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– The poorly-understood role of copper in anemia:
Morley Robbins, MBA, CHC,1 a repeat guest, is the founder of the Magnesium Advocacy Group. He’s best known as the Magnesium Man, and is the author of “Cu-RE Your Fatigue: The Root Cause and How to Fix It on Your Own,” in which he explains the roles of magnesium, copper, iron, vitamins A and D and other essential nutrients.
His Root Cause Protocol2 is the implementation of that information. We’re currently planning to write a book together, which will focus on the little-understood importance of copper and its interaction with iron.
As explained by Robbins, if copper is lacking in your diet, iron will build up in your liver, which changes its physiology and immunoproperties. Liver metabolism is highly dependent on copper and retinol, and there’s not a lot of awareness of that.
“It’s a very sophisticated process of interaction between copper and iron, and if that interaction doesn’t go well, iron is going to start to accumulate in the tissues. It’s going to start in the liver, but it’s going to go elsewhere too,” he says.
“I think that is kind of the takeaway of these conversations — to make sure people know that iron does accumulate, and that iron can be reduced through blood donations. Especially as you get into your 50s, 60s, 70s, it needs to be a regular part of your health routine.”
Three Ways to Measure Iron Status
The clinical term for excess iron in the liver is hemosiderosis, and it’s so pervasive as to be near-universal. But where does the excess iron actually come from? And why is it that many with high iron stores have low serum ferritin?
As Robbins explains, oftentimes, low serum ferritin is not at all a sign of iron deficiency, but rather a deficiency in copper and retinol. The deficiency in copper basically locks iron in the liver and prevents it from being recycled as it should:
“It’s important for practitioners to not measure iron status with just one marker. I think a lot of practitioners are falling into that trap of just using serum ferritin. There are three key ways to measure iron status: Hemoglobin, serum iron and serum ferritin.
The biggest concentration of iron in the body is in our hemoglobin; 70% of the iron is in our red blood cells … Hemoglobin is essential to understand what is going on with the biggest bulk of iron.
The second marker that I really focus on is called serum iron. It’s less than 1% of the iron, but it’s a very important measure of iron because it’s really getting at the iron recycling program. Every second of every day, we have to turn over 2.5 million red blood cells. That’s a lot of activity. In the course of 24 hours it’s 200 billion red blood cells that need to be turned over.
But what’s a surprise is to learn that only 25 milligrams (mg) of iron are needed to support that 24-hour cycle, but 24 of those 25 milligrams, 95% of the iron, is coming from this recycling program. So, it’s a very significant understanding that the serum iron only represents a small percent, but it represents the efficiency of the iron recycling.”
Ideally, hemoglobin should be between 12.5 and 13.5 for women, 14.5 to 15.5 for men. Serum iron should ideally be about 100 for women and 120 for men. The closer serum iron is to these, the more efficient your recycling is.
What You Need to Know About Serum Ferritin
The third iron measure is serum ferritin. There are four different types of ferritin in your body, broadly categorized as heavy chain and light chain. Heavy chain ferritin refers to ferritin protein inside cells and mitochondria that require copper to work properly. Serum ferritin refers to ferritin in your plasma, is outside the cell — and also outside the red blood cells, the hemoglobin.
“What is not well-known is that this ferritin that shows up in the blood is very iron-poor. It doesn’t have iron in it. The iron has been discharged in the liver and then the protein gets secreted out … So, serum ferritin is not representative of iron per se. The iron was discharged in the liver …
I would never use ferritin only as an indication of iron status. You need to see hemoglobin, serum iron, and serum ferritin. You need to see them in relationship to each other …
[When] serum ferritin starts to get high, it’s highly correlated with inflammation or an infection. And again, it makes sense. The liver is taking it on the chin. Iron is not being metabolized properly. Pathogens might be involved. And so, the body starts to secrete the ferritin in a more significant way …
Serum ferritin should be between 20 and 50. That seems to be a nice sweet spot for people. When the serum ferritin begins to get up in the hundreds, there’s a significant likelihood that there’s pathology in the liver that’s causing that …
For women, the serum ferritin red flag goes up at 150. For men, the red flag goes up at 300. It can go up into the 5,000s and even higher, with severe chronic disease and inflammation …
Low ferritin is an indication of metabolic breakdown in the spleen … it’s some kind of parasitic dynamic that’s affecting protein production. The ferritin protein is not getting transcribed properly …
So, low ferritin … means low recycling. Something in the iron recycling system is out of balance and needs attention. I would argue that, almost without exception, it’s a lack of bioavailable copper. The spleen organ is intensely copper dependent. The liver intensely copper dependent. That’s not well known in clinical circles.”
So, to summarize, one of the most common errors doctors will make is to prescribe iron pills when serum ferritin is low. More than likely, what’s needed is copper, retinol and other factors to support iron recycling. Unfortunately, articles and textbooks on iron metabolism rarely if ever mention the copper side, even though copper plays a far more important role in the recycling of iron.
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