W. Thomas Johnson

The last two decades have produced an abundance of nutritional knowledge. New nutrients have been found and new roles have been discovered for well-known nutrients. Recommendations for dietary intakes of fat, carbohydrate, and protein also have been updated. One can hardly pick up a newspaper or magazine that doesn’t contain an article about foods that enhance health, prevent disease, or lead to weight loss.

Clearly, the abundance of nutritional knowledge has led to a pretty well-informed public. However, most people are unaware of the work required to obtain that knowledge. Nutrition articles that appear in reputable newspapers and magazines are usually based on information obtained from scientific research. Historically, scientific research has led to change, and nutrition research is no exception. It is an active endeavor that will eventually change the current state of knowledge. Present dietary requirements and concepts regarding healthy diets, even those that seem written in stone, will probably change in light of new knowledge provided by nutrition research.

How are new ideas generated? An enzyme, called superoxide dismutase--or SOD--serves as an example that shows how scientific thought can evolve. SOD contains both copper and zinc, and past research has shown that copper deficiency lowers the activity of this enzyme. As a result, SOD is often used as an indicator of copper status in humans and animals suspected of being copper deficient. It is also known that SOD helps to destroy highly reactive forms of oxygen that can damage cells. This implies that copper deficiency can lead to cell injury by increasing oxidation.

A few years ago, scientists discovered that mutations in SOD occur in about 2 percent of patients suffering from amyothrophic lateral sclerosis (ALS)--also known as Lou Gehrig’s disease--which is a progressive degeneration of nerve cells that control muscles. This led some nutrition scientists to think that some forms of ALS could be classified as nutritional deficiency diseases. They hypothesized that copper deficiency lowers SOD activity, thereby increasing oxidative damage to the nerve cells. Their hypothesis was based on the assumption that the mutated SOD was less efficient than normal SOD in destroying reactive oxygen. However, subsequent research found that the mutant SOD was quite capable of preventing oxidation. Apparently, something else was causing the mutant SOD to damage neurons.

At this point, nutrition scientists lost interest because the finding did not fit their hypothesis. Very recently, scientists found that zinc is easily detached from the mutant SOD associated with ALS. Furthermore, when mutant SOD loses zinc, it becomes toxic to motor nerve cells and causes them to die. The scientists also found that removing zinc from normal SOD causes it to become toxic to these cells. Although they don’t fully understand why this happens, the discovery may rekindle the idea that some neurological diseases are deficiency diseases.

While the hypothesis that zinc deficiency may start nerve cells on a death plunge by producing a toxic form of SOD is highly speculative, the hypothesis itself serves as an example of how ideas in nutrition science can evolve. If scientists in universities and research laboratories like the Grand Forks Human Nutrition Research Center choose to test the hypothesis, years of research would be required to determine its validity.

If the findings support the hypothesis, then the public will learn about it in newspapers and magazines. They may even find that the research changed the amount of dietary zinc recommended for proper health. If research does not support the hypothesis, the public will never know about the time and effort scientists spent chasing an idea. However, it is important for people to understand that chasing ideas is something scientists do. And, when the chase is successful, it can be beneficial to all.

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