[2017] Lore of Nutrition: Challenging Conventional Dietary Beliefs

by Tim Noakes

  After the talk, the various celebrity speakers and I eagerly signed our books for members of the audience (mine was Challenging Beliefs). Just two years later, at the Discovery Vitality Summit, I was informed that there would be no place for me to sign copies of The Real Meal Revolution, and that it would be neither on sale nor on display at the event.

  It was a clear measure of how far I had fallen in their eyes.

  The ‘debate’ at the Discovery Vitality Summit provided the perfect excuse for University of Stellenbosch–embedded journalist Wilma Stassen to write a second article attacking the Banting/LCHF diet, and me. Published in Health-E News on 11 August 2014, and titled ‘Noakes diet particularly dangerous for Afrikaans population’, the piece clearly originated from the conference, as much prominence was given to Dalby’s personal attack on me.

  Stassen begins her article by implying that my advice is dangerous because ‘some patients with high cholesterol have exchanged their cholesterol-lowering medication (called statins) for the LCHF diet, with detrimental results’.89

  Nowhere in The Real Meal Revolution do I specifically state that people with high cholesterol should abandon their statins and follow the LCHF diet. I may believe that this is exactly what the evidence shows to be the best advice for people, especially women, who have ‘high cholesterol’ levels but no heart disease, but I do not prescribe behaviour. My job is simply to provide evidence.

  Instead of asking me for my opinion, Stassen sets up a straw-man argument. ‘Cardiologist Dr Anthony Dalby describes Noakes’ advice to heart patients to exchange cholesterol-lowering drugs for his diet as “criminal”,’ she writes. Yet, as I have said, I have never advised heart patients to replace their statins with the LCHF diet.

  Stassen continues:

  International obesity expert Professor Tessa van der Merwe says there are ‘many health risks connected with the LHCF [sic] diet’. It could exacerbate heart disease, worsen diabetes and osteoporosis and cause gall and kidney stones, says Van der Merwe, honorary Professor of Endocrinology at the University of Pretoria. ‘If you have got familial hypercholesterolemia (FH), the chances that you will develop a sinister cholesterol profile is a reality,’ she adds. FH is caused by a genetic disorder that causes high LDL (‘bad’) cholesterol. It is particularly common in the Afrikaans-speaking population, where there is a 1:70 occurrence in comparison to a 1:500 in the general population.

  Van der Merwe conveniently fails to acknowledge her conflict of interest: that she works in a medical institution that promotes bariatric surgery over nutrition to manage obesity. She also does not ask how, if the incidences of diabetes, osteoporosis, and gall and kidney stones have all increased since 1977, when humans were told to remove fat from their diet, these epidemics can be attributed to an increased fat intake following the adoption by some people of the high-fat diet after the publication of The Real Meal Revolution in 2013. The cognitive dissonance of the professionals unable to acknowledge this conceptual paradox is addressed in a Credit Suisse report published in 2015, which suggests that: ‘Health care officials and government bodies have been consistently behind developments on the [nutrition] research front.’90

  Then there is this condition called familial hypercholesterolaemia. When a patient presents with an elevated total blood cholesterol concentration of 7.5 mmol/L or greater, cardiologists are quick to diagnose FH. We are taught that FH is a fatal condition that provides the absolute proof that cholesterol is the direct cause of arterial clogging and heart attacks.

  But the truth is vastly different. In fact, it is the exact opposite.

  Almost all conventionally trained cardiologists try to convince us that the best predictor of heart-attack risk is ‘cholesterol load’, which is an individual’s lifetime average blood cholesterol concentration multiplied by their age. Thus, the higher the average lifetime blood cholesterol concentration and the older the individual, the greater the damage to his (mainly, but also her) coronary arteries. So, according to this logic, an elevated blood cholesterol concentration is like an internal time bomb, just waiting to explode.

  This model therefore predicts that heart-attack risk in people with FH increases as they age and as their coronary arteries become progressively more clogged, until they eventually succumb to fatal heart disease by middle age.

  To prove this hypothesis, all we need are studies of the life histories of a large number of people with FH. Fortunately, there are a handful of longitudinal scientific studies that have looked at this, and the results they provide are revolutionary. For my analysis, I have borrowed unashamedly from a blog by Dr Zoë Harcombe on this topic.91

  Harcombe reports that in 1991 the Simon Broome Register Group found that people with FH were at a greater risk of dying between the ages of 20 and 39, but thereafter, this mortality difference lessened, so that mortality was no higher for people with FH aged 60 to 74 than it was for those of the same age without FH.92 A second study derived from the Simon Broome Register Group found that death from CHD was 2.5 times higher for FH sufferers than the general population, but the all-cause death rate was no higher.93 Thus, writes Harcombe, ‘patients with Heterozygous FH were dying more of CHD, but less from cancer and thus the death rate was no higher overall’. Harcombe concludes:

  The combined findings from these two Simon Broome Register Group papers show that, if you genuinely have FH and you are aged 60 or over you should be pleased to know that you have a lower risk of cancer and no greater risk of heart disease. If you have FH and are aged 39 or higher, you are already past the highest risk period of your life for heart disease. Even in the 20–39 age group, there were 6 deaths in 774 person years studied – less than a 1 in 100 incident rate and that’s in 1 in 500 people.

  A Dutch study that traced two centuries of descendants of an ancestor with FH found that mortality in those with untreated FH varied dramatically between individuals and changed with time; mortality was no higher in FH carriers during the 19th and early 20th centuries, yet rose after 1915 to peak between 1935 and 1964, before falling again. The authors noted that: ‘During the decades with excess mortality, survival in the branches of the pedigree differed significantly, ranging from normal life expectancy to severe excess mortality … [so that] such large variation in mortality in two directions (over time and within generations) in a pedigree indicates that the disorder has strong interactions with environmental factors.’94 The authors also suggested that in the 19th century, FH might have conferred a survival advantage against infectious diseases. Another study, published 15 years earlier, also reported normal life expectancy in some people living with FH before 1880.95 And another, published 25 years earlier, found that people with FH did not have a reduced life expectancy.96

  Even more perplexing for the cholesterol activists is the recent finding that in people with FH, blood cholesterol concentration has essentially no predictive value for heart attack or stroke in the next 5–10 years.97 Instead, in order of significance, the following factors increased risk for a cardiovascular event: age (above 60 years), obesity, previous history of CVD, age (30–59 years), overweight, diabetes, use of the drug ezetimibe, high blood pressure, patient on maximum combined therapy, patient on maximum lipid-lowering therapy, male, premature family history of CVD, patient on maximum statin dose, and active smoking.

  In other words, people with FH who are at risk of heart attack are those who have the conventional risk factors, most especially IR and perhaps blood-clotting abnormalities,98 in which total blood cholesterol concentration plays no role. Recent genetic studies confirm that ‘not all FH patients present the same CVD risk and accurate stratification of CVD risk in FH is imperative’. They further suggest that using genetic risk scores ‘could lead to a more personalized approach to therapy’.99

  The key point perhaps is that many people with FH will have a completely normal life expectancy despite living for seven or more decades with ‘criminally elevated’ blood cholesterol concentrations, whereas others with FH will
die young from heart disease. This has important implications for our understanding of how to treat patients with FH, and how we interpret non-randomised studies of treatment outcomes in these patients. What you believe determines what you believe. And there is perhaps no better example of this than the current medical management of FH. Suppose the first patient with FH whom a doctor ever encounters dies at the age of 21 from extensive coronary artery disease and a fatal heart attack. How would that doctor not prescribe statin drugs to every other patient with FH in his practice, especially if everything he reads in the medical literature advertises the dangers of cholesterol in people with FH? For if high cholesterol can kill someone in their 20s, imagine what even moderately elevated cholesterol values are doing to the coronary arteries of all the doctor’s other patients, whether or not they have FH.

  What these studies show is that FH is not a uniformly fatal disease. Rather, there appears to be a ‘protective effect of age’, the opposite of what one would predict if it is solely exposure of the coronary arteries to years of high blood cholesterol concentrations that causes fatal heart attacks. Worse, in our current state of uncertainty, medical science is unable to distinguish between patients with FH who are likely to die at a young age and those who will have a normal life expectancy. All this becomes extremely important when we review the evidence that experts who work closely with the pharmaceutical industry use to convince us that statins are effective in mitigating FH.

  The two trials usually quoted as proof of statins’ effectiveness were neither randomised nor properly controlled.100 As a result, we cannot be certain whether the apparently beneficial effects of statin prescription were simply because the populations studied consisted of older FH individuals (over age 39) with a normal life expectancy. But if you have been taught that (1) elevated blood cholesterol concentrations cause arterial disease; (2) the higher the blood cholesterol values, the sooner death from heart disease will occur; and (3) all people with FH must die young from heart disease, it follows that if a study finds that FH sufferers taking statins can have a normal life expectancy, then statins must be remarkably effective drugs. That an identical outcome could result even if the statins were ineffective will never be considered or conveyed to the medical profession, because it might just be another death blow for the lipid hypothesis (see Chapter 17).

  If ‘high cholesterol’ is the exclusive cause of heart disease, how is it that elevated cholesterol levels suddenly become unimportant when people with FH pass the magical age of 39? The answer must be that it is not cholesterol that is causing arterial disease in those with FH, but something else. Because the blood cholesterol concentrations in people with FH who develop heart disease are no different from those who do not.101 Imagine that: in the disease that we are told provides definitive proof that cholesterol causes heart disease, blood cholesterol concentration cannot distinguish between people who will develop coronary artery disease and those who will not. Then there is the question of why, in those with FH who develop coronary artery disease, it is only the arteries supplying the heart and not the brain that are affected.102 Yet the brain arteries are exposed to the same high blood cholesterol concentrations.

  Clearly something other than cholesterol is causing heart attacks in people with FH. The most probable explanation is that the genetic condition that causes FH is itself benign if it results solely in an increased blood cholesterol concentration. Rather, it is another genetic condition that sometimes, but not always, co-exists with FH and that increases the risk of heart disease. It seems probable that this factor has to do with an increased likelihood for developing blood clots103 or perhaps plaque rupture, or even a co-existing insulin resistance.

  Cardiologists should be telling older patients whose blood cholesterol levels rise on the Banting diet – perhaps exposing their FH genotype – that they are well past the age at which FH confers any increased risk of heart attack. And that they can take some comfort from the fact that, statistically, they are much less likely to develop cancer.

  Returning to Stassen’s article, she goes on to deliver what she clearly considers to be the Dalby knockout punch: the anecdote of the woman who ‘dumped her statins for Noakes’ diet’ and whose blood cholesterol concentration increased from 5.1 to 12.9 mmol/L. ‘But when the 39-year-old woman returned to a normal diet and resumed her medication,’ observes Stassen, ‘her cholesterol dropped substantially to 7.3.’

  Stassen fails to ask Dalby for the evidence that prescribing statins to a woman without any sign of arterial disease will improve her life expectancy. Possibly because the answer is that there is very little evidence that statins improve life expectancy in women whose only abnormality is a raised blood cholesterol concentration.104 The truth is that these drugs carry the risk of serious long-term side effects, including an increased risk for muscle breakdown,105 peripheral neuropathy,106 worsening blood glucose control shown as increasing HbA1c concentrations,107 T2DM,108 liver dysfunction, acute renal failure and cataract,109 Parkinson’s disease,110 cancer,111 and perhaps cognitive problems,112 including transient global amnesia.113 Others argue that statins worsen arterial disease and promote heart failure.114 Hence their indiscriminate use might also be labelled ‘criminal’.

  My favourite author on this topic is cardiologist Barbara Roberts MD, who directs the Women’s Cardiac Center at the Miriam Hospital in Rhode Island. In her book The Truth About Statins, she writes:

  I am seeing more and more healthy women in their thirties being put on this drug because their physicians don’t read the fine print. A healthy woman in her thirties can expect to live another fifty years. It makes no sense at all to go on powerful medicines with the potential for serious, life-threatening side effects – for decades – when they have no proven benefit. Especially since you can get all the benefits of statins without taking them, simply by changing your lifestyle.115

  Further support for the ineffectiveness of statins in treating postmenopausal women comes from a Women’s Health Initiative study, ironically co-authored by Jacques Rossouw.116 It found that postmenopausal women with T2DM had a 39 per cent greater risk of developing heart disease, even when treated with statins – the same risk as those who were not treated with statins. Rossouw did not refer to this in the Centenary Debate, because it further confirms that IR, and not cholesterol, leads to heart disease.

  Which brings me to a point emphasised by Peter Gøtzsche in his book Deadly Medicines and Organised Crime:

  It’s important to realise that drugs are never safe. Life jackets on boats are good to have, as they may save your life. They won’t kill you. Drugs are not like that. Taking a statin may reduce your risk of dying from heart disease, but it will also increase your risk of dying from some other causes. Not much, but one of the statins, cerivastatin (Baycol), was taken off the market after patients had died because of muscle damage and renal failure.117

  Importantly, Dalby fails to mention that at age 39, his patient is approaching the age at which the blood cholesterol concentration is without value in predicting risk of future heart attack.118 Whereas low blood cholesterol concentrations consistently predict increased risk of cancer;119 shorter life expectancy, especially in the elderly120 and, most especially, in the very elderly121 (see Figure 7.4); increased mortality in advanced heart failure;122 increased risk for infection during life,123 including a greater likelihood of contracting124 and dying from HIV/AIDS;125 in some but not all studies, an increased risk for developing dementia or Parkinsonism;126 and increased risk for suicide127 and violent behaviour.128

  So the question becomes: Why would you want to treat an elevated blood cholesterol concentration in a female, especially one over 60 years of age, who has no clinical evidence for heart disease? Why not focus on treating the real causes of ill health, which are the complications caused by IR and persistent hyperinsulinaemia? What if these are of much greater importance than trying to treat a probably meaningless ‘raised’ blood cholesterol concentration?

 
Figure 7.4

  Cumulative survival curves in all 85-year-old participants (A), in men (B) and in women (C) based on the categories of blood cholesterol concentrations – high, intermediate or low. Note that there is a graded effect so that those with the highest blood cholesterol concentrations have the greatest survival. This effect is more marked in elderly men than in women. Reproduced from Takata et al.

  Stassen next invites the opinion of another UCT professor, David Marais, who states: ‘Statins make a tremendous difference in heart-disease risk in people with FH, as they will not be able to control their cholesterol through lifestyle.’ He adds:

  In persons with the common range of cholesterol, there is a definite association with risk but other factors such as age, smoking, hypertension, obesity and others, may predominate in their contribution to risk so that intervention with cholesterol lowering treatment will not have as large an impact as it has in the very high risk of FH [my emphasis].

  What Marais does not add is that hypertension, obesity and diabetes (which he also failed to mention is the strongest risk factor for heart disease other than NAFLD and metabolic syndrome) are merely signs of an underlying insulin resistance in people eating high-carbohydrate diets. And that the most effective treatment of IR is the LCHF diet. If the LCHF diet can reverse obesity, hypertension and metabolic syndrome, as our Canadian study has shown,129 and can effectively manage T2DM, then surely it should be any cardiologist’s first choice in the management of heart disease?