Lore of Nutrition: Challenging conventional dietary beliefs

by Tim Noakes

T2DM patients who received what the American Diabetes Association believes to be the absolute optimum treatment did no better than those who received inferior care.

And even if the disease is perhaps not quite as lethal as the pessimists propose, we can still always blame the patient for any failed outcomes. So treatment failures occur because patients do not fully comply – they fail to take their medications as prescribed, they do not exercise enough, they become too stressed and do not get sufficient sleep, and they eat too much fat and not enough ‘heart-healthy’ carbohydrates.

It is clear that we made a major mistake in recommending the increase of carbohydrate load to >40% of total caloric intake. This era should come to an end if we seriously want to reduce the obesity and diabetes epidemics. Such a move may also improve diabetes control and reduce the risk for cardiovascular disease. Unfortunately,

There is also evidence for the reversal of progressive renal failure with an LCHF diet in an obese diabetic patient, so that the authors question whether ‘obesity caused by the combination of a high-carbohydrate diet and insulin may have contributed to the patient’s failing kidney function’.35 Secondly, there is clear evidence that the primary cause of kidney failure is T2DM.36 And diabetes is caused by high-carbohydrate/high-sugar diets in people with IR. So the advice of these dietitians – to eat less protein and fat and more carbohydrates – can be directly linked to increasing rates of diabetic kidney failure.

By some convoluted (il)logic, their argument – that the moment you stop eating LCHF (which successfully produces weight loss) and reintroduce carbohydrates, you regain all the lost weight, and then some – is meant to cast the LCHF diet as the cause of weight gain, not the reintroduced carbohydrates. But what we should actually deduce is that, to avoid weight gain, humans should limit the amount of carbohydrates they eat (for life), exactly as the LCHF eating plan advocates.

understand how a diet can be balanced if more than 50 per cent of its energy comes from a single nutrient – carbohydrate – for which the human body has no (i.e. zero) essential requirement. Surely a ‘balanced’ diet should contain, for example, one-third fat, one-third carbohydrate and one-third protein? And if not, why not?

Mungal-Singh conveniently forgets to mention that the HSFSA has major conflicts of interest: it accepts funding from three companies that produce highly processed seed oils containing unhealthy omega-6 polyunsaturated fats and, until very recently, even more unhealthy trans fats (see Table 7.1). Among this group is Unilever, the world’s largest producer of polyunsaturated ‘vegetable’ oils and, coincidentally, ice cream.

In fact, they found ‘a 22% higher risk of death for each 30 mg/dl (0.78 mmol/L) reduction in serum cholesterol’. This

‘In meta-analyses, these cholesterol lowering interventions showed no evidence of benefit on mortality from coronary heart disease … or all cause mortality,’ concluded Ramsden and his colleagues.48

the proportion of heart patients who were still alive after two years was significantly less (52 per cent) in the group fed corn oil than in the group who continued to eat as they always had (75 per cent). The authors concluded that ‘under the circumstances of this trial corn oil cannot be recommended in the treatment of ischaemic heart disease’.

blood glucose concentration taken one hour after glucose ingestion was the best predictor for mortality in the intervention group. This is compatible with the theory that IR is the real determinant of ill health. Could

‘polyunsaturated fat and carbohydrate intakes were associated with greater progression’.

Remarkably, a new meta-analysis concludes that: ‘Due to null results and a small number of studies included there is no strong evidence that replacement of saturated fatty acids with unsaturated fatty acids may benefit lipid profiles in this population [my emphasis].’

He should have informed the audience of some of the conclusions that Dr John Ioannidis, professor of medicine at Stanford University and author of many of the definitive articles on the failings of evidence-based medicine,73 has come to: In nutrition, there has been so much observational and mechanistic research that thousands of spuriously significant associations have already been produced and translated in heavily opinionated, debated recommendations. Getting another significant result in a field that is already saturated with so many significant results offers no information gain: we still (think we) know what (we thought) we knew. Conversely, ‘negative’ results offer high information gain, because they change our probably false beliefs about potentially effective interventions … we should hope to get more ‘negative’ results in the future.74

Dalby later fulminated about my ‘criminal’ behaviour, yet he did not mention that in 2009/10, five of the pharmaceutical companies for whom he works in an advisory capacity – Pfizer, Novartis, Sanofi, AstraZeneca and Eli Lilly – were fined a total of $4.7 billion for various fraudulent (i.e. criminal) activities.82 I also wonder if Dalby ever informs patients who participate in the pharmaceutical trials he oversees that their data belongs solely to the company funding the trial, and that the company has the right to do pretty much whatever it likes with that information. Danish physician and author Dr Peter Gøtzsche believes that these trials are so lacking in transparency that an honest patient consent form should read: I agree to participate in this trial, which I understand has no scientific value but will be helpful for the company in marketing their drug. I also understand that if the results do not please the company, they may be manipulated and distorted until they do, and that if this also fails, the results may be buried for no one to see outside the company. Finally I understand and accept that should there be too many serious harms of the drugs, these will either not be published, or they will be called something else in order not to raise concerns in patients or lower sales of the company’s drugs.83

In my lecture, I argued that the single most important factor determining what we should be eating is our individual level of IR. This, I proposed, is the underlying condition causing obesity, T2DM, gout, hypertension and atherogenic dyslipidaemia in those eating high-carbohydrate diets. (Only later would I appreciate that cancer and dementia fall in the same category.) Next I spoke about

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.

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.

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

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.

concluding slides stated the following: Current dietary guidelines based on lipophobia are not evidence-based and are harmful. Adoption of the 1977 Dietary Guidelines for Americans caused the global epidemic of obesity and diabetes after 1980. This can be explained by exposing those with IR to inappropriately high carbohydrate intakes. Carbohydrate-rich diets are the cause of a wide range of modern chronic diseases of lifestyle.