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Should You Supplement?

by Robert A. Jacob, Ph.D.

Diabetes and oxidative damage

Normally, the body maintains a balance between the amount of reactive oxygen species generated and its antioxidant defense. This balance may be tipped, however, by conditions that greatly increase the generation of reactive oxygen species (such as cigarette smoke in the lungs) and/or lack of antioxidant defense due to malnutrition. Many diseases involve increased production of reactive oxygen species, including infections and inflammatory conditions such as arthritis and inflammatory bowel diseases.

There is substantial evidence that people with diabetes tend to have increased generation of reactive oxygen species, decreased antioxidant protection, and therefore increased oxidative damage. Hyperglycemia, or a high blood glucose level, has been shown to increase reactive oxygen species and end products of oxidative damage in isolated cell cultures, in animals with diabetes, and in humans with diabetes. Measurement of the end products of oxidative damage to body fat, proteins, and DNA are commonly used to assess the degree of oxidative damage to body cells and tissues. Most studies show that these measures are increased in people with diabetes.

The activities of key antioxidant enzymes are also found to be abnormal in people with diabetes. In some studies, these enzyme activities are seen to be lower than normal, suggesting a compromised antioxidant defense, while other studies show higher activity, suggesting an increased response to oxidative stress. Some studies indicate that oxidative damage is greater in people with Type 2 diabetes compared to those with Type 1, especially people with Type 2 diabetes and the metabolic syndrome, which involves central obesity, hypertension (high blood pressure), and high blood fat levels along with insulin resistance (decreased effectiveness of insulin in metabolizing blood glucose).

There is evidence that antioxidant protection is decreased and oxidative stress increased in some people even before the onset of diabetes. For instance, increased levels of oxidative stress have been found in people who have impaired glucose tolerance, or prediabetes.

Evidence for antioxidant protection

Overall, the evidence indicates that hyperglycemia creates additional oxidative stress, and that measures of oxidative damage are generally increased in people with diabetes. Therefore, the question arises as to whether antioxidant treatment may delay or prevent diabetes, or delay the onset of diabetes complications that include cardiovascular, kidney, nerve, and eye diseases. Cell culture and animal studies support the hypothesis that antioxidants can protect diabetic cells from some damage. However, two types of human studies must also be examined to answer the question: population studies and clinical trials.

Population studies. Population, or epidemiologic, studies have looked at the relationship between antioxidant intake and the development of diabetes. They have also examined the effects of antioxidant intake on a group of people with diabetes compared to a similar group without the condition.

Examination of the diets of some 4,300 Finnish adults (40–69 years old) without diabetes showed that those with low dietary intakes of vitamin E had a significantly greater risk of developing Type 2 diabetes over the next two decades. There was no relationship between intake of vitamin C and risk of future diabetes development. In another study of 81 male and 101 female Finnish adults at high risk for Type 2 diabetes, dietary carotenoids were associated with improved measures of glucose metabolism (fasting plasma glucose concentration and insulin resistance) in men but not women. In a third study, blood levels of five carotenoids were measured in 1,597 Australian adults that were healthy or had varying degrees of impaired glucose metabolism. Those with higher blood levels of the carotenoids had a healthier profile of glucose metabolism tests—fasting plasma glucose levels, insulin concentrations, and glucose tolerance levels.

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