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DOCTORS often terrify patients out of their wits for no good reason, says University of Cape Town emeritus professor Dr Tim Noakes. Not because doctors\u00a0are bad people. They just\u00a0aren\u2019t all that jacked up on science, and\u00a0how to tell relative from absolute risk, says Noakes, a world-renowned scientist. Many doctors don\u2019t know that\u00a0they don\u2019t know vital\u00a0information about heart disease: that for many\u00a0patients it\u2019s not their tickers but their livers that are the problem. In other words, \u2018it\u2019s the fatty liver disease, stupid\u2019, says Noakes. Harsh? Yes.\u00a0True? \u00a0Well, take a\u00a0look at the science he presents below and make up your own mind. In Part 1, Noakes looked at evidence to show that advice doctors give to patients about low-fat foods protecting them from heart diseaseis all \u00a0wrong. Here he looks at why\u00a0insulin resistance is not spoken about in polite medical circles, and what the most abused term in medicine really is. \u2013 Marika Sboros<\/em><\/p>\nBy Tim Noakes<\/p>\n
Perhaps the most abused term in medicine is \u201crisk factors\u201d\u00a0for the reason that few truly \u2026 understand what the term really means.\u00a0When the doctor tells the patient: \u201cHigh blood cholesterol is a risk factor for heart disease,\u201d the doctor may or may not really understand what (s)he is saying.<\/p>\n
For the patient, the message is abundantly clear. All she\u00a0hears is: \u201cHigh blood cholesterol causes heart disease \u2013 your value is too high. You best lower it immediately. Or you will die.\u201d<\/p>\n
But this is not what \u201crisk factor\u201d, as currently defined, should convey.<\/p>\n
Risk factor is a term \u00a0from epidemiological studies that attempt to determine which factor(s) present in a population \u2013\u00a0an experimental cohort \u2013 observed for a period from years to decades, is associated with the development of specific illnesses of interest.<\/p>\n
Epidemiology is a powerful tool for studying diseases for which there is a singular cause \u2013 for example an environmental toxin such as asbestos or lead, or a bacterium like those causing typhoid, tuberculosis or cholera. \u00a0It is largely ineffective for isolating the precise causative factors in conditions, like nutritional diseases, in which there are likely to be multiple causes.<\/p>\n
Associational studies, performed by observing humans as they go about their daily lives, can only suggest causation \u2013 that is, that an identified \u201crisk factor\u201d actually causes the disease of interest \u2013 when the relationship between the two is statistically too obvious to ignore.\u00a0The\u00a0proper way to prove causation is to undertake randomised controlled trials (RCTs) in which the suspected causative agent is manipulated in the tested population whilst it remains unchanged in the control group.<\/p>\n
If the outcome robustly supports the tested hypothesis, then causation may be assumed.<\/p>\n
The measure of statistical strength in observational (associational) studies is the Hazard (or Risk) Ratio (HR or RR).\u00a0 Only if the HR is greater than 2 and preferably greater than 5 (indicting that the risk factor is present 2-5 times more frequently in those with the condition than in those without it) can one begin to believe that the associated risk factor is the direct cause of the disease of interest.<\/p>\n
Classic examples for high HR values in epidemiological studies include an 1875 study showing an HR of 2000 for scrotal cancer in London chimney sweeps, and a 1950 study that found the HR for lung cancer was 10-30 in smokers depending on how heavily they smoked.<\/p>\n
In 1849 John Snow calculated that the HR for infection with cholera was 14 in those London residents who received their (cholera-infected) water from the Southwark and Vauxhall Company; many argue that his study heralded the beginning of modern epidemiology.<\/p>\n
No one would dispute that these extremely high HRs identify a singular causative agent.\u00a0 There is no need to undertake more expensive RCTs to confirm that this relationship is causal.<\/p>\n
Consider the Parachute RCT analogy:\u00a0 We do not need to have parachute-less skydivers jump from airplanes to prove that parachutes reduce mortality.\u00a0 Some ideas do not require definitive statistical proof to be accepted as true.<\/p>\n
Interestingly the HR for heart attack in cigarette smokers is only 2, which is not high enough, by itself, to prove causation. But intervention RCTs show that stopping smoking immediately reduces heart attack risk, confirming that smoking is one of the factors causing heart attacks.<\/p>\n
To return then to where we began \u2013\u00a0\u00a0cholesterol as a \u201crisk factor\u201d for heart disease.\u00a0 Observational studies show that the HR for the association between the blood cholesterol concentration and heart disease is at best about 1.3, a figure that is far too low to suggest, by itself, that cholesterol causes heart disease.<\/p>\n
But a $40 billion\/year (statin) drug industry based on the still unproven theory that blood cholesterol is the direct cause of heart attack, ensures that this pathetically weak association is never discussed in polite medical circles.<\/p>\n
To do so invites excommunication, as I and a few others, have discovered\u00a0\u2013 to our surprise and dismay.<\/p>\n
By extension of argument, countless associational studies have by now produced a long list of \u201crisk factors\u201d with low to very low HR values that my profession has taught all to fear.\u00a0 This is best described as scare-mongering.\u00a0 For these low HR values simply do not begin to suggest causation.<\/p>\n
And if a \u201crisk factor\u201d is not a proven causative factor for a particular disease, then how can it be described as a \u201crisk factor\u201d, other than if there is malicious intent to mislead.\u00a0 These are merely elements that are co-incidentally and weakly associated with that disease.\u00a0 Just as umbrellas are always associated with rainy weather.\u00a0 But they are not the cause of atmospheric condensation, any more than the attending fire fighters caused the fire.<\/p>\n
This \u00a0brings us to the second and more important fact about \u201crisk factors\u201d.<\/p>\n
For besides being told (without evidence) that blood cholesterol is a risk factor for heart disease, we are also assured that obesity is a risk factor for high blood pressure, diabetes, heart attack, non-alcoholic fatty liver disease (NAFLD), stroke, arthritis, cancer and dementia.<\/p>\n
And in the same breath that diabetes is a risk factor for \u2013\u00a0you guessed it \u2013\u00a0obesity, high blood pressure, NAFLD, heart attack, stroke, arthritis, cancer and dementia.\u00a0 Or conversely, that high blood pressure is a risk factor for heart attack and stroke.<\/p>\n
This is intellectually absurd:\u00a0 how can everything be a risk factor for everything else? Indeed how do we explain the recent finding that the extent of disease in the (coronary) arteries (supplying the heart muscle) predicts an individual\u2019s risk for developing many other chronic illnesses including cancer and dementia.<\/p>\n
The answer can be found in the ignored work of Dr Gerald Reaven, now emeritus professor of medicine at Stanford University, California, USA.<\/p>\n
Reaven has spent the past 60 years studying the condition that intellectually he now owns, insulin resistance.\u00a0 His interest was peaked early in his career when he read that there are 2 forms of diabetes \u2013 the first, insulin-deficient type 1 diabetes mellitus (T1DM) caused by failure of insulin production by the pancreatic beta cells (which are destroyed in an auto-immune process).<\/p>\n
In the second, insulin-resistant type 2 diabetes (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 insulin resistance or carbohydrate intolerance.\u00a0 Persons with insulin resistance have blood insulin concentrations that are elevated most of the time, a condition known as hyperinsulinaemia.<\/p>\n
Reaven\u2019s great contribution has been to show that this persistent hyperinsulinaemia in insulin resistance, whether or not associated with T2DM, produces a collection of grave secondary consequences, listed in Table 1 below:<\/p>\n
Table 1:\u00a0 Consequences of persistent hyperinsulinaemia present in persons with insulin resistance who eat high (>50g carbs\/day) carbohydrate diets.<\/p>\n
\n- Weight gain<\/li>\n
- Increased fat in the abdominal organs (visceral adiposity)<\/li>\n
- High blood pressure<\/li>\n
- Abnormal blood fat, glucose and insulin concentrations (atherogenic dyslipidaemia \u2013 see later)<\/li>\n
- Elevated blood uric acid concentrations (gout)<\/li>\n
- Impaired ability of arteries to dilate (endothelial dysfunction)<\/li>\n
- Whole body inflammation<\/li>\n
- Dysfunction of the mitochondria (cellular organs that produce energy)<\/li>\n
- Progressive increases in insulin resistance (insulin-induced insulin resistance)<\/li>\n
- Impaired exercise performance<\/li>\n<\/ul>\n
But Reaven\u2019s greatest (and bravest) intellectual contribution is to suggest that insulin resistance and hyperinsulinaemia are the necessary biological precursors definitely for four\u00a0\u00a0and perhaps for all six\u00a0\u00a0of the most prevalent chronic medical conditions of our day \u2013 the very 6 that will bankrupt our medical services within the next two decades.\u00a0 Unless we understand the crucial importance of Reaven\u2019s work and begin to\u00a0act without delay.<\/p>\n
These conditions are<\/p>\n
\n- Obesity<\/li>\n
- Arterial disease\u00a0\u2013\u00a0\u00a0 local:\u00a0 Heart attack or stroke, disseminated:\u00a0Type 2 diabetes mellitus<\/li>\n
- High blood pressure<\/li>\n
- Non-Alcoholic Fatty Liver Disease (NAFLD)<\/li>\n
- Cancer<\/li>\n
- Dementia (Alzheimers\u2019 disease, also known at Type 3 diabetes)<\/li>\n<\/ul>\n
In his honour, the term Reaven\u2019s (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 risk of heart attack.<\/p>\n
The key finding from Reaven\u2019s work is that these conditions are not separate \u2013 they are different expressions of the same underlying condition.\u00a0 Thus a patient should not be labelled as having high blood pressure or heart disease or diabetes or NAFLD (or perhaps even cancer or dementia).<\/p>\n
Instead the patient\u00a0\u00a0should be diagnosed with the underlying condition \u2013\u00a0insulin resistance \u2013 with the realisation that the high blood pressure, the obesity, the diabetes, the NAFLD or the heart attack or the stroke are simply markers, symptoms if you will, of the basic condition.<\/p>\n
And that basic condition is insulin resistance which, simply put, is the inability of the body to tolerate more than an absolute minimum amount of carbohydrates eaten each day (without developing hyperinsulinaemia).\u00a0 We now know that for most with more severe insulin resistance, daily carbohydrate intakes of 25-50g are the maximum that can be tolerated.\u00a0 But when Reaven began his work this was not known.<\/p>\n
To determine whether nutritional factors contribute to the development of the 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 insulin resistance and metabolic syndrome.<\/p>\n
So besides establishing the fundamental role of insulin resistance in these chronic diseases, Reaven also discovered the optimum treatment \u2013 carbohydrate restriction. By any measures, Reaven should be a shoe-in for the Nobel Prize in Medicine.\u00a0 But perhaps not.\u00a0 For he failed subsequently to emphasise the curative effects of low-carbohydrate diets in insulin resistance.<\/p>\n
Why not?<\/p>\n
I suspect that during his daily work at Stanford Medical School, Reaven was in close contact with some of the more important cardiologists in the USA and perhaps in the world. They would not have taken kindly to their colleague\u2019s suggestion that, to prevent heart attacks, cardiologists should be prescribing high fat diets instead of the low fat diet dictated, then as now, by the American Heart Association.<\/p>\n
Had he chosen that route, Reaven\u2019s colleagues would have excommunicated him, his research funding would have dried up, and his career would have been over, exactly as happened to Dr John Yudkin in England for his (correct) suggestion in the 1970s that sugar, not saturated fat, causes heart disease.<\/p>\n
So it seems to me that Reaven kept quiet, choosing rather to continue researching insulin resistance without paying much attention to how a low-carbohydrate high-fat diet might \u2013 simply, effectively and at low cost \u2013 prevent and reverse all the medical disguises through which insulin resistance reveals itself.<\/p>\n
One disease, one cause, many symptoms.<\/p>\n
Reaven\u2019s problem is not unlike that faced by Darwin and Galileo whose findings estranged each from religious orthodoxy.\u00a0 For Reaven\u2019s unifying hypothesis of chronic disease must offend not just his colleagues in cardiology.\u00a0 For his hypothesis strikes at the very heart (pun intended) of the pharmacological model that we practice in modern medicine.<\/p>\n
For if obesity, diabetes, heart disease, NAFLD and high blood pressure (and perhaps also cancer and dementia) are in fact all symptoms of the same underlying condition, insulin resistance, 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.<\/p>\n
But what if the cornerstone for the treatment of all these conditions is a low-carbohydrate diet \u2013 the very diet that has now been vilified by my profession for the past 50 years? \u00a0That must be an extremely frightening thought for very, very many.\u00a0 How does one come to terms with the possibility that, by following medical orthodoxy, one may have harmed very many patients?<\/p>\n
It\u2019s the fatty liver disease, stupid.<\/p>\n
More support for Reaven\u2019s unifying hypothesis of chronic disease has recently come from an unexpected source \u2013 from those doctors, hepatologists, who specialise in the study of diseases of the liver.<\/p>\n
It has been known for some time that the added risks associated with obesity depend, in part, on where that extra fat is stored in the body.\u00a0 Thus fat that accumulates under the skin \u2013 subcutaneous fat \u2013\u00a0is far less unhealthy than is fat that accumulates within and between the organs in the abdomen, so-called visceral obesity.<\/p>\n
The hepatologists have now gone one step further to show that the real killer in visceral obesity is the fat that accumulates within the liver causing NAFLD, a disease that is now also reaching epidemic proportions.<\/p>\n
Their work shows that it is NAFLD and not obesity per se that produces the abnormal metabolic state \u2013 the atherogenic dyslipidaemia (Tables 1 and 2) \u2013 that causes heart disease in those with insulin resistance and the metabolic syndrome.<\/p>\n
Table 2: The metabolic features of atherogenic dyslipidaemia present in those with NAFLD and insulin resistance<\/p>\n
\n- Elevated blood glycated haemoglobin (HbA1c) levels<\/li>\n
- Elevated fasting blood insulin levels<\/li>\n
- Elevated fasting blood glucose levels<\/li>\n
- Hyperinsulinaemia and hyperglycaemia (elevated blood glucose levels) in response to carbohydrate ingestion<\/li>\n
- Low blood HDL-cholesterol concentrations<\/li>\n
- High blood triglyceride concentrations<\/li>\n
- Elevated numbers of small dense LDL-particles<\/li>\n
- Elevated blood Apolipoprotein B concentrations<\/li>\n<\/ul>\n
The\u00a0absolutely key point is that dietary carbohydrates and not dietary fat cause NAFLD. For when the insulin resistant eat excess carbohydrates including fructose found in sugar and fruits, they must convert into fat any extra carbohydrate they cannot either use as a fuel or store immediately as carbohydrate in liver or muscles.<\/p>\n
Note that all these options are severely reduced in those with insulin resistance.\u00a0 Instead under the action of insulin \u2013 the fat-building hormone\u00a0\u2013\u00a0\u00a0that fat is stored, initially as fat in the liver.\u00a0 But as NAFLD develops, insulin resistance worsens, hyperinsulinaemia increases, atherogenic dyslipidaemia deteriorates and the seeds for the chronic diseases of obesity, diabetes, heart disease, NAFLD and perhaps cancer and dementia are sown.<\/p>\n
Thus it is that dietary carbohydrates and not dietary fat that is the direct cause of this group of chronic diseases in those with insulin resistance.<\/p>\n
Summary.<\/p>\n
\n- The work of Dr Gerald Reaven \u00a0is as revolutionary to the understanding of medicine as were the works of Newton, Galileo and Darwin to their disciplines.<\/li>\n
- By producing a unifying theory for perhaps sixchronic diseases and by presenting the initial evidence that these conditions are initiated by high carbohydrate diets in those with insulin resistance, he has fundamentally changed our understanding of how these conditions develop and how best they should be treated.\u00a0 And also how they might be prevented.<\/li>\n
- Our challenge is to incorporate this new understanding into our teaching and practice of medicine.\u00a0But time is short. We need to act expeditiously if we are to reverse the progressive slide to ill health, with the ultimate bankruptcy of global medical services.<\/li>\n<\/ul>\n","protected":false},"excerpt":{"rendered":"
In this article, Professor Tim Noakes speculates that high carb diets and insulin resistance are the true causes of: Obesity High blood pressure Non-Alcoholic Fatty Liver Disease (NAFLD) Arterial disease: local:\u00a0 Heart attack or stroke disseminated:\u00a0Type 2 diabetes mellitus And possibly even: Cancer Dementia (Alzheimers\u2019 disease, also known at Type […]<\/p>\n","protected":false},"author":2,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":[],"categories":[44],"tags":[],"_links":{"self":[{"href":"http:\/\/www.frot.co.nz\/design\/dietnet\/wp-json\/wp\/v2\/posts\/1496"}],"collection":[{"href":"http:\/\/www.frot.co.nz\/design\/dietnet\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"http:\/\/www.frot.co.nz\/design\/dietnet\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"http:\/\/www.frot.co.nz\/design\/dietnet\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"http:\/\/www.frot.co.nz\/design\/dietnet\/wp-json\/wp\/v2\/comments?post=1496"}],"version-history":[{"count":2,"href":"http:\/\/www.frot.co.nz\/design\/dietnet\/wp-json\/wp\/v2\/posts\/1496\/revisions"}],"predecessor-version":[{"id":2143,"href":"http:\/\/www.frot.co.nz\/design\/dietnet\/wp-json\/wp\/v2\/posts\/1496\/revisions\/2143"}],"wp:attachment":[{"href":"http:\/\/www.frot.co.nz\/design\/dietnet\/wp-json\/wp\/v2\/media?parent=1496"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"http:\/\/www.frot.co.nz\/design\/dietnet\/wp-json\/wp\/v2\/categories?post=1496"},{"taxonomy":"post_tag","embeddable":true,"href":"http:\/\/www.frot.co.nz\/design\/dietnet\/wp-json\/wp\/v2\/tags?post=1496"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}