[2017] Lore of Nutrition: Challenging Conventional Dietary Beliefs
Page 14
As a result: ‘Consuming a reduced-carbohydrate diet, with moderate fat and high protein intake, may decrease the risk of weight gain in postmenopausal women. However, prevailing dietary recommendations call for limiting fat intake in order to promote optimal health and prevent chronic disease. Our findings therefore challenge prevailing dietary recommendations, suggesting instead that a low-fat (diet) may promote rather than prevent weight gain after menopause [my emphasis].’37
Can it be that the other authors of the WHIRCDMT may finally be dissociating themselves from the scientifically unsubstantiated opinions of the now retired Rossouw?
His current dietary advice differs from the LCHF eating plan only in that he advises people to eat more wholegrains (whatever those are), fruit, legumes, vegetable oils and low-fat dairy products, and to limit the intake of red meat, especially processed meats.
At the end of the debate and in a speech carefully prepared even before he had heard the debate, Volmink concluded the evening, in the words of one columnist present in the audience, ‘by insinuating that Noakes was essentially a “bulls!#&er”’.38
To be fair to Volmink, he did not specifically single me out, but some may have interpreted what he said and the way he said it to indicate that I was his target. He suggested that we need reliable research evidence, which the following do not constitute:
Wild extrapolations from laboratory bench data;
Reckless claims from observational studies;
Cherry-picked studies;
Anecdotal stories; and
‘Bullshit’ provided by people with no interest in the truth and who are simply trying to impress us. They ‘make it all up’.
He concluded by saying that he had ‘heard nothing this evening that convinces me that we are on the wrong path in terms of these dietary guidelines’, and ‘at all costs we must not do harm’. Furthermore, Volmink appeared wilfully oblivious to the implications of the fact that Rossouw’s WHIRCDMT has provided definitive evidence that a low-fat diet is without benefit and may even be harmful. And that the medical faculty of which he is dean serves a community that is at the epicentre of the South African obesity/T2DM epidemic, caused, in my opinion, by the ‘do no harm’ low-fat diet that his friend Rossouw continues unrestrainedly to promote.
So if this debate was not about the truth, then what was it really all about? This would become apparent over the next four years, culminating in the HPCSA hearing against me that began in June 2015.
After the debate, I was interviewed by medical science writer Chris Bateman, who also asked Rossouw and two other UCT-linked professors, Krisela Steyn and Naomi Levitt, for their opinions. The responses were published in the February 2013 issue of the South African Medical Journal (SAMJ).39 For what was supposed to be an academic debate, the professorial responses seemed remarkably un-academic, and rather too personal, setting the tone for what would become the norm over the next five years.
According to Rossouw, my first error was to overstate the importance of carbohydrate intolerance (insulin resistance), because so few in the world suffer from it. ‘The biggest divergence is that Rossouw says he can show that the proportion of truly carbohydrate-intolerant people runs to about six per cent,’ wrote Bateman. ‘Noakes claims it’s at least ten times this.’
But what are the real facts?
In 2012, the American Diabetes Association (ADA) reported that of the US population of 313 million, 9.3 per cent (29.1 million) had T2DM and another 27 per cent (86 million) had pre-diabetes.40 Thus, in 2012, 34 per cent of the US population had been diagnosed with IR, an incidence nearly six times greater than Rossouw is prepared to acknowledge. Note that this includes only those who were diagnosed because they presented with symptoms caused by their IR.
In fact, the incidence of pre-diabetic US citizens will be much greater than 86 million, because no one has yet performed proper testing for IR in a sizeable proportion of that population. This requires measurement of fasting blood glucose and insulin concentrations, at the very least.
To properly diagnose IR, one needs to measure changes in blood insulin and glucose concentrations for two to five hours after the ingestion of 100 grams of glucose, as first described by Joseph Kraft.41 He showed that 75 per cent of 4 030 subjects who had normal glucose tolerance by conventional criteria showed an inappropriate hyperinsulinaemic response,42 indicating that they were insulin resistant, but that their IR was ‘hidden’ if only their glucose response to glucose ingestion was tested.6 These included 117 children aged 3–13 years, 45 per cent of whom had normal glucose profiles but who were hyperinsulinaemic, and 651 teenagers aged 14–20 years, 67 per cent of whom had normal glucose tolerance but who were also hyperinsulinaemic.
Other evidence that the rates of IR must be much higher than Rossouw’s 6 per cent is provided by US obesity statistics. Currently, more than 69 per cent of US adults are considered to be overweight or obese, with rates continuing to rise precipitously.43 The majority of those who are overweight or obese will be insulin resistant.44
My opinion is that, at the very least, 60 per cent of US citizens are likely to be insulin resistant according to Kraft’s definitions.
Rossouw’s response reveals that one of the most senior scientists in the NIH – a man in whom the NIH was prepared to entrust $700 million for the WHIRCDMT study – apparently has neither any reasonable knowledge of nor particular interest in the condition of IR. Fifty years of medical education have seemingly not taught him about the single most important global medical condition.
Or is it simply that the omertà prevents him from acknowledging that IR exists? For once he and his colleagues acknowledge its existence, they have to acknowledge the dangers of sugar and carbohydrates, the value of a low-carbohydrate diet and the intellectual poverty of the diet-heart hypothesis. They have to break the omertà.
As they also cannot acknowledge that IR, and not cholesterol, is the underlying cause of arterial disease, it is understandable why Rossouw and his colleagues chose to go the personal ad hominem route rather than address the science I had presented. They simply had no valid counter-argument. Instead, they chose to shoot the messenger in a way that even the HPCSA specifically forbids. In fact, the HPCSA’s rules on how doctors should interact in public are clear:
Healthcare practitioners should:
Refrain from speaking ill of colleagues or other healthcare practitioners.
Not make a patient doubt the knowledge or skills of colleagues by making comments about them that cannot be justified.
What these three colleagues allowed to be published in the SAMJ clearly breached that rule. Rossouw told Bateman:
I think Tim got diabetes because he was obese. God forbid one of these days that he may have to take medicines made by the evil pharmas – he’s a good scientist in his field, but he’s way outside of his field and comfort zone here. He doesn’t understand the science and the whole concept. He’s cherry picked and misinterpreted and is going down a very dangerous path. Applying dietetic measures, he’s doing harm and flouting the Hippocratic oath.
The article continues:
[Rossouw] said the debate on lowering cholesterol with statins … had been ‘dead for 20 years’. There was now ‘absolute proof’ that cholesterol was causal in heart disease. ‘Most of the people he cites are zombies from that era and they’ve been left behind by science. The more Krisela [Steyn] told me about this, the more concerned I became. Noakes’ theory had the potential to divert people from diets and treatments that were known to do good. Were I still a faculty member I’d be very concerned about this member undoing a lot of good work done in heart disease prevention. If Noakes came up against anyone in this field he would get the same reception he got at his “faculty meeting” [the Centenary Debate]. His perception is he was set up to be discredited. But he’s in the scientific world and his theories have no standing. Any diet that is calorie and energy restricted will reduce weight. They all work … for some people the approach he advocates
may work better. I have no problem with that, but when you generalise and say everyone should be on the diet permanently, eat your fats and no carbs, that’s not right, especially when there are no long-term data on that, while there are data on the conventional diet. Why mess with success? I think five years from now we’ll be able to stand back and say where we are … and the public will have stopped paying attention. I regard this a temporary aberration. Advocating it for wider health promotion will not stand the test of time.’
Yet, in truth, it is Rossouw who is cherry-picking the data, misrepresenting the facts and ‘flouting the Hippocratic oath’. Having spent $700 million of US taxpayers’ money disproving the diet-heart hypothesis, he still travels the world promoting the opposite of what that study found. I doubt that Hippocrates would have condoned this behaviour.
Particularly interesting is Rossouw’s assertion that there is now ‘absolute proof’ that cholesterol is ‘causal in heart disease’. As I show in Chapter 17, this is utterly unfounded. I would also refer Rossouw to the article by Robert DuBroff referenced in Chapter 3, which concludes that the evidence is now overwhelming that lowering blood cholesterol concentrations through diet or drugs ‘does not significantly prolong life or consistently prevent coronary heart disease’.45 All this evidence contradicts Rossouw’s reference to the ‘zombies’ who disagree with the diet-heart hypothesis and his assertion that the diet I promote has no standing in the ‘scientific world’. More telling is his opinion that in five years’ time, ‘the public will have stopped paying attention’.
At the time of this book’s publication, exactly five years since Rossouw made his prediction, it is the diet-heart hypothesis that is in terminal decline. The public, at least in South Africa, cannot get enough information about Banting. Five years later, and the ‘revolution’ Rossouw spent so much effort trying to suppress has exploded into the mainstream,7 while interest in his low-fat, ‘heart-healthy’ prudent diet lessens by the day.
Next up in Bateman’s article was Professor Krisela Steyn, associate director of a multi-university collaboration called the Chronic Disease Initiative for Africa. Under her watch, the prevalence of chronic diseases, especially T2DM, in her home province of the Western Cape, has increased exponentially. Clearly, whatever research and interventions she has initiated have not produced any positive outcomes. Speaking to Batemen about me, she said: ‘Damage is being done here. He’s radically oversimplified things.’
Bateman continues:
[Steyn] said it was ‘sad’ when a good scientist wandered off his area of expertise. ‘He’s lost the plot a little – he’s not basing all his public statements on the best available data. Yes, he’s right to question any scientific statement of any type, but please bring the good data.’ Steyn said she hoped the charismatic Noakes, whose bona fides she does not question, had a good diabetologist looking after him. ‘He’s entitled to punt something he totally believes in. But what’s scary is that he’s damaging patients and the population by insisting on this diet for life, regardless of the cost. My overwhelming emotion is sadness that a person of his stature has made this mistake.’ She cited Linus Pauling, the Nobel Prize winner for chemistry, ‘going on a tirade about vitamin C curing the common cold’, when it was shown that at best it might reduce the duration of the common cold. ‘Then we had Mbeki. The question is how does one get there? If you don’t deal with the academic data, a person with public standing can do a tremendous amount of harm.’ She said the worst time to ‘go to the public with health guidelines’ was when academics were still debating the truth for a position. ‘You go to the public when you have irrefutable evidence that this is the right thing to do.’
Let’s dissect her statements, specifically the latter ones. First, both Linus Pauling and former president Thabo Mbeki promoted hypotheses for which there was no firm evidence or plausible biological explanation. For all we know, Pauling may still turn out to be right. If we have yet to grasp the reasoning behind his hypothesis, it is perhaps because we lack the double Nobel Prize winner’s extraordinary grasp of biochemistry and molecular biology. I have learnt not to dismiss the ideas of genius simply because there is not yet a plausible explanation.
In contrast, there is a large body of peer-reviewed evidence, including Rossouw’s WHIRCDMT, that actually disproves the diet-heart hypothesis. There is also a wealth of evidence showing the value of low-carbohydrate diets. If Steyn is unaware of the evidence, it is because of her unwillingness to break the omertà and to engage with the published literature. This is allied, perhaps, with a reluctance to acknowledge that what she believes and has taught two generations of students is wrong.
Second, Steyn herself has repeatedly over the past four decades ‘gone to the public’ with her ‘irrefutable evidence’ allegedly proving the diet-heart hypothesis, the alleged value of substituting polyunsaturated vegetable oils for dietary saturated fat, and her belief that a low salt intake is essential to prevent high blood pressure. Unfortunately, there is no such ‘irrefutable evidence’ for any of these claims.
For example, a recent analysis concludes that whereas a high sodium intake is associated with increased risk of cardiovascular events (heart attack and stroke) and death in people with hypertension,46 there is no such association in those with normal blood pressures. Furthermore, the same study found that low sodium intakes are associated with increased risk for cardiovascular events and death; a finding also reported in five other studies.47 In other words, advocating a low-salt diet could be causing harm.48
Then there is a new study showing that almost everything we understand about human salt metabolism is wrong. This research was stimulated by the observation that increased dietary salt intake reduced fluid intake, the precise opposite of what we have been taught for decades. Instead, this study found that the ‘kidneys, liver and skeletal muscle form a physiological-regulatory network’ to control the amount of fluid the body retains.49 The point is that a high salt intake produces metabolic changes in the liver and skeletal muscles that no one ever predicted; these changes do not cause body water content to increase – the popular explanation of how a high salt diet supposedly causes blood pressure to rise.
Since this is to some extent the opposite of what we predicted, and if salt does not raise the blood pressure causing hypertension, perhaps now is the time to begin a proper evaluation of whether we need to either reduce or increase our dietary salt intakes. For example, there is more than enough evidence to show that hypertension is a condition caused by diets high in sugar and carbohydrates in those with IR,50 so that by targeting salt rather than sugar we have focused on the wrong ‘white crystals’.51
Will these latest findings lead Steyn to question the wisdom of her decades-long crusade advocating low salt intakes by all South Africans according to the principle of ‘first do no harm’?52 Or will she continue to support what appears to be an industry-directed omertà?8
I invited US science journalist Nina Teicholz and UK obesity researcher Dr Zoë Harcombe – the two people who have provided the most complete bodies of evidence disproving the diet-heart dogma – to provide expert witness on my behalf at my HPCSA hearing in October 2016 (see Chapter 13). Steyn did not avail herself of the opportunity to hear these two world authorities in person, but I hope that she is now aware that her ‘irrefutable evidence’ for the diet-heart hypothesis is nonsense and that she will reconsider her statements. She should ask herself whether the diet she promotes could actually be the cause of the growing ill health of the communities she is employed to serve.
The last to invoke the omertà for Bateman’s report was Professor Naomi ‘Dinky’ Levitt, head of endocrinology and diabetic medicine at UCT and co-director with Steyn of the Chronic Disease Initiative for Africa. I graduated from UCT as a doctor a year ahead of Levitt, and we received our subsequent MD degrees at the same graduation ceremony in 1981.
I often wonder if Levitt thinks back to those years when T2DM was relatively uncommon in the Western Cape.
Today, it is the most common cause of mortality in the province. I also wonder if she ever asks herself whether she played any part in this human disaster and if she could have done things differently. Could she, the professor of endocrinology and diabetes at a premier medical institution in the Western Cape, have slowed the growth of the T2DM epidemic in the province, then in South Africa and, perhaps, even the world?
Or is T2DM, as she teaches her students, a disease of inevitability from which there is no escape; that will require patients to inject insulin or take drugs for the rest of their lives; and which progresses inevitably to death from disseminated obstructive arterial disease, as was my father’s experience, regardless of our best medical efforts? Given this ‘inevitability’, what is a professor meant to do other than criticise anyone who ignores the omertà and proposes that perhaps T2DM does not have to be an ‘inevitable’ disease with unavoidable, fatal consequences.
In the article, Levitt9 described me as ‘irresponsible’, saying:
I think Rossouw showed him up based on science and Tim’s rather superficial understanding of epidemiology. [The debate] highlighted his lack of appreciation of the complexities of fat metabolism. You’d expect better of Tim. He has a good reputation, so this is extremely dangerous.
Perhaps unsurprisingly, Levitt, like Rossouw and Steyn, failed to address the evidence I had presented and the manner in which it disproves cherished dogmas. Clearly, she had not listened to a single word I had said.
Bateman’s SAMJ report ended with the statement that, according to Steyn and Levitt, the Cochrane Centre, under the direction of Volmink, would be releasing a review of all existing data on the subject by the end of February 2013. Eventually published in July 2014, this meta-analysis of ‘low-carbohydrate’ RCTs would become known as the Stellenbosch or Naudé review, which would play a central role in the HPCSA’s September 2014 decision to prosecute me.