Will whole grains make you live longer?

Three! journal articles were published on whole grains in the past couple of weeks; not sure how that happened. Zong et al had this article published in Circulation: “Whole Grain Intake and Mortality From All Causes, Cardiovascular Disease, and Cancer. A Meta-Analysis of Prospective Cohort Studies.” Aune et al had this article published in the BMJ: “Whole grain consumption and risk of cardiovascular disease, cancer, and all cause and cause specific mortality: systematic review and dose-response meta-analysis of prospective studies.” Chen et al had this one published in the AJCN “Whole-grain intake and total, cardiovascular, and cancer mortality: a systematic review and meta-analysis of prospective studies.”

The US Circulation/Harvard team study was the one that dominated the media headlines, not only in the US, but also in the UK, where we were misinformed: “Three slices of wholemeal bread a day slash risk of dying from heart disease by 25%”.

All three studies were meta-analyses of prospective cohort studies. Just to make sense of this – a meta-analysis is generally seen as the highest level of evidence possible. It is a statistical technique to pool together many similar studies, working on the principle that looking at several studies together is more powerful than looking at just one. Prospective cohort studies are also called population studies, or epidemiological studies. These types of studies follow populations over a period of time. At the start of the study they record as many things as possible about the participants’ lifestyle (smoking/alcohol/diet/exercise etc) and they record as many things as possible about the participants’ characteristics (age/gender/education etc) and then they see what happens to the people over the following years. The goal with prospective cohort studies is simply to spot patterns (associations) – do people who drink alcohol get liver disease? Do people who do yoga get fewer diagnoses of stress?

The standard issues

Every time a study hits the headline – e.g. “wearing red socks will reduce your risk of dying from boredom by 25%” – there are two standard issues: association is not causation and relative risk is not absolute risk…

1) Association is not causation.

Observational studies can only establish associations. They cannot say that A causes B. They can only say that A and B are associated. For example, observational studies are good ways of establishing that smoking and getting lung cancer are associated. The next question to ask is – does this have a plausible mechanism? The answer is yes – we have evidence of the ways in which substances in cigarettes damage lungs. We could then test the hypothesis “Smoking causes lung cancer” by conducting a randomised controlled trial where the intervention is smoking vs. not smoking and nothing else changes.

The two studies from last week have shown an association between consuming whole grains and mortality and that’s it. Is there a plausible mechanism? The BMJ article tries to suggest a few (are people who eat whole grains slimmer? Are whole grains anti-inflammatory? Read Dr William Davis’s Wheat Belly book and you’ll conclude the opposite.) There is nothing intrinsically healthy about whole grains, so there is no obvious plausible mechanism. I will suggest below an explanation for the observed association – the marker vs. maker argument.

2) Relative risk is not absolute risk.

I don’t blame the media for this one – I blame the press releases from the journals. These should know better than to put “25% reduced risk” in a press release – knowing that this is misleading relative risk hysteria and not scientific absolute risk information.

European heart data tell us that 33 in every 100,000 men died from coronary heart disease in 2009 and 8 in every 100,000 women died from CHD in 2009. IF eating whole grains were causal and IF eating whole grains could reduce this by 25%, then – taking the women – approximately 7 in 100,000 women in the top whole grain consumption category would be likely to die from CHD and 9 in 100,000 women in the never/hardly ever eat whole grains category would be likely to die from CHD (the difference between 7.1 and 8.9 being just over 25%, while maintaining 8 as the average/mean).

7 vs. 9 in 100,000. Hardly hold the front page now is it?!

The other key points

1) Dietary advice to eat whole grains is not evidence based.

For something to be evidence based, it needs to be based in evidence, If something is based in evidence, the evidence comes first. Advice to consume whole grains dates back to the 1980 Dietary Guidelines for Americans (if not earlier). If you can see the full BMJ article you will notice that only one study that appears in all the meta-analysis results even comes from the last century. This one study, Liu et al, dates back to 1999. All other studies used as evidence are from the year 2000 onwards (a high proportion are from the past couple of years).

Dietary Guidelines have been under serious attack from real food proponents for the past few years. I can understand wanting to try to find retrospective evidence for guidelines in this climate, but it will never make the guidelines evidence based. The evidence didn’t come first and it never will.

2) The comparator group is Jekyll & Hyde.

These studies claim to have found an association between whole grain consumption and reduced mortality (i.e. living longer). The groups that they compared were those in the highest intake of whole grain consumption (more than 3oz per day) vs. those in the lowest intake group. People in the lowest intake group were those who (self) reported “rarely or never” eating whole grains.

The 2010 Dietary Guidelines for Americans tell us: “Less than 5 percent of Americans consume the minimum recommended amount of whole grains, which for many is about 3 ounce-equivalents per day. On average, Americans eat less than 1 ounce-equivalent of whole grains per day.” (p.36)[1]

Hence – both studies have used a very small section of the population as the comparator group (<5%). There are two polarised groups of people in the “never/rare consumers of whole grains”: i) people who avoid all grains and ii) people who eat refined grains instead of whole grains. I would expect whole grain eaters to be healthier than refined grain eaters. The comparison that has not been done is the whole grain eaters vs. the no grains-at-all eaters (the latter, virtually guaranteed, also avoid sugar).

3) Whole grain consumption is a marker, not maker, of a healthy lifestyle.

I would expect people who consume whole grains regularly (the <5%) to: not smoke; not drink; be affluent; do yoga; be slim; shop at Whole Foods/Waitrose; eat at restaurants, not takeaways; have children called Olivia and Tarquin and so on. The whole grain consumption is a marker of good health, not the maker of good health.

The BMJ study noted this as one of the limitations of their research: “People with a high intake of whole grains might have different lifestyles, diets, or socioeconomic status than those with a low intake, thus confounding by other lifestyle factors is a potential source of bias.”

That’s journal speak for “Whole grain consumption is a marker, not maker, of a healthy lifestyle.”

The headlines imply that people just need to up their intake of whole grains and they will “slash their risk of dying from heart disease by 25%!” This could not be further from the truth. It’s not causal, the absolute difference is tiny and it’s a whole lifestyle being depicted in these studies – not a whole grain.

To prove me wrong, the authors of these studies need to give 3oz of whole grains daily to the smoking, drinking, obese, sedentary, aimless, fourth generation unemployed, living-on-benefits, deprived populations in the Welsh valleys and change nothing else. Do you think that will “slash their risk of dying from heart disease by 25%”?!

Me neither.

Posted in Ingredients, Other Diets, Research
Tags: , , , , ,

Eatwell Guide – BJSM Editorial

This editorial in the British Journal of Sports Medicine has just been published (23.30 Monday June 13th 2016). The title is “Designed by the food industry for wealth, not health: the ‘Eatwell Guide.’”

The key points are:

1)      Our advice is being tweaked; it needs to be overhauled.

The UK has had plate pictures intended to represent role model healthy eating since the Balance of Good Health Diagram (1994). This was relaunched as the ‘Eatwell’ Plate in 2007 and it has been relaunched again (March 2016) as the ‘Eatwell’ Guide.

Many of the recent changes have been cosmetic. Details of cosmetic and the segment size changes can be found here.

2)      The plate proportions don’t allow for the difference between food weight and calories.

The plate has (perhaps unintended) consequences. The editorial notes that the segment sizes might be 37% “Potatoes, bread, rice, pasta and other starchy carbohydrates”; 39% “Fruit and vegetables”; 8% “Dairy and alternatives” (soya basically); 12% “Beans, pulses, fish, eggs, meat and other proteins”; 1% “Oils & spreads”; and 3% junk food, but this is by weight. When the vast difference between, say, the c. 40-50 calories for 100 g of fruit and vegetables and the c. 800 calories per 100 g of oils & spreads is taken into account, the plate proportions change dramatically.

I explained this here, with reference to the Eatbadly Plate – the same principles apply to the Eatbadly Guide – only the numbers on the segments have changed.

3)      The group, set up by Public Health England, to review and revise the Eatbadly Plate was dominated by representatives of the fake food industry.

What on earth is Public Health England doing setting up such a group? What does the Association for Convenience Stores representative know about diet and nutrition?! Why did the two least conflicted group members not attend any meetings after the first one?

4)      The guide is not evidence based.

The guide is very specific in proportions, without seemingly knowing the consequence of these proportions (point 2 above). I said in the editorial “There has been no randomised controlled trial (RCT) of a diet based on the Eatwell Plate or Guide, let alone one large enough, long enough and with whole population generalisability.”

Professor Tom Sanders is a regular writer for the Science Media Centre. When a press release is issued by medical journals, the SMC mobilise to counter the article (maybe just the ones they don’t like). (Or rather – maybe the ones that their food, pharma and other funders don’t like). Sanders’ comment on my editorial was: “The claim made that the dietary guidelines are not supported by randomised controlled trials (RCT) is plainly wrong.  The Food Standards Agency and later Public Health England commissioned several large RCTs to underpin current dietary guidelines and I was involved in leading several of these.” He quoted this Reidlinger/Sanders et al study.

It won’t take you long to notice that this is not a study of the ‘Eatwell’ Plate or Guide. It makes no mention of either. There is no attempt to make the intervention diet match the ‘Eatwell’ segments, let alone the proportions. It’s not even a test of the 55% carb/15% protein/30% fat Dietary Reference Values for the UK, since the diet group ended up at 45% carb/18% protein/33% fat (rounding errors). It also wasn’t large enough (160 people) or long enough (12 weeks). It was a study of surrogate end points, not real health outcomes. The control group was not a control group, as in left alone/left as baseline. The control group diet “was based around refined cereals”, “without restriction on salt and sugar”, but “with a limited intake of oily fish (less than once a month).” Incredibly the ‘control’ participants “were supplied with a butter-based spread (35.3 g SFAs/100 g and 2.4 g trans fatty acids/100 g) and a liquid unhydrogenated vegetable oil (palm olein) that contained 40% SFAs.” Crikey – I’m surprised they survived the trans fats alone! Oh, and Sanders declared of himself: “TABS is a trustee and governor of the British Nutrition Foundation and reported a financial interest in respect of payment for attendance at scientific advisory panels for Heinz PLC [ZH – both diet and ‘control’ group were supplied with baked beans!], Global Dairy Platform, Malaysian Palm Oil Board and the Natural Hydration Council, and GlaxoSmithKline and lecture fees from Lilly.”

I emailed Sanders to request details of the “several large RCTs to underpin current dietary guidelines.”He kindly replied by return with the Reidlinger/Sanders study top billing and then this study by Jebb et al. This also had nothing to do with the Eatbadly Plate/Guide, didn’t test for the five segments, let alone precise proportions. It was a comparison of five variations of high and low glycaemic index carbs matched with high saturated fat or high monounsaturated fat or low fat. It studied 548 people at risk of the metabolic syndrome for 24 weeks, so not generalisable even if it had studied the Eatbadly Plate/Guide. It also concluded: “This study did not support the hypothesis that isoenergetic replacement of SFAs with MUFAs or carbohydrates has a favorable effect on Si [insulin sensitivity].” So why send me this?!

I replied “Many thanks for these – was it just the two?” and Sanders came back with “There are moreI just gave two of the ones that are more relevant.”

No need to change this therefore: “There has been no randomised controlled trial (RCT) of a diet based on the Eatwell Plate or Guide, let alone one large enough, long enough and with whole population generalisability.”

Enjoy the editorial and many thanks to the BJSM for the opportunity to write it and to the peers, whoever they may be, who reviewed it.

Posted in Gov. Policy, Media comments, Obesity
Tags: , ,

Obesity Injection (Horizon prog)

The story

On June 7th 2016 overweight and obese people were given a hope – a false hope – that their weight will simply be injected away.

Fast forward ten years, obesity won’t be a problem. They’ll have the injections, they will be painless, no side-effects and actually really inexpensive and freely available.” Sir Steve Bloom, Professor of Medicine at Imperial College, London.

A miracle injection to end the obesity epidemic. How marvellous!

Something else you should know about Sir Bloom is that a company called Thiakis was founded in 2004to develop novel medicines for the treatment of obesity and co-morbidities based on original research of Professor Steve Bloom and his colleagues at Imperial College London.” The main product range being developed was “synthetic versions of the natural gastrointestinal peptide oxyntomodulin”. Look at the bottom line of text: “Wyeth Pharmaceuticals acquires Thiakis in a transaction worth up to £100m.”

That’s a sum worth raving about a product for. It wasn’t mentioned on the Horizon programme, which covered the story on June 7th 2016.

The product

The injection involves three hormones being administered in a jab before each meal: OXM (oxyntomodulin), PYY and GLP1. All three are understood to suppress appetite – here are a couple of articles on this – ooh look who wrote them!

The jab is supposed to work by making people feel full, as with bariatric surgery. Writing in the Daily Mail, Dr Giles Yeo, the presenter of the Horizon programme, said of the injection: “it appears it can indeed mimic gastric bypass and make the brain think you are full, so patients ate less.”

Two other points made by Dr Yeo in this article are important to address:

1)     “Put simply, we eat too much and move too little. It is physics.”

2)     “Gene research shows, however, that some people eat more than others because they feel a little more hungry all of the time.”

Why this injection is NOT going to end the obesity epidemic

1)     Overeating isn’t about appetite.

The Jab is supposed to work by making people feel full – like gastric surgery – but gastric surgery doesn’t work for many people. Men in white coats seem to have no understanding of why people overeat. They don’t seem to understand addiction – both physical addiction & psychological/ emotional addiction. Food is a drug of choice for many people – the most accessible drug of choice. Food is a ‘prop’ – researchers need to understand what happens when that prop is taken away.

The issues that people have with food, and the issues for which food is used, don’t get taken away with an operation or an injection. People with an eating disorder eat WAY beyond feeling full. Feeling full has nothing to do with most weight problems. Feeling less full is going to make no difference to someone who eats for every reason other than genuine hunger.

The ‘benefit’ that gastric surgery has over hormones trying to ‘mimic’ gastric surgery is that people physically can’t eat as much after effectively having their oesophagus attached to their anus! People report being physically sick and/or ‘dumping’ (a collection of very unpleasant symptoms, from nausea to sweating), when more is eaten than can be digested post surgery. There are mechanisms to prevent people from eating as much post bariatric surgery. These are by no means fool proof. People work out how to liquidise chocolate; they find jelly and ice cream easier to digest than meat and vegetables and they ‘graze’, so that the restricted amount they can eat at any one time becomes less relevant.

People find ways around bariatric surgery – finding ways around this injection will be even easier. Plus – an injection before every meal?! (it’s actually four hours before every meal to be precise!) “…painless, no side-effects and actually really inexpensive and freely available…” Seriously?!

2)     The obesity epidemic can’t be explained by genetics.

Yeo’s Mail article covered “gene research”. In the Horizon programme Yeo says: “I believe that genetics play an important part in why some people eat more than others.”

This makes no sense.

UK obesity has increased from 2.7% (men and women) in 1972 to 22.6% for men and 25.8% for women by 1999 (Michael Wadsworth et al., 2006). The UK obesity epidemic has emerged in a generation therefore. Genetics surely can’t explain something that has happened within one generation.

3)     The obesity epidemic can’t be solved by eating less.

We have known since the Benedict study almost 100 years ago (Francis G. Benedict, 1919); through the Minnesota Starvation experiment (Keys et al., 1950) and the Stunkard and McLaren Hume research (Stunkard A, 1959) to the comprehensive Marion Franz review of 2007 (Franz et al., 2007) that eating less does not produce sustained weight loss. A 2015 study of 176,000 people, showed that the chance of someone with a BMI of 30-34.9 achieving normal body weight (in any year of the 9 year study) was 1 in 210 for men and 1 in 124 for women!(Fildes et al., 2015) The 2016 review of the Biggest Loser contestants scientifically confirmed the metabolic changes that defeated dieters long term (Fothergill et al., 2016).

The Horizon programme showed two men (yes two), fed one meal (yes one), and eating 203-240 calories fewer respectively with the TV cameras there. Sorry – after the injection. Dr Yeo is obviously a calorie theory man. He got really excited “Over even a few months, the amount of weight you’d lose would be incredible.” Even IF this injection could achieve less intake (and no evidence was presented that the body wouldn’t just adapt to the injection, as it tries to adapts to all change), and even IF this did lead to weight loss, we have a hundred years of evidence showing that weight lost with a calorie deficit is so rarely sustained.

What might work?

*      As I’ve said so many times before, we need to eat better, not less. This video explains why calories are not equal and why we need to eat fewer of some and likely more of others.

*      If the Holy Grail of dieting is appetite suppression, then we have the solution already. The trouble is, it’s freely available. There’s no £100m company to sell. We eat the most satiating macro nutrients naturally provided – fat and protein – and shun the one – carbohydrate – that is the least satiating and least nutritious. The most common statement made by people on a low carbohydrate diet is “I don’t feel hungry”.

*      The psychological side still needs to be addressed and people need support to find a healthy prop, or to get through life without an addictive-like prop, but the eating strategy is there.

Or, to use Bloom’s own words, but just to change the subject: “Fast forward ten years, obesity won’t be a problem. They’ll have the low carb diets, they will be painless, no side-effects and actually really inexpensive and freely available.”

Now that really would be a miracle!


Fildes, A., Charlton, J., Rudisill, C., Littlejohns, P., Prevost, A. T., and Gulliford, M. C. (2015) Probability of an Obese Person Attaining Normal Body Weight: Cohort Study Using Electronic Health Records. Am J Public Health. Vol.105(9), pp.e54-9.

Fothergill, E., Guo, J., Howard, L., Kerns, J. C., Knuth, N. D., Brychta, R., Chen, K. Y., Skarulis, M. C., Walter, M., Walter, P. J., and Hall, K. D. (2016) Persistent metabolic adaptation 6 years after “The Biggest Loser” competition. Obesity. pp.n/a-n/a.

Francis G. Benedict. (1919) Human Vitality and efficiency under prolonged restricted diet. Carnegie Institution of Washington.

Franz, M. J., VanWormer, J. J., Crain, A. L., Boucher, J. L., Histon, T., Caplan, W., Bowman, J. D., and Pronk, N. P. (2007) Weight-loss outcomes: a systematic review and meta-analysis of weight-loss clinical trials with a minimum 1-year follow-up. J Am Diet Assoc. Vol.107(10), pp.1755-67.

Keys, A., Brožek, J., Henschel, A., Mickelsen, O., and Taylor, H. L. (1950) The biology of human starvation. University of Minnesota Press.

Michael Wadsworth, Diana Kuh, Marcus Richards, and Hardy., R. (2006) Cohort Profile: The 1946 National Birth Cohort (MRC National Survey of Health and Development). Int J Epidemiol. Vol.35 pp.49-54.

Stunkard A, M.-H. M. (1959) The results of treatment for obesity: A review of the literature and report of a series. A.M.A. Archives of Internal Medicine. Vol.103(1), pp.79-85.


Posted in Conflict, Dieting, Media comments, Obesity, Other Diets
Tags: , , ,

Types of fat

There are three different types of natural fat. The chemical structure of fat is shown below with three examples of the different types of fat. Fatty acids are made up of chains of Carbon atoms (C) bonded with Hydrogen (H) atoms. At one of the ends of a fatty acid is a carboxyl group (-COOH).

You can see that the example saturated fat below has all the Carbon atoms bonded to Hydrogen atoms. This fat is described as “fully saturated with Hydrogen atoms” – hence the name saturated fat. This means that no Hydrogen atoms are missing i.e. this is the most stable structure.

The example monounsaturated fat below has one pair of Hydrogen atoms missing, so it has one double bond between Carbon atoms. This makes the monounsaturated fat less stable than the saturated fat. Poly normally means many, but it means just two in the example below. The bottom fat structure has two pairs of Hydrogen atoms missing, so it has two double bonds between Carbon atoms. This makes the polyunsaturated fat less stable than the monounsaturated fat, which is less stable than the saturated fat.



Given that saturated fat is the most stable and therefore the safest to cook with (the safest at high temperatures) and polyunsaturated fat conversely is the least stable and the least safe to cook with, it is rather outrageous that public health ‘experts’ are advising us to favour polyunsaturated fats over saturated fats. i.e. unstable fats, over stable fats.

As the tweet below suggested, we need a change in terminology to make the language clearer, so that people stop thinking that saturated/stable is bad and polyunsaturated/unstable is good…



Further to this tweet, I declare the different types of fat renamed as polyunstable fat; monounstable fat and stable fat. Please use the correct terminology from now on!

Many thanks – Zoë

p.s. Don’t forget that all foods that contain fat contain all three fats: stable, monounstable and polyunstable. There are no exceptions. We cannot eat one without all three in food.

Posted in Gov. Policy, Ingredients
Tags: , , ,

PCSK9 Inhibitors & Statins

Statin side effects pave the way for son of statins…  


In May 2014, two doctors were maliciously attacked by a researcher. The researcher heads up the Clinical Trial Service Unit (CTSU) at Oxford University.

The doctors’ crimes (they were independent, but the same) were to mention that statin side effects might affect approximately 18-20% of takers. Both doctors referenced a peer reviewed article, which said that “the rate of reported statin-related events to statins was nearly 18%.” (The researcher demanded a retraction of both articles and continues to want the journal editor’s head on a plate, so to speak.

The journal commissioned an independent investigation to see if the articles should be consigned to Orwellian thought police archives. The best thing about the investigation was that it emerged that the researcher’s unit had received £268 million from pharmaceutical companies/interested parties. (Are you thinking what I’m thinking?!)

Wind forward to 4th April 2016 and an astonishing paper was published in The Journal of the American Medical Association (JAMA). The paper opened with the words: “Muscle-related statin intolerance is reported by 5% to 20% of patients.”

That’s just muscle-related statin side effects – what do the numbers become when mind, mood, memory, mo-jo and more side effects are added in?!

The study reported in the JAMA paper was funded by Amgen (remember that name). The combined conflicts of the authors covered most drug companies that make cholesterol lowering medications (I couldn’t see any not represented). Even more interesting was the fact that one of the authors, David Preiss, is a member of the CTSU. The same CTSU headed up by the researcher demanding the retractions for even mentioning that statin side effects could be as high as 20%.

What’s going on?

What’s going on is that it has become strategic to attack statins. Statins are now off patent – pharma speak for not being worth as much money any more. In preparation for the end of the gravy train, researchers have been working on other ways to lower cholesterol. The fact that higher cholesterol is associated with lower deaths (for men and women, from heart disease and all-causes) seems to have conveniently escaped their notice.

The powers that be have tried all sorts to find the next blockbuster cholesterol-impairment drug. Most notably they have tried, and failed, to raise HDL, which they think is good cholesterol when it is a lipoprotein. Maybe that’s why they failed.

The one that they have managed to get past drug approval bodies (which is sadly not difficult when most of those are conflicted) is called a PCSK9 inhibitor. (It spell checks to “pesky”, which amuses me).

PCSK9 Inhibitors

If I told you that a drug went on sale on 1st September 2015, which involved fortnightly injections at a cost of £4,000 a year and for which trials on incidents or deaths had not even started, you might be shocked. That’s exactly what happened. A drug named “Repatha” went on sale, having been “granted marketing authorisation” (note marketing authorisation, not drug approval) by the European Medicines agency on 21st May 2015.

Repatha is a PCSK9 inhibitor. One of a human’s estimated 20,000-25,000 protein coding genes is PCSK9. The PCSK9 gene provides instructions for making a protein that helps to regulate the amount of cholesterol in the blood stream. The PCSK9 protein controls the number of low-density lipoprotein (LDL) receptors on the surface of cells. LDL receptors are particularly plentiful in the liver, enabling the liver to remove cholesterol from the blood stream as needed. This is how the body is designed to work.

The company that makes Repatha, Amgen, describes its drug as follows: “Repatha is designed to bind to PCSK9 and inhibit PCSK9 from binding to LDL receptors on the liver surface. In the absence of PCSK9, there are more LDL receptors on the surface of the liver to remove LDL cholesterol from the blood”. Repatha is thus designed to stop the body from working in the way it is designed to work.

Statins were also designed to stop the body doing what it was designed to do. Statins block a vital pathway in the body – the mevalonate pathway. PCSK9 inhibitors impair a genetic/protein production pathway in the body.

My fundamental objection to all drugs that are designed to stop the body doing what it is designed to do, is that I don’t like money-motivated, share-holder driven, pharmaceutical companies ‘playing God’. I trust evolution more than Pfizer and Amgen.

What we need to know about Repatha/PCSK9 inhibitors

There are probably only two key things to know:

1) Repatha has no proven benefit for heart deaths or events.

To quote the European Medicines Agency: “The effect of Repatha on cardiovascular morbidity and mortality has not yet been demonstrated” (p.11 ).

You may want to read that again. Repatha will cost you/the health service £4,000 a year and it has not been shown to have any effect on heart disease or deaths. It will lower your cholesterol and that is it.

The marketing to demonise cholesterol has been so long and effective – it is quite possibly the best marketing campaign that has ever been undertaken – that people think that cholesterol lowering is the end goal – a benefit in itself. This is The Great Cholesterol Con.

In a media article on the eve of the drug going on private sale, it was noted that “While it is proven the drug lowers cholesterol, its manufacturer Amgen is conducting trials involving 27,500 patients in an attempt to show it saves lives, with results expected in 2017”. The crazy mad world, of pharmaceutical companies and drug approval agencies, considers it sufficient that a drug lowers an arbitrary measurement – in this case cholesterol – no actual health impact is required.

No matter the topic of any blog I write, at the end of the post there are more comments about cholesterol than anything else. People fear cholesterol. People are obsessed with lowering it. Otherwise intelligent doctors think “the lower the better”, without having stopped to wonder why the body is making cholesterol 24-7 if it’s so deadly.

Did you know that statins were also marketed on the basis of cholesterol lowering, rather than proven heart health benefit? Here’s a gem of a quotation from Dr Malcolm Kendrick’s book – Doctoring Data. Pfizer are the makers of the biggest drug blockbuster of all time: the statin Lipitor. It earned them $125 billion during its patent lifetime. (That’s the GDP of Ukraine as a guide, or more than the GDP of 70% of the world’s countries to put it in perspective.) As Malcolm shares in Doctoring Data:

For many years Pfizer were forced to include this little snippet at the bottom of their adverts in the US: ‘Lipitor has not been shown to prevent heart disease or attacks.’”

As Malcolm continued: “I would be willing to bet that you did not know that.”

2) The other thing that you probably should know about Repatha/PCSK9 inhibitors is that the side effects are probably unknown and/or under reported.

Given that the side effects of statins were denied to the point of vicious personal attack almost 30 years after their introduction, you should probably not expect the side effects of PCSK9 inhibitors to be researched fully, let alone openly declared. The prize is simply too huge for irritations like side effects to be allowed to get in the way.

Fortunately, patient leaflets have to tell the truth, or CEOs can end up in jail. The Repatha patient leaflet already cautions that there are many common side effects (i.e. those that affect up to one in ten people): “Flu (high temperature, sore throat, runny nose, cough and chills); Common cold, such as runny nose, sore throat or sinus infections (nasopharyngitis or upper respiratory tract infections); Feeling sick (nausea); Back pain; Joint pain (arthralgia); Injection site reactions, redness, bruising or pain; Rash.” I’m not sure I want fortnightly injections, let alone any of those side effects (many, such as aches and pains, are very similar to those found with statins). The International Network of Cholesterol Skeptics (THINCS) has far more sinister predictions of the harm that will likely be done by drugs that inhibit the operations of one of our protein coding genes.


NICE originally rejected Repatha on the basis that the cost/benefit was unproven. On the basis that the cost was £4,000 per patient and the benefit was non-existent, this was the only decision that could be made. It should remain the only decision that can be made, but I suspect that NICE will approve Repatha sooner or later. This will be the inevitable outcome of having the NICE review committee suitably staffed with pro-drug support, as has been the case with statins.

Hence the JAMA article attack on statins. NICE need to be given reason to support a drug that has no proven heart disease benefit and a substantial patient annual cost. The current belief is that PCSK9s are not needed because the world has statins. The world is now ready for the truth about statins, therefore: side effects are serious and affect a significant proportion of people (the desired conclusion being that these people would be better off on PCSK9s). Before long more and more people will be moved onto PCSK9s and the son-of-statins will be crowned.

Armed with the full picture, the JAMA paper ceases to be astonishing and becomes breathtakingly cunning and calculated. The prize from PCSK9s could be more like the GDP of Russia than Ukraine – Bond villains have done worse for less than that. If attacking statins is a necessary step on the road to riches beyond riches beyond wild dreams, then so be it. If that means admitting something that has been denied and defended for three decades, then so be it. If that means apologising to Dr Assem Malhotra and Dr John Abramson – the two doctors attacked – then – don’t hold your breath.

Posted in Conflict, Gov. Policy, Research
Tags: , , , , , , ,

Eatwell Guide – conflicts of interest

The new ‘eatwell’ guide, no longer a plate, was issued on March 16th 2016. This is my view of that guide. This post is about the group behind the guide.

When Unilever take out adverts in national UK newspapers saying: ”We are delighted that unsaturated fats, like the oils found in our spreads, now have a dedicated section of the Eatwell Guide and are recognised as the healthy option…”, you should be alarmed. If your so-called role model healthy eating plate is welcomed by fake food companies, surely you got it wrong. (Many thanks MelanieB for the pic.)

The remit of the group

A group was set up in November 2014 to review the ‘eatwell’ plate. You can follow this link to a number of documents where you will find the Purpose of the group and the Terms of reference as follows (SACN is an abbreviation for the Scientific Advisory Committee on Nutrition and PHE is Public Health England) (the bit in blue is all direct quotation):

Purpose of the group: “At the time of the publication of the draft SACN Carbohydrate and Health report, PHE highlighted action that would be undertaken while the SACN consultation continued. Sugar Reduction – responding to the challenge, included a commitment to review healthy eating messages in light of the draft SACN report. PHE has established this external reference group to provide advice on aspects of the eatwell plate.”

Terms of reference: “To provide advice to Public Health England on potential changes to the eatwell plate in light of draft recommendations from SACN.

* consider approaches to revising the segment sizes for the eatwell plate
* approaches to reviewing the visual aspects of the plate model
* approaches for reflecting messages on foods that should be consumed in limited amounts
* approaches for reflecting hydration messages
* opportunities for promotion of any amended visual.”

The group committed to meeting together, or virtually, up to three times between September 2014 and January 2015. The meeting minutes show that the group met in November 2014, December 2014, February 2015 and June 2015. The SACN report was not published until July 2015, so the group met to respond to the report before it was published – presumably relying on draft SACN guidelines.

The members of the group

If you follow this link, you can see the original documents about meetings, terms of reference etc. Very little information is shared – that’s typical of any bodies subject to the Freedom of Information act, for which I have some sympathy.

The members of the group revising the eatbadly plate were:

Lisa Jackson, AFN (Chair) – Association for Nutrition.

The Association for Nutrition founding fellows can be seen here. Jackson was the main spokesperson on the press release. Two other members of the AFN caught my eye: Anne de Looy – author of this support for the sugar industry and none other than Alison Tedstone, Chief Nutritionist for Public Health England. Probably fair to say, therefore, that PHE set out to ensure that the outcome would meet PHE approval.

Alison Nelson, BDA – British Dietetic Association (Luci Daniels attended the final meeting instead of Alison Nelson).

The BDA sponsor list is not as bad as those of other group members: Danone; Abbott Nutrition – catch em young eh? But you can generally rely on a dietician to defend fake food and they have previously shared with me how “delighted they have been” to work with the sugar bureau.

Karen Tonks, IGD – Institute of Grocery Distribution.

Members are food, drink and grocery manufacturers, distributors, wholesales and operators – the full Monty of the food, drink and grocery world.

Judy Buttriss, BNF – British Nutrition Foundation.

Don’t be fooled by the name – the British Nutrition Foundation have always had one of the worst conflict lists you will see. Members are the who’s who of the fake food industry again: Aldi; ASDA; Birds Eye; British Sugar; Coca-cola; Co-Op; Danone; General Mills; Greggs; Heinz; Kelloggs; KP Snacks; M&S; Mars; McCain; McDonalds; Morrisons; Nestle; PepsiCo; Quorn; Sainsbury;  Slimming World!; Tate & Lyle; Unilever; United Biscuits; Waitrose; Warburtons; and Weetabix.

Andrea Martinez-Inchausti, BRC – British Retail Consortium.

Members include: Aldi; ASDA; Burger King; Costa Coffee; Greggs; Iceland; Lidl; M&S; McDonalds; Morrison; Sainsbury; Spar; Starbucks; Subway; Tesco; Thorntons; Waitrose; and many, many more.

Kate Halliwell, FDF – Food & Drink Federation.

Members are again pretty much the who’s who of the fake food industry: AB sugar; Association of British foods; Allied Bakeries; Alpro SOYA; Batchelors (premier foods); Border Biscuits; British STARCH industry; British oat and barley millers’ association; British sugar; Britvic; Burton’s Biscuit company – that’s just some of the companies under A and B. You can work through C to Z if you like! I highlighted SOYA and STARCH, as they will be especially thrilled with the new plate.

James Lowman, Association of Convenience Stores (Judy Byers attended the Feb and July 2015 meetings instead of James Lowman).

“The Association for Convenience Stores core purpose is to lobby Government on the issues that make a difference to local shops.” The ACS describes itself as the voice of 33,500 local shops. Here is ACS Chief Executive, James Lowman, (the man on the ‘eatwell’ committee) welcoming the failure of the Welsh public health bill, because convenience stores don’t want a tobacco register. Nice!

Modi Mwatsama, UKHF (UK Health Forum) – jolly good!

No conflicts! Ta dah! However, how much impact could one person have, especially when other potentially health orientated members didn’t turn up…

Helen Donovan, RCN – Royal College of Nursing – jolly good!

However, the meeting minutes showed that Donovan did not attend the December 2014, February 2015 or June 2015 meetings, so nurses were not represented.

Esther Trenchard-Mabere, ADPH – Associate Director of Public Health – should be good but also, according to the minutes, didn’t attend any meetings beyond the November 2014 ‘meet and greet’.

Maureen Strong, AHDB – Agriculture & Horticulture Development Board.

The Agricultural & Horticulture Development Board is a statutory levy board. Farmers, growers and others in the supply chain have to pay the levy. The AHDB is supposed to represent: Pig meat; Milk; Beef & lamb; Cereals and oilseeds; and Potatoes. May I suggest that, while cereals, oilseeds and potatoes are celebrating, pig, milk, beef and lamb producers should withhold their levies. Strong certainly did not put in a strong showing on behalf of meat and dairy producers.

The bottom line

The terms of reference tell us that “Public Health England established this external reference group to provide advice on aspects of the eatwell plate.” Public Health England presumably appointed the chair from the same stable as itself (AFN). Public Health England presumably appointed the other reference group members from the fake food industry. Why? Why have one such member? Let alone stack the majority of the group with the who’s who of the fake food industry? How the heck are we supposed to take Public Health England seriously with this kind of behaviour?

What on earth chance did EAT REAL FOOD! have with that External Reference Group?!

Posted in Conflict, Gov. Policy, Obesity, Research
Tags: , , , , ,

Eatwell Guide

The origin of the ‘eatwell’ plate

(Throughout this post, the plate/guide will either be called ‘eatwell’ in inverted commas, to illustrate that it is anything but. Or, I shall use the name that I coined several years ago and used in my 2010 obesity book: The eatbadly plate.)

The ‘eatwell’ plate was launched at a press release on 16 September 2007, by the Food Standards Agency (FSA). It is described in the British Nutrition Foundation video on YouTube as the “healthy eating model for the UK” – suitable for young or old, vegetarian or not and for any ethnic group.

It replaced The Balance of Good Health, which was launched by the UK Department of Health in 1994 and was also a picture of a segmented plate. In April 2000, responsibility for the Balance of Good Health (BOGH) diagram and concept passed to the then newly formed Food Standards Agency (FSA). When the FSA revised the plate in 2007, it summarised the differences between the two plates. The BOGH title was seen as “unfriendly” and “lacking in emotion” and so the title and some colours on the plate rim changed. Food groups were renamed. For example “bread, other cereals and potatoes” became “bread, rice, potatoes, pasta (and other starchy foods)”. In other words, a marketing company made a lot of money making the plate more “friendly” and “emotional”, but, to all intents and purposes, what we know as the ‘eatwell’ plate has been around since 1994. (I share this nonsense, as it has happened again…)

The new ‘eatwell’ guide

A new ‘eatwell’ guide (not plate) was issued on 17 March 2016. This is what the new plate, sorry, guide, looks like. This is a summary of what has changed. It’s been renamed the ‘eatwell’ guide (they don’t use the inverted commas ha ha); the knife and fork have gone; the images are drawn, not photographed; the segment names have been updated – those are the first four changes. Never has the expression “moving the deck chairs on the titanic” been more appropriate! How is any of this going to address epidemics of obesity and diabetes?!

The next four get into the meat of the guide (sorry – meat is largely off the menu): the segments have been resized; the purple segment (the one that used to famously have a red can of cola) now only has unsaturated oils and spreads; high fat, salt and sugar foods have been removed from that purple segment; and there’s a new hydration message.

The segment sizes are not in the launch documents – I phoned the helpline on the press release to be told they would only be given out to journalists. So much for public help, or health! (They’re below – don’t worry). The only real food in the purple segment (butter) has been removed. The biscuits, sweets, cakes, crisps and chocolate have been removed from the purple segment – only to be given a fabulously prominent spot on the eye catching bottom left of the diagram – along with ketchup and ice cream. That’s the fake food industry appeased :-) And not even the hydration message holds water, as Dr Margaret McCartney pointed out in July 2011.

There is so much so wrong with the plate/guide, I hardly know where to start. Let’s focus on the three main issues:

1) The plate/guide is not evidence based

This document (page 2) sets out how it thinks the ‘eatwell’ guide can help (my comments are in red – hover near the underlines to see links):

The Eatwell Guide shows the different types of foods and drinks we should consume – and in what proportions – to have a healthy, balanced diet.
The Eatwell Guide shows the proportions of the main food groups that form a healthy, balanced diet:
• Eat at least 5 portions of a variety of fruit and vegetables every day (This is not evidence based. It was invented in 1991 without evidence base and attempts to post rationalise it have failed)

• Base meals on potatoes, bread, rice, pasta or other starchy carbohydrates; choosing wholegrain versions where possible (This is not evidence based. As Tanner said “Farinaceous and vegetable foods are fattening, and saccharine matters are especially so”…)

• Have some dairy or dairy alternatives (such as soya drinks); choosing lower fat and lower sugar options (This is not evidence based. There is a growing evidence base to the contrary – specifically supporting full fat dairy products).

• Eat some beans, pulses, fish, eggs, meat and other proteins (including 2 portions of fish every week, one of which should be oily) (There is some evidence base for oily fish. Micronutrient evidence should drive us towards meat/fish/eggs/dairy/seeds etc).

• Choose unsaturated oils and spreads and eat in small amounts (There is no evidence that total fat or saturated fat is harmful and some evidence that vegetable oils are harmful.)

• Drink 6-8 cups/glasses of fluid a day (No evidence base).

If consuming foods and drinks high in fat, salt or sugar have these less often and in small amounts.”

The ‘eatwell’ guide encourages consumption of nutritionally poor foods, rather than nutritionally rich foods. The SACN report has been used to try to justify the new guide. This is a dissection of that report.

2) The plate/guide does not understand the difference between volume/weight and calorie intake

In September 2009, when I asked the FSA what the plate proportions were based on, they said weight. In my 2010 obesity book, I did an interesting calculation where I took the average calorie number for each segment and worked out what the plate would look like if the proportions were represented by calorie intake – which is what matters to the body and which is what is used in dietary studies. A savvy calorie counter or nutritionist will be able to do a back of the envelope: fruit and veg is c. 40 calories per 100g; bread is about 260 cals per 100g, grains are about 360 – starchy things will average out therefore; oils are approximately 880 cals per 100g, spreads lower – that will average too. I have a database of foods to which I commonly refer, so I worked it out more scientifically. The precision doesn’t matter much.

I’ve picked the foods to match closest to those on the new ‘eatwell’ guide to calculate the following: Starchy foods average c. 334 cals per 100g; Fruit & veg 43 cals per 100g; Dairy & alternatives (think moobs when you see soya guys!) 157 cals; Beans, pulses, fish, eggs, meat & other proteins, c. 180 cals; Oils & spreads c. 819 cals and the Junk (off the plate but the proportions allow for it) c. 600 cals.

When you recalculate the plate by proportion of calories, this is what happened to the old plate:

OLD ‘Eatwell’ plate % in diagram % by cal intake
Starchy foods 33% 50%
Fruit & veg 33% 6%
Milk & dairy 15% 12%
Non dairy protein 12% 10%
Junk 8% 22%
TOTAL 101% 100%

The starchy foods became 50% of calorie intake; the junk (purple) segment became 22% and fruit and veg plummeted to 6% of calorie intake,

The new ‘eatwell’ guide is arguably worse. These are the proportions with and without junk (small rounding errors)

 With junk included  Without junk
NEW ‘Eatwell’ guide % in diagram % cal intake % in diagram % cal intake
Starchy foods 37% 62% 38% 68%
Fruit & veg 39% 8% 40% 9%
Dairy & alternatives 8% 6% 8% 7%
Beans, pulses, fish, eggs, meat etc 12% 11% 12% 12%
Oils & spreads 1% 4% 1% 4%
Junk 3% 9%

Without junk included, the new plate has a whopping 68% of calories in the form of starchy foods – things that make you fat. When junk is allowed (and it is allowed – I’m being generous here) 71% of calorie intake comes from starch and junk combined. Fruit and veg barely moves from the 6% of calories from the eatbadly plate. Beans, pulses, meat, fish, eggs – crikey – which idiot put almost all of the good stuff in one small category?! – accounts for 11-12% of calorie intake. Dairy is the big loser in the new eatbadly guide – down from 12% of calorie intake to 6-7%. Look at how junk takes such a big chunk of daily calories (still almost 10%) – JUNK HAS NO PLACE ON A ROLE MODEL PLATE OF HEALTHY EATING. There – shouting over (for now).

Nutrition 101 tells us that fat and protein can be used for basal metabolic needs and carbs and fat can be used for fuel (protein too can be used for fuel – and will be as a last resort). Carbs cannot be used for the vast majority of our daily calorie requirement. This video will explain. In a ‘healthy’ eating guide that drives us to consume (using the no junk proportions) 68% of our diet as starchy foods, 9% as fruit and veg (more carbs), 10% as dairy (some carbs) and even the beans/pulses/fish/eggs/meat segment can be taken in carb/protein form (beans/pulses) rather than no-carb form (meat/fish/eggs) – you can see how this guide mandates that we will get insufficient fat/protein and excess carbohydrate. We will be under nourished nutritionally and over fed fuel. In short – we will be sick and fat.

3) The plate/guide is another missed opportunity

Yet again, we didn’t need the committee. We didn’t need all these documents and diagrams and press releases and orange borders and such like. We just needed a three word message to come from Public Health Bodies:


Another three word message therefore comes to mind:


Posted in Gov. Policy, Obesity, Other Diets, Research
Tags: , , ,

Lowering Blood Pressure & SPRINT

Imagine that a doctor said: “I’d like you to take this pill. It will reduce your risk of dying by 30%.” You’d pretty seriously consider it, if not jump at the chance…

The story

I happened to be in the car, with Radio 4 tuned in, last Wednesday (3rd Feb 2016) at 3.30pm. Dr. Mark Porter’s programme, Inside Health (the transcript is below the recording), had just started and I heard a researcher saying that his trial had been stopped just over three years into a five year study because the benefit was already so dramatic. This is the holy grail of randomised controlled trials – ‘we just had to stop the trial because it was unethical not to treat the control group because the intervention group was doing so well’. Having seen this happen more than once, it can also happen, funnily enough, when gaps that had emerged between the two groups start to narrow…

The researcher being interviewed was Dr. Paul Whelton. Whelton is the chair of the SPRINT (Systolic blood PRessure INtervention Trial) steering committee. The full paper for the trial can be seen here. (In Figure 3, the data available at four year shows the intervention and control group lines closer together than at the time the trial was stopped; funnily enough).

The trial enrolled over 9,000 people in the US between the dates of November 2010 and March 2013. There were many inclusion and exclusion criteria. These are very important, because they define the profile of people to which the results can apply. All participants had to be over the age of 50. And they had to have systolic blood pressure (the first number of the two e.g. the 140 in 140/90) between 130 and 180. And they had to have had a significant risk factor for cardiovascular disease (already had cardiovascular disease, already got chronic kidney disease and/or had a 10 year risk of 15% of higher on the Framingham scale). Two exclusion criteria were listed – the participant must NOT have diabetes and they must NOT have already had a stroke.

The aim of the trial was quite interesting – it was not to see if blood pressure medications were better than not taking medications. It was to see if what they called “intensive” blood pressure (BP) lowering treatment (to medicate people to get them below 120 systolic BP) was better than “standard” BP lowering treatment (to medicate people to get them below 140 systolic BP). The goal of this trial, therefore, was to see if giving more meds was better than giving fewer. The idea of not giving meds at all was not part of this trial.

The trial participants were also interesting – older people and sicker people – designed to ensure that there would be a decent number of deaths in a short period of time. This is not underhand – if the trial outcome is deaths, you need people to die!

4,678 were analysed for the intensive treatment group; 4,683 were analysed for the standard treatment group. At the time the trial was stopped, 155 people in the intensive treatment group had died and 210 people in the standard treatment group had died. Table 2 in the full paper has the statistics on this. This was presented as a Hazard (risk) Ratio of 0.73, which can be presented as a 27% difference between the two interventions. Indeed, Whelton presented this on Inside Health as “In fact their total mortality was reduced by close to 30% and I’ve never been in a trial where we’ve seen that before.”

Relative risk

That’s relative risk, which I have frequently explained as highly misleading. The absolute risk of dying in any 1 year of the study was approximately 1 in 100. In the intensive treatment group 1.03 people in 100 died; in the standard treatment group 1.37 people in 100 died. That’s 10 people in 1,000 vs. fewer than 14 people in 1,000. That’s hardly “Stop the trial! People are dropping like flies!”

Who didn’t benefit

Then is when it gets even more fun. Figure 4 in the paper is called a forest plot or a blobbogram. I kind of like the second name. All you need to look for in a blobbogram is whether each horizontal line touches or crosses the vertical line, which is drawn at 1.0. Any horizontal line that touches or crosses that vertical line is NOT significant. It could have happened by chance. You should ignore it.

The blobbogram in this paper tells us that, the intensive treatment made a significant difference for:

– all participants grouped together;
– people who didn’t have previous chronic kidney disease;
– people 75 years old or older;
– men;
– non black people;
– people who didn’t have previous cardiovascular disease; and
– people whose starting blood pressure was under, or equal to, 132.

The intensive treatment made NO significant difference for:

– people who did have previous chronic kidney disease;
– people under 75 years old (that’s 82% of participants for starters);
– women;
– black people;
– people who did have previous cardiovascular disease;
– people whose starting blood pressure was greater than 132 (that was 66% of people).

For the majority of people, therefore, there was no benefit from intensive treatment. (As an aside, is it surprising that lowering BP to below 140 makes no difference to people whose starting BP is already below 132?!)

Thanks to Dr. Margaret McCartney on Inside Health, the programme discussed the numbers needed to treat to impact one person. In McCartney’s words: “you had to treat 90 people in order to delay one death over the three year period of the trial.  Now that is important but it means that 89 out of those 90 people did not get benefit from having their death delayed and were at risk of just getting the side effects from the intervention. Is that worth it or is it not?  That’s for the patient to decide, not for me.”

Which brings us nicely on to…

The down sides

The side effects were serious. A Serious Adverse Event is defined as a “Fatal or life threatening event, resulting in significant or persistent disability, requiring or prolonging hospitalization, or judged important medical event.”

The paper reported: “Serious adverse events of hypotension, syncope [fainting], electrolyte abnormalities, and acute kidney injury or acute renal failure… occurred more frequently in the intensive-treatment group than in the standard-treatment group.” “A total of 220 participants in the intensive-treatment group (4.7%) and 118 participants in the standard-treatment group (2.5%) had serious adverse events that were classified as possibly or definitely related to the intervention (hazard ratio, 1.88; P<0.001).”

If you want to report deaths rates as 30% better than the standard treatment group, you should also report side effects as double that of the standard treatment group. Presenting benefit as 30% (relative) and the side effects as 4.7% (absolute) is naughty at best and deliberately misleading at worst. Some of those side effects are serious and nasty as well – acute kidney injury or acute renal failure? What would happen if the trial were kept to five years long, or extended for longer? Would significant numbers of people in the intensive treatment group die of kidney failure? How many will end up on lifelong dialysis as a result of this trial?

The honest patient conversation

This kind of trial informs medical policy – it is intended to. That’s why drug companies spend so much money funding research, researchers and research institutions. The messages that are best left in the minds of the medical world are 1) the trial stopped early i.e. you must get your patients on this treatment asap or you will be unethical and 2) there was a 30% difference in mortality i.e. you must get your patients on this treatment asap or you will be unethical.

Then the doctor conversation can be: “I’d like you to take this pill. It will reduce your risk of dying by 30%.”

As McCartney suggested, the good doctor sets out the facts in an understandable way and lets the patient decide if absolute benefit is worth the known (side effect) risk. The honest doctor conversation in this case – only even to be considered with patients over the age of 50 – would be:

“If you are male, or over the age of 75, or have no previous chronic kidney disease, or are not black, or have no previous cardiovascular disease, or have current systolic blood pressure under 132, AND over the age of 50 (because we didn’t test younger people), AND don’t have diabetes (because we didn’t test for people with that), AND haven’t had a stroke (because we didn’t test for people with that) … if you then take 3 pills a day (that was the actual number of pills administered) every day for 3.26 years, you have a 1 in somewhere up to 90 chance (Note 1) of delaying death i.e. you might not die within the 3.26 years – you might die the day after, or sometime after, we don’t know. Oh, and by the way, you double your (relative) risk of some serious side effects including acute kidney failure and you might faint here and there, so don’t idle at the top of staircases.”

Now who would jump at the meds?!


One of the key findings from this meta-analysis was that you can’t take six studies of 2,500 sick men and set dietary guidelines for entire populations. (Except that this is what happened – oh – and the studies themselves did not support the guidelines introduced). Research is said to lack “generalisability” if it is undertaken on, and/or shows results for a small or specific part of the population. Put simply, you can’t study people over 50, find significance for men or over 75s only and then apply guidelines to entire populations…

When McCartney joined the debate, so did Tony Heagerty, introduced as “Professor of Medicine at University of Manchester, who has a special interest in treating high blood pressure.”

Closing the debate, Porter asked Heagerty the key question: “Well this is the big question isn’t it Tony – does this one trial, which has come up with this finding and suggestion that we should be aiming at 120 – is that enough to change our current guidance and practice on it?”

Heagerty replied “I believe it does actually… the National Institute for Health and Clinical Excellence scoped out or looked for a reason to change guidelines in 2015 and the guideline writing committee felt there was no new evidence. I think that in 2016 the British guidelines will have to be readdressed with regard to targets for looking at effective blood pressure control.”

The paper’s own blobbogram confirmed that there was no significant difference for people under 75 years old (82% of the study participants). There was no significant difference for people with previous chronic kidney disease, or people with previous cardiovascular disease. There was no significant difference for women. There was no significant difference for black people and, perhaps most incredibly of all, there was no significant difference for people whose starting blood pressure was greater than 132 (66% of participants).

So there are calls for UK wide guidelines to be changed for all people when absolute risk benefit vs. Serious Adverse Effect cost barely holds up for white men over 75 with no previous CVD and already low blood pressure.

This is when John McEnroe’s legendary comments springs to mind: “You cannot be serious”!

(Note 1) the number needed to treat included women/under 75 year olds etc, who we now know will not benefit, so the number needed to treat will change with the caveats spelled out. Even if you leave out the caveats and tell any non-diabetic/non-stroke patient over 50 they have a 1 in 90 chance of benefit and likelihood of side effects – some serious – I suspect they would decline the kind offer.


Posted in Conflict, Gov. Policy, Research
Tags: , , ,

Burning off calories (& food labels)

On 15 January 2016, the Royal Society for Public Health (RSPH) called for the introduction of ‘activity equivalent’ calorie labelling on food and drink. Such labelling would show how much activity would be required to burn off the calories contained in the food or drink. But would it?!

The press release can be viewed here. The call was made in an attempt to help with “the UK’s growing obesity crisis.” According to the press release, the RSPH’s said of activity equivalent labelling: our “own research found two-thirds (63%) of people would support its introduction, with over half (53%) saying it would cause them to make positive behaviour changes such as choosing healthier products, eating smaller portions or doing more physical exercise.” (The RSPH kindly shared by email that the research undertaken involved 2,010 UK adults, aged 18+, surveyed online between 11th and 13th December 2015).

The full position paper is here. The RSPH ‘hopes’ that prominent pictorial icons, alongside front of pack information, would increase consumer awareness of both calories contained within the food/drink and the activity required to burn off those calories. The icons are illustrated in the full position paper. An example bag of crisps is shown with a picture of someone: running; cycling and swimming and the numbers say that these activities would need to be done for 19, 23 and 13 minutes respectively to burn off the 171 calories in this particular bag of crisps.

The problems

1) The first problem is that all of this is based on the calorie theory: the idea that, one pound of fat equals 3,500 calories and humans gain one pound if they have a 3,500 calorie excess and lose one pound if they have a deficit of 3,500 calories. None of this has been sourced, proven, explained – anything. It remains the biggest dieting myth ever invented and perpetuated by human beings.

2) The second problem is that calories are not equal. If we proceed on the correct assumption that calories are units of fuel, nothing to do with weight, we will be on safe ground. This video shows how most of the fuel requirement of the body is determined by basal metabolic rate (the fuel needed by the body if we lie in bed all day) and that this, almost entirely, needs to be met by fat and protein. Carbohydrate is for energy only (and fat can meet energy needs just as well, arguably better).

3) It follows from (2) that all carbohydrate that humans consume must be burned off with activity or it will be stored as fat. It cannot be used for anything else. This means that any activity equivalent label only needs to list carbohydrate calories. This is the fuel that needs to be burned off, or it will be stored as fat (in what ratio, we do not know – certainly not in the 3,500 calorie ratio).

To take an example, 100 grams of Mars Bar contains 17g of fat, 4g of protein and 70g of carbohydrate (the rest will be water). If someone eats 100g of Mars Bar, they need to use up 70g – approximately 280 calories worth – of carbohydrate fuel. The fat and protein can be used by the body for maintenance and repair.

4) This brings us to another problem. We cannot choose what we want the body to burn for fuel – the body mechanisms and physiological state decide this for us. If we eat the Mars Bar and start running at 5 miles per hour, the body will first use any glucose already available in the blood stream. After this? Who knows. Maybe glycogen stored from carbohydrate eaten in the past 24 hours, maybe glucose from the Mars Bar, maybe fat from the Mars Bar (instead of using this for cell repair/maintenance). Who knows? This whole calories in/calories out mythical thinking has led to a lot of erroneous assumptions about food, activity and weight. This initiative perpetuates a lot of this bad science.

5) Notwithstanding that only the carbohydrate calories need considering, the pictorial icons are wildly inaccurate and yet would be taken as accurate by most people. In the full position paper, page 4 has a guide as to how much medium walking vs. slow running a person would need to do to burn off the example foods shown.

The source for the information is this very rough calculator, which doesn’t take gender into account and is not very sensitive to age. I’ve reverse engineered a couple of examples and the numbers seem to be based on a 50 year old (male or female) weighing 76kg (nearly 12 stone). This person would, allegedly, use up 436 calories running slowly for 42 minutes (close to the 445 for the sandwich). Weighing 50 kg, I would need to run for 65 minutes to achieve the same – a 55% margin of error. Other, more accurate, calculators available suggest I may need to run at 5 miles an hour for over 75 minutes to burn off the sandwich.

6) Problem six logically follows three, four and five above: the body needs to burn off all carbohydrate daily, not just snacks consumed. If this labelling route is a good idea, it should apply to every food containing carbohydrate, from fruit to lentils to yoghurt to brown rice.

Government guidelines advise consuming 55% of calorie intake in the form of carbohydrate. I would need to run for three solid hours to burn that off, even before starting the running needed to burn off any extra snacks!

7) Problem seven is huge and not widely known. I wrote about this in a blog in 2010. We don’t use up as much energy as we think. Exercise calculators take into account BMR (Basal Metabolic Rate). Hence, if watching TV requires 68 cals an hour (this is the calculation for a 140lb/10 stone person) and moderate walking burns 200 calories an hour (for the same person), then going for a walk should be viewed as the additional energy needed beyond doing nothing (i.e. 130 calories in this case). Some slimming plans encourage “treats for activity” e.g. jog for 20 minutes, have a (say) 200 calorie confectionery bar. It is quite UNlikely that someone would use 200 calories in 20 mins jogging above what they would need anyway pottering around the house or being at work.

8) Problem eight is that this is music to the ears of the fake food industry. Sure, they won’t like having to change labels if this becomes mandatory, but they would like to make portions smaller, to reduce ‘burn off’ times, while keeping the price the same, to boost profit. This is essentially what has been happening with the government (IR)responsibility deal.

9) The final problem is the same one encountered by all of these different initiatives by different organisations – the opportunity cost of what could be done instead. Instead of going to all this effort hoping that adding complex and inaccurate pictures to every fake food product will encourage people to avoid, or burn off, junk, why not advise people not to have the junk in the first place?

When people ask for my views of traffic light, or other labelling, schemes my response is always the same – our labelling policy should be simple: don’t eat anything that requires a label. Why is it so difficult for public health bodies to simply come out and say “Eat real food”!

No doubt the RSPH initiative is well intentioned, albeit without any evidence that it would have an impact. Sadly it suffers from so many flaws, I cannot see any good coming from good intentions. Well meaning “Eat real food” messages would be far simpler and more effective, yet somehow seem to escape the mind set of public health bodies.

Posted in Media comments, Obesity, Research
Tags: , , , , ,

Sugar the evidence

Just as this page documents recent academic articles questioning current dietary advice, so this page documents recent academic articles about sugar. All the papers are from 2015 onwards except the first two position papers, which are important to capture:

Position statement on Sugar & cardiovascular health: Johnson RK, Lustig RH, et al. “Dietary sugars intake and cardiovascular health: a scientific statement from the American Heart Association”. Circulation. 2009

Position statement on Sweeteners & health: Gardner C, et al. “Nonnutritive sweeteners: current use and health perspectives: a scientific statement from the American Heart Association and the American Diabetes Association.” Circulation. 2012.

Articles from 2015:

Summary of evidence (Cochrane link). October 2015: Public Health England. “Sugar Reduction: The evidence for action.

Fructose & Cardiometabolic health. October 2015: Malik VS, Hu FB. “Fructose and Cardiometabolic Health: What the Evidence From Sugar-Sweetened Beverages Tells Us”. J Am Coll Cardiol.

Sugar sweetened drinks & Hypertension. October 2015: Jayalath VH, et al.”Sugar-sweetened beverage consumption and incident hypertension: a systematic review and meta-analysis of prospective cohorts”. Am J Clin Nutr.

Sugar & Tooth decay. October 2015: Meyer BD, Lee JY. “The Confluence of Sugar, Dental Caries, and Health Policy“. J Dent Res.

Sugar sweetened drinks & Global burden of disease. August 2015: Singh GM, et al; “Estimated Global, Regional, and National Disease Burdens Related to Sugar-Sweetened Beverage Consumption in 2010.” Circulation.

Refined carbohydrates & Depression. August 2015: Gangwisch JE, el al. “High glycemic index diet as a risk factor for depression: analyses from the Women’s Health Initiative”. Am J Clin Nutr.

Sugar, Tooth decay & Obesity. July-Aug 2015: Yeung CA, Goodfellow A, Flanagan L.”The Truth about Sugar”. Dent Update.

Sugar sweetened drinks & Type 2 diabetes, independent of obesity. July 2015: Imamura F, et al. “Consumption of sugar sweetened beverages, artificially sweetened beverages, and fruit juice and incidence of type 2 diabetes: systematic review, meta-analysis, and estimation of population attributable fraction”. BMJ.

Sugar consumption & Addiction. June 2015: Tryon MS, et al. “Excessive Sugar Consumption May Be a Difficult Habit to Break: A View From the Brain and Body”. J Clin Endocrinol Metab.

Sugar sweetened drinks, Diabetes & Kidney disease. June 2015: Yracheta JM, et al. “Diabetes and Kidney Disease in American Indians: Potential Role of Sugar-Sweetened Beverages“. Mayo Clin Proc.

Sugar & Aging. March-April 2015: Ross SM. “Sugar-induced aging: the deleterious effects of excess dietary sugar intake”. Holist Nurs Pract.

Fructose & Type 2 diabetes. March 2015: DiNicolantonio JJ, O’Keefe JH, Lucan SC. “Added fructose: a principal driver of type 2 diabetes mellitus and its consequences”. Mayo Clin Proc.

Sugar sweetened drinks & early onset of menstruation. March 2015: Carwile JL, et al.Sugar-sweetened beverage consumption and age at menarche in a prospective study of US girls”. Hum Reprod.

Sugar sweetened drinks & Snacking. March 2015: Bleich SN, Wolfson JA. “U.S. adults and child snacking patterns among sugar-sweetened beverage drinkers and non-drinkers”. Prev Med.

Sugar sweetened drinks, Hypertension & CVD. March 2015: Xi B, et al. “Sugar-sweetened beverages and risk of hypertension and CVD: a dose-response meta-analysis”. Br J Nutr.

Conflicts of interest in the sugar industry & UK institutions & individuals. February 2015. Gornall J. “Sugar: spinning a web of influence”. BMJ.

Sugar & CVD. Jan-Feb 2015. Ross SM. “Cardiovascular disease mortality: the deleterious effects of excess dietary sugar intake”. Holist Nurs Pract.

Sugars, Metabolic Syndrome & Cancer. January 2015. Das UN. “Sucrose, fructose, glucose, and their link to metabolic syndrome and cancer”. Nutrition.

Sugar & FDA approval: Is it even safe? 2015: Card MM, Abela JF. “Just a Spoonful of Sugar Will Land You Six Feet Underground: Should the Food and Drug Administration Revoke Added Sugar’s GRAS Status?” Food Drug Law J.

(Please note, this is just a selection of articles on sucrose/sugar from 2015. On the date of this post, a pubmed search of (“sucrose”[tiab]) OR “sugar”[tiab])(tiab picks up the words sugar or sucrose in the title or abstract) in humans from 1 January 2015 to 19 January 2016 produced 677 articles. I picked review articles, which looked easier to digest than this one!)

For older articles, see the c.140 references at the end of this post.

Posted in Dieting, Ingredients, Media comments, Obesity
Tags: , , , , , , , , ,