by Tim Noakes
4. Patients with T2DM do not die because of an inadequate supply of glucose to their brains. They die as a result of widespread obstructive disease in all their arteries (and capillaries), including those supplying blood to the heart and brain, causing heart attacks, strokes and blindness; to the kidneys, causing kidney failure, the treatment of which requires expensive but life-saving renal dialysis; and to the limbs, especially legs, leading to infection and gangrene, treatable only by amputation. The incidence of all these conditions is rising exponentially across the globe, like a disease tsunami that is completely out of control.8 But because the certain cause was the misguided adoption of the 1977 Dietary Guidelines for Americans, no one involved in developing those guidelines is keen to acknowledge their contribution to this mounting global catastrophe. And until those responsible own up to their mistake, this global calamity will grow progressively worse.
5. When humans ingest carbohydrate, their blood glucose concentrations rise (see Figure 7.1 on page 136). To limit this rise, the body secretes the hormone insulin to switch off liver glucose production and to remove excess glucose from the bloodstream. However, as I explain more fully in Chapter 17, the rise in blood glucose and insulin concentrations is greatest in those with T2DM (because their tissues, including their livers, are insulin resistant, meaning that insulin is less effective in slowing down the liver’s excessive glucose production and diverting glucose out of the bloodstream for storage in the muscles and liver).
What should be of real concern is that insulin is probably the key driver of most of the pathological changes that occur in those with IR who persist in eating high-carbohydrate diets. I discuss this in detail in Chapter 17.
If the ingested food includes fat and carbohydrate, the response is essentially the same – the blood glucose response is reduced, but insulin secretion is again increased.9 Ingestion of fat alone does not induce an insulin response.10 Interestingly, fat ingestion uniquely produces very large increases in secretion of gastric inhibitory polypeptide, the hormone whose key functions remain partially uncertain.
Figure 7.1
Changes in blood glucose (left panel) and blood insulin concentrations (right panel) in response to ingestion of protein, glucose, and glucose and protein at time 0 in persons with T2DM. Note that whereas protein ingestion did not cause the blood glucose concentration to rise, it did cause a moderate increase in blood insulin concentration (right panel). The co-ingestion of glucose and protein increased insulin secretion substantially, which reduced the blood glucose response (left panel). Reproduced from Nuttall et al.11
Figure 7.1 shows the response of blood glucose and insulin concentrations to a single meal. However, when food is ingested repeatedly during the day, these effects become additive, producing more frequent periods of hyperglycaemia (raised blood glucose concentration) and hyperinsulinaemia (raised blood insulin concentration), as shown in Figure 7.2 on page 137. These biological effects produced every few hours for decades are the cause of the explosion of chronic disease in people eating modern, highly processed, high-carbohydrate, high-sugar diets.
These findings show very clearly why high-fat diets with low-carbohydrate and low-protein contents produce the least insulin secretion and should, therefore, be the logical dietary choice for those with IR and diabetes of either type. Indeed, before the discovery of insulin in 1921/22 by Frederick Banting (no relation to William Banting) and colleagues at the University of Toronto, a diet very low in calories and carbohydrates was the only diet that could prolong the lives of children with type-1 (insulin deficient) diabetes.12
In the 1870s, William Morgan wrote that the aim of treatment of T1DM was ‘avoiding feeding the disease, by selecting a diet devoid of saccharine matter [carbohydrates]’.13 In 1848, the work of Claude Bernard had shown that the ‘HUMAN RACE, like SUGAR-CANES, possess a sugar-manufacturing organ – the liver. In fact, that marvellous gland is as busily and actively engaged, both hourly and daily, in fabricating sugar, as it is in manufacturing and secreting bile.’15 So to clear the urine of glucose, Morgan wrote, ‘a diabetic should exclude all saccharine and farinaceous materials from his diet’.16 He concluded: ‘Theoretically, the Diabetic should be supplied pretty largely with FAT; and practically it is found that its effect is highly beneficial.’17
Figure 7.2
Changes in plasma glucose, insulin, triglyceride, and liver and muscle glycogen concentrations in response to the ingestion of two high-carbohydrate mixed meals in insulin-sensitive and insulin-resistant young men. Note that in response to carbohydrate ingestion, those with IR show similar changes in blood glucose concentrations when compared to insulin-sensitive young men, but larger increases in blood insulin, blood triglyceride and liver triglyceride concentrations, and smaller increases in muscle glycogen concentrations. Reproduced from Petersen et al.14
This advice persisted through the early 1900s: ‘there should be absolute avoidance of carbohydrates and accordingly a diet composed exclusively of fat and meat’;18 ‘10–25gm carbohydrate per 24 hours’;19 ‘the total carbohydrate in the diet of diabetic patients is almost invariably restricted, and seldom exceeds 100 grams [per day]’;20 and, perhaps over-optimistically, ‘If the [diabetic] patient stops overeating and eats less sugar and starch, most of the symptoms of diabetes will vanish.’21 The Michigan Diet for Diabetes22 also restricted carbohydrate intake to about 20 grams per day, and re-analysis of the Allen Diet for Type-1 Diabetes reveals that it typically contained approximately 39 grams carbohydrate per day (8 per cent of calories).23 All this advice was based on the knowledge that it was dietary carbohydrate that raised blood glucose concentrations.
Unfortunately, with the discovery of insulin in the 1920s, physicians caring for patients with T1DM allowed dietary carbohydrate content to increase progressively, decade by decade. Whereas in 1915 the prescribed diet contained only 25 grams carbohydrate per day, by the 1940s this had increased to 172 grams per day.24
6. There are just 5 grams of glucose in 5 litres of human blood. Yet few portions of carbohydrate-rich foods contain less than 25 to 50 grams carbohydrate. This means that every time we eat a reasonable serving of carbohydrates, glucose in amounts of 5 to 10 times greater than the entire glucose-carrying capacity of our blood circulation is suddenly entering our system. This is a metabolic crisis for which humans, as a result of our evolution from an original primate ancestor, are simply not designed (see Chapter 16).
Considered together, these facts do not suggest that carbohydrates should be the primary source of energy in the diabetic’s diet, as the CDE proposes.
Because of significant errors in their understanding of the biology of IR and T2DM, the CDE uses erroneous logic to explain how people with these conditions can and should ingest carbohydrates. The global model of diabetes management currently taught holds that diabetics have the right to eat all the foods found in the ‘heart-healthy’ LFHC diet. This diet is based on an intake of predominantly carbohydrates in the form of cereals and grains, starchy vegetables, fruits and sugar-sweetened beverages. Since the diet allows processed foods, including cakes, biscuits and desserts, it is also sugar-rich and rich in hydrogenated vegetable oils and trans fats. There is no need, we are assured, for those with sugar sickness and IR, and thus with an inability to properly metabolise carbohydrate, to restrict their sugar and carbohydrate intakes any more than those with a normal ability to metabolise carbohydrate.
All this makes the management of diabetes unique. The medical profession has never encouraged people with lactose intolerance to ingest milk; those with gluten or peanut intolerance to ingest wheat or peanuts; or those with alcoholism to keep drinking alcohol. Yet somehow this common-sense rule seemingly does not apply to the treatment of diabetes.
The result is that, when eating these high-carbohydrate/sugar combinations, those with T2DM develop persistently elevated blood glucose and insulin concentrations. But because patients with T2DM are insulin resistant, even this excess insulin production will not be
sufficient to maintain normal blood glucose concentrations (because their livers are insulin resistant and will therefore continue to overproduce glucose regardless of how much carbohydrate is ingested and insulin secreted). So patients with T2DM are told that to lower these (unnecessary) carbohydrate-induced increases in blood glucose concentrations, all they need do is inject more insulin, a hormone that those who are insulin resistant are already secreting in excess and to which their bodies are already resistant (and becoming progressively more so with each passing day). We now understand that insulin, whether self-secreted or injected, further worsens IR (see Chapter 17).25
So the current diabetes advice is simple: Be ‘normal’. Eat carbohydrates, because that is your constitutional right. Inject insulin. And ignore the risk of long-term consequences, because we all know that people with T2DM will die prematurely from their disease anyway.
The long-term consequences of following this advice are well documented. A recent analysis of systematic reviews and meta-analyses of contemporary RCTs concluded that ideal care, which maximises tight glycaemic control, produces no better outcomes than less-good care in patients with T2DM.26 With regards specifically to insulin therapy, another meta-analysis concluded: ‘There is no significant evidence of long term efficacy of insulin on any clinical outcome in T2D. However, there is a trend to clinically harmful adverse effects such as hypoglycaemia and weight gain. The only benefit could be limited to short term hyperglycemia.’27
In fact, the most expensive and intensive prospective study of the management of patients with T2DM – the Look AHEAD trial – was terminated prematurely when the researchers realised there was no prospect of a favourable outcome.28 In all, 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. I doubt whether the authors of these studies ever questioned if their failure to show any beneficial effects of this management approach was because patients on the trial were encouraged to eat LFHC diets. As we will learn, you cannot out-medicate the effects of a bad (high-carbohydrate) diet in those with IR.
Such disappointing outcomes only reinforce the belief that diabetes is an irreversible condition that must inevitably worsen with age. Of course, the pharmaceutical industry is only too pleased by my profession’s promotion of this pessimistic prospect, because each year this gloomy disease model generates millions of new customers for its diabetic products. And with the promise that every customer will, over time, become more dependent on Big Pharma’s increasingly expensive wares, profits for companies specialising in diabetes care are predicted to rise by about 20 per cent per year, essentially forever.
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.
The reason why the CDE’s advice is wrong is because people with T2DM or IR cannot metabolise carbohydrates normally; they are carbohydrate intolerant. As a result, if they persist in eating high-carbohydrate diets, they become progressively sicker and more insulin resistant, requiring more medications, and ultimately die from the effects of widespread obstructive arterial disease caused by the continuous over-secretion (or self-injection) of insulin.
Therefore, logically, the first line of treatment must be to restrict the intake of carbohydrates in those with IR.
Fortunately, failed medical treatments based on fictitious biology cannot succeed forever. The power of social media will in time force change, as patients with IR learn that there is a better and simpler way to ensure their future health.
That same day, 4 April 2012, The Times picked up the story. In an article titled ‘Experts refute Noakes’s diabetes diet claims’, Dr Stan Landau, a senior physician at the CDE, ‘said there is no evidence that low-carbohydrate diets are good for people with type 1 or type 2 diabetes or people at risk. In fact, a low-carbohydrate diet can be harmful to them … Landau also said that Noakes has spoken out about diabetes like it is [a] “sinister and malignant” condition when in fact [it] is a “chronically manageable condition”.’29
Had my opinion been sought, I would have shown that the published scientific evidence does not support Landau’s statements. First, as I have described, the low-calorie, low-carbohydrate diet was the original diet for the management of T1DM before insulin was discovered in 1921/22. The diet was prescribed specifically because it delayed death in insulin-deficient children with T1DM. It was used in the hope that these children could be kept alive long enough for a life-saving ‘cure’ to be discovered.
For example, Diabetic Cookery, a famous cookbook of the day written for diabetics by Rebecca W. Oppenheimer, included lists of the ideal foods for diabetics, as well as lists of foods that should be avoided.
Included in her list of ‘especially valuable’ foods ‘owing to their great nutritive qualities’ are butter, olive oil, cream cheeses, meat, poultry, fish and eggs. In contrast, 29 foods high in carbohydrate are listed as ‘strictly forbidden’. William Morgan provided similar lists in his 1877 publication, Diabetes Mellitus: Its History, Chemistry, Anatomy, Pathology, Physiology, and Treatment. The green list in The Real Meal Revolution includes only those foods Oppenheimer prescribed, while those she prohibited are on the orange and red lists, which include foods to be eaten only occasionally or not at all.
Second, there is no evidence that it is dangerous for modern diabetics to eat LCHF; in fact, quite the opposite. In 2014, Dr Osama Hamdy, medical director at the famous Joslin Diabetes Center, wrote:
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, many physicians and dietitians around the nation are still recommending high carbohydrate intake for patients with diabetes, a recommendation that may harm the patients more than benefit them.30
Figure 7.3
A spread from Diabetic Cookery by Rebecca W. Oppenheimer, first published in 1917
I have since been informed that Landau has modified his views on the optimum diet for people with T2DM. Apparently he is no longer so certain that they should be eating high-carbohydrate diets. In addition, the CDE has initiated a trial of the effects of a very low-calorie diet in the management of T2DM, on the basis of evidence that this intervention may reverse T2DM in some patients.31 For this, Dr Landau earns my deepest respect. There is perhaps nothing more difficult in clinical medicine than admitting an error.
In the same Times article, dietitians Tabitha Hume and Theresa Marais claimed that high-protein diets place ‘undue stress on the kidneys which could lead to long-term damage’. Firstly, the LCHF diet is not a high-protein diet, and there is no published evidence showing that even the extremely high protein intakes of bodybuilders (2.8 grams protein per day) produce any evidence of kidney damage.32
A recent RCT found that a ‘low-carbohydrate diet is as safe as Mediterranean or low-fat diets in preserving/improving renal function among moderately obese participants with or without type 2 diabetes (with mild renal impairment)’.33 Similarly, a retrospective study of more than 11 000 US adults found that ‘[d]iets higher in plants and animal protein, independent of other dietary factors, are associated with cardiometabolic benefits, particularly improved central adiposity, with no apparent impairment of kidney function’.34
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.
Hume also suggested: ‘If one avoids sugar completely the liver has to work overtime to produce glucose from fat and protein and this is unhealthy.’ This is incorrect. My colleagues and I have subsequently shown that liver glucose production from protein and fat (gluconeogenesis) is the same in people eating either high-carbohydrate or high-fat diets.37 Because the fat-adapted body is less reliant on glucose for metabolism, there is no need for the liver to ‘work overtime’ to produce glucose. In fact, the liver is working ‘less hard’. In reality, it is high-carbohydrate diets that damage the liver by causing NAFLD in those with IR.38 NAFLD causes the abnormal blood lipoprotein (lipid) profiles39 that, together with insulin and inflammation, cause arterial damage in people with IR and T2DM.40 Hume is therefore blaming the wrong macronutrient for causing bodily harm.
She also said that ‘a lack of carbohydrates means the brain can struggle to produce serotonin. A lack of serotonin can lead to symptoms of depression such as anxiety, sleep disturbances and sadness.’ Again, there is no published evidence to support this, because there is presently no method by which brain serotonin levels can be measured in living humans.