It is known that the practice of calorie restriction, reducing calorie intake while still obtaining sufficient micronutrients, reduces inflammation in animals. This is one of many beneficial changes in the operation of metabolism observed to result from calorie restriction, and this intervention is well documented to extend life spans in short-lived species. Here researchers show that the same effects on inflammation occur in our species. Chronic inflammation rises with aging as the immune system becomes ever more dysfunctional, and contributes to the progression of all of the common age-related diseases. Inflammation is also produced by visceral fat tissue, however, which is one of the reasons why being overweight lowers life expectancy and increases risk of suffering age-related disease. Reduced amounts of visceral fat are probably an important cause of lower inflammation due to reduced calorie intake.
Restricting calories by 25 percent in healthy non-obese individuals over two years, while maintaining adequate protein, vitamin, and mineral intake, can significantly lower markers of chronic inflammation without negatively affecting other parts of the immune system. "Previous studies in animals and simple model organisms over the past 85 years have supported the notion that calorie restriction can increase the lifespan by reducing inflammation and other chronic disease risk factors, but with mixed results about whether it has a negative or null effect on cell-mediated immune responses. This is the first study to examine these effects over two years on healthy, normal- or slightly over- weight individuals and observe that caloric restriction reduces inflammation without compromising other key functions of the immune system such as antibody production in response to vaccines."
After six weeks of baseline testing, which included metabolic measurements to determine their total daily energy expenditure, and blood collection to evaluate inflammation and cell-mediated immunity markers, 220 eligible individuals were randomized into two groups and further stratified by site, sex, and body mass index. The control group maintained their normal diet for the duration of the study, while the test group was provided with support to maintain a high-satiety diet that restricted their calories by 25 percent including customized behavioral guidance. The test group was also given multivitamin and mineral supplements to prevent micronutrient malnutrition. To maintain a 25 percent reduction in calories the test group's calorie prescriptions were reduced three times through the two-year study to coincide with their weight loss based on body fat, and muscle mass calculations.
The research team found that the test group had a significant and persistent reduction in inflammatory markers with no discernible difference in immune responses from the control group at the end of 24 months. However, while reduction in weight, fat mass, and leptin levels were most pronounced at 12 months they were not accompanied by the significant reduction in C-reactive protein and TNF alpha, both indicators of inflammation, until 24 months. This delay suggests that long-term calorie restriction, at least 24 months, induces other mechanisms that may play a role in the reduction of inflammation.