He sat there, looking woebegone but resigned, and asked the inevitable question. ‘OK, Doc, so tell me — what mustn’t I eat?’ Freshly informed that his cholesterol was high, he awaited the mild note of concerned triumph in his wife’s voice as she pointed out that he really shouldn’t be eating steaks at his club and omelettes with three eggs (although egg-white-only omelettes were, she acknowledged, an Americanism too far).
As a doctor, it always gives me pleasure to be able to reassure someone that life will carry on, perhaps not regardless, but in a recognisably pleasant way after a health warning. Dietary advice about cholesterol is one easy way to achieve this, although in truth, I hide advice about life-enhancing diets under a guise of lowering cholesterol, because lowering cholesterol is not the be all and end all of the matter.
There is a fashion for cherry-picking epidemiological studies that raise questions, rather than provide answers, and then accusing scientific researchers of being similarly biased, closed-minded and in the pay of shadowy plots by ‘big pharma’.
Controversy about the role of low-fat diets has arisen because cohort and randomised, controlled trials do not show a relationship between low-fat diets and deaths from heart disease. Many of these observational trials measured diets by a questionnaire only once at the beginning of studies that may have then followed subjects for up to 16 or 20 years, and few of the randomised trials studied what the subjects ate instead of the fat.
I do not intend to wade deeply into the fat-versus-sugar debate; both to excess seem bad. Saturated fat consumption in the western world has been falling and age-specific death rates from cardiovascular disease have more than halved over the past 30 years, while sugar intake is rising and diabetes and obesity are widespread and growing, literally.
No, I want here to reassure readers that there is finally a gathering consensus about the best food patterns to follow for your heart and the good news is that it does not ban eggs, lean red meat or game and positively endorses seafood, which includes lobster, scallops and oysters. It actually promotes fat in the form of extra-virgin cold-pressed olive oil and nuts — walnuts, hazelnuts, Brazil nuts, and even peanuts (which, I know, are not true nuts… please do not write in). It does not even ban cheese, although the acceptable amounts tend to be those served on the cheeseboard of a three-Michelin-starred restaurant rather than a hearty hunk of ploughman’s cheddar.
Add the known encouragement to eat lots of fibre (aim for double your present intake — this will almost certainly involve more hummus and beans) and plenty of fresh fruit and vegetables and that’s pretty much it. Milk, butter, full-fat Greek yoghurt — all are on the ‘OK in moderation’ list.
At this stage, the hapless patient is generally looking happier, although bewildered: he always understood that heart-healthy diets meant low-fat, low-cholesterol foods — how can everything he thought be so wrong? Well, not everything: pork pies, sausage rolls, doughnuts, fizzy drinks and crème brûlée — there are still foods that should be eaten rarely if at all.
But I do think the ‘experts’ need to raise their hands here — not because of some sinister plot by the food or pharmacological industry but because, in spite of good intentions, postwar dietary advice went too far in the promotion of the ‘low fat’ diet and did not focus sufficiently on what was eaten instead.
The excitement of the past few years, which has spawned so many books on the errors of the low-fat diet, is principally based on very large epidemiological studies following populations over 20 or more years, which suggest that avoiding fat but substituting refined carbohydrates like pasta, bread and sugar does not lower heart disease rates.
This raises a question — why promote wholegrain bread and fruit that is full of sugar when ‘carbs’ are the new evil? I hope we do not fall into the same trap, as with fat, of accusing a single food substance in our diet of being the culprit. Carbohydrates which have been extracted and refined — table sugar, milled flour, even squeezed fruit juice — are rapidly absorbed by the body and produce an intense release of insulin to control the sugar levels in the blood; insulin drives the sugar into our cells and indirectly causes it to be stored as abdominal fat. Consumption of refined sugars has exploded in the last decade, mostly in fizzy drinks and added to ‘low fat’ modified foods and ready-made meals. But whole grains and the fibre in fruit slow down the release of sugar and dampen down the insulin response.
There is remarkably little evidence that a diet including foods containing high levels of cholesterol, such as eggs or prawns, puts up cholesterol levels and there is absolutely no compelling evidence that it is bad for cardiovascular health. This may seem counterintuitive but makes sense, as cholesterol is an essential element in the body. It is the principal constituent of the bioactive membrane around all 37 trillion cells in the human body as well as the main constituent of the myelin sheaths insulating our nerves (30 per cent of all the cholesterol in the body is contained within the brain). What’s more, the body needs cholesterol to manufacture sex and stress hormones — testosterone, oestrogen and cortisol — as well as vitamin D. So life would be a dull, drab affair if we didn’t have it.
It is precisely because cholesterol is so important that we are capable of making it ourselves, mostly in the liver. On a typical diet, we make about 75 per cent of our cholesterol and get the remaining 25 per cent from our food but we can make all of it, if necessary, even on a cholesterol-free diet. The amount is determined to a great extent by genetic predisposition; for the majority of us the more cholesterol we eat, the less our livers produce. Similarly, if we eat less, we make more. I say the majority of us because our response to cholesterol in food is also largely genetically determined; around 30 per cent of the population, known as ‘hyper-responders’, do not make this adjustment and for them, not eating cholesterol may lower serum cholesterol levels.
But even in them, this is not to say that dietary cholesterol is bad; the story is more complex than a simple number. Cholesterol measured in the blood is reported as ‘total serum cholesterol’, the level carried in all the different forms within the blood. Since cholesterol is a waxy, fatty substance and blood is largely water, the body has to coat cholesterol in proteins to make it miscible with blood (a bit like adding mustard to an oil and vinegar dressing). The resulting ‘lipoprotein’ complexes have different functions in the body: low-density lipoprotein (‘LDL’) carries cholesterol from the liver to cells where it is needed and it is an excess of this level in the blood that is associated with the risk of early heart disease; on the other hand, high-density lipoprotein (‘HDL’) transports unused or excess cholesterol back to the liver where it is broken down or excreted into the gut as bile.
This is the origin for the idea of ‘good’ (HDL) and ‘bad’ (LDL) cholesterol and it is self-evident that a number for ‘total cholesterol’ tells us little about risk. Food that raises total cholesterol levels may raise the HDL at least as much as the LDL and so pose little risk to health.
Even this paradigm is overly simplistic if you look deeper — nut intake seems to make the type of LDL change from small, dense and dangerous LDL to big, fluffy, less dangerous LDL — although all would still be measured as LDL — while a high intake of refined carbohydrates lowers HDL cholesterol and shifts the type of LDL towards the small, dense type, at the same time also raising insulin levels, promoting abdominal fat deposition and increasing body markers of inflammation and thrombosis.
One of the best dietary studies was the Predimed study carried out in Barcelona and published in the New England Journal of Medicine last year. In this study, almost 7,500 people aged 55 to 80 and at risk of heart disease were randomised to take one of three diets: a standard ‘low fat’ control diet; a Mediterranean diet (Med-diet) with added nuts (30gm per person/day); and a Med-diet with added extra virgin olive oil (one litre per household per week). The study was stopped early, after less than five years, because those taking the Med-diets had 30 per cent fewer strokes, heart attacks and deaths from cardiovascular disease.
Participants in both Med-diet groups had reduced blood pressure, improved the lipid profile and diminished insulin resistance compared with those allocated to a low-fat diet, and the Med-diet had an anti-inflammatory effect, whereas mediators of inflammation increased after the low-fat diet intervention.
Much more work needs to be done to refine dietary advice and it is highly likely that it won’t be ‘one size fits all’. Perhaps we should try to avoid demonising any single food type but concentrate a little more on putting plenty of the good stuff into our supermarket trolley. Then a steak at the club every week and a soft-boiled egg or two for breakfast is just fine.