[2017] Lore of Nutrition: Challenging Conventional Dietary Beliefs

by Tim Noakes

  Having exposed the true findings of the WHIRCDMT and the reluctance of both the NIH and Rossouw to report those findings transparently, I was certain that my approach would win the day.

  Rossouw began his reply by saying that the error Eenfeldt and I had identified in Figure 3 was clearly a ‘printer’s error’. He failed to explain why he had yet to direct JAMA to correct it. He then started to make his case using the diversionary technique of information overload. My talk, he insinuated, was purely about entertainment; his talk, he promised, would be exclusively about hard science.

  The main evidence he presented was secular trends4 in (declining) heart-disease rates in several countries, including Finland, Poland, northern Sweden, the US, England and Wales. These trends, he implied, proved that the recent adoption of the low-fat diet in those countries was effectively preventing the development of arterial disease in their populations. He believed so strongly in the value of this evidence that after the debate he stated: ‘Why mess with success?’

  Well, let’s consider how other experts without a personal stake in the diet debate interpret the published evidence that Rossouw presented.

  One study, quoted by Rossouw in both the debate and a subsequent publication,13 showed falling heart-attack rates in England and Wales. The authors estimated that about 50 per cent of this reduction was due to smoking avoidance and 40 per cent to improved medical care.14 At best, dietary change could only explain a maximum of 10 per cent, not the 100 per cent Rossouw implies in his presentations and publications.

  The key point is that these secular trends do not constitute definitive proof, because so many variables are changing at the same time; that is why we prefer evidence from RCTs such as the WHIRCDMT, the Multiple Risk Factor Intervention Trial and the Look AHEAD trial, all of which, as Rossouw well knows, disprove absolutely the diet-heart hypothesis.

  If Rossouw had ever been my student, he would have heard me frequently quote Albert Einstein: ‘No amount of experimentation can ever prove me right; a single experiment can prove me wrong.’ If you focus on secular trends in heart disease, you cannot ignore the ‘Japanese paradox’: whereas in Australia, Canada, France, Sweden, the UK and the USA the continuing fall in CHD mortality has been associated with falling blood cholesterol concentrations, the opposite has occurred in Japan. As a result, CHD mortality is 67–75 per cent lower in Japanese men and women than in American men and women, despite higher blood cholesterol concentrations in the Japanese. The authors say that this observation ‘may suggest some protective factors unique to Japanese’.15 What if that factor is nutritional?

  This change has occurred as Japanese people of all ages have reduced the amount of carbohydrate in their diets, replacing it with fat, especially from animal sources, but also from vegetables.16 The point is that for a theory to be true, it must explain all observations, not only those that can be cherry-picked to favour one’s personal scientific bias.

  Rossouw also omitted to mention other evidence from Japan showing that Japanese with low blood cholesterol levels are at increased risk of mortality from stroke, heart disease and cancer.17 Furthermore, higher intakes of saturated fat appear to be particularly beneficial in the prevention of stroke in East Asians,18 another finding Rossouw conveniently ignored.

  In touting the great successes in reversing CHD in the North Karelia province of Finland – an unusual population that suffered the unimaginable stresses of relocation following the Russo-Finnish Winter War of 1939–1940 – Rossouw conveniently failed to discuss the inconvenient finding from the Finnish province of Kuopio. As Rossouw tells it, Finns living in North Karelia have the highest CHD mortality of all Finns, assumed to be due to their high rates of smoking, hypercholesterolaemia and hypertension. Conveniently ignored is the fact that virtually the entire population of East Finland – 400 000 people, including those living in North Karelia – was displaced in 1940 during the Second World War, when Russia took control of Karelia. It seems rather more likely that the much higher rates of heart disease in East Finland compared to West Finland, despite similar intakes of fat and saturated fat, were a direct result of the Russian invasion during the war, which directly affected those living in the east of Finland, including North Karelia.

  In 1972, a community-wide intervention was introduced to reduce these three risk factors – much like CORIS – and the outcome in North Karelia was compared to the neighbouring province of Kuopio, in which CHD mortality rates were equally high, but in which there was no intervention.19

  Five years later, the decline in total and CHD mortality in both men and women was identical in North Karelia and Kuopio, even though the prevalence of the conventional CHD risk factors had initially fallen much more in North Karelia than in Kuopio.20 In particular, there was no change in the average number of cigarettes smoked per day, no change in blood cholesterol concentrations and no change in mean blood pressure in those living in Kuopio. Even more difficult to explain was the finding that in both Kuopio and North Karelia, women showed a much greater reduction in CHD mortality than did men, even though the reduction in risk factors in women was generally negligible or non-existent.21

  Interestingly, as the project continued, the authors combined the results from Kuopio and North Karelia as if both provinces were always part of the original intervention. In that way, an inconvenient truth could be conveniently hidden.

  This study, quoted by Rossouw as evidence for the benefits of an intervention that reverses coronary risk factors, like his WHIRCDMT, failed to prove his contention, because CHD and total mortality fell in both men and women in North Karelia and in Kuopio, whether or not coronary risk factors were reduced by an expensive intervention aimed especially at lowering blood cholesterol concentrations.

  Nor was Rossouw prepared to discuss the ‘Sami paradox’. Specifically, the finding that the Sami reindeer herders living in the northernmost regions of Finland and who, like the Masai and Sambouri, live exclusively on animal products, have exceptionally low rates of CHD, despite blood cholesterol concentrations greater than 6.5 mmol/L, way above values considered to be ‘safe’.22 ‘Our current knowledge of cardiovascular risk factors cannot explain the low mortality from IHD [ischaemic heart disease] in the Sami district of Finland,’ the authors of one study concluded.23 Interestingly, reindeer meat is high in the antioxidants selenium and alpha-Tocopherol, and the monounsaturated fat oleic acid.

  Rossouw was also not brave enough to mention the Roseto Paradox.24 Roseto was an exclusively Italian-American town in eastern Pennsylvania with, in the early 1960s, ‘a remarkably low rate of coronary heart disease among the living, despite the fact that the conventional risk factors were found to be at least as prevalent in Roseto as in the two control communities’25 and that ‘Rosetans eat at least as much animal fat as the average American’.26 Thus:

  The oil intake of the Rosetans was relatively low in olive oil. They used a great deal more lard than the wives of the people in this room use. One of their favorite dishes was fried peppers. They would fry the peppers in lard and they are very good. Then you’d take a piece of Italian bread and rub it around in the gravy that is left and eat that and that’s delicious! The Rosetans were very poor when they came and they are much more prosperous now. They eat everything. I’ve had many dinners with Rosetan families. They usually have more than one type of meat. When I eat ham I cut the rim of fat off and don’t eat it, same way with roast beef. They cut right through and eat it all. We were very elaborate in our study of their diet because we had Ancel Keyes [sic] breathing down our necks.27

  Heart-disease rates and mortality rose over the next 25 years as the population began to move away from its traditional (Mediterranean) ‘values of southern Italian villagers’. This included dietary changes that ‘occurred … in the direction of what the American Heart Association calls “prudent”. There was less consumption of animal fat.’28

  The authors made two substantive conclusions. First, that the lower rates of heart disease in Roseto
in the 1960s were due to the ‘greater social solidarity and homogeneity in Roseto’, without any evidence that coronary risk factors were lower than in those living in the neighbouring communities with higher heart-disease mortality rates.29 Second, that social change over the next 50 years produced the ‘sharply increased rates of heart attack amongst men under the age of 65’.30 This change was not prevented by an increased adoption of the AHA ‘prudent’ diet with a reduction in saturated-fat intake.

  Rossouw’s attempt to explain any and all secular changes in heart-disease mortality rates simply on the basis of reduction in saturated-fat intake is simplistic, indeed opportunistic, in the extreme.

  He also failed to discuss the other extreme, the ‘Israeli paradox’. Israel has replaced dietary saturated fat with higher intakes of omega-6 polyunsaturated fats from vegetable oils so that intakes are 8 per cent higher than in the US and 10–12 per cent higher than in European countries. Israelis suffer from high rates of CHD, hypertension, T2DM and obesity – all markers of IR. Cancer mortality rates are also high, especially in women. The authors of a study looking into the Israeli paradox wondered whether ‘rather than being beneficial, high omega-6 polyunsaturated fat diets may have some long-term side effects, within the cluster of hyperinsulinemia, atherosclerosis and tumorigenesis’.31 I return to this in Chapter 7.

  Clearly, proponents of low-fat diets have simply ignored the evidence for the potentially harmful effects of high omega-6 polyunsaturated-fat intake.

  Rossouw also ignored a serious concern noted by most of the authors of these studies: that although heart-attack rates may have fallen in some countries since the adoption of his ‘heart-healthy’ diet, obesity and T2DM rates are rising in those same countries.

  This brings us to the bigger paradox, which I had yet to identify in December 2012. In all the countries in which heart-attack rates are (or were) falling, the incidence of T2DM is increasing at an exponential rate, as is obesity. But we know that diabetes (by itself or as part of the metabolic syndrome) is the single best predictor of heart-attack risk. There is also the evidence that life expectancy in the US has now reached its peak and will likely decline by the mid-21st century.32 So how can diabetes rates and the prevalence of metabolic syndrome be rising at the same time that heart-attack rates are falling? It makes no sense.

  The answer, which may be relatively simple, provides the crucial missing evidence that finally proves just how damaging the low-fat, ‘heart-healthy’ diet advocated by Rossouw and others is. The key insight comes from understanding how cigarette-smoking causes heart attack.

  Rate of cigarette consumption is the single variable that best tracks US heart-attack rates, including the sudden rise after the First World War and the equally dramatic fall beginning in the 1960s (Figure 4.1). This, too, is paradoxical, because we ‘know’ that arterial disease is a slowly developing disease, occurring over decades.

  Figure 4.1

  The annual number of deaths from CHD in the US began to rise shortly after the end of the First World War. The rise and subsequent fall in heart disease precisely tracks the rise and fall of cigarette consumption in the US. (Data from US National Vital Statistics)

  So how does a change in cigarette consumption produce fairly rapid changes in heart-attack rates if smoking is the direct cause of arterial disease? The answer is that arterial disease – popularly called ‘clogging of the coronary arteries’, but known medically as the development of arterial plaque – is not the immediate cause of a heart attack. Rather, it is when the plaque itself becomes unstable and suddenly ruptures (acute plaque rupture) that a heart attack (or sudden death) occurs.

  Interestingly, the size and extent of any particular arterial plaque does not determine whether or not it will rupture. Small or large arterial plaques seem to have pretty much the same propensity to rupture, which is why coronary bypass grafting or the placement of a stent in a narrowed coronary artery does not guarantee immunity from future heart attacks (see Chapter 3).

  So, if heart-attack rates track changes in population smoking rates without a significant time delay (of decades), then smoking must be acting on plaque stability rather than on the long-term development of arterial plaque.

  Interestingly, there is one study of the diet-heart hypothesis that showed a dramatic effect in reducing heart-attack rates in those with established heart disease. The effect was so rapid that it can only have been due to plaque stabilisation, not removal of the underlying atherosclerosis.

  In the Lyon Diet Heart Study (Figure 4.2), survival was already superior within the first six months in the group fortunate enough to be randomised to eat the ‘Mediterranean alpha-linolenic acid-rich diet’, compared to the standard low-fat, ‘heart-healthy prudent diet’ promoted by Rossouw, the NIH and the American Heart Association (AHA).

  Figure 4.2

  Survival curves after first heart attack in persons randomised to either a ‘Mediterranean alpha-linolenic acid-rich diet’ or the standard AHA ‘heart-healthy prudent diet’. Note that survival is significantly worse in those eating the AHA heart-healthy diet, and that differences in survival on the different diets is already apparent within the first six months on either diet. Redrawn from de Lorgeril et al.33

  There are two reasons why Rossouw and most of his cardiology colleagues must ignore this study.5 First, it shows that the AHA ‘heart-healthy prudent diet’ is not particularly effective in preventing a second heart attack in those who have survived a first. Second, and much more importantly, the dramatic superiority in survival in those eating the Mediterranean diet could not be explained by lower blood cholesterol concentrations, which were identical in both groups. Superior survival on the Mediterranean diet is, therefore, not due to greater reductions in blood cholesterol concentrations, as Rossouw’s model of heart disease demands. So this study provides another paradox that Rossouw seems unwilling to address.

  Although T2DM is clearly a major cause of unstable arterial plaque34 (because it is the best predictor of acute heart-attack risk), the real disease burden of T2DM is the widespread occlusive arterial disease that it causes. This is a progressive, more lethal form of arterial disease that leads to the complete obstruction of flow in the arteries supplying blood to the kidneys (causing kidney failure), the eyes (causing blindness) and the limbs (causing gangrene, requiring amputation), among other organs.

  As heart-attack rates have fallen subsequent to the introduction of the low-fat, ‘heart-healthy’ diet in 1977, low-fat-diet exponents such as Rossouw will have us believe that their diet miraculously prevents all arterial disease. To reach this conclusion, they have to ensure that neither doctors, dietitians nor the public notice the elephant in the room: the exponential increase in the incidence of occlusive arterial disease in those with diabetes, the pathology that will ultimately bankrupt all medical services globally.

  They are able to do this because the medical profession and pharmaceutical industry present T2DM as a disease principally of abnormal glucose metabolism – causing blood glucose levels that are either too high or too low. In reality, T2DM is a disease of progressive occlusive arterial disease, with catastrophic consequences.

  This deception successfully hides the fact that T2DM is by far the worst form of arterial disease. And no one asks: If the low-fat diet prevents arterial disease in the heart vessels, why does it not prevent the form of occlusive arterial disease present at other sites in patients with diabetes? As rates of diabetic arterial disease have increased exponentially since the 1977 low-fat, ‘heart-healthy’ dietary guidelines were introduced, we must conclude that those guidelines are not preventing this form of arterial disease. In fact, an even more likely conclusion is that the 1977 guidelines are the direct cause of the most prevalent form of arterial disease – that which is present in those with IR and T2DM.

  So effective is the industry-directed misinformation campaign that it seems to have become my profession’s primary goal to focus obsessively on the risk that our patients will de
velop heart attacks. What we should really be concerned about is their risk of developing T2DM, the major cause of the most severe form of arterial disease. If we genuinely want to prevent the arterial disease of T2DM, we must understand, as I detail in Chapter 17, that it is the excessive intake of dietary carbohydrates, not dietary fat, in those with IR which causes the progressive, widespread, occlusive arterial disease common in diabetes.

  In December 2012, unfortunately, I was still unaware of this key evidence that irrefutably destroys Rossouw’s arguments in support of low-fat diets.

  Interestingly, in the article he wrote three years after the Centenary Debate, Rossouw seemed to have mellowed on the dangers of LCHF diets:

  It appears that no particular dietary pattern for weight reduction is superior to another. Individual preference determines whether or not to employ a low-fat, high-complex carbohydrate diet; or a low-carbohydrate, high-fat diet, or a diet somewhere in between, provided that the diet also limits energy intake. There is a general agreement that refined carbohydrates, starches and sugars need to be limited, or even eliminated, in diets for weight reduction [my emphasis].35

  The problem with this conclusion is that it conflicts with the evidence from Rossouw’s own study, the WHIRCDMT. That study found that postmenopausal women eating Rossouw’s favoured low-fat US Dietary Guidelines for Americans ‘prudent’ diet gained more weight during the study regardless of whether they began the trial with a normal weight, or if they were overweight or obese. The opposite occurred on the low-carbohydrate diet. The authors concluded: ‘These findings suggest that a low-fat diet may promote weight gain whereas a reduced-carbohydrate diet may decrease risk of postmenopausal weight gain.’36