Janet W. Rankin, PhD and Abigail D. Turpyn
Journal of the American College of Nutrition, Vol. 26, No. 2, 163-169 (2007)
Studied Variable: Dietary Carbohydrate
Variables Measured: Body weight, IL-6, CRP, urinary 8-epi-prostaglandin, FBG, FFA (fasting)
Variables controlled for: Caloric intake
Protocol Summary: Subjects were ed into two groups followed calorie restricted (~1360 kcal/d) diets varied in composition: LC = 58F/12C/30P ; HC = 24F/59C/18P. Weight, inflammatory markers (IL-6 and CRP) and oxidative stress (8-epi) were measured weekly.
Age: adult, premenopausal
Number of Participants: 29
Weight Status: Overweight BMI 32.1 ± 5.4 kg/m2
Health Status: weight stable for at least 6 months, nonsmokers, sedentary, otherwise healthy and unmedicated
Study Duration: 4 weeks
Summary of results:
* LC lost a bit more weight (3.8 ± 1.2 kg LC vs. 2.6 ± 1.7 HC, p=0.04)
* CRP increased an average of 25% in the LC group whereas it decreased 43% in the HC group (p=0.02)
* FBG decreased similarly for both groups
* IL-6 increased similarly for both groups
* 8-epi varied differently between groups but with no consistent pattern.
* Serum NEFA increased for both groups, the increase was greater for LC
Here is a screenshot of the results: (click on image to enlarge)
Researchers' Conclusion: "Diet composition of the weight loss diet influenced a key marker of inflammation in that LC increased while HC reduced serum CRP but evidence did not support that this was related to oxidative stress."
Although apparently not statistically significant, the LC group (~190 lbs) was a bit heavier than the HC group (~175 lbs) to begin with in this study. This could be related to the LC group starting at a higher (although also not indicated as significant) average CRP level.
But look at the CRP graph showing the individual results vs. baseline -- the horizontal axis is the baseline CRP. I find this disturbing. The first thing that jumps out is that almost all of the LC group had increases while all of the HC group had decreases. Also disconcerting is that this effect seems more pronounced for those who had a low level of CRP to begin with -- IOW, LC seems to induce an inflammatory state according to the CRP indicator. This is not seen for HC where in most cases CRP declines. If one looks at the right side of the graph, you have the subjects in the highest baseline "inflammatory state". What happens? Significant decreases in CRP for the HC group, negligible change either way for LC.
Whether or not to be stressed over CRP levels is a matter of continued confusion and controversy, but higher CRP levels are never, as far as I've seen, considered a good thing.
I came across this article while researching plasma free fatty acids (NEFA, FFA) and am concerned with the effect the LC diet had on fasting FFA's. The highest fasting level for the LC group was almost 1.5X (50% higher) than the highest fasting level for the HC group. The high level vs. baseline for LC was ~1.8X vs. ~1.5X for the HC group.
I don't know enough about 8-epi at this time to comment on that aspect of this study.