The dietary research from Framingham also failed to support Keys’s hypothesis. This never became common knowledge, because it was never published in a medical journal. George Mann, who left the Framingham Study in the early 1960s, recalled that the NIH administrators who funded the work refused to allow publication. Only in the late 1960s did the NIH biostatistician Tavia Gordon come across the data and decide they were worth writing up. His analysis was documented in the twenty-fourth volume of a twenty-eight-volume report on Framingham released in 1968. Between 1957 and 1960, the Framingham investigators had interviewed and assessed the diet of a thousand local subjects. They focused on men with exceedingly high cholesterol (over 300) and exceedingly low cholesterol (under 170), because these men “promised to be unusually potent in the evaluation of dietary hypotheses.” But when Gordon compared the diet records of the men who had very high cholesterol with those of the men who had very low cholesterol, they differed not at all in the amount or type of fat consumed. This injected a “cautionary note” into the proceedings, as the report noted. “There is a considerable range of serum cholesterol levels within the Framingham Study Group. Something explains this inter-individual variation, but it is not diet (as measured here).”

“As measured here” encapsulates much of the challenge of scientific investigation, as well as the loophole that allowed the dietary-fat controversy to evolve into Henry Blackburn’s two strikingly polar attitudes. Perhaps the Framingham investigators failed to establish that dietary fat caused the high cholesterol levels seen in the local population because (1) some other factor was responsible or (2) the researchers could not measure either the diet or the cholesterol of the population, or both, with sufficient accuracy to establish the relationship.

As it turned out, however, the Framingham Study wasn’t the only one that failed to reveal any correlation between the fat consumed and either cholesterol levels or heart disease. This was the case in virtually every study in which diet, cholesterol, and heart disease were compared within a single population, be it in Framingham, Puerto Rico, Honolulu, Chicago, Tecumseh, Michigan, Evans County, Georgia, or Israel. Proponents of Keys’s theory insisted that the diets of these populations were too homogenous, and so everyone ate too much fat. The only way to show that fat was responsible, they argued, was to compare entirely different populations, those with high-fat diets and those with low-fat diets. This might have been true, but perhaps fat just wasn’t the relevant factor.