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Eduardo N. Siguel, Medical research PO Box 10187, Gaithersburg, MD 20898
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The data does not appear to accurately calculate the effect of fatty acid composition. According to my research, the fatty acid composition of tissues (using plasma as a biomarker), particularly the relative percents of essential vs. non essential fats (approximated by PUFA vs. NonPUFA) is a (or the) major nutritional predictor of acquired cardiovascular disease. Monunsaturated (MUFA) intake is far less relevant because the body seeks to maintain MUFA levels fairly proportional to PUFA. Humans can make MUFAs from saturated fatty acids. According to my research and models, MUFAs are made by the body to compensate for suboptimal levels of PUFAs. Eating more means the body makes less. Thus, I propose that the major factors accounting for lower cardiovascular disease in some Mediterranean populations is body tissue levels of essential fats (~ PUFA except for polyunsaturates of the w7 and w9 families). Diets high in fish or some vegetables provide adequate omega -3s; olives (and olive oil) provide omega-6s. The Lyon’s heart study achieved huge reductions in risk of myocardial infarction using a diet high in essential fats. I doubt that higher intake of MUFAs has substantial beneficial effects. Instead, the key are the vegetables, nuts and foods high in essential fats (and not excessive calories). References de Lorgeril M, Salen P, Martin J-L, Monjaud I, Delaye J, Mamelle N.
Mediterranean diet, traditional risk factors, and the rate of
cardiovascular complications after myocardial infarction: final report of
the Lyon Diet Heart Study. Circulation. 1999;99:779–785.
Siguel E, Lerman, RH. Altered Fatty Acid Metabolism in Patients With Angiographically Documented Coronary Artery Disease. Metabolism 1994; 43:982-93. Siguel, E. Deficiencies and Abnormalities of Essential Fats in Gastrointestinal and Coronary Artery Disease. Journal of Clinical Ligand Assay 2000; 23:104–11. Siguel, E. Clinical Impact of Methodological Issues in the Diagnosis of Deficiencies and Abnormalities of Essential Fats. Journal of Clinical Ligand Assay 2000; 23:112–21. Competing interests: Author has a patent to measure fatty acids |
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William T Neville, General Practitioner Abbey Road Surgery, 63 Abbey Road, Waltham Cross, Hertfordshire, EN8 7LJ
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This article and the Mediterranean Diet Score unfortunately do not consider one of the major benefits of a Mediterranean diet which is its low Glycaemic Index (GI). The resulting scores and conclusions therefore give an incomplete picture. If the GI were considered, a better explanation of the benefits of a Mediterranean diet would be apparent. GI is a measure of how rapidly carbohydrates are digested. High GI food causes a high, sharp rise in blood glucose and insulin which is harmful. Low GI food causes a low, sustained rise in blood glucose. A low GI diet may prevent or control a variety of conditions including diabetes, cardio-vascular disease, obesity, hyperlipidaemia, Alzheimer’s disease and breast cancer. Due to the high content of fruit, vegetables and legumes the Mediterranean diet has a low GI. Pasta has a low GI which is relevant to the Italian diet. The GI is therefore important for people who wish to improve their health by switching to a Mediterranean diet. If they continue to eat the high GI food typical of a Western European diet they will not benefit. Such high GI food includes potatoes, most rice and most breakfast cereals. White bread, brown bread and even wholemeal bread have a high GI because they are made from finely milled flower. This high GI food needs to be replaced by low GI alternatives for example porridge, muesli, stone-ground bread, granary bread (made with malted or sprouted wheat) or bread containing soya and linseed. Eating fish, unsaturated fat, nuts, legumes, fruit and vegetables are important. But for a Mediterranean diet to benefit a wider population the consumption of high GI food needs to be decreased and replaced with low GI food. References: 1. Kelly SAM, Frost G, Whittaker V, Summerbell CD. Low glycaemic index diets for coronary heart disease. Cochrane Database of Systematic Reviews 2004, Issue 4. Art. No.: CD004467. DOI: 10.1002/14651858.CD004467.pub2. 2. Thomas DE, Elliott EJ, Baur L. Low glycaemic index or low glycaemic load diets for overweight and obesity. Cochrane Database of Systematic Reviews 2007, Issue 3. Art. No.: CD005105. DOI: 10.1002/14651858.CD005105.pub2. 3. Thomas D, Elliott EJ. Low glycaemic index, or low glycaemic load, diets for diabetes mellitus. Cochrane Database of Systematic Reviews 2009, Issue 1. Art. No.: CD006296. DOI: 10.1002/14651858.CD006296.pub2. 4. Jenkins DJ, Wolever TM, Taylor RH, et al. (1981) Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr 34:362–6 Competing interests: None declared |
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Maria G Joyanes, Researcher CNA-AESAN Ministry of Health and Social Policy of Spain, Ingrid M. Outschoorn
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Reading your innovative approach to the individual components of the Mediterranean diet as a mortality predictor, your conclusion with respect to fish and dairy products is well explained. The diet score predictor of ethanol consumption relates to low and high doses, where red wine is the main source. We wonder if one can estimate the contribution of non- nutrients or if one can obtain more information indicating whether the ethanol is via fermentation or distilled, for the remainder of the intake. Finally, in the search for predictive factors, considering the results from other countries, these could be addressed with respect to ethnic and geographic variations. Gene and environment interaction measurements can be based on quantitative measurements of a few paired subjects across a generation? Joyanes M & Lema L. Criteria for optimizing the food composition tables in relation to studies of habitual food intakes. Crit Rev Food & Nutr Sci. 2006 Vol 46, Number 4, June:329-336(8) Zaridze D, Brennan P, Boreham J, Boroda A, Karpov R, Lazarev A, Konobeevskaya I, Igitov V, Terechova T, Boffetta P, Peto R. Alcohol and cause-specific mortality in Russia: a retrospective case-control study of 48 557 adult deaths. Lancet 2009 Jun 27;373(9682):2201-14 Competing interests: None declared |