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American Journal of Clinical Nutrition, Vol. 88, No. 5, 1448, November 2008
© 2008 American Society for Nutrition

LETTER TO THE EDITOR

Reply to CK Chow

Giovanni Ravaglia and Paola Forti

Department of Internal Medicine
Cardioangiology and Hepatology
University Hospital S Orsola-Malpighi
University of Bologna
Via Massarenti 9
40138 Bologna
Italy
E-mail: giovanni.ravaglia{at}unibo.it

Dear Sir:

We thank Dr Chow for his comments on our study (1). Several methods have been suggested and used to adjust serum vitamin E status for serum lipids (2), but the issue has not been standardized. In preliminary analyses, we tested several possible approaches—the ratios of vitamin E to cholesterol, to tryglicerides, or to cholesterol plus tryglicerides—but the results did not differ significantly. Therefore, we chose the adjustment that made it easier to compare our data with the data of the studies we referenced. The fact that significant associations were found only after adjustment for cholesterol values was clearly pointed out in the discussion as a major limitation of the study. However, the plasma concentration of vitamin E varies with the amount of concurrent lipids, and lipid standardization is needed to estimate the biological status of vitamin E (3).

We entirely agree that, because of their cross-sectional design, data on prevalent dementia cannot establish whether serum vitamin E status affects cognitive function or whether cognitive function, via altered dietary habits and blood lipid carriers, affects serum vitamin E status. However, to better clarify this issue, our investigation also provided longitudinal data, which are less likely to be biased by the effect of cognitive function on nutritional status at baseline.

The table provided by Chow does not seem to take into account the fact that we provided absolute plasma concentrations of vitamin E metabolites as supplemental data (see E-Table 1 under "Supplemental data" online at http://www.ajcn.org/cgi/content/full/87/5/1306/DC1). In particular, absolute concentrations of plasma tocopherols were reported in µmol/L, but plasma {alpha}-tocopheryl-quinone and 5-nitro-{gamma}-tocopherol were reported in nmol/L, which means that values must be multiplied by 0.001 to be expressed in µmol/L. Therefore, contrary to the statement of Chow statement and in full agreement with previous literature (4), the plasma {alpha}-tocopheryl-quinone and 5-nitro-{gamma}-tocopherol concentrations in our cohort were much lower than the corresponding concentrations of {alpha}-tocopherol. Finally, our results did not by any means exclude the possibility that variables other than serum vitamin E status may be related to the risk of cognitive impairment. Indeed, this possibility is the reason that we included sociodemographic features, lifestyle habits, cardiovascular risk factors, and previous cognitive status in the analyses as possible confounders.

ACKNOWLEDGMENTS

Neither of the authors had a personal or financial conflict of interest.

REFERENCES

  1. Ravaglia G, Forti P, Lucicesare A, et al. Plasma tocopherols and risk of cognitive impairment in an elderly Italian cohort. Am J Clin Nutr 2008;5:1306–13.
  2. Ford ES, Schleicher RL, Mokdad AH, Ajani UA, Liu S. Distribution of serum concentrations of alfa-tocopherol and gamma-tocopherol in the US population. Am J Clin Nutr 2006;84:375–83.[Abstract/Free Full Text]
  3. Jordan P, Brubacher D, Moser U, Stahelin HB, Gey KF. Vitamin E and vitamin A concentrations in plasma adjusted for cholesterol and triglycerides by multiple regression. Clin Chem 1995;41:924–7.[Abstract/Free Full Text]
  4. Brigelius-Flohé R, Traber MG. Vitamin E: function and metabolism. FASEB J 1999;13:1145–55.[Abstract/Free Full Text]




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