By Tom Johnson
Why do we eat? This seems like a simple question. But when I asked several people, I received a variety of answers: “To nourish my body” or “because I’m hungry” and some far-out answers loosely related to the cosmos and our place in the universe.
While the answer to the question is simple — we eat to get energy — the process of converting food into energy is complicated. The important task of converting food calories into usable forms of cellular energy is shouldered by mitochondria, specialized organelles within cells.
Mitochondria take electrons extracted from the food we eat and push them through a series of steps that ends with the production of a compound called ATP. ATP provides the energy that drives the cellular processes needed for life. But in the process of producing energy, mitochondria also produce potentially harmful substances called reactive oxygen species or ROS. While the concentration of ROS in cells usually is well-controlled, diet can influence mitochondrial function in ways that increase the production of ROS to levels that become harmful to the mitochondria.
In order to understand the relationship between diet, mitochondrial function and disease, it is important to understand how ROS can cause long-term, irreversible damage to mitochondria. Most of us know that cells have DNA that harbors the genes that determine our biological characteristics. Not as well- known is that mitochondria contain their own DNA whose genes determine the ability of mitochondria to use electrons — derived from food — to produce energy.
ROS produced by the mitochondria can damage the mitochondrial DNA. This damage can cause genetic mutations that impair the ability of mitochondria to generate energy. Over time, the accumulation of these mutations can cause mitochondria to lose their ability to produce sufficient energy to meet cellular needs, and as a consequence, disease may follow. Mitochondrial dysfunction resulting from accumulated mutations in mitochondrial DNA has been implicated in heart failure, neurodegenerative diseases such as Alzheimer’s disease, diabetes and cancer. Mitochondrial dysfunction also can contribute to obesity by causing abnormal cellular use of carbohydrates and fats.
Although the food we eat ultimately supplies the electrons that mitochondria use to produce energy, food also supplies other nutrients, particularly minerals such as iron, copper and zinc and certain vitamins, such as biotin, vitamin B6 and pantothenic acid, which support mitochondrial function. These minerals and vitamins are either components of the mechanism that mitochondria use to move electrons through the energy-producing steps or help synthesize the components in these steps.
If dietary intake of these vitamins and minerals is inadequate, electrons derived from food cannot move efficiently through the energy-producing steps. Instead of contributing to energy production, the electrons then help increase the production of ROS, which in turn increases the rate of mutations in mitochondrial genes. It is at this level, the crossroad between mitochondrial energy production and ROS production, that diet can influence the development of disease.
Research being conducted at the Grand Forks Human Nutrition Research Center is helping to determine if low intakes of nutrients needed for mitochondrial function influences the risk for developing certain kinds of heart disease and obesity.
In the U.S., a significant percentage of people — from 10 percent to 25 percent — do not meet dietary requirements for iron, zinc or vitamin B6. Furthermore, among pregnant women, 10 percent do not meet the dietary requirement for copper, more than 75 percent do not meet the dietary requirement for iron, and near 40 percent do not meet the dietary requirement for biotin.
Another important area being investigated “nutritional programming,” which occurs during gestation —where genes are turned on or off in response to various factors, including maternal diet and nutrition. Researchers are investigating whether low intakes of iron, copper or zinc during pregnancy can have long-term effects on mitochondrial function in offspring. Because such nutritional programming can affect susceptibility to health risks later in life, the researchers are studying whether such low intakes during pregnancy can promote disease as offspring age.
Recent results from studies indicate that low copper intakes by rats during pregnancy alters mitochondrial function in the hearts of offspring in a manner that increases ROS production and damage in the heart when the offspring become adults. The ultimate goal is to provide a scientific basis for dietary recommendations that will help reduce the risk for developing diseases that occur as a result of diet-related mitochondrial dysfunction.