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Sydney diet heart

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Information about Sydney diet heart

Published on February 16, 2013

Author: pronutritionist

Source: slideshare.net

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The recovery and re-evaluation of the old data on Sydney Diet Heart Study uncovers unexpected outcomes. However, interpret with care because things have changed since 1970s.
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Sydney Diet Heart Study re-evaluation 2013 Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ 2013;346:e8707.Page 1

Sydney Diet Heart Study ended 1973, the same year when Opera House wasopened. Now after 40 years, the actual results of the study are presented.Photo: BigStockPhoto

Background• Sydney Diet Heart Study was one of the key studies in Diet Heart Hypothesis. It was a randomized controlled study (RCT) with disease and mortality end points.• For some mysterious reason, the original investigators never reported the cardiovascular outcomes of the study, but total mortality rates only. This is rather puzzling as the purpose of the study was to examine the effects of saturated fat (SFA) and polyunsaturated fat (PUFA) on heart disease• Chris Ramsden with coworkers and one original investigator, Dr. Boonseng Leelarthaepin, recovered the original data and analyzed the heart disease mortalityPage 3

Methods (schematic)Randomization of patients(MI survivors/angina, n = 458) Low in SFA, high in PUFA diet. Safflower oil and safflower oil based margarine* n=221 y. 1966→1973 Median follow up: 39 months Control (as at baseline) (normal Aussie diet during 1960s) n=237 *) “Increase PUFA intake to about 15% of food energy and to reduce ntake of SFA and dietary cholesterol to less than 10% of food energy and 300 mg per day, respectively” Page 4

Methods• N= 458, males only.• All participants had symptomatic coronary heart disease at the baseline (secondary prevention)• ~ 70% were smokers at baseline• Total cholesterol was ~ 280 mg/DL, ie. 7,2 mmol/l at baseline• 8,1 % in PUFA group and 5,5 % in SFA group had diabetes at baseline• Blood pressure was around 137/89 mmHg in both groups• BMI was around 25 in both groups• SFA intake at baseline in both groups was around 16 % of energy and PUFA around 6 % in both groups• Intake of carbs was around 40 % of energy at baseline in both groupsPage 5

Results, changes in dietPage 6

Results, changes in cholesterol Δ 7,8%Total cholesterol was 7,8 % lower (ie. 0,59 mmol/l, or 23 mg/DL) in the PUFAgroup at 12 months. No data at the end of the study is available Page 7

Results, coronary heart diseasemortality PUFA Safflower oil/margarine 74 % increased risk in PUFA group Control Diet, high in SFAPage 8

Results, updated meta-analysis (1/2) When all PUFA studies are included, there is no difference in cardiovascular disease mortality between the high SFA and the PUFA groupsPage 9

Results, updated meta-analysis (2/2) In the PUFA studies where considerable increase in alfa-linolenic (ALA) was also achieved, PUFA+ALA/EPA/DHA interventions delivered 21 % decrease in cardiovascular mortalityPage 10

Why did not the reduction in cholesterol bringabout any benefit? My speculations (1/2)• There role of trans fat in the margarine (ie. intervention group)? I don’t think it was of major importance – The control group was allowed to use other commercial margarines available at the time (and they used) – Margarines high in trans fat still deliver better Total Cholesterol/HDL –ratio than butter (Mensink et al. 2003, meta- analysis of 63 feeding trials)• Role of inflammation (Ω-6 FAs → increase in arachidonic acid levels → inflammation story) – Ramsden dismisses the whole concept of inflammation in the discussion even if he has previously been a keen supporter – A recent meta-analysis of RCTs in humans: diet very high in linoleic acid do not cause the increase in inflammation markers in humans (Johnson & Fritsche 2012) – If anything, high doses of SFA are pro-inflammatory according to many recent meal studies and prospective cohortsPage 11

Why did not the reduction in cholesterol bringabout any benefit? My speculations (2/2) • There role of oxidatized linoleic acid metabolites in ox-LDL (OXLAMs) – The number one explanation offered by the authors – This theory is pretty new and non-established and represents a major shift in the thinking of cholesterol sceptics – The theory contradicts the fact that nuts, high in linoleic acid, do consistently decrease the risk of cardiovascular disease in prospective cohorts studies and improve lipid profile in humans (Mozaffarian et al. 2011) • Perhaps, just a coincidence? • Perhaps, the recovery of the old data was not bullet- proof?Page 12

Meta-analysis. My conclusions • Vegetable oils devoid of ALA are not protective against cardiovascular deaths • Vegetable oils, like canola oil (rapeseed oil in Northern Europe) and flaxseed oil, are higher in ALA and lower in linoleic acid, and therefore likely to improve cardiovascular prognosis • Modern margarine are devoid of trans fat, at least in Nordic Countries, and based on canola oil. They are likely to improve health outcomes • Nuts are, in spite of their high linoleic acid content, consistently linked to improved health outcomes and should be used regularly • In a pooled analysis of modern prospective cohorts, a replacement of SFA with PUFA reduced coronary deaths risk by 26 % (Jakobsen et al. 2009) – Using the currently available and popular vegetable oils and margarines seem to protect from coronary deathsPage 13

Thank you Chris Ramsden, Boonseng Leelarthaepin et al!Page 14

Welcome aboard! http://twitter.com/pronutritionist http://www.facebook.com/pronutritionist http://www.pronutritionist.net (Finnish) http://www.pronutritionistblog.com (English) Reijo Laatikainen, Authorized Nutritionist, MBA15 16/02/2013

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