Oslo Diet‐Heart 1966.

Study characteristics
Methods	RCT Oslo Diet‐Heart Trial Summary risk of bias: moderate to high for CVD outcomes, low for all‐cause mortality
Participants	Men with previous MI (Norway) CVD risk: high Control: randomised 206, analysed 148 (at 5 years) Intervention: randomised 206, analysed 152 (at 5 years) Mean years in trial: control 4.3, intervention 4.3 % male: 100 Age: mean control 56.3, intervention 56.2 (all 30 ‐ 67) Ethnicity: ethnicity not mentioned Statins use allowed? Unclear (medications not mentioned as exclusion criteria, most appeared to be on anti‐coagulant medications, statins not mentioned) % taking statins: Not reported (probably none as too early, pre‐1980)
Interventions	Modified fat diet vs control Control aims: no dietary advice but direct questions answered, supplement = 1 vitamin tablet daily Intervention aims: reduce meat and dairy fats, increase fish, vegetables, supplement ‐ 1 vitamin tablet daily, 0.5 L soy bean oil per week (free to 25% of participants), sardines in cod liver oil (free at certain times to encourage compliance) Control methods: usual diet Intervention methods: continuous instruction and supervision by dietitian, including home visits, letters and phone calls Total fat intake: unclear (note ‐ intake of total fat, carbohydrate, protein and sugar was assessed in 17 "especially conscientious and positive" as well as intelligent dieters, but this was not reported here as unlikely to be representative, and lacking control group data) Saturated fat intake: unclear (mean difference unclear) PUFA intake: unclear PUFA n‐3 intake: not reported PUFA n‐6 intake: not reported MUFA intake: unclear CHO intake: unclear Protein intake: unclear Trans fat intake: unclear Replacement for saturated fat: PUFA (based on dietary goals) Style: diet advice and supplement (food) Setting: community
Outcomes	Stated trial outcomes: coronary heart disease morbidity and mortality Data available on total mortality? yes Cardiovascular mortality? yes Events available for combined cardiovascular events: total MI, sudden death, stroke, angina Secondary outcomes: non‐fatal and total MI, stroke, CHD mortality (fatal MI and sudden death), CHD events (MI, angina and sudden death) Tertiary outcomes: weight, total cholesterol, systolic and diastolic BP (but no variance information was provided)
Notes	Study duration over 4 years Study aim was to reduce serum cholesterol by a diet "low in saturated fats and in cholesterol, and rich in highly unsaturated fats", saturated fat intakes during study were not reported SFA reduction aimed (reduction unclear as not measured except in a highly compliant subgroup) Total serum cholesterol, difference between intervention and control, mmol/L: ‐1.07 (95% CI unclear), reduction > 0.20 Weight change from baseline was ‐0.5 kg in the control group (n ~ 155), ‐2.5 kg in the intervention group (n ~ 160) at 51 months Total cholesterol change from baseline was ‐0.46 mmol/L in the control group and ‐1.53 mmol/L in the intervention group at 51 months Systolic BP at baseline was 153.8 mmHg in control and 159.0 in intervention, and mean sBP through trial was 154.3 mmHg in control and 158.2 mmHg in the intervention group. Diastolic BP at baseline was 93.5 mmHg in control and 97.1 mmHg in intervention, through trial mean dBP was 95.5 mmHg in control and 98.6 mmHg in intervention participants Trial dates: Recruitment 1956 to 1958 Funding: Det Norske Råd for Hjerte‐ og karsyk‐dommer, A/S Freia Chokoladefabriks Arbeidsfond for Ernærings‐forskning, JL Tiedemanns Tobaksfabrik Joh H Andresens medisinske fond, plus A/S Farmacöytisk Industri provided a multivitamin free of charge, DE‐NO‐FA and Lillleborg Fabriker provided soy bean oil at reduced prices, the Research Laboratory of the Norwegian Canning Industry, Stavanger Preserving Co and Kommendal Packing Comp provided Norwegian sardines in cod liver oil free to those in the intervention group. Declarations of Interest of primary researchers: none stated, all authors worked for academic or health institutions.
Risk of bias
Bias	Authors' judgement	Support for judgement
Random sequence generation (selection bias)	Low risk	"table of random numbers used", by Prof Knut Westlund
Allocation concealment (selection bias)	Low risk	Randomisation appears to have occurred before medical examination within the study, so was not affected by participant characteristics and was concealed.
Blinding of participants and personnel (performance bias) All outcomes	High risk	Participants were aware of their allocation as was the main trialist.
Blinding of outcome assessment (detection bias) CVD outcomes	Unclear risk	Outcomes were categorised by a diagnostic board, but their blinded status was unclear.
Blinding of outcome assessment (detection bias) All‐cause mortality	Low risk	Blinding is not relevant in assessment of mortality.
Incomplete outcome data (attrition bias) All outcomes	Low risk	The participants who could not be directly followed up for the 5 years were followed until death or study end through personal interviews, or contact with their physicians or relatives.
Selective reporting (reporting bias)	Low risk	Not relevant for primary and secondary outcomes as all trialists were asked for data
Free of systematic difference in care?	High risk	Dietetic input level very different, although medical care appeared similar. See control and intervention methods in the Interventions section of the table of Characteristics of included studies
Stated aim to reduce SFA	Low risk	Aim to reduce SFA stated
Achieved SFA reduction	Unclear risk	SFA intake not reported
Achieved TC reduction	Low risk	Although statistical significance was not reported or calculable, TC in the intervention group was 1.07 mmol/L lower than in the control group, a large fall (and almost certainly statistically significant).
Other bias	Low risk	None noted