Oliver and Boyd 1953 - lessons from the early history of the lipid hypothesis.

The introduction to Hooper et al. 2015 gives a good potted history of the lipid hypothesis. It's well worth reading to get some background as to why this idea that saturated fat causes heart disease took off the way it did. (Hooper 2015)
There's a chain of logic involved. There is cholesterol in atherosclerotic plaques. There was a correlation between high cholesterol and heart disease. Eating saturated fat tends to elevate serum cholesterol. Join the dots.
The assumption is that the high cholesterol that correlates with heart disease and the effect of saturated fat on serum cholesterol are the same thing. 

In 1949 Ryle and Russell in Oxford documented a dramatic increase in coronary heart disease (CHD), and the Registrar General’s Statistical Tables of 1920 to 1955 showed that there had been a 70-fold increase in coronary deaths during this 35-year period (Oliver 2000; Ryle 1949). This sudden surge in coronary heart disease sparked research into its causes. A case-control study published in 1953 of 200 post-myocardial infarction patients and age-matched controls established that those with disease had higher low density lipoprotein (LDL) cholesterol levels (Oliver 1953).

The 70 fold rise seen by Ryle and Russell seems to have been mainly due to vagaries in coding cause of deaths during the period, plus a decrease in mortality; in large part, more people were dying of CHD because more people were living to a suitable age, and CHD was becoming a popular diagnosis, replacing other similar causes on death certificates. CHD almost certainly did rise, but probably not nearly so fast. And of course it's ridiculous to think that people didn't eat much saturated fat before the 1920s. There's a small mistake in Hooper et al.'s citation of Oliver and Boyd 1953; this paper doesn't mention LDL cholesterol, just serum cholesterol. The reviewers would have picked this up if they'd been interested in the early history of the lipid hypothesis.The Plasma Lipids in Coronary Artery Disease. Oliver MF, Boyd GS. Br Heart J. 1953 Oct;15(4):387-92. Free text.
Oliver and Boyd 1953 does show a significant difference in cholesterol levels between MI patients and case-controls. That's true (except that strangely there was absolutely no correlation in women in the 50-59 age group). Peak decade for MI in men (largest % of cases) was 50-59, for women 60-69. 


The subjects were 200 consecutive admissions with coronary artery disease and 200 miscellaneous inpatient controls. In the coronary artery disease group, there was electrocardiographic confirmation of myocardial infarction in 170, and of ischaemia before or after the Master two-step test in 30 who presented clinically with angina of effort; any subject who lacked cardiographic confirmation of coronary artery disease was excluded. Adequate controls were very difficult to obtain from a hospital population, but were carefully selected from convalescent in-patients, who had no history or clinical features of atherosclerosis, cardiac, hepatic, metabolic, or renal disease, nor of any other condition known to influence the plasma lipids.
The coronary artery disease group was completed first, and the mean age of each decade of both sexes was determined; the control group was then completed so that the mean age, and number of cases in each decade, would correspond with the coronary artery disease group.

Does this study indicate in any way that saturated fat in the diet was linked to the high cholesterol associated with CHD?
In a small pilot study an irregular diurnal variation in plasma cholesterol was observed thus it was decided that all samples should be withdrawn between 8 and 8.30 a.m. in the fasting state. No blood sample taken during anticoagulant therapy has been included in this series. Similarly, no blood sample taken within five weeks of the occurrence of myocardial infarction has been included. All subjects were receiving a light ward or weight-reducing diet. 

So - the MI cases had been receiving the "light ward or weight-reducing diet" for at least 5 weeks. The controls were "convalescent", and as convalescence was still a leisurely process in hospitals in the UK in 1953, we can safely assume their exposure to hospital food was similar. Indeed, the study indicates that there was no age-related obesity in controls: 

Hypertension and obesity are more common after the menopause, but neither would seem to influence these observations; all the control subjects had a diastolic pressure of less than 90, and a morphological study employing a ponderal index assessment (Sheldon et al., 1940), did not show any tendency to endomorphy in this decade in the controls.

Though the text is not clear on this, the MI cases were probably more likely to be on the weight reducing diets than controls.

So what does Oliver and Boyd 1953 tell us about saturated fat and heart disease? Surely it demonstrates either 1) that the serum cholesterol level in MI cases has nothing to do with diet, or 2) that the serum cholesterol level in MI cases relates to a response to diet which is unique to MI cases, and which does not go away on light hospital or weight-reducing rations. There are three possible explanations of this; 1) that genetic determinants of serum cholesterol, such as FH phenotype, are related to MI (which seems pretty uncontroversial), 2) that cholesterol is elevated in response to an MI, and that this effect plays out over many weeks, 3) that cholesterol response to diet is influenced by either a recent MI or by genetic conditions predisposing to MI.
That saturated fat can cause heart disease in healthy people doesn't seem a logical conclusion to draw from Oliver and Boyd and is not a possibility mentioned in the text.

Any other explanations? 1953 was one year after the killer smog of London. The Oliver and Boyd study took place in Edinburgh, historically known as Auld Reekie for its air pollution. The Clean Air Act 1956 was the first attempt to limit air pollution in the UK. These and similar later Acts, the publication of and response to Silent Spring (1962), and the decline in cigarette smoking following (in the U.S.) the Surgeon General's report and Consumer Union reports into smoking (1963) seem to match the rapid decline in CHD after 1970 in the English speaking world and those countries that undertook similar public health measures in the same historical period (including Scandinavia and Japan).
Oliver and Boyd didn't ask questions about smoking, which might have been revealing, but they did at least set up their experiment to control for diet. It's just a pity that Keys and Hegsted ignored that.

See also: Flaws, Fallacies and Facts: Reviewing the Early History of the Lipid and Diet/Heart
Hypotheses. Elliott J. Food and Nutrition Sciences, 2014, 5, 1886-1903
http://dx.doi.org/10.4236/fns.2014.519201