BY MORLEY M ROBBINS

Fatigue is the most common health complaint patients report to their physicians. Yet few physicians today know how to help their patients banish fatigue. Knowing how to truly resolve fatigue is simply not in their wheelhouse.

Millions of people continue to struggle with persistent fatigue and a wide range of chronic degenerative health conditions. Instead of addressing root causes, many treatments merely manage symptoms—and in some cases introduce additional side effects.

This disconnect exists because an important biological system that governs energy production is largely overlooked.

The Missing Mineral System

Ceruloplasmin is a protein manufactured principally in your liver but also in many other tissues in your body. It transports copper throughout the body. Up to ninety percent of copper found in the blood is transported by ceruloplasmin, yet that circulating copper represents only about one percent of the copper in the body. The remaining ninety-nine percent is found in our tissues.

When this mineral-regulating system breaks down, iron begins to accumulate where it should not—disrupting cellular energy production and contributing to persistent fatigue.

Misled and Misfed

For more than two decades, I have sought to understand why so many people today—adults and children alike—suffer from chronic fatigue and other degenerative diseases. That search led me to examine how key minerals—magnesium, copper, and iron—along with the protein ceruloplasmin, interact to maintain human health. In the process, I also discovered what happens when these interactions are disrupted—often by widely accepted yet deeply flawed health recommendations.

Many of these insights were described in the medical literature more than one hundred years ago, yet their findings were largely ignored.

At best, these recommendations reflect decades of human error across medicine, government health agencies, agriculture, and the food industry. At worst, they may be due to a more nefarious agenda, one designed to prevent us from achieving the optimal health and abundant energy we all deserve.

Overall, I’ve come to recognize that it’s the first factor—lack of curiosity and human error—that is mostly responsible for the healthcare crisis our nation and other nations face. Dwelling on frustration serves little purpose beyond triggering the body’s stress response, which can rapidly deplete mineral reserves—especially magnesium. Still, understanding how we have been “misled and misfed,” whether intentionally or not, is essential if we hope to restore health.

Ancient Clues About Oxygen

Everybody wants to know what’s new, but understanding what endures is often far more important. One overlooked clue to understanding fatigue lies in what happened when oxygen first began accumulating in Earth’s atmosphere long ago. According to astrophysicists, about 2.45 billion years ago, the Great Oxygenation Event (GOE) occurred, sometimes called the Oxygen Catastrophe, wiping out an estimated ninety-nine percent of existing species as oxygen levels rose from a nearly oxygen-free, “reducing” atmosphere.

Why does this matter for your health today? Because the same oxidative chemistry that once made oxygen deadly for early life is the very process that now “rusts” our tissues and organs, saps energy, and drives disease when oxygen is not properly controlled inside the body.

These events illustrate just how reactive oxygen can be. Oxygen in excess is toxic to aerobic beings as well. Yet that basic biological truth is not properly taught in medical schools.

The second part of the clue is that copper literally saved life as we know it. Once oxygen accumulated, life had to find a way to manage its high reactivity. Copper-dependent enzymes solved this problem by safely converting oxygen into water without generating harmful oxidative byproducts.

That is the gift of copper to our planet—and also to our physiology. We need bioavailable copper—copper the body can absorb and use—to prevent oxidative stress. It does this by safely converting oxygen into water and other usable molecules.

Were it not for copper, life on Earth would be impossible. All life depends on copper-based systems to manage oxygen safely. Without enough bioavailable copper in our bodies, oxygen’s reactive nature begins damaging tissues and mitochondria—the cellular “powerhouses” responsible for energy production. Copper, when naturally working through its network of enzymes, is the only element in the body that works with oxygen cleanly to prevent oxygen from “rusting out” our cells, tissues, and organs.

Copper, Iron, and the “Rusting” of the Body

In addition, copper is the only element that regulates iron’s status, thus preventing iron’s reactions with oxygen, which inevitably lead to this “rusting” process. When oxygen cannot be activated by copper in the mitochondria to produce water and release energy, oxidative stress results—creating free radicals and reactive oxygen species (ROS), highly reactive oxygen-derived molecules that can damage cells. This aligns with the “free radical theory of aging,” first proposed by Denham Harman in the 1950s, which holds that cumulative oxidative damage contributes to aging and disease.

Cholesterol’s Surprising Role

At almost the same time that the GOE occurred, cholesterol first made its appearance. Contrary to popular belief, cholesterol is not a toxin or a cause of disease. In fact, it takes eleven molecules of oxygen to make one molecule of cholesterol.

Cholesterol is really an oxygen sink for humans and any other organism that doesn’t have enough copper to activate oxygen to make energy in the mitochondria or to deactivate the oxidants to prevent oxidative stress.

For billions of years, cholesterol has served as a buffer, helping organisms that lack enough bioavailable copper survive in an oxygen-rich environment.

Among its many functions, cholesterol acts as a governor, regulating how much oxygen passes through cell membranes into cells. The less bioavailable copper you have, the more your body will produce oxidative stress, which will then cause an increase in cholesterol levels for this very reason. And that rising oxidative stress will “rust” the cholesterol. It was never the level of cholesterol that caused health problems. It was always about the amount of iron.

How does that relate to your health?

When Iron Becomes Trapped

Very simply: inert or bound iron in your tissues and organs also captures oxygen, causing them to “rust” or oxidize. In order to be healthy and have all of the energy you need, iron in your body needs to be mobilized and circulating, so that it can carry oxygen to all of your organs, tissues, cells, and ultimately to the mitochondria to be turned into energy, rather than remaining bound in the tissues.

That is what iron is designed to do—deliver more oxygen. But once it becomes immobilized and bound (stuck) in tissues, health problems begin as levels of oxidative stress rise from failed energy production and failed oxidant elimination.

That’s why copper is so important. Just as it rescued life on the planet billions of years ago, so, too, is it safeguarding our health as long as we do all that is necessary to enable it to do so.

Copper and Cellular Energy

The first principle to understand if you want to regain your energy and improve your health is that we humans can’t work with oxygen on its own. Copper interacts with oxygen to do two things: first, it activates oxygen to create two molecules of water, which then allows for the release of energy, and second, it deactivates oxidants to clear metabolic exhaust.

That’s the unique gift of copper. Copper enables energy production in mitochondria through key enzymes such as cytochrome c oxidase, the enzyme that drives the final step of cellular energy production.

Energy production also generates metabolic exhaust. Copper is able to run a whole series of enzymes, including ceruloplasmin, that are designed to take the sting out of the oxidants produced by the activation of oxygen. Without ceruloplasmin, these “accidents with oxygen” turn into free radicals that “rust” out our tissues and organs. Mitochondria are the source of ninety percent of the body’s energy and ninety percent of its exhaust.

Now you can see why copper is such an important part of mitochondrial function. No or low bioavailable copper inevitably means no or low energy. Despite the oft-repeated phrase that we are “copper toxic,” the reality is just the opposite.

Even though we are all different, all of our cells are designed to engage in two fundamental actions: create energy and clear exhaust. To do that, all our cells rely on a balance of three key minerals (magnesium, copper, and iron), along with ceruloplasmin, to function properly. The fact that many people struggling with fatigue have never heard these concepts should itself be a clue.

Much of this information has been known in scientific literature for decades. Yet these mineral and metabolic truths are being overlooked, misunderstood, and, worse yet, not taught to doctors and other health practitioners.

Early Scientific Evidence

Research dating all the way back to 1928 proves that the lack of bioavailable copper causes iron accumulation in the tissues, especially in the liver. When copper is insufficient, iron accumulates in tissues where it does not belong, triggering oxidative stress that disrupts cellular energy production.

The scientific literature from around the world—though not widely discussed in conventional medicine—is clear and consistent. Persistent fatigue—and many chronic diseases—are driven by oxidative stress. Oxidative stress arises when cellular function breaks down due to an imbalance among copper, iron, magnesium, and the copper-dependent protein ceruloplasmin. This prevents our ability to metabolize energy, recycle iron in the mitochondria, and, therefore, prevents harm caused by iron’s inevitable interactions with oxygen in our tissues and blood.

Copper harnesses oxygen much the same way chefs harness ingredients to create a delicious meal. Iron’s function, by contrast, is to transport oxygen in much the same way that a waiter carries the meal to the diners in a restaurant.

Much of what you “know” about your health condition, especially your fatigue, is flawed by “missing information.” Without understanding the roles of copper, iron, magnesium, and ceruloplasmin, the basic physiology behind fatigue remains hidden.

Many discoveries documented throughout the twentieth century remain poorly communicated in modern healthcare. We want to trust our doctors and health practitioners, but unfortunately, through no fault of their own, they are not taught this fundamental information about how the cells in our body work. As a result, many people struggle to regain the energy and vitality their bodies can produce.

Ceruloplasmin: Your Own Sun

In the same way that the sun is the center of our solar system, I’ve come to regard ceruloplasmin as the “sun” of our bodily universe of metabolic activity. This most vital protein is pivotal for regulating iron, copper, and oxygen status in the body, and it expresses up to twenty or more enzyme functions.

In addition, there are ceruloplasmin receptors throughout the human body, including in all of the body’s endothelial cells, which line the inner walls of the blood vessels. The purpose of these receptors is to serve as a docking station for ceruloplasmin to download copper into these cells to support metabolic and antioxidant functions.

This calls into question one of the cornerstones of chronic disease, which is built around endothelial dysfunction—the breakdown of the thin cellular lining that regulates blood vessel health. The function and metabolic integrity of the endothelium are based upon bioavailable copper, which, in turn, depends upon ceruloplasmin and the ceruloplasmin receptors. Yes, endothelial dysfunction certainly does occur, but only in the absence or deficiency of these two “partners in health.”

To understand why ceruloplasmin is so important to our health, we need to consider how our body’s cellular processes are designed to both produce energy and repair itself, and to contain and eliminate toxins. Our cells need to be able to both create energy and clear “exhaust” as energy is produced by our mitochondrial power grid. This is one of the key roles that ceruloplasmin plays.

As our cells produce energy, ceruloplasmin—along with other copper-dependent enzymes—keeps the oxidants generated during this process in check, preventing the oxidative stress that contributes to chronic disease.

Without ceruloplasmin—and the network of cuproenzymes—the oxidants turn into free radicals that “rust” out tissues and organs.

Just as importantly, it is ceruloplasmin that makes copper available to our cells, tissues, and organs. An apt analogy is that ceruloplasmin is the “taxi” that drives copper to where copper needs to go. There is no greater need for copper than in our mitochondria.

Ceruloplasmin belongs to a family of proteins and enzymes known as multicopper oxidases (MCOs). In this capacity, ceruloplasmin regulates the transportation of iron into red blood cells and other essential iron-containing proteins involved in cell growth. Because ceruloplasmin carries copper, it helps regulate iron metabolism and prevents the oxidative stress and inflammation that occur when iron becomes unbound and reactive in our tissues. And it provides similar protection against unchecked oxygen. (Oxygen is essential for cellular energy, but when it is not properly regulated by ceruloplasmin and other copper-dependent enzymes, it can generate damaging free radicals.)

Ceruloplasmin supports cellular energy production while helping prevent the formation of damaging oxidants through its copper-dependent activity. Studies show that ceruloplasmin scavenges and inhibits the production of hydroxyl radicals, superoxide radicals, and lipid peroxides, all of which are types of oxidants that are dependent on iron ions. If energy is falling and oxidative stress is rising, then our body lacks bioavailable copper or ceruloplasmin.

Copper is the key to ceruloplasmin’s ability to regulate iron metabolism through its ferroxidase activity, which prevents iron from becoming reactive. Research shows that mutations in the ceruloplasmin gene can prevent copper from being incorporated into the protein, disrupting iron metabolism and leading to iron accumulation. Studies have shown that defective ceruloplasmin, lacking copper, is a factor in a wide range of disease conditions.

These defects can lead to neurological symptoms such as impaired movement, memory problems, and speech difficulties. The medical literature consistently shows that ceruloplasmin keeps iron in its proper chemical state and helps it circulate through the body via key transport proteins. Scientists like to refer to this action as cellular iron efflux, which is a fancy way of saying “keep iron moving.”

Circulating iron is the ideal state for iron. It is not meant to be stored. That is why measuring iron in its storage state, via the serum ferritin protein, makes little sense. It is akin to selecting a car based solely on the size of its trunk while ignoring the size and efficiency of its engine.

It is also known that ceruloplasmin levels become elevated as an acute-phase reactant in response to inflammation. Yet instead of recognizing that elevated ceruloplasmin—and the antioxidant activity of the copper it carries—is an appropriate response to infection and inflammation, Big Pharma is applying the same misinformation strategy used against cholesterol since 1955. Like cholesterol, they want us to see ceruloplasmin as the “bad guy” and recommend that we do what we can to “lower” it.

This makes little sense, because elevated ceruloplasmin during inflammation is a sign that the protein is doing what it is meant to do—helping bring inflammation under control. Entirely missing in this drama is knowing the activity of this key protein. Knowing the level of ceruloplasmin is not the same as knowing its enzyme activity, just as knowing someone’s height is not the same as what they are physically capable of.

What Pharma and physicians who accept this myth-guided approach overlook is that ceruloplasmin must contain adequate copper and properly folded amino acids to function fully as a master antioxidant enzyme. Because ceruloplasmin’s ferroxidase activity regulates iron status and movement, lowering ceruloplasmin disrupts this process and can lead to serious health consequences.

As one scientific paper put it, “It should be remembered that the protein [ceruloplasmin] is an acute phase entity so that its concentration in the plasma increases twofold to threefold [emphasis added] at the onset of infection or wounding. Under these circumstances, the multi-functionality may be highly important. There is no ‘may’ about it: ceruloplasmin’s multi-functionality is highly important.”

Ceruloplasmin: The Body’s Defense System

Another example of ceruloplasmin’s multi-functionality is the role it plays in helping the body fight infections. Like copper, ceruloplasmin is important for enabling neutrophils to kill harmful bacteria. For neutrophils to do this effectively, iron must remain in the proper chemical state to regulate an enzyme called myeloperoxidase (MPO), which can otherwise interfere with immune defense. Research proves that ceruloplasmin, by regulating iron valence, inhibits MPO.

This is important because MPO promotes oxidative stress during inflammation and infection by producing a substance called hypochlorous acid (HOCl). Ceruloplasmin helps shield the body from oxidant production by regulating the MPO response. It does this by managing iron so that it remains in the right state and stays active.

Ceruloplasmin’s ability to keep MPO in check is also of significance to anyone who engages in endurance exercises, such as marathons. Endurance exercise depletes our minerals, especially magnesium. This depletion can trigger inflammation, including in the heart, and cause MPO levels to rise.

In athletes with low ceruloplasmin, rising MPO levels can degrade heme in hemoglobin, releasing iron that accelerates oxidative stress and further depletes magnesium. In extreme cases, this chain reaction may help explain why some long-distance runners suffer fatal cardiac events near the end of races.

By now, it should be clear how vital copper, magnesium, and ceruloplasmin are to maintaining energy and protecting the body from oxidative stress. When these minerals and proteins work together, the body can generate energy efficiently, recycle iron properly, and keep oxidative damage in check.

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Morley M Robbins is the creator of the Root Cause Protocol, designed to ignite energy in our metabolism, and the author of the popular book [Cu]re Your Fatigue. Also known as “Magnesium Man,” he is a recognized expert on mineral metabolism and the delicate dance that copper plays with iron, magnesium, and calcium.

He received his BA in Biology from Denison University in Ohio and holds an MBA from George Washington University in healthcare administration. Morley has completed numerous wellness certification programs, is a certified health coach, and has been a podcast guest on over 300 health programs.

Well Being Journal adapted the above excerpt from [Cu]re Your Fatigue, Second Edition: The Root Cause and How to Fix it On Your Own by Morley M Robbins. Copyright © 2025 by Morley M Robbins. Printed with permission from BenBella Books, Inc.