FEW EPIDEMIOLOGISTS could be better suited to deliver tomorrow’s Geoffrey Rose Lecture on Population Sciences than Kay-Tee Khaw, Professor of Clinical Gerontology at the University of Cambridge. Khaw was a medical student of Geoffrey Rose back in the 1980s at St Mary’s Hospital in London, and it was here, she says, that her defining principles in preventive cardiology were established. ‘In fact,’ she admits, ‘it was because of Geoffrey that I went in to epidemiology in the first place. He was the basis of my career.’
As a prelude to today’s eponymous lecture on ‘old and new challenges’ in preventive cardiology, Khaw cites Rose’s much repeated claim that the real challenges in cardiovascular medicine today lie not with the treatment of acute conditions but with the wider environments which encourage their development.‘But don’t forget,’ Khaw reminds us, ‘that Rose’s population philosophies began with clinical medicine, asking first, how do I treat this patient, and then, how can we prevent this happening.’ It was from an answer to the second question that Rose developed his view that, while high risk individuals must be treated, the real gains in CVD prevention would be derived from changes in whole populations. The prevalence of those at high risk would thus depend on where the whole population distribution of risk lies.
Even today, says Khaw, in the age of genomics, exactly the same philosophy applies. The challenge is still to identify what people can do collectively to change their risk profiles, explaining that ‘a very small change can have a massive effect on prevalence in populations’. Today, for example, 93 susceptibility genes and gene variants have been identified for coronary heart disease. But even if genomic analysis can identify those people at very high genetic risk of CHD, their absolute numbers are so small that individual treatment will have little impact on overall population risk, such is the distribution of genetic risk throughout populations. Indeed, she adds, the distribution of genetic risk is no different from that of hypertension or high cholesterol.
It’s for these reasons, she explains, that lifestyle changes rather than individual high-risk strategies have guided prevention policies over the past two decades. Such an approach is exemplified in patterns of stroke for which incidence and mortality rates were already declining well before the widespread introduction of antihypertensive medications.
Professor Khaw’s research in population science has been largely concentrated on a prospective study of more than 25,000 men and women in Norfolk - a region of eastern England - a part of the European Prospective Investigation into Cancer (EPIC). Participants originally completed a health and lifestyle questionnaire with information on smoking, alcohol, physical activity, social class, and education. BMI and blood pressure were measured and blood samples were assayed for vitamin C and lipids (and other biological markers). Data from the latter prompted one of Khaw’s most widely cited reports (from 2012), which showed that plasma concentrations of saturated fatty acids were positively associated with CHD and omega-6 polyunsaturated fats inversely related. ‘These findings,’ she says, ‘were consistent with evidence of a protective role of omega-6 fats substituting for saturated fats for CHD prevention.’
However, in terms of lifestyle change, she still describes the dietary fat story as ‘complicated’, noting conflicting study results from both observational and randomised studies. For example, the $260 million Women’s Health Initiative trial (in postmenopausal women) found no evidence that those allocated to a low fat diet had no lesser risk of CHD than controls. However, while such studies might suggest no beneficial cardiovascular effect from lowering total fat intake, Khaw’s EPIC-Norfolk study suggested that the balance between high saturated and low polyunsaturated fat is important. ‘When you reduce saturated fat, it’s critical what you replace it with,’ she says, suggesting that a profile of high saturated and low polyunsaturated fat would indeed increase CHD risk. Such an explanation, she adds, might also explain the long seen observations (and apparent paradoxes) of the Mediterranean diet - that, while consumption of unsaturated fats is high, this is also a high fat diet. So different types of fat have differing biological and metabolic effects.
The study thus proposed that dietary recommendations should focus on patterns of food intake rather than individual nutrients, and the balance between different nutrients in foods. ‘Early guidelines to prevent CHD recommended reductions in saturated fat but little consistency as to what might be substituted: other fats, protein, or carbohydrate,’ the study concluded. ‘Our results add to the accumulating evidence that substitution of saturated fat by polyunsaturated fat may have more CHD benefits.’
Such ‘controversial’ conclusions on dietary guidance as public health policy bring us back to Geoffrey Rose, Professor Khaw’s mentor, and the population strategy of CVD prevention by the control of incidence rates. ‘The prior concern,’ said Rose, when comparing the high risk and population strategies, ‘should always be to discover and control the causes of incidence.
’Optimising cardiovascular health: old and new challenges, 30 Aug 17:20-18:00 Regents Park - The Hub
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