5 Steps to prevent Heart Disease

Wednesday, August 20, 2014

Paradigm Change in Fatty Acid science

Paradigm Change in Fatty Acid science

http://www.ncbi.nlm.nih.gov/pubmed/22658146#

J Clin Lipidol. 2012 May-Jun;6(3):216-34. doi: 10.1016/j.jacl.2012.04.077. Epub 2012 Apr 13.

Fatty acids in cardiovascular health and disease: a comprehensive update.

Source

Miller School of Medicine, University of Miami, Miami, FL 33136, USA. sjbaum@fpim.org

Abstract

Research dating back to the 1950s reported an association between the consumption of saturated fatty acids (SFAs) and risk of coronary heart disease. Recent epidemiological evidence, however, challenges these findings. It is well accepted that the consumption of SFAs increases low-density lipoprotein cholesterol (LDL-C), whereas carbohydrates, monounsaturated fatty acids (MUFAs), and polyunsaturated fatty acids (PUFAs) do not. High-density lipoprotein (HDL)-C increases with SFA intake. Among individuals who are insulin resistant, a low-fat, high-carbohydrate diet typically has an adverse effect on lipid profiles (in addition to decreasing HDL-C, it also increases triglyceride and LDL particle concentrations). Consequently, a moderate fat diet in which unsaturated fatty acids replace SFAs and carbohydrates are not augmented is advised to lower LDL-C; compared with a low-fat diet, a moderate-fat diet will lower triglycerides and increase HDL-C. Now, there is some new evidence that is questioning the health benefits of even MUFAs and PUFAs. In addition, in a few recent studies investigators have also failed to demonstrate expected cardiovascular benefits of marine-derived omega-3 fatty acids. To clarify the clinical pros and cons of dietary fats, the National Lipid Association held a fatty acid symposium at the 2011 National Lipid Association Scientific Sessions. During these sessions, the science regarding the effects of different fatty acid classes on coronary heart disease risk was reviewed.


 More articles:


1- 4-Mozaffarian D et al. PLoS med 201023: 7 e10000252 Meta-Analysis of Randomized Controlled Trials- Displacing with PUFA, Carbohydate, MUFA
2- Am J Clin Nutr. 2010 Mar;91(3):502-9. Epub 2010 Jan 20.
Saturated fat, carbohydrate, and cardiovascular disease.
Siri-Tarino PW, Sun Q, Hu FB, Krauss RM.
3-Cochrane Database Update
WITHDRAWN: Advice on low-fat diets for obesity.
Summerbell CD, Cameron C, Glasziou PP.
4-Regular egg consumption does not increase the risk of stroke and cardiovascular diseases.
Qureshi AI, Suri FK, Ahmed S, Nasar A, Divani AA, Kirmani JF.5-Epub 2011 Jan 26.
Astrup A Dyerberg J, Elwood P, Hermansen K, Hu FB, Jakobsen MU, Kok FJ, Krauss RM, Lecerf JM, LeGrand P, Nestel P, Risérus U, Sanders T, Sinclair A, Stender S, Tholstrup T, Willett WC.
The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010?
"Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk."
6-Epub 2010 Jan 20.
Saturated fat, carbohydrate, and cardiovascular disease.

Siri-Tarino PW, Sun Q, Hu FB, Krauss RM.
"An independent association of saturated fat intake with CVD risk has not been consistently shown in prospective epidemiologic studies, although some have provided evidence of an increased risk in young individuals and in women."
7-Epub 2010 Mar 31.
Saturated fat and cardiometabolic risk factors, coronary heart disease, stroke, and diabetes: a fresh look at the evidence.
Micha R, Mozaffarian D.
"Compared with carbohydrate, the TC:HDL-C ratio is nonsignificantly affected by consumption of myristic or palmitic acid, is nonsignificantly decreased by stearic acid, and is significantly decreased by lauric acid."
"Evidence for the effects of SFA consumption on vascular function, insulin resistance, diabetes, and stroke is mixed, with many studies showing no clear effects,"

3 comments:

  1. 1) The articles down the right-hand side of your your blog are Google Documents. Please copy these into blog posts, to allow for comments. I have comments.

    2) Siri-Tarino et al and Chowdhury et al (not mentioned above) are meta-studies that produce a null result, due to their selection criteria. There are two studies showing statistically-significant RR for CHD greater than 1 for high sat fat intakes (Mann et al & Boniface et al), but these are drowned-out by a large number of low sat fat intake studies and a study on dairy sat fat which has a RR for CHD less than 1.

    3) The Krauss studies showing reducing LDL particle size with increasing %E from carbohydrate used a 50:50 mixture of complex carbs and sugars. If the complex carbs were maltodextrin or amylopectin (very high GI), they would have been equivalent to feeding glucose. The Krauss studies are therefore extremely suspect.

    4) There are carbs, there are carbs and there are carbs. A diet containing Whole Food "wet" carbs gives high satiety, with minimal disturbance to BG level in people with Impaired Glucose Tolerance & T2DM. According to Discussion on Physiological Factors Influencing the Action of Insulin - Himsworth, a certain minimum amount of carbohydrate (~150g?) must be eaten each day, in order to maintain High Insulin Sensitivity. LCHF diets don't meet this requirement. NK diets definitely don't meet this requirement.

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  2. Nigel, the Himsworth article is from 2-11-1936? Anything more recent on this subject?

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    Replies
    1. You KNOW you want to spend hours rummaging through PubMed! ;-)

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