ORLANDO, FLA. — Low dietary magnesium may elevate serum levels of C-reactive protein, but high vitamin E intake does not reduce levels of the inflammatory marker among at-risk individuals, according to two separate studies.
Both studies were conducted by researchers at the Medical University of South Carolina in Charleston and were presented at the annual meeting of the North American Primary Care Research Group.
Recent clinical studies have uncovered structural changes in C-reactive protein (CRP) linked to dietary magnesium intake, said Dana King, M.D. To assess the validity of that association, she and her colleagues at the university studied 5,021 adults in the National Health and Nutrition Examination Survey (NHANES) database.
The current recommended dietary allowance (RDA) for magnesium is 400 mg/day. Of the study population, 75% consumed less than 309 mg of magnesium per day—the lower end of adequate, Dr. King said. Regression analysis showed these adults to be 55% more likely to have elevated CRP levels, compared with those adults who met the RDA for magnesium.
After the investigators controlled for the various factors associated with low magnesium intake in this population, including older age, female gender, nonwhite race, nondrinker status, and reduced exercise, low magnesium intake was still a significant predictor of elevated CRP.
The subgroups at highest risk for elevated CRP linked to low magnesium included adults over age 40, those with a body mass index over 25 kg/m2, and those who consumed less than 50% of the RDA for magnesium. “The inverse association was clearly linear. The lower the magnesium intake, the greater the risk for elevated CRP,” Dr. King noted.
The findings are important given that most Americans consume magnesium at levels well below the RDA, and because CRP is a marker of risk for ischemic heart disease—the leading cause of death in developed countries, said Dr. King. “It is possible that increasing dietary magnesium to adequate levels can reduce heart disease risk substantially,” she added.
Because of the limitations of the cross-sectional study design, “the relationship between magnesium and CRP should be further evaluated in prospective studies,” Dr. King concluded.
The second study investigated the possible link between vitamin E intake and CRP concentrations. Because individuals with a combination of high ferritin and high LDL cholesterol levels tend to have elevated CRP levels due to increased oxidative stress, investigators at the Medical University of South Carolina hypothesized that higher intakes of vitamin E, because of its antioxidant properties, might help mitigate the CRP elevation in these people.
Using data from the 1999-2000 NHANES database, Brian Wells, M.D., now of the Cleveland Clinic, and colleagues, stratified a random cluster sampling of 4,204 adults aged 25 years and older by daily vitamin E intake. The researchers used logistic regression to determine predicted levels of CRP and divided the study population into quartiles by daily vitamin E intake.
As expected, those at-risk individuals with elevated levels of both ferritin and LDL cholesterol had significantly higher levels of CRP than did those individuals with normal iron and cholesterol measures. Within both the at-risk group and the general population, vitamin E intakes equal to or greater than the high end of intakes seen in the general population—about 50 IU—were not significantly associated with CRP levels, said Dr. Wells.
“Having high iron and LDL means having a lot of cholesterol available to be oxidized. Our hypothesis was that if oxidized LDL causes an inflammatory response leading to increased CRP, the antioxidant might mitigate that response,” he said. “What we saw was that vitamin E intake at the high end of normal levels in the diet was not linked with a reduction in CRP.”
It is possible that much higher levels of vitamin E, “or another antioxidant entirely,” could have an effect on CRP, said Dr. Wells, and these possibilities should be the focus of future research.