Applied nutritional investigationAssociation between dietary glycemic index, glycemic load, and high-sensitivity C-reactive protein
Introduction
Cardiovascular disease and diabetes are two leading causes of morbidity and mortality in the United States and worldwide. According to the Centers of Disease Control and Prevention in 2005, it was estimated that 25.6 million non-institutionalized Americans have some form of heart disease and more than 20 million have diabetes [1], [2]. Among those with diabetes, 65% will die from heart disease or stroke [3].
High-sensitivity C-reactive protein (hs-CRP), a marker of inflammation, has been recognized as a risk factor for future cardiac events [4], [5], [6], [7], [8], [9], [10], [11], [12]. Although very high hs-CRP levels are likely the response to acute inflammation, slightly elevated levels are indicative of chronic inflammation present in such diseases as cardiovascular disease and diabetes. High-sensitivity CRP values are useful in determining disease progression or the effectiveness of treatments, and because many of these diseases are modifiable by lifestyle, tracking hs-CRP can be quite informative. It is important to identify which lifestyle factors have the greatest impact because lifestyle factors may provide an important intervention opportunity to beneficially influence hs-CRP levels to reduce the risk of cardiovascular disease and diabetes.
Diet is one of the many modifiable risk factors for cardiovascular disease and diabetes. There is increasing evidence that quantity and quality of carbohydrate can modify disease risk [13], [14]. One method to evaluate the quality of carbohydrate is the glycemic index (GI), a measurement of the blood glucose response to 50 g of carbohydrate from a particular food [15]. Glycemic load (GL) is the GI of a food multiplied by its carbohydrate content in grams (quality by quantity). The present study examined the relationship among GI, GL, and hs-CRP, a marker of inflammation, in a population of healthy adults.
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Materials and methods
Data for this study was obtained from a 1-y prospective observational study designed to examine seasonal variations in blood lipid levels in a disease-free population in central Massachusetts [16]. The study began in 1996 with 641 eligible participants enrolled at baseline. Eligibility requirements included an age from 20 to 70 y, literacy in English, and not planning to leave the area within the next year [16]. Exclusion criteria included 1) using or planning to use lipid-lowering drugs, 2)
Results
A total of 641 participants with 2795 observations were available for analysis. Because our goal was to examine the longitudinal effect of dietary GI or GL on hs-CRP, participants with data available for fewer than two time points were excluded (n = 49 observations). An additional 617 observations were excluded because dietary measurements and hs-CRP were not available at the same quarter. We excluded 65 observations where hs-CRP was >10 mg/L because such elevated levels are likely to be caused
Discussion
In this 1-y observational study, we did not observe a positive association among dietary GI, GL, and hs-CRP. Although the literature reporting the relationship between GI or GL and hs-CRP is limited, the results from this study are not in agreement with a previous study that reported a significant positive association between dietary GL and hs-CRP [25].
One explanation for the difference in findings may be due to differences in the study populations. Among 244 middle-aged female participants in
Conclusion
In this prospective observational study, we found no association between dietary GI or GL and hs-CRP. This is a surprising finding, given a previous study's positive findings and the observation by our group that fiber, in agreement with other studies, was inversely associated with hs-CRP in our study population [23]. This is interesting because fiber is a very strong factor in the determination of GI, and one would expect that GI would also be associated. Due to the limited number of studies
Acknowledgments
The authors thank Laura Robidoux and Priscilla Cirillo for their assistance with study recruitment and data collection; Kelly Scribner for coordination of the 24HRs; and dietitians who conducted the 24HRs: Susan Nelson, Christine Singelton, Pat Jeans, Karen Lafayette, Deborah Lamb, Stephanie Olson, and Eileen Capstraw; Dr. Nader Rifai for his assistance with hs-CRP measurements; and Dr. Eric Rawson for his contribution in the development of the hs-CRP project. They also thank Drs. Charles
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This work was supported by grants R01-HL52745 and 1 R21 HL074895-01 from the National Heart, Lung and Blood Institute. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the National Heart, Lung and Blood Institute.