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LETTERS TO THE EDITOR |
Mary Emily Clinical Nutrition Research Unit
School of Dietetics and Human Nutrition
McGill University, Macdonald Campus
21,111 Lakeshore Road
Ste Anne-de-Bellevue, PQ H9X 3V9
Canada
E-mail: jonesp{at}macdonald.mcgill.ca
Dear Sir:
We are writing in reference to the article by Joki et al (1) that was recently published in the Journal. The reported objective of the study was to investigate lipid and sterol metabolism in children with food allergy who were given restricted diets. Outcome measurements included concentrations of serum cholesterol precursors, plant sterols, and lipids. The authors concluded that allergic children have low dietary intakes of cholesterol and low serum cholesterol concentrations. The authors also concluded that serum plant sterol concentrations increased, probably as a result of plant sterols in the rapeseed oil supplement. A careful review of the article by Joki et al identified certain fundamental problems in the study design that severely compromise accurate interpretation of the results.
First, the inclusion of rapeseed oil supplementation confounds the hypothesis of the study. As the authors themselves stated, rapeseed oil is known to contain substantial amounts of plant sterols. Plant sterols are widely known to significantly lower plasma cholesterol concentrations and alter plasma plant sterol concentrations when consumed with the diet. Therefore, what this study actually examined was lipid and sterol metabolism in allergic children supplemented with or without plant sterol-containing rapeseed oil for 3 mo in combination with a restricted diet. This question is very different from the originally intended question about the metabolic effects of a restricted diet alone.
Second, interpretation of the results raises some important questions. The authors report that only 40 of the 52 children were supplemented with the rapeseed oil. It remains unclear to the reader why the supplement was given at all and why only a portion of the children received the supplement. More troubling is the fact that, as the data are presented, we do not know how many children in each group (food allergic and nonallergic) received the supplement or whether those children were the ones contributing the most to the decreased mean cholesterol concentrations. The authors do state that the subjects who received supplementary rapeseed oil had higher plant sterol concentrations than those who did not, but, in the Discussion section, changes in plant sterol concentrations are discussed by comparing allergic subjects with nonallergic subjects. Therefore, it is not clear from the results how many of the allergic and nonallergic subjects were supplemented, which makes it impossible to conclude whether it was the supplementation or the allergic condition that influenced serum plant sterol concentrations.
Third, the authors discuss the importance of cholesterol as an essential lipid molecule for growing children and state that one of the goals of their study was to determine whether the low concentrations of serum cholesterol in their subjects were due to insufficient cholesterol synthesis or absorption or to low intakes of cholesterol and saturated fat. In patients whose cholesterol absorption and intake may be compromised, it seems even more illogical that a supplement with known cholesterol-inhibitory properties would be prescribed. Not only would that predispose the patient to even lower serum cholesterol concentrations, but it also would no longer allow the researcher to accurately assess the hypothesis regarding cholesterol absorption and serum concentrations in allergic children given restricted diets.
Fourth, the authors' rationale for using serum plant sterol concentrations to predict changes in cholesterol absorption is not scientifically sound. Under steady state conditions, plant sterol concentrations in serum are positively related to the efficiency of cholesterol absorption (2-4). However, plant sterol concentrations cannot be used as predictors when the serum concentrations of sterols are in a state of flux as a result of supplementation. When stanols are supplemented in the diet, there is a resultant decrease in plasma campesterol concentrations, which appears to mimic the decrease in cholesterol absorption. Similarily, when sterols are supplemented, cholesterol absorption decreases, but serum concentrations of plant sterols actually increase. Some researchers in the field of phytosterols have inappropriately used the campesterol-to-cholesterol ratio as an indicator of changes in cholesterol absorption efficiency after plant stanol supplementation (5-7). Joki et al also incorrectly refer to this method when assessing changes in cholesterol absorption. In addition, they draw 2 contradictory conclusions regarding cholesterol absorption. First, they conclude that, because the campesterol-to-cholesterol ratio was higher in the allergic subjects than in the nonallergic subjects, cholesterol absorption was not affected, from which they draw the inference that the allergic subjects had no bowel inflammation. Second, they conclude that, because there was an increase in cholesterol synthesis, cholesterol absorption must have been reduced. The authors cannot have it both ways—either cholesterol absorption was altered or it was not.
We feel that the results of the study by Joki et al do not reflect the hypothesis and that this discrepancy is due to flaws in the study design. Moreover, the discussion regarding serum plant sterol concentrations and cholesterol absorption is inconsistent through the article and shows a poor understanding of the metabolic effects of plant sterols. To render this study meaningful to the scientific community, the authors need to restate the hypothesis so that it includes plant sterol supplementation, express the data clearly in terms of allergic and nonallergic subjects and in terms of which subjects from each group were supplemented, and, finally, rework the discussion with a stronger understanding of the effects of plant sterol consumption on metabolism generally and on cholesterol metabolism specifically.
REFERENCES
This article has been cited by other articles:
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  F. Briand, S. Serisier, M. Krempf, B. Siliart, T. Magot, K. Ouguerram, and P. Nguyen Atorvastatin Increases Intestinal Cholesterol Absorption in Dogs J. Nutr., July 1, 2006; 136(7): 2034S - 2036S. [Full Text] [PDF]
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