National cholesterol month

I was at a dinner party recently when the subject of cholesterol came up. Every (lay) person around the table turned out to be an expert: “Cholesterol is bad”, said one. “Well actually there’s good and bad cholesterol”, clarified another. “Our cholesterol shouldn’t be higher than five”, volunteered one sage. Five what? They had no idea. Why is cholesterol bad? Not a clue. If ever there were a substance vilified with the utmost ignorance – cholesterol is it.

This month, October, is national cholesterol month in the UK. September was national cholesterol month in the US. Call me cynical, but staggering the months gives one sixth of the year when the increasingly global on-line world is being manipulated to have cholesterol front of mind. Leading the charge in the UK appears to be Heart UK – an organisation masquerading as a charity, which more accurately should be seen as a voice piece of the cholesterol lowering industry. Here are Heart UK’s backers.

This is what we should be told in national cholesterol month and these are the things that my fellow diners should have been saying about cholesterol:

1) Cholesterol is utterly life vital

Every human being would die instantly without cholesterol. Every single cell in the human body depends upon it. We would have no digestion or hormone function without cholesterol. Cholesterol is critical for brain and memory functions – even though the brain is only 2% of the body’s weight, it contains approximately 25% of the body’s cholesterol (Ref 1). Cholesterol is essential for bones and all the roles performed by vitamin D. We could not reproduce without this life vital substance. Hence, not only would humans die without cholesterol, the human race would die out.

2) Cholesterol is so vital that our body makes it

It cannot be left to chance that we would need to get cholesterol from an external source, such as food. One of the key reasons that we need to spend approximately one third of our lives sleeping is to give the body time to produce cholesterol, repair cells and perform other essential maintenance.

3) There is no such thing as good and bad cholesterol

The formula for cholesterol is C27H46O. There is no good or bad version. Ignorant people call HDL ‘good’ cholesterol and LDL ‘bad’ cholesterol. Neither HDL nor LDL are even cholesterol – they are lipoproteins. HDL is High Density Lipoprotein and LDL is Low Density Lipoprotein. HDL is smaller than LDL and is therefore higher in density. Lipoproteins carry cholesterol, protein, phospholipids and triglyceride around the blood stream to undertake vital roles.

4) The cholesterol blood test is a guess

The standard blood test can only measure total cholesterol & HDL. So we have one equation, four unknowns, only two of which can be measured:

Total cholesterol = LDL + HDL + Triglycerides (VLDL)/5

Any GCSE maths student will tell you that this is insolvable.

Your best option is not to get your cholesterol ever tested and then you can never be a victim of the cholesterol lowering machinery that will kick in if your guestimate fails the following test…

5) There is no science behind the number “5”

Even after years of artificial intervention, the average cholesterol level in the UK is somewhere between 5.6 – 6.3 mmol/l (Ref 2) (216-244 mg/dl). The powers-that-be have decided that this should be 5mmol/l (193 mg/dl). This is like saying that the average height for a woman is 5’4” and we have decreed that it should be 5’1”. We could then stop the body from performing a natural function (growth) by administering drugs to stop growth hormones from doing their job. I trust that this analogy disturbs you. It is, however, frighteningly similar to what we are doing with attempts to lower average cholesterol levels.

6) “There’s no connection whatsoever between cholesterol in food and cholesterol in blood. And we’ve known that all along.” Ancel Keys

Dietary cholesterol is only found in animal foods – meat, fish, eggs and dairy. Ancel Keys spent the 1950s feeding humans high levels of animal foods to see if dietary cholesterol had any impact on blood cholesterol levels. He concluded unequivocally that it did not. He never deviated from this view. While exonerating cholesterol, Keys also exonerated animal foods at the same time – and any substance contained therein. If large intakes of animal foods have no impact on cholesterol levels, then neither animal foods per se or any component of these foods (water, protein, cholesterol, saturated or unsaturated fat) have any impact on cholesterol levels!

Unaware of this irrefutable logic, diet ‘experts’ will tell you that saturated fat raises LDL and unsaturated fat raises HDL. They won’t tell you how. I have yet to find a biochemist who can explain how this can happen – let alone that it does. As every food that contains fat contains all three fats (saturated, monounsaturated and polyunsaturated) you cannot consume any food that has saturated and not unsaturated fat, or vice versa.

Even if the very small 3 grams per 100 grams of unsaturated fat in sirloin steak (Ref 3) could raise HDL and even if the even smaller 2 grams per 100 grams of saturated fat in sirloin steak could raise LDL – where would this leave our insolvable equation?!

The US dietary guidelines are due to be re-issued this year. The draft report announced in February 2015 that “cholesterol is no longer a nutrient of concern” (Ref 4). It never was you Muppets!

7) Low cholesterol is associated with higher mortality. High cholesterol is associated with lower mortality

I have analysed cholesterol levels and death rates for all 192 countries for which the World Health Organisation has data. You may need to read this carefully. The lower the cholesterol levels, the higher the death rate; the higher the cholesterol levels, the lower the death rate. This holds for men and women and for heart disease deaths and total deaths from any cause – for all the countries in the world. Knowing how utterly vital cholesterol is to human life, this makes complete sense (Ref 5).

8) Follow the money

Why would humans put so much effort into stopping the body from doing something that it is designed to do – make cholesterol?

Statins are drugs that impair the body’s production of cholesterol. One statin alone, Lipitor, has been worth $125 billion to Pfizer since 1997 (Ref 6). This statin is the most lucrative drug in the world. It is not the only statin.

Thankfully statins don’t work perfectly. If they stopped the body producing cholesterol altogether they would have a 100% death rate.

An entire low-fat spread industry, worth billions, has emerged simply by adding plant sterols to margarines because the brainwashed public will buy anything with “cholesterol lowering” properties. These plant sterols compete in the human body with human cholesterol and the overall impact on heart health is serious (Ref 7). I trust my body to make the cholesterol it needs. I’m not going to replace this with a foreign compound.

Back to the dinner party: While my healthy heart sank at the nonsense being asserted by intelligent acquaintances, there was an upside to their naive acceptance of propaganda: When the cheese course arrived, there was plenty to be enjoyed by the enlightened!


Ref 1:

Ref 2:

Ref 3:

Ref 4:

Ref 5:

Ref 6:

Ref 7:

Posted in Conflict, Gov. Policy, Media comments, Research
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Butter or margarine?

Another paper has been produced by the Harvard team, which likes to analyse data for associations between food and health. This one is entitled “Saturated Fats Compared With Unsaturated Fats and Sources of Carbohydrates in Relation to Risk of Coronary Heart Disease: A Prospective Cohort Study”.

The researchers have looked at data already collected for two large studies: the Nurses’ Health Study (84,628 women) and the Health Professionals Follow-up study (42,908 men). The nurses were followed from 1980 to 2010 and the men from 1986 to 2010. All were free from diabetes, cardiovascular disease and cancer at baseline. Diet was assessed by a food frequency questionnaire every four years i.e. not very accurately.

The study results were that there were 7,667 incidents of coronary heart disease (CHD) in 24 – 30 years of follow-up. The results reported that:

Higher intakes of polyunsaturated fat (PUFAs) were significantly associated with a lower risk of CHD. Comparing the highest with the lowest quintile (fifth) gave a hazard ratio (HR) of 0.80 (0.73 – 0.88).

Higher intakes of carbohydrates from whole grains were significantly associated with a lower risk of CHD. Comparing the highest with the lowest quintile gave a hazard ratio (HR) of 0.90 (0.83 – 0.98).

Higher intakes of carbohydrates from refined starches/sugars were associated with a higher risk of CHD. HR was 1.10 (1.00 – 1.21).

The team then went on to claim that replacing 5% of energy intake from saturated fats with equivalent energy intake from PUFAs, monounsaturated fats or carbohydrates from whole grains was associated with a 25%, 15% and 9% lower risk of CHD respectively.

The overall conclusion of the study was “Our findings indicate that unsaturated fats, especially PUFAs, and/or high-quality carbohydrates can be used to replace saturated fats to reduce CHD risk.”

Issue 1

The first point to always remember is that this is association, not causation. Could it be the case that people who eat more fish (PUFAs) and/or eat more cous cous (whole grains) are generally healthier than those who eat fries and burger buns? This would make PUFA and whole grain consumption a MARKER of health, not a MAKER of health.

Issue 2

The numbers are always presented as relative risk, which is misleading and should not be done. Responsible researchers present absolute risk, full stop.

There were a total of 127,536 people studied. There were 7,667 incidents of CHD over a 24-30 year period (use 27 as an average). The chance of any person having an incident in any one year was 0.22% (about 1 in 450 people). Given that the nurses were 34-59 in 1980 (and therefore 64-89 in 2010) and the men were 40-74 in 1986 (and therefore 64 – 98 in 2010), I’m surprised that the incident rate wasn’t way higher than this. And I bet it was massively correlated with age, as heart disease always is.

The data

Table 1, baseline information, was quite interesting. It presented basic data about the participants in the five quintiles of saturated fat (SFA) intake, from lowest to highest. This informed us that those in the highest SFA group consumed almost double the total fat of the lowest SFA group and almost double the monounsaturated fat (MUFA) of the lowest SFA group. The highest SFA group also consumed almost double the trans fat intake of the lowest SFA group. I expect this adversely affected the health of the highest SFA intake group. This also tells me that the highest intake SFA group were eating processed food – another confounding issue.

Table 1 also told us that total carbohydrate intake ranged from 34.2% of energy intake (for the highest fat intake women) to 55.1% of total energy intake (for the lowest fat intake men). The carb intake from whole grains was as low as 0.72% – 1.2% of daily calories for the women and slightly higher at 2-5.2% for men. The whole grain results have been calculated on a tiny base, therefore.

The three key results presented above (on PUFAs, whole grains and refined carbs) came from Tables 2 and 3 in the paper. Table 2 also found the following, but this wasn’t included in the findings:

Higher intakes of total fat were significantly associated with a lower risk of CHD. Comparing the highest quintile (fifth) with the lowest quintile gave a hazard ratio (HR) of 0.88 (0.80 – 0.96).

Higher intakes of trans fat were significantly associated with a higher risk of CHD. Comparing the highest quintile (fifth) with the lowest quintile gave a hazard ratio (HR) of 1.20 (1.09 – 1.32). This was the single most significant result of the paper, but not mentioned in the press release or the abstract.

Higher intakes of saturated fat were (not statistically significantly) associated with a lower risk of CHD. Comparing the highest quintile (fifth) with the lowest quintile gave a hazard ratio (HR) of 0.93 (0.82 – 1.05).

The swapping sat fat for something else bit

The researchers estimated that the effect of replacing 5% of energy intake from saturated fats with equivalent energy intake from PUFAs, monounsaturated fats or carbohydrates from whole grains was associated with a 25%, 15% and 9% lower risk of CHD respectively.

First of all – that relative risk applies again. Remember that the incident rate for any person in any one year was 0.22%. Even if we take these relative risk estimates at face value, the incident rate would be 0.17%; 0.19% or 0.20% vs. 0.22%. Not exactly hold the front page now eh?

Second – replacing 5% of energy intake from saturated fats may not sound like much, but it’s huge (it’s not 5% of 9.6% – it’s taking 5% away from 9.6%). The intake of saturated fat (Table 2) ranges from 9.6% to 16.9% of total energy intake. The lowest quintile would need to more than halve saturated fat intake (from 9.6 to 4.6%) and the highest quintile would need to reduce it by approximately one third (to 11.9%).

Third – what would people actually be cutting back on if they cut saturated fat significantly? Figure 3.4, page 26, of the 2010 US dietary guidelines shows that the main sources of saturated fat are processed food: pizza; grain-based desserts; dairy desserts (ice cream); KFC; hot dogs; burgers; tortillas; candy; potato chips etc. Butter accounts for 2.9% of saturated fat sources and milk 7.3%.

Do you think health would improve if people halved their intake of saturated fat by halving their intake of this kind of junk? Of course it would. Would health improve by removing eggs, meat and dairy products from grass living animals from the diet? Quite the opposite.

The press release “Butter is not back” is therefore an inaccurate, misleading, cheap shot from a university that should know better. Doing this gave the ‘Harvard kings of association nonsense’ the headline they were looking for “Butter isn’t better than marg”.

Remember the most significant, not-reported, result in the whole paper? The one about transfats? Check out how liquid vegetable oils are processed into an unnaturally solidified butter-like substance and you’ll realise how dangerous this press release was.

What do we take away from this?

Sensible dietary advice remains unchanged – eat real food; don’t eat processed food. Butter, churned from natural food sources, is far better for you than hydrogenated (or some other solidifying process), bleached, deodorised, emulsified, coloured, gunge (a.k.a. margarine). Additionally: association studies, which selectively report relative risk, especially those that emanate from the Harvard ‘got it in for butter’ team are potentially bad for your health.

Posted in Ingredients, Media comments, Research
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Coca-cola, exercise & conflicts

The last couple of weeks have seen Coca-Cola in the news quite a bit. Coca-Cola has been having a tough time recently. This summer’s business news reported that revenues for the past year (2014) were down $2 billion from 2012 figures (although what’s a couple of billion when you’re still getting $46 billion?!)

The exposé

It looks like the NY Times was the first newspaper to break the latest story. Anahad O’Connor was the journalist who reported that Coca-Cola was funding ‘scientists’ to reiterate the message to focus on exercise, and not calorie intake, in the war on obesity.

One of the tools in this collaboration is a new organisation called the Global Energy Balance Network, which has the mission “healthier living through the science of energy balance.” Their vision is a world in health energy balance. For this, read ‘a world in which Coca-Cola sales stop falling, but human beings get off their lazy backsides to burn off the calories in those cans of Coca-Cola’. How they explain the fact that calorie-free, diet drinks are associated with long term weight gain/waist increase, I know not.

When asked why the web site was registered to Coca-Cola, the President of the Global Energy Balance Network (GEBN) replied that the group’s members didn’t know how to register a web site. That is probably the scientific equivalent of a child being caught with their hand in the cookie jar saying “it wasn’t me”! Even the GEBN site admits: “GEBN has received support from… blah, blah, blah… and an unrestricted gift from The Coca-Cola Company”. How kind of Coca-Cola to help these ‘scientists’ with their web site and to give them unrestricted funds at the same time.

The four key names listed on the GEBN website are James Hill; Steven Blair; Gregory Hand and John Peters. Shame on all of them for being industry whores (no – that’s not too strong a word), while trying to masquerade as scientists. The NY Times discovered that Coca-Cola donated $1.5 million in 2014 to launch the GEBN organisation. It can’t cost much to run a web site that Coke set up, so I wonder how much of the unrestricted funding is personally enjoyed by these four puppets? Anahad O’Connor further discovered that Coca-Cola provided approximately $4 million in funding to two of the GEBN founding members: Steven Blair and Gregory Hand. Coca-Cola clearly chooses its targets well, as Steven Blair’s work has formed much of the basis of US federal guidelines on physical activity.

Blair also got a ‘money-can’t-buy’ reward from Coca-Cola. He was invited to carry the Olympic torch at London 2012. (Am I the only one wondering if Blair is just too darn lazy, or has he been having too much of his sponsor’s produce?!)

Coca-Cola’s relationships

Coca-Cola’s relationships with obesity and health organisations are widespread. They are a premier sponsor of the American Dietetic Association. This is additionally worrying in America as dietitians have a legislated monopoly on giving dietary advice – check out their other sponsors in case you ever wondered where American official dietary advice comes from.

Coca-Cola is a sustaining member of the British Nutrition Foundation. The National Obesity Forum “was secretly paid £50,000 by Coca-Cola to promote low-calorie sweeteners”. The Association for the Study of Obesity has received Coca-Cola funding in the past.

The International Life Sciences Institute (ILSI) describes itself as “a nonprofit, worldwide organization whose mission is to provide science that improves human health and well-being and safeguards the environment”. ILSI receives its funding from its industry members, governments, and foundations. The president of the ILSI is Rhona Applebaum representing The Coca-Cola company USA.

The Scientific Advisory Committee on Nutrition (SACN) recently published a report on carbohydrates and health. As this blog pointed out at the time, the chair of this working group is Professor Ian MacDonald, and his research interests include nutritional and metabolic aspects of obesity, diabetes and cardiovascular disease. An excellent candidate for chair you would think, except that the SACN 2008 annual report lists Professor MacDonald’s declared interests as Mars Europe and Coca-Cola Europe.

The Olympics have long been a wonderful platform for Coca-Cola to promote their products to a global audience, as one of the official sponsors of the games. Coca-Cola’s association with sport and slim, athletic looking people, reinforces their desired message – drink Coca-Cola, exercise and you won’t get fat. As Coca-Cola says on its website, they are “proud to be the longest continuous corporate partner of the Olympic Games” – an involvement that dates back to the Amsterdam games of 1928.

Even the World Health Organisation is not immune. They were ‘outed’ in 2012 as a recipient of Coca-Cola’s profit.

And finally, the UK government promotes Coca-Cola as role model healthy eating. A red can of cola is prominently featured on the Eatbadly plate.

The defence

James Hill, President of the Global Energy Balance Network hit back by saying: “Funding from the Coca-Cola Company will help build the infrastructure for an international consortium of scientists and representatives from a variety of sectors dedicated to battling obesity. The food, physical fitness, healthcare and other industries all must play a role in the solution.”

I disagree. We will never solve the obesity epidemic by thinking that fake food can help. Fake food is the problem, not the solution. We finally made progress in the tobacco war, not by working with the cigarette companies, but by doing everything we could to legislate against them.

I found the Coca-Cola response far more honest (although ‘feet’ and ‘shooting in them’ came to mind). Dr. Ed Hays, Chief Technical Officer of The Coca-Cola Company wrote a statement to set the record straight. The key words of interest in this statement are these ones: “Our business strategy is for more people to enjoy our products more often…”

At last, something with which I agree. Coca-Cola is in business to make money; to maximize returns to shareholders. It is not Coca-Cola’s job to resolve the obesity epidemic. Never has been; never will be. In the fight against the obesity epidemic, Coca-Cola is the enemy, not a private army. We know this. Coca-Cola knows this. Their response to this unfortunate truth is to try to keep their enemies closer still. We need to keep ours as far away from our citizens as possible.

Posted in Conflict, Exercise, Obesity, Research

SACN report: Carbohydrates & Health

Seven years!

On Friday 17th July 2015, a report was issued by the Scientific Advisory Committee on Nutrition (SACN). This report was initiated seven years ago: In 2008, the Food Standards Agency and the Department of Health asked SACN to provide clarification of the relationship between dietary carbohydrates and health and to make public health recommendations.

Terms of reference

The Terms of reference of the working group were four fold. “To review:

1)    the evidence on dietary carbohydrate and colo-rectal health in adults (including colo-rectal cancer, irritable bowel syndrome, constipation) and in childhood and infancy;

2)      the evidence on dietary carbohydrate and cardio-metabolic health (including cardiovascular disease, insulin resistance, glycaemic response and obesity);

3)      the evidence on dietary carbohydrates and oral health;

4)      the terminology, classification and definitions of types of carbohydrates in the diet.”

It would have been far better to give an independent panel (we’ll come to conflicts) a free remit on food and health and then they may have been able to spot a connection between the change in dietary guidelines (1983 UK) and the concomitant epidemics of obesity and diabetes. They may also have been able to look at recommended micro nutrient intakes and worked out that the most nutrient dense foods are not ‘healthy whole grains’.

Overall summary and conclusions

Chapter 12 has the overall summary and conclusions. You can look at the whole report yourself. I’ve extracted key conclusions on carbohydrates and the health measures that fell within the terms of reference. The summary is presented for: total carbohydrate; sugars and sugar-sweetened foods and beverages; starch and starch rich foods; and dietary fibre.

Total dietary carbohydrate

12.8 “Overall, the evidence from both prospective cohort studies and randomised controlled trials indicates that total carbohydrate intake appears to be neither detrimental nor beneficial to cardio-metabolic health and colo-rectal health.”

i.e. we spent seven years looking at evidence on carbohydrates and we can’t say that it’s harmful or helpful. That’s quite funny – unless you’re the poor sod who funded all of this. Hang on a sec – that’s me, as a UK taxpayer!

Sugars and sugars-sweetened foods and beverages

12.9 “Prospective cohort studies indicate that sugars or sugars-sweetened beverage intake is not associated with the incidence of colo-rectal cancer. There is no association between the incidence of type 2 diabetes mellitus and total or individual sugars intake, but a greater risk is associated with a higher intake of sugars-sweetened beverages. There is insufficient evidence to enable conclusions to be drawn in relation to cardiovascular disease endpoints.”

i.e. observational studies clear sugar of all charges except that sugary drinks are associated with type 2 diabetes.

12.10 “Trials examining cardiovascular risk factors, inflammatory markers and risk factors for type 2 diabetes mellitus demonstrate no effects of increasing sugars intake. There is also insufficient evidence to assess the link between individual sugars and sugars-sweetened foods and beverages and cardiometabolic outcomes.”

i.e. what trial evidence we looked at clears sugar of all charges.

12.12 “Overall, there were very few studies on individual sugars, such as glucose, fructose or sucrose, which met the inclusion criteria for this report. Prospective cohort studies indicate that higher consumption of sugars and sugars-containing foods and beverages is associated with a greater risk of dental caries.”

i.e. there isn’t much evidence on sugar (that’s because research is funded where it can benefit the funder; the government should fund research into the health effects of sugar, but it doesn’t. It funds seven year coffee meetings instead!) The worst we can find is that sugar is bad for teeth. The latter was firmly established in the 1983 National Advisory Committee on Nutritional Education (NACNE) report, so there’s nothing new here.

Starch and starch-rich foods

12.13 “Prospective cohort studies indicate no association between starch and refined grain intake and cardiovascular disease endpoints and type 2 diabetes mellitus. There is a lack of evidence relating colo-rectal cancer and oral health to starch and starch-rich foods intake. There is insufficient evidence to draw a conclusion on the association between starch intake and weight gain.”

i.e. starch and even refined grains are also cleared of all charges. We don’t have evidence for starch and weight gain, so we have to let starch off for that one as well.

Dietary fibre

12.15 “Prospective cohort studies indicate that a diet rich in dietary fibre is associated with a lower incidence of cardiovascular diseases, coronary events, type 2 diabetes mellitus and colo-rectal cancer.“

i.e. we’ve seen an association between fibre intake and lower incidence of the conditions we were asked to look at. However, cohort studies can only suggest association – Randomised Controlled Trials are needed to show causation. And…

12.16 “Randomised controlled trials indicate no effect of (total, mixed) dietary fibre intake on cardiovascular or type 2 diabetes mellitus risk factors considered in this report.”

i.e. … proper intervention trials showed nothing. Zippo. Zilch.

12.19 “Overall, randomised controlled trials in adults indicate that supplementation with non-digestible oligosaccharides improved blood lipid concentrations, increased faecal mass and bacterial content. Resistant starch supplementation increased faecal mass and short chain fatty acid content. Polydextrose and polyol supplementation increased faecal mass.”

i.e. giving adults things that they can’t digest generates lots of poo.

Key Recommendations

I’ve not listed all recommendations. Because the fourth term of reference was about terminology and classification, some of the recommendations are about terminology and classification and this is pretty dull.

S.16 “It is recommended that the dietary reference value for total carbohydrate should be maintained at an average population intake of approximately 50% of total dietary energy.”

i.e. despite the fact that even an active person only needs c. 25% of their intake in the form of energy and that this can come from carbohydrate OR fat, we recommend that everyone has half their intake in the form of the only macronutrient for which we have zero requirement: carbohydrate.

S.18 “It is recommended that the average population intake of free sugars (Defined at end – Ref 1) should not exceed 5% of total dietary energy for age groups from 2 years upwards.”

i.e. people should have no more than 5% of their dietary intake in the form of sugar but, because all carbohydrates are, or break down into, sugar they should have 50% of their dietary intake in the form of sugar (S.16).

S.22 “It is recommended that the dietary reference value for the average population intake of dietary fibre for adults should be 30g/day.”

i.e. there is no evidence for the current recommendation of 18g/day but we will increase this substantially to another number for which there is no evidence: 30g/day. (There is big love for fibre emanating from this 384 page document – the word “fibre” appears 717 times. They clearly haven’t read “Fiber Menace”).

S.23 “It is recommended that the average population intake of dietary fibre for children aged 2 to 5 years should approximate 15g/day, for children aged 5 to 11 years 20g/day, for children aged 11 to 16 years 25 g/day and for adolescents aged 16 to 18 years about 30g/day.”

i.e. we’ve made up numbers for adults so why not make them up for children and teenagers too. Good luck parents with your little darlings literally full of cr@p.

Background on health outcomes (disease prevention)

Chapter 4 shares the headlines of what the committee (in various forms – people came and left over seven years) learned about each of the conditions they were asked to look at:

Cardiovascular disease

4.3 notes that atherosclerosis is influenced by elevated blood glucose. And what elevates blood glucose? Try carbohydrates.


4.5 shows the belief system held by the committee about obesity – not the insulin/hormone model of the thinkers in this field, but the classic greed and sloth model: “Obesity occurs when energy intake from food and drink consumption is greater than energy expenditure through the body’s metabolism and physical activity over a prolonged period, resulting in the accumulation of excess body fat.”

Type 2 diabetes

4.7 “It is important to identify which dietary aspects improve glycaemia, insulinaemia and insulin resistance in individuals with normal or moderately compromised glycaemic control to further elucidate the role of diet in the prevention of type 2 diabetes mellitus.”

It is important to identify!? I thought that was the committee’s job? I think you’ll find: dietary fat has no impact on blood glucose or insulin; protein has no impact on blood glucose and carbohydrate wrecks havoc with both blood glucose and insulin.

Colo-rectal health

The learnings here were presented in seven sections (4.8-4.14) – not one of which mentioned carbohydrate or sugar. Fibre was mentioned only once – in the context of “an intake of about 25g/day dietary fibre” will help defecation.

Oral health

About the worst they could say was (4.16) “Sugars in the diet exert an effect after eruption when the teeth are exposed to the oral environment.” Whatever that means.


The conflicts of interest among panel members long preceded this report. Channel 4 ran a programme on the 20th January 2014 highlighting the food industry funding received by “the chief scientist looking at the sugar question” – Professor Ian MacDonald of Nottingham University. Channel 4 Dispatches discovered that since 2012 he had resumed working for two food and drink giants: sitting on two advisory boards for Coca Cola and one for Mars. As the programme released noted: “He also receives funding from Unilever which is the world’s largest ice-cream manufacturer.”

Hannah Sutter did a fuller expose of other committee members here. Notice Jordan cereal – they’ll love the fibre love-in. Mars and Coca-Cola will be really happy that sugar has largely been exonerated and Sainsbury’s will be happy that 80% of the current aisles have been given a health tick.

You’ll have to search hard for the declared conflicts. I asked Public Health England and was directed to the annual report. Check out Annex 5.

The SACN report has a preface by Dr Ann Prentice, Chair of the Scientific Advisory Committee on Nutrition. Here are her declared interests. I’ve highlighted a few:

Action Medical Research; Aarhus University Hospital; Aquapharm; Arch Timber Protection; Boden Institute for Obesity; British Dietetic Assoc; BUPA Treasury; Cambridge University Hospitals; Christie NHS Foundation Trust; Coca Cola; Cranfield University; Danish Brewers’ Association; Diabetes UK; Electro Sci. Industries; European Molecular Biology Laboratory; HS Pharma; Institute of Brewing and Distilling; Ikon Informatics; Iron Therapeutics Switzerland AG; Kellogg Company; King’s College Hospital LLR-G5 Limited; National Safety Assoc; National Centre for Social Research; Nestle; Playerthree; Shield Holding AG; Thermo Fisher Scientific; Weight Watchers Int; World Cancer Research Fund; The Rank Prize Funds; Thrombosis Research Institute; UCL Consultants; Universitat Rovira; Weight Watchers; York Teaching Hospital NHS Foundation Trust; pSiMedica.

(I find myself wondering if any of those make toilet paper!)

Closing view:

My first and lasting thought is – why did this take seven years and 384 pages? It takes fewer than seven seconds and three words to issue sound dietary advice: “Eat real food!” (“All-bran doesn’t count”, may be helpful in the circumstances).

My other key points are:

1)      All carbohydrates are, or break down into, sugar. The report is littered with the words monosaccharides (saccharide meaning sugar), disaccharides (sugar), polysaccharides (sugar), fructose (sugar), glucose (sugar), maltose (sugar) … They must know that they are talking about sugars all the time – just sugars in different forms. Yet, the key recommendations can be summarised as “eat less sugar and eat more sugar.” I just don’t get it.

2)      There is no evidence for any of these recommendations:

–        50% of the diet in the form of carbohydrate sugars – why? Why not 5%? Why not 95%?

–        5% of the diet in the form of free sugars – why? Why not 10%? Why any?

–        18g of fibre had no evidence; 30g has no evidence. Why 30? Why not 10? Why not 50? Why not just tell people to eat food for the micronutrients they need and then fibre won’t get a look in?

3)      The sugar industry could barely have dreamed of such a favourable report, but then when your chair of the SACN and your chair of the SACN carbohydrate working group are/have been funded by Coca-Cola and Nestle and Coca-Cola and Mars respectively, the sugar industry should never have been that worried.

Ref 1: S.17 gives the definition of free sugars as: “It is recommended that the definition for ‘free sugars’ be adopted in the UK. This comprises all monosaccharides and disaccharides added to foods by the manufacturer, cook or consumer, plus sugars naturally present in honey, syrups and unsweetened fruit juices. Under this definition lactose when naturally present in milk and milk products is excluded.”

Posted in Conflict, Gov. Policy, Research

Chocolate & cardiovascular disease

On Tuesday 16th June 2015 we woke up to the news: “Two chocolate bars a day ‘reduce risks of heart disease and stroke‘”.

The claim for stroke and coronary heart disease together (what is termed cardiovascular disease – CVD) was a 14% risk reduction.

Here’s the full study (not sure it’s still on open view sadly – it was at the time). Table 3 is where they get the headline numbers from, for those interested.

I’m not going to do the usual association vs. causation and work out the absolute risk this time. I need a break from doing the same thing over and over and hopefully you feel the same!

What I will look at is four things: i) the implications of headlines like this ii) is there a plausible mechanism? iii) what could really be going on here and iv) a recent chocolate study that fooled the world.

The implications of headlines like this

The previous week’s headlines on nuts may make people think ‘I just need to eat a couple of brazil nuts a day and I can compensate for all the bad lifestyle choices I make…’ Following this story, people may be thinking ‘I can carry on eating two Mars Bars a day and not only is it not bad for me – it will reduce my risk of dying.’

That’s the implication of this headline, because there was no claim that very dark chocolate, with high cocoa content, was being measured here. Indeed the study noted (p7): “Milk chocolate was more frequently consumed than dark chocolate in this cohort; however, we still observed a reduced risk of CVD.”

This makes no sense. When researchers find something, they have to offer what is known as a plausible mechanism (a sensible explanation for how, in this case, confectionery might be able to lower CVD risk).

Is there a plausible mechanism?

The attempt to offer a plausible mechanism can be found in the “Discussion” part of a paper and the discussion in this one is well worth a read. First, the researchers explore the limitations of dietary questionnaires, which are known to be very unreliable. You can see this for yourself – try to write down now everything you’ve eaten for the past 7 days and see how accurate you think it is. Bearing in mind you will be more likely to think it is accurate because you will trust your memory. You are more likely to remember actual meals than grazing, snacking and leftovers.

Option 1:

The discussion claims that under-reporting occurs “particularly among women and participants who are obese.” No judgement! The discussion continues by suggesting that sweets and snacks may be less likely to be declared by those with greater CVD risk such as the obese and physically inactive. So now ‘women; fatties and couch potatoes’ are being singled out for under-reporting!

Being judgmental would have some scientific validity if it were true. Under-reporting generally does not offer a plausible mechanism for the observed link between chocolate consumption and incidence of CVD unless – as the researchers note – those with greater CVD risk under-report. (If those with greater CVD risk under-report, then those with lower CVD risk look like they eat relatively more). If this were the case, we would expect the baseline characteristics of the lowest chocolate intake group to show a higher BMI and lower activity. There is some difference in activity levels (18% active in the lowest intake group vs 20% active in the highest intake group) but no difference in BMI (average BMI of 26 in all groups).

Option 2:

Is it the case that chocolate has some nutritional properties that would reduce the risk of CVD? The researchers did explore the dark vs. milk chocolate issue – that dark chocolate has been found previously to be the one with benefit. They suggested that not only the flavonoids in chocolate (more abundant in dark chocolate), but also other compounds possibly related to milk constituents such as calcium and fatty acids may provide an explanation for the observed association. No evidence was found for any great properties of confectionery, however, and this would need to be countered by the substances in confectionery known to be unhealthy – like sugar, sweeteners, additives, vegetable oils and possibly hydrogenated fats.

That was about it for possible explanations, leading the researchers to conclude: “… this observational study cannot provide evidence on the potential causality of the observed association.” i.e. we’ve explored a few options, but we don’t have a clear plausible mechanism.

If a study found that people who support Manchester United wear red socks, this would have a greater plausible mechanism than Mars Bars reduce your risk of strokes!

What could really be going on here

I always start with baseline characteristics (Table 1) when I look at studies like these and one line jumped out immediately. The chocolate consumption was divided into five, fairly evenly sized, groups of approximately 4,000 people in each. The name for one of any five groups is “quintile”. The lowest quintile (lowest intake of confectionery) had a 4.6% incidence of diabetes. The highest quintile (highest intake of confectionery) had a 0.7% incidence of diabetes.

The lowest quintile was in fact the group of all the people consuming no chocolate whatsoever. Their daily intake was zero grams of confectionery. The immediate obvious thought is – people with diabetes don’t eat confectionery. They would be mad to do so. The 0.7% of people with diabetes in the highest intake group are the ones risking their health.

The researchers showed that they too had spotted this with the following comment in the discussion: “It is possible that part of the observed association could be explained by reverse causality in that people with a higher risk profile, including those with obesity, diabetes mellitus, or prevalent CVD, eat less chocolate-containing foods than people who have a perceived healthy risk profile.”

That would be my most obvious “what’s really going on here”. “People with diabetes avoid confectionery.” As a finding, that would hardly grab the headlines.

Talking of headline grabbing, it was very interesting to note that the average intake for the highest quintile was 24.9 grams per day. That’s half a Mars Bar – not two bars. Why the discrepancy? The range of consumption in the top group was from 16 to 99 grams per day. That’s a third of a Mars Bar to two Mars Bars. This was presented as the more headline grabbing “two chocolate bars a day”. “Half a Mars Bar” would not have had the same effect, I guess.

The chocolate study that fooled the world

It was somewhat unfortunate for this Scottish study that it came on the back of a scam that went viral on the internet. In December 2014, a journalist called John Bohannon was approached by a German TV reporter called Peter Onneken. He and his colleague, Diana Löbl, were working on a documentary film about the junk-science diet industry. They set about doing a genuine clinical trial with the end in mind of a headline “Chocolate helps weight loss”.

A GP in on the scam ran the clinical trial. 5 men and 11 women were recruited (aged 19 to 67). One group followed a low carb diet. Another followed the same low carb diet with 1.5 oz (42g) of dark chocolate daily and the rest (the control group) made no change to their usual diet. The trial lasted 21 days.

You can immediately see that this will work. The low carb diet will make the difference and the dark chocolate has been added to this at such a level that it will have little adverse difference. Indeed, both treatment groups lost about 5lb; the control group lost nothing. The headline was achieved. (The link goes through just how the trial could be stacked in the researchers’ favour so that it would give statistically significant results).

The story was accepted by a journal! This was the journal. If you search on chocolate, or Johannes Bohannon, nothing is returned, suggesting that the humiliated journal has removed the original article. Here it is for posterity.

The story made the front page of Bild, Europe’s largest daily newspaper. The Daily Mail ran the story as “Pass the Easter Egg! New study reveals that eating chocolate doesn’t affect your Body Mass Index”. The headline is still there, but the text has been changed to cover a different, Australian, study. There is a note at the end of the article “A previous version of this article made reference to a German study which claimed a link between cocoa diets and weight loss. We have removed this reference as the study was subsequently revealed to be incorrect.” The study wasn’t incorrect – the study was perfectly correct – the reporting was poor. Thankfully not the UK team, but someone for Daily Mail Australia.

At least the Daily Mail has updated the story. As has the Huffington Post. Their original article: “Excellent news: Chocolate can help you lose weight” has been updated to “Chocolate weight loss study’s authors reveal report was fake (UPDATE).”

At the time of writing this post, The Express site had not revised the story “Chocolate accelerates weight loss: Research claims it lowers cholesterol and aids sleep”. The original article is still up quoting Johannes (not John) Bohannon, “research director of the nonprofit Institute of Diet and Health” (the ”Institute of Diet and Health” was also made up for the scam.)

The Times of India is still reporting: “Need a ‘sweeter’ way to lose weight? Eat chocolates!”.

The final thought

We clearly need to apply a common sense filter to all media reports about nutritional studies. Will two brazil nuts a day extend your life? No. Will two Mars Bars a day reduce your risk of cardiovascular disease? More likely the opposite. Will chocolate help you to lose weight? Sadly not! Will there be another nonsense nutritional study before next week? You can bet your life on it.

Posted in Ingredients, Obesity, Other Diets, Research
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The British Nutrition Foundation, Food Giants and our Children

We had dinner with friends recently – the proud parents of 11 and 13 year old boys. Mum could not wait to share her outrage that she was being ‘told off’ by school staff for not putting bread or snacks in the boys’ lunch boxes.

Both boys are the picture of health. They have grown up eating real food. They don’t want bread or sugary cereal bars. They want Parma ham, goat’s cheese and olives. They’re OK with berries and cream, but would choose meat over fruit any day. The only issue I see with this diet is expense and expectations. Developing a penchant for fillet steak and scallops, before reaching teenage, comes at a purse cost and sets the boys up for a shock when they leave home and pay their own bills.

Our mum friend also shared that her 11 year old had just done ‘cooking’ at school. He was asked to take in a pre-made flan base, a tin of custard and a tin of pineapple rings – they were going to ‘make’ a flan. I tweeted this and Twitter came back full of similar stories – bring in a jar of pasta sauce as we’re ‘making’ pasta tomorrow. Bring in some chopped chicken pieces and a jar of curry sauce, as we’re ‘making’ curry. One mum said on twitter that they should be called “stirring” lessons, not cooking lessons!

I was chatting to a GP about this, who was similarly alarmed by the appalling messages being given to young people that she is having to counter in her work with children. Following our conversation, I looked into how it could be that school staff felt that they had such a mandate to impose dietary advice. It turned out to be a very interesting exploration and a huge thanks to Jon Ungoed Thomas at The Sunday Times and Justin Stoneman for their investigation leading to this article on Sunday 24th May 2015.

The ‘eatwell’ plate

The ‘eatwell’ plate (what I call the eatbadly plate) was launched at a press release on Sunday 16 September 2007. 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. We’ll come to the British Nutrition Foundation soon.

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 newly formed Food Standards Agency. The FSA web site details 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)”. May I suggest that 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.

Everything starts with this plate. The link to the NHS web site confirms that the plate “doesn’t apply to children under the age of two” but, “Between the ages of two and five, children should gradually move to eating the same foods as the rest of the family, in the proportions shown on the eatwell plate…” From the age of two, therefore, the eatbadly plate is the role model for healthy eating.

If you look at the detailed advice offered, you can see that the carbohydrate dominant advice starts from the minute babies put anything other than breast milk or formula in their mouths. From six months, first foods are advised to be “mashed or soft cooked fruit and vegetables like parsnip, potato, yam, sweet potato, carrot, apple or pear… Or soft fruit like peach, melon, soft ripe banana or avocado … Or baby rice or baby cereal mixed with your baby’s usual milk.” Carbs, carbs, carbs, carbs and more carbs.

The advice at 8-9 months looks remarkably like the eatbadly plate: “Your baby’s diet should consist of a variety of the following types of food: fruit and vegetables; bread, rice, pasta, potatoes and other starchy foods; meat, fish, eggs, beans and other non dairy sources of protein and milk and dairy products.” Only the junk segment is not mentioned – Mars Bars can come later eh I guess.

Parents have also contacted me to say – not only are they incensed by school staff telling them how to feed their own children, they get pretty furious when their little ones come home full of news about this plate – having been taught about it at school. One even said “Mummy – you’re wrong – we should be having pasta for tea.”

How has this plate become embedded in our children’s education?

The national curriculum

The British Nutrition Foundation (BNF) worked with the Food Standard Agency (FSA) – before the FSA was relieved of its food advice duties – to embed the eatbadly plate in the national curriculum. As this web site informs us, in 2007, the FSA and BNF launched Core Food Competences for children aged 5-16 years.

The site further tells us that the BNF initiated a review of the original framework – along with Public Health England (PHE), FSA Northern Ireland, FSA Scotland and the Welsh Government. The updated framework can be seen here.

The core competencies are set out as follows:

By the age of 7, children should:… be aware that we all need a balanced and varied diet to grow, be active and maintain health, and that we need to eat more of some foods than others, e.g. as depicted in the eatwell plate.”

By the age of 11, children should: … make food choices based on the current healthy eating advice and understand that a healthy diet is made up from a variety and balance of different food and drinks, as depicted in the eatwell plate.”

By the age of 14, children should: … use current healthy eating advice to choose a varied balanced diet for their needs and those of others.” [my note – presumably we no longer need to reference the eatbadly plate – it would be so ingrained by now.]

By the age of 16, children should: … be able to apply current healthy eating recommendations, and understanding of people’s needs, to their own diet and those of others, e.g. before and during pregnancy, breastfeeding.” [my note – remember – the eatbadly plate is for everyone for every life stage.]

The British Nutrition Foundation

When I do presentations about conflicts of interest, the slide that gets the biggest gasps is the British Nutrition Foundation list of members. Here it is:

British Nutrition Foundation Conflicts

The members of the British Nutrition Foundation are the who’s who of the fake food and drink world from Tate & Lyle to Coca-Cola with everything from Weetabix to McCain (oven chips) in-between. Most of the major UK grocery retailers are also members – even M&S, but then they are one of the worst for placing sweets at child eye level at checkouts, so we shouldn’t be surprised.

The BNF initiates a review of the school nutrition core competencies and these are the organisations behind the BNF. That’s why the Sunday Times headline “Pupils taught cola is part of a healthy diet” now makes sense.

The BNF members and the eatbadly plate

The fake food companies just love the plate. Sugary cereal is prominently featured. Junk food has its own entire segment – only supposed to be 8% by weight/space on the plate – but that ends up being 22% of daily energy intake. Don’t worry about the fruit and veg a) we can promote baked beans as one of your five a day and b) all that volume only ends up being 6% of daily energy intake. 50% of dietary intake ends up being cereals, bread, etc – no wonder Kelloggs, General Mills, Weetabix, Greggs and Warburtons are right behind it. Real food barely gets a look in – nothing much on this plate to support farmers or fishers.

You should know that your healthy eating plate is anything but when it is featured on junk food web sites:

Nestlé want you to “Use the Eatwell plate to help you choose the right foods and proportions”.

Walkers are keen to show you how “The Government’s Healthy Eating guide, The Eatwell Plate, shows how snack foods can be part of an overall balanced diet”.

United Biscuits and the Institute of Grocery have a case study to show how “The healthy eating messages collated within the Best practice guide, such as the Eatwell Plate, are used in UB’s in-house Health and Nutrition training for employees as well as on their website”.

Kellogg’s want to make sure pregnancy features plenty of their products, as supported by the ‘eatwell’ plate.

And Sainsbury’s are only too happy to promote the ‘eatwell’ plate‘.

So parents, next time your pride and joys come home raving about bread and cereals, you may want to educate them about which foods really are the most nutritious and then give them a lesson about conflicts of interest. Clearly, this is something they need to know about from the age of 5.

Posted in Conflict, Gov. Policy, Media comments, Obesity
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Food Groups

There must be something about the number five and public health dietary advice. First the myth of five-a-day, then five times a week (that’s the exercise nonsense) and now five food groups.


The role model plate for healthy eating in the UK – the ‘eatwell’ plate – (or the eatbadly plate, as I call it) informs us that there are five food groups (my notes in blue):

– Fruit and vegetables; (fruit and vegetables are so different, they should never appear in the same category together)

– Bread, rice, potatoes, pasta and other starchy foods; (should be called “things that make you fat”)

– Milk and dairy foods; (milk is a dairy food, duh!)

– Foods and drinks high in fat and/or sugar; (this is not a food group; it’s a description and of two polar opposites) and

– Meat, fish, eggs, beans and other non-dairy sources of protein. (everything other than pure fats & sucrose contain protein, so virtually every non-dairy food falls into this category).


The US My Plate also thinks that there are five food groups – just different ones:

– Fruit;
– Veg;
– Grains;
– Protein; and
– Dairy.

My note – protein is a macro nutrient, not a food group. The other four food groups all contain protein (and fat and carbohydrate – just to list all three macro nutrients). This is ignorant in the extreme. I’ve dissected it here.


Australian children are also taught by Healthy kids Australia that there are five food groups – different ones again:

– Dairy;
– Fruit;
– Grain (cereal foods);
– Lean meats and poultry, fish, eggs, tofu, nuts and seeds; and
– Vegetables, legumes and beans.

My note – this is slightly better in that it doesn’t confuse a macro nutrient with a food group. However, lumping the most nutritious foods into one group and specifying lean meats is bad advice.

Food groups

There is no definitive list of food groups, so I’ll propose one:

– Meat;
– Fish;
– Eggs;
– Dairy;
– Vegetables;
– Fruit;
– Nuts & seeds;
– Legumes (beans, pulses, etc); and
– Grains.

That would make nine groups.

Meat could further break down into red meat, game, poultry. Fish could be categorised as oily fish, white fish, seafood. Starchy vegetables (potatoes, root vegetables) could be set aside from green leafy vegetables and so on. However, as basic food groups go, the nine work well.

As for fats: butter comes under dairy products; lard and meat juices are by-products of (cooking) meat; and oils can be derived from fruit (avocado, olive), seeds (sesame, sunflower), legumes (peanut), or nuts (coconut) etc and hence haven’t been assigned to a separate category.

Dieticians seem to get quite exercised about cutting out whole food groups (notwithstanding food groups having been wrongly defined). They don’t seem to mind when vegetarians cut out meat and fish or even when vegans cut out meat, fish, eggs and dairy. However, they don’t like people cutting out starchy foods – the things that make us fat.

Most people should be OK including some foods from all food groups. Some people (of Asian origin especially) have lactose intolerance and are well advised to avoid dairy.

The most nutritious food groups to choose from are meat/fish/eggs/vegetables/seeds and dairy if you are OK with it. We can get every nutrient we need from meat, fish, eggs, vegetables and seeds. We have no need for fruit, legumes and grains, although they can make enjoyable and versatile additions to our diet, if we can tolerate a higher level of carbohydrate.

There is some debate as to how ‘real’ some of these nine food groups are – dairy and grains are relatively recent additions to our diet. As a general rule, the longer we have been eating something (animals), the more natural/real it is as a food source.

I have yet to meet a human being who benefits from eating wheat (see Wheat Belly and Grain Brain to discover why), but wheat isn’t a food group – it’s one grain and there are better grain choices if you do eat grains, such as brown rice, natural oats, quinoa etc.

Note that sucrose is not in a food group anywhere – nor is much of the cr@p on the UK eatbadly plate – sugary cereal, cola, cakes, biscuits, baked beans, white bagels, chocolate, fruit in syrup, soya drink etc.

My dietary advice

My three key messages are:

1)     Eat real food!

Every food from the nine food groups should be eaten in its most natural form – meat with the skin/fat on; whole vegetables, not juice; whole fruits, not dried fruit or juice; brown rice, not white refined etc.

2)     Three times a day.

That’s an ideal maximum – if two meals work for you, fine. If your lifestyle demands four, OK. But, unless you are a cow, or want to be the size of one – STOP GRAZING!

3)     Manage carb intake.

If (1) and (2) don’t get you to natural weight and optimal health, manage your carb intake. If you are diabetic or very obese, manage your carb intake from the outset. The Harcombe Diet® gets people into the habit of having ‘fat’ meals (based on meat/fish/eggs/dairy) or ‘carb’ meals (based on legumes, grains, starchy veg, fruit). Non starchy veg can be eaten with any meal. Have no more than 1, possibly 0, carb meals a day if very carb sensitive/insulin resistant/diabetic/very obese (Note below).

I hope that this helps to provide a better definition of food groups and far more concise and effective dietary advice than you’ll get from the millions of pages of public health documents and non-science (aka nonsense).

(Note: diabetics should work with their doctors before making any dietary changes. A good doctor will work with a patient to reduce carbs and meds.)

Posted in Dieting, Gov. Policy, Obesity
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High protein diets, weight & death

On May 8th 2015, The Independent, and a few other newspapers, reported “High-protein diets increase risk of weight gain, study finds”.

The abstract can be found here. Sadly the full article is not on open view, but I’ve got a copy to dissect it for you below.

The PREDIMED study

In this study, the researchers used the PREDIMED (PREvencion con DIeta MEDiterranea) data to look at the association between protein intake and weight and then protein intake and deaths.

I’ve written about this study before. PREDIMED is actually a randomised controlled trial, rather than a population study, as the 7,447 participants were divided into three groups at the start of the study. Two groups were put on a diet called “The Mediterranean Diet”, which was described as follows: “The traditional Mediterranean diet is characterized by a high intake of olive oil, fruit, nuts, vegetables, and cereals; a moderate intake of fish and poultry; a low intake of dairy products, red meat, processed meats, and sweets; and wine in moderation, consumed with meals.” This is not what people actually eat in the Mediterranean. They eat a diet high in: meat, especially red and cured; fish, especially oily; dairy products, especially cheese; eggs; vegetables; and fruits in season. They also eat potatoes and white grains (bread, rice, pasta) and they drink red wine – not sure about the moderation!

The control group was put on a low-fat diet (that was an adverse intervention, not a control, therefore). The other two groups were put on this Fictitious Mediterranean Diet (FMD from now on) and they were also told to avoid soda drinks, bakery goods, spreads, red and processed meat (apart from the red meat, this is excellent advice). The low-fat diet group was told to have at least three servings a day of bread, pasta, potatoes, rice etc – those nicely fattening products that raise triglyceride levels. The FMD groups were told to have oily fish. The low-fat group was told to avoid it. One of the intervention groups was encouraged to add 50g or more of olive oil daily to their FMD and the other FMD group was given 30g of mixed nuts per person per day.

Of the 7,447 people in the study, 57% were women. The women were aged 60 to 80 and the men were aged 55 to 80. The participants had no previous cardiovascular disease at enrollment, but they were deemed “at-risk”, as only people with type 2 diabetes or at least three other “major risk factors” (smoking, obesity, family history of heart disease etc) were included in the study.

This particular study using PREDIMED data

7,216 of the original 7,447 subjects were included in this protein study. 231 people were left out for having extremely high or low energy intake and/or incomplete dietary data. The 7,216 people were placed into five groups in order of average energy from protein intake – low to high. There were 1,443 people in each group (1,444 in the middle group). The lowest protein intake group averaged 83 grams per day and the highest 96.6 grams, so we’re talking a couple of eggs difference between highest and lowest protein intake here, or 50 grams of tuna.

There were some striking differences in the five groups. They were similar for age, BMI and waist circumference, but the highest protein group were healthier for smoking and drinking: 72% of the highest protein group had never smoked vs 47% of the lowest protein group; 1.1% of daily calories came from alcohol for the highest protein group (HPG) vs 4.5% for the lowest protein group (LPG).

However, some other substantial differences were working against the HPG. Prevalence of diabetes was 60% in the HPG vs 37% in the LPG. Family history of cardiovascular disease was 25.1% vs 19.6%. 40% of the HPG were taking oral anti-diabetic drugs vs 24% of the LPG and three times as many of the HPG were taking insulin as the LPG. The HPG also did less activity than the LPG.

The energy intake of the five groups was one of the most striking differences: an average of 1,972 calories per day in the HPG and 2,453 calories per day in the LPG. The substantial difference in calorie intake impacts the percentage of energy from protein intake (the denominator effect for the mathmos). The article thus claims that the lowest calorie intake group was at greater risk of weight gain!

Model 1 in the paper adjusted for age, smoking, exercise, alcohol and similar lifestyles factors (and for the PREDIMED intervention!) Models 2 and 3 further adjusted for health conditions and medications, but they also played around with other macro nutrients (fats and carbs), as we’ll see.

After the baseline differences, the next interesting thing was that the study defined weight change as those who lost or gained ≥ 10% of body weight. That’s a lot in study terms. A weight change of 5% is more typically used as a measure. Everyone else was put in the “maintained weight” category. This high bar meant that, during a median follow-up of 4.8 years, 186 cases of weight loss were recorded and 149 of weight gain. So, the headlines about weight gain are immediately based on 149 people, not 7,447.

Then, of these 149 people who gained weight, 93 were in what was considered a normal protein intake range, 37 had protein intake lower than this and 19 had protein intake higher than this. Now we’re down to the headlines being based on 19 people. (This part of the paper looked at just three groups – low/normal/high – not the original five).

For the raw data facts, 2.1% of the lower protein group gained 10% or more of their starting body weight; 2.1% of the normal protein group gained 10% or more of their starting body weight and 1.9% of the higher protein group gained 10% or more of their starting body weight. The higher protein group thus had a lower incidence of weight gain (fractionally) than the other two groups.

When it came to losing 10% or more body weight, this was achieved by 2.6% of the lower protein group, 2.4% of the normal protein group and 3.5% of the higher protein group.

So the higher protein group had a lower incidence of weight gain and a higher incidence of weight loss. None of these results was statistically significant, but they make a mockery of the media headlines.

The one significant result

When protein intake alone was looked at, using the standard measure of grams of protein per kilogram of body weight (with data unadjusted or fully adjusted), not one significant result could be found for weight gain, or weight loss, or waist circumference increase, or waist circumference decrease. Nothing. Zippo. Zilch.

The researchers should have stopped there. Or reported that protein intake has no impact on weight or waist circumference either way when 7,216 people are followed-up for an average 4.8 years.

But no. They decided to adjust for fat intake, which allowed the claim that the higher protein intake must be at the expense of carbohydrate and they adjusted for carbohydrate intake, which allowed the claim that the higher protein intake must be at the expense of fat. They looked at all protein options possible (total protein intake, animal protein intake, vegetable protein intake, the ratio of animal to vegetable protein intake), for weight loss, weight gain, waist circumference increase, and waist circumference decrease. That’s a total of 128 different options that they looked at. Seven showed a significant difference and only one of these was reported in the abstract:

1) The one statistically significant finding reported in the abstract was that, when protein replaced carbohydrate the hazard ratio was 1.9 with the confidence interval being 1.05-3.46 – 1.05 being so close to the non-significant 1.0. (The confidence intervals are wide because of the very small numbers we’ve ended up with – 19 people).

2) The six statistically significant findings in the body of the article, but not the abstract or headlines, were all related to low intake of vegetable protein. They were that:

i) People with the lowest intake of vegetable protein were less likely to lose weight (in both the carb and fat ‘replacement’ models). The opposite didn’t help – people with higher vegetable protein were not more likely to lose weight.

ii) People with the lowest intake of vegetable protein were less likely to have a reduction in waist circumference. They were also less likely to have an increase in waist circumference. Again – this was the case for both the carb and fat ‘replacement’ models – making four statistically significant, but rather irrelevant and unexplained, results.


I haven’t repeated all of the above for deaths. The hazard ratios for deaths are presented in Table 2 of the paper. Let’s take the raw data again (Note below): There were 69 deaths (among 1,443 people) from any cause during the follow-up in the highest protein group (HPG). There were 95 deaths (among 1,443 people) from any cause during the follow-up in the lowest protein group (LPG).

If we play the association, relative risk game that is usually played, that could be presented as 40% higher deaths in the lowest protein group. The fact is that the absolute death rate in the HPG was 4.8% and it was 6.6% in the LPG. Cardiovascular death rates were 1.0% in the HPG and 1.7% in the LPG. Cancer death rates were 1.9% in the HPG and 2.6% in the LPG.

The researchers noted U-shaped patterns in the data (the middle group tended to be the low point and either side tended to be higher). Instead of comparing low protein intake with high, they compared everything to the middle group and then only reported how bad the high protein intake was. The low protein intake was arguably worse.

(Note – the adjusted models don’t make intuitive sense: smoking & alcohol work in favour of the HPG, but diabetes and meds – especially insulin – work against the HPG. Model 1 adjusts for the lifestyle factors, so I would expect the results for Model 1 to swing against the HPG – and they do. However, Models 2 and 3 further adjust for medical conditions and medications, so I would expect these to swing back in favour of the HPG and they don’t).


The actual study conclusion was “Higher total protein intake, expressed as percentage of energy, was significantly associated with a greater risk of weight gain when protein replaced carbohydrates.”

The headline should have been: “There is not even an association between protein intake, weight gain, weight loss, and/or change in waist size.” The supplementary headline should have been “When we play with numbers to try to get a result, we still can’t find anything in 121/128 cases and the other 7 are nothing to write home about.”

Or: “People with low protein intake are 40% more likely to die.” ;-)


Protein is in all foods except pure fats (oils/lard) and pure carbohydrate (sucrose). Protein is in lettuce, apples, bread, steak – every other food. There is no pure protein food on the planet. Skinless chicken breasts and white fish are the closest we get to being able to eat protein alone. Hence eating more protein in a natural (real food) diet means eating more carbohydrate (beans, pulses, fruits, vegetables, potatoes, oats) or more fat (meat, fish, eggs) or both (dairy products, nuts, seeds). Eating more protein unnaturally would mean removing the skin from chicken – or worse – protein shakes etc.

I do think that an unnaturally high intake of protein is potentially harmful. Protein shakes etc will place unnecessary strain on the kidneys, deplete vitamin A and may have long-term harm. However, unnaturally high protein diets have a metabolic advantage (thermic effect of nutrients) and would be expected to have a positive impact on weight while having a negative impact on health. Death within 4.8 years I would find highly unlikely, unless the protein intake was extreme, which was not the case in this study (83-96.6 grams/day).

That’s a general point – it’s not what this study is about. I’m afraid that this study reinforces a trend that has been taking place for some time – researchers playing with numbers and over-emphasizing any slightly significant finding, while ignoring the truer picture that there was no finding, to grab headlines. The bar for nutritional studies needs to be substantially raised and adhered to.

Posted in Media comments, Other Diets, Research
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Being overweight reduces dementia risk?

The headline on Friday 10th April 2015 was “Being overweight ‘reduces dementia risk’”. The original article is here. Sadly on pay per view only, so it cost me $31.50 for 6 pages.

I tweeted early on Friday morning “Being overweight may be associated with reduced incidence of dementia but ‘reduces risk of’? Really?”

I couldn’t see a plausible mechanism and nor could the researchers, who confessed to having been “surprised”. As the BBC article noted, “Any explanation for the protective effect is distinctly lacking.”

However, twitter being the marvel that it is, served up a plausible mechanism, from a Seattle physician, within minutes of my tweet. We’ll get the study and the usual pitfalls out of the way first and then see what could really be interesting about this finding.

The study

The study was the usual “let’s examine lots of data” format, which is the most common method for grabbing headlines at the moment. Data from almost two million people (1,958,191) was reviewed. The average age at the start of study was 55. The average length of follow-up was 9 years. Hence this was a huge review with almost 20 million person years of data.

There were 45,507 cases of dementia recorded during the follow-up period. The paper presented this as 2.4 cases per 1000 person years (i.e. their calculation, not mine).

BMI (body mass index) was recorded at the start of the study for each participant. This measurement was taken some time between 1992 and 2007 – when the participants reached the age of 40 or older. We know nothing about what happened to weight over the average nine years of follow-up. Those who were underweight at the start of the study could have been obese by the time they developed dementia and vice versa – we know none of this.

The study confirmed that dementia was strongly associated with age and so age needed to be adjusted for in the analysis of the data.

The numbers in the newspaper headlines came from Table 2 in the paper and from the top set of numbers (adjusted for age and sex only). However, even when the researchers adjusted for everything they could think of (smoking, diabetes, medications, alcohol etc) the numbers hardly changed, so we can see these as valid figures.

The Table 2 numbers took normal BMI as “healthy weight” and gave that a reference base of 1.0. They then presented the incident rate of dementia, relative to 1.0, as follows for the different weight categories:

– Underweight (BMI <20) = 1.34 (this was where the “34% higher risk” headlines came from).

– Overweight (25-29.9) = 0.82 (this was where the “18% lower risk” came from).

– Obese (30-34.9) = 0.76 (this was where the “24% lower risk” came from).

– Very obese (BMI >40) = 0.71 (this was where the “29% lower risk” came from).

The common pitfalls

We should know these really well by now:

1) This is association not causation.

We may have observed that people who wore red socks to the baseline health check went on to develop dementia. We should not jump to the conclusion that wearing red socks increases the risk of dementia.

2) This is relative risk, not absolute.

The fact that there were 2.4 cases of dementia per 1,000 person years means that I’m not worried about any of this already. Applying this 2.4 number to the incident rate in each of the different weight groups, results in the following:

– The incident rate for underweight people becomes 3.2 cases per 1,000 person years.

– The incident rate for overweight people becomes 2.0 cases per 1,000 person years

– The incident rate for obese people becomes 1.8 cases per 1,000 person years

– The incident rate for very obese people becomes 1.7 cases per 1,000 person years

2.0 per 1,000 person years vs. 2.4 per 1,000 person years suddenly doesn’t seem quite so dramatic, don’t you think? But those are the actual real, absolute, incident rates behind the headlines.

Possible things going on

It could be the case that more obese people died and were therefore not available for follow-up (and not alive to develop dementia). An interesting study on weight and mortality here was covered in a much more readable way by the brilliant Dr Malcolm Kendrick here. The study showed that obesity was associated with more deaths, but that being overweight wasn’t. Hence, this cannot serve as an explanation for this dementia weight finding, which showed that the incidence of dementia was lower with every increase in weight category they measured from underweight to very obese.

The researchers themselves offered the possible explanation that heavier people may have taken in more nutrients and that some of these may have had mind protection benefits. I’m not sure that there is any evidence for this (and they didn’t seem that convinced by it). When I heard the lead researcher on Radio 4 on Friday morning, he really did hold the view that he was surprised and couldn’t explain the findings.

The plausible mechanism

A Seattle physician, called Theodore Naiman, who tweets as @tednaiman may have been able to help the research team. In response to my “Really?” tweet, questioning plausible mechanism, he replied:

@zoeharcombe Obesity-resistant persons take more glycation damage hit as their adipocytes don’t protect them by sucking up all extra glucose.”

A quite excellent use of 140 characters! If you need a bit more explanation…

If we view the underweight, not unreasonably, as those most resistant to obesity – these are the people not storing excess glucose in fat cells. They are not laying down fat. It could be that they are underweight because they rarely ingest glucose. However, it is likely that the majority of this group do consume glucose, but their underweight status indicates that they are not storing it. The glucose still has to ‘go/stay’ somewhere and it can therefore be found/spend longer in other parts of the body, where we know sugar causes cell damage.

Conversely, the most obese people are extremely good at storing away excess glucose in fat cells. They may find this attribute undesirable, but it is actually very desirable for the body to ensure that potential glucose (glycation) damage can be minimised with glucose being whizzed away into fat cells very efficiently.

We know throughout evolution that the ability to store fat would have given a human a survival advantage. The fleshy people would out-live the lean people in times of scarcity. It would appear that the ability to store fat most efficiently may have benefit in today’s times of plenty – saving us from sugar damage to brain and body alike.

It doesn’t mean, therefore, that we should try to gain weight to avoid dementia. I did an interview with Radio Tees on Friday morning and the presenter, Mike, wondered if this were license to eat biscuits. No! The direction of causation – if this is the actual mechanism – would be that obese people would have natural dementia protection. The obesity would be the indicator that they have this protection – not the cause of it per se.

Now that’s plausible to me! Tiny absolute risk – but plausible!

Posted in Media comments, Obesity, Research
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Where does the 3500 calorie theory come from?

The simple answer is “I don’t know” and nor do any of the public health bodies/obesity organisations that use it, as this post comprehensively confirms. The “Prove it or stop using it” post invites anyone to source/prove the calorie formula. The challenge was first thrown out in my 2010 obesity book and still goes unanswered.

This post is to share the earliest reference that I have found to the formula (although it doesn’t actually state it). I’d be very interested in anything earlier that anyone can find and even more interested in proof. There is enough counter evidence already that I can guarantee that proof cannot and will not be found.

Lulu Hunt Peters (1918)

In a book called Diet and Health by Lulu Hunt Peters (1918),[i] Hunt Peters states “Five hundred Calories equal approximately 2 ounces of fat. Two ounces per day would be about 4 pounds per month, or 48 pounds per year. Cutting out 1000 Calories per day would equal a reduction of approximately 8 pounds per month, or 96 pounds per year.”

An article from the Chicago Daily Tribune (Sept 15, 1959) asserts “a pound of fat is lost whenever the body burns up 3,500 calories by diet or exercise”.[ii] The way that this is asserted, suggests that it is already a well known ‘fact’ by this date, but did Hunt Peters start it or perpetuate it?

A couple of extracts in Diet and Health make me think that it is plausible that Hunt Peters did effectively originate “The Calorie Formula”:

1)  On the opening page, Hunt Peters says: “I am sorry I cannot devise a key by which to read this book, as well as a Key to the Calories, for sometimes you are to read the title headings and side explanations before the text. Other times you are supposed to read the text and then the headings. It really does not matter much as long as you read them both. Be sure to do that. They are clever. I wrote them myself.” (Hunt Peters own emphasis in italics).

2)  Chapter 2 “Key to the calories” has the following: [Sidenote: Pronounced Kal’-o-ri]. So calories were so little known at the time, that Hunt Peters needed to tell people how to pronounce them. If only we had stayed so blissfully ignorant about calories, or at least had come to see them as fuel for the body – which is all that they are.

If Hunt Peters had the right to be proud of her ‘cleverness’ and if she really did break something revolutionary to the women of Los Angeles in 1918, we may indeed have one woman to ‘thank’ for “The Calorie Formula”, which is the foundation of weight loss advice to date. If anyone else knows of a reference earlier than 1918, I would be most interested for research sake, but it actually matters less from where this originated and more that it has held as ‘fact’ for almost a century and yet it cannot be proven to hold true.

p.s. I know the background to the estimated calories per gram (which are wrong) and how the 1lb is assumed to be 3500 (which is also wrong). I’m looking for the first reference to the calorie formula/theory (the two parts being: 1lb = 3500 cals; to lose 1lb you need to create a deficit of 3500 cals) or an earlier application of the theory – without actually stating it – than Lulu Hunt Peters. It’s a very specific statement, which has pervaded virtually all dieting literature and which millions, if not tens/hundreds of millions of people are following right now. And we know not from whence it came!

[i] Lulu Hunt Peters, Diet and Health (with key to the calories), published by Chicago The Reilly and Lee Company, (1918).

[ii] T R Van Dellen, “How to keep well”, Chicago Daily Tribune, (15 September 1959).

Posted in Dieting, Gov. Policy, Obesity, Research
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