For your convenience, here’s a list of peer reviewed studies and journal articles, challenging current dietary advice, since March 2013.
The papers are listed in reverse chronological order and I’ll try to keep this updated. Please post a comment with those I’ve missed and I’ll update.
February 9th 2015: Harcombe et al. “Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis.” BMJ Open Heart. 2015.
February 1st 2015: Nathalie Genevieve Puaschitz et al. “Dietary Intake of Saturated Fat Is Not Associated with Risk of Coronary Events or Mortality in Patients with Established Coronary Artery Disease.” The Journal of Nutrition. (Many thanks to Ted Hutchinson for this one).
November 24th 2014: Sean C Lucan and James J DiNicolantonio: “How calorie-focused thinking about obesity and related diseases may mislead and harm public health. An alternative.” Public Health Nutrition. 2014.
November 21st 2014: Brittanie M. Volk, Laura J. Kunces, Daniel J. Freidenreich, et al. “Effects of Step-Wise Increases in Dietary Carbohydrate on Circulating Saturated Fatty Acids and Palmitoleic Acid in Adults with Metabolic Syndrome”. PLoS One 2014.
November 17th 2014: Malhotra A, Maruthappu M, Stephenson T. “Healthy eating: an NHS priority A sure way to improve health outcomes for NHS staff and the public.” Postgrad Med J 2014.
October 8th 2014: Lamarche, B., and Couture, P. “It is time to revisit current dietary recommendations for saturated fat.” Applied Physiology, Nutrition, and Metabolism. pp.1-3. 2014 (Many thanks to Gaby in comments for this one).
September 2014: Bazzano LA, Hu T, Reynolds K, et al. “Effects of Low-Carbohydrate and Low-Fat Diets A Randomized Trial”. Ann Intern Med 2014; 161(5): 309-18.2
August 2014: Harcombe Z, Baker J. “Plant Sterols lower cholesterol, but increase risk for Coronary Heart Disease.” Online J Biol Sci 2014; 14(3): 167-9.
June 2014: Feinman RD, Pogozelski WK, Astrup A, et al. “Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base.” Nutrition (Burbank, Los Angeles County, Calif) 2014.
April 2014: Schwingshackl L, Hoffmann G. “Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression“. BMJ Open 2014; 4(4).
April 2014: Hansen A. “Swedish health advisory body says too much carbohydrate, not fat, leads to obesity“. BMJ 2013; 347.
March 2014: Chowdhury R, Warnakula S, Kunutsor S, et al. “Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis“. Ann Intern Med 2014; 160(6): 398-406.
March 2014: Georgina E. Crichton and Ala’a Alkerwi. “Whole-fat dairy food intake is inversely associated with obesity prevalence: findings from the Observation of Cardiovascular Risk Factors in Luxembourg study.” Nutrition Research. (Many thanks to Evonne in comments for this one).
February 2014: Ravnskov U, DiNicolantonio JJ, Harcombe Z, Kummerow FA, Okuyama H, Worm N. “The Questionable Benefits of Exchanging Saturated Fat With Polyunsaturated Fat.” Mayo Clinic proceedings Mayo Clinic 2014. (Viewable here thanks to Dr Michael Eades)
January 2014: DiNicolantonio JJ. “The cardiometabolic consequences of replacing saturated fats with carbohydrates or Ω-6 polyunsaturated fats: Do the dietary guidelines have it wrong?” Open Heart 2014; 1(1).
December 2013: Schwingshackl L, Hoffmann G. “Comparison of effects of long-term low-fat vs high-fat diets on blood lipid levels in overweight or obese patients: a systematic review and meta-analysis”. Journal of the Academy of Nutrition and Dietetics 2013; 113(12): 1640-61.
October 2013: Malhotra A. “Saturated fat is not the major issue”. BMJ 2013; 347.
May 2013: Malhotra A. “The dietary advice on added sugar needs emergency surgery“. BMJ 2013; 346.
May 2013: Glen D.Lawrence: “Dietary Fats and Health: Dietary Recommendations in the Context of Scientific Evidence.” Advances in Nutrition. 2013.
March 2013: Z. Harcombe, J. Baker, B. Davies. “Food for Thought: Have We Been Giving the Wrong Dietary Advice?” Food and Nutrition Sciences 2013; 4(3): 240-4. (This is the second most popular paper for the journal Food & Nutrition Sciences, confirming the interest in progressive, rather than conventional, thinking.)
And, of course, none of these should have been necessary as Uffe Ravnskov ended the debate in May 2010 in this book - viewable here.
If I told you that a private company had instructed me to remove this video, I would expect you to be shocked. What do you think about the same private company instructing me to stop saying this: “the calorie theory and conventional weight loss advice is wrong” and this: “weight gain and loss also depends far more on carbs consumed, than calories, or fat, consumed“? Appalled? Outraged?
That’s exactly what has happened, over the past year. The private company is the Advertising Standards Authority.
* You probably think that the Advertising Standards Authority (ASA) is an official body. You would be wrong. It is a self-appointed, self-regulated, upholder of the opinions of another non-official, self-appointed, self-regulated body: the Committees of Advertising Practice (CAP).
* CAP make up ‘the Codes of Advertising Practice”; the ASA apply them. Think of CAP and the ASA like Simon and Louis in the X Factor, only not as entertaining: Simon makes up the rules, Louis follows them.
They are two sides of the same coin; partners in crime. One has a red web site; the other has a blue web site – look how similar they are. Well, they do live at the same address: Mid City Place, 71 High Holborn, London, WC1V 6QT. They even publish a shared annual report.
* Both bodies use the tag line “Legal, decent, honest, truthful.” These are not legal bodies, (as in set up by law) let alone decent, honest or truthful. These two organisations are more misleading per se than any misleading advert I have seen. The most misleading thing is that they lead you to believe they are official bodies. They aren’t. They write to you as if they have legal powers. They don’t. You can’t even lodge a complaint about them being misleading because they are accountable to no one.
* CAP/ASA decided in 2010 that they will extend their self appointed remit to the internet. As someone who does not place adverts and does not allow adverts on any of my web sites, I would not expect to have anything to do with either body. CAP and the ASA have different views. They have decreed that, if you are connected to ‘a product’ in any way e.g. author of a book, web pages that they decide are connected with that book shall be deemed adverts.
* CAP have opinions. They have opinions on things you may not even think warrant an opinion. They have opinions on global warming, fat burning, the calorie theory, current dietary advice, cholesterol, stripograms (yes, really!) and religious organisations, just as examples.
* In my world of diet, health and nutrition, CAP believe that the current dietary advice is correct. They believe the calorie theory. They believe that Flora gunge is good for the heart and that cholesterol is bad. They have no evidence for any of this – but they are a self-appointed regulator, so they do whatever they like.
* A troll writes to the ASA and complains that you say things on your web site like “the calorie theory and conventional weight loss advice is wrong“. The ASA then writes to you saying:
i) We have decreed that your web page is an advert;
ii) You are in breach of the CAP code; and
iii) You must stop saying things that CAP don’t like, or we will put you on our naughty boys’ list.
Hence – we are now on the naughty boys’ list. Or, as Dr Malcolm Kendrick says, we now have a badge of honour!
This blog is about censorship. This blog is about one unofficial body trying to silence any views that are different to the opinions of their partner unofficial body, which you can assume to be conventional. It’s also about the scum levels that troll cowards are stooping to, to try to silence progressive thinking.
We asked CAP for evidence for their codes. The full exchange can be seen here. The bottom line is that CAP have no evidence for their opinions, against which they are judging us and in the field in which they are demanding evidence from us.
I wrote to the ASA chair, Rt Hon Lord Smith of Finsbury, and the CAP chair, James Best, and asked them four questions:
1) What gives the ASA/CAP (you are two parts of the same) the right to try to censor free speech?
2) Who gave the ASA/CAP the power to police any debate on the internet (including, but not limited to, health, nutrition, climate change etc) upon which CAP holds an opinion for the ASA to enforce?
3) How do you justify demanding evidence from me when a) you have none of your own (in my area of expertise anyway – see Appendix) and b) when the ASA are not able to consider our evidence because it differs from CAP’s opinions?
4) What will you do about this case, now and ongoing, given that I will not remove content from the World Wide Web, which challenges the status quo, just because CAP holds a conventional view?
I have not yet received a reply from CAP. The ASA chair did not deign to reply, but the head of casework replied on his behalf. Her response was as follows:
1) “Marketers have a right to express their opinions freely so long as they do so in line with the rules set out in the CAP code.”
i.e. you can freely express your opinions so long as they are the same as CAP’s. CAP holds conventional opinions and thus any non-conventional views are not allowed.
2) “Our authority to regulate marketing materials derives from an agreement from Government through which the ASA is designated as the ‘established’ means for administering the Consumer Protection from Unfair Trading Practice Regulations 2008 (the CPRs), which prohibit unfair, misleading or aggressive marketing to consumers.”
This is misleading. It implies that the ASA have been appointed by the Government to regulate adverts, which they have not. All that they have is access to the Office of Fair Trading (now abolished, by the way), which everyone else in the UK also has. They have no government authority to impose their opinions across the internet and to silence debate.
3) “It is not for the ASA to disprove a claim that a marketer has made and we are entitled to base our rules on generally accepted public health advice in the interest of consumer protection.”
i.e. we don’t have to provide evidence. We don’t have to disprove your evidence. We “are entitled” to rely on conventional thinking and insist on any non-conventional views being removed.
4) “If you refuse to comply with the advertising code following an ‘Upheld’ ASA adjudication, our Compliance team has a range of sanctions that include posting your name on our wall of non-compliant advertisers.”
i.e. if you do not allow yourself to be censored, we will put you on our naughty boys list.
That’s censorship and bullying and all sorts of other contemptible behaviour.
Logic & futility – you cannot win
To use one of our examples, a troll objected to this video “as it implied that conventional weight loss advice was wrong.” You bet it does!
The ASA decreed that the video is an advert for the book The Obesity Epidemic: What caused it? How can we stop it? That’s tenuous enough – but go with it. They then say that you’re not allowed to imply that conventional weight loss advice is wrong (because CAP have decreed that it is right) and therefore you must remove your ‘advert’ a.k.a. the video. Yes – seriously folks – George Orwell was way more prophetic than he/we realised.
If my site contained details of a book that reflected CAP’s opinions, there would be no issue. The Simon and Louis, Yin and Yang, of CAP and the ASA would not be trying to censor me. The ‘but for’ is therefore my content, not the notion that I am ‘advertising a book’.
To use another of our examples: This is a direct quotation from ASA correspondence:
“The claim “In no way is the body as simplistic as energy in = energy out – and, therefore, we do not need to put less energy in and/or try to get more energy out. We need to eat better, not to eat less” in ad (e) [ZH – that’s a web page] and comparison in ad (g) [ZH – that’s the video] misleadingly implied that conventional weight loss advice was wrong.” Again – you bet it does!
The ASA have decreed that this is i) in breach of CAP’s opinions (sorry – the CAP code) and ii) misleading. We pointed out to the ASA that – IF the web pages are adverts (and we have never accepted this – they are my editorial content) then we have two options:
i) Write conventional nonsense, which makes CAP happy, but then site visitors would be misled because the book is anything but conventional; or
ii) NOT mislead visitors and make site content clear that I do NOT subscribe to conventional wisdom, but then CAP would put you on the naughty boys list.
You cannot win in the ASA/CAP world of Alice in Wonderland.
The bottom line
We shared the attempt to elicit evidence from CAP with the ASA and asked a specific question:
“Please can you let us know how the ASA can review evidence submitted, in a “legal, decent, honest and truthful”, way when you exist to impose the opinions of CAP and the evidence submitted is counter to the opinions of CAP?”
The ASA replied back “As you are aware, it is the role of CAP to write, and review as necessary, the rules and it is the ASA’s role to apply them. Whilst I have noted your comments, because the ASA simply apply those rules I would not be able to consider as part of the investigation the evidence base or validity of those rules.”
And there you have it ladies and gentlemen. CAP admit they have no evidence. The ASA admit they have no choice but to administer the opinions of CAP. If someone complains to the Alternative-view Silencing Agency about you, don’t waste a second of your time submitting evidence. It makes not one iota of difference. Knowing this – you may like to choose your response more appropriately. From now on, ours will be “to ignore”.
“Freedom is the right to tell people what they do not want to hear.” George Orwell.
p.s. I always like to check conflicts of interest. To quote the ASA: “The ASA is funded by advertisers through an arm’s length arrangement that guarantees the ASA’s independence”. Ha ha. Check out P35 of the 2013 Annual Report, Unilever had 3 of the top 6 most complained about adverts. None were upheld by the Alternative-view Silencing Agency. Don’t bite the hand that feeds eh!?
The Royal Society for Public Health (RSPH) published a press release on 31st October 2014 calling on the drinks industry and the newly appointed EU Health Commissioner to introduce calorie labelling for alcoholic drinks. The RSPH claimed that there was strong public backing for this to happen and a general lack of awareness among consumers about the calorie content of alcoholic drinks.
The RSPH commissioned a polling company, Populus, who interviewed a random sample of 2,117 British adults, online, between 10-12th October 2014. The results were as follows (Please note – the press release claims “two thirds of the public”/”over 80% of the public”, but claims can only be made on behalf of those interviewed – not the Great British public):
– Two thirds (67%) of those interviewed supported the addition of calorie labels on packaging of alcohol drinks (we don’t know how this was positioned in the survey);
– Over 80% of those interviewed didn’t know, or guessed incorrectly, the calorie content of a large glass of wine (we don’t know what margin for error was allowed);
– Almost 9% didn’t know, or incorrectly estimated, the calories in a pint of lager (ditto).
(As an aside, this blog, by the RSPH chair said that 80% of 500 people “didn’t know the calorie content of their favourite tipple”. 2,117 or 500? How many people were interviewed?)
The European Commission is due to make a decision by December 2014, about extending nutrition labelling (including calorie labelling) on alcohol. (Alcoholic drinks are currently not recognised as food and are therefore exempt from food labelling.)
The Chief Executive of RSPH, Shirley Cramer CBE, was quoted in the press release as saying:
“Calorie labelling has been successfully introduced for a wide range of food products and there is now a clear public appetite for this information to be extended to alcohol to help individuals make informed choices. With 2 in 3 adults overweight or obese and given that adults who drink get approximately 10 percent of their calories from alcohol, this move could make a major difference to waistlines of the nation.”
I’m familiar with the UK Family Food Survey, so the “10 percent of their calories from alcohol” didn’t sound right. (Check the 2012 document – Table 24.4, page 18 – and you can see that alcohol accounts for 58 calories out of 1,990 – 2.9% of calorie intake.)
I emailed the communications manager to ask for the source of the 10% claim and she replied by return to say that it was from p17 of this. Start on p16 and notice that averages (means) for all adults (or in a couple of cases children) are reported for: fruit and vegetables; oily fish; all energy; total fat; saturated fat; transfats; Non Milk Extrinsic Sugars; non-starch polysaccharides; vitamins and minerals. Only one intake is reported differently. Alcohol is not reported as a mean intake of all adults, but as an average of those who drank alcohol in a four-day recording period: “58% of adults aged 19 to 64 years and 52% of adults aged 65 years and over consumed alcohol during the four-day recording period. Adults aged 19 to 64 years who consumed alcohol during the four-day recording period obtained 9% of energy intake from alcohol; older adult consumers obtained 7%.”
That’s how Cramer manipulated the figures to make the ‘prize’ of alcohol calorie reduction look larger than it is. Even then, 7 and 9% became “approximately 10%.” This is disingenuous.
Alcohol and calories
As followers of this blog/recipients of this newsletter will know, there are fundamental issues with calories in general: thermodynamics not being about calories or weight; the calorie theory being unsourced and unproven, etc. There are additional issues with alcohol calories…
The assignment of calories to different foodstuffs is generally credited to Wilbur Atwater (1844-1907) and Max Rubner (1854-1932). Their work around the turn of the 19th-20th century developed the first calorimeter and this enabled them to estimate that carbohydrate, protein and fat had approximately 4.1, 4.1 and 9.3 calories per gram respectively.[i] (Rubner recorded the calorific value for olive oil as 9.4, so even his 9.3 was an average of four fats reviewed. This has never been a precise science).
Atwater was concerned about helping American working men to fuel their physical labour and he discovered that alcohol had approximately 7 calories per gram. This was much to the joy of the liquor industry, giving rationale for alcohol consumption for its calorie value. It’s ironic that, just over 100 years later, the powers-that-be are trying to curtail alcohol consumption for its calorie value.
Those who know about the thermic effect of nutrients and the work of Jequier,[ii] Feinman and Fine,[iii] know that macronutrient calories behave very differently within the human body. Alcohol calories even more so. The body sees alcohol as a toxin and wants to get rid of it. Some is got rid of as acetic acid. (When you drink, you wee – yes?) Alcohol digestion takes place mostly in the liver and the kidneys, not in the digestive system – big clue there. So alcohol calories don’t count in the same way as sugary drink calories. Those RSPH pictures claiming a glass of wine = a slice of pizza – also disingenuous.
Arguably, given that alcohol calories are not properly digested – the more Brits drink and the less they eat, the slimmer they will be!
Calorie labelling and choices
Let’s be honest – what is really going on here is that the Royal Society for Public Health is trying to stop people drinking alcohol. Frightening people with health scares hasn’t worked, so they are now trying the calorie angle to see if this will curb drinking instead. And it might. Women especially are more calorie aware/obsessed than men and may choose a lower calorie drink. But this won’t necessarily lower alcohol – which is the end in mind, is it not?
The RSPH web site accompanying the press release has a picture of a Pina Colada (scroll down), claiming that it has 450 cals. It has 2 units of alcohol. On the same web page, I can see that I could have 2.5 x 250ml glasses of wine with a total of 8.2 units of alcohol for the same 450 calories. The law of unintended consequences could take effect here. On the RSPH’s own video here (bottom one) a woman says she won’t drink less – she may choose lower calorie alcohol options.
Alcohol and weight
You can download the RSPH’s position paper on alcohol here.
Here is the paragraph on alcohol and weight in the position paper:
“There is evidence that heavy drinkers (drinking four or more drinks per day) are at a greater risk of obesity than moderate or non-drinkers. The odds of being overweight or obese are also significantly higher among binge drinkers than among those who consume the same amount of alcohol over multiple sessions. (Ref 14) Weight gain from drinking alcohol is also greater in individuals who are already overweight or obese and there are individual differences in the impact of alcohol consumption on weight. (Ref 15) Drinkers dependent on alcohol, however, due to the propensity to substitute alcohol for meals, may experience weight loss (Ref 16).”
Ref 14 can be seen in full here. This is the results section of the abstract:
“Current drinkers had lower odds of obesity (Adjusted odds ratio = 0.73, 95% CI: 0.55, 0.97) as compared to non-drinkers. The odds of overweight and obesity were significantly greater among binge drinkers and those consuming four or more drinks/day. However, those who reported drinking one or two drinks per day had 0.46 (95% CI: 0.34, 0.62) and 0.59 (95% CI: 0.41, 0.86) times the odds of obesity, respectively. Similarly, the odds of obesity were significantly lower among those who reported drinking frequently and consuming less than five drinks per week.”
Did you get that? Current drinkers had lower odds of obesity. Those drinking one or two drinks per day had approximately half the incidence of obesity compared to non drinkers. The odds of obesity were significantly lower for the frequent drinkers. Look at Table 2 in the paper to see that you do not want to be a non drinker, or even in the first quartile of drinking days per year. Those in the second, third and highest quartiles of drinking days all had a significantly lower incidence of obesity. The average drinks per week data shows that you want to be having more than 15 drinks a week (a drink was counted as a 12oz beer or 4oz wine), rather than 10-14 drinks a week. Although the only statistically significant findings on the drinks per week section was those drinking up to 5 drinks a week had significantly lower levels of obesity than teetotalers.
The only finding in favour of alcohol intake and obesity was the one quoted by the RSPH position paper. This is disingenuous.
Ref 15 (abstract) can be seen here. The paper title is: “Is alcohol consumption a risk factor for weight gain and obesity” and it opens by noting “Epidemiologic data showed a positive, negative, or no relationship between alcohol intake and body weight.” Again – only the circumstance in favour of the RSPH’s anti-alcohol position has been cited: “Weight gain from drinking alcohol is also greater in individuals who are already overweight or obese.”
What about those not overweight or obese? You can either buy the paper ($54) or assume that – had there been any more ammunition from this paper, the RSPH would have used it.
Ref 16 doesn’t try to offer evidence for an association between weight and alcohol intake – other than an inverse one. It admits that very heavy drinkers tend to drink rather than eat and therefore tend to experience weight loss. This is further evidence for the notion that replacing food calories with drink calories could actually aid weight loss. (I think it would, but I am not advising it as an overall health strategy).
And that’s it. So we don’t actually have evidence presented by the RSPH for the implication that reducing alcohol consumption will reduce calories will reduce weight. It’s all just inferred. So what is the evidence for alcohol and weight?
Here is where you should do yourself a favour and get this fab little read from amazon. Tony Edwards has gone through reams of evidence on alcohol and all important conditions, from weight to heart disease and cancer to diabetes, so that you don’t have to. There were a couple of summary articles at the time of publication. Try this or this.
In Chapter 7 of his book, Edwards runs through the major studies reviewing alcohol and weight over the past 25 years: Wang et al 2010 studied 19,220 women, their drinking habits and weight for almost 13 years. Approximately 9,000 gained significant weight over the study. The study concluded: “Compared with non-drinkers, initially normal-weight women that consumed light-to-moderate amount of alcohol experienced smaller weight gain and lower risk of becoming overweight and/or obese during 12.9 years of follow-up.”
Then there’s the findings of a 5-6 year long Danish study, involving 43,500 people, where daily drinkers had the smallest waistlines. Then there’s the 8 year long University College London study of nearly 50,000 women, which showed that women who drank 30 grams of alcohol daily were less likely to put on weight than teetotalers. Then there’s the 10 year study, of 7,000 US adults, showing that drinker gained less weight than non drinkers. And so on.
Please note that this is all still association, not causation; relative, not absolute risk. Nonsense on top of nonsense therefore but not even the underlying association is supporting the RSPH position.
Don’t forget in all of this that the unit guidelines were plucked from thin air. Although Richard Smith wasn’t popular with the Royal College of Physicians for saying so.
Has the RSPH proven that calorie labelling on alcohol would reduce alcohol consumption? No.
Has the RSPH proven that alcohol and weight are even positively associated? No.
Has the RSPH proven that labels would have any impact on any health condition that alcohol is claimed to be associated with? No.
There’s just been a lot of insinuation, inference and disingenuity. And a lot of media hot air. Talking of hot air…
Here’s a final thought for you…
Coal apparently has 7,000 calories (kcal) per kg. That’s 7 kcal per gram – the same as alcohol. Do you think that a gram of coal would make you fat?! Well then…
[i] Max Rubner, “Zeitschrift fur Biologie,” Festschrift zu Voit, (1901).
[ii] Eric Jequier, “Pathways to Obesity”, International Journal of Obesity, (2002).
[iii] Richard Feinman and Eugene Fine, “A calorie is a calorie violates the second law of thermodynamics”, Nutritional Journal, (2004).
Michael Mosley was back on our screens last week (15 October 2014). I do like MM. I like his bedside manner. I like his preparedness to self-experiment and he’s becoming more and more aligned with the real foodie way of thinking, as shown with his confession on exercise here and on fat here.
However, he and the other doctors on Trust me I’m a doctor (TMIAD), are being badly let down by whoever is advising them on nutrition. Doctors receive barely a few hours of training in nutrition, despite Hippocrates’ advice “Let food be thy medicine and medicine be thy food.”
The carb experiment
Dr Chris van Tulleken, one of the twins who did the Horizon fat vs. sugar experiment in January 2014, is one of the TMIAD presenters. He took part in a ‘ground-breaking’ experiment, in an Italian restaurant, with the positioning statement: “starchy foods, like potatoes and pasta, have lots of calories but can you make these goods better for you?”
The study lead was Dr Denise Robertson from the University of Surrey. The 10 participants were given 100g (cooked weight) of pasta (with a tomato based sauce), 3 days in succession. On day one the pasta was hot, just cooked; on day two the pasta was cold, having been chilled overnight; and on day three they had the chilled pasta re-heated. This is a good experiment design, as the same subjects are used for all three interventions thus minimising any impact of different people responding differently to the same circumstances. The participants took their own blood samples every 15 minutes for the 2 hours following the pasta consumption.
Robertson’s hypothesis was that cooking the pasta differently would “reduce its calories.”
Tulleken narrated: “starchy foods like this are very quickly broken down into sugars … high sugars, and the resulting insulin, are unhealthy and they may make you feel hungry soon after a meal. And that’s the problem with refined sweet sugars, but it’s also true for things like pasta, potatoes, white rice and white bread.”
A graph was shown of the rise in blood glucose levels after eating first the freshly cooked pasta.
The average fasting blood glucose level is 5.6 mmol/L, but the normal range is wide and most people fall into a fasting blood glucose range of 3.3-7.7 mmol/L. The starting average blood glucose level for the group of 10 was 4.6 mmol/L (reading from the graph on the TV as accurately as possible). The peak blood glucose level occurred after 30 minutes – 6.6 mmol/l. At 120 minutes, the mean blood glucose levels were 5.3 mmol/L.
The chilled pasta peaked at about 6.4 mmol/L and the peak was slightly later than the freshly cooked pasta. However, the graph shown on the programme put the fresh pasta and chilled pasta alongside each other. I don’t know about you, but I found the difference between the green and blue lines completely underwhelming.
Robertson explained what had happened as follows: “We know that when a starch, such as potato or pasta, is cooked in water and then it’s allowed to cool, you’re changing the structure of that starch. You’re changing it in such a way, it becomes resistant to the normal enzymes that we have within our bodies. And, because the enzymes don’t work on it, it releases less glucose and so you get a lower glucose response.”
Tulleken clarifies “So it’s good for you because you get a lower blood sugar.”
Robertson: “You do and it’s now called resistant starch. And resistant starch, because you’re not digesting it will move down your intestine; it will end up in your large bowel and it becomes part of your dietary fibre.”
It got a bit more interesting when the two-day-old chilled pasta was re-heated. The graph for this one led Tulleken to exclaim: “astonishingly, it reduces the rise in glucose by another 50% making it even healthier.” You can see the second graph below
The blood glucose peak for the re-heated pasta is 5.7 mmol/L. The 50% is a relative claim, using the 4.6 mmol/L starting blood glucose level and is highly misleading. The red line is more different from the green line than the blue line is, but it’s not ground-breaking and here is why…
The programme could have produced a flat line – none of the ‘bad’ rise in glucose, sugar peak and insulin production by either 1) giving the subjects meat or fish or 2) giving them the pasta packaging to eat!
What this experiment has done is to make food less digestible so that it doesn’t produce the physiological changes that occur when the body registers that we have eaten food. The ultimate indigestible substance would be the cardboard box from which the pasta came. “But that would be stupid – it has no nutrients“, I hear you cry and you would hit the nail on the head. This experiment seems to completely disregard the reason why we eat. We eat food because we need nutrients to survive: essential fats; complete proteins; vitamins and minerals. This experiment is celebrating indigestibility – the pointlessness of eating something.
White pasta has little enough nutrition to start with. When it has been boiled once, chilled in a fridge overnight, left for another day and then re-boiled – how many nutrients do you think survived? I don’t know. I can tell you what it had after it was first cooked. And then compare it to the meat or fish that the participants could have enjoyed in the same Italian restaurant:
|(All per 100g of cooked product)
|Calories per 100g
|TOTAL (Ash makes up remainder)
|A (3000 IU)
|B1 (1.2 mg)
|B2 (1.3 mg)
|B3 (16 mg)
|B5 (5 mg)
|B6 (1.7 mg)
|Folate (400 mcg)
|B12 (2.4 mcg)
|C (90 mg)
|D (600 IU)
|E (15 mg)
|K (120 mcg)
|Calcium (1000-1200 mg)
|Magnesium (420 mg)
|Phosphorus (700 mg)
|Potassium (4,700 mg)
|Sodium (1,500 mg)
|Copper (0.9 mg)
|Iron (18 mg)
|Manganese (2.3 mg)
|Selenium (55 mcg)
|Zinc (11 mg)
As you can see from the table, the pasta has no essential fats, no complete protein and is pretty pointless for vitamins and minerals – manganese being an unimpressive exception. And this was before it was chilled, left and re-heated – no doubt destroying more of these paltry nutrients. The essence of this part of the programme was that a researcher managed to reduce the nutritional content of pasta by making it less digestible and this was considered a good thing?!
The really interesting points from this experiment are:
1) It shows how deeply and completely ingrained the belief is that we should be basing our meals on starchy foods. At no point did a nutritional scientist (Robertson) or a doctor (Tulleken) – both very bright people no doubt – question the wisdom of eating starchy carbohydrates in the first place. Especially in the context of the discussion about blood glucose and insulin response being desirable to avoid.
2) It was a fun admission that a calorie is not a calorie. Those who think that there is only one law of thermodynamics (and even this one doesn’t say energy in = energy out) will be beyond distressed trying to work out where the missing calories have gone.
Those who know that the second law, entropy, must be taken into account will enjoy the example of what entropy is all about – calories being lost and calorie being used in making available energy.
Those who really understand thermodynamics will know that it says nothing whatsoever about weight anyway – it is entirely about the movement of heat – and therefore it says no more about 100g of pasta than it says about 100g on the bathroom scales.
3) It was a wonderful admission, from a doctor, that starch is sugar. The starch that our government tells us to eat is sugar.
And those were the real lessons from the experiment.
The fat investigation
Later on in the programme, Mosley addressed the nutritional issue that led to the advice that we should eat more carbohydrate – the demonisation of fat. Mosley explained that he grew up in the 1960s when “medics declared war on saturated fat.” He shared that this had led to an increase in consumption of margarine and then we realised that the trans fats in spreads “are fantastically bad for the heart and they are being phased out“. Mosley described this as an example of “a public health campaign which had an unfortunate consequence.” But – Mosley set out to ask – how bad was the original advice on saturated fat?
In the introduction to this part of the programme, Mosley made all the errors that can be made in relation to fat in just a few words: “Saturated fatty acids, as they are technically known, are found in animal fats… and also in some vegetable oils, like palm and coconut, while other oils such as olive and sunflower contain polyunsaturated fatty acids.”
1) Saturated fatty acids are found in every single food that contains fat – not just animal foods – there are no exceptions.
2) Saturated fatty acids are found in all vegetable oils – not just palm and coconut – there are no exceptions.
3) Oils, such as olive and sunflower, and palm and coconut, do contain polyunsaturated fatty acids. They also contain saturated fatty acids and monounsaturated fatty acids because all foods with fat contain all three fats – there are no exceptions.
Mosley then sets off to try to answer the question” Does saturated fat really increase the risk of heart disease, as is widely believed?” But what hope does he have when he doesn’t even know what saturated fat is?!
Mosley interviews Professor Kay-Tee Khaw, from the Department of Public Health at Cambridge University, who was part of the study group that did a systematic review of 49 observational studies and 27 Randomised Controlled Trials (RCTs) with the conclusion “Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”
Professor Christian Drevon, from the Department of Nutrition at Oslo University, was the BBCs classic counter-balance interview. He still thinks that “saturated fat in the diet is one of the major risk factors for Coronary Heart Disease“. This is where Mosley’s ignorance didn’t help, as he wasn’t armed with the right questions to challenge Drevon, who should have been asked: What is saturated fat? How can we obtain the essential fats, complete protein, vitamins and minerals that we need to survive without eating saturated fat? (and quite a lot of it) Why do you tell people to favour vegetable fats over animal fats when a tablespoon of olive oil has nearly three times the total fat and twice thee saturated fat of a 100g pork chop? And so on…
From a lack of basic understanding, it was perhaps not surprising that Mosley’s announced that his personal conclusion on saturated fat is: “These days I do eat butter and drink milk, but it’s not an excuse to pour down double cream because, whatever it’s doing to your heart, fat is very rich in calories.” Where the heck did calories come in?!
Trust me I’m a doctor?
I did enjoy the programme. The evidence for acupuncture having a visible effect under MRI, but without the mechanism being known, was honest and interesting. The paralysed patient being able to stand and move his limbs again was utterly inspirational and hugely significant for spinal cord injuries. The vitamin D study was interesting – mostly for the fact that less than half of a group of office workers had adequate vitamin D levels – more so than the discovery that sun, vitamin supplements or oily fish would work equally well and quickly at restoring those levels. There was much of value in the programme. However, it sadly showed that, when it comes to nutritional science, you may not want to trust your doctor.
The ink has barely dried on the Iona Heath independent panel report into the demands from Rory Collins that two papers, which dared to reference another peer-reviewed paper that mentioned statins having side effects, be retracted. Heath’s panel very sensibly concluded that the papers should not be withdrawn and the panel admonished Collins for trying to buck the open and transparent BMJ system for handling such issues.
Collins complained about the articles by email to Fiona Godlee, editor of the BMJ, at the end of October 2013. He insisted on a private meeting, which was held in December 2013. Collins was asked by Godlee to express his concerns in a rapid response to the BMJ or an article – as is the normal process for open debate on matters of wide importance. Collins never did this. Instead he continued to try to use private channels to censor that which he did not want published.
The new stunt
On September 18th I received an email forwarded from a doctor specialising in heart disease.
Date: Thu, 18 Sep 2014 10:46:50 +0100
Subject: BCS Statins Survey<
IMPORTANT: STATIN SURVEY
The British Cardiovascular Society is keen to know of any potential adverse effect on cardiovascular disease prevention which may have resulted from recent media stories and articles such as those published in the BMJ (1,2) and in an open letter to NICE (3).
We would be grateful if members would complete this short survey. Your response will be anonymous and the link below is unique to you allowing you to complete the survey once only.
The survey closes on 30th September and results will be made available subsequently on the BCS Website and in the BCS newswire.
(1) Abramson JD, Rosenberg HG, Jewell N, Wright JM. Should people at low risk of cardiovascular disease take a statin? BMJ 2013; DOI:10.1136/bmj.f6123.
(2) Malhotra A. Saturated fat is not the major issue. BMJ 2013; DOI:10.1136/bmj.f6340
PLEASE CLICK HERE TO COMPLETE THE SURVEY
The two papers referenced just happen to be the ones that Collins didn’t like. The ones that he wanted removed from the BMJ altogether. Having failed, a society that you have probably never heard of, The British Cardiovascular Society, is trying to stir up trouble to smear the authors of these papers and the letter to NICE.
The end in mind
This is not an open and genuine survey – honestly interested in evidence based medicine. This is a loaded and leading survey with a clear end in mind. The British Cardiovascular Society (BCS) are not interested in any positive outcomes from the publicity surrounding Collins vs. The BMJ. They are not interested in Mrs Jones, who decided to come off statins, having heard about the side effects, who now finds that she can walk again. They don’t care about Mr Smith whose libido may have come back – along with his mind, mood and memory. They are only interested in adverse effects and anecdotes about adverse effects.
As Dr Malcolm Kendrick explained here: “Now, why would they be doing this? I do not think it is that difficult to work it out. The BCS is trying to gather evidence that the articles by Abramson, Malhotra and the open letter to NICE have caused harm to patients. They will be asking their members if they know of people who have stopped taking statins, or who will not go on statins, because of what they have read in the BMJ and suchlike.
Once they have done this, they will then extrapolate the raw figures to the entire population of the UK, in order to claim that ‘Thousands have died.’ Abramson will be attacked, along with Malhotra and the BMJ. I will get a few attacks as well for drafting the letter to NICE. This is a very unsubtle variation of the ‘You’re killing my patients’ tactic which is regularly used to silence any who dares criticise currently medical opinion.”
Who are the British Cardiovascular Society?
The May 2013 annual report tells us that “The British Cardiovascular Society is dedicated to the promotion of cardiovascular health.” (Download from this page).
The web site thanks its main partner: “The British Cardiovascular Society (BCS) is grateful to the generous support of its Industry Partner, Bayer PLC.” I bet it is.
The office address is 9 Fitzroy Square, London, W1T 5HW. Remember this.
I emailed BCS on September 24 to ask:
On your web site you share that “The British Cardiovascular Society (BCS) is grateful to the generous support of its Industry Partner, Bayer PLC.”
Please can you help with the following:
– Do any other pharmaceutical companies provide funding, directly or indirectly to the BCS?
- How much does Bayer donate?
I have had no response.
A web of conflict
I started to look at the “Officers of the Society” for individual conflicts of interest and I started to recognise some names from previous conflicts of interest research. What emerged was a glimpse into a web of conflict involving a large number of self created organisations/charities, in the field of heart disease, with connections to and funding from pharmaceutical companies. I suspect that I have barely scratched the surface.
There are individual organisations, such as the BCS and/or Heart UK (the ultimate voice piece of the statin industry) and then a representative from each of them meet together as a body called the Joint British Societies. The president of BCS, Iain Simpson, is a member of the Joint British Societies (JBS). He declares no conflicts of interest at JBS. His thought process must go something like – I’m at JBS representing BCS and so I don’t have to declare the fact that BCS is funded by Bayer? No, that doesn’t work for me either.
The Joint British Societies
The representatives from other organisations, which form the JBS, are as follows. Where Declarations Of Interest (DOI) have been made, they derive from this document, which is dated March 2014. Where declarations have not been made, I have searched for them and referenced the source:
Prof John Deanfield Represents the British Heart Foundation and claims “No DOI”, despite the fact that the BHF is in bed with Flora margarine.
Dr Susan Connolly Declares “Travel grant and advisory board for Merck Sharp Dohm”.
Prof Patrick Doherty Represents BACPR – the British Association for Cardiovascular Prevention & Rehabilitation. Despite being supported by the BHF (Flora) and being “an affiliated group of the BCS” (Bayer), Doherty declared “no DOI.” The address for the BACPR is also 9 Fitzroy Square, London, W1T 5HW.
Prof Keith Fox Declares funding from: “British Heart Foundation; Medical Research Council; Wellcome Trust” and “Additional Grant Funding and honoraria: Sanofi Aventis, Lilly, Bayer/Janssen, Astra Zeneca, GSK.”
Prof Richard Hobbs Declares consultation and speaking engagements with BI, Bayer, BMS/Pfizer, Medtronic all in non-prevention of CVD areas.
Prof Aroon Hingorani Declares that he is on the advisory board for Roche.
Prof Steve Jackson Co-representing the British Hypertension Society, one of the British Cardiovascular Society affiliates. Jackson declared “no DOI.” Really? Daiichi-Sankyo, Boston Scientific and Omron Healthcare are friends of the society.
Dr Catriona Jennings Represents another of the British Cardiovascular Society affiliates: British Association for Nursing in Cardiovascular Care (BANCC). She is President of this society, which also has 9 Fitzroy Square as its address. She states “No DOI.” Pfizer and Astra Zeneca are declared here, however.
Prof John Potter Declares that he has served on the Advisory Boards of several Pharma companies including Merck Sharp Dohm and Bayer, from whom he has received honoraria.
Prof Naveed Sattar Has consulted for: Amgen, Sanofi, Astrazeneca, BMS, Roche, UCB and Boehringer Ingelheim. Speaker Bureau for Lilly, Merck Sharp Dohm.
Dr Fran Sivers Has worked with Unilever on HeartAge and has advised a Medical Charity called Dipex.
Prof David Spiegelhalter Claimed no DOI. Yet on his own web page he states “I have acted as a paid statistical consultant to a variety of organisations, including the Healthcare Commission, World Anti-Doping Agency, Novartis, and GlaxoSmithKline.”
Prof Gerard Stansby Claimed no DOI. This page clarifies “GS has received research funding and fees for speaking and chairing meetings from a number of pharmaceutical companies.”
Dr Paul Stevens Claimed “No DOI”. In CG182 here, Appendix D has the declarations of interest for this NICE development group. Stevens are listed as “Honoraria for lectures and attendance at international meetings for Ortho Biotech, Bayer, Amgen, Pfizer and Hoffman La Roche and a research grant from Roche UK for developing an expert system for the management of chronic kidney disease.”
Prof Peter Weissberg Represents the British Heart Foundation and claims “No DOI.” Not even Flora?
Dr David Wheeler Declared consultancy Fee/Honoraria from: Amgen, Janssen, Astellas, Baxter, Merck Sharp Dohm, Vifor Pharma, Otsuka, Fresenius, Shire Research grants: Genzyme, AstraZeneca.
Prof Bryan Williams Claimed “No DOI.” He’s Chair of Medicine at the Institute of Cardiovascular Sciences. Can you imagine that being free from pharma funding? Here’s a throw away comment on his bio page “He holds grant awards from the NIHR, MRC and the BHF as well as collaborative grants with industry.”
Dr Peter Winocour Served on clinical expert advisory boards supported by Novo Nordisk, BI, Sanofi Aventis, Merck Sharp Dohm, and received support to attend meetings from Novo Nordisk and BI.
Prof David Wood Declared honoraria for Advisory Boards (Merck, Sharp & Dohme) and invited lectures (including AstraZeneca) Unrestricted research grants to the European Society of Cardiology from several pharmaceutical companies (AstraZeneca, Bristol-Myers Squibb/ Emea Sarl, GlaxoSmithKline, F. Hoffman-La Roche, and Merck, Sharp & Dohme).
There are two more members, whom we will come to shortly.
The position of the JBS
The Joint British Societies – when declarations are fully made – reads like a pretty comprehensive representation of the statin making pharmaceutical industry. Sure enough, this is the Joint British Societies view on Lipid lowering therapy:
* Intensive statin therapy is recommended in all patients following MI, in the absence of a contraindication or intolerance, irrespective of initial cholesterol values.
* Statins should be prescribed with a ‘lower is better’ approach to achieve values of at least <2.5mmol/L for non-HDL-c (equivalent to <1.8mmol/L for LDL-c).
At the end of this article, the Competing interests are declared as follows: “There are no significant competing interests.”
Did you spot the address for correspondence for the Heart journal? Yes – Heart is the publication of the British Cardiovascular Society, 9 Fitzroy Square, London, W1T 5HW.
The Connection to the NICE statin guidelines.
My newsletter back in February 2014 shared that the Guideline Development Group (GDG) had serious conflicts of interests, which should have led to the exclusion of 8 out of 12 panel members from the group. NICE showed that it really couldn’t care less about this and went ahead with their ‘everyone should be on statins‘ advice.
Two of the members of the Joint British Societies were on the NICE statin GDG:
Alan Rees as a member of the JBS declared “Advisory Board and talks for: Aegerion, AstraZeneca, Merck Sharp Dohm, Sanofi-Aventis, Pfizer, BMS and Novo Nordisk.”
Dermot Neely declared that he was representing Heart UK and that he had “No DOI”. This whole DOI thing is getting beyond a joke. These are the partners of Heart UK – how are these not conflicts of interest? The declaration for the NICE GDG also included “In the past 12 months I have participated in one-off advisory boards for pharmaceutical companies developing lipids modifying therapy for specialist use in poorly treatment responsive and/or severe inherited lipids disorders, including Roche Pharma (dalcetrapib), Genzyme (mipomersen), and Aegerion (lomitapide).” Not relevant?
What started as research into the British Cardiovascular Society, for a leading and loaded survey, with a clear and underhand end in mind, ended up as a discovery of a web of organisations, charities and affiliates with pharmaceutical funding, shared addresses and what seems to be an extensive network of statin pushers.
I can think of two reasons:
1) It gives the appearance of a number of ‘respectable’ organisations/charities all believing in the same thing. In this case that “Intensive statin therapy” should be enforced with a “‘lower is better’ approach.”
2) It creates a ‘once removed’ structure, so that the pretty much universally conflicted members of the Joint British Societies group seem to think that it’s OK that they put their names to a “lower is better” policy as members of the JBS and then ‘forget’ that they are funded by the companies who will benefit from this exact policy.
Conflict is conflict. I often say that liver is the most nutritious food on the planet, because that’s what nutrient analysis shows. If I received any funding whatsoever from a liver association/organisation/producer – you should know about it. And it should not matter which meeting I am attending one day or the next – the liver conflict would prevail and should always be declared. Given my abhorrence towards conflicts of interest you won’t be surprised to know that I have received no such payments from any organisation and never will I sell my soul in this way. It’s just disgraceful that this position is not shared by people in positions of power and influence.
I got a call at 8.30am today (Sept 11th 2014) to ask if I’d go on Radio 5 live between 10-11am to talk about ‘the fat shaming’ story. What fat shaming story?!
The Daily Mail headline was “Telling someone they’re fat makes them eat MORE: People made to feel guilty about their size are six times as likely to become obese.” The Telegraph went with “Fat shaming ‘makes people eat more rather than less‘”. The Guardian got a teeny bit more accurate, but not much, with “‘Fat shaming’ does not help people lose weight, study finds.”
Here’s the link to the original study (Dr Jackson very kindly whizzed me over a copy this am).
The article & press release
Please note from the outset the title of the study and the objective set out by the researchers.
Title: “Perceived weight discrimination and changes in weight, waist circumference and weight status” (my emphasis).
Objective: “To examine associations between perceived weight discrimination and changes in weight, waist circumference and weight status” (my emphasis again).
The press release was undeserving of an academic study – the usual headline grabbing, sensationalist, misleading at best and disingenuous at worst, which we have sadly come to expect. “‘Fat shaming’ doesn’t encourage weight loss.”
The study was not an intervention. It was an observational study using the English Longitudinal Study of Ageing (ELSA) for data. As the ELSA is a study of people aged 50 years or older and as the initial sample of participants was drawn from responses to the Health Survey for England (HSE) in 1998, 1999, and 2001, this is not a study of the general adult population. This was a study of people with an average age of 66 at baseline.
2,944 people were studied over 4 years.They had BMI and waist circumference recorded in 2008-09 and 2012-13 and they were asked for their perceived weight discrimination in 2010-2011 in response to five (subjective) questions.
‘In your day-to-day life, how often have any of the following things happened to you:
1) you are treated with less respect or courtesy;
2) you receive poorer service than other people in restaurants and stores;
3) people act as if they think you are not clever;
4) you are threatened or harassed;
5) you receive poorer service or treatment than other people from doctors or hospitals.
On the basis of these questions, 5% of participants perceived that they had experienced weight discrimination. The study has just become a study of 150 people perceiving discrimination against a control group of 2,794. This is not a study of weight discrimination among 2,944 people.
The perception of weight discrimination ranged from 0.7% in the normal weight category to 35.9% of those classed morbidly obese. Men and women reported similar levels.
This is interesting. I see two shop assistants chatting rather than helping me and I just think that they’re rude. If I were morbidly obese, would I perceive that they were treating me differently because of my size?
Weight: Those who perceived weight discrimination started the study almost 22kg heavier than those who didn’t.
Those who reported weight discrimination gained, on average, wait for it, 0.95kg – not even 1 kilogram! During a four year study.
Those who didn’t report weight discrimination lost, on average, wait for it 0.71kg – that’s about how much dark chocolate I eat in a week. During a four year study.
Another interesting thing – which was completely swept under the carpet – check figure 1 in the paper. There were 6 categories that were studied: normal weight at baseline; overweight at baseline; obese (BMI 30 or higher); obese class I (BMI 30-34.9); obese class II (BMI 35-39.9); and obese class III (BMI 40 or higher). The only groups that gained during the study were the normal weight and overweight people who perceived weight discrimination. All the obese categories – whether they perceived discrimination or not – lost weight on average during the study and the normal/overweight people who did not perceive discrimination lost weight or experienced no change.
Table 1 tells us that there were 7 normal weight people who perceived weight discrimination and 15 overweight people who perceived weight discrimination. Today’s world-wide nonsense is thus based on the perceptions and negligible weight change for 22 people.
From the numbers in the paper, I calculate that the Daily Mail headline about “six times more likely to become obese” derives from the following… The paper reports that “Among participants who were not obese at baseline, perceived weight discrimination was associated with higher odds of becoming obese (25.2 vs. 4.4% OR=6.67).” There were only 22 participants who were not obese at baseline who perceived weight discrimination. To achieve 25.2%, 5.5/22 of these became obese (not sure how). There were 2,102 participants who were not obese at baseline who didn’t perceive weight discrimination. To achieve 4.4%, 92.5/2,102 became obese. So, 5.5 people became obese in one group and 92.5 in the other group. The significant thing that differs is the group size. A couple of people makes a big difference in the group with 22 people. Plus – two thirds of the small group were already overweight, compared with half the large group. It is far more likely that overweight people became obese than normal weight people – in a four year period – and thus the group of 22 had another factor stacked against them. Do you think 5 people justify the Daily Mail headline?
Waist circumference: Those who perceived weight discrimination started the study with an almost 20cm greater waist circumference than those who didn’t.
Those who reported weight discrimination gained, on average, wait for it, 0.72cm – not even a centimeter! During a four year study.
Those who didn’t report weight discrimination lost, on average, wait for it 0.4cm – I doubt you could measure my waist to a 0.4cm degree of accuracy from one day to the next. Again, during a four year study.
I mean – seriously journos – do you ever look beyond the press release?!
Association, not causation.
AND this is – as always – association not causation.
Dear Daily Mail, we have no evidence that anyone was told that they were fat, just that they perceived being treated differently.
Dear Daily Mail & Telegraph, we have no evidence that people ate more. We do have evidence that obese people lost weight whatever their perception of weight discrimination. Maybe they ate less? Maybe they ate more, but better? Who knows.
Dear The Guardian, obese people did lose weight, whether ‘fat shamed’ or not.
Nothing MADE 150 people do anything. There was an association between gaining less than a kilo and losing less than a kilo and the subjective answers to 5 questions in 22 normal weight/overweight people and not even this association in 128 others.
I have been told by many people of all ages, male and female, about the abuse experienced by obese people – particularly morbidly obese people. During the Radio 5 live discussion, “Zanita” made me gasp out loud when she shared comments that had been directed towards her. “Jenny” had been insulted by someone close to her. I’ve just been on BBC Radio Tees and Mike Parr shared comments made to him. Such behaviour is completely unacceptable, rude and ignorant.
Insulting people for any personal attribute – gender, age, diversity, size, attire, anything – is gross human behaviour and it says way more about the abuser by a margin that the abused. I think that people know if they need to lose weight. I know that they want to lose weight. I believe that our current eat less/do more advice sets them up to fail. I think that food is addictive and that obesity is a complex problem, which no insult or abuse is going to help.
BUT – a bag of sugar either way affecting 22 people in a study who perceived that they had been treated differently between two weigh-ins four years apart. Really?!
On September 2nd 2014 a story broke in the field of diet and nutrition, but it barely made it across the pond. The New York Times headline was “A call for a low carb diet that embraces fat.” The Huffington Post covered the story, but didn’t devote a whole article to it. Instead they combined the findings of this study with another to report “What can we really learn from that low-fat vs. low-carb study?”
The BBC ignored it. The Mail did an on-line only piece “Time to throw out the bread! A low-carb diet IS the most effective way to lose weight – and it cuts the risk of heart disease, too.” Great headline, but you wouldn’t have come across the article by chance. I had to do a very specific search on the mail site to see if they had covered it. Similarly the Guardian had an on-line story “Low-Carbohydrate Diet Protects Against Heart Disease Study Shows.”
This is the link to the original article “Effects of low-carbohydrate and low-fat diets.” Dr Michael Eades has very kindly dropped it in his box for you to be able to see the full article.
Start, as usual, with any conflicts of interest. The study was funded by the National Institutes of Health, which is very interesting in itself. It’s the first study I’ve seen funded by a public body to review the effect of low-carb diets, let alone as compared to low-fat diets – the latter typifying public health advice. There is a full conflict of interest form, covering all authors involved in the study here. It is unusually and refreshingly completely void of any conflicts whatsoever. Oh to find a drug or food item study so genuinely independent.
The study was simple in design and meticulous in execution. Many of the medical site reviews of the study detailed and/or complimented the care that had been taken to make the trial as controlled as possible.
The study involved 148 men and women without cardiovascular disease or diabetes. The men and women were aged 22 to 75 years and had a BMI of between 30 and 45, so that they had sufficient weight to lose over the study period. The participants were recruited from the general public through open adverts. This generated more response from females than males, resulting in 89% of the subjects being female. The study was undertaken in New Orleans, Louisiana. 51% of the participants were black, 45% were white and the remainder were Asian and Hispanic.
73 of the participants were randomly allocated to the low-fat diet and 75 were randomly allocated to the low-carb diet. Table 1 in the paper shows the baseline characteristics of the participants. This is where we can check that the randomisation ‘has worked’ and we are equally like to have similar numbers of females in each diet group, similar numbers of different ethnic origins, similar starting weights and so on. The low-fat group were a couple of years older than the low-carb group and they were 1.6kg heavier on average (i.e. more weight to lose), but, Table 1 overall is reassuring that the groups started off from a very similar baseline.
The study noted that there have been very few attempts to study low-carbohydrate diets and none had ticked two important criteria of 1) actually being a low-carb diet and 2) studying a diverse population. The Gary Foster (2003) study did compare an actual low-carb diet (Atkins) to a low-fat (government advice) diet, but this did not involve a diverse/carefully randomised population. This study, covered in the BBC Horizon programme about The Atkins Diet, concluded that Atkins was better for weight loss and cholesterol measures. The usual attempt to study a ‘low-carb’ diet has involved carb intake in the 100-200g range. That’s a high-carb diet to the low-carb world!
This was different. The low-carb diet group target was less than 40g of carbohydrate a day. The low-fat diet group target was less than 30% of daily energy intake from total fat and less than 7% from saturated fat – model government advice therefore. I emphasised the word target because the discussions on-line about the study didn’t pick up the actual intake reported in the paper.
Table 2 reported the actual intakes of carbohydrate and fat for the two groups:
The low-carb group were supposed to consume <40g carb per day. They did in fact consume, on average: 97g carbohydrate/day at 3 months; 93g/day at 6 months and 127g/day at 12 months. The low-carb group thus substantially missed their targets.
The low-fat group, in contrast, did hit their total fat targets (they recorded saturated fat intake of between 8-9% during the study). They were supposed to consume less than 30% of their daily intake from fat and they achieved this: 27.5% at 3 months; 27.9% at 6 months and 29.8% at 12 months.
The researchers reported that 5 people dropped out of the low-fat group and 5 people dropped out of the low-carb group after 3 months. By the end of the study (at 12 months), 13 people in total had dropped out of the low-fat group and 15 had dropped out of the low-carb group. That was an 18% drop out in the low-fat group and a 20% drop out in the low-carb group. That’s a reasonably low drop out rate for a diet study and a number dropped out due to life stressors and/or pregnancy – understandable with a largely female group 22 years old and above.
The results fell into two main areas: weight and what the researchers called “cardiovascular risk factors.” One of these I value (weight), the other I don’t (cardiovascular risk factors – apart from to wave at people who do value it).
Weight: To quote verbatim from the study: “Weight loss was greater in the low-carbohydrate group than in the low-fat group at 3, 6, and 12 months.”
The main results are worth capturing in a little table (this is an extract from Table 3 in the paper).
|Body weight (kg):
|- at 3 mths
|- at 6 mths
|- at 12 mths
|Lean mass (%):
|- at 3 mths
|- at 6 mths
|- at 12 mths
|Fat mass (%):
|- at 3 mths
|- at 6 mths
|- at 12 mths
This tells us many interesting things:
1) As the researchers reported, weight loss was greater in the low-carb group at 3, 6 and 12 months – at least double at all three checks. This was despite the fact that the low-fat group achieved their dietary target of <30% fat and the low-carb group did not achieve their target of <40g carb a day – not even close.
2) Lean mass increased more, at every checkpoint, with the low-carb group.
3) Fat mass decreased more, at every checkpoint, with the low-carb group.
4) Even with the low-carb group missing the 40g/day target quite substantially, this group continued to have good results for weight, lean mass and fat mass at 12 months. Notice the low-fat group displaying the classic 6 month turnaround – with regain following. This was clearly illustrated by Marion Franz’s 2007 review of 80 studies involving 26,455 people. The classic graph from this study can be seen here. By 12 months, the low-fat group had regained 50% of the weight loss at 3 months and started to decrease lean mass and increase fat mass.
5) Perhaps most interesting of all – this study disproves the calorie theory (not that any study has ever proven the calorie theory – every study proves it wrong). The low-fat group were consuming, on average, 2,034 calories at base line and the low-carb group were consuming 1,998 on average. At 3 months, these averages had dropped to 1,418 and 1,258. At 6 months, these averages were 1,481 and 1,324. At 12 months, these averages were 1,527 and 1,448.
I’ve calculated what the 3,500 calorie theory says each group should have lost and it works out as follows:
– The low-fat group should have been 7.3 kilograms (multiply by 2.2 for an approximate conversion to pounds) lower at 3 months; 13.9 kg lower at 6 months and 25.9 kg lower at 12 months. They were, in fact, 1.8 kg lower at 12 months.
– The low-carb group should have been 8.8 kilograms lower at 3 months; 16.8 kg lower at 6 months and 29.8 kg lower at 12 months. They were, in fact, 5.3 kg lower at 12 months.
Remember that the calorie theorists say that low-carb diets only work because people eat less. Both groups did eat fewer calories, but the calorie theory was as ridiculously inaccurate as it always is.
The saddest finding for me, working in the field of obesity, was how little both groups lost, on average, over the course of a year with heavily supported and well monitored conditions. There was no mention of real or processed food in the study, so continuance of processed food in both groups may have hindered weight loss. I would also have loved to see the results for a group that actually achieved the 40g/day carbohydrate intake target, as this could have been impressive. As I find, and so do many others in the world of real food/managed carb, results can be substantially better than 5 kilograms a year.
Cardiovascular risk factors: I will report these rather than discuss them because, as people who know me will know, I have no time whatsoever for the notion that cholesterol is a risk factor in anything. It requires one to assume that the body makes cholesterol to kill the host – quite possibly the most absurd assumption that one can hold. Notwithstanding this, as most of the medical world is obsessed with total cholesterol and the lipoproteins LDL and HDL (while thinking that these are bad and good cholesterol and not lipoproteins ha ha), here are the results from the cholesterol jury:
At 6 months (comparing the period in which the low-carb group were at least below 100g/day):
– The low-fat group had higher total cholesterol, the low-carb group had lower total cholesterol.
– The low-fat group had higher LDL, the low-carb group had lower LDL.
– The low-fat group had lower HDL at 3 months and no change at 6 months, the low-carb group had higher HDL at both checkpoints.
– The low-fat group had higher triglycerides at 3 months and virtually no change at 6 months, the low-carb group had lower triglycerides at both checkpoints.
The only good thing about all this is that people who believe the diet-heart hypothesis say that low carb (by definition higher fat) diets raise cholesterol, LDL, triglycerides etc and NONE of this was found to hold true.
Perhaps the biggest story of all, however, was that the UK largely ignored this. Let not the evidence get in the way of public health advice eh?!
I was on the circulation list for a recent email entitled “Breast cancer: 2 peaches/week 41% lower risk”.
The email opened by saying :
“Women who ate two servings of peaches per week had a 41% lower risk of breast cancer over the next 24 years according to a study from the Harvard School of Public Health in Boston, Massachusetts, USA.
“Women who ate one serving of blueberries per week had a 31% lower risk of breast cancer over the next 24 years.
“This study followed 75,929 women (part of The Nurses’ Health Study), 38- to 63-years-old at baseline, and followed them for up to 24 years.”
Here is the original paper. (Ref 1)
My first reply was
Association, not causation.
Relative risk, not absolute.
Nonsense, not science!
The more considered reply develops these further
Association, not causation
As Dr Malcolm Kendrick beautifully says “Association does not prove causation, but lack of association disproves causation”.
The way that science should work is that epidemiology/observational studies suggest association and then possible associations should be tested in a sufficiently powered, long enough, randomised controlled trial to see if there could be causation – changing the hypothesised thing alone. We have largely abandoned this step in science since, and including, the Seven Countries Study. We now see an overweight sedentary person and assume that being sedentary made them overweight. What about being overweight made them sedentary? What about a lousy high-carb-following-gov-advice diet made them both overweight and low in energy? What about a thyroid condition led to both?
If we observe association, we should look for a plausible mechanism to see if the intervention would be worth testing. If (to use another Dr Malcolm fab example) we push someone out of an airplane without a parachute we can do an n=1 to say that being pushed out of an airplane without a parachute causes death and jumping out of a plane with a parachute rarely causes death and so the parachute has a plausible mechanism in life extension.
What is the plausible mechanism with peaches and breast cancer?! I would not be surprised if women eat more peaches then men and substantially more women develop breast cancer – so where does that leave us? Is it antioxidants? Coffee and cocoa powder are massively higher in antioxidants than fruit so there could be a better intervention. Is it general nutrition? Fruit is pretty rubbish for nutrients compared to animal foods and dark green veg. I can’t even see a plausible mechanism.
Relative vs. Absolute risk
This study followed 75,929 women, 38- to 63-years-old at baseline, for up to 24 years. During this time there were 792 cases of post-menopausal breast cancer recorded. The study title did clarify that it was solely looking at post-menopausal cancer. The email I received didn’t clarify this.
That’s an incident rate during the 24 year study of 1.04%.
In any one year, the incident rate was 0.043%. Can you even get your head round such a tiny number?
So now we introduce the relative risk. The following table is extracted from Table 3 in the paper. It tells us the incidents among consumers of peaches/nectarines – don’t forget the nectarines.
The study used women who never eat peaches/nectarines as the base line. The baseline is given a risk ratio of 1.0. Relative to this group, those who had peaches up to a couple of times a month had exactly the same risk ratio – 1.0. Those who had peaches more than a couple of times a month but fewer than once a week had virtually the same risk ratio: 0.98. Those who had peaches between once and twice a week had a risk ratio of 0.87 BUT the confidence interval was 0.66-1.15, which includes the baseline number of 1.0 and thus we can’t be sure that we are not seeing the same result as at baseline and therefore we call this not significant.
The only significant result (where the confidence interval excludes 1.0) is the two or more peaches/nectarines a week:
||Up to 2/mth
||>2/mth to <1/wk
||1/wk to <2/wk
|Breast cancer cases
|Adjusted relative risk (RR)
1.0-0.59 = 0.41, which is where the 41% headline comes from.
The incidents and person years tell us the following:
We know from the overall numbers (792 incidents from 75,929 women in 24 years) that, in any one year, the incident rate was 0.043%.
This incident rate was 0.062% for never eat peaches and 0.038% for eat more than 2 peaches a week.
Are you any more able to get your head round those numbers?
No – me neither.
Now how does the 41% risk headline, with no explanation offered, look?!
Table 3 also tells us that they did not adjust for education, which is a well known marker for being better off…
If this study told us anything (apart from the fact that researchers continue to NOT understand association vs causation and relative vs absolute risk) it may have confirmed what we already know, which is that better off people enjoy better health.
Take UK regional life expectancy. The lowest for men and women occurs in Glasgow with life expectancy of 71.6 and 78 years respectively. The highest for men and women is found in Kensington and Chelsea – 85.1 for men and 89.8 for women.
Another interesting finding of the study was that there was not even an association with breast cancer and other fruits and vegetables. None. Zippo. Only peaches/nectarines and blueberries have magic breast cancer prevention plausible-mechanism-unknown properties. Peaches are posh fruits – P for posh. Passion fruit, Papaya, PawPaw, Pequi, Persimmon, Pewa, Pineapples, Pitahaya, Pitomba, Pomegranates, Pashminas (ho ho).
Q) Would you more likely find peaches in a fruit bowl in Kensington and Chelsea or in Glasgow?
Did the researchers not think – we’ve just reinforced better off = better health? And we should research health inequalities? No – the researchers want to carry on researching nonsense.
The abstract ends with these words: “These results are considered exploratory and need to be confirmed in further studies.” That’s academic speak for “we need funding, so please give us some money.” Bet the Blueberry Association has been in touch already.
Ref 1: Fung TT, Chiuve SE, Willett WC, Hankinson SE, Hu FB, and Holmes MD. Intake of specific fruits and vegetables in relation to risk of estrogen receptor-negative breast cancer among postmenopausal women. Breast Cancer Res Treat, 2013 Apr; 138(3): 925-930.
This is a short blog about a new game, as I see it…
The headlines on 6th August 2014 were that millions more people should be taking aspirin daily for a minimum of 5 years, ideally 10, heck – make that for ever…
The original article is here. The BBC reported the story as “Daily aspirin ‘cuts bowel and stomach cancer deaths.'” Of course nothing cuts deaths – we are all going to die – but let not the facts get in the way of the story.
The article is interesting in that it’s the first that I’ve seen to detail explicitly how many people might be saved and how many might be killed by taking aspirin. Yes, killed. Check out figure 1 and the researchers have estimated how many men and women they claim will be saved by taking aspirin and how many deaths they forecast “due to stroke, GI bleeding or peptic ulcer caused by aspirin.”
On balance, they say more will be saved than killed and so an aspirin a day for loads of people will kill a few here and save more there. And here’s the big point. Aspirin is as cheap as chips, cheaper than chips no doubt, so why would you not want to put every over 50 year old on aspirin (the age will no doubt get lowered) if you can save more than you kill?
Conflicts of interest
The first thing I check in any article is declarations of interest. If someone tells me walnuts are going to save lives and they and/or the study were funded by the walnut foundation, I am inclined not to take much of what I read very seriously.
In this article the disclosure states: “JC [that’s the lead author – the one who was on the TV that day]: Member of the Bayer advisory board. JB: Consultancy for Bayer Pharma. Research funding from Bayer Pharma. A stockholder and medical director in QuantuMDx, a new medical devices company which will develop point of care pharmacogenetic testing. Aspirin sensitivity is one of company’s targets. JAJ: Consultant to Astra-Zeneca, Dr Falk Pharmaceuticals, Chief investigator of AspECT trial and ChoPIN trial. PMR: Has received honoraria for talks, advisory boards and clinical trial committees from several pharmaceutical companies with an interest in antiplatelet agents including Astra-Zeneca, Bayer, Boehringer Ingelheim, Sanofi-BMS, Biotronic, Johnson & Johnson and Servier, and is on the executive committee of the ARRIVE trial. Research funding from Boehringer Ingelheim. All remaining authors have declared no conflicts of interest.”
If all the companies with an interest in antiplatelet agents (things that aim to prevent blood clotting) – Astra-Zeneca, Bayer, Boehringer Ingelheim, Sanofi-BMS, Biotronic, Johnson & Johnson and Servier etc – were seen to be behind a paper saying “give millions of people antiplatelet agents”, we would probably see through this and wonder about the drug cost and not just the cost of those ‘killed’ by stroke and stomach bleeds weighed up against those ‘saved’ from cancer.
So here’s the plan:
1) Do a paper about the benefits of the cheap, generic, everyone-has-it-in-the-medicine-cabinet, friendly, aspirin.
2) Call for millions of people to be given cheap aspirin for years and years and a humongous medication opportunity has just been created.
3) As soon as possible after the aspirin prescribing occurs, show that the expensive, branded, drug company antiplatelet agents are so superior to aspirin that to keep people on the generic, cheap aspirin would be a crime. Particularly, I suspect, having highlighted the stomach bleed/ulcer problems – these branded drugs will no doubt be better at avoiding stomach problems. Then millions of people will be switched to the patented drugs and stay on them for decades.
4) Make riches beyond wild dreams.
Watch this space…
The CTSU is the Oxford Clinical Trial Service Unit. Where this ends and the CTT (Cholesterol Treatment Trialists) Collaboration begins or where CTT ends and where Sir Professor Rory Collins and Colin Baigent and co. begin or end, I know not. One gets the impression that the web between the parties is not intended to be clear.
This is the group that promotes statins. This is the group that holds data on statin side effects, which it won’t share with doctors and patients who would like to know about these statin side effects. Pause to digest that for a second. There is clinical trial information about what the most prescribed drugs in the US and UK could do to humans and researchers refuse to share it.
It was the lead member of this group, Sir Professor Rory Collins, who recently attacked the BMJ for publishing two articles that referenced the same peer review article finding about statin side effects. Not only did Collins attack the BMJ he went entirely outside the journal’s normal process and demanded that the two articles be retracted. The first was by John Abramson, Harriet Rosenberg, Nicholas Jewell and James M Wright; the second was by Dr Aseem Malhotra.
I covered Collins’ attempt at censorship in this post (after the Dr Maryanne Demasi Catalyst bit). In writing the post I found a declaration of interest involving over £115 million by CTSU member, Colin Baigent, repeatedly mentioning Collins/CTT/CTSU. This is in fact less than half the funding that the CTSU has received from commercial organisations. The MRC (Medical Research Council) and BHF (British Heart Foundation) funding, which they declare more readily, is in addition to the eye watering sums that they get from the hands that feed them.
The documents published as part of the panel review
The BMJ’s editor, Dr Fiona Godlee, called for an independent panel to be set up to investigate Collins’ demands. The full report of the panel is here, (published 1 August 2014). The outcome was that the panel found that neither the Abramson et al paper nor the Malhotra paper should be retracted.
The far more interesting outcome was the supplementary information that was published alongside the panel’s full report, in the BMJ spirit of openness and honesty. In particular, some “not for publication” letters written by Collins. If you make such serious demands, that a world regarded journal retract two papers, you don’t get to call the shots on what remains hidden. Hence much “Supporting Documentation” has been published by the panel called upon to investigate Collins’ demands.
Letter SP17, dated 31 March 2014, has an interesting “P.S.” (direct Collins’ quotations in blue and italics for ease of reading).
“P.S. Conflicts of interest: There have been a number of comments in the BMJ and elsewhere about potential conflicts of interest in this area, so it may be helpful to provide you with some background. CTSU’s coordination of the Cholesterol Treatment Trialists’ Collaboration (CTTC) has been funded by the Medical Research Council and British Heart Foundation, without any commercial funding.”
You can read the full P.S., for it is quite long. It ends as follows:
“As we are all aware, a range of potential conflicts of interest exist and it is important that there is transparency (as, for example, with the BMJ’s advertising and sponsorship revenue from vaccine manufacturers which it inadvertently omitted to report when commenting on the MMR vaccine and autism story). With respect to CTSU, we have had a policy for more than 20 years of not accepting honoraria, consultancy or other payments directly or indirectly from industry, except for research grants and reimbursement of travel and accommodation to take part in scientific meetings (see attached)… Please could you let me have details of all conflicts of interest that have been declared by the authors of the Abramson and Malhotra papers (including the size of all payments that they have received for any statin-related work)?”
The conflicts of interest for the Abramson article were openly declared at the end of the article (as is BMJ policy) (JDA is John D. Abramson and NJ is Nicholas Jewell):
Competing interests: JDA and NJ serve as experts for plaintiffs’ attorneys in litigation involving the drug industry (including a statin). JDA has received payment for lectures from several universities, medical schools, and non-profit organisations. He was formerly executive director of health management for Wells Fargo Health Solutions.
The conflicts of interest for the Malhotra article were openly declared at the end of the article (as is BMJ policy). There were none to declare.
Competing interests: None declared.
Letter SP18, dated 14 April 2014, reiterated demands for the conflicts of interest of Abramson and Malhotra to be declared. “Please would you let me have the details of all conflicts of interest for Abramson et al and Malhotra, including the amounts of any payments that they have received for any statin-related work? This is information that should quite properly be in the public domain. In a spirit of reciprocity, I have attached the details of all grants from industry to CTSU for our research covering the past 20 years and more…” You’ll find this item – SP21 - in the supplementary information. If you open one link in this whole blog, make sure it’s this one.
This is priceless. “In a spirit of reciprocity, I have attached the details of all grants from industry to CTSU for our research covering the past 20 years and more…” Just look at that list. It doesn’t even include funding from the MRC, Cancer Research-UK or the BHF. It’s difficult keeping track of all the millions but I got to £268 million give or take a few hundred thousand. Plus, as Hannah Sutter discovered here, (point 4 especially), the MRC seems to be an indirect delivery mechanism for further pharmaceutical funding.
Who is being open and honest here?
Abramson & Malhotra declared their interests openly in their original articles, the latter having nothing to declare.
On 31 March 2014, Collins demanded “details of all conflicts of interest for Abramson et al and Malhotra” when all he needed to do was read them at the end of the articles to which he so objected. In the same letter, Collins told the BMJ “CTSU’s coordination of the Cholesterol Treatment Trialists’ Collaboration (CTTC) has been funded by the Medical Research Council and British Heart Foundation, without any commercial funding” (my emphasis).
Just two weeks later, Collins sent the BMJ “all grants from industry to CTSU for our research covering the past 20 years and more…” “In a spirit of reciprocity...” The commercial funding came to c. £268 million.
Does that seem open and honest to you?
In the most recent statin article listing Collins as an author on pubmed, scan all the way down to “funding” and the funding declaration opens with info on the China part of the study. The bit relating to Collins/CTSU etc states “the Clinical Trial Service Unit and Epidemiological Studies Unit (CTSU) at Oxford University also receives core funding for it from the UK Medical Research Council, the British Heart Foundation, and Cancer Research UK.” What about the £268 million?
Does that seem open and honest to you?
I thought I’d see when Collins last wrote for the BMJ and what he declared when he did so. He wrote about confidential data of all things! Sadly not on open view, but I have seen a copy of the full paper. At the end of the article we see the following:
Competing interests: None declared.
What, not even the fact that you have commercial agreements in place prohibiting the sharing of data? i.e. keeping that data confidential?
Does that seem open and honest to you?
The real scandal
I have followed this saga with interest because it has been a saga – of arrogance, accusations and demands. We must not let the Eastenders style drama detract from what the real scandal is here. The real scandal is that a research body holds data, which could provide vital information for patients and doctors about the serious adverse effects for the most widely prescribed drugs in the Western world and the body will not release the data. This blog confirms this fact. See the email from Colin Baigent to Dr Maryanne Demasi (the Catalyst Programme presenter who has also been censored) on 24 Sep 2013 10:44:01: “It is important to recognise that data from participating trials are not owned by the Collaboration [CTT], but remain the property of the trial sponsors, so we are not able to provide unlimited access to the combined database.”
I interpret this as – we receive £268 million from trial sponsors and it is not in their interests for side effect data to be shared. And if some patient loving cardiologist, with no such conflicts of interest, dares to suggest that statins have side effects (when we hold that information and won’t tell him) we’ll bypass the BMJ process and demand retraction.
My contempt for Collins, Baigent, the CTSU and the CTT – wherever the web lies – knows no bounds.