Uffe Ravnskov

A selection of my newsletters 

 

For several years I have sent newsletters to people who have shown interest in the many contradictions of the cholesterol hypothesis and/or the work of our group THINCS, The International Network of Cholesterol Skeptics. Here comes a selection of these letters. If you want to become a recipient of my newsletters, please click here.  

 

October 2004        About those who write the guidelines 
December 2006
     About treatment of type 2 diabetes and a vicious attack on me
January 2008        About Pfizer and Merck and their criminal behavior
April 2008
              About the unsuccesful statin trial named ENHANCE
November 2008     About the misleading and dangerous advices for statin treatmen
March 2009
           About Harvard and their industry-sponsored prfessors
September 2009   About all the "goods" associated with statin treatment
December 2009
    About WHO/FAO experts unable to draw correct conclusionss
April 2010
             Medical journalists with open eyes
June 2010
             The new trial regulations and their surprising effects
July 2010
              About Colin Campbell and his misleding book "The China Study"
September 2010
   More intelligent jouralist 
October 2010
        How researchers try to exlain away their own results
December 2010
     About critical researchers and journalists
January 2011
        About the Cochrane report and statin treatment of healthy people
April 2011
              More fraudulence; about Alzheimer, and funy youtube programs
May 2011
               A brilliant talk by our member, Professor David Diamond
June 2011              Humorous comments and a revealing study from Sweden
July 2011
               A report about statin adverse effecs and how editors close their eyes
September 2011
    More false conclusions and the diet revolution in Sweden

Sept-Oct 2011
       About Unilever and their "heart-healthy buttery spread
Oct 2011                The "miraculous" statin drugs
November 2011     How to mislead the medical profession
December 2011
     
Low cholesterol, cancer and infections
January 2012         About writing letters to medical journals

February 2012
       Statin treatment and the risk of getting diabetes
March 2012            About red meat and about obesity
April 2012              More about statin side effects
 
May 2012             
There is light in the tunnel ahead
July 2012               About bad muscles and a fraudulent dietary study
August 2012         Egg yolk, bad science and scientific fraud
Sept  2012           
Fraudulent advertising for food containing plant sterols.
Oct 2012               Right and wrong about statin treatment
December 2012    Does statin treatment prevent cancer?
January 2013       Scary news, bad news and good news
February 2013     The scandalous dietary gudelines
February 2013     Light ahead in the tunnel?
March 2013          Fraud is allowed, but not questioning
May 2013             Statins or not? Red meat or not?


 

 

October 2004   

How to convert healthy people into patients

You have probably heard about the new guidelines issued a few months ago by the National Institutes of Health and according to which “normal” cholesterol now is considered to be far below the mean value in most populations. Bingo thus for the drug companies (and the authors of the guidelines).   
     But luckily there is a growing number of sceptical scientists. A few days ago the Center for Science in the Public Interest, an American non-profit consumer advocacy organisation, send a petition to the NIH and a number of politicians and institutions asking for a neutral evaluation of the studies that have been used as an argument for introducing these guidelines. Read the petition and also the response from Barbara Alving, acting director of the National Heart, Lung, and Blood Institute, sent to a reporter on British Medical Journal:  
     Please note that while the petition is backed up by relevant references to the scientific literature, Alving´s response has nothing of the kind. Malcolm Kendrick has a comment to this story, “Conflict of Interest – Time to Count The Spoons” 

     Read also the BMJ reporters own comments

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December 2006  

About lowcarb diet and diabetes

Recently Heine and coworkers published a review in British Medical Journal about the treatment of type 2 diabetes without mentioning a word about the many succesful low-carbohydrate trials. The strong resistence against these trials is of course due to the cholesterol campaign according to which we shall eat carbohydrates instead of fat, an advice that has been given to diabetic patients as well. Read the many comments to that study in BMJ, including my own (the last one).

If you want to read more about the lowcarb diets I can recommend these papers, freeely available on the web:  

Arora SK, McFarlane SI. The case for low carbohydrate diets in diabetes management.

Westman EC, Volek JS, Feinman RD  Carbohydrate restriction improves the features of Metabolic Sydrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction

 

Ridicule instead of answer

As readers of my newsletters or my books know there is no evidence whatsoever that saturated fat has anything to do with atherosclerosis or coronary heart disease. But do you know that there is no evidence either that saturated fat raises the cholesterol concentration in the blood? A recent paper by Krauss and coworkers is a further confir- mation, but their finding, clearly recorded in a table, wasn´t mentioned in the discussion or in the abstract. This is a common observation when researchers come up with results that go counter to the cholesterol paradigm. Therefore I sent a letter to the editor My letter was commented in a vicious editorial by Martijn Katan, one of the most eager proponents of the cholesterol campaign. You can read more about this discussion here.

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      January 2008  

     Pfizer fraud

Pfizers new cholesterol-lowering drug Torcetrapib was a failure; instead of lowering the risk of heart disease, it resulted in more heart attacks, although in addition to lowering LDL cholesterol, it also raised the "good" HDL. 

Now it appears that Merck´s Vytorin is just as bad. Instead of halting the progress of atherosclerosis the trial directors of ENHANCE noted an increased progress, although cholesterol was lowered more than ever before. Here is a comment in New York Times

But there are more curious facts about that trial. Read for instance a comment in The Guardian

A new article about statin treatment has just been published on the web by our member Sandy Szwarc. 

...and here are more critical articles published in Bloomberg Businessweeek:

Do Cholesterol Drugs Do Any Good?
In the Real World, a Slew of Side Effects from Statins
False Promises on Alzheimer's

Critical comments have also been aired by Gary Taubes and Tara Parker-Pope, both of them in New YorkTimes.  

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                  April 2008  

                  An unsuccesful statin trial

In this week´s issue of The New England Journal of Medicine the report from the unsuccesful ENHANCE trial was published, almost two years after it had been terminated. Not unexpectedly, at least for those who have been informed by THINCS´ members, a further lowering of cholesterol by a non-statin drug did not improve the angiographic changes of the coronary arteries; on the contrary. Read Sandy Szwarc´s report!

In that trial cholesterol was lowered in two groups of people with familial hypercholesterolemia. Unexpectedly, at least to the trial directors, angiographic progress was the same in both groups, although cholesterol was lowered much more in those who were treared with two cholesterol lowering drugs. There is a logical explanation to that, unknown to most people, and it may remain so, at least for a while, because the editor of the New England Journal of Medicine didn´t find my comment of sufficient interest to their readers. The explanation is that it is not the high cholesterol that causes a few of the people with familiar hypercholesterolemia to die at a young age.    Read my rejected letter  

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              November 2008  

             ...and  another one

First, you have probably heard about the new statin trial JUPITER. According to its authors their new super statin drug Crestor may soon eradicate cardiovascular disease.

Not so – we are again misled by industry-paid socalled researchers. Here are two excellent comments; the first one by Dr. Michael Eades, the second one by one of our members Sandy Szwarc

                Scary news

According to the new guidelines for cholesterol lowering even children should be treated with statins. Fortunately a host of critical comments have appeared in various media. Here are two from Tara Parker-Pope, the wise medical reporter on New York Times: 8-Year-Olds on Statins? A New Plan Quickly Bites Back

…and one from Sandy Szwarc: Is it for real? Cholesterol screening in toddlers and statins from elementary school age?

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                   March 2009     

              Why the bad things aren´t told

Here are some cuttings from an article by New York Times reporter Duff Wilson:

...In a first-year pharmacology class at Harvard Medical School, Matt Zerden grew wary as the professor promoted the benefits of cholesterol drugs and seemed to belittle a student who asked about side effects. Mr. Zerden later discovered something by searching online that he began sharing with his classmates. The professor was not only a full-time member of the Harvard Medical faculty, but a paid consultant to 10 drug companies, including five makers of cholesterol treatments.
...about 1,600 of 8,900 professors and lecturers have reported to the dean that they or a family member had a financial interest in a business related to their teaching, research or clinical care. The reports show 149 with financial ties to Pfizer and 130 with Merck.
...David Tian, 24, a first-year Harvard Medical student, said: "Before coming here, I had no idea how much influence companies had on medical education. And it's something that's purposely meant to be under the table, providing information under the guise of education when that information is also presented for marketing purposes."  

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September 2009  

The statins are better than snake oil

It is often said that statins are good for almost any human disease. The method used to ‘prove’ that is to compare people on statin treatment with untreated people. Most people in the latter group have of course low cholesterol, and not only low, but very low cholesterol, because as you know the upper limit for normal has been lowered again and again through the years. It is well-known that low cholesterol is a risk factor for many diseases; to mention only infectious ones and cancer. What these researchers have shown is therefore that high cholesterol is beneficial because people in the statin group have had high cholesterol most of their life. One of the allegations is that statin treatment protect against pneumonia. Recently researchers compared 1125 patients with pneumonia with 2235 healthy people of the same age and sex. What they found was that more of the pneumonia patients were on statin treatment, not less. Their result was recently published in British Medical Journal

 

Recomended reading

If you think that the statin trials have proved that cholesterol lowering is beneficial I recommend you to read two important books written by people with inside information about how we are conned by the drug industry. The first one is “The Truth About the Drug Companies” by Marcia Angell, former editor-in-chief of New England Journal of Medicine, one of the world’s most respected medical journals. The other one is “The Trouble With Medical Journals” by Richard Smith, former editor-in chief of British Medical Journal,  another great and respectable publication.

You should also listen to Beatrice Golomb. She is an associate professor of medicine at the University of California, San Diego and has devoted many years studying the side effects of statin treatment. Here is a youtube talk she gave recently entitled Pharma corruption of medical science

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December 2009  

A dietary U-turn

Those of you who have followed our work already know that saturated fat isn´t a menace to human health. Recently WHO and FAO published a new report, Fats and Fatty Acids in Human Nutrition.  

Now, finally, their experts have  come up with the same conclusion; go to pages 191 and 239. However, they havern´t changed their recommendations! You can read more about that paper here  (from my new book Ignore the Awkward! How the Cholesterol Myths Are Kept Alive)                                                                                                                                     

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                                      April 2010  

                       The press is awakening

The press is awakening. Here you will find interesting articles from major newspapers and journals:  

John von Radowitz, (The Independent):
85% of new drugs 'offer few benefits'
Christopher Hudson (Telegraph): Wonder drug that stole my memory.

Statins have been hailed as a miracle cure for cholesterol, but little is known about their side effects. Read also the 140 comments, but beware, they are scary.  

Melinda Wenner Moyer (Scientific American): It's Not Dementia, It's Your Heart Medication: Cholesterol Drugs and Memory. Why cholesterol drugs might affect memory.

Tom Naughton: Big Fat Fiasco:  how the misguided fear of saturated fat created a nation of obese diabetics. A humourous speech with a serious content. Five parts, on Youtube  

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June 2010  

No more fraudulent trials?

After the Vioxx scandal new clinical research regulations have come into force.  Trials that begin enrolment of patients after 1 July 2005 must register before their start in a recognised trials registry to be considered for publication and they must be published within 90 days after the ending regardless of whether the results are positive, negative or inconclusive.
   Curiously, almost all of the major trials that have been published since then have failed. How can we explain the discrepancy between the the older positive trials and the negative recent ones? This is a crucial question put by the French researcher and THINCS member
Michel de Lorgeril

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July 2010  

The China Story - from Alice in Wonderland?

Have you been mislead by Colin Campbell? Here is an excellent analysis by our member Stephanie Seneff of his book The China Study. It is sad that this book has had such great impact on people's  dietary habits.

September 2010

More revelations  

More and more people realize that the cholesterol campaign is built on bad or fraudulent research. Here are a number of recent eye-opening articles:

Steven Lewingston (Washington Post): Ike and the war on meat
Tom Naughton: Bad News for Statins
Jo Willey (Daily Express): Statins Can Be Risk To Health

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October 2010  

How to get the desired results

A colleague of mine asked about my view on an article in Science Daily. Here you can read that ”A new study by researchers at Harvard School of Public Health (HSPH) provides the first conclusive evidence from randomized clinical trials that people who replace saturated fat in their diet with polyunsaturated fat reduce their risk of coronary heart disease

The paper, the main author of which is Dariush Mozaffarian from the Channing Laboratory at Harvard Medical School, is available here.

The article in Science Daily also tells about another recent review co-authored by Frank B Hu and Ronald M Krauss, two other well-known US scientists. They concluded that ”there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.” The abstract of that paper is available here. Their conclusion was explained away by these words: ”Some of these mixed findings may relate to absence of prior focus on the specific replacement nutrient for saturated fat.”

How did Mozaffarian and his coworkers reach to their contradictory conclusion, you may ask. It is particularly curious because Mozaffarian himself has published a study that contradicts his new paper. What he and his coworkers found was that progress of atherosclerosis was less pronounced the more saturated fat the participants had eaten.

Let me tell you how Mozaffarian succeded with turning around:

By including the Finnish Mental Hospital study, a dietary trial that did not satisfy the most elementary requirements for a correctly performed trial. For instance, it was neither controlled, randomised or blind. 

By excluding two trials where mortality increased in the treatment groups and a third where no effect was achieved. (You can read more about these trials in my books).

Furthermore, they included the DART trial, where the only group that improved had increased their intake of fish as the only dietary measure.

What proponents of polyunsaturated fat forget is also that today, most of such fat comes from corn, soy and sunflower oil. Here the main type of polyunsaturated fat is omega-6, and there are numerous papers having shown that an excess intake of omega-6 polyunsaturated fats has many serious adverse effects.  

A humorous talk about serious matters

Recently Tom Naughton gave a speech at the local library entitled "Big Fat Fiasco:  how the misguided fear of saturated fat created a nation of obese diabetics."  Luckily a photographer was there, because it is both funny and serious, and it is now available on Youtube in five parts

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December 2010

Fraud revealed

Do you believe in medical science? Do you think that what has been published in the major medical journals reflects the truth and nothing but he truth? Then read this article by John Ioannidis entitled ”Lies, damned lies and medical science” published recently in The Atlantic.

Ioannidis has spent his career challenging his peers by exposing their bad science. Here is a quotation from the article: ”We could solve much of the wrongness problem, if the world simply stopped expecting scientists to be right. That’s because being wrong in science is fine, and even necessary—as long as scientists recognize that they blew it, report their mistake openly instead of disguising it as a success, and then move on to the next thing, until they come up with the very occasional genuine breakthrough.” 

More and more journalists have realized that the drug companies aren’t thrustworthy either. Read for instance this article by Stephen Adams from the British newspaper The Telegraph. Or the document from Public Citizen

Good news

For many years  Walter Willett, head of the world´s largest dietary study situated at Harvard, has warned against saturated fat. This is most curious because none of the many Harvard studies has ever found that those who gorge in saturated fat are at a higher risk than those who follow the offical guidelines.
   But now, in an
interview by Marni Jameson in LATimes, he admits that fat is not the problem!  

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January 2011

How to cover up the bad news

You have probably read about the new report from the Cochrane Collaboration mentioned in many of the major media recently (for instance The Telegraph, BBC, Boston Globe, CBC News, LA Times, and Reuters. The aim of the Cochrane authors was  to assess the effects, both harms and benefits, of statins in people with no history of CVD. For that purpose they had analysed randomised controlled trials of statins with minimum duration of one year and follow-up of six months, a total of 14 including 34272 participants.

The authors concluded that ”although reductions in all-cause mortality, composite endpoints and revascularisations were found with no excess of adverse events, there was evidence of selective reporting of outcomes, failure to report adverse events and inclusion of people with cardiovascular disease. Only limited evidence shed that primary prevention with statins may be cost effective and improve patient quality of life. Caution should be taken in prescribing statins for primary prevention among people at low cardiovascular risk.”

As mentioned in the Cochrane report the low number of side effects is unlikely. To mention only that independent researchers have found that muscular problems are seen, not in less than 1 percent as reported in all statin trials, but in about 25 % of those who exercise regularly. 

But it is worse than that. As the authors had included only trials with a length of one year or longer, they have missed the first statin trial, named EXCEL. It included more than 8,000 healthy individuals (named ‘patients’ in the trial reports, because of their moderately elevated cholesterol) who received one of four different doses of lovastatin (Mevacor®) or a placebo. The trial was terminated already after 48 weeks of treatment. 

The reason?

Because the authors only wanted to see if the ”patients” tolerated the drug, and they did, at least according to the trial report.

In the abstract you look in vain after the clinical outcome. In the text you can read that total mortality was 0.2 percent in the control group and about 0.5 percent in the four treatment groups. The total number of deaths was 36, but as nothing was said about the exact number of participants in each group (they were ”of similar size”), it is impossible to calculate if the higher number of deaths in the treatment groups was statistically significant or not. However, it would most likely have become significant had the trial continued.

It is also worth mentioning that whereas all statin trials with a positive outcome are freely available on the web, this is not the case with EXCEL.  

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April 2011

Cholesterol and the brain

Although members of THINCS since long have warned against the harmful cerebral effects from cholesterol lowering, few doctors know about it and nothing is mentioned on the drug labels. Here is a thorough review about this issue by Emily Deans, MD, a clinical instructor in psychiatry at Harvard Medical School. 

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May 2011

Obesity - a man-made problem

More and more scientists realize that the cholesterol campaign is the greatest medical scandal of modern time. Here you can listen to a brilliant talk "How Bad Science and Big Business Created the Obesity Epidemic" by our member Professor David M Diamond from the Departments of Psychology and Molecular Pharmacology and Physiology, Center for Preclinical and Clinical Research on PTSD in Tampere.   

 

June 2011

How to explain away bad results

Using a new technique named strain imaging US researchers have found that statin treatment decreases myocardial function.  This is not new knowledge, of course; just consult the writings of our members Alena and Peter Langsjoen. Do we expect official warnings now?
     Of course not. Here is a comment by Malcolm Kendrick (from our internal discussions):   

You make the mistake of believing that peer reviewers actually read the papers they are sent....
   And, of course, criticising statins in public would be the end of any self-respecting cardiologists career. So we have now reached the point where it is clear that statins damage heart function - but this is a good thing. Statins sure as hell work in a mysterious way. Even when they are doing harm they are doing good. In fact the more harm they do, the better it is.It may be worth writing a book on statin theology:
     'Father, if statins are so powerful and good, how can they let bad things happen? I do not understand.
     'Ah, my son, the ways of the statin are beyond human understanding. We must not question their great power. All we can know is that Statins are great in their endless love for us all. To ask such things isis to question the greatness of Statination itself....etc.'

Another solution is to create an ad-hoc hypothesis. If you don´t know what that means, read Tom Naughton´s explanation!  

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The statins are bystanders only

 A new problem for the cholesterol campaign has appeared: There is no association between the decrease of heart disease and the use of statins.This has been shown by Swedish researchers who compared the two measures in all Swedish districts.

No association! In some districts heart disease went down and statin use increased but in just as many it was the opposite.

You can read the paper here to be published in Journal of Negative Results, meaning that very few will take notice, unless of course you tell about it whenever you have the possibility.

Again, this is no surprise for those who have followed the literature with a critical eye. If you want a detailed explanation why cholesterol is not the enemy, read this review by one of our members Stephanie Seneff. Its title is How Statins Really Work Explains Why They Don't Really Work.  

 

Alzheimer and low chlesterol

Researchers paid by the drug industry are eager to tell us that people with Alzheimer´s disease should be prescribed a statin drug. How do they explain that all the blood lipids are lower in such patients, lower the more advanced the Alzheimer has progressed? You can read more about that here  

 

A funny video

  LCHF is the shit! 

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July 2011

Scary statin news, but editors, please keep quiet!

Half a year ago I told you about the new Cochrane report the authors of which concluded that the benefit from statin treatment of people without heart disease is questionable. What I didn´t tell about was the results from a report by Hippisley-Cox and Coupland published last spring in British Medical Journal. The reason was that I hadn´t observed it myself at that time.

In the QResearch database 368 general practices in England and Wales had supplied data from more than 2 million patients of whom 225,922 were new statin users. By analysing these data Hippisley-Cox and Coupland concluded that whereas the total number of prevented coronary events, almost all of which were non-fatal, was less than 3 per cent, the total number of adverse effects was more than 4 per cent. The adversities were not harmless either, but consisted of acute renal failure, cataract, and serious liver and muscle damage.

You may probably ask yourself if statin treatment of healthy people has been stopped after the publication of this scary report. The answer is no. Neither the practicing doctors nor common people know about these figures, possibly because the British report is difficult to understand for people without thorough knowledge about epidemiology and statistics. But what about the experts? Why haven’t they reacted? Are they anxious to loose their research money and their other financial benefits from the drug industry?

Together with two highly qualified members of THINCS (Professors Paul J Rosch and Morley C Sutter; see our list of members) I sent a paper to British  Medical Journal about this issue. In the paper we showed in many details that the number of adverse effects must have been even higher because liver disease was recorded only if the substance that reflects liver damage was three times higher than the upper limit of normal, and muscle disease was recorded only if the substance that reflects muscle damage was four times higher. In accordance independent researchers have reported that 20-25% of statin-treated people experience muscle pain or weakness. We also pointed out that several types of adversities were not recorded at all. It is well known for instance that diabetes occur in about 0.5% of statin-treated people and that 20% of the male patients become more or less impotent after a few months treatment. Reviews taking all cholesterol-lowering trials together have also shown a significant increase in death from accidents, suicide, or violence, and there are numerous reports about memory loss and other cerebral disturbances.

Worst of all is that the risk of cancer has been ignored by all experts although there is much scientific evidence that cholesterol lowering may result in cancer (you can read much more about that in my recent book Ignore the Awkward!).

A few days later I received the following message from the editor: 

Thank you for sending us your paper. We read it with interest but I regret to say that we have decided not to publish it in the BMJ. Although we are sympathetic to the general point that the downsides of statins are underappreciated, we think that we have covered the point enough. Indeed, we published the Hippesley Cox article that you draw heavily upon.


But neither the editor nor the authors have drawn the relevant conclusion that healthy people should stop taking statins. We therefore send our paper to The Lancet instead, but got an immediate answer from the editor:

 

Dear Dr. Ravnskov, Many thanks for submitting your manuscript to The Lancet. We have considered your manuscript, but our decision is that it would be better placed elsewhere

We tried Archives of Internal Medicine, but with the same result: 

Dear Dr. Ravnskov, Your manuscript has been reviewed by the senior editors of Archives of Internal Medicine. I regret to inform you that its priority rating is not sufficiently high to warrant our considering it further for publication. Based on our initial review, we will not be sending the paper for additional outside editorial review

Today millions of healthy people are on statin treatment without knowing about the imbalance between benefits and risks. How should we inform them when the experts and the medical journals don´t? We haven´t given up and we shall try other journals. The problem is however, that few medical journals are able to survive without their income from the drug industry, and editors are therefore reluctant to publish papers like ours.

In Sweden we have succeeded in informing the public by publishing an article in Dagens Nyheter,  the largest and most influential Swedish newspaper. An English version is available on the web. Click also on the text in the upper. right hand corner: Svenska Dagbladet: Debate on reignited.  

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September 2011

Shuffle the cards and the reader will believe you!

Misleading papers about the benefits of statin treatment published by research groups from prestigious universities are countless. Here is an example.

In 2003 the results from a large, multinational statin trial named ASCOTT-LLA (Anglo-Scandinavian Cardiac Outcomes Trial—Lipid-Lowering Arm) including 10305 patients, half of whom had received statin treatment. All of them had three risk factors, but none of them had had a heart attack. The trial was planned to continue for five years, but was stopped already after 3.3 years because of its “large reduction in major cardiovascular events”. Fatal and non-fatal myocardial infarction was reduced by 36 %, seemingly an impressive figure.

However, the absolute figures were 1.93 % “heart events” in the statin group against 3 % in the untreated control group, thus a difference of only 1.07%. The figure 36% is correct, however, because 1.07 is the difference between 3 and 1.93, and 1.07 is 36 % of 3.The difference in mortality was even lower. 3.6 % died in the statin group against 4.1 % among the untreated. You could also say that the chance of being alive after 3.3 years without statin treatment is 95.9 %, but if you take a statin drug every day you can increase your chance to 96.4 %.

You have to consider the risk of adverse effects, however. In the statin group 3.8 % either got diabetes, renal failure or life-threatening heart arrhythmia, against 3.2 % among the untreated. None of these adverse effects had increased with statistical significance, but perhaps they would, had the trial continued for the planned five years. Nothing was said about other adverse effects, although there are many reports about muscle damage, impotency, cancer, bad memory or temper, to mention just a few, and some of them have been reported in much larger number. More about that in my previous newsletter. 

Now to the amazing news. Eight years after the discontinuation of the trial the outcome of the British participants was analysed. To their surprise the researchers found that among those who had been on statin treatment eight years before, fewer had died from an infectious or respiratory disease compared with the untreated control individuals. Only 1.6% of those, who had been on statin treatment, had died from these diseases against 2.44% among the untreated.

The authors were excited, and the news were spread to many newspapers and professional websites; for instance Science Daily, Daily Mail, Pulse, Netdoctor and The Heart to mention a few.

The authors had a number of reservations. But what they didn’t consider was the fact that the number of statin-treated individuals after these eight years was almost the same in the two groups. To cite the authors:


“…there was substantial drop-in and drop-out of statin therapy among those originally randomized to placebo and atorvastatin, respectively. Consequently, at the closure of BPLA (the follow-up analysis; my comment), of those originally assigned atorvastatin, 63% were still taking it, and of those originally assigned placebo, 56% were taking atorvastatin.”


The crucial question is of course the following: Why did the original treatment group stop taking statins? Could the reason be unpleasant adverse effects? And isn´t it possible that some of those who started statin treatment during these eight years had not yet decided to stop because of unpleasant symptoms? If so, no conclusions can be drawn from these findings. That cholesterol-lowering should prevent infectious diseases is also highly unlikely, because the lipoproteins protect against all kinds of infectious diseases, an issue that I have described in detail in my books.   

 

More brave journalists

Now to the good news. Skepticism against the cholesterol campaign is growing. A few days ago medical journalist Lois Roger published a critical article about this issue entitled Big Fat Lies in the Sunday Times. Unfortunately it is not available without paying, but somebody has sent it to a website named Active Low-Carber Forums

Another eloquent journalist and researcher is Roy Moynihan. In the August 15 issue of BMJ he published a new, critical paper entitled “Surrogates under scrutiny: fallible correlations, fatal consequences”. Those who have read my books are of course familiar with the issue. Here are a few quotations for those who haven´t, as it is not available for nonsubscribers:



According to the 2010 Institute of Medicine report, although the methods used to determine blood cholesterol are reliable and reproducible, they do not directly measure LDL cholesterol and so have “limitations.” In addition, though LDL cholesterol is “hypothesised” to have a causal role in the atherosclerotic disease process, it has “not been conclusively proven.” And…lowering LDL cholesterol “does not always correlate with improved patient outcome.”The report points out there are over 200 coronary risk factors, and that cholesterol, while currently considered by many to be a valuable biomarker for heart disease, is only one of “multiple determinants” and “numerous other mediators. 

…The benefits of long term preventive therapies like cholesterol lowering drugs are usually portrayed as relative reductions in risk, but when the risks are considered in absolute terms, a different picture emerges. For example, based on a Cochrane review of trials for primary prevention, there has been recent enthusiasm that for people without a history of heart disease statins can reduce premature deaths by 17%, coronary heart disease by 28%, strokes by 22%, and revascularisation by 34%. Yet a close reading of the tables from that systematic review suggests the estimated absolute risk reductions with around four to five years of drug taking are 0.5% for death, 1.9% for coronary heart disease, 0.5% for stroke, and 0.7% for revascularisation.    
…A major rethink of the role of surrogates in medicine is timely. Routinely approving and prescribing therapies on the basis of their effects on someone’s numbers, rather than their health, is increasingly seen as irresponsible and dangerous. And even when evidence suggests clinical benefits of popular “preventive” medicines for those at lower risks, a rational assessment reveals many people must be treated to prevent one adverse event, so most users gain no direct benefit despite years of treatment. 

…The magic of numbers may help corporate profits and professional pride, but at what cost to the health of ordinary people who mistake a numerical benefit for a genuine one? Surely it’s time to ask if there might be a healthier new model for medicine based on far less harmful and costly ways to try to reduce human suffering.”

 

 

A Swedish revolution

In Sweden there is an increasing understanding that meat, eggs and dairy products have nothing to do with atherosclerosis or heart disease. The story began the year 2005. Lars Erik Litsfeldt, a Swedish lawyer contacted me to tell me about his success with a lowcarb, high fat (LCHF) diet. A few years earlier he was an overweight diabetic with heart problems, but after a few days on the LCHF diet his blood sugar became normal and he could stop his medication, and soon after his body weight was back to normal. Our discussions about fat and cholesterol  inspired him to wrote a book “Fettskrämd” (Scared by fat). 

The same year a book was published by Sten Sture Skaldeman, a journalist, who had almost halved his body weight (141 kg; 311 lb) by eating a LCHF diet. He had followed the usual dietary recommendations in vain; his body weight increased more and more. When he got diabetes and heart failure he realised that his life could end very soon and he therefore decided to eat the food he enjoyed the most, eg. fat food. To his surprise he noted that week after week he lost weight and all his ailments disappeared.  

However, what really created attention was what happened to Annika Dahlquist, a general practitioner in Northern Sweden.  When she experienced the same benefit on herself from this diet, she started recommending it to her patients as well. Two local dieticians accused her for misconduct and reported her to The National Board of Health and Welfare (Socialstyrelsen) and her chief prohibited her from giving dietary advice. However, two years later The National Board acquitted Annika; although her dietary advice went contrary to the official guidelines, as they wrote, they were supported by science. 

Annika wrote a book herself, which became a blockbuster. Today every Swede knows Annika Dahlquiost and her message. She has appeared in several television shows and she has given numerous lectures for lay people all over the country  She has been followed by another general practitioner, Andreas Eenfeldt, who has written a blockbuster book as well and started an LCHF blog that has become the largest health blog in Sweden.  

Together with eight colleagues I have backed up the LCHF movement by criticizing The National Food Administration for giving unhealthy dietary advices, both in the newspapers and in the Swedish medical press. Here is an excerpt from my book “Ignore the Awkward!” about one of our papers, published in Dagens Medicin, a popular medical newspaper:      
                

 Recently, the Swedish Food Administration published a list of seventy-two studies, which they claimed were in support of their warnings. Together with eleven colleagues I scrutinized the list and what we found was the following:   Eleven studies did not concern saturated fat at all. 

Sixteen studies were indeed about saturated fat, but they were not in support.

Three reviews had ignored all contradictory studies. 

Eleven studies gave partially or doubtful support.         

Eight studies were reviews of experiments, where the treatment included not only a ‘healthy’ diet, but was combined with weight reduction, smoking cessation and physical exercise. So how did they know whether the small effect was due to less saturated fat or to something else? Furthermore, all of them had excluded several trials with a negative outcome. 

Twenty-one studies were about surrogate outcomes. In most of the studies the authors claimed that saturated fat raises cholesterol. We should note that high cholesterol is not a disease. 

Twelve studies were listed because they had shown that people on a diet, which included a high proportion of saturated fat and little carbohydrates, reacted more slowly to insulin than normally. From that observation, the authors claimed that saturated fat causes diabetes, but decreased insulin sensitivity is a normal reaction. When you cut the intake of carbohydrates radically, your metabolism is changed to spare blood glucose and it works by reducing your insulin sensitivity. That saturated fat produces diabetes is also contradicted by several experiments on patients with early or manifest type 2 diabetes. They have shown, that a diet with much saturated fat and little carbohydrates normalises the level of blood sugar and insulin and many of the patients are able to stop their medication.2

Another contradiction is, that for many years the consumption of saturated fat has decreased in many countries, while during the same time period we have seen a steady increase in the incidence of type 2 diabetes.”

I assume that you are curious to know how the Swedish Food Administration responded to our criticism. They did respond, but we couldn’t find an answer to our questions about saturated fat. Indeed, we could not even find the term saturated fat in their text. Instead you could read statements such as:

Our dietary guidelines are based on science… they are a synthesis of thousands of studies… they are based on the WHO guidelines.

According to a recent poll almost 25% of the Swedish population has changes their dietary habits in the LCHF direction and in today´s local newspaper you could read that there is lack of butter in all districts in Sweden.

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Sept-Oct 2011

False and dangerous advertisements from Unilever

Recently David Jenkins and 16 colleagues published the results from a dietary trial in JAMA (The Journal of the American Medical Association). They had compared the usual low−saturated fat diet with a diet that included plant sterols, soy protein, fibers, and nuts. They succeeded in lowering LDK-cholesterol by about 13% with the plant sterol diet, but only by 3% with the usual low-fat diet.

What is a plant sterol, you may ask.

Cholesterol is an important constituent of plants as well, although the molecule looks a little different. There are several types of plant cholesterol; together they are named plant sterols. A typical Western diet contains 400-500 mg plant sterols, but little is taken up in the gut. Human and plant cholesterol compete for uptake in the gut. If you eat much plant sterol, your intake of normal cholesterol goes down. This fact got Unilever the idea to add plant sterols to their food products; in the first hand to margarine. The product is named Promise Active in the US, and Flora Pro.active or Becel Pro.active in other countries. And this was also the product that was given to the participants in the plant sterol group.

 It is correct that cholesterol goes down if we eat much plant sterol, but that doesn’t mean that it is able to prevent heart disease, because no one has ever tested that in a scientific experiment. What happens is that our own cholesterol is exchanged with a foreign type of cholesterol, not only in the blood but also in our cells and cell membranes.

Is it really a good idea? Isn’t it likely that the molecular differences between animal and plant sterols have a meaning? I think so, and science is in support of my view.

Several studies have shown that even a mild elevation of plant sterols in the blood is a risk factor for heart disease, and the findings in people with a rare inborn disease named sitosterolemia are in accord. These people absorb much more plant sterols than normally and they also become atherosclerotic much earlier in life than normal people.

Statin treatment lowers blood cholesterol, but at the same time it raises the level of plant sterols. In the 4S-trial about 25 % of the patients had a mildly elevated level of plant sterols before treatment. In this group statin treatment resulted in a further increase of plant sterols and the number of heart attacks was twice as high compared with the patients with the lowest plant sterol levels. This means that for about 25% of the many millions of people on statin treatment, their risk of heart disease may increase, not decrease.

In spite of that, Unilever still advertise their margarine and other food products with high contents of plant sterols: Enjoy heart healthy buttery spread with Promise!

I became upset when I read that paper and I therefore sent a letter to the editor of JAMA with the following text: 

       Questionable conclusions from a dietary trial

It is well known that an addition of plant sterols and soybean products to the diet may lower cholesterol by 10-15%. The findings in the dietary trial performed by Jenkins et al.(1) are therefore no surprise. It is questionable, however, if a lowering of cholesterol by dietary means is equivalent with a lowering of the risk of coronary heart disease (CHD) because hitherto no unifactorial dietary trial has succeeded in lowering cardiovascular or total mortality (2,3). What the authors also ignore is that an increased intake of plant sterols is associated with an increased cardiovascular risk. In at least four cohort studies a high intake or a high plasma level of plant sterols were independently associated with a higher risk of  CHD, and in experiments on mice a dietary supplementation with plant sterol esters equivalent to a commercial spread induced endothelial dysfunction (4).

 
References

1.   Jenkins DJ, Jones PJ, Lamarche B et al. Effect of a Dietary Portfolio of Cholesterol-Lowering Foods Given at 2 Levels of Intensity of Dietary Advice on Serum Lipids in Hyperlipidemia: A Randomized Controlled Trial. JAMA. 2011:306(8),831-839.

2.   Ravnskov U. The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. J Clin Epidemiol. 1998;51(6):443-460.

3.   Hooper L, Summerbell CD, Higgins JP et al. Dietary fat intake and prevention of cardiovascular disease: systematic review. BMJ. 2001;322(7289):757-763.

4.   Weingärtner O, Böhm M, Laufs U. Controversial role of plant sterol esters in the management of hypercholesterolaemia. Eur Heart J. 2009;30(4):404-409.   

A month later I got the following answer from the Editor:   

Dear Dr. Ravnskov:

 

Thank you for your recent letter to the editor. Unfortunately, because of the many submissions we receive and our space limitations in the Letters section, we are unable to publish your letter in JAMA.

    After considering the opinions of our editorial staff, we determined your letter did not receive a high enough priority rating for publication in JAMA. We are able to publish only a small fraction of the letters submitted to us each year, which means that published letters must have an extremely high rating.

    We encourage you to contact the corresponding author of the article, although we cannot guarantee a response. We do appreciate you taking time to write to us and thank you for the opportunity to look at your letter.

 

Sincerely yours,

 

Jody W. Zylke, MD

Senior Editor, JAMA

Letters Section Editor   

I haven´t contacted the corresponding author of the paper, as suggested by Dr. Zylke, by the simple reason that nothing would happen. According to the Conflict of Interest Disclosures ten of the authors were supported financially by Unilever and several other producers of the food types used in the trial. Here is for instance Dr. Jenkins´ list: 

“Dr Jenkins reported serving on the Scientific Advisory Board of Unilever, Sanitarium Company, California Strawberry Commission, Loblaw Supermarket,Herbal Life International, Nutritional Fundamental for Health, Pacific Health Laboratories, Metagenics, Bayer Consumer Care, Orafti, Dean Foods, Kellogg’s, Quaker Oats, Procter & Gamble, Coca-Cola, NuVal Griffin Hospital, Abbott, Pulse Canada, Saskatchewan Pulse Growers, and Canola Council of Canada; receiving honoraria for scientific advice from the Almond Board of California, International Tree Nut Council Nutrition Research and Education Foundation, Barilla, Unilever Canada, Solae, Oldways, Kellogg’s, Quaker Oats, Procter & Gamble, Coca-Cola, NuVal Griffin Hospital, Abbott, Canola Council of Canada, Dean Foods, California Strawberry Commission, Haine Celestial, and Alpro Foundation; being on the speakers panel for the Almond Board of California; receiving research grants from Loblaw Brands Ltd, Unilever, Barilla, Almond Board of California, Solae, Haine Celestial, Sanitarium Company, Orafti, International Tree Nut Council, and Peanut Institute; and receiving travel support to meetings from the Almond Board of California, Unilever, Alpro Foundation, and International Tree Nut Council.”   

In addition Unilever Research and Development provided the donation of margarines used in the study.

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October 2011  

Misleading scientists - once again

Statins cure almost everything. This is the message we are told again and again in the scientific press; at least from researchers supported by the drug companies. Here is a new example. 

In European Heart Journal Peter S Sever and his coauthors claimed that statin treatment also lower mortality from infections and respiratory diseases.  How did they come up with this surprising result? It is surprising because as readers of my books know, the lipoproteins, the carriers of cholesterol, is an important part of our immune system. If we lower cholesterol, we lower the lipoproteins as well.  

Their argument comes from a large statin experiment called ASCOTT-LLA. This trial included more than 10,000 patients with hypertension, half of whom were treated with atorvastatin. The trial was stopped prematurely in 2002 after three years because of the allegedly obtained benefit at that time.  In the treatment group 3.58% had died; in the untreated group 4.13%.  

After that the treated participants decided for themselves whether they wanted to continue the treatment or not, and the untreated were offered treatment. About a third in the first group stopped or had already stopped treatment, and more than half of the others started. Eight years later more had died from infections and pulmonary diseases in the control group. 

But how could they know whether the difference was due to statin treatment? As I wrote in a letter to the journal: It is not too farfetched to assume that those who stopped the treatment, did it because of unpleasant adverse effects, and that many of those, who had started it, not yet had recognized that possible adverse effects were caused by the treatment. 

The analyses were supported by an unrestricted grant from Pfizer and two of the authors, including Peter Sever, had served as consultants or received travel expenses, or payment for speaking at meetings, or funding for research from one or more pharmaceutical companies that market blood-pressure-lowering or lipid-lowering drugs, including Pfizer for ASCOT. 

If you want more information about the many misleading ways we are informed about the statins, read this paper by Stephanie Seneff. Stephanie is a senior scientist at Massachusetts Institute of Technology (MIT) and a member of THINCS 

And if you think that the lipid guidelines are written by independent researchers, please read this article by Larry Husten.

Recently, the Danish government committed an act of extreme folly: They taxed saturated fat, ostensibly ‘to prevent obesity’. And in so doing, they got it disastrously wrong. Why? Because saturated fat is not only not fattening; it is actually one of the best slimming agents.  If you understand the Scandinavian languages, you can read why that is a bad idea in my chronicle in Berlingske Tidende, one of the major Danish newspapers. (You can get an approximate translation using Google´s language tool). To prevent similar mistakes by other governments Members of THINCS are just now preparing a similar paper in seven different languages to be sent to newspapers in other countries. We are not too optimistic because articles critical to the cholesterol campaign are rarely accepted for publication.

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November 2011

How to cheat with complicated calculations

The New England Journal of Medicine recently published the results of the SATURN trial. It was designed to study the effect of atorvastatin (Lipitor) vs. rosuvastatin (Crestor) on the volume of atheroma in a coronary artery. It was hoped that the volume would be reduced, demonstrating that high dose statins can decrease the burden of atherosclerosis.

Initially 1578 patients were selected for the trial, but after a run-in period of 2 weeks where they were treated with half-maximal doses of either atorvastatin or rosuvastatin, 193 patients were excluded. The rest were treated either with 80 mg atorvastatin or 40 mg rosuvastatin. After 2 years of treatment a further 346 patients had disappeared.

Before and after the trial the patients underwent intravascular ultrasonography to measure the lumen diameter and the total diameter of a coronary artery. Subtracting the lumen area from the total area of the artery is thought to reflect the total atheroma volume, (represented as the percentage atheroma volume). The primary endpoint was to measure the reduction in percent atheroma volume

After the treatment the lumen had increased on average by 0.99 % in the atorvastatin group, and by 1.22 % in the rosuvastatin group, and the per cent atheroma volume (eg. the area of the arterial wall) had decreased by 1.1 % and 1.3 % respectively.   

There was also a secondary end-point. However, I must admit that I did not understand what it meant, and if anyone does, please explain it to me. Here is what the authors wrote:


A secondary efficacy end point, normalized total atheroma volume (TAV), was calculated as follows:

TAVnormalized = Σ (EEMarea − lumen area    x       median no. of

                      no. of images in pullback         images in cohort

 
For TAV, the summation of the EEM area minus the lumen area is performed first. This value is divided by the number of images in the pullback and then multiplied by the median number of images in the cohort. The average plaque area in the pullback was multiplied by the median number of images analyzed in the entire cohort to compensate for differences in segment length between subjects. The efficacy end point of change in normalized TAV was calculated as the TAV at 104 weeks minus the TAV at baseline. Regression was defined as a decrease in PAV or TAV from baseline.

Anyway, the critical measure was the difference between the inner and outer area of the artery. Unfortunately, there is no evidence that the figure from this calculation reflects atheroma volume. For example, vascular dilation will increase the inner diameter, without having any effect on the thickness of the arterial wall. But this would result in an apparent decrease in atheroma volume. To further understand what I mean, read the following section from my book Fat and Cholesterol are GOOD for You!  

The anguish of angiography  
Let us still have in mind, that a change of the coronary diameter is nothing but a surrogate outcome.  It is assumed that a widening of a coronary vessel on an X-ray means less atherosclerosis and thus a better chance to avoid a heart attack, but this is only an assumption.  

    
Artery walls are surrounded by smooth muscle cells. When such cells contract, the artery narrows. When they relax, it widens. Various factors may stimulate the
smooth muscle cells of the corona­ry arteries. Most important, mental stress, anxiety, exposure to cold, and even a sustained handgrip may lead to contrac­tion. The latter effect was studied six years earlier by Dr. Greg Brown, the same Dr. Brown who led the angiogra­phic trial mentioned above (1). He found that a handgrip sustained for a few minutes was followed by a 35 per cent decrease of the vessel diameter.  

    
Consider that the changes seen in the trials were only a few per cent on average. What do you think you would do yourself if
somebody were to put a long catheter all the way from your groin up to your heart and into your coronary vessels? If you are not a stuntman or an astronaut I think that you probably would have gripped the nurse's hand or something else very tightly.  
    
Also, drugs which relax the coronary vessels, and which are used by almost all coronary patients, may have disturbed the study. In the trial Dr. Brown and his coworkers were aware of that problem. The use of such drugs was "dupli­cated as exactly as possible."  This can't have been too easy be­cause the level of any drug in the blood depends on a large number of factors, which are difficult to standar­dize. And Dr. Brown and his colleagues didn't write anything about duplica­ting possible handgrips or anxious feelings because such duplica­tion is, of course, impos­sible. So, any factor which may influence the state of the smooth muscle cells in the coronary vessels may have influenced the vessel diameter much more than the possible appearance or disap­pearance of a tiny amount of cholesterol.  
    
There are more uncertainties. Dr. Seymor Glagov and his colleagues from University of Chicago studied the hearts of 136 deceased individuals and found that when vessels become sclerotic, they widen to compensate for the narrowing brought about by the deposition of choleste­rol in their walls (2). In fact, this widening overcompensates for the deposition until the cholesterol deposits occupy about 40 per cent of the area beneath the muscle wall. Only thereafter does the vessel become steadily narrower. In other words, an increase of vessel diameter may be due to disap­pearance of cholesterol in a highly sclerotic vessel, but also to a compen­satory widening during the first stages of cholesterol deposition. How could the trial directors know whether the increase of vessel diameter was due to a disappearance of deposited cholesterol, or to a compensatory widening due to an appearance of deposited cholesterol or due to less anxiety at the second angiography?  


References
1. Brown G and others. Reflex constriction of significant coronary stenosis as a mechanism contributing to ischemic left ventricular dysfunction during isometric exercise. Circulation 70:18-24, 1984
2. Glagov S and others. Compensatory enlargement of human atherosclerotic coronary arteries. The New England Journal of Medicine 316:1371-1375, 1987.

In short, the degree of arterial dilation is a massive and uncontrolled variable in the SATURN study. This problem could have been solved if the investigators had included a placebo group (a group of patients who unknowingly received an ineffective pill). However, “It was not considered ethically possible to measure disease progression in placebo-treated patients”, as they wrote.

There were other major problems with this study. The issue of drug related adverse events is extremely important. This was virtually dismissed within the paper. “Both agents had acceptable side-effect profiles”.

Can this be true. A more detailed review of adverse events reveals that “new proteinuria”, defined as an excretion of more than twice the amount of protein in the urine during the follow-up, in 1.7 and 3.8 %, respectively in the two groups. An increase in proteinuria is a measure of progressive damage to the kidneys. This trial only lasted two years, so we don´t know what would have happened in the longer term.

Equally it was stated that less than two per cent had laboratory signs of liver damage. However, liver damage was only recorded if the laboratory signs were at least three times higher than the upper limit of the normal range. And whilst less than two per cent had muscular damage, this was only reported if the laboratory signs were at least five times higher than the upper limit of the normal value. What do you think will happen with the liver and muscles of patients whose laboratory signs were “only” twice or four times higher, respectively?

In the end a further 22 % of the patients had disappeared. The reasons were said to be preference of patient (7.7% and 7.8 %), adverse effects (7% and 6.5 %), loss to follow-up (1.3% and 2.9 %) and noncompliance (2.3% and 1.9 %). What they meant with “preference of patient” I don´t know, but I am confident that “non-compliance” and perhaps also “loss to follow-up” represent those who could not tolerate the medication. Thus, whilst the authors claimed that ‘both agents had acceptable side effect profiles,’ the reality is that 12% could not tolerate these agents at the start of the study, and another 23 % dropped out – most likely to due to intolerable adverse events.

My summary of the SATURN study would be that it used a primary end point that has never been properly validated, and can be affected by a host of confounding variables e.g. stress . This variability could only have been controlled for by including a placebo arm, which was not done. Therefore, the result is rendered meaningless.

More importantly, it would appear that the burden of adverse events from using high doses of statin drugs is unacceptably high. It is likely that more than a third of patients will be unable to tolerate 80 mg Atrovastatin, or 40 mg of Simvastatin. All of this suffering in order to have an uncertain effect on a surrogate end-point, which may or may not mean anything.

Finally, I should mention that the study was supported by AstraZeneca, and most of the results were in favour of their drug rosuvastatin, although most of the differences were not statistically significant. I shall leave you with a list of the authors´ conflicts of interest:

 

Dr. Nicholls reports receiving consulting fees from Roche, Esperion, Merck, Omthera, Sanofi-Aventis, and Boehringer Ingelheim, serving as an unpaid consultant for Abbott, Pfizer, LipoScience, Novo Nordisk, AtheroNova, and CSL Behring, receiving grant support from Eli Lilly, AstraZeneca, Novartis, Anthera, LipoScience, Roche, and Resverlogix and lecture fees from AstraZeneca and Roche; 
Dr. Ballantyne, receiving grant support from Abbott, Astra-Zeneca, Bristol-Myers Squibb, Genentech, GlaxoSmithKline, Kowa, Merck, Novartis, Roche, Sanofi-Synthelabo, and Takeda, consulting fees and honoraria from Abbott, Adnexus, Amarin, Amylin, AstraZeneca, Bristol-Myers Squibb, Esperion, Genentech, GlaxoSmithKline, Idera, Kowa, Merck, Novartis, Omthera, Resverlogix, Roche, Sanofi-Synthelabo, and Takeda and lecture fees from Abbott, AstraZeneca, GlaxoSmithKline, and Merck; 
Dr. Barter,
holding an advisory board position for AstraZeneca, Merck, Roche, CSL Behring, and Pfizer, receiving grant support from Merck, consulting fees from CSL Behring, and lecture fees from AstraZeneca, Kowa, Merck, Pfizer, and Roche; 
Dr. Chapman, receiving grant support from Merck and Kowa, consulting fees from Merck and Pfizer, and lectures fees from Merck and Kowa; 
Dr. Erbel, receiving grant support from the Heinz Nixdorf Foundation and the German Research Foundation and support for travel, accommodations, or meeting expenses from Biotronik, Sanofi, and Novartis; 
Dr. Libby, serving as an unpaid consultant for Novartis, Johnson & Johnson, Amgen, and Roche, serving in unpaid leadership roles for clinical trials sponsored by AstraZeneca, GlaxoSmithKline, Novartis, Pfizer, Pronova, and Sigma Tau, and having previously received royalties from Roche for the patent on CD40L in cardiovascular risk stratification; 
Dr. Raichlen
, being an employee of and owning stock in AstraZeneca; and 
Dr. Nissen
, receiving consulting fees from Eli Lilly, grant funding from AstraZeneca, Pfizer, Novartis, Karo Bio, Novo Nordisk, Takeda, Resverlogix, and Omthera, and support for travel, accommodations, or meeting expenses from Novo Nordisk, Takeda, Karo Bio, Eli Lilly, Pfizer, Novartis, and Amgen. 

No other potential conflict of interest relevant to this article was repo
rted.


It is a sad fact that this report has been accepted for publication in The New  England Journal of Medicine considered  the leading medical journal in the world Either the editors and referees did not do their jobs, are not qualified for their tasks, or they have been blinded by Mammon.  

Should children lower their cholesterol???

There are more miserable news. Recently an expert panel appointed by the National Heart, Lung and Blood Institute and endorsed by the American Academy of Pediatrics has published new guidelines according to which every child in the United States should be tested for high cholesterol between ages nine and 11 so steps can be taken to prevent heart disease later on.

Such crazy thoughts have been aired several times in the past. In a letter to The Lancet (published on January 1, 2000; a good start of the new millennium). I tried to explain why this is a most dangerous idea, but obviously the letter made no impact.

How can an expert panel produce such malicious recommendations, you may ask. Because they are paid by the industry, of course. Read for instance  Larry Hustens report  or the one from the non-profit organisation Integrity in Science

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December 2011

Bad statin news aren´t welcome

In many western countries more and more get cancer although at the same time more and more people stop smoking, one of  the most cancer provoking factors. Members of Skeptics think that the reason is the increasing use of cholesterol lowering drugs. Those who promote such treatment argue that no analysis of the statin trials have shown any association and some even claim that the statins protect against cancer.

There are many ways to cover up the fact that lowering cholesterol may lead to cancer, but there are also numerous observations that point to low cholesterol as the villain. 

But how can low cholesterol lead to cancer? This is a good question, and there is an answer. Because the liporoteins partake in the immune defense system, and because many cancers are caused by virus or bacteria.

Together with two members of THINCS, Kilmer McCully, the discoverer of the association between homocysteine and atherosclerosis, and Paul Rosch, President of the American Institute of Stress, I have tried to present the facts around this issue. The paper has finally been published in Quarterly Journal of Medicine Before that, we sent the paper to six different medical journals (not at the same time of course), all of which rejected it. Here are their arguments


Archives of Internal Medicine:

 I regret to inform you that its priority rating is not sufficiently high to warrant our considering it further for publication. Based on our initial review, we will not be sending the paper for additional outside editorial review.  

 

CA: A Cancer Journal for Clinicians
Thank you for submitting your proposal for an article on "Low cholesterol, cancer and the role of lipoproteins" to CA: A Cancer Journal for Clinicians. It is our editorial policy to concentrate on articles that address cancer more broadly (treatment modalities used for many cancer types, current treatment of common types of cancer, public health issues relevant to several cancer types, etc.). For these reasons, we cannot consider your article for publication in CA. However, you may want to consider submitting your article to CANCER, another peer-reviewed American Cancer Society journal, which publishes more focused papers such as the one you have described  

 

Cancer
Thank you for your recent manuscript submission of "Low cholesterol, cancer and the role of lipoproteins" (CNCR-11-2485) to Cancer.  Your paper has undergone initial review. I am sorry to report that it was not deemed to be of broad enough interest to our readership to merit further evaluation.   

 

JAMA
Thank you for your inquiry. However, JAMA is not able to consider your manuscript for publication.

 

Journal of the National Cancer Institute

I am sorry that we shall not be able to use the above-titled manuscript. After careful evaluation, the Editorial Board did not accord it a priority sufficient for further consideration.  

 

Scandinavian Cardiovascular Journal:  
Thank you for submitting the manuscript # SCAR-2011-0151 entitled "Low cholesterol, cancer and the crucial role of lipoproteins" to the Scandinavian Cardiovascular Journal. The questions raised are important, indeed, and deserve a thorough analysis and discussion. Admittedly not being an expert on this field, my impression is that the present manuscript is polemic in style, and biased. This view was shared by one leading cancer epidemiologist; he/she finds the present selection and interpretation of the literat
ure superficial and subjective. Hence I choose not to forward your manuscript to our reviewers.

Read our paper yourself and tell me if the paper is not "of broad enough interest" or if it is "polemic in style" or if "its priority rating is not sufficiently high"

What I have told you here is no exception. Many of our members including myself can tell you about how difficult it is to publish papers that goes counter to conventional wisdom. On oe of our websites you can find many examples of rejected papers and comments.

 

Statin treatment and infections

Several researchers have claimed that statin treatment prevents infections. Recently a Dutch group published an analysis of the statin trials where the authors had reported the number of infections. Not unexpectedly they didn´t find any difference between the statin groups and the controls (those who got an ineffective placebo pill).  

In an editorial in the same issue of British Medical Journal, where the Dutch report was published, Beatrice Golomb commented the study. It was certainly not expected either because, as she wrote, a number of relevant factors may distort the results. One of them is the fact that among 632 statin trials, only eleven reported the number of infections, and ”most authors declined to provide the omitted information when approached”. “The best evidence, she concluded, “is that statins should not be used to forestall infection or its consequences.” 

There is even evidence of the opposite. As mentioned, and as Golomb also pointed out, low cholesterol is a risk factor for infection, and as we have a plausible mechanism to propose, we send a letter to British Medical Journal, now published as a Rapid Response

Most Rapid Responses are available on the web ony. If you sympathize with our letter, you are most welcome to vote (on the right hand side of the letter). Many positive votes may possibly increase its chance to become published in the paper version as well.

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January 2012

A misleading statin report

In my November newsletter I told you about the misleading SATURN trial. Together with two of our members, Paul Rosch, Professor of Medicine and Psychiatry at New York Medical College and President of The American Institute of Stress, and Stephanie Seneff, Principal Research Scientist at MIT, I sent the following letter to New England Journal of Medicine:

     Questionable conclusions from the SATURN trial

To define the relationship between the external and internal diameter of an artery as percent atheroma volume1 is problematic, since dilation of the artery per se would be interpreted as a decrease of atheroma. This is hardly a trivial bias, because irrelevant factors may cause a significant dilation of the arteries without changing atheroma size. Brown et al. found that an isometric handgrip sustained for a few minutes during cardiac catheterization increased the luminal area by 35%,2 and drugs as well as emotional factors that affect arterial tone may also be confounding factors. Furthermore, when arteries become sclerotic, they often widen. This widening can overcompensate for the increase of the atheroma until it occupies about 40 per cent of the wall area.3 Thus, an increase in vessel lumen could be due to diminished atheroma volume, compensatory widening in response to arteriosclerosis, vasodilating drugs, or the patient may be less stressed at the second investigation and therefore less prone to grip the nurse´s hand or something else.

 

1. Nicholls SJ, Ballantyne CM, Barter PJ et al. Effect of two intensive statin regimens on progression of coronary disease. N Engl J Med 2011 Nov 15.

2. Brown BG, Lee AB, Bolson EL, Dodge HT. Reflex constriction of significant coronary stenosis as a mechanism contributing to ischemic left ventricular dysfunction during isometric exercise. Circulation 1984;70:18-24.

3. Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med !987;316:1371-5.

  A few days later I got the following letter from the journal:

     Dear Dr. Ravnskov,

I am sorry that we will not be able to print your recent letter to the editor regarding the Nicholls article of 01-Dec-2011.  The space available for correspondence is very limited, and we must use our judgment to present a representative selection of the material received.  Many worthwhile communications must be declined for lack of space.

Thank you for your interest in the Journal.

Sincerely,

    Gregory Curfman, M.D. Executive Editor

It is of course embarrassing that the editors accepted the SATURN report for publishing in one of the world´s most respected medical journals, but shouldn´t they have the guts to admit their mistake? Or has even this journal become dependent on the money from the drug companies? They have lots of them; take a look for instance at the short movie with three of our members as actors.

How to meet criticism

A few months ago Jan Pedersen and coworkers, all of them strong supporters of the diet-heart idea, published an editorial in British Journal of Nutrition entitled The importance of reducing SFA to limit  CHD.

I was astonished, because more and more researchers have realized that there is no scientific support for the claim that saturated fat is dangerous to health. On the contrary, many studies have shown the opposite.

Together with four members of THINCS I se
nt a letter to the journal explaining why the arguments presented by Pedersen and his coworkers are invalid.

Pedersen and his co-workers published a response to our letter without answering any of our objections (To read their response, click on the blue field in the upper right corner). Their answer is almost identical with a response I got a few years ago from Martijn Katan, one of Pedersen´s co-workers. You can read my letter and Katan´s response on Michael Eades blog  together with Michaels comments.

A positive interpretation of our correspondence is of course that when supporters of a questioned paradigm start ridiculing their opponents instead of arguing in a scientific way, a
paradigm shift is approaching.

An interview with me

Recently I was interviewed by Patrick Timpone on One Radio Network. It is available
here (Click on the arrow at the middle of the site). Although my spoken English is not too good, I think you can understand most of it.

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February 2012

Diabetics - don´t eat statins!

It is well established that patients with diabetes run a greater risk of developing cardiovascular diseases. In Sweden and in most other countries cholesterol-lowering treatment is therefore prescribed routinely to all diabetics, whether their cholesterol is high or low and failure to do so is seen as professional misconduct. But there are a number of observations that should have stopped this habit long ago. 

First, at least fourteen studies have shown that high cholesterol is not a risk factor for patients with diabetes. If you are in doubt, go to chapter 4 in my book “Ignore the Awkward!, there you will find the references to these studies. The reason is probably the fact that high cholesterol may protect against infections, a common problem for diabetic patients. As readers of my books know, there is strong evidence that the lipoproteins are able to bind and inactivate all kinds of bacteria and virus. You can read more about that in a paper that I published together with Kilmer McCully.

A critical and well-informed reader may possibly say that the small effect from statin treatment is not due to cholesterol lowering, but to their other effects, and this is true. If so, statin treatment perhaps may benefit a diabetic in other ways. But here comes the next warning: Statin treatment may cause diabetes!

Several of the statin trials ended up with more diabetics in the treatment group. For instance, in the JUPITER trial 3 per cent got diabetes, but only 2.4 per cent among the untreated control individuals.


The authors wrote that this small risk was more than balanced by the benefits. Then what was the benefit?


In the control group 2,7 % died, in the treatment group only 2.2 %!


The trial was stopped already after less than two years because of the good results. The question is, how many would have gotten diabetes after ten years? Let us take a look at a recent report from a study called Womens Health Initiative

More than 150,000 US women age 50-79 were followed for 7-12 years. At follow-up about ten per cent of the women were on statin treatment. Almost ten per cent of the statin-treated women had diabetes, but only six per cent among the non-users. And please recall that no statin trial has ever succeeded in lowering mortality for women.

There is a logical reason why cholesterol lowering may lead to diabetes. Like all other organs and structures, the insulin-producing cells need cholesterol, and when less cholesterol is available, less insulin is produced. This was recently demonstrated by a group of researchers from Toronto

What happens with those who already have diabetes when they start statin treatment? We don’t know because nobody has analysed this question.

Is it really wise to treat diabetic patients with a drug that worsen the function of their insulin-producing cells? And is it wise to lower the risk of cardiovascular diseases in other people with a treatment that may cause a disease, which increases the risk? Or, as you know from my december newsletter, may result in cancer in the long run, not to mention the risk of the many other unpleasant side effects.

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March 2012

Is read meat a deadly  poison?

Recently a new report has been published from the famous Channing Laboratory at Harvard. Here, a number of researchers headed by Walter Willett have studied the dietary habits for many years in more than 100,000 men and women. Again and again they have warned us against saturated fat, although none of their many studies have found that heart patients have eaten more of such fat than have other people. However, as I told you in my December Newsletter Willett has changed his mind

This time the message, published in Archives of Internal Medicine, is that you will shorten your life if you eat too much unprocessed read meat. Two population groups, the Health Professionals Study that included 37698 men, and the Nurses’ Health Study that included 83644 women, were followed for 22 and 28 years, respectively. At the start and every 4 year they filled in a dietary questionnaire.

At follow-up almost 24,000 had died. The authors divided the participants into five parts (quintiles) after their intake of read meat. The first quintile included those who had eaten the least, and the fifth those who had eaten the most. Fromthemfiguresmgiven in the tables it is possible to calculate the mortality in each group.

The pattern was similar in both groups, but for simplicity I give you the figures for the Health Professionals´ Study only. Here 1.23 per cent had died each year in the first quintile; and 1.29 per cent in the fifth quintile. Thus, during the 22 years the total mortality in these two groups was 27.1 and 28.4 per cent, respectively.

But it was only 21.8 per cent in the third quintile! So, what shall we do? If we eat too much, the risk increases, but so it does if we eat too little. How can we know whether we eat too much or too little?

However, there were many factors that could have skewed the result. For instance, those with the lowest intake were more physically active, fewer smoked, they ate more fruits, vegetables and fish, and fewer had diabetes and high blood pressure compared with the other groups. These life style factors were particularly bad in the fifth quintile.

But as mentioned, the risk of dying was about the same in all groups. You could also say that even if you smoke, eat too little fruits, vegetables and fish, and even if you have diabetes or high blood pressure, then you may live almost as long as people with a healthier lifestyle if you gorge in unprocessed read meat.

The authors concluded otherwise, however, because their statistician has made some serious errors. After having corrected for the uneven distribution of the various factors, they found that the risk of dying was lowest in the first quintile and it increased step by step from the first to the fifth quintile. Their conclusion was that if you consume less than 42 gram unprocessed meat per day, you could lower your risk to die the next 22-28 years by about 8 per cent.

It is not possible to know the exact mortality after their corrections, because it is expressed in a statistical term called hazard risk. But let us assume that the risk after the corrections was 30 per cent for those with the highest intake and 27.6 per cent for those with the lowest. These figures are of a similar magnitude as those that we can calculate ourselves from the original figures. The difference between 30 and 27.6 is 2.4, meaning that you can only lower your risk of dying by 2.4 per cent. Then how can they conclude that we can lower it by 8 per cent? Because 2.4 is 8 per cent of 30.

There are more curious data. The body weight of the participants was pretty normal in all groups. To be precise, BMI varied between 24.7 and 26.0. But whereas the high-consumers on average ate about 2200 calories per day, the low-consumers ate only 1659. In the  Nurses’ Health Study,  where BMI varied between 23.9 and 24.7 the high-consumers ate 2030 calories and the low-consumers only only 1202! These figures are of course highly unlikely. People who have eaten only 1202 calories per day for 28 years cannot have the same body weight as people who have eaten 2030 calories per day.

Thus, the statistician must have made some serious miscalculations. But let us assume that the figures are correct. Should we really bother? Let me calculate it in another way.

If you eat as much unprocessed read meat as you like, your chance to be alive after 22 years is about 70 per cent, but if you avoid it as much as possible you can increase your chance to 73 per cent at most. But again, this is true only if the data published by Hu and his coworkers are correct, and this is very unlikely.

You can learn more about this paper by reading a detailed comment by one of our members  Zoë Harcombe. She also asked Frank Hu, if he could explain the curious result. Here is his answer:

Thanks for your interest in our paper. Unfortunately, the crude mortality rate is misleading because the mean age in the first quintile (Q1) was older than other quintiles. Therefore, the crude mortality rate in the first quintile would be artificially higher than other quintiles. In this analysis, age was a stronger confounding factor than other lifestyle factors. 

 

Hope this helps.

 

Frank Hu

This answer is nonsense of course, because there were only minor differences in age between the five quintiles. In HPFS it varied between 52.2 and 53.8, and in NHS between 45.3 and 47.3 years. For instance, compare these small differences with the fact that in the fifth quintile there were almost three times more smokers than in the first; and only 17 percent were physically active against 27 percent in the first.

Professor David Diamond, another member of THINCS, sent him a letter as well, but hitherto Frank Hu hasn´t answered him.

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Do you become fat by eating fat?

A last question: Do you suffer from obesity? Then listen to this brilliant lecture by Zoë Harcombe.

 

 

April 2012

"New" statin side effects

Those of you, who have read our member Duane Graveline´s book ”Thief of Memory” know that bad memory is one of the many serious side effects from statin treatment. According to Dr Graveline thousands of reports about cognitive problems that have occurred during statin treatment and have disappeared after its discontinuation, have been sent to FDA since the introduction of these drugs. A few months ago FDA finally have officially admitted in a New safety alert that such problems may occur. You can read more about that in several newspapers, for instance NY Times, Edmonton Journal and Boston Globe  

You may probably ask, how come that it took more than ten years? Let me cite a few words from Marcia Angell´s book ”The Truth About the Drug Companies. How They Deceive Us and What to Do About It”. Marcia Angell is the former editor in chief of The New England Journal of Medicine. 

”Congress also put the FDA on the pharmaceutical industry´s payroll . . . Fees . . . soon accounted  for about half the budget of the agency´s drug evaluation center. That makes the FDA dependent on an industry it regulates.” (page 208)

 

”The FDA is subject to industry pressures through its eighteen standing advisory committees on drug approvals. These committees, which consist of outside experts in various subspecialities, are charged with reviewing new drug applications and making recommendations to the agency about approval. The FDA almost always takes their advice. Many members of these committees have financial connections to interested companies . . . Members of FDA advisory committees are said to command unusually high consulting fees from drug companies.” (pages 210-211).

More and more are realizing the dangers of statin treatment. Here is a warning from Sylvia Booth Hubbard, NewsMax Media (Peter Langsjoen, who is mentioned in the article, is a member of THINCS).  

And here is a scary video from an insider , who has worked for 15 years in the drug industry

In a previous newsletter I told you about statins and the risk of cancer. Our article about this issue has now been published in the paper version of Quarterly Journal of Medicine. 

Kim Greenhouse from a Los Angeles Radio named ”It´s Rainmaking Time” interiewed me recently. You can listen to it here.

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May 2012

There is light in the tunnel ahead

A few months ago two well-known US scientists Rodney Hayward and Harlan Krumholz published an open letter entitled Three reasons to abandon  low-density lipoprotein targets in the medical journal Circulation: Cardiovascular Quality and Outcome.  In this paper they criticized the updated clinical guidelines to be published this year by the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. They showed that there is no scientific support for the idea to treat to a certain LDL value: “The dogma that treating to target is based on clinical trial evidence belies the fact that no clinical trial has yet tested this strategy”. …not all drugs that improve lipid profiles reduce patient risk”. 

Another argument was that “clinical trials demonstrate that the relative effects of statin therapy are not substantially related to a patient’s pretreatment LDL” 

Or said in another way: High LDL-cholesterol is not a risk factor for cardiovascular disease. But this conclusion would of course have been too provocative to be published in a journal owned by the American Heart Association.

You can also listen to his message on Youtube

Since then Professor Krumholz has gone further. In a recent issue of the same journal he has published a new paper entitled A Note to My Younger Colleagues...Be Brave. By that he means that if they have discovered something, grounded in science that goes counter to common belief, they should not avoid to speak truth to power.

This is not too easy. Let me cite Professor Krumholz: 

”Unfortunately, our profession does not often reward those who question dogma. In fact, there are many episodes throughout the history of medicine and science in which truth was resisted and dogmatic beliefs, however poorly supported by evidence, were imposed by those in a position to do so. If we are to accelerate innovation in medicine, eliminate wasteful practices, and improve the depth and effectiveness of how we care for patients, then there must be room to question traditional approaches and to introduce new and better ways of prevention, diagnosis, and treatment. We are now at that critical juncture.”

There are a few who dare. Listen for example to this radio show where the host Alex Jones  talks with Dr. Russel Blaylock, a retired neurosurgeon and author, about the dangers of statin drugs and how they are causing serious brain disorders and increasing the incidence of dementia.

And here is a short video, where Beatrice Golomb is interviewed on ABC News about memory loss and cognitive side effects from taking Lipitor and other statins. After a few minutes ABC News´ medical editor Tim Johnson try to calm the viewers by telling them that ”only” two per cent of the users experience memory loss. As in the US alone at least 30 million people are on statin treatment, it means that more than half a million suffer from memory loss. Hopefully there aren´t too many pilots or bus or train drivers among them.

Listen also to this audio where our member Zoe Harcombe, author of The Obesity Epidemic is interviewed on BBC by Steve Wright.

On Youtube Malcolm Kendrick MD, author of The Great Cholesterol Con and another member of THINCS, reveals the disturbing results from a large study performed by WHO, one among numerous studies that contradict the cholesterol hypothesis and which have been ignored by the proponents of the cholesterol campaign. 

Mary Vernon , former president of the American Society of Bariatric Physicians (doctors specializing in treating obese patients), is another curageous researcher. She has published several papers about the miraculous results from treating diabetic patents with a low-carb, high-fat diet. In this interview by Swedish doctor Andreas Eenfeldt she tells about her experiences. Andreas himself has been one of the leading proponents of the lowcarb diet in Sweden. His blog is the most visited health blog in Sweden and is available also in English

Here is a new book about an old issue: How Statin Drugs Really Lower Cholesterol and Kill You One Cell at a Time by James and Hannah Yoseph. I have now read it and although I have studied this issue for more than 20 years, I found much new and shaky information about the criminal way the statins have been introduced. Even the Nobel Prize winners Goldstein and Brown, those who discovered why cholesterol was very high in familial hypercholesterolemia, seem to have participated in this scandalous process. 

A British film producer Justin Smith and his co-workers are just now preparing a critical movie about the cholesterol campaign entitled  $29 Billion Reasons to Lie About Cholesterol. The film will be finished by August this year and is planned to have the first screening in August in London. A short trailer, recently renewed, is available. It is also possible to preorder a copy of the DVD. Several cholesterol critics have been interviewed, among them are John Abramson MD, author of Overdosed America, Professor Paul Rosch, President of The American Institute of Stress and a member of THINCS, Malcolm Kendrick, MD, Peter Langsjoen, MD, world expert on Q10 and also a member of THINCS, and myself.

I wonder if the increasing number of critical researchers (there are many more) have made the drug industry desperate. Recently The Cholesterol Treatment Trialists’ (CTT) Collaborators, most of whom are paid by several drug companies, published an analysis in The Lancet, According to the authors their analysis provides strong evidence that the reduction in vascular risk with statins is at least as great in low-risk patients as in high-risk patients. 

They have analysed the data from almost 175,000 participants in 27 statin trials. According to their analysis, statin therapy caused a consistent reduction in the relative risk for major vascular events even for healthy low-risk people. Therefore, they wrote, the study suggests that current guidelines might need to be reconsidered, meaning, according to a commentary in the same issue, that all people above fifty should take statins.

I am sure that the crucial question for most people is not whether they can avoid a non-fatal heart attack by lowering their cholesterol, but whether they can prolong their life, and whether they can do it without risk of getting serious adverse effects from the treatment. From table 3 in the Lancet paper it is possible to calculate that the chance to be alive after five years for people without vascular disease and whose 5-year risk of a major vascular event is lower than 10% is the same, whether they are on statin treatment or not and whether they have a vascular disease or not. 

There is a benefit for people whose risk lies between 10% and 20%, but it is trivial at most. According to the table their chance of being alive after five years without treatment is 89.9%. If they take a statin every day they can increase their chance to 90.7%.


Do this small benefit really exceed any known hazards of statin therapy, as the authors wrote? I doubt. As I mentioned in a previous newsletter more than four per cent run a risk of moderate or serious adverse effects from the muscles, liver, kidneys or eyes. As I explained in my letter, these numbers were even underestimated, and the authors had not examined the frequency of diabetes, impotency or cerebral symptoms either.

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July 2012

Statin treatment and bad muscles 

In my books I have given many examples of adverse effects after statin treatment that have been downplayed or ignored by the drug industry. One example is muscle pain and weakness which according to the industry is seen in less than one per cent of the treated patients, but which according to independent researchers occur in 20-25 per cent. 

Beatrice Golomb, associate professor in medicine and her co-workers at the University of California, San Diego has published a report about this issue. They performed a regularly controlled double-blind trial in women who were treated with identical capsules containing either a placebo or a statin drug and found that 40 percent in the statin group got muscle problems, which were serious in 10 percent. You can read more about the trial in Daily Mail.

A Fraudulent dietary study

Recently Swedish-American scientists published a report in British Medical Journal, where they claimed that women should eat as much carbohydrates and as little proteins as possible to lower their risk of getting a cardiovascular disease. The paper seemed convincing, published in a respectable medical journal and four of the authors were professors. Many newspapers around the world also took in the message.

I wonder if the editors of British Medical Journal have gone on an early holiday. Not only was the methods used highly questionable, but the benefit of this advice was exaggerated, to put it mildly and the most important result was ignored.

The authors sent a questionnaire to 96,000 Swedish women aged 30-49 year. They should answer how much of eighty different foods and drinks they had consumed per day during the preceding six months, but only 49,000 of the women responded.

Fifteen years later the authors looked into the national quality register for health and health care to see, how many who had suffered from a cardiovascular disease. The results were then compared with the participants intake of protein and carbohydrates.

How many of you are able to recall what you have eaten yesterday in every detail, not to mention what you ate half a year ago? And do you eat the same food the next fifteen years?

As an example I shall mention that the intake of calories varied between 442 and 2992. Most people need about 2500 calories per day to stay in metabolic balance; manual workers much more. How many people do you think are able to survive with an intake of 442 calories per day without ending up as a skeleton? 

If the information about the daily intake of calories was so inaccurate, why should we believe in the reported intake of carbs and protein? And don´t other foods play a role?

The authors claimed that at least four similar studies had been performed using the same methods and with a similar result, but this is not true. One of them, the largest of all such studies which has been performed at Harvard for may years, hasn´t come up with any evidence that a high intake of proteins is dangerous to health. What they have noted is that people who gorge in carbs have a higher risk of dying from a stroke or a heart attack, but contrary to the new study, they had asked the participants about their dietary habits regularly during the follow-up period. In addition, several reports, ignored by the authors of the new study, have been published with a similar result.

To draw conclusions about the effects of a low-carb diet is not possible from the data presented in the Swedish-American study because very few ate such a diet. Among the ten per cent who had the lowest intake, the carbs accounted for about 40 per cent of the total intake of calories. The benefits from a low-carb diet cannot be achieved, unless the intake is lower than 40 per cent; the lower, the better. This has been demonstrated in more than twenty experiments on people with type 2 diabetes or its precursor the metabolic syndrome. Their body weight goes down dramatically, their blood pressure and blood glucose becomes normal, their blood lipids improve and many of the patients are able to quit their antidiabetic medicine.

Critics of the low-carb diet claim that the high intake of saturated fat may be dangerous in the long run. It is true that we have not yet any long-term studies of the low-carb diet with cardiovascular disease or mortality as outcome, but it seems highly unlikely that a diet able to reduce most of the factors associated with a higher risk of cardiovascular disease should increase the risk. Besides, as I have documented in my books and in my scientific papers, no study has ever shown that a high intake of saturated fat leads to cardiovascular disease. On the contrary, at least six studies have shown that people with stroke have eaten less than healthy people.

But the study I tell about here included only women below the age of 50, and it is very rare that anybody die from the complications of type 2 diabetes in this age group. Why didn´t they include older women? Had they done that, the result would with all certainty have become much worse.

But let us assume the very unlikely possibility that their results are correct and that they are relevant. What was the benefit from eating as little protein and as much carbs as possible?

Using the figures in one of the tables it is possible to calculate that only 2.5 per cent got a heart attack or a stroke during these fifteen years, whereas this happened for 3.5 per cent among those who gorged in protein and ate little carbs.

However, I think, that the most important question is, if whether we can prolong our life by dietary measures. There are good reasons to assume that mortality was not affected in the study, because any researcher, who discover a method to lower mortality with statistical significance would report that eagerly.

However, in a report published from the same study, when the authors had followed the participants for twelve years only, they told that mortality was 37 per cent higher among those who ate the “dangerous” diet compared with those who ate as much carbs and as little protein as possible.

Most readers probably clap their hands, but to report an effect in per cent rather than in percentage points is highly misleading. However, this method is used by many researchers, when they try to exaggerate a trivial effect of a new treatment. Results from statin treatment for instance are always given as percentage. Let me exemplify how this method may mislead.

If only one patient die in a treatment group, which includes one hundred patients, but two die in an untreated control group of the same size, you can claim that mortality has been lowered by fifty per cent, because the difference between one and two is one, and one is fifty per cent of two. However, the true difference is of course only one percentage point.

Using the figures in one of the tables in the 12-year report we can calculate that for those who ate the dangerous diet, the chance not to die from a cardiovascular disease was 99.58 per cent, whereas the chance for those who ate the beneficial diet was 99.87 per cent. Thus, the benefit of 37 per cent corresponded to only 0.29 percentage points.

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August 2012

Is egg yolk dangerous to health?

On August 1 the medical journal Atherosclerosis published a paper by three Canadian researchers saying that eating egg yolks was just as dangerous to health as cigarette smoking. Unfortunately, many newspapers have reported the message from this study uncritically. (Read what the investigative reporter Jon Rappoport, once nominated for a Pulitzer Price, has to say about uncritical journalism). 

But there are exceptions. In The Atlantic Kristin Wartman has given a more balanced view. For instance she has discussed the paper with MIT researcher and senior scientist Stephanie Seneff, a member of THINCS. 

The authors' warnings against egg yolk is of course pure nonsense. Egg yolk contains everything needed to create a living warmblooded creature, and no previous study has ever been able to show any health problems associated with the intake of eggs. Their "scientific" argument for avoiding egg yolk is also flawed. You can read more about that study on Zoê Harcombe`s homepage. Zoê is a member of THINCS  and the author of several books about diet and obesity.

Statin Nation - a new film 

On September 10 Justin Smith releases his new film Statin Nation, where he has interviewed a number of experts about the fraudulent way the cholesterol campaign has been concerted. Among the interviewees are five members of THINCS including myself. It has already been shown for a selected public and has been commented in three British newspapers. You can read about the film, its producer Justin Smith and the participants in this press kit and you can also look at a trailer and order the film.

If you still think that health care and medical science are honest and respectable enterprises, then read the recent newsletter from The American Institute of Stress written by its president professor Paul Rosch, also a member of THINCS. Go to page 11 ("Physician and Medical Facility Fraud").

A calorie is a calorie

...or is it? Here is a humorous youtube about the low-carb/high-fat diet, the diet that is able to cure type 2 diabetes and the metabolic syndrome in a few months.top

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September 2012

Fraudulent advertising for food containing plant sterols. 

For many years Unilever has marketed its margarine Becel pro-activ (Flora pro-activ) and certain yoghurt products with the argument that they lower cholesterol. The cholesterol-lowering effect is due to the addition of plant sterols extracted from soya beans and Finnish timber using extraction petrol. The effect is that less normal cholesterol and more plant sterols are taken up by the gut resulting in higher levels of plant sterols and lower levels of human cholesterol in the blood 

Now to the problem. Several studies have shown that an increased level of plant sterols is associated with an increased formation of atherosclerosis, heart disease and premature death. In the following I shall mention the most important of these studies. I have also included the web address for these studies.  

High levels of plant sterols in the blood characterize a rare inborn disease named sitosterolemia, and patients with this disease develop xanthomas already in childhood. Xanthomas are benign tumours situated in the skin consisting of cholesterol and are seen in many patients with extremely high cholesterol, so-called familial hypercholesterolemia. In sitosterolemia these tumours also contain many plant sterols (reference 1).  

Several researchers have documented that patients with sitosterolemia become atherosclerotic in early childhood and may die from a coronary already as teenagers (references 2-5).  

There are of course good reasons why animals and human beings are using the cholesterol molecule instead of plant sterols to build cell walls and to produce bile, various hormones, vitamin D and other useful substances. It is therefore no surprise that exchanging our own cholesterol with plant sterols are harmful as has been demonstrated in experiments on rats fed large amounts of plant sterols. Not only was this diet harmful to their cells; it shortened their life as well (reference 6). 

In an analysis of one of the first statin experiments researchers led by Finnish scientist Tatu Miettinen found that 25 percent of the patients had an elevated level of plant sterol in their blood. These patients did not benefit from statin treatment; on the contrary their risk of heart disease increased (reference 7). 

In a review from 2003 all trials using food rich in plant sterol were analysed. The review was sponsored by Unilever, the main author´s research was also paid by Unilever; two of the other authors have patents on margarine containing plant sterols, and one of them had shares in the Finnish company Raisio, which produces margarine containing plant sterol. The authors concluded that plant sterols are harmless referring to animal experiment as evidence ignoring the rat study mentioned above (reference 6). They dismissed the studies reporting early atherosclerosis and cardiovascular death in sitosterolemia with the following argument: “This risk is believed to be largely hypothetical, and any increase due to the small increase in plasma plant sterols may be more than offset by the decrease in plasma LDL”. 

In their review the authors claimed that a study has shown that patients with sitosterolemia can eat plant sterols without risk. That study was included in a list of 33 similar experiments with the aim to measure the effect of plant sterol intake on the plasma lipids in human beings. With one exception all of them had a duration of less than nine weeks, almost all of them were performed for 3-4 weeks only. One wonder why it has been necessary to do 33 experiments (most of them paid by Unilever) with the only purpose to show that plant sterols lower cholesterol. Why has nobody performed a five-year controlled experiment to study the effect on cardiovascular events? 

The authors of reference 8 also ignored Miettinens previous study (reference 7) showing that statin treatment increases the risk of heart disease in people with raised plasma levels of plant sterols, although Miettinen was a co-author of the review. 

In some of their advertisements Unilever uses a report from European Food Safety Authority published in 2008 (reference 8) as support, but the authors of that report have not considered possible adverse effects either. They conclude that the plant sterols lower cholesterol, but also that “there are no human intervention studies demonstrating that plant stanols reduce the risk of coronary heart disease.”  

In this connection it is relevant to mention that many studies have shown that the effect of the statins do not depend on the very lowering of cholesterol because the benefit is the same whether cholesterol is lowered a little or very much. This fact explains why the patients in the 4S trial, whose plant sterol levels were high, did not benefit from statin treatment, although their cholesterol was lowered just as much or more than the other participants´. Therefore the argument that plant sterols lower cholesterol is misleading, because most people think that cholesterol lowering is synonymous with a lowering of cardiovascular risk.  

A few weeks ago I sent this report to the Swedish Consumer Ombudsman with the purpose to stop the promoting of food enriched with plant sterols. You are most welcome to send it to a similar governmental authority in your own country 

Here follow the references to the scientific studies mentioned above (click on the authors name to read the full paper) together with a selection of quotations from these papers:  

1. Bhattacharyya and Connor 1974Sitosterolemia and Xanthomatosis. A newly described lipid storage disease in two sister. 
“Although the usual diet may contain 150-250 mg of plant sterols, chiefly f8-sitosterol, only trace amounts of these sterols have heretofore been found in human or animal blood and tissues. We now report elevated plant sterol levels in the blood and tissues of two sisters with extensive tendon xanthomas but normal plasma cholesterol levels. Besides. P-sitosterolemia and xanthomatosis, no other physical, mental, or biochemical abnormalities were detected..... We suggest that increased absorption of P-sitosterol must be considered as one cause of this disease. The reason for the extensive xanthomatosis in these two patients remains unknown. Perhaps in some way plant sterols initiated the development of xanthomas with otherwise normal plasma cholesterol levels. Clinical atherosclerosis has not yet occurred.”  

2. Beaty et al 1986Genetic Analysis of Plasma Sitosterol, Apoprotein B, and Lipoproteins in a Large Amish Pedigree with Sitosterolemia.
”We previously reported the finding of phytosterolemia, xanthomatosis, and hyperapobetalipoproteinemia (hyperapoB) in five siblings in a large Amish pedigree ascertained through a 13-year-old boy who died suddenly from advanced coronary atherosclerosis…..The plasma levels of total and low density lipoprotein (LDL) sterol remain normal or moderately elevated in sitosterolemia [1-9]. Each of the 16 reported cases developed tendon xanthomas before the age of 10 years, and atherosclerosis of the coronary arteries, aorta, and aortic valve (producing aortic stenosis) occurred as early as the second decade of life [1-9].”

3. Salen et al. 1985: Lethal atherosclerosis associated with abnormal plasma and tissue sterol composition in sitosterolemia with xanthomatosis.
“These results indicate that cholesterol, plant sterols, and 5a-stanols are deposited prematurely and are associated with accelerated atherosclerosis in subjects with sitosterolemia with xanthomatosis.”

4. Assman G. et al. 2006: Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: Results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study. 
“Conclusions: Elevations in sitosterol concentrations and the sitosterol/cholesterol ratio appear to be associated with an increased occurrence of major coronary events in men at high global risk of coronary heart disease.” 

5. Weingärtner et al. 2009Controversial role of plant sterol esters in the management of hypercholesterolaemia.
”Summary points: Currently there are no data available indicating that functional foods supplemented with plant sterol esters reduce cardiovascular events. Findings in patients with the hereditary disease of sitosterolaemia, data from epidemiological studies, as well as recently published in vitro and in vivo data suggest that plant sterols potentially induce negative cardiovascular effects. Prospective clinical studies testing relevant clinical endpoints are needed, before a diet supplementation with plant sterol esters can be recommended.”  

6. Walisundera et al. 2000Vegetable Oils High in Phytosterols Make Erythrocytes Less Deformable and Shorten the Life Span of Stroke-Prone Spontaneously Hypertensive Rats.
”This study suggests that the high concentration of phytosterols in CA and the addition of phytosterols to other fats make the cell membrane more rigid, which might be a factor contributing to the shortened life span of SHRSP rats.”

7. Miettinen TA et al. 1998. Baseline serum cholestanol as predictor of recurrent coronary events in subgroup of Scandinavian simvastatin survival study. 
“The risk of recurrence of major coronary events increased 2.2-fold (P<0.01) by multiple logistic regression analysis between the lowest and highest quarter of cholestanol….Conclusions: Measurement of serum cholestanol concentration revealed a subgroup of patients with coronary heart disease in whom coronary events were not reduced by simvastatin treatment.” (No, it increased; my comment).
 

8. European Food Safety Authority 2008. SCIENTIFIC OPINION. Plant stanol esters and blood cholesterol
”There are no human intervention studies demonstrating that plant stanols reduce the risk of coronary heart disease….The product may not be nutritionally appropriate for pregnant and breastfeeding women and children under the age of five years. Patients on cholesterol lowering medication should only consume products with added plant stanol esters under medical supervision.”

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October 2012

Right and wrong about statin treatment

Statin treatment accelerates atherosclerosis 
Recently two separate studies showed that people on statin treatment develop atherosclerosis more often than untreated people. One of them was published in Diabetes Care, the other one in Atherosclerosis. You can get more details about this shocking finding in Dr. Mercola´s interview with senior scientist researcher Stephanie Seneff from MIT, who also is a member of THINCS. Read also Dr. Mercola´s comments about statin treatment.

Does statin treatment protect against cancer?
Ask any statinist and the answer is yes. In numerous studies the authors have claimed that statin treatment protect against all kinds of cancers. But all of them have made a serious error. Their evidence comes from comparisons between people on statin treatment and non-treated people. What all of the authors have ignored, unknowingly or deliberately, is that low cholesterol predispose to cancer. As most people on statin treatment have lived most of their life with high cholesterol, and as most untreated people have  low cholesterol, there is an obvious risk of bias.

Here comes a section from my book Ignore the Awkward! to give you more details about this question Just exchange the word Alzheimer with the word cancer.  

The statins cure everything

Statins are said to be useful against more than heart disease, e.g. cancer, lung disease, heart failure, hip fractures and much more. The way in which researchers have studied these alleged benefits is confounded with a serious error. As an example I shall analyse the allegation that statin treatment prevents Alzheimer’s disease.  The idea goes against common sense. Today we know that not only is the brain the cholesterol-richest organ in the body; cholesterol is also vital for its function, because the creation of nerve impulses demands a steady production of cholesterol.

     First, the evidence for this alleged effect does not come from trials. Instead, researchers have counted the number of patients with Alzheimer’s disease among people with low cholesterol and among people treated with statins. Because the upper limit for normal cholesterol has been lowered more and more, we can be confident that the untreated people’s cholesterol was not only low, it was very low. The fact that most Alzheimer patients were identified in this low-cholesterol group is seen as a proof that statin treatment prevented those in the other group.

     What has been forgotten is that low cholesterol is a frequent finding in people with various types of mental disturbances. For example, people whose cholesterol is lower than 200 are much more likely to decline in functional performance tests such as walking, turning around and dressing themselves.23 In addition, people with high cholesterol develop Parkinson’s disease and dementia less often than people with low cholesterol.24,25  Detailed records of the ability of people to learn, to reason, to concentrate and to organize their thoughts have also shown that, on average, the smartest people have the highest cholesterol.26  That statins should prevent Alzheimer’s disease is also contradicted by the finding that people with high cholesterol do not develop Alzheimer’s disease more often than people with low cholesterol.23       

     Not unexpectedly, researchers who are not employed by the pharmaceutical industry have even found negative effects from cholesterol reducing treatment. One of them is Matthew Muldoon, an American professor of internal medicine. Already after six months he noted that the memory of patients had declined.27 Later on in my book I shall tell the reader about more serious, cerebral disturbances caused by statin treatment.          

     Now to the crucial question. If Alzheimer´s disease is seen more often in untreated people than in people on statin treatment, is it because they have had low cholesterol for many years or is it because they have not received statin treatment? And if Alzheimer’s disease is seen less often in statin-treated people, is it because they have lived most of their life with high cholesterol, or is it because they have received statin treatment? Nobody knows.

 

A more scientific version, recently published in Quarterly Journal of Medicine by me and two colleagues of mine, Paul Rosch and Kilmer McCully, is available. Two of us have also mentioned it shortly in the coming film Statin Nation mentioned in my August Newsletter and hopefully presented for the public next month. Part of the section about cancer is available on Youtube.

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December 2012

Does statin treatment prevent cancer?

In my October newsletter I told you how it is possible to manipulate our minds to think that statins protect against almost everything. Here is another example.

Last month Danish researchers published a paper in New England Journal of Medicine entitled Statin use and reduced cancer-related mortality. They had studied how many people who had got the diagnosis cancer in Denmark between 1995 and 2007, how many who had died from cancer and how many of them who had been treated with statins before the cancer was discovered. What they found was that fewer had died among those who had got a statin prescription during this period. Therefore they concluded that statin treatment protects against cancer.  

What they ignore is, that at least four studies have shown that people with low cholesterol had a greater risk of getting cancer 20-30 years later, and that people with familial hypercholesterolemia has a lower risk of cancer.

What they also ignore is that three statin experiment resulted in more cancer in the treatment group an with statistical significance. What they also ignore is that several studies of cancer patients and patients without cancer have shown that the cancer patients had been treated much more often with statins than the control individuals.  

What they also ignore is the Japanese study the authors of which treated more than 40,000 patients with a low dose simvastatin. Seven years later three tomes more among those whose cholesterol had been lowered the most had died from cancer compared with those whose cholesterol was unchanged.  

Those who advocate statin treatment deny the cancer risk by referring to reviews of the statin trials, which have found no increase of cancer. There is a serious error in these reviews because they have excluded skin cancer from the calculations, although skin cancer is the first cancer type we should expect to see, if statin treatment is carcinogenic, because it is easy to diagnose at an early stage. Indeed, in the two first simvastatin trials 4S and HPS skin cancer was seen more often in the treatment groups, and if the figures from the two trials are calculated together the increase was statistically significant. Since then the number of skin cancer has not been recorded in any statin trial.  

The reason why cancer was seen less often among statin-treated people is probably because they have lived most of their life with high cholesterol, which, as I mentioned, protects against cancer, whereas the untreated have lived most of their life with normal or low cholesterol, and low cholesterol is, as mentioned, a risk factor for cancer. Furthermore, nobody knows how many of the statin-treated patients who really took the drug. A Canadian study found for example that most old people who have been prescribed statin treatment have stopped the treatment after two years  

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January 2013

Scary news, bad news and good news

In my april 2012 newsletter I referred to Duane Graveline´s report about memory loss due to statin treatment. Duane has researched further in FDA´s archive and I can tell you, it is much, much worse. Anyone who is on statin treatment and any doctor who prescribe these drugs must read Duane Graveline´s report

The number of people with Alzheimer´s disease has been inceasing for several years. One explanation may be the increasing use of statin treatment, but there is another way that leads to this deplorable condition: eating a carbohydrate-rich food. Three THINCS members, Stephanie Seneff, Glyn Wainwright and Luca Mascitelli have recently published a scientific paper, where they have explained the mechanism. 

Here comes the crazy news. Recently a Danish research group published a report in which they claimd that young men, who eat too much saturated fat, lower the quality of their sperms. Their message was spread uncritically in many newspapers. I feel it necessary to quote what Drummond Rennie had to say about such reports, when he was the deputy editor of JAMA: 

“There seems to be no study too fragmented, no hypothesis 
too trivial, no literature citation too biased or too egotistical, no design too warped, no methodology too bungled, no presentation of results too inaccurate, too 
obscure, and too contradictory, no analysis too self-serving, no argument too circular, no conclusions too 
trifling or too unjustified, and no grammar and syntax too offensive for a paper to end up in print.” 

If you think this description of medical science is an overstatement, read our member Zoë Harcombe´s comment to the sperm paper. 

But there are good news also. At first a sensational report from our member Jørgen Vesti-Nielsen. He was one of the first scientists to show that the best way to treat type 2 diabetes is to eat a low-carb, high-fat diet. The benefit of this diet has now been verified by at least twenty well-performed trials on patients with impaired insulin sensitivity or manifest type 2 diabetes. Their blood glucose level became normal, they lost weight, their blood pressure went down and many of the participants were able to quit their insulin and pills. And please note, nothing “bad” happened with their blood lipids. On the contrary, the “good” HDL went up a little and their triglycerides plummeted. You can find the references to these studies in a report of mine. It is in Swedish, but click on the word Litteratur, and you will find the references (numbers 6-26). 

But the same diet can be used in type 1 diabetics as well. This is what Vesti-Nielsen and his co-workers have documented in a new report. About half of forty-eight type 1 diabetics were able to follow this diet, which resulted in a major improvement of their laboratory values, and they were also able to reduce their insulin doses. We can only guess how much this may reduce their risk of future complications, but remember, that blindness, gangrene, heart disease and other side effects of diabetes are strongly associated with bad laboratory values. 

In a previous newsletter I told you about “STATION NATION – the Great Cholesterol Cover-Up”, a new film produced by the British medical journalist Justin Smith, in which among others a number of our members, including myself, have been interviewed. Hopefully this film may be able to inform many people about what I use to characterize as the greatest medical scandal in modern time. The producers have had some technical problems with the film, but everything has been solved, and you can now buy the film together with several additional interviews here. Justin himself has been interviewed in a British radio program. The interview starts at 8.05

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February 2013

The scandalous dietary guidelines

According to the current dietary guidelines we shall exchange saturated fatty acids with polyunsaturated fatty acids to avoid cardiovascular disease. But what is the difference between saturated and polyunsaturated fatty acids you may ask. 

The main part of a fatty acid is composed of a core of carbon atoms to which hydrogen atoms are attached. When the number of hydrogen atoms is optimal, as in saturated fatty acids, their electrons form stable pairs with those of the carbon atoms. Saturated fatty acids are saturated with hydrogen atoms. 

Unsaturated fatty acids are missing hydrogen atoms. Monounsaturated fatty acids are missing two atoms; polyunsaturated fatty acids (named PUFAs in the following) are missing four or more. Therefore, instead of sharing one pair of electrons with each other, some of the carbon atoms are sharing two pairs of electrons with their neighbour carbon forming a so-called double bound. Lack of hydrogen atoms makes the fatty acids unstable; they go easily rancid. The more double bonds they have, the more unstable they are. 

Two of the PUFAs, linoleic acid and alfa-linolenic acid are essential, meaning that we cannot produce them ourselves, but require small amounts in our food. The first one is an omega-6 PUFA, the second one is an omega-3. (The name omega refers to the placement of the double bound). 

Seafood is rich in omega-3 PUFA and oils from corn, sunflower and soybeans are rich in omega-6 PUFA:. To be very short (the PUFA biochemistry is complicated) omega-6 PUFA stimulates inflammation and omega-3 lowers it. Inflammation is a useful process, for instance if we become infected, but not if it goes too far. This explains why eating much omega-6 is associated with various human diseases, for instance asthma, arthritis, vascular disease, thrombosis, immune-inflammatory processes, and tumour proliferation. Now to the scary issue of this letter. 

Thirty-five years ago a dietary experiment was performed in Sydney, Australia. About half of 458 male patients with heart disease were given a diet low in saturated fat and cholesterol and with a high content of linoleic acid. The others ate as usual. 

Five years later 17.2 per cent in the diet group had died from a cardiovascular disease, but only 11 per cent in the control group. As only total mortality was reported in the original report (17.6 versus 11.6 per cent), the results were published recently once again in British Medical Journal, because the authors wanted to warn against eating too much omega-6 polyunsaturated fat. 

For that purpose they included an analysis of the combined result from four similar trials, where saturated fat was exchanged with omega-6 PUFA, and in all of them mortality was highest in the treatment group. They also analysed four trials, where the diet was composed of both omega-3 and omega-6 PUFA, and in these trials mortality was a little lower in the treatment groups.  

At a closed consensus meeting in 2010 in Copenhagen invited scientists (no, I was not invited; researchers with a controversial view are never invited to consensus conferences in this field) concluded that “the evidence from epidemiologic, clinical, and mechanistic studies is consistent in finding that the risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids.” You can read more about that in a paper authored by seventeen international experts

As I have shown in my books, in my papers and in my newsletters, there is no such evidence whatsoever. Read also what was written by authors of one of the sections in the recent WHO/FAO report (p 191): “The available evidence from cohort and randomised controlled trials is unsatisfactory and unreliable to make judgement about and substantiate the effects of dietary fat on risk of CHD”. However, in spite of the result of their review, they found no reason to change the current advice.

Most PUFAs in our food to-day are of the omega-6 types. Nothing is mentioned in the guidelines or in the mentioned paper about which type of PUFAs we shall eat, meaning that if you ask people to eat more PUFA, they automatically end up with eating much more omega-6 than omega-3 PUFAs, and those who produce sunflower, corn and soybean oils clap their hands, of course, as do researchers that are sponsored by the industry.

Already in 1991 Scott Grundy, one of the main actors in the cholesterol campaign, warned against eating too much omega-6 PUFA. According to Grundy there was no epidemiological support for this advice; it suppressed the immune system; it lowered the “good” HDL, it promoted LDL oxidation, and it increased the risk of gallstones. Of special concern was that linoleic acid might promote carcinogenesis in humans, as it does in laboratory animals. Since then many studies have confirmed his warnings. Associations have been found between omega 6 PUFA and prostate, pancreas, colon and in particular breast cancer. One of he first and longest dietary trials, where saturated fat was exchanged with PUFA also resulted in cancer. Fewer died from a heart attack but more died from cancer. (That fewer died from a heart attack could at least partly be explained by the fact that there were many more smokers in the control group).

After the introduction of the dietary guidelines for Americans in 1977 our intake of saturated fat has decreased and our intake of carbohydrates has increased. A few years later an obesity and diabetes epidemic started, and it has continued up to today in many countries. Are we going to see a cancer epidemic as well? The question is relevant because cancer may also be an effect of statin treatment

A few weeks ago I was invited to a conference in Oslo by The Norwegian Heart and Lung Patient Organization. I took up this problem at the end of my talk, which is available on Youtube

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February 2013

Light ahead in the cholesterol tunnel?

Many interesting things are happening just now, so therefore I send you yet another February newsletter. Let me start with the French professor Philippe Even, whose book "La Vérité sur le cholestérol" (Editions du Cherche-Midi) is going to be published today. In this week´s issue of Le Nouvel Observateur their journalist Anne Crignon has written two articles based on interviews with Even and myself. Eight pages of the magazine are devoted to cholesterol, and her articles have made a tremendous impact in France. Use this link, and you will find several hundred links to various newspapers, magazines and blogs that have cited or commented this issue. If you are not familiar with the French Language, you can translate the text using Google Translate

Another interesting book is The Great Cholesterol Myth: Why Lowering Your Cholesterol Won't Prevent Heart Disease-and the Statin-Free Plan That Will by Jonny Bowden and Stephen Sinatra. Their book inspired Dr Oz to interview the authors in a program, which he called “the most important show I have ever done on cholesterol”. (However, his demonstration of how atherosclerosis is created using balloons filled with a yellow fluid is nonsense). Here is part 1 and here is part 2

In my August 2012 newsletter I told you about Justin Smith´s film Statin Nation, a film that should be able to stop the cholesterol campaign immediately if it could be shown on the major television channels. If you haven´t seen it already, take a look at a few excerpts available on Youtube:

Here is an excerpt about the so-called good and bad cholesterol. Here is an excerpt about the lowcarb-highfat diet, 

Here is an excerpt about statins and cancerAnd here is a short presentation of Justin Smith himself

But please see the whole film - You can rent it here.

There are other critics out there. Here is a short review about the many serious side effects of statin treatment. Probably you may react, when Raymond Francis tells you that statins do not prevent heart attacks, but just continue, and you will know what he means. 

A ketogenic diet is an extreme variant of the lowcarb-highfat diet. It has been used for many decades to treat children with epilepsy and with great success, but have you heard that it even may cure cancer? We are still waiting for a correctly performed scientific trial, but there are already many case stories about the success of that diet published in medical journals. Here is a television program from CBN about this issue

Dominique D´Agostino, one of our members, has recently started such a trial

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March 2013

Fraud is allowed but not questioning

One of the most cited papers in support of the official dietary guidelines is “Seven Countries” by Ancel Keys. Those of you who have read my books know, that Keys was a cheat. For instance, in his paper from 1953, the one that started the war against fat, he excluded data from sixteen out of twenty-two countries, data that did not fit with his idea.  

The results in “Seven Countries”  study did not support his conclusions. For instance, heart mortality was 16-17 times higher on Corfu than on Crete, although they ate the same amount of saturated fat on the two islands. To say that he cheated in that study is perhaps to go too far, because the figures were given in the tables.

But in a recent review (the second article down for March) our member Zoë Harcombe has made a deeper analysis of Seven Countries and of other arguments used by the creators of the dietary advices. Did you know for instance that in the Seven Countries study as well as in the NICE guidelines biscuits, ice-cream, cakes, pastries and savoury snacks are classified as saturated fats? And there is much more.

According to the directors of the cholesterol campaign one of the strongest arguments is that people with inherited high cholesterol, so called familial hypercholesterolemia die from a heart attack at a young age. There are some very curious facts about this disorder. Did you know for instance, that the numbers who die from a heart attack is trivial; these people´s average life span is the same as for other people; more die from a heart attack, but fewer die from cancer. It isn´t the high cholesterol that causes the early death; many studies have shown that cholesterol of those who die from a heart attack is not higher than the cholesterol of those who do not. The risk factors are instead inherited high levels of prothrombin, factor VIII and fibrinogen, substances that participate in the coagulation processes.

You can read more about that in a letter I sent to British Medical Journal . Obviously my view on this issue is too controversial to become published in the paper version of the journal; therefore it is only available on the web as a “Rapid Response”, and few read these letters  

A few days ago I got an email from Robert Bramel, who has familial hypercholesterolemia. Here is what he wrote:  

“I have FH  so I joined a discussion group at theFHFoundation.org.  I asked the group why no one seems to understand why it is some FHers have significant disease and some have none. That was met only with "danger, danger, danger. Start taking statins". I then offered Sijbrands study that FH isn't all that hazardous and reported my personal negative experience with statins and how much better life is without it.Today I was told I had been dropped from the discussion group with this message: 

"The FH Foundation is made up of committed individuals who have FH and National thought leaders in the field of lipidology. It is our mission to raise awareness of Familial Hypercholeaterolemia and encourage proactive treatment of this life-threatening genetic disorder. Your understanding of the scientific data does not match that of our 11 renown physicians or respected public health organizations such as the CDC. We respectfully ask that you find another venue for your thoughts"  

For some people, keeping a monolithic story is much more important than getting it right. I looked up the funding for these doctors. According to propublica.org, five of ten received $250,000 pharma funding (total) over two years.” (end of letter)

I participate myself in CardioExchange, a discussion group of cardiologists in the hands of New England Journal of Medicine. A few months ago I received the following letter:  

“Dear Dr. Ravnskov,  

I am writing on behalf of the editors of CardioExchange. As you know, we encourage a free discussion of ideas about cardiology on the website, but we also reserve the right to shape or curtail that discussion when necessary to maintain an atmosphere that welcomes contributions from all of our members.

 

Although we appreciate your contributions to the site, we are writing to request that you refrain from the constant repetition of the same points (ie, rejection of the lipid hypothesis). Please feel free to contribute comments to the site, but, to be clear, every mention of lipids, cholesterol, or statins on the site should not be used as an occasion to educate other members about the shortcomings of this field. Constant repetition around such points only serves to drive members away, which doesn't serve anyone\'s interest.

 

Best,

 

Matt O\'Rourke

Director, Product Development, NEJM Group”  

More news.

Our member Malcolm Kendrick has started a blog

Hundreds of videos about statin treatment are available on Youtube; most of them are warning against such treatment. There are also some who recommend it because of “the great benefit”. Do not believe them!

If you do, please listen to the interview with the whistleblower Gwen Olsen, who has worked in several drug industries for many years .  

Here is a sad story about the effect of statin treatment, and this is not a rare case; I have received many letters with similar stories  

Justin Smith, the creator of the revealing film Statin Nation, has now uploaded the first thirteen minutes of the film

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May 2013

Is the Cochrane Collaboration still reliable?

Doctors and researchers have great confidence in the Cochrane Collaboration. It is a non-profit organization consisting of a group of over 28,000 volunteers in more than 100 countries and said to be independent. The group conducts systematic reviews of randomized controlled trials of health-care interventions, which it publishes in the Cochrane Library 

Hitherto no statin trial has succeeded in prolonging the life of healthy people whose only “disease” is high cholesterol, or who have risk factors for heart disease, but who have never had any heart problem. As mentioned in one of my previous newsletters Cochrane Collaboration published an analysis of these trials in 2011. When all results were taken together they found a minimal risk reduction. However, their conclusion was, that “only limited evidence showed that primary prevention with statins may be cost effective and improve patient quality of life. Caution should be taken in prescribing statins for primary prevention among people at low cardiovascular risk. 

But in a recent Cochrane report about the same issue, the authors conclude that Reductions in all-cause mortality, major vascular events and revascularisations were found with no excess of adverse events among people without evidence of CVD treated with statins.

How come they have changed their mind, you may ask. Because the minimal benefit in the second review was a little better. Let us take a look at the figures.

The first Cochrane analysis included about 28,000 “patients”. In the control group 3.06 % had died; in the treatment group only 2.58%; a difference of 0.48 % You can also say, that without statins your chance to be alive after a few years without treatment is 96.9 %, but if you take a statin drug every day, you can increase your chance to 97.4 %.

In the new analysis, that included about 48,000 “patients”, the result was a little better. In the control group 5.17 % had died; in the treatment group only 4,41 %; a difference of 0.76 %. You can also say, that without statins your chance to be alive after a few years without treatment is 94.8 %, but if you take a statin every day you can increase your chance to 95.6.    

These small effects were even exaggerated, because in both analyses, the authors had excluded EXCEL, the first trial performed on healthy people. It included more than 8000 people, but it was stopped after 48 weeks, because, as Merck explained to me in a letter, they were only interested to know, if the “patients” tolerated their drug, which they did. 

The trial included three treatment groups, and the mortality in these groups were 0.5 %; in the control group only 0.2 %. This is not mentioned in the abstract; you have to calculate it yourself from figures given in the text. 

The reason for excluding EXCEL was that they only accepted trials with a length of at least one year, and as mentioned EXCEL was stopped after 48 weeks.

Without the data from EXCEL the new analysis seems to have shown a benefit because, as the authors wrote, there was no excess of adverse events. Obviously they had forgotten what they wrote in their previous report: There was evidence of selective reporting of outcomes, failure to report adverse events and inclusion of people with cardiovascular disease.

And they were right. In my newsletters and in my books I have given many examples of the fraudulent way the industry-sponsored trial directors have downplayed the adverse effects from statin treatment. Let me just mention that at least 20 % get muscular problems, just as many become impotent, at least 4 % get diabetes, about 1 % cataract, and an unknown number polyneuropathy or mental disturbances such as memory loss, depression, sleep disturbances and aggressive behaviour. Duane Graveline has also written about this issue, and you can read about the influence of low cholesterol on brain function here.

Most serious is the risk of cancer. Together with Kilmer McCully and Paul Rosch, two of our most respected members of THINCS, I have given detailed arguments in a paper for the view, that statin treatment, or rather low cholesterol, is carcinogenic. 

More about red meat

For several years we have been told that red meat causes both cancer and cardiovascular disease. However, most studies of this issue have calculated the outcome for intake of red meat and processed meat  taken together in their calculations, and as I told in a previous newsletter there were serious errors in the few studies that found unprocessed read meat to be unhealthy. 

Recently Sabine Rohrman and 46 co-authors published the results from EPIC (European Prospective Investigation into Cancer and Nutrition), a large dietary study conducted in 23 centers in 10 European countries.

The authors organized interviews of 448,568 men and women about their habitual diet  habits during the previous year; and in most countries an extensive self-administered dietary questionnaire was used as well. After that the participants were followed for 12-13 years. After correcting for confounders they found that intake of red meat is harmless; not unexpected it is the intake of processed food that may be harmful.  

 

Note: If you want to receive my newsletters, click here 

If you are not familiar with the scientific language used here and there in the above, You can read about most of the issues taken up in the above in a more popular way in my books. In the most recent one I have also described how it has been possible to seduce a whole world for many decades by ignoring all conflicting observations; by twisting and exaggerating trivial findings; by citing studies with opposing results in a way to make them look supportive; and by ignoring or scorning the work of critical scientists. Both of them are available from amazon, the latter one also in a Kindle version.

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