[2017] Lore of Nutrition: Challenging Conventional Dietary Beliefs

by Tim Noakes

  Unimpressed, Van der Nest remarked to Pienaar: ‘Your petticoat of bias is showing.’

  Pienaar eventually conceded that he should not have used the word ‘wise’.

  Pienaar’s poor performance under cross-examination was not entirely his fault. It was glaringly obvious that the HPCSA had not briefed him properly. He was unfamiliar with the full context of the tweeted exchange between Leenstra, Noakes, Strydom and Ellmer. Van der Nest described it as a ‘mystery’ and ‘inexplicable’ that the HPCSA had withheld crucial information from its own witness.

  After cross-examination, members of the Professional Conduct Committee were invited to ask questions. Dr Janet Giddy asked Pienaar whether, as a bioethical expert, he would recommend that the HPCSA charge Ellmer and Strydom as well – or did he have ‘different rules for different people’? Clearly floundering, Pienaar said there were ‘many, many perpetrators’, but given Noakes’s high profile, he should be singled out.

  Giddy found that sentiment disturbing and repeated her question: ‘I am asking you, as an ethicist, what is the ethical, right thing to do? … We know in this particular case there were other, what you called perpetrators, which is quite a loaded word, if I might say. But what I am hearing you are saying, it is good to make an example of one perpetrator, but you are not worried about the other perpetrators?’

  Pienaar confirmed his opinion that the HPCSA had to make an example of someone, and that it should be Noakes.

  Thus, the HPCSA’s case ended in even deeper trouble than it had been in November 2015. Pienaar, like all the other expert witnesses before him, had failed to sustain the claim of a doctor–patient relationship. He had also failed to uphold the argument that Noakes’s tweet constituted medical advice, and not just information. And, just as crucially, he had conceded that there was no evidence of any harm.

  *In an email to his superiors at the NIH, Rossouw refers to Noakes as ‘a South African physician promoting the low carb high fat diet for all that ails mankind’. In refusing an interview with me, he calls me ‘a shill for the physician’. Thus an interview will be ‘mishandled’, he claims.

  12

  Finally, Noakes Speaks

  ‘The greatest enemy of knowledge is not ignorance, it is the illusion of knowledge.’

  – Daniel J. Boorstin, American historian

  On the afternoon of Wednesday 10 February 2016, two years and six days after the tweet that started it all, Professor Tim Noakes began his defence in what the public had by now dubbed ‘the Nutrition Trial of the 21st Century’.

  Local and international interest in the hearing was high. At stake were Noakes’s reputation, distinguished career and right to freedom of speech as a scientist. Costs for both sides were already in the stratosphere, perhaps more so for the HPCSA, which had recently acquired an expensive team of external lawyers. The HPCSA also appeared to have pockets as deep as its desire to find Noakes guilty. According to a reliable source, Advocate Ajay Bhoopchand would submit a bill of close to R1 million (the equivalent of around $62 500 at the time) for the eight-day hearing alone.

  By the time Noakes began testifying, Bhoopchand and instructing attorney Katlego Mmuoe would have known that their client’s case was possibly in terminal decline. None of their expert witnesses had held up well under cross-examination. Their only hope was for Bhoopchand to undermine the defence’s evidence. It was a tall order: Noakes’s evidence alone consisted of 6 000 pages, 1 200 slides, and more than 350 publications and articles. It would take him almost 40 hours to present, over two sessions, concluding on 17 October 2016.

  An expectant silence settled over the room in the Cape Town conference centre as Advocate Rocky Ramdass led Noakes through his CV. At over 100 pages, it was the longest and most fecund CV, scientifically speaking, of the trial so far. Noakes sped through it, punctuating his words with an ironic smile – Ramdass would call it his ‘habitual smile’. To the uninitiated, it could have seemed that Noakes was blowing his own trumpet – critics, and even supporters, sometimes accuse him of arrogance – but in this case, he was sending a signal to the HPCSA and the world that he was here to deliver a loud and clear message. It was one that his qualifications and knowledge gave him every right to dispense.

  His credentials, research experience and A1 rating by the NRF dwarfed the prosecution witnesses’, including the dietitian who had started it all, Claire Julsing Strydom. Next to Noakes’s ruddy scientific pedigree, Strydom’s looked positively anaemic. She was also conspicuous by her absence. Noakes later described her failure to attend as both ‘disappointing and a lost opportunity’. Strydom might have learnt something. (Bhoopchand later said that he had advised Strydom not to attend, but would not say why.)

  In going through his CV, Noakes said that he had ‘to some extent started sports science and sports medicine’ in South Africa. That was an understatement. Noakes is well known for his generosity of spirit in readily acknowledging the work of others. Among those is former South African rugby captain Morné du Plessis. In the early 1990s, Noakes and Du Plessis teamed up to found the Sports Science Institute of South Africa to fund research into sports performance and to house the laboratories of the UCT/MRC Research Unit for Exercise Science and Sports Medicine (ESSM), which Noakes had helped found and which he directed for 25 years. The application of this research would provide sportspeople of all disciplines with the evidence-based means to improve performance. Noakes and Du Plessis also wanted to use it as a platform to build public interest in the country’s top sportspeople and build state pride. They achieved those aims and more.

  Noakes listed key aspects of his work and experience spanning decades. This included supervision of the research of PhD and master’s students, and his own extensive research in fields ranging from insulin and carbohydrate metabolism (not just glucose, but fructose as well), and cholesterol and triglyceride (blood fats) responses, to the modification of risk factors for heart disease through diet and peripheral artery disease as it relates to T2DM. As far back as 1978, Noakes’s areas of scientific exploration at SSISA/ESSM have covered glucose metabolism (glycaemic control), lipid profiles and fat metabolism, and diabetes. All this was decades before his spectacular about-turn on the role of carbohydrates and fats at the end of 2010. His ESSM unit was also one of the first to investigate low-carb diets, including ketosis, for sports performance. In one fell swoop, Noakes decapitated the HPCSA’s contention that his scientific knowledge and experience of nutrition was narrow and restricted to adults and athletes.

  Noakes spoke eloquently about the effects the HPCSA hearing was having on him and his family. ‘I would have done anything in my power to stop [this trial] happening because of the cost to me personally, and to my family,’ he said. He choked up when he spoke of his family’s support, in particular that of his wife, Marilyn. He also paid tribute to his legal team. (From the outset, Van der Nest and Ramdass had offered their services for free.) ‘I wouldn’t have got through it without them,’ he said. ‘It has been a tough time, financially very, very taxing. People just do not understand what the costs of an action like this are.’ Noakes’s critics gleefully took to social media to claim that he had ‘broken down’ while giving evidence, and the press picked up and ran with it. That was not true. As Noakes later explained, it was nothing more than cathartic relief that brought him close to tears – the relief of finally being able to speak up for himself and the enduring passion that drives him professionally: the search for scientific truth.

  Noakes then outlined the framework within which he would present his evidence. He said that it would include describing his own data, which was ‘relatively important to this whole case’. In Chapters 16 and 17, he gives an overview of the rigorous science that he presented in his own defence. Thus, it would be needless repetition here. Instead, I have identified key themes in his evidence and highlighted how he used the science to rebut the HPCSA’s case against him.

  The public had compared the HPCSA hearing to a modern-day Spanish I
nquisition, and Noakes to Galileo. He took up the comparison with dramatic effect, quoting at length from Galileo’s Middle Finger by American bioethicist Alice Dreger:

  Science and social justice require each other to be healthy, and both are critically important to human freedom. Without a just system, you cannot be free to do science, including science designed to better understand human identity; without science, and especially scientific understandings of human behaviors, you cannot know how to create a sustainably just system … I have come to understand that the pursuit of evidence is probably the most pressing moral imperative of our time. All of our work as scholars, activists, and citizens of democracy depends on it. Yet it seems that … we’ve built up a system in which scientists and social justice advocates are fighting in ways that poison the soil on which both depend. It’s high time we think about this mess we’ve created, about what we’re doing to each other and to democracy itself.1

  Using Dreger, Noakes placed scientific evidence at the heart of the hearing: ‘Evidence really is an ethical issue, the most important ethical issue in a modern democracy. If you want justice, you must work for truth. And if you want to work for truth, you must do a little more than wish for justice.’2

  ‘You have to look at the totality of the evidence,’ Noakes said. ‘That’s what I am doing. I am a totalist. I have obsessive compulsive disorder with facts. That’s why I write like I do. If anyone tells me there’s no evidence to support low-carbohydrate diets, I tell them they haven’t read the literature.’

  Reciting one of his favourite quotes, Noakes said: ‘Everyone is entitled to their own opinion, but not to their own set of facts.’

  ‘I tell my students that when a single strand of evidence conflicts with their beliefs, they better start questioning their views,’ he said. Only those who refuse to look at the totality of evidence could conclude that his views on LCHF are ‘unconventional’.

  It was clear from the evidence Noakes presented that he had a dual purpose. He wanted to educate those who had charged him and to demolish the pillars of the charge. Using his natural teaching instincts and chatty style – which held the attention of his ‘audience’ throughout – he began to reveal why there are so many endocrinologists and cardiologists among his most vociferous critics: he had dared to challenge medical orthodoxy and the industries that had grown up around conventional treatment protocols for obesity, diabetes and heart disease.

  In particular, he contradicted the pessimistic outlook of orthodox doctors and dietitians towards T2DM. They see diabetes as a chronic, degenerative condition that increases the risk of heart disease, kidney problems, blindness and amputation. Noakes challenged this thinking, as well as the orthodox medical model that has diabetics taking drugs for the rest of their lives. Optimism in the face of a T2DM diagnosis was a key theme of his evidence. Noakes has never called LCHF a ‘cure’ for diabetes. He has, however, said that it is a safe, effective and cheap method that can reverse all the symptoms of the condition. It’s a matter of semantics, really, and many people around the world who use LCHF to manage their T2DM say that it is as close to a ‘cure’ for the condition as modern medicine has come thus far.

  Noakes’s evidence was a powerful mix of the personal and the professional. One of the first slides he presented was a photograph of him and his parents at his graduation in 1981. He had just received his Doctor of Medicine (MD) degree – a PhD equivalent that allowed him to teach and set up a sports-science course at UCT. His father, Reginald ‘Bindy’ Austin Noakes, had been diagnosed with T2DM a few months earlier. At the time, Reginald also had high blood pressure and other features of IR and the metabolic syndrome. He was the same age then (68) as Noakes is today. Within six years, he would lose his foot from the consequences of diabetic PAD. Within eight years, he would lose both legs and surrender his mind to the disease.

  That faded photograph spoke volumes about what drives Noakes as a scientist, a medical doctor and an ordinary mortal: the search for truth and the desire to help people improve their health. It spoke particularly of Noakes’s mission to save diabetics from the grim fate that had befallen his father after following orthodox dietary advice. At the time of his father’s illness, dietitians and doctors (Noakes included) believed that diabetics needed regular carbohydrates to ensure there was enough glucose for the brain. Noakes did not blame the dietitian, Joan Huskisson, who advised his father. She gave advice that she thought was right at the time. She based her advice on a hypothesis that many doctors and dietitians still hold dear today: when prescribing diets for patients with T2DM, the sole consideration is that the brain requires glucose to function (see Chapter 7). ‘This hypothesis is wrong,’ said Noakes. The information that Huskisson gave his father was therefore ‘utterly and completely false, a wrong assumption that has to lead to the wrong advice’.

  Noakes had helped Huskisson to develop teaching in dietetics at UCT. Her advice was the same that experts continue to give diabetics today: eat a low-fat, high-carb diet. Huskisson wrote a book in 1990, funded by SASA, titled Food: What’s In It For You? She gave Noakes a copy, in which she had inscribed: ‘Tim – Thank you very much indeed for the ongoing support! It really is appreciated tremendously … and No! I don’t get royalties for copies sold.’ (That highlighted another theme running through the hearing: the sugar industry and its toxic influence on dietary advice.)

  In his evidence, Noakes quoted from a more recent book, by South African registered dietitian Hilda Lategan: ‘Carbohydrates are an important source of energy in the body and glucose, which is the product of the digestion of carbohydrates … is the only energy source for the brain … It is, therefore, crucial for diabetics to include carbohydrate-rich foods at each meal.’3

  Since his Damascene moment, dietitians have frequently accused Noakes of being antagonistic towards them and dietetics in general, and ADSA in particular. Neither is true. If anything, the HPCSA’s witnesses showed that it is ADSA that has a ‘beef’ with Noakes, not the other way round.

  Noakes related how devastated he was when he realised that his father had died not because he was not getting enough glucose to his brain, but because he had disseminated (widespread) arterial disease, which is now recognised as the cornerstone of diabetes. Reginald Noakes would also have had NAFLD, commonly known as ‘fatty liver’, although no one knew it at the time. Noakes presented robust research showing that high-carbohydrate diets cause NAFLD in people who are insulin resistant/diabetic. He also showed that NAFLD causes blood-fat abnormalities, and that it is these blood-fat abnormalities that, together with high blood insulin levels and inflammation, lead to disseminated arterial disease. Thus, he showed that T2DM is ultimately a condition of progressive, disseminated arterial disease. It progresses over decades, he told the hearing. It leads ultimately to complete obstruction of blood flow to the eyes, kidneys and lower limbs. The consequences couldn’t be more severe: blindness, kidney failure and gangrene (and eventually amputation) of the limbs. This same arterial disease can lead to heart attacks and strokes, although these represent a ‘fundamentally different process’.

  Ultimately, Noakes said, the high-carbohydrate diet killed his father. He spoke with profound sadness about the consequences of not knowing what really ailed his father. If he had known then about NAFLD and its crucial role in T2DM and heart disease, he could have examined his father. ‘We would have seen that my father had fatty liver with certain cholesterol abnormalities,’ he said. ‘These are called lipoprotein abnormalities, which are specific to NAFLD. We could have treated him, because what he needed to do was the opposite of the advice that was given.’ Noakes said that hepatologists (liver specialists), and not cardiologists, would probably be the ones to treat heart disease in the future. It was the first of many gauntlets he’d throw to cardiologists in his evidence.

  Another theme in Noakes’s evidence was the diet-heart hypothesis that saturated fat causes heart disease. The hypothesis, which became a pillar of the HPCSA’s case against him,
is the platform on which drug companies built the multibillion-dollar statin industry. Statins are cholesterol-lowering drugs. They are also the world’s most prescribed drugs. It’s an understatement to say that Noakes is no fan of statins. While evidence shows that statins may have some use in secondary prevention (i.e. after a first heart attack or stroke), they don’t work well for primary prevention. They also come with a long list of side effects, many severe enough to offset any benefits.

  Noakes gave evidence in the hearing to show that the diet-heart hypothesis is currently unproven and therefore, by definition, should be considered unconventional and unscientific. He outlined how the hypothesis had spawned the lipophobia (fear of fat), demonisation of fat (especially saturated fat) and glorification of carbohydrates that began in the late 1970s. He described saturated fat as the victim of possibly the ‘biggest scam in the history of modern medicine’.

  ‘Carbs and insulin are driving obesity,’ Noakes stated, ‘not saturated fat.’ When food-makers took saturated fat out of the diet, he said, they had to replace it with something to make food more palatable. That something was sugar and carbohydrates, two highly addictive substances. The consequences for global health have been nothing short of catastrophic: a pandemic of lifestyle diseases.

  It is true that heart-attack rates have been falling in some countries since the late 1960s. Some scientists claim that this is proof that the low-fat diet prevents arterial disease. But Noakes offered an alternative explanation in his evidence: a reduction in smoking in these countries has reduced the number of patients experiencing the sudden plaque ruptures that cause heart attacks and strokes, he said. But while fewer people are dying of heart attacks, many more are developing T2DM as a consequence of LFHC diets. The disease burden of arterial disease has therefore simply shifted to the obstructive form found in T2DM. If the low-fat diet really prevented arterial disease, it should also have prevented the now much more prevalent obstructive form found in type-2 diabetics.