109. Cochrane Collaboration Evaluates Statins for Primary Prevention of Heart Disease

The Cochrane Collaboration has established a unique reputation for the publication of reports on a variety of topics in the medical field. This is an area where there are very powerful vested interests and the quality of much of the research is questionable. Therefore the contribution of the Collaboration has proved to be extremely valuable with respect to decisions on treatment and policy formulation.

In recent years the Collaboration has produced two reports which focus on the use of statins for the primary prevention of heart disease. In the first one it was concluded that caution should be taken in prescribing statins for primary prevention among people at low cardiovascular risk (1). However in the second on e published 2 years later, the conclusion was that the totality of evidence now supports the benefits of statins for primary prevention(2). In this blog I will attempt to discover why and how there has been such a radical shift in position.

At the outset I should emphasise, that I consider the critical information to assess the value of these drugs is all-cause mortality. First of all, there can be no argument about the validity of the “diagnosis”. Secondly, this is what most patients will wish to know. It not much comfort if a reduction in the risks of death from heart disease is counterbalanced by an increased risk of dying from another disease. It is also important to have reliable information on adverse side-effects. Many patients are likely to question the value of an extra few months on this earth if the quality of life is made miserable by the drugs.

The first report which was released in January 2013 included research up to September 2007. This was based on 14 trials (with 16 trial arms) involving 34,272 participants. The mean age of the participants was 57 years (age range 28-50), 65.0% were male. However data on all-cause mortality was only provided in 8 trials. Furthermore in 2 trials which accounted for over one quarter of the participants were stopped prematurely.

The report noted that all but one of the trials had some form of pharmaceutical industry sponsorship. Research has shown that the results of trials sponsored by the pharmaceutical industry- are more likely than non-industry-sponsored trials to report results and conclusions that favour drug over placebo because of biased reporting and/or interpretation of trial results (3). As a consequence:

“In primary prevention where world-wide the numbers of patients eligible for treatment are massive, there might be motivations to use composite outcomes and early stopping to get results that clearly support intervention.”

The authors concluded that the review:

highlights the shortcomings in the published trials of statins for primary prevention. Selective reporting and inclusion of people with cardiovascular disease in many of the trials included in previous reviews of their role in primary prevention make the evidence impossible to disentangle without individual patient data. In people at high risk of cardiovascular events due to their risk factor profile (i.e. 20+% 10-year risk), it is likely that the benefits of statins are greater than potential short term harms although long-term effects (over decades) remain unknown. Caution should be taken in prescribing statins for primary prevention among people at low cardiovascular risk.”

As soon as the report was published, there was an objection from Rory Collins and Colin Baigent of the Cholesterol Treatment Trialists’ (CTT) Collaboration at the University of Oxford. Their concern was the report had stated that the CTT collaborators had not published information about the proportional and absolute benefits of statin therapy among people with no prior history of vascular disease. They referred specifically to a paper published in The Lancet in 2010.They also objected to a statement in the press release announcing the release of the report which was as follows:

Given that low cholesterol has been shown to increase the risk of death from other causes, statins may do more harm than good in some patients”.

In reply the lead author Shah Ebrahim pointed out that the CTT Lancet paper of 2010 was not available at the time the review was completed. However he insisted that the estimate of the effects of lowering LDL cholesterol with respect to major vascular events, contained in the review, was similar to that of the CTT. He also re-iterated his surprise that the CTT did not provide more information on other outcomes among participants taking statins for primary prevention. He drew attention that others have raised the issue of all-cause mortality in primary prevention trials (4) and that there are particular concerns about increased risk of diabetes in people who take statins (5).

With respect to the press release, the point was accepted and a correction was issued.

Now we come to the second report which was published in January 2013 (2). This included research which was published up to the beginning of January 2012 and was based on 18 trials (with 19 trail arms) with 56,934 participants. The mean age was 57 years and 60.3% were men.

Thirteen trials with 48,060 participants recruited reported on total mortality. In the statin group 1077 out of 24,408 people died (4.4%) whereas in the control group there were 1223 deaths out of 23,652 (5.1%). This translates into an Numbers Needed to Treat (NNT) of 96 which means that 96 people have to be treated for 5 years for one to benefit. Furthermore it is crucial to appreciate that this means 96 people have to be treated for 5 years for one to benefit.

There was a reduction in various end-points related to cardiovascular disease (CVD) which were associated with falls in total cholesterol (TC) and LDL cholesterol in trials which reported these outcomes. The review concluded that adverse side-effects were not excessive although not all trials reported these fully. . Patients’ perception of quality of life was reported in only one trial and this showed limited benefit.

It is also interesting to note that in this report it was stated that:

“there was low risk of bias ….though all trials were either fully or partially funded by pharmaceutical companies”

What is especially noteworthy is that this review makes detailed reference to the work of the CTT.

In particular:

  • The CTT Collaboration has published analyses focusing on the comparison between high and low doses of statins which demonstrate that more intensive treatment lowers LDL cholesterol more, resulting in greater benefits with no excess risk of non-vascular mortality (6).
  • Strong evidence of the absence of any adverse effects on cancer risk is also confirmed by a further CTT Collaboration report (7).
  • The Cochrane estimates of the effects on all-cause mortality are in agreement with those of the CTT (8). Although it does accept that there is an increased risk of myopathy and rhabdomyolysis in those treated with statins especially in those treated with high (9). These benefits equate to an NNT of 167 for people with a <5% five year risk for heart disease and 67 for those with a 5-10% risk. This means that for those with the lower risk 167 people have to be treated for 5 years for one to benefit and 67 for those with the higher risk

The final conclusion is that benefits of statins outweigh any serious adverse effects. Hence earlier claims that statins provide no overall benefit in primary prevention in terms of all-cause mortality can no longer be substantiated.

This represents an about turn in the space of 2 years. Here are a few comments which I believe are worth addressing if you are mystified by this complete reversal in the position reached by the Cochrane authors.

It is evident that the research from the CTT has been highly influential with the authors when coming to their final conclusion. I just wonder if they were aware of the criticisms of the work of the CTT by Dr David Newman (10). He points out that the CTT does not compare those who were on statins with the corresponding controls. Instead they selected those individuals in which the statin treatment reduced the LDL Cholesterol 1 mmol/L or 40 points in US terms. As Dr Newman describes it:

“…they shifted the data so that their numbers corresponded precisely to patients whose cholesterol responded perfectly.”

He continues:

 “Patients whose cholesterol drops 40 points are different than others, and not just because their body had an ideal response to the drug. They may also be taking the drug more regularly, and more motivated. Or they may be exercising more, or eating right, and more health conscious than other patients. So it should be no surprise that this analysis comes up with different numbers than a simple comparison of statins versus placebo pills. Ultimately, then, this new information tells us little or nothing about the benefits someone might expect if they take a statin. Instead it tells us the average benefits among those who had a 40-point drop in LDL.”

Furthermore the LDL Cholesterol drop cannot be predicted because the effect of the statins is unknown. This means that the conclusions of this analysis have absolutely no relevance to patients and doctors who have to decide if statins should be prescribed.

Here is a final quote from Dr Newman:

“Perhaps never has a statistical deception been so cleverly buried, in plain sight. The study answers this question: how much did the people who responded well to the drug benefit? This is, by definition, a circular and retrospective question: revisiting old data and re-tailoring the question to arrive at a conclusion. And to be fair they may have answered an interesting, and in some ways contributory, question. However the authors’ conclusions imply that they answered a different, much bigger question. And that is not a true story.”

It seems to me that this is a very valid criticism because the CTT studies do not include those who were on statins but failed to lower their LDL Cholesterol. I am not aware that anyone has answered Dr Newman’s critique. Incidentally this would explain why the CTT does not agree with other analyses which find that the use of statins as a preventive measure does not reduce all-cause mortality.

The CTT data on side- effects are entirely dependent on the results which were obtained from trials. Serious doubts have been raised. Rather ironically the second Cochrane report accepted that the reporting of adverse events in these trials is generally poor, with failure to provide details of severity and type of adverse events or to report on health-related quality of life. It then went on to conclude rather complacently:

“However, it seems unlikely that any major life-threatening hazards associated with statin use exist”.

Recently Sir Richard Thompson , President of the Royal College of Physicians and colleagues wrote to NICE expressing concern about the proposal to extend the use of statins to those with a low risk of developing CVD (11). The letter commented specifically on side-effects as follows:

“I am in no doubt, both personally and from the reported experience of my patients, that statin side-effects are consistently under-reported. This occurs two ways; firstly, doctors airily dismiss symptoms reported by patients (“statins could not possibly cause that!”), and secondly it is unusual for well-recognised side-effects such as rhabdomyolysis or even non-specific muscle pains to be yellow-carded. In my view the potential severity of muscle symptoms justifies extreme caution”

The argument was supported by information on the number of adverse side-effects in various stain trials, which is shown here in Table 1.

Table 1 Adverse side-effects reported in various statin trial

Trial, Name of statin Side-effects, statin treatment,% Side-effects,control,%
AFCAPS/TEXCAPS Losartan 13.6 13.8
4S simvastatin 6.0 6.0
CARDS atorvastatin 25.0 24.0
METEOR rosuvastatin 83.3 80.4
LIPID Pravastatin 3.2 2.7
JUPITER Rosuvastatin 25.0,discontinuation,

15.0,serious side-effects

25.0, discontinuation,

!5.5, serious side-effects

WOSCOPS Pravastatin 7.8 7.0

Note: The values shown refer to “total adverse effects” unless otherwise indicated

What is quite remarkable about these figures is the similarity between those for the group treated and those for the controls. Furthermore the variation is huge. In one the values are as low as 3% but in another it is over 80%. The reality is that the companies have little interest in collecting data on side-effects. The information shown above clearly demonstrates the information on side-effects obtained in clinical trials simply lack credibility.

The letter also referred to the fact that independent researchers do not have access to raw data and noted that:

“…the data driving NICE guidance on statins comes almost entirely from pharmaceutical company funded studies. Furthermore, these data are not available for review by independent researchers, only those who work for the Oxford Cholesterol Treatment Trialists Collaboration (CTT).

The CTT has commercial agreements with pharmaceutical companies which apparently means that they cannot release data to any other researchers who request to see it. Which, in turn, means that the latest reviews of the data by NICE and also by the Cochrane group are totally reliant on the CTT 20121 meta-analysis analysis of this concealed data?”

It is highly relevant that in the recent BMJ controversy it has emerged that the CTT at Oxford University has had funding from drug companies of about £268million as Zoe Harcombe has revealed (12).

There have to be very strong suspicions that the Cochrane authors have allowed themselves to be bullied into submission by the actions of Rory Collins and Colin Baigent. It is evident from the information I have presented here that they have ignored key considerations, which ought to have had an impact in reaching their conclusions. Perhaps they should have studied another Cochrane publication entitled “Eminence v Evidence” (13) which makes some extremely pertinent comments.

This is a great pity because if ever there was a need for a body which can conduct an authoritative evaluation of the evidence it is now. It is to be hoped that the powers that be in Cochrane will take these points on board. Above all its contributors must stand up to bully boy tactics of the very powerful vested interests. Many will be familiar with the fact that Rory Collins tried the same tactic with the BMJ. To her great credit Fiona Godlee , the editor-in-chief was not intimidated by Collins and effectively took appropriate action which put him in his place. Cochrane could well to learn some lessons from this.

Finally, even if the conclusions of the second Cochrane report are genuine, let us consider this from the perspective of those who will be prescribed statins in accordance with the latest NICE guidelines. These mean that those with a 10% risk of developing CVD will be advised to go on statins. Effectively this means everyone over 50, because no matter how fit and healthy a person is, when the time comes there must be at least a 1 in 10 chance that the cause of death will be heart disease. Cochrane states that 67 people will have to be treated for 5 years for one person to benefit. Although according to Mark Baker of NICE, 77 will have to be treated for 3 years. Whatever the figure the chances are very small. Cochrane comments:

These NNTs are well within the range considered worthwhile in primary prevention

Well I have got news for the authors and for the medical professions as a whole if this is statement is an accurate reflection of its opinion. It is certainly not acceptable to me and I strongly suspect to the vast majority of patients. In my experience most people believe that if they are prescribed a drug it will effective for them personally. They might be prepared to accept that there may be less that 100% certainty, possibly as low as 20%, which is an NNT of 5! It is crucial that we are concerned here with prevention. I recognize that it is rather different for a person with a serious illness, who will clutch at anything that may be effective. But prevention is a new ball game and in my opinion, there would be very few who would agree to statins if they were aware that there was only a 1 in 67 chance that it would do them any good.

For anyone who is concerned that their risk of CVD is high and they wish to lower them, what should they do? Here are some suggestions:

  • If you smoke cigarettes, stop immediately
  • Take regular exercise, If you can walk at least 1 mile per day, this will certainly imlrove your life expectancy
  • Make adjustments to your diet. There is now very convincing evidence that restricting the intake of sugar and refined carbohydrates will reduce the risks not only of CVD but also of diabetes, cancer, Alzheimer’s Disease as well as lowering blood pressure and achieving weight loss

There is absolutely no doubt any benefits derived from statin treatment will be insignificant when compared those which can be achieved by implementing the measures outlined above. Furthermore, any side-effects will be minimal compared to those experienced by people on statins.

So whatever way you look at it, the case for statins just does not stack up. The truth is that the fundamental objective is the profitability of the drug companies and improving public health simply does not feature. In fact, if statins were only used to treat patients suffering from CVD, this could be a critical step towards good health. It would definitely release funds which could be better in spent in other ways, such as employing more nurses.

It is a matter of great regret that this particular Cochrane team did not follow the example of the one led by Tom Jefferson, which considered neuraminida inhibitors including Tamiflu (14). The background has been explained in an article in The Guardian by Ben Goldacre (15). An earlier Cochrane report had concluded that these ‘flu drugs do reduce the rate of complications of conditions such as pneumonia. However a paediatrician in Japan pointed out that the Cochrane report was based on the results of 2 published trials of which only one showed a positive response. In fact there were another 8 trials, for which the results had never seen the light of day and all of these had been negative!! As a direct result of this Tom Jefferson realised that in the 2008 report they had made a mistake in relying on the published data. So he decided to see if he could get hold of the information. There was a long battle with Roche, which by this time controlled the data, before the company eventually sent documents containing excerpts, which did not provide adequate information to assess the benefits and the adverse side-effects. It was also not possible to consider the details of the trial procedures, which is essential if the quality of the data is to be evaluated.

Consideration of the work of various regulatory agencies such as the FDA in the USA and EMEA in the EU indicated that there were serious flaws in the procedures. As Cochrane had not been provided with the detailed information it needed to do its review properly, it decide to exclude all this data from the analysis. Effectively it was unable to reach a conclusion and explained the position in a further review published in December 2009. This was followed by a long period of prevarication by Roche, including claims that some of the Cochrane researchers had made untrue statements about the drug and the company and allegations questioning their independence. Finally under pressure from the BMJ which supported the Cochrane investigators, Roche agreed to release all the data but it had taken 5 years for this to happen.

When this information was evaluated, the review was finally published in April 2014. Because the team now had the clinical study reports (CSRs) from the manufacturers it was able to compare the information with that which had been submitted to the regulatory authorities. Rather significantly it was decided not to use results which appeared in scientific journals because in previous versions of this review unresolved discrepancies in the data presented were identified in published trial reports. Substantial publication bias was also uncovered.

Based on these assessments of the regulatory documents (in excess of 160,000 pages), it was concluded that there were substantial problems with the design, conduct, reporting and availability of information from many of the trials. As a consequence, there were doubts about the reliability of the results. The review was based on 20 trials with zanamir (Relenza, from GSK) and 26 trials with oseltamir (Tamiflu fom Roche). It was found that:

both drugs shorten the duration of symptoms of influenza-like illness (unconfirmed influenza or ‘the flu’) by less than a day. Oseltamivir did not affect the number of hospitalisations, based on the data from all the people enrolled in treatment trials of oseltamivir. Zanamivir trials did not record this outcome. The effects on pneumonia and other complications of influenza, such as bronchitis, middle ear infection (otitis media) and sinusitis, were unreliably reported, as shown by the case report form in the trial documents. Some forms showed limitations in the diagnostic criteria for pneumonia. Regulatory comments noted problems with missing follow-up diary cards from participants. In children with asthma there was no clear effect on the time to first alleviation of symptoms.

Prophylaxis trials showed that oseltamivir and zanamivir reduced the risk of symptomatic influenza in individuals and households. There was no evidence of an effect on asymptomatic influenza or on non-influenza, influenza-like illness, but trial conduct problems prevent any definitive conclusion.

Oseltamivir use was associated with nausea, vomiting, headaches, renal and psychiatric events; these last three were when it was used to prevent influenza (prophylaxis). Its effect on the heart is unclear: it may reduce cardiac symptoms, but may induce serious heart rhythm problems. In adult treatment trials of zanamivir there was no increased risk of reported adverse events. The evidence on the possible harms associated with the treatment of children with zanamivir was sparse.”

This is not exactly impressive. Roche put out a press release contesting these findings but did not provide any reasons. When the benefits are balanced against the side-effects, it is difficult to justify their use. It was certainly a huge waste of money by the government to spend £500 million to stockpile supplies of this drug. But that is what happens when all the relevant data to make an informed decision is not available.

When this episode is compared with the performance of the team dealing with statins, a sad state of affairs emerges. In contrast to Tom Jefferson, the statin team seems to have just submitted to the power and influence of the industry and its supporters. There has been a total failure to insist on getting access to the primary data. As the Tamiflu review clearly demonstrates  when the original reports become available for assessment, the perspective is completely different. In the light of this, there have to be very strong suspicions that if and when the relevant statin data is released generally, we will find that the benefit/adverse side-effects ratio is very much worse than we have been led to believe.

Commenting on the Tamiflu review, Dr David Tovey, Editor-in-Chief of The Cochrane Library said:

“We now have the most robust, comprehensive review on neuraminidase inhibitors that exists. Initially thought to reduce hospitalisations and serious complications from influenza, the review highlights that [NIs are] not proven to do this, and it also seems to lead to harmful effects that were not fully reported in the original publications. This shows the importance of ensuring that trial data are transparent and accessible” (17).

Let’s hope that one day he will be able to say the same about statins.


  1.  http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD004816.pub4/full
  2. http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD004816.pub5/full
  3. http://jama.jamanetwork.com/article.aspx?articleid=197132
  4. http://archinte.jamanetwork.com/article.aspx?articleid=416105
  5. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(09)61965-6/abstract
  6. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)61350-5/fulltext
  7. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0029849
  8. Lancet 2012;378:doi:10.1016/S0140-6736(12)60367-5
  9. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(07)60716-8/fulltext
  10. http://cardiobrief.org/2012/05/27/guest-post-data-drugs-and-deception-a-true-story/
  11. http://drmalcolmkendrick.org/2014/06/27/another-backlash-begins/
  12. http://www.zoeharcombe.com/2014/08/ctsu-funding-from-drug-companies/
  13. http://www.cochrane.org/news/blog/eminence-vs-evidence
  14. http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD008965.pub4/full
  15. http://www.theguardian.com/business/2014/apr/10/tamiflu-saga-drug-trials-big-pharma
  16. http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD008965.pub4/abstract;jsessionid=D0952B85723A29FF11B3087DB5F71938.f03t02
  17. http://www.cochrane.org/features/tamiflu-and-relenza-getting-full-evidence-picture




108. Swedish Expert Committee: A Low-Carb Diet Most Effective for Weight Loss

In September last year, the Swedish Council on Health Technology Assessment released a report entitled “Dietary Treatment for Obesity” (1) which has accepted much of the revised thinking on the relationship between diet and health.

This blog is by the Diet Doctor, Andreas Eenfeldt, who has an excellent website at http://www.dietdoctor.com/

I am very grateful to Andreas for permission to post this article here.

The original can be sourced at


Which diet is the most effective for weight loss?

This could be a historic day in Sweden (23 September 2013). Today it became official. After over two years of work, a Swedish expert committee published their expert inquiry Dietary Treatment for Obesity (Google translated from Swedish).

This report from SBU (Swedish Council on Health Technology Assessment) is likely to be the basis for future dietary guidelines for obesity treatment within the Swedish health care system.

The health care system has for a long time given general advice to avoid fat and calories. A low-carbohydrate diet such as LCHF (2) has often been dismissed as a fad diet lacking scientific foundation. The time has now come to update knowledge in this area.

According to SBU, the only clear difference among different dietary recommendations is seen during the first six months. Here a low-carbohydrate diet, such as LCHF, is clearly more effective than today’s conventional advice.

From fad diet to best in test.

Here are some more highlights from the report:

Health Markers

In addition, health markers will improve on a low-carbohydrate diet, according to SBU. You’ll get:

…a greater increase in HDL cholesterol (“the good cholesterol”) without having any adverse affects on LDL cholesterol (“the bad cholesterol”). This applies to both the moderate low-carbohydrate intake of less than 40 percent of the total energy intake, as well as to the stricter low-carbohydrate diet, where carbohydrate intake is less than 20 percent of the total energy intake. In addition, the stricter low-carbohydrate diet will lead to improved glucose levels for individuals with obesity and diabetes, and to marginally decreased levels of triglycerides.

So, all important health markers improved or unchanged on a stricter low-carbohydrate diet. Just like an international review of all research in the area showed last year (3).

Long-term Uncertainty

Long term, studies show no statistically significant differences among different diets, and the differences decrease with time. The SBU suggests that this is because of decreasing compliance with time. People simply tend to fall back to old habits.

The more studies we add, the better we can see the clear advantage of low-carbohydrate diets. Unfortunately SBU has excluded all studies examining both obese and overweight people. If you include studies on weight loss where overweight people are included – to get a greater scientific basis – a clear advantage for the low-carbohydrate diet was seen even after a year (4)

A well-designed study, which for the same reason as above, was dropped from the SBU report’s analysis, still showed a persistent advantage for the LCHF-like diet (Atkins) after two years, despite the difficulty with such long-term diet studies.

For the long-term effect, if you keep to a strict low-carbohydrate diet, there are only anecdotal reports on weight and cholesterol levels (5).

Physical Activity

SBU also kills the idea that exercise plays an important roll in weight loss. Exercise may be very good for health, but:

Systematic reviews of the literature show that the addition of physical activity to a dietary intervention for individuals with obesity have, if any, a marginal effect on weight loss at the group level.

The effect of exercise on weight in studies is in other words marginal or non-existent (6).

Warnings Against LCHF Dismissed

There’s a great lack of knowledge today on what dietary guidelines are best for long-term health. We simply don’t know.

Recent cautions on low-carbohydrate diets are at best based on statistical associations derived from food questionnaires from people who didn’t (!) eat a low-carbohydrate diet. The SBU also dismisses these warnings:

Most of these studies suffer from major shortcomings, which make them difficult to interpret. The foremost shortcoming in these studies is that it’s often impossible to determine whether those with the lowest intake are knowingly eating a moderate low-carbohydrate diet for health reasons, or if they are high consumers of fast-food.

The breakdown of carbohydrates, fat and protein, which in such studies are imaginatively labeled “a low-carbohydrate diet” is usually very similar to the macronutrient distribution in a hamburger with fries and soda…

Towards the Future

What will be the consequences of today’s report?

Advice on a low-carbohydrate diet is however very rare, if we look at the practice survey. It’s not clear how common it is to actively discourage patients from the strict low-carbohydrate diet. A low-carbohydrate diet, even the stricter form, will lead to a greater weight loss in the short term than the low-fat diet, and studies have indicated no adverse effects on blood lipids, provided that the weight stays low. One possible consequence of this report will therefore be an increased use of a strict low-carbohydrate diet for short-term weight reduction.

SBU will always express itself very carefully. But it can’t be said much clearer: It’s high time for the health care system to take seriously advice on LCHF for weight loss!

This is also interesting:

…it’s not possible to draw any conclusions about the relationship between a low-carbohydrate diet – regardless of fat content – and cardiovascular disease. Here we could apply the precautionary principle, and advise some restraint on saturated fat intake, as long as the documentation of the long-term effects are inadequate.

Many health care workers will no doubt (without any better reasons than preconceptions) be wary of dietary advice on more saturated fat. I was once scared of saturated fat myself.

I think that SBU is keeping a reasonable attitude here, as it isn’t even necessary to give advice on a lot of saturated fat for a low-carbohydrate diet. You can eat even a strict low-carbohydrate diet (such as LCHF) emphasizing unsaturated fats (3). This has been shown to be effective in several studies (7,8,9)

It would be wonderful if the health care system started to apply the benefits of a low-carbohydrate diet, even before the outdated fear of butter has melted away everywhere.

The SBU-report Dietary Treatment for Obesity is a gigantic step towards more effective dietary guidelines within the health care system. This is a historic day in Sweden.


  1. http://www.sbu.se/upload/Publikationer/Content1/1/Diets_among_obese_individuals.pdf
  2. http://www.dietdoctor.com/lchf
  3. http://onlinelibrary.wiley.com/doi/10.1111/j.1467-789X.2012.01021.x/abstract;jsessionid=7396D07C42DB2B84642D35158B132AF9.d04t04
  4. http://www.dietdoctor.com/new-analysis-lchf-best-for-long-term-weight-and-health
  5. http://www.dietdoctor.com/will-lchf-work-long-term-say-four-years
  6. http://www.dietdoctor.com/how-to-lose-weight#13
  7. http://www.nutritionj.com/content/7/1/30
  8. http://www.nytimes.com/2009/06/09/health/09diet.html?ref=health&_r=1&
  9. http://www.sciencedaily.com/releases/2009/06/090608162426.htm



107. Support for Diets High in Fat and Low in Carbohydrates Gathers Momentum

There is a growing body of scientific evidence and personal experience which demonstrates that the high content of sugar and refined carbohydrate foods is one of the main factors responsible for the rapidly increasing levels of obesity and diabetes. This in turn increases the risks of conditions such as heart disease, cancers and Alzheimer’s Disease. Conversely those who make adjustments to their diet in order to reduce the carbohydrates and increase the fat consistently find that they can achieve significant improvements in their health.

A recent paper has pulled together much of the relevant information and provides a valuable summary of the current state of knowledge (1).

There are 12 key points which are as follows:

  1. Hyperglycaemia is the most salient feature of diabetes. Dietary carbohydrate restriction has the greatest effect on decreasing blood glucose levels.It is universally accepted that dietary carbohydrate is the main dietary determinant of blood glucose and restriction shows the greatest reduction in blood glucose concentrations as well as HbA1c(Glycylated haemoglobin, which gives the average blood sugar level over the previous few months)
  2. During the epidemics of obesity and type 2 diabetes, caloric increases have been due almost entirely to increased carbohydrate. In the USA, there were increases in the carbohydrate content of the diet of about 7% of calories with concomitant reductions in the intake of fat between 1970 and 2000. Similar changes have been recorded for Great Britain
  3. Benefits of dietary carbohydrate restriction do not require weight loss. This is crucial because many diabetics are not overweight and many who are overweight are not diabetic. In fact the obsession with weight per se has not been particularly helpful because most people have great difficulty in losing weight by the conventional calorie control approach. Paradoxically the switch to a diet which is low in carbohydrates is often accompanied by weight loss even when this has not been a specific objective
  4. Although weight loss is not required for benefit, no dietary intervention is better than carbohydrate restriction for weight loss. In a British study it was found that those on a low carbohydrate diet were more successful in losing weight than a comparable group who followed a conventional Healthy Eating diet. On the other hand low fat diets have produced very poor results. In the Women’s Health Initiative (WHI) the low fat intervention group was encouraged to consume a diet with 20% fat, which was rich in fruits, vegetables and grains (2). Although they lost 2.2 kg in the first year, this was regained by the end of the 7-year study.
  5. Adherence to low-carbohydrate diets in people with type 2 diabetes is at least as good as adherence to any other dietary interventions and is frequently significantly better. In a study of The Active Low-Carber Forum, an on-line discussion group with over 150,000 members, a common assertion was that a low-carbohydrate regimen provides the greatest degree of satisfaction. Provided the carbohydrate reduction is maintained, there is no need to restrict total food intake, which is necessary on a low fat diet.
  6. Replacement of carbohydrate with protein is generally beneficial. Although it is generally recommended that carbohydrate is replaced by fat, a number of systematic studies have found that high-protein-low carbohydrate diets have a more favourable effect on weight loss and cardiovascular risk factors than fat reduced diets.
  7. Dietary total and saturated fat (SFA)  do not correlate with risk of cardiovascular disease (CVD). Despite massive investigations it has not been possible to demonstrate that SFA is a risk factor for heart disease. One meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD (3,4). Although recommendations to lower SFA are an integral part of many national nutrition policies, the lack of evidence is now so compelling governments will eventually have make fundamental changes to official strategies.
  8. Plasma SFAs are controlled by dietary carbohydrate more than by dietary lipids. It is now becoming clear that the concentration of SFA in the blood is determined by the amount of carbohydrates rather than the SFA in the food. A diet low in carbohydrates is more effective in reducing the blood triglycerides than one which is low in fat.
  9. The best predictor of microvascular and, to a lesser extent, macro-vascular complications in patients with type 2 diabetes, is glycaemic control. In the United Kingdom Prospective Diabetes Study (UKPDS) it was found that the key controlling variable was HbA1c. As HbA1c increased, there was a corresponding increase in fatal and non-fatal myocardial infarction events. By contrast, there was a 14% decrease in myocardial infarction for every 1% reduction in HbA1c.
  10. Dietary carbohydrate restriction is the most effective method (other than starvation) of reducing serum triglycerides and increasing high-density lipoprotein (HDL). Compared with other diets, a low-carbohydrate diet achieved the greatest decrease in triglyceride, as well as decrease in weight, HbA1c and glucose and a greater increase in HDL.
  11. Patients with type 2 diabetes on carbohydrate-restricted diets reduce and frequently eliminate medication. People with type 1 usually require lower insulin. Dietary carbohydrate restriction, because of its increased effectiveness in glycaemic control, frequently leads to reduction and often complete elimination of medication in type 2 diabetes. Similarly, patients with type 1 typically require lower medication on low-carbohydrate diets.
  12. Intensive glucose lowering by dietary carbohydrate restriction has no side effects comparable to the effects of intensive pharmacologic treatment. It has been established that not only is the use of drugs to treat diabetes ineffective but there are also proven hazards. By contrast the change of diet definitely works and there are no known dangers.


When all the information is collated there is a very convincing case for choosing diets which are low in carbohydrates. It is becoming more and more obvious that the decision to advise a reduction in fat (and an increase in carbohydrates) was totally misguided. As a consequence huge numbers of people have developed chronic diseases. Unfortunately the wrong advice is still being promulgated in most countries. We have now reached the point where the evidence is overwhelming and that policies must be changed radically and without delay. The single exception is Sweden, where a recent official report clearly recognised the extensive benefits of a diet which is low in carbohydrates and high in fat. This topic will be covered in the next blog (5).


  1. http://www.nutritionjrnl.com/article/S0899-9007(14)00332-3/fulltext
  2. http://jama.jamanetwork.com/article.aspx?articleid=202138
  3. http://ajcn.nutrition.org/content/91/3/535
  4. http://ajcn.nutrition.org/content/91/3/502
  5. http://vernerwheelock.com/?p=542

106. Bad Science and Big Business Responsible for Obesity Epidemic

Dr David Diamond is a neuroscientist who was overweight with high values for his blood cholesterol (TC) and triglycerides, which indicated that he was a prime candidate for heart disease. He was therefore typical of those who are recommended to be prescribed statins on the grounds that this treatment will lower the TC and therefore reduce the risks that they will suffer a heart attack. In this case Dr Diamond decided against statins but elected to change his diet and follow the official recommendations which were supposed to reduce his TC and triglycerides. Essentially he cut down on animal products such as meat, butter, cheese and eggs in order to reduce his intake of saturated fat (SFA). His diet consisted of skinless chicken, low fat foods (cheese, yogurt), olive oil, bread,vegetables, fruit, nuts, cereal and potatoes In addition he increased the amount of regular exercise.

After a couple of years, he found out that this regime not only failed to reduce his risk for heart disease, it actually increased it. His triglycerides and the ratio of TC/HDL Cholesterol got even worse. His cardiologist told him he needed to go on statin drugs immediately and that he was deluding himself by believing diet could change anything.

Instead Dr Diamond decided that he would do his own research into the scientific literature and become an expert in heart disease. This meant that during the day he was a neuroscientist, but in the evenings and weekends he was studying about heart disease. He tells his own story in a public lecture given at the University of South Florida where he is employed (1). It is available on You Tube and although it lasts for about an hour it is well worth watching. Here is a summary of some of the key points he makes.

He begins by recalling the experience of William Banting, a London undertaker, who in 1862 at age 66 years weighed 200 pounds even though he was only 5 foot 5 inches high. Although he tried cutting down on his calorie intake coupled with vigorous exercise, he was unable to lose weight. A surgeon named William Harvey recommended a diet rich in animal foods and vegetables but limited in sugar and starch. So he ate 3 meals a day consisting mainly of meat, fish or game. As far as possible he avoided bread, milk, beer, sweets and potatoes. Between August 1862 and May 1863 he had lost 35 pounds which increased to 50 pounds by the beginning of 1864.He wrote a pamphlet describing his experience which was widely disseminated. He lived well into his eighties.

More recently in the 1940s and 1950s Alfred Pennington in the USA found that those who consumed fresh meat with no restriction on fat but avoiding bread flour, sugar and sweets had no difficulty in controlling their weight.

In 1963, it was reported that weight loss could be achieved satisfactorily by a diet which was low in carbohydrates (2). The patients felt no hunger. They could eat as much meat, butter and fat as they wished, provided they restricted their consumption of foods containing carbohydrates. More recently the Atkins’ Diet has been the subject of much controversy but effectively there is no major difference between this diet and the one which Banting had adopted over 100 years earlier.

Despite all the claims that a diet low in carbohydrates can have all kinds of effects which are deleterious to health, these have proved to be totally unfounded. Research reported in 2006 confirmed that a diet low in carbohydrates not only facilitated weight loss but also moved other indicators of risk towards the normal/healthy levels (3). This included triglycerides and the TC/HDL ratio. Furthermore the blood glucose levels, which indicate diabetes were reduced considerably.

As a result of his investigations, Dr Diamond altered his own diet to one with eggs, butter, beef, chicken (with the skin), full fat cheese, coconut, dark chocolate, nuts and vegetables (especially broccoli), small quantities of fruit, bread, potatoes and sugar. This certainly worked and all the usual indicators reverted to the values consistent with low risks for various disease and general good health, not to mention the fact that he lost weight.

So what has gone wrong? Dr Diamond recounts the role of Ancel Keys, who was a very influential character from the 1950s when Americans were obsessed with the fact that they had one of the highest rates of heart disease in the world. Keys claimed that the higher the fat (and SFA ) intake in a country the greater the death rate from heart disease. However a relationship like this certainly does not demonstrate that the fat/SFA is the cause of the heart disease. In reality, the truth reveals that Keys was selective in his use of data, because other researchers pointed out that he had only used data from 6 countries, whereas if he had used all the data at his disposal (from 22 countries) it was evident that there was no relationship whatsoever. In fact Keyes was a fraud. Despite opposition from many experts, he managed to prevail. He was effectively supported by Senator George McGovern, who chaired a Senate Committee which devised dietary guidelines for the USA. These endorsed the advice to limit the intake of meat/meat products, partly because they were regarded as a source of SFA but also because they were a source of cholesterol. There was never any justification for either of these concerns (4, 5). However the Senate Committee report provided the rationale for the official US dietary recommendations which advised that the most of the diet should consist of carbohydrates, but that animal foods especially those which contain fat should be restricted.

Dr Diamond is just one of a long list of individuals who have evaluated the evidence objectively and come to the same conclusion. There is convincing evidence that the increased intake of sugar and refined carbohydrates is the fundamental cause of obesity, heart disease, diabetes, Alzheimer’s Disease and various cancers. Because the official advice is wrong, we have the paradox that those who follow it carefully are damaging their own health. As Dr Diamond found out, when he discovered that his risks of developing heart disease had increased, the treatments/advice offered were completely ineffective and actually exacerbated his condition. There is absolutely no doubt that this scenario is all too common. It is not just confined to the US because the guidelines devised there have been adopted by the WHO. Consequently the official policies on nutrition are essentially the same in most countries. This is a scandal of immense proportions, which is made worse by the fact that there is huge reluctance by the mainstream public health professionals to admit that there is a need for a profound change in national policies.


  1. http://healthimpactnews.com/2014/how-bad-science-and-the-pharmaceutical-industry-created-most-modern-diseases/
  2. E S Gordon et al (1963) http://jama.jamanetwork.com/article.aspx?articleid=666850
  3. http://link.springer.com/article/10.1007/s11010-005-9001-x
  4. http://vernerwheelock.com/?p=270
  5. http://vernerwheelock.com/?p=105



105. Statin critics cleared. Top statin advocate knuckles’ rapped

Recently I have devoted several posts to the topic of statins (1,2,3). It is obvious that there are many serious doubts about the official/conventional approach to the use of these drugs which have been highlighted by the recent controversy in the BMJ. The results of the special inquiry established by Fiona Godlee, the editor-in-chief of the BMJ, have just been announced.  So I am delighted to post this article by the medical journalist Jerome Burne. I am very grateful to Jerome for permission to publish here. The original can be sourced at:


The long running spat between senior statin advocate Professor Sir Rory Collins and the British Medical Journal has come to a very satisfactory conclusion. His demand – that two papers challenging his claims about the safety and effectiveness of statins – be withdrawn, has been rejected by a committee specially set up to consider it.

Instead the report, just out, makes several low key but sharp criticism of the way Sir Rory has been dealing with his data. (For more background details on what has been going on see here – Eminence medicine defends status quo and here – Statin debate the ultimate two minute guide)

Sir Rory had been particularly incensed that both the BMJ articles had challenged his claim that statins were effective in healthy patients and caused very few side effects. His specific complaint concerned a minor error in reporting the percentage of side effects contained in another article. This was rapidly corrected

The two authors he was attacking – Dr Aseem Malhotra and Dr John Abramson – had their own concerns about Sir Rory’s work. Notably that his conclusions were based on placebo controlled trials of the drugs run by the drugs companies that kept the data they had collected hidden.

The secret statin data

Since the published results of drug company trials are notoriously unreliable, it’s now widely agreed that independent researchers should be able to look over the data that had been collected on each patient.

The research centre that Sir Rory heads – the Cholesterol Treatment Trialists (CTT) in Oxford – holds the biggest collection of statin data in the world, but no one outside the organisation has been able to study it for 20 years – CTT the house of statin secrets. The committee’s report made it clear that this was no longer acceptable.

‘It is very clear,’ it said ‘that statin trial data is not available for assessment,’ going on to note that this ‘may contribute to uncertainty about the risks and benefits’ of the drugs. That was a damming point since the basis for Sir Rory’s demand for a retraction was that questioning his results from randomised controlled trials was killing people by stopping them taking the drugs. In the committee’s view the issue was still uncertain.

The report picked up on another example of Sir Rory’s eccentric approach to evidence and to normal scientific debate. It noted that despite being asked to write an article rebutting Malhotra and Abramson’s claims and to participate in the rapid responses to the articles, all his correspondence arrived marked ‘not for publication’. ‘This was unlikely’ the report drily observed ‘to promote open scientific dialogue.’

Evidence based medicine not delivering

But there is a much bigger issue here than Sir Rory’s ‘grand old man’ style. While he behaved as if the RCT was an unimpeachable source of information, what has emerged from this battle is that the evidence based medicine project is in intensive care if not already expired. Statins are the most widely prescribed drugs ever and quite possibly the subject of more RCTs than any other.

Yet here we are 20 years on and there is widespread agreement that we still don’t really know how effective they are at preventing heart attacks in healthy people – the group who get by far the most statin prescriptions – or what the true side-effect rate is. Part of the problem is the drug companies’ well-known habit of fiddling of statistics, hiding of unfavourable results, selecting trial subjects most likely to produce favourable results and so on.

The unreliability of RCT’s has recently been acknowledged by one of evidence based medicine’s most enthusiastic supporters – Dr Ben Goldacre. “…We lack reliable information from randomised controlled trial on common symptomatic side effects of statins,’ he wrote in a BMJ editorial last month.

This is something of a volte-face for Dr Goldacre since it was only a few months earlier that a research paper with his name on it concluded that statins didn’t really have any side effects at all; reports saying they did were largely due to a sort of reverse placebo effect – people expected pains and other problems so sure enough they felt them.

A tarnished gold standard

In fact Dr Goldacre has become something of a flip-flopper. It was only a year ago that he wrote a good book (4) – Bad Pharma – that explained in great and forensic detail why results of commercial drug trials couldn’t be trusted because of drug company fiddling.

Yet his statin side effect trial was based on entirely on results from commercial trials. So Dr Goldacre who spent years jeering at any and all non-drug treatments for their lack of RCTs, now admits that even several dozen RCTs can’t decide on the effectiveness or safety of a single drug. It’s a gold standard that is looking fatally tarnished. The debate over how best to fix it wil be covered in another post.

RCT’s unreliablity is particularly unfortunate for patients on statins since waiting in the wings is a new generation of super statins that lower cholesterol even more powerfully and are expected to cost around 20.000 dollars a year – Beware new cholesterol drugs coming. How are we going to decide if they are worth it?

Meanwhile we may be on the verge of having a firm decision about one of statins’ long terms effects – type 2 diabetes. Nearly a thousand women have so far begun legal proceedings against the pharmaceutical giant Pfizer, claiming that their best-selling cholesterol lowering statin Lipitor caused them to develop diabetes – Thousand woman lipitor lawsuit

If they win, and there is considerable evidence to suggest there is a link, then NICE’s decision to recommend the drugs for another four million people or so, along with Sir Rory’s iron clad confidence that there are no side-effects worth worrying about, will look careless, arrogant and dangerous.


  1. http://vernerwheelock.com/?p=385
  2. http://vernerwheelock.com/?p=432
  3. http://vernerwheelock.com/?p=481
  4. Ben Goldacre (2013) “Bad Pharma: How Medicine is Broken, and How We Can Fix It”. Fourth Estate: London



104.Left Alone To Cope With Statin Side Effects

This is a guest post of an article by Francois Lubbe, editor for The HealthierLife, which originally appeared at:


I am very grateful to Francois for permission to publish here.
Recently, Dr. John Briffa, contributing editor for The Cholesterol Truth blog,(1) wrote an article about how pro-statin doctors have gone on the offensive against other mainstream medical experts who have expressed concerns about the effectiveness of cholesterol-lowering statin drugs, their harmful side effects and the over-prescription of these drugs (2).

The heat is on

If you ask me, it looks like the statin camp is dividing fast — those against and those in favour — and chances are, things are going to get pretty heated.

It’s about time.

Recently, mainstream medical experts wrote a letter, reported widely in the press, in which they detailed objections about the mass-medicalization of millions of healthy individuals with statins. They also highlighted the unreliability of the evidence regarding the adverse effects of statins and the fact that almost all the evidence supporting statin drugs is industry-funded (and therefore liable to bias). Another source of bias is the fact that multiple conflicts of interest exist on the ‘expert committee’ that decides on the prescription guidelines of statin drugs. If you want to read more about this, see ref (3).

These are serious concerns and should not be taken lightly.

As expected, the pro-statin zealots (and those probably benefiting the most from these drugs being pushed) published their counter argument in the BMJ (British Medical Journal), a few weeks ago. See also (4,5).>

Among the objecting medical experts were Professor Sir Rory Collins, head of the Cholesterol Treatment Trialists collaboration, and Professor Peter Weissberg, medical director of the British Heart Foundation. (I can already see why they would object vehemently.)

Professor Collins said that “misrepresenting the evidence” will have a negative impact on people who are at high risk of cardiac events. He also added that rates of myopathy — one of the most reported and most damaging side effects of satins resulting in severe muscle loss and fatigue — are much lower than some people state. As Dr. Briffa states on his blog post in response to Prof. Collins’ comment: “His definition of myopathy appears to be pinned to quite extreme muscle damage, levels of the enzyme used to assess muscle damage (creatinine kinase) are at least 10 times the upper limit of normal. Are we to assume that Professor Sir Rory Collins is disinterested unless muscles are in near-meltdown?”

Professor Weissberg simply said that “…the critics are wrong. They’ve retracted, they’re wrong.” In fact, the retraction Prof. Weissberg refers to, was the misleading representation of statin side-effects, reported in one single piece of research. That certainly has been retracted… the other major objections against statins still stand firm. To read Dr. Briffa’s complete article see ref (6)
Let’s face it, the statin pushers and the pharmaceutical companies manufacturing these drugs have an awful lot to protect… because if their bubble bursts and the truth comes out, not only will they lose a multi-billion cash cow, but their reputations will also be tarnished and they will have to answer to an awful lot of patients who have been negatively affected by these drugs.

One person, who’s already looking for answers, is one of our dedicated readers who left the following comment on our Facebook Fanpage, The Healthier Life:

“…My muscles did melt down and I would like Professor Sir Rory Collins and Professor Peter Weissberg to physically examine me and see for themselves the damage Lipitor/statins has done to my muscles. The muscle wasting in my neck, shoulders, arms/wrists and legs/ankles/feet are clear to see and I have photos taken in 2008 to prove it. The photos also show severe skin damage: thinning, drying and bleeding of the skin. Most doctors are in denial and turn a blind eye to the statin horrors unfolding. And most fail to report ADRs to the MHRA so the statistics held are unreliable.

  1. Why has the NHS [UK National Health Service] covered up the life-threatening statin-induced adverse reaction that I reported on 6 March 2008 when this dangerous drug was stopped? I had taken the drug for 2 years (long term) but it was too late; the damage was done. I have been abandoned by the NHS and left alone to cope with the irreversible serious side effects. It is cruel and inhumane.
  2. Why have I been stonewalled since receiving a letter dated 8 April 2013 from the ICO [Information Commissioner's Office] in response to my request for an investigation into why the Department of Health and the Home Office will not release to me a copy of the test results of an animal statin drug trial on 145 rats ”Statin effects on heart and muscle/Home Office” that took place from 2006-2011?

Until I get answers to these questions and a diagnosis of my drug-induced injuries the public cannot believe a word either of these ‘medical experts’ say. I have been struck off 4 GP practices altogether to keep a lid on this medical horror story/scandal.

[The] Ethics and morality, as a code of practice by which to follow in the workplace, no longer applies to the NHS. What sort of health service and society is this in which corruption rules OK? Collins and Weissberg need to invest in a copy of Ethics For The Real World P.19, authors Ronald A Howard and Clinton D Korver, Harvard Business Press…”(7)

Put that in your pipe and smoke it!

Of course, this reader is just one of the millions (no exaggeration) who have been affected by these dangerous and side effect ridden drugs.

So, it looks like the heat is on and like we’ve said many times before, statin drugs might just prove to be the biggest pharmaceutical scandal in history.

… and another thing

Still on the topic of statin drugs…

Most of our readers have heard all the cholesterol-lowering statin drug horror stories, but maybe you’re new to the train wreck of statin therapy. If so, I’ll recap on just three of the most troubling adverse effects linked to statins…

  1. Statins may increase risk of type 2 diabetes.
  2. Statins may cause muscle damage.
  3. Statins may deplete CoQ10, the antioxidant that’s indispensable to heart health.

I could add to this list and mention increased risk of cataracts, cognitive impairment, kidney failure, liver dysfunction and depression.

Sorry. I couldn’t resist.

Until next time,

Francois Lubbe


  1. http://www.thecholesteroltruth.com/statin-prescribing-widely-available/
  2. http://www.bmj.com/content/348/bmj.g349
  3. http://www.thecholesteroltruth.com/statin-prescribing-widely-available/
  4. http://www.bmj.com/content/349/bmj.g4694
  5. http://vernerwheelock.com/?p=432
  6. http://www.thecholesteroltruth.com/statins-cholesterol-side-effects/
  7. Ronald A. Howard and Clinton D. Korver (2008) “Ethics for the Real World: Creating a Personal Code to Guide Decisons in Work and Life.” Harvard Business Press

103. Should Everyone Avoid Dairy Because of Results with Breast Cancer?

In the previous blog I explained how Jane Plant successfully cured breast cancer by changing her diet. Essentially she stopped eating milk and dairy products as well as any foods which contained them. (1)

However it is absolutely crucial to appreciate that the experience of Jane does not provide evidence to recommend that everyone should refrain from consuming dairy products. While I accept that the case for not smoking it extremely convincing, we have a long way to go before the same can be said of cows’ milk and any products derived from it.

First of all, although I do not question the success of the strategy for Jane, this certainly does not prove that it will work for everyone else. It is possible that this is so but it is equally possible that it may work for 50%, or 5% or 0.5%,.we simply do not know. Secondly, Jane was receiving chemotherapy at the same time, so did this treatment have a role? Thirdly were there special features about Jane that had a bearing on the outcome. She tells us she used to consume plenty of dairy produce so it may be that eliminating dairy produce from the diet is only effective in such people.

Milk is a very complex food, which consists of a wide range of different constituents. As the elimination of all dairy products prevents breast cancer, we still do not know which particular constituents of milk actively contribute to the development of the cancer. It is important to recognise that there is good evidence that some nutrients present in cow’s milk are particularly valuable. These include the short chain fatty acids which meet the demand for energy quickly and efficiently. Milk fat, especially from cows which have been fed a grass-based diet is one of the few good sources of vitamin K2. Recent research has demonstrated the critical role of Vitamin K2 in the effective utilisation of Vitamins A and D, as well as the mineral calcium (2, 3).

In a meta-analysis based on 6 studies it was found that those with the highest dairy consumption had a reduction of 13% in all-cause mortality compared with those who had the lowest consumption (4). With heart disease an analysis based on 9 separate studies also found a small reduction in death rate for those with a high intake of milk and milk products. For both ischaemic and haemorrhagic strokes the death rates were reduced in those with the highest dairy consumption. There were 5 different studies on the relationship between dairy consumption and diabetes: all of them found that there was a reduction in the incidence with a relatively high intake of milk and milk products. In the light of the totality of these results the authors commented that:

The similarity of the estimates of risk is remarkable and, although conclusions have to be tentative, it seems not unreasonable to conclude that there is no evidence that dairy foods as a total group are associated with harm to health either in terms of death, heart disease, stroke or diabetes, but are probably beneficial in relation to these disease outcomes.”

What is undoubtedly true is that Jane’s result raises many questions which can only be answered by major projects. To the best of my knowledge these have not been started and I doubt if any are planned for the near future. The fundamental problem as Jane herself recognises is that the research emphasis is in finding a drug which is a “magic bullet”. To quote her:

“…modern medical research in general, and especially in the case of cancer research , is aimed at trying to find pure form of a chemical compound which….can be administered in quantitative doses and shown in statistically designed clinical studies to significantly affect the outcome of the disease.”

She goes on to question the validity of this approach and concludes that if this is so, no amount of research and no amount of expenditure will produce the answer. The record to date suggests that she is correct because despite the enormous expenditure on cancer research, the progress achieved has been disappointing to put it mildly.

As mentioned above, the health professionals which Jane encountered showed little interest or understanding of the causes of her breast cancer. This type of attitude seems to be very widespread within the NHS. In fact it is characteristic of most of the medical establishment, especially in the USA, which has a major impact on medicine generally in the West. Nevertheless it is self-evident that unless the actual causes are removed as far as possible then the risks that the cancer will return remain high. In fact these risks may be increased even further by radiotherapy and chemotherapy which damage the immune system and therefore impair the body’s ability to deal with any incipient cancers which occur.

The reality is that the present focus in both research and treatment of cancer is on curing the disease. However if real progress is to be made there must be much greater emphasis on identifying the causes so that preventative action can be taken. It is highly relevant that one of the few areas has been with lung cancer where smoking where smoking tobacco was shown to be a major cause. Consequently the incidence has fallen in men as a result of a decline in the numbers who actually smoke cigarettes. Rather ironically the opposite applies to women, as more and more of them take up the habit.

Finally I must re-iterate the success achieved by Jane Plant. So despite what I have said here, I certainly would not wish to dissuade anyone from eliminating dairy from their diet in an attempt to cure or to prevent breast cancer. In the final analysis it is imperative that individuals makes up their own mind about what will be most suitable for each person.


  1. http://vernerwheelock.com/?p=522
  2. http://vernerwheelock.com/?p=169
  3. http://vernerwheelock.com/?p=173
  4. http://vernerwheelock.com/?p=243



102. The Jane Plant Approach to Breast Cancer

Jane Plant is Professor of Geochemistry at Imperial College in London. For 5 years she was the Chief Scientist for the British Geological Survey. In 1987 she was diagnosed with breast cancer, which recurred 5 times and by 1993 had spread to her lymph system. She was not prepared to accept the advice of the conventional medical profession about the treatment and prognosis of her condition without question. Instead she applied her scientific training and expertise to try to identify the actual causes of the disease. As a result she devised simple changes to her diet and lifestyle which produced a complete cure. Her book describes how the story unfolds and contains details which may be used to cure or prevent cancers of the breast and prostate (1).

In this blog I will highlight some of the key points.

As a result of her initial investigations, Jane was astonished to learn how much had been discovered about breast and prostate cancer which was not generally available to the public. In reality there is knowledge of many ‘controllable’ risk factors which could be used to provide advice on how to make simple lifestyle changes that would help to prevent or treat these cancers. In the UK, the risk of developing breast cancer has been increasing progressively for years and would affect about 1 in 12 women at the time the book was written. By contrast, the risks were 50% or more lower in the Far East.

After the breast cancer was diagnosed, Jane agreed to have a mastectomy. While she was visiting the hospital, she repeatedly asked the medical staff what actually caused the cancer so that she could take steps to prevent a recurrence. As she had been advised that excess oestrogen was one of the causes she requested a diet which would reduce her oestrogen levels. Since doctors and nurses had difficulty in answering these questions she was referred to a dietitian, who did not keep a promise to investigate further and failed to respond to telephone calls.

Subsequently Jane made changes to her diet based her work on diets which were considered to be anti-cancer. Despite this about 5 years later, she became aware of a large hard lump under her left arm. This was removed by surgery, followed by a similar procedure to remove another one 2 weeks later. Although there were no signs that the cancer had spread, she agreed to a course of radiotherapy but this did not prevent the development of a small hard lump in a lymph node. After surgical removal, Tamoxifen was recommended, which Jane declined because she was aware it increased the risk of other types of cancer and had known several women on the drug who had died. Unfortunately the cancer re-emerged and this time it was decided that chemotherapy would be the treatment. The procedure involves tests on blood and urine so that the dose can be determined. On one occasion the doctor writing the prescription made a mistake and doubled the previous dose. This was noticed by Jane and a correction was made. However if this had not been detected, she may well have died of liver or kidney failure. The chemotherapy continued and Jane measured the size of the lump regularly, which did not show any decrease.

At this point, Jane decided to approach the problem using all her scientific training and expertise. A study of the different rates of cancer demonstrated the huge differences in the incidence of breast and prostate cancer throughout the world. In particular, the rates for breast cancer in rural China were only about 1/7 the rate of the UK. The difference for prostate cancer is even greater. Even in the industrialised areas of China and Japan the rates are still very much lower. Jane and her husband looked in detail at the information from the China-Cornell-Oxford project based on surveys conducted by a team led by Colin Campbell of Cornell University in the USA. They considered that the differences in cancer rates could be due to the high consumption of soya in the typical Chinese diet but doubted if this was the critical factor. However they then had the bright idea that perhaps milk and milk products would provide the answer to the puzzle. Working on the basis that the part of the body which is diseased is the key to the cause, they concluded that consuming a powerful biochemical from the mammary gland of one species might be sending the wrong signals to the mammary gland of another species, namely the human breast.

Prior to the initial diagnosis of breast cancer, Jane had consumed lots of dairy produce, including skimmed milk as well as low-fat cheeses and yoghurt. Although Jane had made adjustments to her diet, this contained milk, yoghurt and ghee (clarified butter). At this point Jane decided to cease eating all dairy produce immediately, including all other products which use milk or milk products as an ingredient, such as soups, biscuits, cakes.

Although the chemotherapy had not been effective up to that point, within days of commencing the new dietary regime the lump started to shrink. One week after she had eliminated dairy produce from her diet the lump began to soften and reduce in size. Jane continued to monitor the lump and remarkably found a straight line graph between size and time, which indicated that it would disappear completely. Sure enough, after 6 weeks she could find no sign of it. A couple of days later this was confirmed by her cancer specialist. Although the chemotherapy continued at the same time as the altered diet, none of the specialists had ever observed this effect from this type of treatment over a period of 20 years, so the effect must have been caused by the change of diet.

Jane is totally convinced that the link between dairy produce and breast cancer (and probably prostate cancer) is similar to that between smoking and lung cancer. There are some epidemiological studies which are consistent with this conclusion but this type of evidence does not prove “cause and effect”. Nevertheless the experience of Jane certainly cannot be discounted. She is a reputable scientist and there is absolutely no reason to doubt the veracity of her story.


  1. Jane A Plant (2000) “Your Life in Your Hands: Understanding, Preventing and Overcoming Breast Cancer”. Virgin: London




101 More News from Australia

As I explained in the previous blog (1) Robert Clark has now submitted his report, following the Inquiry he conducted into the actions of Jennie Brand-Miller and Anthony Barclay at the University of Sydney set up in response to allegations made by Rory Robertson. Robertson has now had an opportunity to analyse the report and his comments have just been posted on his website (2).here are some of the key points he makes:

  1.  Five of seven of Professor Clark’s “Preliminary Findings of Fact” are factually incorrect.
  2. Clarke concluded that Statements made by the Complainant alleging that the United Nations FAO has falsified data are serious, and do not appear to be based on detailed evidence or inquiry”.However it is clear from the email correspondence between Robertson and officials at the FAO that this conclusion cannot be substantiated. Quite simply the only relevant information available to the FAO was that produced by the Australian Bureau of Statistics (ABS). Data up to 1999 was produced by the ABS but was discontinued after that because the organisation was not satisfied that it could prepare reliable figures. No doubt this means that there were question marks about the figures which were released for some years prior to this. However as Robertson makes clear the data which FAO produced for the years after 1999 were based essentially on that 1999 value. All of these points were put the FAO in a long and detailed email to FAO officials in December 2012. Apparently there was no reply. As the FAO is obviously using ABS data that lacks credibility, Robertson’s case is compelling and Clark has not provided a valid justification for his conclusion.
  3. Although Clark interviewed Brand-Miller and Barclay he did not interview Robertson. This is rather surprising as it is essential that an even-handed approach is adopted in any investigation of this type. When this is related to the fact that some of the key documentation was apparently not consulted there must be serious questions about the objectivity of the inquiry.
  4. Robertson’s prime objection is that the quality of the data, which have been used to conclude that the consumption of sugar has declined, is poor. This “fact” is absolutely crucial to the formulation of the “Australian Paradox”. This in turn has major implications for the food industry and for the formulation of public health policy.
  5. Clark failed to investigate properly misrepresentation of the information on the changes in soft drink consumption. In the original paper there is a graph which clearly shows that the consumption of sugary soft drinks increased from 35 to 45 litres per person per year between 1994 and 2006. It is obvious to anyone that this is an increase of about 30%. Nevertheless, the authors somehow conclude that there is actually a decrease of 10%. Clearly this is a blatant misrepresentation of what is straight forward information. There was a decline in sugar consumption between 2002 and 2006 which Brand-Miller and Barclay calculated to be 600g per person per year. In fact the correct value is only 150g per person per year. Even if there was small reduction in sugar from soft drinks between 2002 and 2006 this certainly does not conflict with the fact there was an increase of 30% between 1994 and 2006. It is surprising that Clark did not refer to this issue.

Now that I have had a chance to go through the report of the investigator in some detail and also have the benefit of the initial response from the complainer, I am forced to the conclusion that it is not the hard-hitting independent investigation that was needed. It certainly comes across as a “get us out of a hole” report. When questions were first raised it was evident that the authorities in the University of Sydney were not impressed and tried to play things down and hope that Rory Robertson would go away. It is difficult to understand why the academics were given the opportunity to present their case in person but Robertson was not. Furthermore the failure on the part of the investigator to ignore some of the documentation submitted makes one suspect that he did not do a totally thorough job.

Whenever dubious behaviour is alleged or suspected, a very good maxim is to “follow the money”. In this case, there is absolutely no doubt that Charles Perkins Centre is a major part of the University of Sydney operation. It represents a huge investment and the work on glycaemic index is very good income source for the University. It is perfectly understandable that the senior management will be keen to protect it. It is highly likely that Robertson will have been regarded as a bit of a nuisance to be swatted away. As it happens he is made of stern stuff and was not going to go away without a fight.

In these days universities have to fight hard for finance but they also have a responsibility as centres of learning and a duty to uphold standards of integrity and scholarship. The longer this controversy goes on the harder it will be to reach a satisfactory solution. The reality is that this incident has done enormous damage to the reputation of the University of Sydney. The fact that this blog is based at the other side of the world demonstrates the impact is not just restricted to Australia. Robert Clark talks about lessons to be learned but makes no comment about how this has been managed by the University. In fact, the University has a really big problem. It has to clean up this mess. Because of the failure to address the allegations when they were made originally, “the powers that be” will have to consider not just the roles of Brand-Miller and Barclay but also the handling of the issue by the senior management. Above all, they would do well to act on the famous advice of Denis Healey “When you are in a hole, the first thing to do is stop digging!”.


  1. http://vernerwheelock.com/?p=513
  2. http://www.australianparadox.com/pdf/RR-response-to-inquiry-report.pdf
  3. http://www.australianparadox.com/pdf/FAOfalsifiedsugar.pdf


100. Australia: Report on Inquiry into Allegations against University of Sydney Academics

In my previous blog (1) I explained the background to the allegation against Jennie Brand-Miller and Alan Barclay by Rory Robertson. Essentially he argued that the so-called Australian Paradox which claimed that the increased incidence of obesity was not related to an increased consumption of sugar. Robertson concluded that the information showing that the sugar intake had fallen, over the period when obesity had increased was fundamentally flawed.

The University of Sydney commissioned Professor Robert Clark, Chair of Energy Strategy and Policy at the University of New South Wales and a former Chief Defence Scientist of Australia to conduct an Inquiry. He had just delivered his report, which is available on the internet although parts of it have been redacted (2).

The key statement in the Australian Paradox paper is that:

This analysis of apparent consumption, national dietary surveys and food industry data indicates a consistent and substantial decline in total refined and added sugar consumption by Australians over the past 30 years”(3).

Robert Clark dismissed 6 of the 7 allegations which Rory Robertson had made. On the face of it, this might appear to be a satisfactory outcome as far as the academics were concerned. The only allegation which was substantiated referred to the decline in sugar intake from sugar sweetened soft drinks between 2002 and 2006. In the paper Brand-Miller and Barclay has used a value of 600g per person. This figure was wrong. It should have been only 150g.

Nevertheless a close reading of the report shows that all in the garden is not rosy and that there are many lessons to be learned. In particular Clark was not impressed by the quality of the original “Australian Paradox” paper. He concluded that the paper was not tightly written and contained a number of arithmetic errors. He expressed the view that important new findings would usually be published in a high-impact, rigorously peer-reviewed journal. Subsequently the results would be considered in special edition publications of conference journal format. Clearly this had not been done as the original was published in what was regarded as a ‘soft’ journal, where the quality controls are less stringent. As a consequence it was recommended that a new one be prepared which specifically addresses the key factual issues raised in the inquiry. Furthermore this paper should be written in a constructive manner which respects the issues relating to the quality and reliability of data, raised by Rory Robertson.

The crux of the dispute is the conclusion in the Australian Paradox Paper which claims that there has been a decline in the consumption of the sugar from 1980 to 2003 during which time there has been a substantial increase in the incidence of obesity. This is fundamental to the Paradox, which is that the obesity is not caused by sugar, a phenomenon which contrasts with that of many other countries, including the USA and the UK.

However as Robertson has pointed out repeatedly the sources used by Brand-Miller and Barclay are subject to many criticisms. This raises serious questions about the reliability of the data and therefore casts doubt on the conclusions drawn.

The body providing the relevant information is the Australian Bureau of Statistics (ABS). Clark was provided with data from the ABS which showed that there had been a decline in the per capita consumption of sugar between 1975/6 and 1998/9. So the critical issue is to determine the reliability of these data. In correspondence between the ABS and Clark it is accepted that some errors may not have been taken into consideration. More specifically, in order to compute a value for the amount of sugar in the food supply it is essential to have information on all the different sources of sugar. These include all the different foods, especially those which are manufactured, which contain sugar. So in order to work out the total supply, the sugar content of all these foods must be known. This is extremely complicated because there must be variability within products and from time to time. Product formulation is continually changing. A good example is the growth in products which are promoted as “low fat”. Very often these are devised by removing the fat and replacing it with sugar. After 1998/9 the ABS discontinued publication of the figures. One of the reasons was that the ABS believed these conversion values were no longer appropriate. The inevitable question, of course, is “Were they ever accurate and reliable?” On top of all this, all the evidence amassed by Robertson, an experienced economist well used to number-crunching, shows that the trend is UP not DOWN

In view of the absolutely critical importance of the conclusions inherent in the Australian Paradox, it would have been incumbent on the authors to provide a cast-iron case. Clearly they have not done so and it is regrettable that Clark did not reach that conclusion. Furthermore he made no attempt to place this issue in the context of the growing appreciation of the role of sugar in the development of a range of different diseases. Of much greater concern than obesity is Type 2 diabetes (T2D) which in Australia has increased more than 3-fold in the past 30 years or so (4).

It is also becoming clear that sugar intake is a key factor leading to the development of heart disease, many cancers and Alzheimer’s Disease. The evidence continues to accumulate (5). The presence of fructose may be especially damaging to health (6).Bodies such as the World Health Organisation and the American Heart Association now accept that current levels of sugar consumption are not compatible with good health. Hence official recommendations are being reduced significantly.

Despite the somewhat unequivocal findings of Robert Clark there is no doubt that Rory Robertson’s campaign has had a genuine impact and that the credibility of the Australian Paradox has been seriously undermined as shown by some of the local media coverage (7).


  1. http://vernerwheelock.com/?p=510
  2. http://sydney.edu.au/research/documents/australian-paradox-report-redacted.pdf
  3. A W Barclay & J Brand-Miller(2011) “The Australian Paradox: A Substantial Decline in Sugar Intake over the Same Timeframe that Overweight and Obesity Have Increased” 3. pp491-504
  4. http://embryology.med.unsw.edu.au/embryology/index.php?title=Abnormal_Development_-_Maternal_Diabetes
  5. http://vernerwheelock.com/?p=325
  6. http://vernerwheelock.com/?p=234
  7. http://www.abc.net.au/radionational/programs/backgroundbriefing/independent-review-finds-issues-with-controversial-sugar-paper/5618490