Sunday, December 22, 2013

The Oslo Diet Heart Study

Studies Associated with the Trial

The effect of plasma cholesterol lowering diet in male survivors of myocardial infarction. A controlled clinical trial (1966) [1] (no access)
The effect of a cholesterol lowering diet in male survivors of myocardial infarction. (A controlled clinical trial) (1967) [2] (in Norwegian)
The effect of plasma-cholesterol-lowering diet in male survivors of myocardial infarction. A controlled clinical trial (1968) [3]
The Oslo Diet-Heart Study: Eleven-Year Report (1970) [4]
Prevention of coronary heart disease: some results from the Oslo secondary and primary intervention studies (1989) [5] (no access) 

Participants and Diets 

412 men aged 30 to 64, who had previously had a heart attack, were randomised to two groups: an experimental group and a control group.  The control group consumed their regular diet, while the experimental group was instructed to consume a diet low in animal fats and cholesterol and high in vegetable oils.  Dietary information from only 17 participants in the experimental group was reported.  The groups were similar at baseline, except the experimental group had slightly higher blood pressure [3] 

The papers I had access to only had pretty basic information on the diet, which came from only 17 participants in the experimental group 

Energy (kcal)
2400
Protein (g)
92
Fat (g)
SFA/MUFA/PUFA (g)
P/S Ratio
104
22/27/55
2.4
Carbohydrate (g)
Sugar (g)
269
51
Dietary Cholesterol (mg)
264

Results 

Cholesterol levels decreased in the experimental group [3]


The number of major CHD relapses can be calculated using the table below from the total number of CHD relapses - angina.  CHD mortality can also be calculated using the table below from the number of fatal myocardial infarctions (10 vs. 23) and the number of sudden deaths (27 vs. 27) [3].  CVD mortality and total mortality are reported more simply in a paper [4] and the results are presented in my table below. 



Experimental
Control
Major CHD Events [3]
70
91
Total CHD Events (P = 0.011*) [3]
80
120
CHD Mortality [3]
37
50
CVD Mortality (P = 0.09) [4]
38
52
Total Mortality (P = 0.13) [4]
41
55

At the end of the 5 year diet period: “the surviving dieters were advised to adhere to the cholesterol lowering diet in the future. The surviving controls were informed that a reduced fat intake possibly might be beneficial, but they received no detailed dietary instructions.”The men were followed for an additional 6 years to track mortality [4].  After 11 years the mortality is as follows:

 [4]
Experimental
(n=206)
Control
(n=206)
Total Cardiovascular Mortality (p=0.13)
88
102
Other Mortality
13
6
Total Mortality (p=0.35)
101
108

So far, this looks to be one of the more favourable studies for the diet heart hypothesis, but even though I don’t have access to the data other people do.  The meta-analysis by Ramsden, et al discussed how the Oslo Diet Heart Study isn’t a simple omega 6 vs. SFA trial, but rather is multifactorial in favour of the experimental diet:

  • The experimental diet was higher in omega 3.  Meats and eggs were replaced with fish, shellfish and ‘whale beef’.  The experimental group was supplied with considerable quantities of Norwegian sardines canned in cod liver oil, which proved to be popular as a bread spread”.  And also soybean oil has some plant omega 3 
  • The experimental diet was higher in vitamin D, which is a more important source of vitamin D for Norwegians.  The fish and cod liver oil supplied 610 IU of vitamin D 
  • The experimental group was encouraged to eat more nuts, fruits, and vegetables; to limit animal fats; and to restrict their intake of refined grains and sugar 
  • The experimental diet was lower in trans fats.  Paraphrasing from Ramsden, et al: in the two decades before the ODHS, Oslo males had a 7-fold increased incidence of an initial heart attack, which coincided with a rapid rise in partially hydrogenated fish and vegetable oil margarines.  In the control group, about 6.9% of total calories came from these margarines, whereas they were “entirely restricted” in the experimental group

With the trial being so multifactorial in favour of the experimental group I don’t think one should use it as evidence for the diet heart hypothesis or for recommendations for omega 6 to replace SFA.

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