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
Tags: , , , , , ,

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
Tags: , , , , ,

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
Tags: , , , , , ,

Worried about cholesterol and/or statins

The vast majority of comments I get on my blogs are about cholesterol and/or statins. I find myself saying the same things over and again, so this post is the one that I’ll now refer queries to – it should answer most of the worries that people seem to have. My top tip is: don’t have a cholesterol test and then you’ll have one fewer thing to worry about.

Worried about high cholesterol

Many of the comments start with people saying that they have high cholesterol. First of all – do you? Or are you part of the scam to make you think that your cholesterol is high because normal has been re-defined? This post may help.

If your cholesterol is anywhere on those normal charts (2-10 mmol/l = 77-387 mg/dl) – you may like to stop worrying.

You should also be aware that the blood cholesterol test doesn’t actually measure LDL (the thing they call ‘bad cholesterol’ – which is not even cholesterol – it’s a Low Density Lipoprotein) – they guess it. See point iv here. You should also be aware that even the total cholesterol, which they do try to measure, is known to be out by as much as 19%.

If you actually have high cholesterol (e.g. 10 mmol/l = 387 mg/dl or above) OR your cholesterol is high for you (i.e. relative to what you know yours normally is – your normal – not the made up normal), remember that your body makes cholesterol for good reason and consider the following: are you injured? stressed? pregnant? recovering from an operation? illness? Any of these will encourage your body to make more cholesterol.

Have you had a cholesterol test taken at the end of winter? in the heart of winter? Vitamin D is made by sunlight synthesizing cholesterol on the skin when you expose your skin to sunlight. Your cholesterol may simply be ‘high’ right now because you haven’t turned it into vitamin D (it’s the low vitamin D that will harm you – not the ‘high’ cholesterol – the high cholesterol can be a sign that you’re lacking vitamin D). Have another test at the end of the summer and make sure you give your body the chance to make some vitamin D with healthy sun exposure (not too much, not burning).

If you know that you have Familial Hypercholesterolemia (FH) – check out the section on FH on this blog post. It may give you a different perspective on FH. High LDL can be the symptom – not the problem – the problem can be the exact opposite of what is assumed – that LDL is not getting to the cells (including heart cells) where it is vitally needed.

Check out these charts too – read them carefully – yes HIGH cholesterol is associated with LOW deaths and LOW cholesterol is associated with HIGH deaths for men and women, CVD deaths and all-cause mortality. (It’s the same for saturated fat, by the way).


I’m the wrong person to ask about statins – that’s your decision. It’s the easiest decision in the world for me – a statin will never pass my lips. This may help explain my position – and the fact that I know the utterly vital role that cholesterol plays in the human body and I trust my body to do what it was designed to do WAY more than I trust pharmaceutical companies to forgo profit in my best interests.

You may also like to read this. If you are in the highest risk group possible (men of a certain age who have already had a heart attack), for every 100 of these men given statins for five years, 1.8 men will live, on average, an extra 6 months and 98.2 will gain no benefit. The intelligent thinking in the world of cholesterol is that any ‘benefit’ of statins for this small, very high risk group, results from anti-inflammatory properties of statins; the cholesterol reduction being a serious and unwelcome side effect.

To look at this another way, some September 2015 research showed that you can take statins for years and you might gain an extra 3 days. Again – likely an anti-inflammatory effect; the cholesterol lowering being a serious price to pay.

Talking of side effects, these are substantially understated and those who mention statin side effects are viciously attacked. In March 2014, The Guardian reported Professor Rory Collins as saying “We have really good data from over 100,000 people that show that the statins are very well tolerated. There are only one or two well-documented [problematic] side effects.” Myopathy, or muscle weakness, occurred in one in 10,000 people, he said, and there was a small increase in diabetes.

As a result of the fall-out from this attack on two doctors who dared to mention statin side effects, it was revealed that Professor Rory Collins’s CTSU team, working on statin (and other) studies, has received c. £268 MILLION from pharmaceutical companies that make statins. If you want to know about statin side effects, just read a patient leaflet – by law they have to be more honest than researchers who withhold side-effect data:

The patient leaflet for Lipitor – the most lucrative statin, indeed the most lucrative drug ever in the history of mankind, states the following:

“Common side effects (may affect up to 1 in 10 people) include:

inflammation of the nasal passages, pain in the throat, nose bleed

allergic reactions

increases in blood sugar levels (if you have diabetes continue careful monitoring of your blood sugar levels), increase in blood creatine kinase


nausea, constipation, wind, indigestion, diarrhoea

joint pain, muscle pain and back pain

blood test results that show your liver function can become abnormal

You may also want to google “Statin diabetes lawsuit” to see how that one is gathering pace in the US. Fancy type 2 diabetes with your statin?! Other statin side effects include loss of libido (hello boys?!), loss of energy, muscle fatigue, muscle aches, weakness, loss of memory, loss of cognitive ability – generally feeling that your get up and go has got up and gone – and taken your mind with it. Former NASA astronaut Dr Duane Graveline has written of his experience here and here.

Do also check the patient leaflet for the over the age of 70 caution. I don’t think many doctors are aware of this. If you’re wondering about whether or not you should be on a statin and you’re over the age of 70/approaching this age – even the leaflet will caution against this. That will be because HIGH cholesterol is known to be particularly associated with LOW deaths in more elderly people (and LOW cholesterol with HIGH deaths).

Watch this (just half an hour) to see a doctor tear apart the nonsense in the cholesterol, statins, dietary fat world.

More reading?

If you’d like more free reading, check out anything on cholesterol/statins on Dr Malcolm Kendrick’s site and/or Dr John Briffa’s site.

For books, check out The Great Cholesterol Con; The Great Cholesterol Myth; Ignore the Awkward; Fat and cholesterol are good for you; just for starters – there are many more.

I hope that this answers most of the queries!

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

Did a low fat diet beat a low carb diet for fat loss?

A story emerged on March 5th 2015 from the annual meeting of the Endocrine Society in San Diego. It was not widely covered, but James Gallagher, Health Editor for BBC online, wrote about it here and The Times picked it up (firewalled).

The study

The study presented at the conference was undertaken by Kevin Hall and colleagues working in Maryland, US. Hall has done some brilliant mathematical work looking at the 3,500 calorie formula.

The purpose of this study was to see if restricting fat or restricting carbohydrate, by the same number of calories, would have more impact on body fat lost.

The study involved 10 men and 9 women who were obese. The average age of the participants was reported as 24 in one part of the briefing paper that I saw and 34 ± 2 in another part. The average BMI was 36.

The participants were contained in a metabolic ward during the study, making this far more rigorous than any ‘free-range’ study, where subjects are expected to stick to a diet from home/work. For 5 days the subjects were given “the exact number of calories they needed to maintain their body weight” in the composition of 50% carbohydrate 35% fat and 15% protein. (This is slightly different to the US guidelines to have 55% carbohydrate, 30% fat and 15% protein, but the study was not designed to test current guidelines.)

For the following 6 days, the participants were randomly assigned to one of two groups where they received a 30% reduced-energy diet by having either their fat or carbohydrate intake restricted. Two to four weeks later (to allow everything to settle back to normal after the first experiment), the participants were readmitted and they repeated the same 5-day diet to maintain weight: 50% carbohydrate 35% fat and 15% protein. Those who had done the 6-day reduced fat diet in the first phase were put on the reduced carbohydrate diet, and those who had eaten the reduced carbohydrate diet were given the reduced fat diet.

This was what we call a “cross-over” trial therefore – all subjects did both interventions. This is an ideal design for this kind of short-term intervention, as it overcomes individual differences of some subjects responding better to one intervention or another. Everyone tried both interventions and so the individual responses are much compensated for.

The results

The results were presented as “Compared to the reduced carbohydrate diet, the reduced fat diet led to a roughly 67% greater body fat loss.” Wow – 67% – how impressive is that? Completely unimpressive as it turns out…

The calorie requirement established during the first five days of 50% carbohydrate, 35% fat, 15% protein was considered to be 2,720 ± 50 calories. This would be my first challenge. My weight is stable and yet my calorie intake is different every day to the next. I don’t see how a fixed calorie intake number can be established at all, let alone in five days.

Notwithstanding this, the study reduced calorie intake by 30% for the subjects for the next 6 days – the reduction to either come entirely from fat intake or entirely from carbohydrate intake.

If someone is having 2,720 ± 50 calories in the percentages 50% carbohydrate, 35% fat, 15% protein, they are having 1,360 carb calories, 952 fat calories and 408 protein calories. The study reported removing 790 ± 20 calories from both diets – all of these to come from carbohydrate intake for the LC group and all 790 ± 20 calories to come from fat in the LF group. This resulted in the following balance of macro nutrients:

The LC group ended up with a diet comprising 30% carbohydrate, 49% fat, and 21% protein.

The LF group ended up with a diet comprising 72% carbohydrate, 7% fat, and 21% protein.

The problems

You can immediately see one of the problems. This should have been called RC and LF – Reduced Carb and Low Fat. The fat intake at 7% is absurdly and unnaturally low; the carb intake at 30% is way higher than any genuine low carb diet. Hence this was not comparing a low carb with a low fat diet. It was comparing a reduced carb diet with an unnatural fat intake.

The body fat loss for the 6-day intervention was calculated as 394 grams for the low-fat group and 236 grams for the reduced-carb group. The difference is 158 grams – about the weight of an apple. However, 158 grams divided by the smaller of the 2 numbers (236) = 67% and that’s where the 67% comes from.

Even more disingenuous is the method of calculation. I wondered how body fat lost could possibly even be calculated to that degree of accuracy (because it can’t). The briefing paper shared the methodology: “The researchers measured the amount of fat eaten and the amount of fat burned, and the difference between them determined how much fat was lost from the body during each diet.”

What?! The researchers have assumed that dietary fat has no other use within the body – any eaten needs to be burned and that’s all that can happen. That is a completely invalid assumption. Fat is the most versatile macro nutrient to the body. It can be used for energy and it can (and is) used for the maintenance and growth of every cell in the body.

The low fat group consumed hardly any fat during their intervention – 135 calories of fat daily, which is about 15 grams. The reduced carb group maintained the same fat intake as in the weight maintenance phase – 952 calories = 106 grams. There was a 91 gram difference in daily fat intake. If we average the grams of fat claimed to have been lost over the 6 days, the LF group allegedly lost 66 grams a day and the RC group allegedly lost 39 grams a day. But the difference is more than three times accounted for by intake.

The low fat group consumed barely any dietary fat to be used for cell maintenance and repair. The entire fat intake of the restricted carb group could have been used up in body maintenance and growth.

Even if the calculation is as simple as grams of fat eaten – grams of fat burned = grams of fat lost, and it isn’t, we can reverse engineer the numbers to show that the reduced carb group were burning 145 grams of fat a day vs. 81 grams of fat a day being burned by the low fat group. So the headline could have been “reduced carb diet burns almost twice as much fat as low fat diet.”

Weight loss vs. fat loss

The headline could also have been “reduced carb dieters lost 46% more weight than low fat dieters”. This was a finding of the study – the average weight loss with the reduced carb diet was 1.9kg in 6 days; the average weight loss with the low fat diet was 1.3kg in 6 days – that’s a difference of 46% if you want to play the misleading relative numbers again. A genuinely low carb diet (under 10% carb intake) could have achieved a 2-3kg loss in 24 hours, as approximately 500g of glycogen would have been depleted and approximately 2kg of water along with it.

Where does this leave us?

The briefing paper did at least acknowledge: “Long-term extrapolation of our results is fraught with difficulties.” However, this didn’t hold the researchers back from the conclusion: “While fat oxidation during prolonged LF and LC diets would be expected to slowly wane over time, our data suggest that the greater fat imbalance is likely to persist with the LF diet leading to more long-term body fat loss than with the LC diet.”

Hall also shared with James Gallagher the challenges of the diet – even in just six days: “It’s not easy, these folks had to eat the same meals every day. This was very strictly controlled and they had to eat the food provided and nothing else, the diets got pretty boring pretty quickly.”

Could a 7% fat diet be done ‘free-range’? Highly unlikely. Should it be done ‘free-range’? Absolutely not. The reality is that a diet with 72% carbohydrate intake and 7% fat intake is unhealthy in the medium, let alone long, term. It would not deliver the essential fatty acids and fat soluble vitamins, A, D, E and K, so vital for human health and survival, let alone the macro nutrient requirements for body maintenance and repair.

While this was a well designed and controlled study, therefore, it is difficult to see how this leaves us with anything useful to take away. Surely the time would have been better spent studying a diet that could actually be recommended and sustained, if shown to be of any benefit, and to report results more scientifically than a headline-grabbing relative risk based on an invalid assumption that comes down to the weight of an apple.

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

Saturated fat & CHD in Europe

This post shows that, for all 192 countries in the world, for men and women, for CVD deaths and all-cause mortality, the HIGHER the cholesterol levels, the LOWER the death rate; the LOWER the cholesterol levels, the HIGHER the death rate. The Pearson correlation coefficient gets higher as we move from male CVD deaths to female CVD deaths to male all deaths to female all deaths.

This blog repeats the exercise of examining the association between heart disease (this time CHD) and an accused causal agent (this time saturated fat). The data is available for Europe here [Ref 1]. As you can see below, the association is again inverse – the higher the saturated fat intake, the lower the CHD death rate for males…

and females…


The correlation for males (r) is 0.545 and it is even stronger (0.62) for females.

The top and bottom seven

In the brilliant “The Great Cholesterol Con”, Dr Malcolm Kendrick reviewed the top and bottom seven countries for saturated fat intake in Europe and the countries with the highest and lowest levels of heart deaths. He used the MONICA data from c. 1998. I repeated this for the 2008 data [Ref 1].

* The 7 countries with the LOWEST saturated fat intake were Bosnia & Herzegovinia; Georgia; Azerbaijan; Tajikstan; Moldova; Croatia; Armenia.

Their saturated fat intake ranged from 3.9-7.3%. The average was 5.8% – all way below the recommended 10% saturated fat limit set by dietary guidelines.

* The 7 countries with the HIGHEST saturated fat intake were Austria; Finland; Belgium; Iceland; Netherlands; Switzerland; France (France is the single country with the highest saturated fat intake in Europe and the lowest rate of CHD deaths).

Their saturated fat intake ranged from 13.9-15.5%. The average was 14.7% – all way above the recommended 10% saturated fat limit set by dietary guidelines.

* The 7 countries with the LOWEST saturated fat intake had the following death rates:

– Male deaths per 100,000 ranged from 73-178, with an average death rate of 117.

– Female deaths per 100,000 ranged from 17-67, with an average death rate of 41.

* The 7 countries with the HIGHEST saturated fat intake had the following death rates:

– Male deaths per 100,000 ranged from 22-65, with an average death rate of 39.

– Female deaths per 100,000 ranged from 4-13, with an average death rate of 9.

Death rates for men were 3 times higher in the lowest saturated fat intake countries than the highest.

Death rates for women were 4.5 times higher in the lowest saturated fat intake countries than the highest.

As Malcolm found from the 1998 data – every single country in the top 7 saturated fat intake countries had a lower death rate than every single country in the bottom 7 saturated fat intake countries. This held for men and women. It holds again with the data from 10 years on.

The nutrition

Two facts are not widely enough known about fat/saturated fat and this explains much of the nonsense claimed about saturated fat. If people knew what saturated fat actually is, they would find their allegations about this life-vital nutrient as absurd as they are:

1) All food that contains fat contains all three natural fats (saturated, monounsaturated and polyunsaturated). There are no exceptions.

Meat, fish, eggs, dairy, nuts, seeds, olives, avocados – all of these foods contain all three fats. It is completely impossible to eat unsaturated fat without saturated fat, or vice versa.

2) The only food group that contains more saturated than unsaturated fat is dairy products. Meat has more unsaturated than saturated fat; eggs have more unsaturated than saturated fat; LARD has more unsaturated than saturated fat – not that any real fat is better or worse than any other – but just to set the record straight.

So – if you want a row about saturated fat – you’re having a row about dairy products and you may want to bear this in mind: There is evidence of a re-emergence of rickets and osteoporosis is rising [Ref 2]. The Family Food survey has reported that the present UK diet is deficient in retinol and vitamin D, providing less than one third of the UK Reference Nutrient Intake and barely a fifth of the recently revised American RDA for vitamin D [Ref 3].

As our 2013 paper suggests: “Using a 100 g steak, as an example, with 5.4 g of fat, it is difficult to accept that the 39% of the fat which is saturated is damaging to the cardiovascular system while the 61% of the fat which is unsaturated is protective. Keeping in mind that the total fat content of the steak will provide all but 3 of the 13 vitamins and 16 minerals that are a pre-requisite for the maintenance of good health.”

[Ref 1] Allender S, Scarborough P, Peto V, Rayner M. European Cardiovascular Disease Statistics: British Heart Foundation Health Promotion Research Group, 2008.
[Ref 2] S. H. Pearce and T. D. Cheetham, “Diagnosis and Management of Vitamin D Deficiency,” BMJ, Vol. 340, 2010, p. b5664. doi:10.1136/bmj.b5664
[Ref 3] DEFRA (The Department for Environment, Food and Rural Affairs), “A National Statistics Publication, the Family Food Survey,” The Department for Environment, Food and Rural Affairs, London, 2010.

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

Competing interest?

After the success of this paper and the huge media interest it generated, a backlash was inevitable. It came in the form of a personal attack on me that I had not declared a ‘competing interest’. What competing interest? I was accused of “the advice on this web site [the one you’re on now] on dairy fat consumption (it contains essential fats, complete protein and invaluable quantities of vitamins and minerals) being similar to the conclusions published in your study on Monday.”

I replied: “I have been doing a PhD examining the evidence base for dietary fat guidelines at the University of West of Scotland since September 2012. This paper is a systematic review and meta-analysis of randomised controlled trials available in 1983. The article was not about meat or dairy products – it does not mention them. The paper expressed no author views about dietary advice – it examined the evidence base for guidelines introduced over 30 years ago. There were no conclusions about dairy fats; I reiterate they were not even mentioned, in the published study from Monday. The media ran with a butter/dairy story, which had no more evidence base from our paper than dietary guidelines had from RCTs.”

Had I, or any of the other six authors, or us collectively as a research team, written a glowing article about dairy products and had any of us/we collectively been funded by the dairy industry to do so, this would absolutely have been a conflict of interest requiring declaration. We sought no funding for this paper. We received no funding for this paper.

One response of the CTSU, (which we now know has received £268 million from pharmaceutical companies that make statins), when challenged about their pro-statin papers and refusal to share Serious Adverse Effect data has been to sling mud back “but so-and-so has written a book on the topic.” As one recipient of this attack, Dr Malcolm Kendrick, said  “If you write in books what you write in papers, that does not make you conflicted, it makes you consistent.”

I considered it completely INappropriate to mention that I also write books at the end of a team academic article, which had nothing to do with “The Harcombe Diet” and which could be seen as a plug. I checked probably the most well known author connected to Open Heart, who is also an associate editor, Ben Goldacre, and there was no mention of his books. It would thus have been inappropriate to mention mine.

After a number of discussions with BMJ Open Heart and the whole research team (there are seven of us) yesterday, there will be a statement added to the paper. Not least, as this is already the most downloaded paper on BMJ Open Heart, this could, of course, generate book/diet interest/sales, completely counter to my intent or wishes.

Posted in Media comments

US and UK dietary advice on fats “should not have been introduced”


Dietary guidelines were introduced in the US in 1977 (ref 1) and in the UK in 1983 (ref 2). The dietary recommendations in both cases were to reduce dietary fat intake; specifically to i) reduce overall fat consumption to 30% of total energy intake and ii) reduce saturated fat consumption to 10% of total energy intake.

The recommendations were made in the belief that dietary fat generally, and saturated fat particularly, caused coronary heart disease (CHD).

The evidence available to dietary committees at that time comprised epidemiological studies and randomised controlled trials (RCTs). The most comprehensive population study undertaken was the Seven Countries Study by Keys et al (ref 3). This reported that CHD “tended to be related” to serum cholesterol values and that these in turn “tended to be related” to the proportion of calories provided by saturated fats in the diet (ref 4). Keys acknowledged that epidemiological studies could reveal relationships, not causation (ref 3). RCTs provide the best evidence (ref 5).

Although a number of reviews of RCTs have been undertaken (refs 6-8), no review has examined the RCT evidence available at the time dietary fat guidelines were introduced. Furthermore, these guidelines have not been changed since they were announced; making the validity of their evidence base as relevant as at the time of introduction.

In our paper, we undertook a systematic review and meta-analysis to find the RCTs available to the committees and to review the findings.

The dietary trials

There were only five trials undertaken to test dietary fat interventions before the US recommendations were introduced in 1977 (ref 9-13). A further study was available to the UK committee, but was published after the US guidelines were introduced (ref 14).

None of these trials studied women. Only one of these trials included healthy subjects (ref 12). The other five were secondary studies, which means they only included men who had already had myocardial infarction. The death rate across all the studies was 30%, reflecting the fact that one of the single biggest causes of death is already having had a heart attack.

Table 1 in the paper summarises the dietary interventions that were tested. Rose et al gave one intervention group 64g of corn oil daily and another intervention group 58g of olive oil (both groups had targets of 80g of oil daily, but the participants found the oil ‘unpalatable’) and compared these to a control group of men receiving no oil. During the two year study, five men died in the corn oil group; three men died in the olive oil group and one in the control group.

The Research Committee low-fat diet compared 123 men randomly allocated to a low-fat diet (no more than 40g of fat daily) and 129 men randomly allocated to continue their normal diet. There were non-significant differences in deaths between the groups.

For just over 3 years, the MRC soya-bean oil study followed 194 control patients who continued their normal diet. The 199 men, randomly allocated to the experimental group, were required “as far as possible” to remove saturated fats from the diet and were instructed to consume 85g of soya-bean oil daily. The intervention group was allowed up to 85g of lean meat daily, any fish, skimmed milk, and clear soups. They were not allowed to consume butter, other margarines, cooking-fat, other oils, meat fat, whole milk, cheese, egg yolk, and most biscuits and cakes. This was not a single dietary intervention, therefore. There were slightly more deaths from any cause in the control group and slightly fewer deaths from CHD in the control group. Neither result was statistically significant.

The Dayton/LA Veterans study was undertaken in a veteran’s home and thus meals were served in a controlled environment. The intervention group was to have no more than 40% of their intake in the form of fat and two thirds of their fat from vegetable oils. There were non-significant differences in deaths between the groups.

The Leren/Oslo study also allocated the intervention group no more than 40% of their intake in the form of fat. This time, 72% of the fat was to come from soya-bean oil. There was nothing of significance in all-cause mortality. The deaths from CHD were lower in the intervention group (significant to a p value of 0.1 but not 0.05).

The Sydney diet heart study was the first to test either of the actual dietary recommendations introduced. It tested 10% saturated fat (and 15% polyunsaturated fat) in the intervention group vs. 14% saturated fat and 9% polyunsaturated fat in the control group. There were significantly more deaths in the intervention group from both all-causes and from CHD.

The key conclusions of our review

*      2,467 males participated in 6 dietary trials: 5 secondary prevention studies and 1 including healthy subjects.

*      No randomised controlled trial had tested government dietary fat recommendations before their introduction. (Woodhill tested the 10% saturated fat recommendation after the US guidelines were introduced. The death rate from all-causes was 18% in the intervention group vs. 12% in the control group).

*      There were 370 deaths from any cause in both the intervention and control groups. The risk ratio (RR) from meta-analysis was 0.996 (95% CI 0.865 to 1.147).

*      There were 207 and 216 deaths from coronary heart disease (CHD) in the intervention and control groups respectively. The risk ratio was 0.989 (95% CI 0.784 to 1.247).

*      There were no differences in all-cause mortality and non-significant differences in CHD mortality, resulting from the dietary interventions.

*      Mean serum cholesterol levels decreased in both control and intervention groups. The reductions in mean serum cholesterol levels were significantly higher in the intervention groups. This did not result in significant differences in CHD or all-cause mortality.

*      Recommendations were made for 276 million people following secondary studies of 2,467 males, no study of women and no study of only healthy people.

*      RCT evidence did not support the introduction of dietary fat guidelines.

The studies’ own conclusions

These are the verbatim conclusions from each of the studies:

1965 Rose Corn & olive oil: “It is concluded that under the circumstances of this trial corn oil cannot be recommended as a treatment of ischaemic heart disease. It is most unlikely to be beneficial, and it is possibly harmful.” (ref 9)

1965 Research Committee Low-fat diet: “A low-fat diet has no place in the treatment of myocardial infarction” (ref 10) [heart attack].

1968 MRC soya-bean oil: “There is no evidence from the London trial that the relapse-rate in myocardial infarction is materially affected by the unsaturated fat content of the diet used.” (ref 11)

1969 Dayton LA Veterans study: “Total longevity was not affected favorably in any measurable or significant degree… For this reason, and because of the unresolved question concerning toxicity, we consider our own trial, with or without the support of other published data, to have fallen short of providing a definitive and final answer concerning dietary prevention of heart disease.” (ref 12)

1970 Leren Oslo Diet Heart study: “Epidemiological studies have demonstrated several factors associated with the risk of developing first manifestations of coronary heart disease. Blood lipids, blood pressure and cigarette smoking are such risk variables… In spite of the small numbers this observation lends some support to the view that the multi-factorial approach is the best way to the solution of the coronary heart disease problem.”(ref 13)

1978 Woodhill Sydney Diet Heart Study: “Survival was significantly better in the P [control] Group.” “It must be concluded that the lipid hypothesis has gained little support from secondary intervention studies.” (ref 14)

Only one study, the Leren Oslo study, suggested that there was “some support” for considering diet as part of many other factors. No other study suggested that any evidence had been found for “the diet-heart hypothesis” and many voiced extreme concern about repeating their dietary interventions. There are few stronger cautions than: “a low-fat diet has no place in the treatment of myocardial infarction.”

As our paper says: “The present review concludes that dietary advice not merely needs review; it should not have been introduced.”


  1. Carter J.P. Eating in America; Dietary Goals for the United States; Report of the Select Committee on Nutrition and Human Needs US Senate. Cambridge, MA, USA: MIT Press 1977.
  2. National Advisory Committee on Nutritional Education (NACNE). A discussion paper on proposals for nutritional guidelines for health education in Britain. 1983.
  3. Keys A. Coronary heart disease in seven countries I. The study program and objectives. Circulation 1970; 41(I-1-I-8).
  4. Keys A. Coronary heart disease in seven countries Summary. Circulation 1970; 41(I-186-I-195).
  5. Barton S. Which clinical studies provide the best evidence? The best RCT still trumps the best observational study. BMJ 2000; 321(7256): 255-6.
  6. Truswell AS. Review of dietary intervention studies: effect on coronary events and on total mortality. Aust N Z J Med 1994; 24(1): 98-106.
  7. Hooper L, Summerbell CD, Higgins JPT, et al. Dietary fat intake and prevention of cardiovascular disease: systematic review. BMJ 2001; 322(7289): 757-63.
  8. Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med 2010; 7: e1000252.
  9. Rose GA, Thomson WB, Williams RT. Corn Oil in Treatment of Ischaemic Heart Disease. BMJ 1965; 1(5449): 1531-3.
  10. Research Committee. Low-fat diet in myocardial infarction: A controlled trial. The Lancet 1965; 2(7411): 501-4.
  11. Medical Research Council. Controlled trial of soya-bean oil in myocardial infarction: Report of a research committee to the Medical Research Council. The Lancet 1968; 292(7570): 693-700.
  12. Dayton S, Pearce ML, Hashomoto S, Dixon WJ, Tomiyasu U. A Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing Complications of Atherosclerosis. Circulation 1969; 40(1S2): II-1-II-63.
  13. Leren P. The Oslo Diet-Heart Study. Circulation 1970; 42: 935-42.
  14. Woodhill JM, Palmer AJ, Leelarthaepin B, McGilchrist C, Blacket RB. Low fat, low cholesterol diet in secondary prevention of coronary heart disease. Advances in experimental medicine and biology 1978; 109: 317-30.


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

Horizon: What’s the right diet for you?

Last January Horizon had a diet programme. This January they had three – all on the same topic – the idea that there are three different types of (over)eaters and therefore three different diets that they should be on. It was described as “a personalised approach to dieting based on genetics, hormones and psychology”.

Hundreds of people” were invited to assessment centres in Glasgow, Manchester and London. From these hundreds, 75 were selected for the programme – no doubt the 75 that best fitted the three groups upon which the programme was based: “Feasters”; “Constant Cravers” and “Emotional Easters”. I assume that the groups were decided upon before the recruitment started.

Further tests were undertaken when the 75 people were invited to Liverpool Hope University – where they were residential for a few days.

The questionnaire

The questionnaire to find out which type you are can be found here. The 12 questions are as follows (the options for responses are in brackets):

1) Do you have the desire to eat when you are irritated or when someone lets you down? (Very often, often, sometimes, rarely, never).

2) At the end of a typical meal, how often do you feel like you haven’t had enough to eat? (All the time, often, occasionally, never).

3) Sometimes when I start eating, I just can’t seem to stop. (All the time, often, occasionally, never).

4) Do you have a desire to eat when things are going against you or when things have gone wrong? (Very often, often, sometimes, rarely, never).

5) If you pass a plate of biscuits or a bowl of crisps, how often will you pick one up? (Always, most of the time, very occasionally, never).

6) How often do you feel hungry? (Almost always, often between meals, sometimes between meals, only at meal times).

7) Do you eat large portion sizes? (All the time, often, occasionally, never).

8) It seems like I have food on my mind a lot (Strongly agree, agree, agree somewhat, agree a little, don’t agree at all).

9) Do you have a desire to eat when you are feeling lonely? (Very often, often, sometimes, rarely, never).

10) When you are preparing food are you inclined to eat something? (Very often, often, sometimes, rarely, never).

11) When you are going through a stressful or upsetting time, what happens to your eating? (I go off food completely, I eat a little less than usual, I eat more than usual, I eat a lot more and find it difficult to control my eating).

12) When you’re out at a meal with friends, do they all seem to get full before you, even when you’re eating the same thing? (Most of the time, often, haven’t noticed, never).

I suggest that questions 1, 4, 9 and 11 are for ‘Emotional Eaters’. Questions 2, 3, 7 and 12 are for ‘Feasters’ and 5, 6, 8, 10 are for ‘Constant Cravers’. I answered the questionnaire honestly and the conclusion was “you’re not in any diet category”. I tested giving the strongest positive response to each question and it said “You are a mix of diet groups: 33% Constant Craver; 33% Feaster and 34% Emotional Eater.”

I also suggest that this questionnaire is about as scientific as asking someone if they smoke and then telling them that they smoke if they say yes.

The confirmation tests

The initial tests at assessment centres were supposed to indicate which group the 75 people would be in and then tests were run at Liverpool Hope University to confirm the predicted group. The Feasters were apparently identified at the initial assessment through gut hormones, GLP1 particularly. We weren’t given any details about the differences in hormone levels across the hundreds of people tested, or whether they were statistically significant.

Introducing the first test for the first diet group, as Chris Van Tulleken (CVT) narrated: “The sushi supper is testing the first group: we’re calling them the Feasters”. This experiment involved all 75 people having a sushi supper together. They could take as many sushi plates as they liked from a conveyor belt in the dining hall. The seating was not random – name cards on the tables told people where to sit.

The outcome of the experiment was that none of the non-Feasters ate more than 14 plates of sushi; while 9 of the Feasters ate more than 14 plates. What’s the significance of 14? Why not average the plates consumed by the assumed Feasters vs. non Feasters? What about the other 16 Feasters (assuming 25 people in each group)? 9 vs. 16 out of 25 suggests that two thirds of the Feaster group disproved the experiment. However, here’s the key issue – all 9 people, who consumed the most plates of food – were seated within the boundaries of the conveyor belt, as this screen grab shows below.

As David Curry, @dac101, also noticed on twitter “gave up on the ‘science’ then they “proved” group were feasters in an experiment where seating plan biased food availability.”

The Emotional Eaters were identified at the initial recruitment by psychological assessment alone (back to asking someone if they eat when they are stressed/let down/lonely and then telling them they eat for emotional reasons). They were confirmed with an experiment where they were put under stress with a simulated driving test. Cortisol levels rose (in everyone) and the Emotional Eaters consumed more biscuits, chocolate and crisps than the non-Emotional Eaters. There were other items on offer – did the non-Emotional Eaters eat more sandwiches for example? The non-Emotional Eaters should, in theory, have been Constant Cravers or Feasters – why was this not an occasion where they wanted to satisfy their constant cravings or desire to feast?

The Constant Cravers were predicted in the initial assessments from genetic tests (details were not given). As CVT explained, Constant Cravers have genes that “trick their fat stores into constantly thinking they need replenishing. The result? They’re hungry all the time.” This one was tested with a grip test where all 75 people were given a “hearty lunch” and then 2 hours later they were given a grip meter and they had to indicate how much they wanted a particular food. Constant Cravers pulled harder for 5 out of 8 foods. How much harder? What about the other foods? We don’t know. For scientific experiments, this was all very unscientific.

The theory

I just don’t buy that there are different types of obese people as described in this programme. 2.7% of UK men and women were obese in 1972 and this had risen to 22.6% of men and 25.8% of women by 1999. To explain the proportion of people who have become obese, it is necessary to explain what changed. The claim in this programme is that gut hormones, genes and psychology provides the answer. I just don’t buy this. We (humans and our ancestors) managed to stay slim for 3.5 million years and then hormones, genes and psychology went awry within a couple of decades and created an obesity epidemic? It just doesn’t make sense.

The ‘but for’ is surely processed food. Would the ‘Feasters’ feast on the animals and vegetation of our evolutionary diet? Would the ‘Constant Cravers’ constantly crave wildebeest and berries? Would the Emotional Eaters be satisfied by salmon and green beans, or are they uniquely drawn to crisps, chocolate, biscuits, cake and other junk? I just don’t accept that these three types override the ultimate issue, which is the processed food dominating modern diets.

The diets

The diets recommended for the three types were:

Feasters were advised to follow “a diet that makes them feel as full as possible as long as possible” – a high protein (fish, chicken, low fat milk were shown), low Glycaemic Index GI (pasta, lentils and basmati rice) diet. The group was specifically told to avoid potatoes and most rice and breads.

Emotional Eaters were advised to have group support and to follow a diet club programme (one clip showed people attending Slimming World).

Constant Cravers were put on the 5:2 diet. They were told to have no more than 800 calories a day for 2 days a week.  CVT narrated “crucially, they need to avoid carbohydrates, like bread and pasta.” Professor Susan Jebb added “fruit’s off; it’s essentially meat, fish, eggs, veg.” Perfect Paleo! Back to CVT “the other 5 days, they don’t have to diet, but they should eat healthily.” (i.e. they’ll need to diet or the 2 days will be wasted). (The fasting days were started while the participants were at Liverpool Hope University. One man was in tears approximately 18 hours into the fast – he was no doubt suffering from withdrawal symptoms from processed carbohydrates,  but he was given no warning of this or advice as to how to ride it though.)

Even if you buy that obesity can be explained by Feasters, Emotional Eaters and Constant cravers, what would be the best diet for each type?

Feasters find it hard to stop eating, so prescribe them a diet where quantities don’t matter…

Emotional Eaters want to comfort eat when life is stressful, so prescribe them a diet where quantities don’t matter…

Constant Cravers want to eat all the time, so prescribe them a diet where quantities don’t matter…

Whichever type you are (if you believe in these types) the best answer to all of them is a diet that allows unlimited amounts of meat/fish/eggs/veg and eliminates (e.g. Paleo) or limits (e.g. Harcombe) other carbohydrates. Any version of Low Carb High Fat (LCHF) is going to be better than all three options assigned – all of which are calorie deficit diets in different forms.

What is weight loss?

The presentation team even showed that they know this:

One of the programme advisors, Dr Giles Yeo, did a urine test with the Constant Cravers to try to encourage them to stick to the punishing regime by showing that they’re burning fat.

CVT explained the only thing that this programme needs to state – what weight loss actually is: “When we eat, our bodies convert our food into sugars, like glucose, but when we fast, and there are no sugars left, our bodies turn to our fat reserves. They burn them, for energy instead, which is why we lose weight.”

Dr Giles Yeo perfectly reinforced this, referring to what was happening when he observed ketones in the urine of the fasters: “When all the sugars are gone, they start to burn fat.”

So the Constant Cravers didn’t need to be starved; they simply needed to be starved of carbohydrates (sugars). The Feasters didn’t need to be put on chicken, beans, lentils and basmati rice. They needed to be allowed to feast on pork crackling, steak, omelettes, butter and cream and they would burn fat beautifully in the absence of sugars and in the absence of hunger. The Emotional Eaters could similarly turn to fat-rich/carb-poor foods when they needed comfort. The universal solution is to limit carbs, to enable body fat to be burned. Chris and Giles say so and then the programme turns back to the overriding calorie theme that is never far away…

The sushi bowls are measured in calories. The 5:2 dieters get a depressing calorie target for 2 days a week. The exercise expert arrives, Dr Jason Gill, and everything comes down to calories – even Swiss rolls are produced to show the calorie equivalent of exercise that has been undertaken. There’s a shopping experiment (message – don’t shop when you’re tired) – it’s all measured in calories. Some of the guinea pigs have their metabolic rates checked – the calories that they needed pre-diet and the calories they need now are the numbers of interest. There’s a test involving a burger – we are told how many calories it has. ‘Morgan’ uses 40 calories doing some shopping. The calorie obsession is omnipresent, despite the inescapable fact that weight loss is about body fat burned, is about absence of carbohydrate/sugars.

What we can still take from this programme

The first thing that we can take is the message that weight loss is about body fat burned is about absence of carbohydrate/sugars. I cannot emphasise this enough because it is all that anyone needs to know about dieting. There were some other interesting and useful take homes from this series of programmes:

1) In Episode 2, Dr Jason Gill was called in to help with an exercise plan (all 3 types were encouraged to exercise). His guinea pigs were given a sophisticated “accelerometer”. The first week they were advised to do whatever they normally do, to establish their baseline activity. Then a personal trainer arrived and the (handful of) people were put through 3 exercise sessions in week 2. The accelerometer measured the steps clocked up by the group on the exercise days and the days in-between.

The baseline showed that the small group had a baseline average of 7,829 steps.  This increased to 11,271 steps on the exercise days, but then dropped back to 6,694 on the days in-between. This meant that the overall average number of steps for week 1 was 7,829 and the average for week 2 was 8,655 – not such a big difference for all the effort that people put in. This has been a key finding of the Peninsula diabetes study, where this ‘compensation’ for activity with subsequent reduced activity, has been repeatedly demonstrated.

Professor Tanya Byron followed this finding by narrating “While exercise is really good for your overall health, the most effective way to lose weight will almost always be to change your diet.” This point was crucial and could have been emphasised much more.

2) In Episode 3 there was an interesting and useful focus on “Mo”. He actually used the words “pissed off” to describe how he felt when he was putting in so much effort and losing half a pound. In Episode 2, Professor Susan Jebb had stated that losing weight requires great effort and mental energy, which I agree with, but only to an extent. I think that sticking to a calorie deficit (eat less/do more) requires way more effort and mental energy than ditching processed food, and the cravings for junk that go with consuming it, and enjoying unlimited real food instead.

The insights, throughout the programmes, from the real dieters showing the extremes of emotions that come with dieting, from hope to despair, were worth watching – if only to remind ourselves that the real food route has got to be an easier way.

3) Finally – my favourite experiment of all. In Episode 3, Professor Paul Aveyard and Professor Tanya Byron, did an experiment with the Emotional Eaters. I am confident that the outcome would apply to all dieters. 8 people were involved in the experiment which involved baking cakes. A cake was produced early on in the experiment and everyone had a slice. 4 of the group were told the truth – that the cake had 700 calories a slice; the other 4 people were told that the cake had 190 calories a slice. Later on that afternoon, they were able to eat cake that they had baked.

The group who thought they had blown their diet by having a 700 calorie piece of cake earlier, ate whatever they liked. “I’ve blown it, so I’ll eat what I want” mentality. The group that thought they were still doing well for the day, hardly ate any further cake at all. The ‘blown it’ group got through almost 2 kg of cake between the 4 of them; the other 4 got through an eighth of that – barely 200g of cake between 4. This was not new. I described the ‘all or nothing mentality’ in my 2004 book Why do you overeat? When all you want is to be slim – and how to overcome it, but this was a great visual illustration of this common behaviour.

There was a final interesting take away from the programme. The weight loss goal for the programme was an average 5% of body weight lost in 12 weeks. As an example, that would be 10lb from a 200lb (14 stone) person. That would be expected in a couple of weeks on LCHF diets. The overall 12 week loss was 8% of body weight, which was better than expected. As with other TV weight loss programmes – Biggest Loser, Fat Club Celebrity Fit Club etc – people do better on TV weight loss programmes – at least for the time they are on TV. The regain after the programme is likely as consistent as the regain experienced by other calorie deficit dieters who have not been on TV. However, for the duration of the programme, the pressure of being in the public gaze has an impact. Sadly this is not scalable.

The most important thing to take away from this programme, however, is what Chris Van Tulleken said about 40 minutes in to Episode 1: “When we eat, our bodies convert our food into sugars, like glucose, but when we fast, and there are no sugars left, our bodies turn to our fat reserves. They burn them, for energy instead, which is why we lose weight.”

So don’t cut food – cut carbs.

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

Katie Hopkins: My Fat Story

The starting aim and metrics

“Katie Hopkins: My Fat story” was a programme aired in two parts on TLC on January 2nd and January 3rd 2015.

Katie Hopkins set out the rationale for the programme in the opening words: “To make a point to the two thirds of Brits who are overweight, I’m going to put on three stone and then prove how simple it is to lose weight.”

Katie started the experiment in June 2014 and she aimed to put on three to four stone by the end of August. Her starting weight was 8 stone 13lb and she is 5’ 7”, so her starting BMI was 19.6 – close to clinically underweight. She described herself as a fitness fanatic and the measurements recorded at the start of the experiment showed that she had 15% body fat, which is extremely low (24% being the low end of normal body fat for a 39 year old female).

One of the first scenes in Programme 1 of 2 showed Katie going in to her local rugby club in a bikini to ask some rugby hunks what they thought of her body. The consensus was that she was “underweight”, “skinny”, had “no bum or boobs” and would look much better if she gained a stone or a stone and a half.

The Programme

The programme was shown in two parts, each an hour long with adverts, so there was probably 90 minutes of content in all. The necessary content – Katie gains three stone and then Katie loses quite a bit less than three stone (sorry to give the punch line away) – took up a very small proportion of the programme because, even with Katie doing a video diary, there’s actually not much of interest in eating more/doing less and then eating less/doing more.

Programme 1 was taken up with repeated visits to a doctor to have measurements taken and to have the “we advise you not to do this blah blah” compulsory disclaimer. The stocking fillers in Part 1 were: the rugby club visit; a visit to America – the home of overeating and let’s meet a 57 stone woman while we’re there; a visit back in the UK to a mum of 3 who had had gastric surgery in 2008 and dropped to 9 stone 7lb but was now back up at 14-15 stone (and upset by excess skin); a visit to a psychologist; and a visit to the Miss British Beauty Curve competition in July 2014, where Katie was an unlikely judge.

The programme didn’t flow – it was a series of sketches – and the key insights were largely missed. The most interesting aspect of the visit to the 57 stone woman in North Carolina was that her slim and fit boyfriend was clearly a ‘feeder’. The control psychology of this would have been interesting to explore, but this didn’t happen. The visit to the bariatric surgery mum could have been an interesting exploration of classic weight rebound, following calorie deficit dieting, but this didn’t happen.

The most interesting part of programme 1 for me was the fleeting coverage of Katie meeting a psychologist and sharing that she has epilepsy. The psychologist suggested to Katie “you can’t control your epilepsy but you can control your weight.” Katie admitted that she has no compassion for herself (and the public observes her having no compassion for others). Katie also shared “It’s a lot easier to be tough me when I’m slim.”

There were many twitter comments that this programme gave us the most insight to date into (apparently) Britain’s most hated woman. The twitter support was especially strong during the second programme where general themes were: “I didn’t think I would agree with anything that Katie said, but I do”; “She’s only saying what’s right”; and “I’m seeing a different side to Katie.”

What Katie thinks she proved and what she did prove

Katie claimed at the end of Part 1 “I have proved if you sit on your bum and eat you will get fat.”

Wrong. Katie showed that, for n=1 (i.e. an experiment with 1 subject), someone who has previously eaten carefully and healthily and (over) exercised will gain weight if they stop exercising and consume doughnuts, chocolate milk, crisps, sweets and other junk at the rate of 400+ calories an hour for 16 hours a day. Had Katie sat on her bum for three months and eaten no junk whatsoever, there is no reason why she should have gained weight.

Katie did an #AskKatie on twitter after both programmes. Two further comments made during Friday’s #AskKatie were of interest:

1) “You have to find the exercise you love. It’s not about diet, it’s about working out.”

2) “My show is not pointless – it proves there are no excuses for obesity. It’s simple maths.”

Wrong and wrong again.

1) Katie stopped exercising as soon as she started the experiment and yet she gained no weight for the first two weeks. She realised that she had to massively increase her food intake to achieve weight gain. Similarly in Part 2, had Katie started exercising and continued to eat 6,000 calories a day of junk, she would have made next to no difference to her weight. Weight is about diet; it’s not about working out.

At the end of the 12 week eat less/move more phase, Katie had lost 2 stone 3lb – she was 11lb heavier than at the start of the experiment. The programme tried to gloss over this by saying she was underweight before and looked better with a fuller face. True and true, but that doesn’t change the fact that Katie failed to lose weight gained deliberately and quickly. She failed to lose 26% of her gained weight to be precise – despite doing 20,000 steps a day and running three times a week. Had she ditched the junk, she may have shown us the power of eating clean.

2) Katie didn’t prove the simple maths – she disproved it, assuming that by “simple maths” she is referring to the calorie theory. Programme 1 stated that Katie had consumed 504,000 calories in 12 weeks. During that time she went from 8 stone 13lb to just under 12 stone – a 3 stone (42lb) gain.

The average calorie requirement for a female is 2,000 calories. Over 12 weeks, this would add up to 168,000 calories. Katie consumed an excess of 336,000 calories in 12 weeks. According to the calorie theory, she should have gained 96lb of fat alone and more on top in water and lean tissue. She gained less than half of the 96lb of fat, let alone the c. 110lb of weight that she should have gained.

The show was pointless, as n=1 is not an indication of the general population and a three month binge and correction is in no way a reflection of the obesity paradox (people so desperately wanting to be slim and yet two thirds not being).

What Katie showed was that, for n=1, where n is a lifelong slim person, quickly on = quickly off when it comes to weight (although not all of it necessarily). Indeed for anyone at a fairly constant weight, normal or otherwise, any weight quickly gained (due to illness/holiday) can be just as quickly lost (again – not all of it necessarily as some serial holiday gainers will know).

What Katie absolutely did not prove is that someone who has been, let’s say, overweight since childhood and obese in adulthood can lose weight and keep it off with a calorie deficit diet. All the evidence since Benedict (1917), Keys (1950), Stunkard & McLaren Hume (1959), Franz (2007) shows that weight lost with a calorie deficit is, in almost all circumstances, regained and often more. This was exactly what the bariatric surgery mum was trying to share, but it was lost on Katie who just thinks that people need to eat less and move more.

As a relevant comparison, if Katie had smoked for 3 months and then quit, would this have shown that a lifelong smoker had no excuse for giving up? We know that the maximum smoking cessation odds are 2%, which can be doubled by quitting with a friend/support group and can be doubled again to 8% with smoking cessation products (reference – I worked for SmithKline Beecham when patches were first launched!) We similarly know that 95-98% of diets fail.

If Katie proved anything beyond quickly on = (mostly) quickly off with this experiment, she proved the set point theory of weight. The evidence from the work of Benedict to Franz mentioned above shows that calorie deficits lead to a short term deviation from the starting weight and then a return to that starting weight, or higher, in the medium to long term. The Franz review of 26,000 people in 80 different weight loss studies, showed that six months is the key marker. Up to six months, calorie deficits lead to weight loss and then the weight starts to be regained around the six month point and most people are back where they were within 48 months or sooner. The greater the calorie deficit, the greater the short term loss and the greater the subsequent regain.

Just as Katie went from c. 9 stone to c. 12 stone and back to c. 10 stone, supporting the set point theory of weight, so another person could have gone from 12 stone to 9 stone and back to 12-13 stone in little more than that time. Katie may, somewhat ironically, have proven the futility of eating less and doing more. The only way to escape the known outcome of calorie deficit dieting is never to do it and to sign up to eating better instead.



Francis G. Benedict, Human Vitality and efficiency under prolonged restricted diet, (study 1917, published 1919).
Ancel Keys, The Biology of Human Starvation, (study 1944-45, report 1950).
Albert Stunkard and Mavis McLaren-Hume, “The results of treatment for obesity: a review of the literature and report of a series”, Archives of Internal Medicine, (1959).
Marion J. Franz, Jeffrey J. VanWormer, A. Lauren Crain, Jackie L. Boucher, Trina Histon, William Caplan, Jill Bowman, Nicolas Pronk. “Weight Loss Outcomes: A Systematic Review and Meta-Analysis of Weight Loss Clinical Trials with a Minimum 1-Year Follow-Up”, Journal of the American Dietetic Association, (2007).


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