Which additional factors may influence the maintenance of vitamin D status?

1503 LETTERS TO THE EDITOR REFERENCES 1. Tholstrup T, Hjerpsted J, Raff M. Palm olein increases plasma cholesterol moderately compared with olive oil in healthy individuals. Am J Clin Nutr 2011;94:1426–32. 2. Hayes KC, Khosla P. Dietary fatty acid thresholds and cholesterolemia. FASEB J 1992;6:2600–7. 3. Ng TKW, Hayes KC, DeWitt GF, Jegathesan M, Satgunasingam N, Ong ASH, Tan D. Dietary palmitic and oleic acids exert similar effects on serum cholesterol and lipoprotein profiles in normocholesterolemic men and women. J Am Coll Nutr 1992;11:383–90. 4. Choudhury N, Tan L, Truswell AS. Comparison of palm olein and olive oil: effects on plasma lipids and vitamin E in young adults. Am J Clin Nutr 1995;61:1043–51. 5. Ng TK, Hassan Khalid, Lim JB, Lye MS, Ishak R. Nonhypercholesterolemic effects of a palm-oil diet in Malaysian volunteers. Am J Clin Nutr 1991;53(suppl):1015S–20S. 6. Voon PT, Ng TKW, Lee VKM, Nesaretnam K. Diets high in palmitic acid (16:0), lauric and myristic acids (12:0 1 14:0), or oleic acid (18:1) do not alter postprandial or fasting plasma homocysteine and inflammatory markers in healthy Malaysian adults. Am J Clin Nutr 2011;94:1451–7. 7. Katan MB, Deslypere JP, van Birgelen APJM, Penders M, Zegwaard M. Kinetics of the incorporation of dietary fatty acids into serum cholesteryl esters, erythrocyte membranes, and adipose tissue: an 18-month controlled study. J Lipid Res 1997;38:2012–22. doi: 10.3945/ajcn.112.036145. Reply to TKW Ng finding that palm oil raises cholesterol is in agreement with the majority of results of studies conducted over the past decades. The author had no conflicts of interest related to this letter. Tine Tholstrup Department of Human Nutrition Faculty of Life Science Copenhagen University Rolighedsvej 30 1958 Frederiksberg C Denmark E-mail: REFERENCES 1. Tholstrup T, Hjerpsted J, Raff M. Palm olein increases plasma cholesterol moderately compared with olive oil in healthy individuals. Am J Clin Nutr 2011;94:1426–32. 2. Keys A, Anderson JT, Grande F. Serum cholesterol response to changes in the diet. IV. Particular saturated fatty acids in the diet. Metabolism 1965;14:776–87. 3. Mensink RP, Zock PL, Kester AD, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr 2003;77:1146–55. 4. Bonanome A, Grundy SM. Effect of dietary stearic acid on plasma cholesterol and lipoprotein levels. N Engl J Med 1988;318:1244–8. doi: 10.3945/ajcn.112.037671. Dear Sir: We thank Ng for his interest in our Danish (not Dutch) study, in which we compare the effects of palm oil, olive oil, and lard (1), but we would like to point out that some of the points he raises are based on misconceptions. He writes that the study ‘‘underscores the fact that when linoleic acid requirements are met, the cholesterol-raising potential of dietary palm oil is only minimal in normocholesterolemic healthy individuals.’’ In fact, the aim of our study was to compare effects of refined palm oil, olive oil, and lard on blood lipids in healthy individuals when these fats replaced part of the energy content of the habitual diet. We found that palm oil raised plasma LDL cholesterol compared with olive oil, as one would expect in light of the established knowledge (2, 3). As Ng points out, the cholesterol-raising effects of palm oil can be counterbalanced by a given intake of linoleic acid. If we had added linoleic acid to the palm oil diet, we should have added it equally to the olive oil and lard diets. This would have resulted in lower plasma LDL-cholesterol concentrations after all test diets; however, the overall difference between plasma LDL-cholesterol concentrations after test periods would be equal to that found in our study. However, this consideration was not part of our aim or design, which simply was to investigate the effects of palm oil, olive oil, and lard. Ng emphasizes ‘‘that it is important that the test fats investigated should provide more than half of total dietary fat calories.’’ But why is this important when the majority of people consume less than half of the calories? Surely the effects of any quantity of fat may be investigated as long as the analyses answer the questions raised in the hypothesis? Only if the aim is to show that palm oil does not raise LDL cholesterol do specific conditions have to be met. The last point we would like to address is that Ng considers the study periods to be too short. However, there is general agreement that steady state of blood cholesterol is reached within 14 d (4), and for this reason no one else has questioned the duration of the test periods. This double-blind, crossover study was appropriate to answer the questions posed in the hypothesis, and our Which additional factors may influence the maintenance of vitamin D status? Dear Sir: I read with great interest the recent findings of Farrar et al (1) that the recommended amount of summer sunlight exposure did not result in sufficient circulating vitamin D concentrations in adults of South Asian origin living in the United Kingdom. In addition to receiving rigorously standardized UV radiation (UVR) doses, equivalent to brief, regular sun exposure at 53.5°N latitude, subjects also completed food diaries to provide an estimate of vitamin D intake to control for any confounding effect on serum 25-hydroxyvitamin D concentrations. Indeed, although the dietary vitamin D intake in both the white and South Asian groups was low, it was significantly lower in the South Asian group. The authors concluded that ‘‘casual sun exposure at UK latitudes plays a much smaller role in maintaining vitamin D status in pigmented groups than in light-skinned groups.’’ Given that there is no clear evidence that dark-skinned individuals have less ability to produce vitamin D, when exposed to increased UVR doses to compensate for decreased UVR penetration due to pigmentation (2), the extent to which additional factors play a role in contributing to and/or sustaining vitamin D status remains uncertain. In this context, 2 additional factors, one long recognized and one just emerging, may play important roles. First, an association has been reported between low dietary calcium intake, increased phytate (inositol hexaphosphate) consumption, and vitamin D deficiency in individuals from southern India (3). Increased dietary phytate intake has also been reported in both adults and children of Asian origin living 1504 LETTERS TO THE EDITOR in the United Kingdom (4, 5), partially due to chapatti consumption as a staple source of carbohydrates. Interestingly, increased dietary phytate intake was associated with rickets in Indian and Pakistani immigrants to the United Kingdom almost 4 decades ago (6). The mechanism or mechanisms by which phytates may affect vitamin D status are not well understood but may include effects on intestinal calcium abso (...truncated)