162. Another Desperate Attempt to Defend the Conventional Dietary Guidelines.

In the light of the excellent paper by Zoe Harcombe and her team which demonstrated conclusively that there was no reliable evidence on which to base the official dietary guidelines when first devised in the USA and in the UK, the BBC has featured this issue in a radio programme (1). This includes interviews with Zoe herself and Aseem Malhotra who explained why the advice to reduce total fat and especially saturated fat (SFA) is fundamentally flawed and has been a crucial factor responsible for the current high levels of obesity and Type 2 Diabetes (T2D). These were followed by what I can only describe as an extraordinary interview with Simon Capewell, who is Professor of Clinical Epidemiology at the University of Liverpool. He also has roles in which he advises the British Heart Foundation, the European Society of Cardiology, Heart of Mersey, National Institute of Clinical Excellence, Public Health England and the World Health Organisation. In his opinion the research by Zoe Harcombe is flawed because it failed to consider the totality of evidence. He goes on to say that there have been “over 1000 papers” since then which support the current guidelines. He cites the work of his own research team which claims it has established that there is a fall in the intake of SFA which is correct. Then he goes on to say there has also been a fall of 20% in the levels of blood cholesterol (TC) from which he concludes that this proves the advice has been responsible for the fall in the death rates from heart disease. To his credit the interviewer points out that this is all based on epidemiology, which cannot demonstrate “cause and effect”. The interviewer quite rightly suggests that there may have been other factors which have contributed to the decline in deaths from heart disease, such as the reduction in smoking and the improvements in treatment. It is true that the mortality due to heart disease has fallen and improvements in treatment and care have had a major impact. According to British Heart Foundation statistics, the percentage of women aged 55-59 years old dying after a heart attack almost halved between 1968 and 1998 while that for men aged 60-64 fell by a third (2). This report comments that measuring morbidity is much more problematic than monitoring mortality so we cannot be sure that there has actually been a genuine decrease in the chances of suffering from heart disease and if so the magnitude of the change.

Anyone who considers that lowering TC is beneficial must be deluded. Just watch this You Tube video (3).

Simon Capewell goes on to imply that Ancel Keys was correct when he concluded that there was a direct correlation between the amount of fat/SFA in the diet of different populations, the level of cholesterol in the blood (TC) and the death rate due to heart disease. In fact he even states that Keys has been vindicated by subsequent studies. This position is absolutely remarkable. The fact is that the work of Keys was full of inconsistencies, was based on data from 6 different countries and made the fatal mistake of assuming that an association is evidence of cause and effect. The work of Keys has been totally discredited by Zoe Harcombe (4), Malcolm Kendrick (5) and most recently by Nina Teicholz (6). The reality is that when information is obtained from many different countries there is no relationship. It just so happened that Keys conveniently omitted:

  • Countries where people eat a lot of fat but have little heart disease, such as Holland and Norway
  • Countries where fat consumption is low but the rate of heart disease is high, such as Chile.

I would strongly recommend that if you really wish to understand what went on then have a look at these references. It is absolutely disgraceful and it simply beggars belief that anyone should even attempt to justify this rubbish!

Simon Capewell states that the dietary guidelines were “prophetic and solid” and “that history has demonstrated how very sound they were”. This is unbelievable! How on earth can anyone reach this conclusion, when we look at the current state of public health in the UK, the USA and most of the rest of the world????

Obesity is an obvious issue of concern but a more accurate indication of public health is shown by the incidence of T2D, which in the UK had doubled in the last 15 years. Those with T2D have a reduced life expectancy and an increased risk of retinopathy, stroke, kidney failure, heart disease, cancer, Alzheimer’s Disease and amputation of limbs.

A man diagnosed with diabetes at age 40 will lose almost 12 years of life and 19 Quality Adjusted Life Years (QALYs) compared with a person without diabetes. A woman of the same age will lose about 14 years of life and 22 QALYs (7).

T2D is caused by excess glucose in the blood. This stimulates the pancreas to produce insulin. The continuous production of high amounts of insulin cause damage to the various body organs which can result in many different chronic diseases. The solution is obvious…..lower the blood glucose by reducing the consumption of sugar and the other foods that contain carbohydrates, which are broken down to produce glucose. These foods, primarily potatoes, bread, rice and pasta must be replaced by other foods, especially those animal products such as meat, dairy and eggs, all of which contain fat. This is direct contrast to the current guidelines which Simon Capewell praises so highly.

The evidence has been very neatly summarised in a recent paper (8). There is absolutely no doubt that this approach works very effectively. At least one of the authors, Dr Jay Wortman, has been able to cure his T2D by altering his own personal diet along these lines. There are literally hundreds of individuals who have achieved exactly the same result (9). The presentations at the recent Low Carb Summit in Cape Town showed just how persuasive our knowledge is at present. Several practising clinicians showed how successful the Low Carb High Fat (LCHF) diet with their own patient records (10).

So we have now reached a point where we have the knowledge not only to halt the current inexorable rise in the incidence of chronic disease but to reverse it. Regrettably the official approach by government and the NHS in the UK is making things worse with the result that millions are suffering unnecessarily and many of these are dying prematurely. It is imperative that there is a complete re-evaluation of public health policy. We have to accept that what is being done at present is one of the main reasons why things are deteriorating.

To identify why there is so little progress, we only have to consider the views expressed by people like Simon Capewell who seem to defend the status quo come what may. Because of his role with so many key organisations, he has enormous influence. But in order to maintain his stance he has to manipulate and misinterpret the evidence.

If we are ever to make the break-through, it is essential the Simon Capewells of this world are tackled at every possible opportunity. His errors are so fundamental that you do not need to have specialised knowledge to do so and I would encourage all those who are aware of the benefits of LCHF, especially those with personal experience, to make your views known to anyone in a position to make the changes. For a start the forthcoming General Election in the UK is a timely opportunity to force the issue on the political agenda. If enough of us rally round then maybe the message will begin to get through.


  1. http://www.bbc.co.uk/programmes/b054t9hn
  2. https://www.bhf.org.uk/~/media/files/research/heart-statistics/bhf-trends-in-coronary-heart-disease01.pdf
  3. https://www.youtube.com/watch?v=i8SSCNaaDcE
  4. Zoe Harcombe (2010) “The Obesity Epidemic” Columbus p 87
  5. http://drmalcolmkendrick.org/2013/03/13/the-untainted-mind/
  6. Nina Teicholz. (2014) “The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet” Simon & Shuster New York
  7. http://jama.jamanetwork.com/article.aspx?articleid=197439
  8. http://www.nutritionjrnl.com/article/S0899-9007(14)00332-3/pdf
  9. http://vernerwheelock.com/?p=422
  10. http://vernerwheelock.com/?p=729


161. More Reflections on the Cape Town Low Carb Summit: Old Mutual Shows the Way Forward

If anyone had doubts about why the current official dietary recommendations which emphasise the benefits of a diet low fat and high carbohydrates are fundamentally flawed, they should have been at the recent Low Carb Summit in Cape Town. When all the available scientific evidence is collected together it is abundantly obvious that the existing approach has been absolutely disastrous. In addition, there are an enormous number of individuals, who have improved their own personal health by switching to a diet which is high in the right type of fats and low in carbohydrates (LCHF, widely referred to as the Banting diet). All of these simply cannot be written off as anecdotal. To do so is to imply these people are all charlatans!
At the end of the conference the following statement, endorsed by all the speakers was issued:
“The mainstream dietary advice that we are currently giving to the world has simply not worked. Instead it is the opinion of the speakers at this convention that this incorrect nutritional advice is the immediate cause of the global obesity and diabetes epidemics.
This advice has failed because it completely ignores the history of why and how human nutrition has developed over the past three million years. More importantly, it refuses to acknowledge the presence of insulin resistance (carbohydrate intolerance) as the single most prevalent biological state in modern humans.
Persons with insulin resistance are at an increased risk of developing a wide range of chronic medical conditions if they ingest a high carbohydrate diet for any length of time (decades).”
Or to put it another way:
“Excessive insulin in the body causes damage to the internal organs, which in turn leads to chronic diseases/conditions including Type 2 Diabetes (T2D), obesity, high blood pressure, fatty liver, heart disease, Alzheimer’s Disease and cancer. The insulin production is stimulated by the high level of glucose in the blood, which is caused by the consumption of sugar and refined carbohydrates. Hence a diet which is low in carbohydrates and has fat as the main sources of energy will result in better health and a reduced risk of developing many diseases.”
The key message from the conference is that the time for debate is over. The emphasis now must be to focus on how the message can be disseminated to all those people who could benefit by altering the composition of their diet. Ideally national policies should be re-vamped but there is so much entrenched opposition and built-in inertia in most governmental systems that this approach is unlikely to be successful in the short term. In the real world, the starting point has to be with the grassroots. As awareness of the effectiveness of the LCHF gathers momentum, there will be opportunities for businesses to capitalise and generate further impetus.
This is already happening in South Africa and some other parts of the world. One of the most significant aspects of the Cape Town conference was the sponsorship by Old Mutual, which is an international investment and insurance company. One of the keynote speakers was Dr Peter Bond who is the company’s Chief Medical Officer. In particular, he described how the standards of public health across the globe are deteriorating because of the increasing incidence of T2D, obesity and the various related diseases. According to company estimates, 3.5 million South Africans have T2D and 50% are unaware of the condition, which is often only diagnosed when an insurance examination is done. As a consequence the application may be declined or subjected to an additional mortality or morbidity loading. Seven out of 10 women and 4 out of 10 men are overweight or obese, which is double the global rate of almost 30%. It is evident that current strategies are not working. Data collected by Old Mutual confirms that total cholesterol (TC) is NOT an effective measure of mortality risk. If currents trends are maintained, then the costs of health care will continue to rise. From the company perspective, this means that the premiums will have to be increased and therefore customers may allow their policies to lapse and it becomes much more difficult to get new business. Old Mutual sells critical illness products: so if those who purchase these policies can be persuaded to adopt lifestyle changes such as a LCHF diet, everyone benefits. The costs of pay-outs will be reduced, which results in lower premiums and increased profitability. From the individual perspective, a reduction in the chances of a serious illness equals better health and quality of life.
Although Dr Bond stated that he was not endorsing any particular diet or way of eating the company has clearly recognised the significance of the event and the impact that the Banting approach is already having in South Africa. All the indications are that the response to the Old Mutual involvement has been very positive.
The crucial factor is that the business understands there is a powerful incentive to encourage people to follow a healthy lifestyle. This may prove to be of huge significance in promoting the benefits of a Banting diet to a much wider audience. The fact that Old Mutual operates in many different parts of the world could be vital. If the initiative in South Africa is a success, then we may expect to see it repeated in many other countries. Assuming this happens, competitors are likely to follow suit. Ultimately governments will wake up to the fact that there are actually ways of halting the apparently inevitable increases in the costs of health care.
This approach is in stark contrast to many other businesses currently involved in health care where consistent poor health equates to the continued demand for drugs and use of the various tests and procedures. As one cynic has pointed out, drug companies derive little benefit if their products successfully cure patients. The ideal for them is to have patients who remain ill and therefore continue to purchase their products. However the reality is that many drugs show absolutely no benefit and are a waste of money (1).
The LCHF approach has tremendous potential to reverse the current disastrous trends in chronic disease patterns and it is imperative that all possible opportunities are exploited so the basic messages are disseminated as widely as possible and as quickly as possible.
1. http://vernerwheelock.com/?p=587

160. Tim Noakes Answers His Critics

This is a repost from Karen Thomson’s Blog. The original can be sourced at

I am very grateful to Karen and Tim for permission to re-post.

By Karen Thomson, February 25, 2015

Written by Prof Tim Noakes
My critics have called me deluded and dangerous. In the South African Medical Journal in 2013, they said I have cherry picked, misinterpreted data, I don’t understand the science, I’ve lost my way, flouted the Hippocratic Oath, and I’m damaging patients and the population.
Last year, for the first time in the history of the University of Cape Town, no senior academic has ever been criticized as publicly as I was. Senior colleagues, including the Dean of the Medical Faculty at UCT (who has since moved upwards and onwards – a reward for his bravery perhaps) sent a letter to the Dean of all South African medical schools and to the press, saying:
“There is good reason for concern that this diet may rather result in nutritional deficiencies, increased risk for heart disease, diabetes mellitus, kidney problems, constipation, certain cancers and excessive iron stores in some individuals in the long-term.”
They said I was “making outrageous unproven claims about disease prevention, and maligning the integrity and credibility of peers who criticize his diet for being evidence-deficient and not conforming to the tenets of good and responsible science. This goes against the University of Cape Town’s commitment to academic freedom as the prerequisite to fostering responsible and respectful intellectual debate and free enquiry.”
The letter ended: “UCT’s Faculty of Health Sciences, a leading research institution in Africa, has a reputation for research excellence to uphold. Above all, our research must be socially responsible. We have therefore taken the unusual step of distancing ourselves from the proponents of this diet.”
The authors didn’t stop there. They ran a website in which they collected extraneous material, selected what they said was my argument, and threw in blogs by people unrelated to the topic, all without giving me the right of reply.
Clearly their goal was to prove that I’m deluded and dangerous. Rather than attacking the science, they attacked me personally and said I was practising junk science.
These are not ugly, horrible people. They were saying what they believed out of a deep sense of conviction.
Are they right, or am I right? We can’t both we right.
I will present the evidence to show that my opinion is scientifically based, does not break any of the rules of good science, that I have a right to that opinion, and that my critics are the ones who are practising junk science, and are endangering people’s health.
They don’t understand causation science, hazard ratios, insulin resistance as well as the special role of gluten, the leaky gut and non-coeliac gluten intolerance in human ill-health.
The key problem is that both sides believe the facts sit with them. At the first international low-carb, high-fat summit in Cape Town, we spent three days discussing evidence for and against low-carb, high-fat diets to treat insulin resistance.
We need to begin by looking at the quality of the evidence.
My critics say low-carb diets are proven not to work and saturated fat is proven to increase the risk of cardiovascular disease (CVD). They say we only have anecdotal evidence for low-carb, high-fat diets for the treatment of insulin resistance (IR) and diabetes.
That’s not correct. We have the evidence: all randomized, controlled trials (RCTs) either show that high-fat outperforms low-fat diets, or long-term RCTs show no evidence that a low-fat diet does any good.
My critics have ignored all the RCTs and other evidence that dispute their theories. In so doing, they have not practised good science according to the rules laid down by Sir Austin Bradford Hill, who is revered as the “father of medical statistics”.
Bradford wrote a series of article in 1937 in the Lancet describing the use of statistics in medical science. It was a completely new science. He was one man who really understood it, and he laid down levels of information for causation, starting from anecdote (case history), and including cross-sectional study, randomized, controlled, prospective, clinical trials, and finally systematic review and meta-analysis.
He explained that it was possible to prove causation from associational studies, but only if certain criteria were met. He listed nine such considerations, but I have focused in this paper on only two: coherence and strength of association.
He wrote in 1965: “Here then are nine different viewpoints from all of which we should study association before we cry causation. What I do not believe…is that we can usefully lay down some hard-and-fast rules of evidence that must be obeyed before we accept cause and effect.
“None of my nine viewpoints can bring indisputable evidence for or against the cause-and-effect hypothesis and none can be required as a sine qua non. What they can do, with greater or lesser strength, is to help us make up our minds on the fundamental question – is there any other way of explaining the set of facts before us, is there any other answer equally, or more likely than cause and effect?”
Bradford Hill designed and completed the first RCT in 1950 (Streptomycin in TB meningitis) and with Sir Richard Doll “proved” that smoking causes lung cancer initially from an associational study (which cannot prove causation). He found that the Hazard Ratio for lung cancer in smokers was 10-30 times higher than in non-smokers. Such a high value could only indicate causation in his opinion.
He wrote: “On the other hand the death rates from coronary thrombosis in smokers is no more than twice, possibly less, the death rate in non-smokers (ie Hazard Ratio of 2 or less). Though there is good evidence to support causation it is surely much easier in this case to think of some features of life that may go hand in hand with smoking – features that might conceivably be the real underlying cause or, at the least, an important contributor, whether it be lack of exercise, nature of diet or other factors.
“But to explain the pronounced excess in cancer of the lung in any other environmental terms requires some feature of life so intimately linked with cigarette smoking and with the amount of smoking that such a feature should be easily detectable. If we cannot detect it or reasonably infer a specific one, then in such circumstances I think we are reasonably entitled to reject the vague contention of the armchair critic ‘you can’t prove it, there may be such a feature’”.
Bradford Hill has since died, and many researchers have ignored his criteria and flipped into a model of junk science – the scientists who are more interested in getting funding and more work, not discovering how to make people healthier.
In science, the bar has dropped to the lowest level of scientific “proof” conceivable – so low that researchers now ignore what Bradford Hill taught and accept any Hazard Ratio above 1.0 as definitive evidence of causation. Poor Bradford Hill turns in his grave with every new publication.
That means just about anything can be proved to cause anything. The result is that have grown an entire discipline of nutritional science based on this improper understanding of Bradford Hill’s doctrines. And we wonder why we have got it all so very, very wrong.
So all the associational nutritional studies used to justify the 1977 USDA (low fat) Dietary Guidelines are based on studies with Hazard Ratios usually between 0.7-1.3. Bradford Hill would not have accepted any of these studies as evidence for causation, or allowed them to be used as the sole justification for novel global dietary guidelines. In fact studies using such feeble criteria for causation are simply scare-mongering, the ultimate junk science.
Since most such studies originate from departments of epidemiology that consider themselves at the forefront of hard science, author James Le Fanu proposes a simple solution: “Meanwhile the simple expedient of closing down most university departments of epidemiology could both extinguish this endlessly fertile source of anxiety-mongering while simultaneously releasing funds”.
Interestingly, a recent report – A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart disease – used four Bradford Hill criteria (strength, consistency, temporality and coherence) to evaluate all the evidence from dietary studies. The study showed strong evidence for vegetables, nuts, “Mediterranean” and high quality dietary patterns for “protective effects against CHD”. These are exactly the components that the Banting high fat diet promotes. They also showed strong evidence that trans-fatty acids and foods with high glycaemic index or load (ie high carbohydrate diets) as “harmful effects promoting CHD”. These are exactly the foods that the Banting high fat diet does not allow. The study found insufficient evidence for: Saturated and polyunsaturated fatty acids; total fat; alpha linolenic acid; meat; eggs; milk.
So if my critics were steeped in the science as they claim, they could only have concluded in their letter to the Deans of all the Medical Schools and to the media, that my advice was completely compatible with the most rigorous science currently available. That I am also correct to argue that there is no evidence that a high fat diet causes anything. Instead they concocted an argument based on evidence that Bradford Hill would have rejected. And this from leading scholars at a leading medical institution in this country.
In his book, The Rise and Fall of Modern Medicine, James Le Fanu says: “Bear in mind Sir Austin Bradford Hill’s insistence that statistical inferences by themselves have no meaning unless they are internally coherent, that is to say, when several different types of evidence for an association between an environmental factor and disease … are examined, they (must) all point to the same conclusion.”
“Put another way, no matter how plausible the link between dietary fat and heart disease might seem, just one substantial inconsistency in the statistical evidence effectively undermines it.” There is now more than one substantial inconsistency that should long ago have relegated the low fat diet to the dust bin of bad science.
My critics also like to say that we only have anecdotal evidence for the benefits of low-carb, high-fat diet. That’s simply not true. There is significant anecdotal evidence, and all of science begins with anecdote. But we also have a wealth of RCT evidence for the superiority of low-carb, high-fat diets of low fat, high carbohydrate diets.
A speaker at the summit, Canadian Dr Jay Wortman, told how he became diabetic 12 years ago, cut carbs from his diet (as a doctor he knows that carbs raise blood sugar), within days his symptoms had improved, and he has been without evidence of diabetes ever since.
Two of my clients attended the summit: Billy Tosh weighed 163kg in July 2012, was close to a heart attack, and had type 2 diabetes and hypertension. By March 2013, Billy had lost 84kg, his hypertension has gone, and he is free of symptoms of diabetes and hypertension. Brian Berkman weighed 153 kgs in July 2011, was diabetic, hypertensive and considering bariatric surgery. By January 2013, he had lost 82kg and is free of symptoms of diabetes, is no longer hypertensive, and avoided bariatric surgery.
Is that all just anecdote? Probably not. I don’t claim they are cured, but they don’t require medication and are without evidence for diabetes.
There are many other case histories of spontaneous recovery from type 2 diabetes, a condition that my profession teaches is irreversible, will require increasing medication for life and has, in essence, a hopeless outlook with the only certainty – more drugs, more illness, more disability.
How many subjects do you require in a trial to prove an effect?
In his book, The World Turned Upside Down, author Richard Feinman said: “It depends on how many people recover spontaneously.”
If there has never been a reported reversal of Type 2 diabetes mellitus (T2DM) in patients following conventional medical advice (which there has not), then a single case is not an anecdote. It is a black swan – in other words something that contradicts our previous beliefs, for example that all swans must be white to be classified as swans. The presence of a black swan requires the immediate funding of a proper scientific study – a randomised controlled clinical trial – to test whether it is possible to reverse T2DM with a low carbohydrate diet.
A key question has been: you can’t prove causation without randomized controlled trials (RCTs). But as I’ve already shown you can in fact surmise causation in cross-sectional study if you fulfill certain strict Bradford Hill criteria. And when applied to cross-sectional dietary studies, the Hill criteria support the health benefits of the low carbohydrate diet. But let’s first consider the evidence from RCTs.
One of my fiercest critics was involved in the most significant RCT: The Women’s Health Initiative Randomized Controlled Dietary Modification Trial, published in the JAMA in February 2006. It was a large trial of 48,836 post-menopausal women, followed over 8.1 years looking at the effects of low-fat eating and costing about $700 million. The study concluded: “Over a mean of 8.1 years, a dietary intervention that reduced total fat intake and increased intakes of vegetables, fruits, and grains did not significantly reduce the risk of CHD, stroke, or CVD in postmenopausal women and achieved only modest effects on CVD risk factors, suggesting that more focused diet and lifestyle interventions may be needed to improve risk factors and reduce CVD risk.” Another two very expensive low-fat RCTs have come to the same conclusions.
The WHI study authors should have designed their study as the test of a null hypothesis: Specifically, if you reduce your fat intake, you will reduce heart attacks and cancer rates. If the results don’t support the hypothesis, then the hypothesis is clearly wrong and must be abandoned (if one is practicing good rather than junk science).
Instead, when the authors discovered that the data did not support their original hypothesis, they simply added an ad hoc modification. So in a news release, Dr Elizabeth Nabel then head of the National Institute of Health – the statutory body that had funded the study with tax payers’ money – suggested that the findings “could have been due to chance”, and that the participants could still have been eating too much fat.
Actually no, Dr Nabel. That’s not science. The study disproves your hypothesis. When the hypothesis is disproven, you have to come up with a new one and then attempt to disprove it.
Albert Einstein said: “No amount of experimentation can ever prove me right;
a single experiment may at any time prove me wrong.”
The WHI study should have been considered the definitive disproof of the authors’ hypothesis that eating less fat will prevent heart disease. But instead the authors and the NIH marketed it as if it supported their hypothesis. That is not science. That’s science driven by industry or governments that are determined to find an outcome that supports their position, regardless of the facts. Why bother to do research if you “know” the outcome before the start? Of if you will interpret any outcome to support your ingrained prejudices?
But the finding that low-fat diets did not reduce the risk of cardiovascular disease is entirely predictable as a high carbohydrate diet produces a specific atheroma-generating metabolic profile in those who are metabolically vulnerable because they have insulin resistance.
For example, there is one study that looked at the progression of
coronary atherosclerosis (narrowing of the coronary arteries) in postmenopausal women by Harvard researcher David Mozaffarian and others, and published in the American Journal of Clinical Nutrition in 2004. The study concluded: “In postmenopausal women with relatively low total fat intake, a greater saturated fat intake is associated with less progression of coronary atherosclerosis, whereas carbohydrate intake is associated with a greater progression.” In other words the study found that higher intakes of “healthy” carbohydrates and “healthy” polyunsaturated fats was associated with more rapid disease progression, whereas women who ate the most saturated fat showed NO disease progression. Naturally this study has been buried, never to be heard of again. More recently, a study in the Journal of Nutrition in February 2015, confirmed that “ Dietary intake of saturated fat is not associated with risk of coronary events or mortality in patients with established coronary artery disease.”
But the strongest evidence against this fake hypothesis has been provided by Nina Teicholz in her riveting book, Big Fat Surprise: Why Butter, Meat and Cheese belong in a Healthy Diet. Teicholz reviews the absence of science behind the hypothesis that saturated fat causes disease. Dr Richard Smith, a former editor of the BMJ, had this to say about this book which should be required reading for all:
“The title, the subtitle, and the cover of the book are all demeaning, but the forensic demolition of the hypothesis that saturated fat is the cause of cardiovascular disease is impressive.
“Indeed, the book is deeply disturbing in showing how overenthusiastic scientists, poor science, massive conflicts of interest, and politically driven policy makers can make deeply damaging mistakes.
“Over 40 years I’ve come to recognise what I might have known from the beginning that science is a human activity with the error, self deception, grandiosity, bias, self interest, cruelty, fraud, and theft that is inherent in all human activities (together with some saintliness), but this book shook me.”
At the Old Mutual Health Summit, Zoe Harcombe presented more novel evidence against the fake hypothesis. She asked the question: What evidence was available from RCTs in 1977 and 1983 to support the adoption of those novel low fat guidelines. Her study reported in the BMJ Open Heart journal one week before the Summit concluded that “Recommendations were made for 276 million people following secondary studies of 2467 (ill) males with reported identical all-cause mortality. RCT evidence did not support the introduction of dietary fat guidelines.”
So now we know that there was no evidence available in 1977 to support the change in dietary advice that became the global standard. And we also know that no evidence has accumulated in the past 40 years to show retrospectively that those guidelines are correct and supported by the most rigorous science.
And more global experts are beginning to weigh in their support almost on a daily basis. Thus in an editorial in Diabetes Management in 2014, Dr Osama Hamdy, Medical Director of Joslin Obesity Centre’s Obesity Clinical Programme, wrote:
“It is clear that we made a major mistake in recommending the increase of carbohydrates load to >40% of the total caloric intake (especially for person with type 2 diabetes mellitus). 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 dieticians across the nation are still recommending high carbohydrates intake for patients with diabetes, a recommendation that may harm their patients more than benefit them.”
Yet my critics continue to ignore all the evidence that favors the health benefits of high-fat diets and the absence of evidence supporting low fat diets.
Could be due to the Upton Sinclair Theorem, which states: “It is difficult to get a man to understand something, when his salary depends upon his not understanding it”.
Perhaps the most important reason why the value of low carbohydrate diets are not yet properly appreciated especially by my profession is because we do not appreciate the importance of the condition of insulin resistance (IR) which is perhaps the single most important biological condition across the globe. So it is my argument that the global epidemics of obesity, diabetes, hypertension, gout, and atherogenic dyslipidaemia (high triglycerides, low HDL-C, increased number of small LDL-C particles, and increased triglyceride-rich remnant lipoproteins) and perhaps also cancer and dementia, are really the tip of the iceberg – the markers of an underlying biological predisposition that becomes apparent in those exposed to high carbohydrate diets and then presents as one of more of those conditions.
So it is my thesis that IR is the most prevalent biological condition in the world. It remains hidden as long as diets are not high in sugar and refined carbohydrates. But in the face of a high carbohydrate diet eaten for decades, the IR leads to all the common chronic diseases that we face today. But the problem is that IR is not taught in many medical schools or schools of dietetics and nutrition and this perhaps is the key problem. For if we don’t recognize the single most important factor predisposing to chronic ill health across the globe, then we are not likely ever to be able to cure or reverse those diseases. Especially if the cure is to remove the cause which is a high carbohydrate diet.
Ignoring IR undermines the modern practice of chronic medicine. If all the conditions linked to IR are caused ultimately by high carbohydrate diets – that is by a nutritional factor, as I believe they are, we don’t need medication, and the pharmaceutical industry that is designed to market its drugs to treat those conditions. For these are not conditions caused by the lack of a specific pharmaceutical chemical. They are caused by too many carbohydrates in the diet.
We fuel the fire with carbohydrates, and try to put it out with pharmacologic drugs that do not address the real cause.
Our critics’ views are based on the belief that all humans can metabolise carbohydrates equally. The condition of IR disproves that idea. Instead IR shows that for some even the smallest amounts of carbohydrate eaten for decades are enough to seriously damage our health in the long term.
In Black Holes and Baby Universes and Other Essays, Stephen Hawking says: “People are very reluctant to give up a theory in which they have invested a lot of time. They usually start by questioning the accuracy of the observations. If that fails, they try to modify the theory in an ad hoc manner. Eventually the theory becomes a creaking and ugly edifice.
“Then someone suggests a new theory in which all the awkward observations are explained in an elegant and natural manner.”
At the low-carb, high-fat summit in Cape Town, I believe that’s what we have done. We have exposed the creaking, ugly edifice of conventional wisdom on nutrition, and explained an alternative in an “elegant and natural manner”.

159. Report on the Low Carb Summit in Cape Town

I have just returned from Cape Town where I was attending the first International Summit Low Carb Summit.
This was a unique event hosted by Professor Tim Noakes and organised by Karen Thomson and her colleagues. It is the first time that most of the leading figures in the world from a variety of disciplines and backgrounds came together to share their experience and knowledge. It was a great privilege for me attend and have the opportunity of meeting so many of the people who are making such a huge contribution towards the relief of suffering and improvement in the standards of public health.
In this blog I will discuss and explain the implications of the meeting. If you are interested in a summary of the main points made by the speakers then I recommend the report prepared by Markia Sboros (1).
There is absolutely no doubt that virtually every country is faced with a huge public health issue because of the continued rise in the incidence of obesity. What is of even greater significance is Type 2 Diabetes (T2D) which is not only a very nasty disease in its own right but also an indication that the person concerned has an increased risk of developing many common chronic diseases including heart disease, cancer and Alzheimer’s Disease. There is convincing evidence that this has been caused by the official dietary recommendation to reduce fat, especially saturated fat (SFA) and to increase the complex carbohydrates. Because this advice has been actively promoted by health professionals and the food industry the habitual diet in most countries has altered by reducing the intake of fats, which has effectively been replaced by carbohydrates. If this rationale is accepted then it follows that the way to improve public health is to reverse the changes in diet which have occurred during the past 30-40 years. Essentially this means consuming a diet which is low in carbohydrates and high in the right types of fat (LCHF).
This was precisely the message which came through loud and clear from all the speakers, irrespective of their background or professional expertise. In fact, many of them have been working on their own for years and found it extremely encouraging to meet others who quite independently had reached the same conclusions. They can take great heart from the fact that they have been able to establish a network which will be mutually beneficial and provide the momentum to promote the concepts of LCHF.
Here is a statement issued at the end of the Summit which was endorsed by all the speakers:
“The mainstream dietary advice that we are currently giving to the world has simply not worked. Instead it is the opinion of the speakers at this convention that this incorrect nutritional advice is the immediate cause of the global obesity and diabetes epidemics.

This advice has failed because it completely ignores the history of why and how human nutrition has developed over the past three million years. More importantly, it refuses to acknowledge the presence of insulin resistance (carbohydrate intolerance) as the single most prevalent biological state in modern humans.

Persons with insulin resistance are at an increased risk of developing a wide range of chronic medical conditions if they ingest a high carbohydrate diet for any length of time (decades).” (2).
From my own perspective, the various contributions have made it clear that the basic concepts are really quite clear and simple. Inevitably there are complexities when researching the detailed biochemistry and physiology. By contrast, for theindividual who just wishes to deal with an illness and find out about a healthy life-style, things should be very straight forward. Dr Jason Fung was absolutely categoric: T2D can be cured! Excessive insulin is damaging the internal organs. So it follows inevitably that the first step towards recovery is to reduce the amount of insulin being produced by the pancreas. Therefore it is essential to reduce the intake of sugar and other sources of carbohydrates. Consequently less glucose will enter the blood stream and the requirement for insulin will be reduced. INSULIN SHOULD NOT BE PRESCRIBED! This will only add fuel to the fire and certainly will not cure the patient. How many sufferers of T2D are treated in this way even though there is scientific evidence that this type of treatment does not work. Furthermore, the conventional dietary advice is to reduce fat and INCREASE CARBOHYDRATES, which will make things even worse! This approach is incompetent and irresponsible.
Despite the strong body of research which underpins the rationale for an LCHF diet, the vast majority of health professionals remain firmly committed to disseminating the “old advice” which has been totally discredited. In South Africa, Tim Noakes has been subjected to vituperative attacks which state that he has been making outrageous unproven claims about disease prevention (3). In the final session Tim delivered a devastating response to his critics, which effectively demolished the allegations against him. This is definitely worth reading and it is available here at the next Blog which is 160(4). What I find particularly appalling is the way in which the critics ignore any evidence which supports the case for the LCHF approach and then make unsubstantiated predictions about the risks associated with a LCHF diet, without a shred of evidence in support. The reality is that many of the critics are incapable of assessing the science in a genuinely objective fashion, lack the scientific integrity to admit they have been wrong in the past and feel threatened by the current developments. Nevertheless there can be no excuse for this kind of behaviour. These people must be challenged at every opportunity because while they continue to influence events, patients are being denied life-saving treatments.
The good news is that Tim and his supporters are having considerable success in South Africa. ”The Real Meal Revolution” has been a runaway success having been the best seller for over 20 weeks. This explains the basis for the LCHF diet (also referred to as the Banting diet, following the success of the London undertaker William Banting with weight loss on a diet high in fat) (5). There are many restaurants which are dedicated to serving meals which comply with the LCHF principles. Other restaurants include Banting items on their regular menus. It is clear that the message is getting through to many people and that they are benefitting from it. In the conference Andreas Eenfeldt, the diet doctor, reported on the progress being made in Sweden, where many are adopting LCHF diets. As a consequence, the consumption of butter is back to where it was before people started worrying about their fat intake. This has been accompanied by a slow-down in the rate at which obesity is increasing. At present no information is available on the incidence of T2D. If it can be shown that this is being controlled then this would be very compelling case. Finally Sweden seems to be the one country where the official stance recognises the value of the LCHF diet.
I wish to congratulate all those involved in this initiative in Cape Town. I hope in a few years’ time we can look back on this a major landmark in the efforts to improve public health globally by making changes to the patterns of food consumption.

1. http://www.biznews.com/lchf-health-summit/2015/03/01/marika-sboros-tim-noakes-banting-myth-madness-magic/
2. http://www.nofructose.com/2015/02/24/mission-statement-from-the-first-international-low-carb-high-fat-health-summit-cape-town-2015/
3. http://vernerwheelock.com/?p=565
4. http://vernerwheelock.com/?p=731
5. http://vernerwheelock.com/?p=630

158. Support for Conventional Dietary Guidelines


Despite the recent report (1) by Zoe Harcombe and her team which demolished one of the main planks used to justify the original advice to reduce the saturated fat (SFA), there are still individuals who are not prepared to accept that the conventional dietary guidelines were fundamentally flawed. One of these is Professor Christine Williams, who holds the Hugh Sinclair Chair in Human Nutrition at the University of Reading. In an article in the New Scientist she states that:
“Claims that dietary fat guidelines in the US and UK were not based on good scientific evidence are misguided” (2).
In her view the use of Randomized Controlled Trials (RCTs) are inappropriate for the development of recommendations which are for the population as a whole.
She then attempts to justify the current recommendations on the basis that it has been demonstrated that SFAs increase the level of cholesterol in the blood (TC) based on animal studies, comparisons of health outcomes between countries with differing diets, and long-term observational studies of large numbers of people.
Professor Williams then goes on to argue that because statins have been shown to lower cholesterol and reduce TC, it must follow that this also works for diet.
This is absolutely bizarre since RCTs have been used to do the studies on statins and it certainly cannot be assumed that the diet will have the same effect as the drugs.
But these factors are of little consequence. The fundamental rationale which she uses in defence of the conventional dietary guidelines is as follows:
• TC is a risk factor for heart disease
• SFA increases TC and hence increases the risk of developing heart disease
• Therefore lowering SFA will reduce the risk of heart disease.
The reality is that this is a load of rubbish! Although much of the research on TC has focussed on heart disease, my view is that the critical indicator must be all-cause mortality. I really cannot get excited if I can reduce my chances of suffering from a heart attack but that comes with a cost of an increase in the risks of dying from cancer. If TC is an accurate reflection of the risks of heart disease then those with low values must have a lower death rate than those with higher values. It so happens this information has been provided in a major study conducted in Norway, in which 52,087 men and women aged 20-74 years were followed over a 10-year period (3). TC levels were measured and details of any deaths which occurred were recorded. In both men and women there was no statistically significant increase in the risk of death at higher TC levels (Table 1). Individuals with a TC of 7.0 mmol/L or higher were no more likely to die of cardiovascular disease than those with levels below 5.0 mmol/L.
In men, there was no increase in the all-cause mortality with raised TC. Those with a TC level between 5.0 and 5.9 mmol/L had the lowest death rate, which was 23% lower than those with a TC below 5.0 mmol/L.
For women the pattern is different. The higher the TC, the lower the risk of dying from all causes. Compared with those with a TC below 5.0 mmol/L, those with the highest TC levels were 28% less likely to die from all causes.


                                                 Hazard ratio
TC, Mmol/L (mg/100ml) Men Women
  All-cause CVD All-cause CVD
<5.0          (<194) 1.00 1.00 1.00 1.00
5.0-5.9     (194-228) 0.77 0.80 0.92 0.90
6.0-6.9     (232-267) 0.84 0.87 0.84 0.81
>7.0          (>270) 0.98 1.05 0.72 0.74

This detailed break-down shows that as expected most deaths occur after the age of 60 years (Tables 2 and 3). Although the optimum TC level for men aged 60-69 is in TC range 5.0 to 5.9 mmol/L, for those over 70 the lowest death rate is in the higher TC level of 6.0 to 6.9 mmol/L. For women it is very clear that the death rate for the over 60s decreases as the TC increases. For this age range it is evident that the highest death rates are for those with a TC level which is below 5.9 mmol/L. The relatively high death rates for those aged 60+ years at low TC values should also be noted (4).


                               (TC LEVELS, mmol/L(mg/100ml)
MEN, ages <5.0(<194) 5.0-5.9(194-228) 6.0-6.9(232-267) >7.0(>270)
20-29 1.10 0.38 0.30 0.00
30-39 0.80 0.57 0.72 0.47
40-49 2.22 1.38 2.27 3.37
50-59 4.54 4.93 6.22 5.74
60-69 20.31 16.20 17.37 18.47
70-74 49.18 40.37 37.93 41.25



(TC LEVELS, mmol/L(mg/100ml)

Women, ages        
20-29 0.35 0.30 0.24 0.60
30-39 0.31 0.43 0.82 0.69
40-49 0.89 1.85 1.69 1.12
50-59 2.95 3.59 3.53 3.79
60-69 22.31 10.32 10.47 9.51
69-74 31.46 22.50 21.58 19.23


The authors commented as follows:‘’If our findings are generalizable, clinical and public health recommendations regarding the ‘dangers’ of cholesterol should be revised. This is especially true for women, for whom moderately elevated cholesterol (by current standards) may prove to be not only harmless but beneficial.’’They went on to conclude:‘’Our results contradict the guidelines’ well-established demarcation line (5 mmol /L) between‘good’ and ‘too high’ levels of cholesterol. They also contradict the popularized idea of a positive, linear relationship between cholesterol and fatal disease. Guideline-based advice regarding CVD prevention may thus be outdated and misleading, particularly regarding many women who have cholesterol levels in the range of 5–7 mmol/Litre and are currently encouraged to take better care of their health’’(4).
In my experience, I have yet to find anyone who is made aware of these results who would wish to lower their TC.
There are lots of other studies which confirm that TC or even the so-called “bad” LDL Cholesterol levels are poor indicators of the risks of developing heart disease (5). It is also highly relevant that in the Lyon Heart Study there was a 74% reduction in the death rates of those on the “healthier diet” but the TC levels were virtually identical in the controls and the treatment groups (6). In a comparison between Belfast and Toulouse, it was found that although the TC levels were the same in both cities, the CVD death rate in Belfast was 4 times that of Toulouse (7).One final point about statins which is highly relevant. According to NICE, 77 people with heart disease have to be treated with statins for 3 years for one to benefit (8). However for those who did not have previous heart trouble, who are the target for the dietary guidelines
• None were helped (life saved)
• 1 in 104 were helped (preventing heart attack)
• 1 in 154 were helped (preventing stroke).
On the other hand
• 1 in 50 were harmed (develop T2D)
• 1 in 10 were harmed (muscle damage) (9).
If we accept that the statin argument has some merit, the benefits to be expected are negligible. Statins may well do more harm than good.
It will be clear that case presented by Professor Williams lacks any kind of credibility. If we are to make progress then it is vital that these bogus defences of the status quo are exposed so that the authorities are forced to recognize the fundamental flaws in the current official advice. How many more people will have to suffer and die prematurely before reason prevails?

1. http://www.bmj.com/content/347/bmj.f6340
2. http://www.newscientist.com/article/dn26949-official-diet-advice-on-fat-stands-despite-new-study.html#.VN3V_mezVy1
3. H Petursson et al (2012). Journal of Evaluation in Clinical Practice 18 (1) pp 159-168
4. H Petursson et al (2012). Journal of Evaluation in Clinical Practice 18 (1) pp 170-171
5. http://vernerwheelock.com/?p=105
6. http://vernerwheelock.com/?p=259
7. http://vernerwheelock.com/?p=256
8. http://vernerwheelock.com/?p=503
9. http://www.thennt.com/nnt/statins-for-heart-disease-prevention-without-prior-heart-disease/





157. Could this be the breakthrough?

A paper entitled:
“Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis” by Zoe Harcombe and colleagues has been picked up by the press in a big way (1). Here are some examples of the headlines:
• Daily Express:
“FAT is the key to living longer: Previous diet advice was WRONG, say experts” (2)
• The Times:
“Saturated fat diet advice not backed by evidence” (3)
• Guardian:
“Fat guidelines lacked any solid scientific evidence, study concludes” (4)
• Irish Times:
“Advice to cut intake of fat and saturated fat ‘wrong’” (5).

The research paper has taken the data from those reliable trials which were available prior to the development of the dietary recommendations to reduce saturated fat (SFA). There were only 6 studies which looked at the relationship between dietary fat, serum cholesterol, and the development of coronary heart disease that were considered to be satisfactory. And all but one focused on secondary rather than primary prevention. The pooled data revealed a total of 740 deaths from all causes, and 423 from coronary heart disease. There was no difference in deaths from all causes between the ‘treatment’ and comparison groups, with 370 deaths in both. And there was no significant difference in deaths from coronary heart disease, with 207 in the ‘treatment’ groups and 216 in the comparison groups. Although there was a reduction in the levels of blood cholesterol (TC) in the treatments groups with reduced intake of SFA this not associated with corresponding reduction in deaths. As all the participants were men, it follows that there was absolutely no information for women.
So the reality is that there was absolutely no justification in 1984 for the official Committee on Medical Aspects of Food Policy (COMA) to recommend that the SFA intake should be reduced from 20% of food energy to 15% as part of a strategy to reduce cardiovascular disease (6). As it happens this target was reached by 2000 (7). Currently the amount of SFA in the British diet is 12.7% of energy. Over this period the incidence of obesity has continued to increase. In men it has doubled since 1993, which is when detailed information was first collected (8). What is especially disturbing is that since 1994 the incidence of diabetes has more than doubled for both men and women (9). It is quite obvious that the expected results have not materialised and that the standard of public health have deteriorated.
These results will come as no surprise to anyone who has taken the trouble to review the evidence or to read any of the books written by independent researchers/journalists such as Gary Taubes, Barry Groves, John Briffa, Zoe Harcombe, Malcolm Kendrick or Nina Teicholz.
Publishing this report in a prestigious journal which has open access may prove to be a master stroke as it has clearly been picked up by the press and is certainly having an impact. But what is disturbing, but not surprising, is the response from the establishment. Here are a few examples:
• Dr Rahul Bahl in an editorial in the same issue of BMJ Openheart claims that:
“Epidemiological and ecological evidence suggests a link between fat consumption and heart disease. The seven countries cohort study by Keys referred to by the authors did find that higher serum cholesterol tended to be related to coronary heart disease incidence and that higher saturated fat consumption tended to be related coronary heart disease incidence. These findings were consistent in long-term follow-up” (10).
Nutritional policy has had numerous failures due to the reliance on epidemiological evidence which by itself cannot provide sound evidence on the relationship between diet and health/illness. It is outrageous that anyone can rely on this study by Keys which has been totally discredited (11).
• Dr Alison Tedstone, chief nutritionist at Public Health England, said:
“This paper is not critical of current advice on saturated fats but suggests the advice was introduced prematurely in the 1980s.” (12).
This really is being disingenuous. We just cannot get away from the facts that there was no reliable basis for the introduction of the recommendation to reduce SFA in the first place, that it has not worked and that no studies have provided any justification in the meantime.
• Victoria Taylor, senior dietician at the British Heart Foundation (BHF), said
“Understanding the true relationship between diet and our health is not simple. It would be all but impossible to carry out a research trial where you controlled the diets of thousands of people over many years. We continue to recommend switching saturated fat for unsaturated fat.” (13).
This position is simply untenable. There is very convincing evidence that many of the individual SFAs are actually important nutrients in their own right (14). Furthermore there is simply no case for increasing the intake of the polyunsaturated fats (PUFA) because this will increase the requirements for the omega-3 fatty acids and will probably also have deleterious effects such as increasing the risks of inflammation (15). It is rather ironic that the BHF commissioned research on SFA which concluded that there is not enough evidence to support the current dietary recommendations to reduce SFA and increase PUFA in order to reduce the risk of heart disease (16). Despite this the organisation could not resist putting their own spin on the research by making this statement on their website:
“We know there are good biological reasons for encouraging a Mediterranean-style diet, where we eat more unsaturated than saturated fat, that lower our levels of ‘bad’ LDL cholesterol” (17).
Surely the position adopted by the BHF has nothing to do with the support it receives from the manufacturers of Flora which is promoted on the grounds that it will “reduce cholesterol”? (18).
The fundamental problem is that when the dietary guidelines were first devised, the decision to recommend that the fat and the SFA in particular should be reduced was wrong! The focus of attention should have been on sugar and the refined carbohydrates. As a consequence the SFA intake has fallen and there has been a corresponding increase in the intake of sugar and carbohydrates. This is primarily why public health is deteriorating as shown by the rise in obesity and diabetes. The only way to address the issue is to reverse the current trends. Although there is growing recognition of the dangers of sugar, there will be little progress until it is accepted that SFA is a crucial nutrient and that it is actually beneficial to increase it.
Hence it is absolutely appalling that so many of the “great and the good” in the medical and public health professions continue to try to put forward rather pathetic justifications to support the official advice even though it cannot be substantiated. To persist in the light of the evidence is completely irresponsible because it is condemning a huge number of people to a life of misery and early death. It is about time these “deniers” faced up to reality and have the intellectual honesty to admit that they have been wrong. Surely that is the least we can expect?
Finally, congratulations to Zoe and her colleagues for a wonderful initiative. Let’s hope this triggers the breakthrough many of us have been anticipating!

1. http://openheart.bmj.com/content/2/1/e000196.full.pdf+html
2. http://www.express.co.uk/life-style/health/557220/Avoid-low-fat-products-packed-sugar-eat-natural-fat-instead
3. http://www.thetimes.co.uk/tto/health/news/article4349211.ece
4. http://www.theguardian.com/lifeandstyle/2015/feb/10/fat-guidelines-lacked-any-solid-scientific-evidence-study-concludes
5. http://www.irishtimes.com/news/health/advice-to-cut-intake-of-fat-and-saturated-fat-wrong-1.2096666
6. Department of Health and Social Security (1984) “Diet and Cardiovascular Disease” London: HMSO
7. http://webarchive.nationalarchives.gov.uk/20130103014432/http://www.defra.gov.uk
8. Health Survey of England 2010 Adult Trend Tables
9. Health Survey for England 2009
10. http://openheart.bmj.com/content/2/1/e000229.full
11. http://vernerwheelock.com/?p=554
12. http://www.express.co.uk/life-style/health/557220/Avoid-low-fat-products-packed-sugar-eat-natural-fat-instead
13. http://www.independent.co.uk/life-style/health-and-families/health-news/dietary-advice-from-the-1970s-found-to-be-a-big-fat-mistake-10034786.html
14. http://vernerwheelock.com/?p=155
15. http://vernerwheelock.com/?p=370
16. http://vernerwheelock.com/?p=381
17. https://www.bhf.org.uk/media/news-from-the-bhf/fats-in-your-diet.aspx
18. http://www.zoeharcombe.com/2013/01/the-british-heart-foundation-flora-pro-activ-an-unhealthy-relationship/

156. Yorkshire Food Revolution

Reducing the risk of heart disease, diabetes and obesity
There is a wide variety of high quality foods produced in Yorkshire, especially meat and meat products as well as butter, cheese, cream and yoghurts which are based on milk from cattle and sheep. Unfortunately many of these are regarded as “unhealthy” because they usually contain saturated fat (SFA). According to the official dietary recommendations SFA is a risk factor for heart disease and so we are advised to limit the amount we eat. The Government has a Responsibility Deal with the food manufacturers and retailers which puts pressure on the industry to reduce the SFA in the food chain. This is encouraging food companies to remove SF from existing products in order to devise “low fat” versions.
During the past few years the rationale used to justify the advice to reduce SFA has come under intensive scrutiny and it is now abundantly clear that it is fundamentally flawed. The reality is that SFA does not represent a threat to health: in fact, certain individual saturated fats are actually important nutrients in their own right! By contrast, it is the sugars and refined carbohydrates which should be the cause for concern. During the past 15 years the incidence of Type 2 Diabetes (T2D) has doubled. Those with T2D have an increased risk of heart disease. Essentially T2D is excess sugar (glucose) in the blood. This is caused by consuming too much sugar and carbohydrate-rich foods like potatoes, rice, bread and pasta which contain starch. These are broken down during digestion to produce glucose which is absorbed into the blood and if there is an overload the result is T2D. Furthermore, soft drinks including fruit juices invariably contain a high content of sugar. In addition, sugar is present in many processed foods. Despite the protests from the vested interests, there is little doubt that current poor standard of public health as shown by the figures for T2D and obesity is primarily because of the high content of sugar and carbohydrates in the typical diet.
It is somewhat ironic that many shoppers choose the “low fat” variants believing them to be healthy. Regrettably this is not the case. By removing the fat a valuable source of nutrients is lost. As the fat is often replaced by sugar the consumer suffers a double whammy!
Although the Government is still pushing a discredited policy, a growing number of consumers recognise that the way forward is to reduce the carbohydrates and increase the amount of fat in the diet. More and more people are finding out for themselves that this actually works and makes them feel better. There is convincing evidence that this type of diet improves health for most people. With respect to weight loss, the effect is noticeable within a matter of weeks. There are literally hundreds of personal case histories on the internet from individuals who have overcome T2D. Many of them have been able to stop using drugs completely
All of this is great news for many Yorkshire food producers. What it means is that foods which have been branded as “unhealthy” should now be regarded as “healthy”. However the most significant development is that even though the Government persists with policies which are doing more harm than good, the message is being picked up by more and more ordinary consumers. This represents a huge opportunity for all those producers of specialised foods here in Yorkshire.
There is no doubt that the time is ripe and things could really explode any time. This has already happened in South Africa. Professor Tim Noakes of the University of Cape Town and colleagues have written a book on this precise issue entitled “The Real Meal Revolution” which has been a phenomenal success. Initially 3,000 copies were printed but it has already sold over 120,000 and has been top of the best seller list for over 20 weeks. Restaurants have devised menus which are in line with the new thinking and are trading extremely well.
Here in Skipton, Malcolm Weaving of The Rendezvous and the Craven Branch of the Federation of Small Businesses have co-operated to organise an event which focused on these exciting concepts. It was held at The Rendezvous on Friday 30th January 2015. The format consisted of:
• A tasting menu of 7 different courses all designed and prepared from ingredients sourced in Yorkshire wherever possible and selected to fit in with the latest thinking on Healthy Eating
• After each course Chris Wildman of the Town End Farm shop described the provenance of the ingredients, the procedures applied to ensure that quality standards are maintained and how the foods can be sourced
• Finally Verner Wheelock, Chairman of Verner Wheelock Associates, specialists in nutrition and food safety training and consultancy to the food industry, discussed the basic principles which underpin these new ideas and how they can be put into practice.
This event was attended by almost 70 people who hopefully now appreciate how it is possible to improve the nutritional quality of the diet by consuming foods that are not only tasty and good to eat but are also produced to the highest ethical standards in the glorious Yorkshire country

155. What Happens to the Cholesterol when the Dietary Fat is Altered?

The official dietary recommendations continue to advise a reduction in saturated fat (SFA) and an increase in the polyunsaturated fat (PUFA). The justification is that the SFA will reduce the Blood cholesterol (TC) and therefore lower the risk of developing heart disease. The same rationale is used to justify the advice to increase the intake of PUFA, which should also reduce the TC. It is therefore relevant to consider the results of some studies which investigate the effects of changes in the dietary fat on the TC.
Way back in the 1960s members of the Anti-Coronary Club in New York volunteered to participate in a trial (1). A total of 814 men aged between 40 and 59 years old were placed on the “Prudent Diet” which involved a very substantial reduction in their intake of animal fat, which is rich in SFA, and a corresponding increase in that of PUFA. A separate group of 463 men which carried on as normal was used as the control for comparison.
In this investigation there is no question that the TC was lowered. However there were 9 deaths due to heart disease in those on the Prudent Diet but not a single death in the control group. Even more worrying was the fact that the total mortality was about 2.5 times greater in those consuming the “healthier” diet!
A trial conducted in London under the auspices of the MRC investigated the effect of a cholesterol-lowering diet diet in the prevention of relapse in men aged under 60 years recently recovered from their first myocardial infarction. 199 men recently discharged from hospital were randomly allocated to the experimental group were given a diet low in saturated fats and containing 85 gm of soya-bean oil daily. There was a control group of 194 men who consumed their usual diet. All of them participated for at least 2 years but some continued for over 6 years. Those in the experimental group lowered the TC from a mean initial figure of 272 to 213 mg. per 100 ml. at six months (22% fall). The level in the controls fell from 273 to 259 mg. per 100 ml. (6% fall). Suspected relapses were assessed at regular intervals by a review committee unaware of the patient’s diet group.
Although there were 45 major relapses in the test group and 51 in the controls, those which resulted in death were 25 in each. It was concluded that relapses were not related to initial TC level, to change in cholesterol level during the trial, nor, in any consistent way, to observance of the dietary regimen (2).

The Sydney Diet Heart Study (SDHS), conducted between 1966 and 1973 was a randomized control trial in which the intervention group was advised to replace the SFA with safflower oil. It is an excellent opportunity to study the impact of increasing the PUFA. In the original report, deaths due to cardiovascular disease and coronary heart disease were not shown. In an analysis of the data conducted recently by Chris Ramsden and colleagues it has been possible to gain insight into the effects of the different types of fats (3).
The participants were 458 men aged 30-59 years at the outset who had experienced a coronary event shortly before the commencement of the trial.
The intervention group received instructions to increase their PUFA intake to about 15% of food energy, and to reduce their intake of SFA to less than 10% of food energy. To achieve this target, intervention participants were provided with liquid safflower oil and safflower oil polyunsaturated margarine. The control group received no specific dietary instruction. However, some participants began replacing butter with margarine if they had suffered a coronary event.
The results show that the PUFA content of the diet in the intervention group more than doubled and the SFA content was reduced to below 10% of total energy. Compared with the control group, the intervention group had an increased risk of all-cause mortality (17.6% v 11.8%; hazard ratio 1.62). The corresponding values for cardiovascular mortality (17.2% v 11.0%; 1.70) and for coronary heart disease), and mortality from coronary heart disease (16.3% v10.1%; 1.74) were similar. This study demonstrates that selectively increasing PUFA resulted in an increase in rates of death from cardiovascular disease, coronary heart disease, and all-cause mortality compared with a control diet rich in SFA from animal fats and common margarines. This investigation must be regarded as highly relevant because the changes are precisely those which are being recommended by the authorities in the UK and in most of the world. It is obvious that the favourable results confidently predicted have not materialized.
It is also important to note that although there was a decline in the TC levels of both groups it was much greater in the intervention group. This provides further confirmation that lowering TC does not result in a corresponding reduction in the coronary death rate.

Although the TC levels in both groups fell but the decline was much greater in the intervention group than it was in the control group. The cholesterol theory predicts that the death rate attributed to heart disease would be therefore be less than in the control group. In reality it was 70% GREATER than in the control group and only slightly less for all-cause mortality. This is further evidence that the benefits which have been claimed for lowering cholesterol simply do not materialize in the real world.
The case for reducing SFA and increasing PUFA is full of holes as far as the impact on the blood cholesterol levels are concerned. When researchers have attempted to confirm it, they have failed totally. Although the TC has been lowered successfully there certainly has not been the improvement in health so confidently predicted by those who formulate and implement the current policies. Despite this the advice from the NHS and health professionals here in the UK and in most other countries continues to emphasise the importance of limiting the intake of SFA. Furthermore there are many products on the market which are actively promoted on the grounds that that they are high in PUFAs and will therefore “lower cholesterol”!


1. G Christakis et al (1966) Journal of the American Medical Association 198 (6) pp 597-604
2. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(68)90746-0/abstract
3. C E Ramsden et al (2013) British Medical Journal 346:e8707

154. The Acidity of the Body

These days we are given all sorts of advice on healthy eating. There is much controversy about what actually constitutes a healthy diet. Readers of these blogs will know that there are many criticisms of the current official recommendations. There is a convincing case that complying with these will do more harm than good. Furthermore there is considerable variation in how individuals respond to a particular diet. Therefore it would be very helpful if there was a simple test which would enable people to assess their progress towards achieving good health.
In fact there is evidence which indicates that this can be done by monitoring the pH, which is a measure of the acidity/alkalinity of the body. The pH is a log scale with the range from 0 to 14. Low values are acid and high values are alkaline. A value of 7 is neutral (neither acid nor alkaline). The body pH can be measured using litmus strips on a sample of saliva or urine. The optimum value is about 7.5 which is slightly alkaline. The strips are readily available and inexpensive. It is quite easy for individuals to check their own pH themselves.
Metabolic syndrome (MetS) is defined as a condition characterised by a number of metabolic features including low HDL Cholesterol, raised triglycerides, hypertension, obesity and insulin resistance. These are invariably associated with common chronic diseases such as diabetes, heart disease, various cancers and all-cause mortality. In a recent study with 148 participants it was found that as the number of MetS features increased the pH of the urine decreased progressively. For those with no features the pH was 6.15 but for those with 4 features it had fallen to 5.7 (1).
In a recent European study a total of 66,484 women were followed for 14 years. During this period there were 1,372 cases of type 2 diabetes (T2D). It was found that those with a high acid-forming potential had a much higher incidence of T2D than those with a low value. Interestingly the difference was greater for those with a “normal” Body Mass Index (BMI) than for those who were “overweight“ with a BMI >25 (2). This was the first time that a large prospective study has demonstrated that the dietary acid load was positively associated with T2D risk, independently of other known risk factors,
Other studies have shown that the incidence of T2D is higher in people with a low pH in their urine when compared with those who have a higher urinary pH. The low pH was associated with the uric acid and the presence of stones in the urine. It was found that this condition was prevalent in patients with glucose intolerance and T2D (3).
The famous German Nobel Prize winner, Otto Warburg, discovered that there is only one cause for cancer which is the replacement of the respiration of oxygen in normal body cells by the fermentation of sugar. All normal body cells meet their energy needs by the respiration of oxygen but cancer cells depend on sugar as a source of energy for the fermentation process. Because of this crucial difference between cancer and normal cells, this knowledge can be utilised to devise methods of curing the disease. Protocols which deprive the body of sugar are proving to be effective in this context. Furthermore the fermentation causes the immediate environment of cancer cells to become acidic and therefore reduce the pH below the optimum value of 7.4.
In a highly significant investigation it was noted that the pH range of tumours in mice was between 6.5 and 6.9 (compared with 7.2-7.5 for normal tissue). When the pH was raised by treatment with sodium bicarbonate (baking soda) this resulted in significant reductions in the number and size of metastases to the lungs, intestine and diaphragm (5). The tumours used were models for breast and prostate cancer in humans. This is a practice which has been used successfully for the treatment of various forms of cancer.
Consequently there is considerable interest in understanding the relationship between various foods and their impact on the pH. Various attempts have been made to determine the impact of different foods on the pH of the body.
Chris Woollams has spent years developing his Canceractive website which contains an enormous amount of reliable information which relates to the prevention and curing of cancers. People diagnosed with cancer invariably have an acidic pH and there are strong indications that the consumption of a high proportion on of foods which are known to be alkaline can help to prevent and even cure cancer (6).
These include:
Beetroot, Cabbage, Carrots, Cauliflower, Celery, Cucumber, Fresh green beans, Lettuce
Mushrooms, Parsnips, Potatoes, Spinach, Swede, Watercress
Fresh fruits
Apple, Avocado, Blackberries, Blackcurrants, Cherries, Grapes, Lemons
Olives, Pears, Olives, Raspberries
Fresh ginger, Fresh juices, Green tea, Olive oil, Seeds
By contrast, here are some of the foods which are acidic producers:
Brussel sprouts, Lentils, Peanuts, Rhubarb, Tomatoes
Bananas, Grapefruit, Oranges, Plum, Prunes
All alcohol, Coffee, Fizzy drinks, Sauce, Sugar, Sweets

The above list is certainly not meant to be comprehensive and the degree to which individual foods can exercise their effect on the pH does vary and of course will be influenced by the amount consumed.
For those whose pH levels are in the acidic range it should be possible to raise it into the alkaline range by making adjustments to the diet. The alkaline-producing foods should be reduced at the expense of the acid-producing ones. However it is critical to understand that it is the balance that is important. While there are some acid-producing foods which should be kept to a minimum such as fizzy drinks and sugar, there are others such as Brussel sprouts and tomatoes which should be include in a healthy diet. The above information is simply a guide which hopefully will enable a person to try out different possibilities and discover what actually works and what is feasible.
The significant advantage of the pH is that it provides a means by which anyone can monitor their progress in response to dietary adjustments. As things stand at present we do not have absolute proof that the rationale is sound but it is certainly worth trying. There is no suggestion that attempting to alter the pH by dietary means will cause any possible harm. On the face of it, pH should be a routine check as already applies to body temperature or blood pressure. It would be extremely valuable if the research could be instigated which would explore how this could be achieved.

1. N M Malouf et al (2007) Clinical Journal of the American Society of Nephrology 2 (5) pp883-888
2. G Fagherazzi et al (2013) Diabetologia doi:10.1007/s00125-013-3100-0
3. K Sakhaee et al (2002) Kidney International 62 (3) pp 971-979
4. http://www.healingcancernaturally.com/warburgcancer-cause-prevention.html
5. I F Robey et al (2009) Cancer Research 69 (6) pp 2260-2268
6. http://www.canceractive.com/cancer-active-page-link.aspx?n=978


153. Public Accounts Committee Report on Tamiflu and Publication of Drug Evaluation Results

A report from the House of Commons Public Accounts Committee concludes that information is routinely withheld from doctors and researchers about the methods and results of clinical trials on treatments currently prescribed in the United Kingdom (1). Invariably the bodies responsible for the approval of new drugs only have access to the results of studies which present the drug under investigation in a positive light which those which do not as well as those which show no benefit or even undesirable effects may never be revealed. Essentially this means that the regulatory authorities do not have the total picture which is needed if sound decisions regarding approval for usage are to be made. Although this problem has been recognised for many years there has been a failure on the part of government, industry and the professional bodies to take the necessary action to deal with it. It was recommended that the full methods and results are available to doctors and researchers for all trials on all uses of all treatments currently being prescribed.

The report considered what happened with Tamiflu, which had been stockpiled between 2006-07 and 2012-13, on the basis that it would be needed in the event of a pandemic of influenza. During this time the Department of Health spent £560 on antiviral medicines, of which £424 was for Tamiflu and £136 for Relenza. Valuable insight into the background to this policy can be gained from some of the evidence presented to the Committee by Ben Goldacre author of “Bad Pharma” and Fiona Godlee, editor-in-chief of the British Medical Journal.

With respect to Tamiflu, Fiona referred to the work of a team at the Cochrane Commission led by Tom Jefferson who discovered that there had been about 123 trials conducted on Tamiflu and that the pharmaceutical company Roche was aware of 74 completed trials. Of those, it appears that the European Medicines Agency (EMA) had access to only 15 incomplete accounts. In the UK, the National Institute for Health and Care Excellence (NICE) had received 4incomplete accounts of trials.

She described those involved in Cochrane Commission reviews as

“slightly obsessive and very scientifically determined people”

While it might be expected that the regulatory bodies would require all the evidence to be provided for evaluation in practice according to Fiona they do not ask for it even though they are entitled to have it. Because they are under-resourced and stretched they tend to take the manufacturer’s word for it. By contrast, in Germany, manufacturers have a legal obligation to provide the Institute for Quality and Efficiency in Healthcare (IQWIG), which performs a similar role to NICE, with a full list of clinical trials and supporting clinical study reports.
In a letter to the Chair of NICE, Sir Michael Rawlins, Fiona described the response from IQWIG when it discovered that had not been provided with all the relevant data on reboxitine, a drug produced by Pfizer(2). The company was told it would only approve the drug for reimbursement if all the results were made available to the Institute. The full dataset showed that the drug was ineffective and possibly harmful. This illustrates very effectively how the regulatory bodies can actually be misled and in reality manipulated by the drug companies.
The report implied that those responsible for the expenditure involved in stockpiling the Tamiflu did not have the evidence which clearly demonstrated the efficacy of the drug, especially in the light of the Cochrane report cited above. Hence it is particularly relevant that when the Chief Medical Officer, Dame Sally Davies, was presenting evidence to the Committee she attempted to cast doubts on the credibility of the Cochrane conclusions. In particular she claimed that the Cochrane group

“extracted data from 25 studies but excluded 43 and took no data from published studies.”

The reply to this comment included the following points:
• Not all the trials on conducted on Tamiflu, produced by Roche had been published in the scientific literature
• Not all of those published have been totally accurate. The original results are contained in “Clinical Study Reports” which are extremely detailed and comprehensive. The experience of the Cochrane group has provided examples of discrepancies between the information in these Clinical reports and what appeared in the scientific paper. The group cited 2 examples which stated that:
“there were no drug related serious adverse events”
“No serious adverse events were noted in the major trials and no significant changes were noted in laboratory parameters”

However, the equivalent clinical study reports for these two trials describe 10 serious adverse events (in nine participants), some of which were classified as “possibly” related to Tamiflu. They also discovered many of the authors of the scientific papers had not actually seen the raw data. At least one paper had been ghost written.
As a consequence the team decided that there were serious doubts about the reliability of the scientific papers from Roche and that they should restrict their analyses to the original Clinical Study Reports, a strategy which seems entirely reasonable
• There was one study, which was the largest treatment trial of Tamiflu, where the only published information was a 300-word abstract of a conference presentation. The author, Professor Treanor did not participate in the original study and admitted on Channel 4 News that he could not even remember presenting it at a conference in 2000
• Hence it was not correct for Dame Sally to conclude that 42 studies had been excluded. The position was that for 42 studies it was possible to obtain sufficient information to determine their suitability for further assessment and analysis in the review… a very different context

The work of the Cochrane team was fraught with difficulties and in some cases the information was only released in response to Freedom of Information requests and even then there was great reluctance to provide it. The claims of the regulators that they had all the information needed to make sound decisions just do not stand up to rigorous examination.
There is absolutely no reason to doubt the Cochrane conclusion its review has had access to the most extensive data set ever used in these particular drug types and therefore provides a transparent assessment. Consequently it has not been possible to draw conclusions about its effect on complications or transmission. Accepting that it is incomplete at this stage, it is certainly the best that has been produced so far and must carry mush more weight than anything from the regulators who have not had access to such comprehensive evidence.
The Government and the officials in the Department of Health would do well to take note of the Public Accounts Committee Report.

1. http://www.canceractive.com/cancer-active-page-link.aspx?n=978
2. http://www.bmj.com/tamiflu/nice