treat copper toxicity?

This is how I lowered copper the first time, in between my first and second hair tests:

• 50 mg zinc three times a day with meals, 150 mg per day zinc total
• 1 mg molybdenum three times a day with meals, 3 mg molybdenum total
• stopped consuming outrageous quantities of high copper foods
• DMSA chelation – probably not a very significant factor based on comments by Andy Cutler.

Some additional things I’m considering now include:

• vitamin C 1 g five times a day (prevents lipid peroxidation caused by copper overload)
• melatonin – because it protects against copper-mediated free radical damage
• liposomal glutathione – seems to be involved in metabolism of copper and its excretion

Here are the copper chelators:

• BAL – toxic
• DMSA – works through the kidneys and increases excretion of copper minimally according to Dr. Cutler
• DMPS – I tried this and reacted badly to it even at low quantities (maybe because it was pulling loads of copper)
• D-penicillamine (DPA)
• triethylenetetraamine (Trientine)
• tetrathiomolybdate (TTM) – still experimental. I got very excited about it at first but then read about some sheep whose lives were saved from copper poisoning – but the sheep died a few years later and were found to have high TTM concentrations in their glands.

Studies of excretion of Cu from sweat and urine and found that sweat is the most efficient way of eliminating Cu from the body – apparently 100x more Cu eliminated from sweat than from urine. This would be very exciting for me if I were not exercise and heat intolerant!

I’m not too interested in DPA and Trientine considering the side effects. Who wants to mess with new risky substances when minerals like zinc and molybdenum can do the job?

What does Andy Cutler say about high copper?

• stopped taking high doses of zinc and molybdenum prematurely
• while chelating with ALA (which reduces copper excretion in bile)
• and tested for copper too infrequently

This is why you really want a coach to help you through chelation if you can afford it. I goofed!

A few excerpts and other comments made by Dr. Cutler:

• “the half-life of copper in the body is about a month. As copper excretion bile is reduced, the half-life lengthens. Interventions to modify copper body burden take more or less a month . . . to show their beneficial effects.”
• “Zinc inhibits copper absorption as does vitamin C.”
• “Supplements that increase bile flow will increase copper excretion.”
• “Copper toxic people who don’t have mercury have “normal looking” hair analyses with high copper. People with high copper and high mercury probably aren’t making enough bile and need to pay attention to getting their liver to do this.”

What can I learn on FDC about high copper?

• B6- 100 mgs. 2x day
• B5- 500 mgs. 2x day
• Vitamin C- I take 1000 mgs. 5x day
• Vitamin E- 400 is’s 2x day
• Vitamin A- 20,000 iu’s per day”

Why did my copper fall dramatically from test 1 to test 2?

I believe it was due to:

• 50 mg zinc three times a day with meals, 150 mg per day zinc total
• 1 mg molybdenum three times a day with meals, 3 mg molybdenum total
• stopped consuming outrageous quantities of high copper foods

Why did my copper climb again?

I foolishly stopped taking the high quantities of zinc and molybdenum before testing to make sure my copper was down all the way to healthy levels. I did this because Dr. Cutler talks about how fast copper drops and recommends hair testing once a year roughly. He might say somewhere to test more frequently with high copper but if so, I failed to pay attention. I assumed that my low copper diet would do the trick after seeing my good progress on the first test. You know what they say about assumptions.

On the other hand… there is this guy Fernando who has been getting tested for three years and his copper and mercury levels have been going up steadily at the same time as he has been feeling better and better through nutritional balancing. He’s saying that the hair test copper going up shows that his detox is working. My situation is probably a mixed one.

How badly did I screw up?

Badly enough that I wanted to cry and didn’t sleep the first night after receiving my results. I might have prolonged my suffering by close to a year. On the other hand, it’s very possible I would not have discovered liver and colon cleansing and maybe most importantly oxygen therapy. These are therapies that will help me have a more complete recovery and I’m certain will benefit my family in powerful ways as well.

How about a little entertainment here too:

There exists a high copper personality.  Positive traits include a warm, caring, sensitive, emotional nature, often with artistic orientation and a child-like quality.  Often high-copper people are young-looking.  Many traditionally feminine traits are associated with copper such as softness, gentleness and intuitiveness.

Do I really want to lose my personality? Imagine my wife’s surprise when I turn into an athlete and a jerk after my recovery!

What should I do now?

I’ve already gone back on the high molybdenum/zinc protocol and also removed mushrooms, avocado and kale from my diet. This time, I’m not going to stop this protocol until I have proof that my copper is in range.