If you research either vitamin D or copper enough, you’re bound to come across Morley Robbins contrarian views eventually. I tend to listen to people who seem to have deep knowledge in tightly confined areas especially when they say everyone else is wrong. So about a year ago, I stopped trying to take vitamin D and stopped giving it to my family because of Morley Robbins.
Ray Pete’s writings convinced me to stop taking fish oil at some point. Not much happened when I stopped and I’ve since restarted the fish oil, albeit at much lower doses.
I don’t like feeling like the Lone Ranger so this year I consulted Rick Malter on my copper toxicity picture. Then for good measure I sought out Morley Robbins for a second opinion (my most recent HTMA on the right). Rick thought I was mostly on the right track but wanted me to be a little less aggressive with my copper detox because of the risk of cardiac arrest.
Morley Robbins had a very different opinion for me, saying “It’s the iron, stupid”. Okay, he didn’t say it exactly like that, but pretty close. I’m going to try to summarize his case here for my own benefit and maybe for yours. In a nutshell, my iron levels are double what they should be. This causes tremendous amount of oxidative stress in my body and most critically disables my liver preventing it from resolving other secondary toxicities.
“Think of your health problems as a Ferris wheel”, he says. Oh, but it’s not spelled Ferris, it’s Ferrous with ‘ous’. Your copper toxicity, heavy metal toxicity, tendonitis, fatigue etc are all represented by the chairs hanging on the wheel. The axle at the center of everything is your iron overload. Here’s what that looks like on my recent Labcorp test results:
There is some convincing science that iron accumulation is a very underappreciated problem. It seems to be highly correlated with degenerative brain function and disease and this has been proven by studies comparing men and women and postmenopausal women. What? You mean a woman’s menses protects her brain function? Yes.
The quickest thing you can do to start lowering high iron is to give blood. This is one point on which Dr. Cutler and Morley Robbins agree. Too bad you can only do it every eight weeks. I also found quite a few other ways to lower iron which I will go over further down.
One of those ways happens to be cholestyramine… what a coincidence since I started taking it regularly a week ago. And that got me thinking, it’s possible my CIRS diagnosis is actually not a mold thing. Maybe it’s the iron.
Out of curiosity I went back and looked at my old old blood test results and guess what? My ferritin jumped from 75 ng/mlL in 2004 to 141 in 2006. That just happens to be the time period in which I went over the cliff with my health. Coincidence? Note, the normal range according to Labcorp is 30-400. Morley says to ignore that because “those ranges are for healthy people”. Some say “as a rule 25-75ng/mL is an acceptable range for most”.
Here’s what I think happened – unaware of my genetics, I inadvertently exposed myself to mold, VOCs and heavy metals. With its poor natural methylation, my body was unable to eliminate the toxins and they accumulated, resulting in deranged mineral transport and manganese depletion. That knocked out my sugar control. Or it’s possible that I had a mild accumulation of iron going back decades which worsened my sugar control.
Anyway, being the really smart dude I am (or was), I started eating very low glycemic index foods. I couldn’t fall asleep without eating, so every night I ate large quantities of teff. That prevented me from gaining too much weight and saved my adrenal glands from the huge blood sugar spikes caused by eating bread.
BUT… teff is packed with iron and copper. I ate a little more than 1 cup every day for several years and before you know it, my health was so poor, I was essentially disabled. By the way, I was ordering my teff in 25 pound bags and each would only last me a couple months.
So, how did I get from eating a lot of teff to disabled? Again, it’s genetics.
Seems to me that I may have enough genetic copper related flaws (ATP7B & GPHN) to give me a mild case of Wilson’s disease and enough iron related flows to give me a mild case of hemochromatosis. It’s likely that iron overload caused an acceleration of copper accumulation. That’s because when the liver starts accumulating iron it stops performing its duties which include producing ceruloplasmin, the main copper transport protein.
I don’t know whether iron overload came first, or copper or heavy metals. Maybe it was just a perfect storm and it was all happening together with some surges now and then from one contestant or another. In fact, Chris Kresser in this fascinating video mentions that VOCs contribute to copper accumulation.
Watch this video and you’ll note that the mainstream medical community won’t recognize such a thing as ‘a mild case of hemochromatosis’ or ‘a mild case of Wilson’s disease’. And that’s how I got really really sick, because the MDs I sought out, believed in those lab work “normal” ranges:
To be really fair, I have to tell you all so that my parents both have low ferretin numbers now. So I’m not at all blaming my illness entirely on genetics. It’s just one factor among many.
I’m pretty sure I can pursue both copper and iron reducing protocols at the same time and I don’t like to get bogged down in abstract or unsolvable mysteries. I want to get healthy and don’t think I need to know everything to get there. When my iron and copper are greatly reduced, then I’ll start working on the heavy metals.
The Ferris wheel also illustrates another choice Morley Robbins wants us to make, in addition to avoiding vitamin D supplements. He says that healers divide into two camps: in the first group are the ones that want to attack the chairs on the Ferris wheel – Dr. Cutler for example who says you have to get the mercury out (or Dr. Shoemaker who says you have to get the mold toxins out).
And in the second group you have mineral balancing experts like Robbins and Malter who want to strengthen the host (you). According to Morley, when my iron levels normalize, my body will regain it’s natural abilities to detoxify and thrive on its own.
Now for the details. If you want to go to the source, visit Morley Robbins website and read his toxicity of iron posts 35, 36, 37, 38, 39, 40, and 41. If you’re a scientist or want to be a scientist, read Sir Douglas Kell’s Iron behaving badly article. Or checkout life extension’s overview on iron and brain degeneration.
Here, I’ll try to summarize Morley Robbins posts for you. Here goes:
The average doctor will only look at your ferritin levels. All this measures is the iron you’ve got in storage. But we should be concerned about active iron metabolism. If your ferritin is high, it means that your liver, spleen, bone marrow and probably brain have already filled in with iron. You’ve waited too long to do something about it and you’re already ill.
The vast majority of all practitioners also recommends high dose of vitamin D which is actually a hormone so should be called hormone D. High-dose vitamin D (and sunshine) depletes vitamin A, which in turn causes iron anemia.
So you’re thinking I should just take a lot of vitamin D and that will solve my iron problem. Here’s the catch, taking high-dose vitamin D causes iron anemia by lowering ceruloplasmin which reduces bioavailable copper and iron. That’s going to make me sicker. How does this happen? The vitamin D depletes vitamin A which is a precursor to ceruloplasmin.
If you’re like me, you’re now thinking “Why not take vitamin D with vitamin A to get the benefits of D without lowering ceruloplasmin?” well according to Morley the answer is that vitamin D is a powerful hormone and causes other problems: increases calcium, lowering potassium slowing the thyroid. Decreases magnesium agitating the adrenal glands. In a nutshell, it’s a can of worms.
Back to iron. Each ferritin molecule can hold as many as 4,500 iron atoms resulting in tremendous oxidative stress in your body.
Ferritin is mostly contained or stored iron. It is the free iron that is not contained or unbound that is dangerous to us.
It’s dangerous because free iron overload:
- lowers cell pH to acidic levels
- lowers cellular oxygen (optimal oxygen occurs at pH 7.4)
- lowers production of ATP in the mitochondria
- damages organs
- nourishes harmful bacteria, fungi and protozoa
- can change DNA
- can help to spread cancer
Most of us are more familiar with the dangers of low iron or iron anemia, right? Well, Morley has a lot to say about that too and I’m glad because my wife and one of my daughters have very low ferritin.
He says we have known since the 1860s that iron anemia (and low hemoglobin) is a clinical indication of copper deficiency which you should read as ‘low bioavailable copper’. But iron anemia is not the only trouble caused by low bioavailable copper. It’s more of a train wreck situation because bioavailable copper plays a key role in:
- the creation of EPO in the adrenals which is a hormone that signals for new red blood cells in bone marrow
- the production of heme
- the insertion of iron into heme
- the creation of hemoglobin
- the recycling of iron
So, if you have low ferritin, low serum iron and/or low iron saturation, there’s a good chance you have copper deficiency as well.
At this point, it’s time to talk about ceruloplasmin (cp). If you know a little bit about it, you’ll remember that it’s the major copper carrying protein in the blood. If you have a copper deficiency, you most likely have low cp and need to increase it. But now you should not be surprised to learn that cp is also an iron transporter making sure that iron is in active circulation around the body where it should be.
Morley says “Ceruloplasmin GUARANTEES Iron Mobilization.” So I wonder if it wouldn’t be more accurate to say that the axle of the Ferris wheel is actually ceruloplasmin.
Want to read the science behind this? This report titled Metabolic crossroads of iron and copper shows the interactions between copper and iron are complex and far from understood at this point. The biggest take away from reading it for me is that your liver is at the center of this universe. I’m going to start doing liver flushes again on a regular basis, maybe aiming to do them quarterly…
Can I go off on a little tangent here? My wife also has Hashimoto’s thyroiditis which Morley says is caused by copper deficiency. Partly I mention this because Hashimoto’s is so widespread, affecting up to 10% of the population in the US and possibly 20% of women in the US according to Dr. Izabella Wentz.
So now I’ve got copper toxicity myself, my wife has copper deficiency and low ferretin, my oldest daughter has very low ferritin and my youngest daughter has high RBC copper. So you can see I’ve got a lot of interest in ceruloplasmin now.
Summarizing a little, you understand that we need adequate levels of cp to bind and transport both copper and iron so that it’s bioavailable. You understand that inadequate levels of cp cause iron and copper to get stored and circulate in a dangerous and harmful free state.
So now, Morley wants us to ponder what happens to the person with copper deficiency or iron anemia who takes copper or iron supplements. Some of them may have healthy levels of ceruloplasmin and those people will probably respond well to supplementation.
But the vast majority probably have low levels of ceruloplasmin, just like my wife and I.
So , given ALL of the above, WHY in the world do practitioners — of ALL flavors — mindlessly administer IRON, given that it will ONLY CAUSE the Oxygen levels to DROP EVEN FURTHER, given the fact that Unbound Iron LOWERS pH?!? And not one single word is EVER mentioned about Copper status, Ceruloplasmin status or the status of B-Vitamins that are very much a part of Iron metabolism…
For the record, my MD and functional medicine doc are both very open-minded and supporting me wholeheartedly in my battle for recovery! Without them, I’d be nowhere because the lab work costs a fortune if you have to pay for it out-of-pocket. THANK YOU.
So what can we do to raise cp? Here are a few things:
- supplement magnesium
- avoid taking vitamin D supplements
- take cod liver oil which provides natural forms of vitamin D and A
- get vitamin E in your diet with wheat germ oil
- take diatomaceous earth (DE)
- eat lamb, beef liver, goat, goat milk, pork,venison and rabbit because it has high nutrient density (a perfect balance of copper, zinc, iron, retinol, b vitamins and choline) to help rebuild the liver (cp is made in the liver)
- take milk thistle
- lower your manganese if it’s high
And a few things to avoid:
- the citrate form of vitamins/supplements
- artificial forms of vitamin C like ascorbic acid
- high-doses of vitamin C (1500 mg or more?)
- high doses of zinc (more than 15 mg?)
- iron supplements or supplements containing iron
- DMPS (if you have high iron)
- binging on high copper/iron foods
This is just an overview and I recommend getting a hair test analysis and personal consulting with Morley Robins. If your iron is high like mine, you may also want to read the Life Extension guide for hemochromatosis, a genetic condition that causes chronic iron overload.
After studying the natural methods for lowering iron I’ve decided on these:
Cholestyramine – Iron is excreted in bile so any binder that prevents the recirculation of bile by moving out of the body will reduce iron (I also use charcoal which does adsorb bile). This one is not so natural, I know. My MD prescribed it for CIRS so I was already taking it.
IP6 – Phytic acid—also called inositol hexaphosphate, or IP6—is comprised of six phosphorus molecules and one molecule of inositol. In foods, phytic acid binds to iron and other minerals in the digestive tract and may interfere with mineral absorption. As a purified extract of rice bran, taken between meals so it will not bind to minerals in the digestive tract, phytic acid is readily absorbed into the bloodstream, where it acts as a potent mineral chelator. Phytic acid binds to any free iron or other minerals (even heavy metals such as mercury, lead and cadmium) in the blood, which are then eliminated through the kidneys. Phytic acid removes only excess or unbound minerals, not mineral ions already attached to proteins. Phytic acid is such a potent—but safe—iron and mineral chelator that it may someday replace intravenous chelation therapy such as the mineral-chelator EDTA or iron-binding drugs such as desferrioxamine (Desferal). Because of its ability to bind to iron and block iron-driven hydroxyl radical generation (water-based) as well as suppress lipid peroxidation (fat-based), phytic acid has been used successfully as an antioxidant food preservative.
Lactoferrin – Lactoferrin’s primary role is to sequester free iron, and in doing so remove essential substrate required for bacterial growth. Antibacterial action of lactoferrin is also explained by the presence of specific receptors on the cell surface of microorganisms. Lactoferrin binds to lipopolysaccharide of bacterial walls, and the oxidized iron part of the lactoferrin oxidizes bacteria via formation of peroxides. This affects the membrane permeability and results in the cell breakdown (lysis).
An iron-binding protein analogous to the iron transporter transferrin; it binds and sequesters iron in areas outside of the bloodstream such as the mucous membranes, gastrointestinal tract, and reproductive tissues (Jiang 2011). It is present at high concentrations in milk, and is secreted by immune cells (neutrophils) as an antibacterial compound at sites of infection or inflammation (Paesano 2009; Brock 2012).
Experiments also suggest lactoferrin may have antioxidant and anti-inflammatory properties, and may influence the expression of inflammatory genes (Scarino 2007; Paesano 2009; Mulder 2008). Evidence suggests low-iron apolactoferrin may be protective against iron-mediated free radical damage; it reduced iron-catalyzed formation of hydroxyl radicals in vitro (Baldwin 1984). Dairy inhibits iron absorption because it contains lactoferrin. It can decrease or eliminate the side effects of nausea and constipation caused by iron supplementation.
Contrary to the antiviral and antibacterial actions of lactoferrin, very little is known about the mechanism of its antifungal action. Lactoferrin seems to bind the plasma membrane of Candida albicans inducing an apoptotic-like process.
Each lactoferrin molecule can reversibly bind two ions of iron, zinc, copper or other metals. It is demonstrated that lactoferrin is involved not only in the transport of iron, zinc and copper, but also in the regulation of their intake. Presence of loose ions of zinc and copper does not affect the iron binding ability of lactoferrin, and might even increase it.
Rutin – Polyphenols such as chlorogenic acid (Kono 1998), quercetin, rutin, chrysin (Guo 2007), punicalagins (from pomegranate) (Kulkarni 2007), and proanthocyanidins (from cranberry) have been shown to bind iron in vitro (Lin 2011). In an in vitro binding study of 26 flavonoids (a type of polyphenol) isolated from a variety of sources (including tea catechins, hesperidin, naringenin, and diosmin), several were nearly as effective as desferoxamine at chelating ferrous iron when supplied at a 10:1 flavonoid/iron ratio.
If reading this has piqued your interest in copper, please have a look at my next post about fighting copper toxicity with copper.
So, what do you think? Am I on the verge of a breakthrough?
UPDATE – Feb 9th, 2018:
After writing this post, I made lots of changes to my supplements and my sleep deteriorated steadily. I had been sleeping well 10 to 14 nights per month, but that dropped down to one good night of sleep per month. After nine months without sleep, I started experimenting, searching for the cause of my lost sleep. It’s now February 2018 and I’ve narrowed it down considerably and believe the issue is vitamin A deficiency.
When I wrote this post I was taking 20,000 IU vitamin A daily based on the Carl Pfeiffer Treatment Center protocol for copper toxicity. I just restarted taking vitamin A so I don’t know for sure what will happen. BUT, it’s worth noting that the liver is one of the primary storage centers in the body for both vitamin A and copper. And, they are antagonistic to each other. There are a bunch of studies about this in rats, but it’s hard for me to make sense of it.
Here’s what I think happened in my body – copper in my liver antagonizes the vitamin A that I get from food leaving me deficient in vitamin A. The next step is also way over my head, but I can see there is a clear link between glucose metabolism and vitamin A (fatty acid metabolism too, which has also been an issue for me). The bottom line – if gluconeogenesis doesn’t happen properly in your liver, I don’t think you can get a good nights sleep. Finally, I started high dose vitamin D in an attempt to improve my sleep.
Ironically, my sleep did not improve but my ceruloplasmin went up, not down! Moral of the story? Don’t fix what ain’t broke. And maybe don’t fall for everyone pushing an alternative viewpoint. And one more thing, my MD says high ferretin is a natural consequence of inflammatory processes – just ignore it and focus on the underlying infections. When you’ve solved the core issue, your ferritin will come back to normal. And that core issue for me and others with copper toxicity could be the CBS upregulation SNP.