Why Battle? Simply because the whole hypothesis linking elevations of certain lipid moieties causally with an increased propensity to the development and progression of coronary and other vascular atherosclerotic disease has not been as secure as one would imagine.

The so-called, “Diet-Heart” hypothesis began in the 1950s under the compelling and persuasive personality of Dr Ancell Keys. Keys exercised tremendous influence in the American post-war establishment, for example the combat rations for the American army were known as, ‘K rations’ after Keys, who had invented them. There was an epidemic of coronary artery disease raging in the United States, and considerable pressure was felt on the medical and governmental agencies to come up with solutions. In this environment, Ancell Keys published his, ‘Seven Countries Study”. By relating the intake of saturated fat to heart attack frequency in six countries, he showed a close relationship between the two-and the, “Diet Heart Hypothesis” was born.

He was obviously a great salesman, and despite the many an obvious flaws in his theory found great resonance in the scientific, political and administrative communities-ultimately, convincing even the medical profession. He managed to make the front cover of Time magazine twice in two decades.

Unfortunately, despite its appeal, manipulation of the saturated fat intake in America as elsewhere did little if anything to stem the rising tide of heart attacks. Sceptics found plenty of flaws, and even some creative statistical manipulation in Keys’s data on the saturated fats/heart-attack relationship. It must be admitted that the study had other laudable conclusions, e.g. the relationship between cigarette smoking and heart attacks etc.

In the 1970s, The Diet Heart Hypothesis was under serious threat. Just when it was about to be discredited, a new dimension for treating high cholesterol emerged-the HMG co- reductase inhibitors, aka “Statins”. These immensely potent drugs lowered LDL-cholesterol two levels only dreamed of by the dietary interventionists. They also had a wide range of other effects e.g. on vascular inflammation, endothelial function, clotting via action on fibrinogen which could have mediated their undeniable beneficial effects on coronary and stroke mortality and morbidity. However, the cholesterol entity was readily measurable and the Diet Heart Hypothesis was so firmly entrenched, that all statins benefits were viewed through the perspective of LDL reduction. The previous guidelines concentrated heavily on reducing LDL to very low levels. Individuals who had a high calculated risk of developing atherosclerotic vascular disease or were diabetic, were encouraged to reduce their LDL-cholesterol two levels below 2.0 mmol per litre. This often required high-dose statins therapy as well as not infrequently, combination with other lipid-lowering agents.

The latest, 2013 ACCAHA guidelines make several radical departures from the previous one. Firstly they do reiterate the use of high-dose statins therapy equivalent to 40 mg atorvastatin for the highest risk cases. More controversially, even asymptomatic patients with a calculated risk using a new calculator of greater than 7.5% risk of ischaemic events in 10 years would merit statins therapy. This would increase the pool of patients eligible for statins therapy by a substantial amount. No provision exists for retesting lipid levels once therapy has been initiated.

These guidelines do not sit well with a large number of practitioners and only time will tell the degree of acceptance they will enjoy.