Further response from Hoenselaar

摘要

I wish to thank Pedersen et al. for their comments in response to my letter to the editor'2). The articles they refer to may indeed cast some doubt on the use of HDL-cholesterol as a predictor of CHD. The authors then continue their letter by summarising the evidence linking SFA to CHD risk. However, their conclusions may not in all cases be a valid representation of the scientific literature. The authors provide evidence that SFA intake decreased and PUFA intake increased in the USA and state that there are also reports of declining SFA intake concomitant with the reduction in CHD mortality in several other populations, referring to five articles'3-71. However, the link between SFA intake and CHD mortality was not examined in the articles referredto; what these articles actually described were trends in fat intake over different time periods for three different populations. Two reports described fat intake in the USA0,41. The changes in SFA and PUFA intake were accompanied by a decrease in MUFA intake1"*1. Since these three changes were of equal size and took place at the same time, it will take other data to put them in perspective before they can be possibly directly linked to CHD. Two other reports described fat intake in Nordic countries, with an emphasis on Finland'5,61. Again, changes in SFA and PUFA intake took place in the same time frame. This time, these changes were accompanied by a decrease in trans-fat (TFA) intake. The New Zealand report is the only article which might suggest a direct link between SFA and CHD(7). It shows a trend in decreased CHD rates over time, and (in another part of the text) it is mentioned that SFA consumption decreased over time. However, no direct correlation was examined.