W. Thomas Johnson

Millions of years ago when the first organisms appeared, the earth's atmosphere was low in oxygen. However, this condition changed when some of these early organisms developed the ability to use light for splitting water into hydrogen and oxygen. The oxygen generated by these organisms raised the oxygen content of the Earth's atmosphere. Today, the atmosphere is 21% oxygen and supports many diverse life forms that need oxygen to live. However, oxygen is toxic. Primitive organisms needed to develop defensive mechanisms that would protect them from oxygen toxicity and assure their survival. While the evolution of these defensive mechanisms allowed organisms to cope with oxygen, it also allowed them to begin using oxygen in metabolic processes.

At some point in time a primitive organism evolved that could generate energy efficiently by using oxygen. This was fortunate for us because each of our cells contain mitochondria which are the remnants of this primitive organism that now serve as the power plants supplying the energy needed to drive cellular metabolism.

What does this have to do with nutrition? During evolution, copper was incorporated into several of the defensive and metabolic processes that allowed life to exist and even prosper in an oxygen-rich atmosphere. The dependence of these processes on copper has persisted through the ages and is the reason that copper is now classified as an essential nutrient. For example, one of the components in the mitochondrial energy producing mechanism is a copper-containing enzyme called cytochrome c oxidase.

This enzyme is very responsive to dietary copper. Research at the Grand Forks Human Nutrition Research Center and other laboratories around the world has shown that the consumption of diets that are low in copper reduces cytochrome c oxidase activity in the mitochondria of humans and animals. My research has shown that reduction in the enzyme's activity is accompanied by changes in the way cells produce energy as well as by damage to their mitochondria from highly reactive types of oxygen. These findings have important implications for human health.

Although a diet that supplies 2 milligrams of copper a day is considered adequate, about 30% of diets in North America and Europe provide less than 1 milligram of copper on a daily basis. Studies at our Center indicate that this is insufficient to maintain normal cytochrome c oxidase activity in some types of cells. A growing body of evidence from several laboratories has shown that changes in cytochrome c oxidase and oxidative injury to mitochondrial components, particularly mitochondrial DNA, contribute to some common degenerative disorders including Alzheimer's disease, heart failure and diabetes. Could the legacy of copper dependency instilled in us because of ancient changes in atmospheric oxygen haunt us now as the degenerative diseases that we are all so familiar with? If so, what amount of dietary copper is needed to slow or prevent the degenerative process? The answer to these questions is the goal of some of the research currently being conducted at the Grand Forks Human Nutrition Research Center.