by Tim Noakes
I suspect that the only way infants can lay down fat in this way is if they follow the same pattern as hibernating bears, which put on weight in the autumn before winter hibernation. They do this by developing (reversible) IR – becoming hyperinsulinaemic in the autumn and during the winter hibernation, but returning to normal insulin sensitivity during the spring and summer.63 Recall in Chapter 16 I discussed the work of Professor Richard Johnson, who has investigated the role of sugar consumption in turning on the ‘fat switch’ to produce this metabolic change.
It is, therefore, not unreasonable to suggest that a heightened level of IR was programmed into human newborns sometime in the past six million years specifically to ensure that they became fat in the final 12 weeks of gestation; this fatness was then essential to generating the ketone bodies needed for the development of the large infant brain during the first two years after birth.
But we also know that infants born to mothers who develop gestational diabetes – a reversible form of T2DM that goes into remission immediately after the infant is born – are over-fat and at increased risk of developing obesity and T2DM. This indicates that infants exposed to continuously elevated maternal blood glucose concentrations become even more insulin resistant, and are pre-programmed to have higher levels of IR even before they are born.
So the infant in utero lives on a knife-edge: insufficient IR, and the infant will have inadequate body-fat stores to maximise its brain development during the first two years of life; too much, and the infant will likely develop obesity/T2DM, perhaps even in adolescence. But there is more.
Bears reverse their IR by fasting during their period of hibernation. But human infants, especially those born to mothers with gestational diabetes, will likely be weaned onto the same high-carbohydrate foods that caused their (insulin-resistant) mother’s gestational diabetes in the first place. In this way, the environment converts a normal biological advantage, built into humans for the purpose of developing our large brains, into a trap for T2DM.
This interpretation has relevance to my HPCSA trial. By advocating weaning infants onto an LCHF diet, I was specifically trying to help mothers avoid this environmental diet trap.
My hypothesis is that, in order to produce the large brains that made us human, our evolution required that our babies develop (reversible) IR in the final 12 weeks before birth. When we lived in a low-carbohydrate environment this was fine, because infants would be weaned onto high-fat and moderate-carbohydrate foods similar in composition to breast milk. But with the introduction of modern convenience foods for infants by the Fremont Canning Company in Freemont, Michigan, in 1926 (to become Gerber in 1928), babies began to be weaned onto high-carbohydrate foods. Amy Bentley writes: ‘By the postwar period, refined white rice cereal, introduced by Gerber in the 1940s, had become the iconic first food American families fed to their infants.’64 As a result, the period of foetal and neonatal IR would have extended from the final 12 weeks of foetal life to beyond the neonatal period and, after the 1977 US dietary guidelines came into effect, into adolescence.
2. IR is the common condition that causes chronic diseases in those eating high-carb diets
Dr Gerald Reaven, now emeritus professor of medicine at Stanford University, has spent the past 60 years studying the condition that intellectually he now owns, insulin resistance. His academic interest was stirred early in his career, when he read that there are two forms of diabetes. The first, insulin-deficient T1DM, is caused when the pancreatic beta cells (which are destroyed in an autoimmune process perhaps related to wheat exposure causing leaky-gut syndrome) fail to produce insulin.65 In the second, insulin-resistant T2DM, insulin must be secreted in abnormally high amounts, because the target cells on which the insulin normally acts are resistant to its action; hence the condition of IR or carbohydrate intolerance.
Reaven’s great contribution has been to show that this persistent hyperinsulinaemia present in people with IR who eat high-carb diets (more than 50 grams per day), whether associated with T2DM or not, produces a collection of grave secondary consequences:66
Weight gain
Increased fat in the abdominal organs (visceral adiposity)
High blood pressure
Abnormal blood fat, glucose and insulin concentrations (atherogenic dyslipidaemia – Table 16.3 on page 314)
Elevated blood uric-acid concentrations (gout)
Impaired ability of arteries to dilate (endothelial dysfunction)
Whole-body inflammation
Dysfunction of the mitochondria (cellular organs that produce energy)
Progressive increases in IR (insulin-induced IR)
Impaired exercise performance
But Reaven’s greatest (and bravest) intellectual contribution was to suggest that IR and hyperinsulinaemia are the necessary biological precursors for at least four, but perhaps for all six, of the most prevalent chronic medical conditions of our day67 – the very six that will bankrupt our medical services within the next two decades, unless we understand the crucial importance of his work and act without delay. The six conditions most likely caused by high-carbohydrate diets in those with IR are:
Obesity
Arterial disease
Local: Heart attack or stroke
Disseminated: T2DM
High blood pressure
NAFLD
Cancer
Dementia (Alzheimer’s disease, also known at type-3 diabetes)
Reaven’s (Metabolic) Syndrome refers to the combination of obesity, diabetes, abnormal blood lipid levels and high blood pressure existing in the same individual. It is this singular combination that best predicts heart-attack risk.
The key finding from Reaven’s work is that these conditions are not separate – they are different expressions of the same underlying condition. So patients should not be labelled as having high blood pressure or heart disease or diabetes or NAFLD. Instead, they should be diagnosed with the underlying condition – IR – with the understanding that the high blood pressure, obesity, diabetes, NAFLD, heart attack, stroke, perhaps even cancer or dementia, are simply markers, symptoms if you will, of the basic condition.
And that basic condition is IR, which, simply put, is the inability of the body to tolerate more than an absolute minimum amount of carbohydrates each day (without developing hyperinsulinaemia). We now know that for patients with more severe IR, a daily carbohydrate intake of 25–50 grams is the maximum that can be tolerated. But when Reaven began his work, this was not known.
To determine whether nutritional factors contribute to the development of metabolic syndrome, beginning in the 1980s, Reaven completed a number of RCTs of the effects of low-carbohydrate diets in patients with this condition. Without exception, his studies showed that removing carbohydrates from the diet uniformly improved all measures of health in those with IR and metabolic syndrome. This led him to the following conclusions:
These results document that low-fat, high-carbohydrate diets, containing moderate amounts of sucrose, similar in composition to the recommendations of the American Diabetes Association, have deleterious metabolic effects when consumed by patients with NIDDM [non-insulin-dependent diabetes mellitus] for 15 days. Until it can be shown that these untoward effects are evanescent, and that long-term ingestion of similar diets will result in beneficial metabolic changes, it seems prudent to avoid the use of low-fat, high-carbohydrate diets containing moderate amounts of sucrose in patients with NIDDM.68
The results of this study indicate that high-carbohydrate diets lead to several changes in carbohydrate and lipid metabolism in patients with NIDDM that could lead to an increased risk of coronary artery disease, and these effects persist for >6 [weeks]. Given these results, it seems reasonable to suggest that the routine recommendation of low-fat high-carbohydrate diets for patients with NIDDM be reconsidered.69
In NIDDM patients, high-carbohydrate diets compared with high–monounsaturated-fat diets caused persistent deterioration of glycemic control and accen
tuation of hyperinsulinemia, as well as increased plasma triglyceride and very-low-density lipoprotein cholesterol levels, which may not be desirable.70
So, besides establishing the fundamental role of IR in these chronic diseases, Reaven also discovered the optimum treatment: carbohydrate restriction. Yet he subsequently failed to emphasise the curative effects of low-carbohydrate diets that his studies had so clearly shown. Why is this?
I suspect that during his daily work at Stanford, Reaven was in close contact with some of the most influential cardiologists in the US and perhaps the world. They would not have taken kindly to their colleague’s suggestion that, to prevent heart attacks, cardiologists should prescribe LCHF instead of the low-fat diet dictated, then as now, by the Dietary Guidelines for Americans, the AHA and the ADA. Had he chosen that route, Reaven’s colleagues would have excommunicated him, his research funding would have dried up and his career would have been over, exactly as had happened to Dr John Yudkin for suggesting in the 1970s that sugar, not saturated fat, causes heart disease. So it seems to me that Reaven kept quiet, choosing rather to continue researching IR without paying much attention to how an LCHF diet might – simply, effectively and cheaply – prevent and reverse all the medical conditions caused by IR.
3. One disease, one cause, many symptoms
Reaven’s problem was not unlike that faced by Darwin and Galileo, whose findings estranged them from religious orthodoxy. Reaven’s unifying hypothesis of chronic disease not only offends his colleagues in cardiology; it strikes at the very heart (pun intended) of the pharmacological model practised in modern medicine.
If obesity, diabetes, heart disease, NAFLD, high blood pressure, and perhaps even cancer and dementia are, in fact, all symptoms of the same underlying condition – IR – then our current model of medical management must be wrong, requiring, as it does, specific but different pharmacological treatments for each separate condition, overseen by different hierarchies of medical specialists. And what if the cornerstone for the treatment of all these conditions is a low-carbohydrate diet, the very diet that has been vilified by my profession for the past 50 years? It must be an extremely frightening thought for many medical professionals. How do you come to terms with the possibility that, by following medical orthodoxy, you may have harmed many patients?
By producing a unifying theory for perhaps six chronic diseases, and by presenting the initial evidence that these conditions are initiated by high-carbohydrate diets in those with IR, Reaven has fundamentally changed our understanding of how these conditions develop, how they should be treated, and also how they might be prevented. Our challenge now is to incorporate this new understanding into our teaching and practise of medicine.
But time is short. We need to act expeditiously if we are to reverse the progressive slide to ill health and the ultimate bankruptcy of global medical services.
In Chapter 4, I explained why the current low-fat dietary advice does not prevent arterial disease, for example, of the coronary arteries supplying the heart. Instead, by causing atherogenic dyslipidaemia (as shown by Reaven’s three studies and many others71), it is the direct cause of an unprecedented epidemic of arterial disease that threatens to overwhelm global medical services within the next 10 to 20 years.
In my HPCSA testimony, I presented one local study that clearly establishes the extent of the catastrophe facing South African medicine and why my profession is reluctant to acknowledge the existence of the IR that underpins it. T.E. Matsha and colleagues studied 1 198 local volunteers from Bellville, Western Cape.72 Importantly, the volunteers were all ‘healthy’ members of the community; they were not from a population being treated in hospital, for example.
Crucially, the researchers did not simply measure the volunteers’ blood cholesterol concentrations according to the hopelessly incorrect theory that heart disease is the sole threat to the health of people living in the Western Cape. Rather, they measured a decent range of markers of IR and pre-diabetes (Table 17.5). The aim of the study was to determine whether these metabolic risk factors worsened with increasing levels of NAFLD, measured by the blood levels of the liver enzyme gamma-glutamyl transferase. It is known that blood GGT activity provides an excellent measure of the severity of IR and NAFLD.73
Table 17.5: Metabolic and other risk factors in 1 198 residents of a South African community grouped according to level of NAFLD (GGT) activity
Quarters of GGT
Variables
Q1
Q2
Q3
Q4
Number of subjects
292
272
318
316
Mean GGT (IU/L)
14
22
32
56
Mean age (years)
52.8
54.2
53.5
51.3
Mean systolic blood pressure (mmHg)
120
126
126
129
Mean diastolic blood pressure (mmHg)
73
76
76
79
Use of blood pressure–lowering agents (%)
32
40
42
42
Mean body mass index (kg/m2)
28.6
29.5
31.1
30.3
Mean waist circumference (cm)
92.4
95.8
99.3
98.3
Current smoking (%)
33
42
41
46
Mean fasting blood [glucose] (mmol/L)
5.9
6.2
6.6
6.6
Median fasting blood [insulin] (uU/ml)
5.4
7.4
9.4
9.7
Mean HbA1c (%)
6.1
6.2
6.4
6.4
Mean blood [triglyceride] (mmol/L)
1.2
1.4
1.5
1.8
Mean blood [HDL cholesterol] (mmol/L)
1.3
1.3
1.2
1.3
Mean blood total [cholesterol] (mmol/L)
5.4
5.5
5.6
5.7
Median blood [C-reactive protein] (mg/L)
1.9
3.7
4.9
4.9
% with different features of the metabolic syndrome
High waist circumference (%)
71
78
82
81
High blood pressure (%)
66
78
81
83
High fasting blood [glucose] (%)
34
49
51
56
High blood [triglyceride] (%)
15
27
31
39
Low blood [HDL cholesterol] (%)
43
47
56
51
Three components or more (%)
47
60
67
65
[ ] = concentration
Data from T.E. Matsha et al., ‘Gamma-glutamyl transferase, insulin resistance and cardiometabolic risk profile in a middle-aged African population’.74 Note that Q1 were the 25 per cent of the study population with the lowest blood GGT activities; Q4 had the highest values and so the highest prevalence of NAFLD
The data clearly shows that the risk factors worsen across the table from left to right, indicating that increasing levels of NAFLD are associated with a worsening risk profile, as predicted by Reaven’s model. The result is that the percentage in each group with Reaven’s (Metabolic) Syndrome increases from 47 per cent in the group with th
e least NAFLD to 65 per cent in the group with the worst. But more frightening is the true incidence of diabetes in this group.
Even the ‘healthiest’ group (Q1) has elevated fasting glucose and insulin concentrations, as well as mean HbA1c concentrations of 6.1 per cent, indicating that essentially all in this group are already profoundly insulin resistant and will develop one or more of the serious consequences of IR in the next decade or so. Average HbA1c levels of 6.4 per cent and fasting blood glucose concentrations of 6.6 mmol/L in Q3 and Q4 indicate that the majority of people in these groups already have T2DM, although the authors fail to make this point in the table.
From the work of Reaven, Volek and their colleagues, and from my own study,75 we know that the only chance these groups have of escaping the deadly complications of IR and T2DM is to drastically reduce their daily carbohydrate intake to below 50 grams per day. Those with T2DM should reduce to below 25 grams per day.
The problem is that because so many of these typical South Africans have blood cholesterol concentrations ‘dangerously elevated’ at more than 5.01 mmol/L, when they finally present themselves to conventionally trained physicians or cardiologists who believe that cholesterol causes heart disease and who do not understand IR, the majority will be prescribed a cholesterol-lowering statin drug and referred to a dietitian, who will prescribe the usual ‘prudent, heart-healthy, low-fat diet in moderation’.
But statins will increase the risk for developing T2DM (Chapter 7), and the low-fat diet will expedite the development of T2DM and all its complications in the vast majority of these South Africans, whose IR is already so far advanced that their future development of T2DM is now an inevitability.
This is why I refused to run away from the HPCSA trial, no matter the cost to me, my wife and our family.