As I gulp my twice daily dose of metformin and obsessively monitor my blood glucose concentration, sometimes continuously 24 hours a day, I often wonder why did this happen. Why did I develop type 2 diabetes mellitus (T2DM)? Where did I, or perhaps my education, or even my educators go wrong? Or was it all simply inevitable, an unavoidable consequence of the hectic modern lifestyle that many of us choose?
After thinking about it for the past 3 years, I have drawn a number of conclusions. These have substantially changed my understanding of the causation of that group of chronic diseases that, in our abysmal ignorance, we incorrectly label “chronic diseases of lifestyle”. These ideas offer exhilarating opportunities for improved medical practice. We might, for example, be able to force some chronic diseases into remission. But they also raise important challenges for the future of our profession.
If we continue to deny the existence of this evidence and these ideas, we will continue to harm the health of a significant number of our patients.
More about my medical condition and myself.
First I continue to secrete some insulin. Thus I have insulin-resistant, not auto-immune (type 1), diabetes.
Second, my father died from the complications of T2DM. Only now do I appreciate that this places me at a 10-fold greater risk of developing the same condition. My father was always a large and powerful man, winning the Shot-put event at his Birkenhead High School (Liverpool) Sports Day in both grades 11 and 12. In reflection he ate relatively little carbohydrate other than that from bread, potatoes, occasional desserts and some alcohol, preferring meat including offal, eggs, fish and dairy, which were the mainstays of his diet. (Sadly after his diagnosis he increased his daily carbohydrate intake on the advice of his caregivers – advice, which I now know, hastened his death). My conclusion is that to develop ultimately fatal T2DM despite a relatively low carbohydrate intake, my father must have carried a particularly toxic combination of the genetic polymorphisms that cause insulin resistance.
Third, inheriting most if not all of my father’s toxic polymorphisms placed me at very high risk of developing T2DM even though I was much more health conscious than was he. I ate the healthy, “prudent”, low fat diet for 33 years after 1977; I remained physically active competing in hundreds of running races including more than 70 marathons/ultra marathons; I did not ever smoke and I maintained an acceptable body weight until my early fifties after which I suspect my insulin resistance (IR) began to manifest itself clinically (but the obvious signs of which, in my ignorance, I failed to detect).
My key personal error I now believe was to change my diet in 1977 by adopting the dietary advice of the Cape Heart Foundation (subsequently the Heart Foundation of South Africa) of which I was one of three founding doctors. As a result I began to minimize the fat in my diet, replacing it with the prescribed 6-11 daily servings of “healthy” cereals and grains, at the same time substituting “healthy” margarine containing an abundance of polyunsaturated and trans-fats, for the “artery-clogging saturated fats” in butter. I stuck religiously to this diet for more than 3 decades until my instant of epiphany on December 12th 2010 when by complete chance, I re-discovered the seminal work of Drs Volek, Phinney and Westman and their book The New Atkins for a New You. There I unearthed the evidence that had been overlooked in my education: That eating a carbohydrate-restricted, high fat, moderate protein diet would allow me to control my weight effortlessly without hunger provided I restricted my daily carbohydrate intake to between 25-50 grams. So I learned that because I have severe IR, to be truly healthy I would need to replace the “healthy” carbohydrates in my diet with unhealthy “artery-clogging” fats. I discovered too that Dr Robert Atkins, the creator of the Atkins Diet (1), should have been embraced as one of the most important figures in modern medicine. Instead he was scorned – a travesty.
During the first year of my personal experiment I effortlessly lost 15kg of excess body fat, reduced my 21km half-marathon time by more than 40 minutes, cured myself of a sleigh of minor but persistent medical conditions including recurrent weekly headaches (have not had a single headache since my dietary change – likely due to removal of all wheat from my diet); continuous dyspepsia (cured within the first month); irritable bowel syndrome (which began when I changed my diet in 1977); episodic exercise-induced wheezing, rhinitis and bronchitis (all of which required brief periods of inhaled steroids for treatment every few months); was again able to read both books and lecture slides without glasses (Bruce Fordyce reported the same experience) and, most importantly for me, re-kindled my joy of running. I also began a new relationship with food ridding myself of sugar addiction, uncontrollable hunger and binge eating especially when I returned home in the evenings. Instead I lost all hunger and now eat larger meals infrequently (usually a maximum of 3 per 48 hours) whilst snacking on high fat/protein foods a maximum of twice a day.
In time I had to accept that the low carbohydrate diet had not normalized my abnormally elevated blood glucose concentrations so that I would need to treat my T2DM with medication. Once I started on metformin, my weight dropped a further 5 kg for a total weight loss of 20kg. The metformin substantially improved my blood glucose concentrations, which I now control between 4.5 and 6.0mmol/L almost all the time. The sole exceptions are when lecturing on nutrition or watching the UCT Ikey Tigers Varsity Cup rugby team (especially in the epic 2014 Cup Final) when rather higher values (up to 7.5mmol/L) can occur. It turns out that my emotional state and not my (low carbohydrate) diet is the key driver of any episodes of elevated blood glucose concentrations that I now develop.
In time my change of diet was exposed to the South African public and I was forced to explain why I had changed (2). At first, the more I spoke and wrote about what I had done, the greater was the outcry, especially from certain sectors of our profession and from those institutions that promote the dietary advice that I have abandoned. Initially I was uncertain that what I had done would prove irrefutably true, or that the remarkable benefits I had achieved would occur in many others.
But as I read more (>100 books on nutrition and thousands of scientific articles) and most especially became aware of the massive global on-line community promoting this type of dietary change, I became increasingly certain that the 1977 dietary advice that I had initially embraced too readily, is based on “junk” science (3) and that its uncritical adoption has had catastrophic consequences for our health because it has addicted many of us to a high sugar, highly processed, high carbohydrate diet for which most humans, especially those with IR are not adapted.
And the consequence is a truth hiding in broad daylight – the epidemic rise of obesity and T2DM that began across the globe after these new dietary guidelines were introduced in 1977.
The intellectual drivers of modern nutritional advice.
The opposing theories of what causes heart disease – The diet-heart (cholesterol) hypothesis versus the insulin hypothesis.
Ultimately our beliefs of how different diets affect the risk of heart disease determine the dietary advice that we as medical practitioners or dieticians provide our clients. This is not particularly logical but the historical explanation is clear.
The key driver of the 1977 United States Department of Agriculture (USDA) fat-loathing Dietary Guidelines was the acceptance of American biochemist Ancel Keys’ Diet-Heart hypothesis. According to this theory fat in the diet raises the blood cholesterol concentration, which “clogs” the coronary arteries leading to heart attack. This theory, first advanced in 1953, was adopted and institutionalized within the next decade by a series of key players including the American Heart Association, the American Dietetics Association and the US National Institute of Health in the absence of any clear evidence that it is actually correct (3). This institutionalization protected this unproven hypothesis from the scrutiny of a sceptical science, gilding it with the godlike authority of absolute certainty. Only very recently has investigative journalism exposed the junkiness of the science on which this hypothesis is based (3).
By demonizing cholesterol (and dietary fat) as the key drivers of heart disease, this institutionalized “truth” immediately invited the development of cholesterol-lowering drugs to prevent heart disease. These drugs (amongst many other very powerful forces) have irrevocably changed the nature of nutritional education at our Universities. Because the protection of a >$40 billion a year “blood cholesterol lowering” industry based on the unproven diet-heart theory, insures that a contrary hypothesis cannot easily be taught by any institution that benefits from the largesse of the companies producing those drugs. The outcome is that we will continue to teach our students that fat in the diet is bad because it causes heart disease even when it is absolutely clear that this hypothesis is false (3,4).
Indeed I can write this only because I am at the end of my professional academic career, the conduct of which has never been dependant on the largess of the pharmaceutical industry.
The opposite theory, the insulin model of heart disease, is the work of another American, physician Gerald Reaven of Stanford University. Reaven’s genius was first, to develop a method to quantify the level of IR in humans, second to show that the extent of IR differs by a factor of 6 in different humans, and third to establish that IR is the key determinant of a cluster of medical conditions originally named Syndrome X but now termed the Metabolic Syndrome. The key conditions included in the MS are abdominal obesity, hypertension, T2DM, gout and atherogenic dyslipidaemia, comprising elevated concentrations of blood triglycerides and triglyceride-rich remnant lipoproteins, reduced blood HDL-cholesterol concentrations and increased small dense LDL-cholesterol particle numbers. Importantly MS is present in ~70% of persons with coronary heart disease indicating that it is, by far, the best clinical predictor of risk for future heart disease. Unfortunately many in the medical profession fail to understand the seriousness of a diagnosis of MS, in part because we currently do not offer any treatment options that can drive these conditions into remission (5).
Reaven argues that IR causes coronary atherosclerosis by producing a state of continuous insulin hypersecretion (hyperinsulinaemia) in response to carbohydrate ingestion. Continuous hyperinsulinaemia overstimulates those tissues that retain their insulin sensitivity including (i) adipose tissue (causing increased storage of ingested carbohydrate as fat in adipose tissue leading to abdominal obesity. Hyperinsulinaemia also prevent the mobilization of that fat for use as energy. Hence the concept that insulin is the hormone of fat or energy storage); (ii) liver cells (causing de novo lipogenesis, fatty liver, hypertriglyceridaemia, reduced production of “good” HDL-cholesterol with increased production of small dense LDL-cholesterol particles (Pattern B) as well as triglyceride remnant lipoproteins – the key markers of atherogenic dyslipidaemia); and (iii) the sympathetic nervous system (causing increased peripheral vascular resistance leading to hypertension, aided by the action of insulin in increasing sodium retention in the kidney). All these abnormalities are sufficient to explain how chronic hyperinsulinaemia promotes the development of heart disease.
Ultimately in response to continuous overconsumption of carbohydrate, the pancreas fails in most people with IR causing the development of T2DM. When this happens continuously elevated blood glucose concentrations worsen the arterial disease through the production of advanced glycation end-products.
In describing IR – probably one of the most important medical discoveries of the recent past – Reaven should, in my opinion, be a strong contender for the Nobel Prize. But I suspect he will be overlooked in the short-term because he may have failed to understand that IR is simply the substrate without which MS cannot occur.
But it is not the direct cause of MS. For that something else is necessary – the continual ingestion of a high carbohydrate diet for some decades (6)
The pharmacological model of disease development.
My medical training in the early 1970s occurred before teaching and research in medicine became so dependent on funding from the pharmaceutical industry. The outcome in my view is that we have subliminally accepted what seems to be a strange model of disease – one which holds that diseases occur because of the absence in the body of one specific chemical, different for each disease, and which can only be provided by drugs designed and marketed by the pharmaceutical industry.
The problem with this model is that for most diseases it simply does not work. It is not possible to reduce complex diseases to such a simple explanation. Worse this model fails to cure the “chronic diseases of lifestyle” including heart disease, T2DM, obesity, hypertension, dementia and MS. Yet we seem reluctant as a profession to acknowledge that much of what we prescribe, based on this pharmacological model, is palliative and does not address the real causes.
It is my argument that nutritional factors, in particular a life time of eating a high carbohydrate diet including too much sugar and fructose, is the driver of MS and probably many other conditions in those with IR.
To this should be added the role of wheat-based products inducing zonulin secretion in the gut leading to the “leaky gut syndrome”. According to another challenger for the Nobel Prize, Alessio Fasano, this mechanism – a wheat-induced “leaky gut” syndrome – allows the absorption of bacterial proteins which induce an antigenic response that causes a wide range of diseases through this “auto-immune” mechanism (7).
I interpret this as the mechanism explaining why my health improved so dramatically when I removed all wheat from my diet.
The role of the internet in determining the future of modern medicine.
The key change that will influence the future of medical practice is the growth of social media and the Internet. This will produced a fundamental change in the authority of medicine and all its practitioners.
When patients had access to only one source of knowledge – for example their general practitioner – it mattered not if that physician prescribed treatments that did not work. The patient would never know if more effective treatments exist. But the growth of social media and the Internet has irrevocably changed that.
Today through social media and the Internet, patients have access to the experiences of hundreds of millions of others producing what has been termed The Wisdom of the Crowds. The result is that treatments that work will be promoted on the Internet just as much as those, which do not work, will be ruthlessly exposed. And it will matter not who provides the treatments that work – in future patients will seek out those health providers regardless of their credentials or whether or not they attended an accredited institution of higher learning.
In this way the Wisdom of the Crowds will undermine and ultimately surpass The Power of the Anointed.
We live now in a society in which knowledge has been democratized. No longer can the Anointed – those directing our education at the world’s leading institutions – expect that the general public will simply accept their advice on the basis of the institution from which it comes or the professional credentials of those promoting it.
Now it is only the advice that works that has long term credibility.
The sooner our profession understands this, the better.
The key to understanding MS is that it is not a condition of excess calorie consumption that can be magically reversed by telling the patient to eat less and exercise more. MS is a disease of excess fat accumulation. It occurs in persons with insulin resistance who eat high carbohydrate diets and who are constantly hungry. The treatment of MS requires the prescription of a diet that will simultaneously treat the insulin resistance and reverse the hunger. A high fat carbohydrate-restricted diet is the only one that is able to achieve both these outcomes. Persons who change to the low carbohydrate diet are amazed by their improved satiety and their loss of hunger. Successful adapters to this diet now ask each other: What was the exact day on which you lost your hunger?
Those who understand the answer to this question, understand how to manage obesity and related conditions. Those who do not, may be less able to help patients with these conditions.
By focusing his attention on the biological changes in IR and ignoring his own studies showing that a very low carbohydrate diet reverses all the manifestation of MS in those with IR, Reaven may sadly have missed his date with medical immortality. Had he continued with his early studies showing the remarkable benefits of carbohydrate restriction in T2DM, in my view Reaven would have been an inevitable winner of the Nobel Prize (for describing the mechanisms causing the most important medical condition of our time). But had he promoted a high fat low carbohydrate diet he might have evoked the wrath of his colleagues both at Stanford University and at other elite US and other institutions and might even have damaged his chances for continued research funding. Apparently this may have been more than he was willing to chance.
His life work is best described in these two publications:
Kraemer F, Ginsberg HN. Diabetes Care 2014; 37: 1178-1181
Reaven G. Insulin resistance and CHD in non-diabetic subjects. Atheroscler Throm Vasc Biol 2012;32:1754-59
Fasano A. Zonulin and its regulation of intestinal barrier function. Physiol Rev 2011;91:151-175
(Published in The Cape Doctor 2014)