Location: Human Nutrition Research Center on Aging
Title: The effect of caloric restriction and glycemic load on measures of oxidative stress and antioxidants in humans: results from the calerie trial of human caloric restriction Authors
|Meydani, Mohsen -|
|Das, Sai Krupa -|
|Band, Michael -|
|Epstein, Susanna -|
|Roberts, Susan -|
Submitted to: Journal of Nutrition Health and Aging
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 27, 2010
Publication Date: June 1, 2011
Citation: Meydani, M., Das, S., Band, M., Epstein, S., Roberts, S. 2011. The effect of caloric restriction and glycemic load on measures of oxidative stress and antioxidants in humans: results from the calerie trial of human caloric restriction. Journal of Nutrition Health and Aging. 15:456-460. Interpretive Summary: As we breathe, our body constantly interacts with oxygen from which our cells produce energy. Due to this oxygenation, we produce free radicals, molecules that interact with other molecules within cells and cause (oxidative) damage to proteins and genes. This damage may cause many diseases including cancer. To offset oxidative stress, the body produces substances called antioxidants to counteract these effects, but each individual’s ability to produce antioxidants varies according to factors such as lifestyle, genetics, and quality of environment. Aside from causing disease, an increase in oxidative stress and a decrease in antioxidant defense are factors associated with aging. Calorie restriction (CR) has an anti-oxidative function, which is believed to counteract the harmful effects of oxidative stress on the cells and DNA. Therefore it can be suggested from studies that calorie restriction lengthens life span in various animals. In humans, CR studies are limited. The present study was designed to determine the effects of CR on measures of oxidative stress and antioxidant defense system in humans participating in the Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy (CALERIE), the first CR human trial conducted at Tufts University. A total of 46 moderately overweight volunteers, ages 20-42, were given either a high glycemic (HG) or low glycemic (LG) diet. High glycemic foods break down quickly, causing blood sugar levels to rise quickly; low glycemic foods release glucose slowly. Caloric intake was decreased at either 10 percent or 30 percent. All food was provided to participants for 6 months. We found that both 10 percent and 30 percent CR in the moderately overweight subjects affected some but not all of the oxidative/antioxidative markers. While significant decrease in body weight and body mass (BMI) resulted from CR in this study, there was an absence of a strong effect on markers of oxidative stress/defense, which may be due to the short period of CR and a limited number of subjects in each group. Our results still suggest, however, that CR in humans alters some of the biomarkers of oxidative stress and antioxidant defense, indicating a natural way to impede aging and perhaps to prevent certain diseases associated with oxidative stress.
Technical Abstract: Reducing oxidative stress and increasing antioxidant defense is suggested as one mechanism by which caloric restriction (CR) increases longevity in animals. A total of 46 moderately overweight volunteers (BMI: 25-30 kg/m2), ages 20-42 yr were randomized to either high glycemic (HG) or low glycemic (LG) dietary load CR regimen at either 10 percent (n=12) or 30 percent (n=34) of basal caloric intake. All food was provided to participants for 6 mo. Overall, after controlling for CR levels and dietary regimen for 6 mo, plasma glutathione peroxidase activity increased (p=0.04) and plasma protein carbonyl levels decreased (p=0.02) and a non significant decrease in plasma 8-epi-prostaglandin F2alpha level was observed (p=0.09). No significant change was observed in other plasma antioxidants such as superoxide dismutase and catalase. These findings indicate that short term CR (10 percent or 30 percent) in moderately overweight subjects modulates some but not all measures of antioxidant defense and oxidative stress.