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…
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.
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.
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.
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.”
- 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.
- National Advisory Committee on Nutritional Education (NACNE). A discussion paper on proposals for nutritional guidelines for health education in Britain. 1983.
- Keys A. Coronary heart disease in seven countries I. The study program and objectives. Circulation 1970; 41(I-1-I-8).
- Keys A. Coronary heart disease in seven countries Summary. Circulation 1970; 41(I-186-I-195).
- Barton S. Which clinical studies provide the best evidence? The best RCT still trumps the best observational study. BMJ 2000; 321(7256): 255-6.
- 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.
- Hooper L, Summerbell CD, Higgins JPT, et al. Dietary fat intake and prevention of cardiovascular disease: systematic review. BMJ 2001; 322(7289): 757-63.
- 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.
- Rose GA, Thomson WB, Williams RT. Corn Oil in Treatment of Ischaemic Heart Disease. BMJ 1965; 1(5449): 1531-3.
- Research Committee. Low-fat diet in myocardial infarction: A controlled trial. The Lancet 1965; 2(7411): 501-4.
- 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.
- 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.
- Leren P. The Oslo Diet-Heart Study. Circulation 1970; 42: 935-42.
- 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.
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 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.
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 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.
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 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).
The Denmark case
In 2010, Karsten Kaltoft, a Danish childminder, brought an employment law case for unfair dismissal against his employer, a Danish city council. Kaltoft had been working for 15 years looking after children in his own home in Billund, when his employment contract was terminated in 2010. Kaltoft claimed that obesity was part of the reason that he lost his job and that it amounted to unfair dismissal. Billund city council denied the claim.
This case was referred by the Danish courts to Europe for guidance, making it a test case. The European Union Court of Justice was asked to rule on two matters:
i) Does EU law forbid discrimination on the grounds of obesity?; and
ii) Can obesity be considered a disability?
On 17th July 2014, Niilo Jääskinen – the advocate general, who advises the European court in Luxembourg – ruled that EU law does not forbid discrimination on the grounds of obesity but that EU law offers general protection against discrimination on the grounds of disability.
There were two specific judgements given by Niilo Jääskinen, which were of great importance. First, he gave a guide that morbid obesity (officially defined as a BMI of 40+) could be considered a disability. “If obesity has reached such a degree that it plainly hinders participation in professional life, then this can be a disability,” Jääskinen said. (Kaltoft had a BMI of 54 and one of the work related examples cited in reports about this case was that he was unable to help children tie their shoelaces, although this has been denied by Kaltoft who said that he was able to do all aspects of his job).
Second, Jääskinen dismissed the notion that a “self-inflicted” disability could be any less worthy of protection, saying “the origin of the disability is irrelevant”.
The EU ruling was made on 18th December 2014. The substantial difference between the final ruling and the July position from the advocate general is that the December final ruling did not specify a particular BMI at which disability could be a consideration.
The ruling upheld the advocate general’s view that, in principle, obesity in itself is not a disability – but that if someone had a long-term impairment because of their disability, then they could be protected by disability legislation.
Following this ruling, Kaltoft’s particular case will revert to the Danish courts to decide whether it meets the criteria for disability under the ruling. Interestingly – this case will come down to whether or not there were aspects of Kaltoft’s job that he was unable to undertake. As mentioned above, the initial reporting of this case claimed that Kaltoft was unable to do certain aspects of his job – tie the childrens’ shoe laces.
In this article Kaltoft said that he had no such problems. I heard Kaltoft on the BBC 1pm news on 18th December 2014 saying the same – that he had no problems fulfilling the requirements of his role. This means that he will fail on his disability claim! It will not be his size, per se, that determines the case, but whether or not his size has created a long-term impairment. If it hasn’t, he can’t be protected by disability discrimination law.
The UK law & the consequences of the Danish case
The Equality Act 2010 defines disability as “a physical or mental impairment that has a ‘substantial’ and ‘long-term’ negative effect on a person’s ability to do normal daily activities”.
For as long as the UK is part of Europe we are bound by European employment law judgements. Once Europe has judged a case, it then becomes case law.
I have not yet seen if the “self-inflicted is irrelevant” aspect of Jääskinen’s judgement has been reinforced in the ruling. Assuming that it has been, these are the principles that have been established by the ruling:
1) Morbid obesity will not be a disability in itself, but is someone has a long-term impairment because of their disability, then they could be protected by disability legislation. (There is no BMI guideline for this; it will vary by person, by situation – Christmas for lawyers).
2) Employers will not be allowed to argue that the disability is “self inflicted”. As Jääskinen said “The origin of the disability is irrelevant”.
3) Disability legislation already requires employers to make ‘reasonable’ adjustments for disabled people to be able to participate in the workplace. Examples include: making sure that the workplace is accessible (entrance; canteen; toilets etc); providing hearing/sight impairment support as needed; adjusting chairs/desks/equipment as necessary etc.
The implications of the Danish case are that all European employers will need to make reasonable adjustments for obese people (employees and visitors). This case has wider implications too, as providers of goods and services will also need to make reasonable adjustments.
One of the examples cited by Clive Coleman, the BBC’s legal correspondent, during media discussions today (and here) was that it would probably be considered reasonable for a Premiership football club to be able to offer an obese person two seats, while a small, non-league club, with a few hundred seats would not be obliged to do so.
It wasn’t so long ago that Air France introduced a policy of people needing to pay for two airplane seats if they needed two seats. This ruling would see Air France fall foul of the law if they did not offer a second seat for free!
I used to be a VP for Human Resources. This case is thus the perfect marriage of my past and current lives. I’m going to focus on two interesting points from a human resources point of view:
Is the protected characteristic avoidable?
The big debate in discrimination law has historically been – is the protected characteristic avoidable? Sex and race were the first attributes to fall under discrimination protection because it was held that someone could not change their gender or race and therefore to judge someone for something they could not change was unfair. Interestingly, we can now change gender and we have since protected gender change under discrimination law.
The debate that preceded sexual orientation and religion being added to “protected attributes” centred around – were these choices or characteristics that someone could do nothing about. The debate that preceded age was one of the most interesting. It must be a fact that we can do nothing about the age we are – we can’t ‘help’ being 18 any more than we can ‘help’ being 80. However, age is an interesting one because it is the only protected attribute that every one of us will experience. If we live long enough, we will be 18 and 80 and every age in between. It was the first protection, therefore, for everyone, but applying differently at different times of our lives. The law says we should no more be excluded from a job because we are 18 than if we are 80. If we can do the job, we should be given the same opportunity as anyone of any other age.
The Jääskinen judgement was most interesting for his comments about the origin of the disability. By stating that “self-inflicted” is no defence for an employer (or provider of goods and services), Jääskinen pre-empted this ‘avoidable or not’ debate for obesity. He effectively declared irrelevant the debate about whether or not the condition is avoidable.
Can the person do the job?
The second, even more interesting, point for me is that discrimination legislation has always been about discrimination. That sounds obvious, but it’s a critical point – let me explain… Discrimination legislation has protected against prejudice. It has protected someone from not being given the same opportunity and treatment because of some protected characteristic e.g. a person not being given a job because of their race; gay men not being able to stay at a Christian B&B etc (the latter is doubly problematic as both religion and sexual orientation are protected, so which protection trumps the other?)
In every aspect of discrimination legislation to date, the ability to do the job has been the founding principle. Indeed discrimination can only be found where the ability to do the job is not in question. A white person applies for a job and gets an interview; an Asian person with the same qualifications applies for the job and doesn’t get an interview – that’s discrimination. If the Asian person is not qualified for the job and doesn’t get an interview, there’s no discrimination case.
This obesity ruling has turned this entire principle upside down. It has declared that disability will only apply where the person is unable to do the job. Can you imagine this applying to the other protected characteristics? A man can’t do this particular job but, this being the case, if we don’t give him the job we will be discriminating against him, so we must make reasonable adjustments so that he can do the job?! Seriously?
The huge implication of this ruling for employers is that they cannot reject someone for not being able to do a job if the reason for not being able to do the job is their weight. My friend’s niece has just gone through rigorous medical tests to be a police officer – weight, fitness and all sorts. Do the police now have to make reasonable adjustments for anyone to be a police officer, regardless of their ability to chase a criminal? There has always been a height requirement for the forces and air stewards (one needs to be able to reach the overhead lockers). Will there now still be a height requirement but, if someone can’t move easily down the aisles, easyJet needs to make reasonable adjustments?
The radio debates today have been about obese people. Can obese people do anything about their condition? Will there be resentment if obese people are given blue badges. I’ve even heard people saying – “giving them blue badges won’t help – because they won’t walk as far and will get more obese”. The debates have been dominated by the usual “greedy”, “lazy” ignorant kinds of opinion.
For me, the most interesting outcome of the ruling is that, for the first time in discrimination history, protection has been given to only those unable to do a particular thing (carry out particular work, sit in one seat etc). Additionally the onus is now on employers and providers of goods and services to work out how they get around this. I anticipate some extraordinary case law to follow from this unprecedented and possibly unworkable decision.
For your convenience, here’s a list of peer reviewed studies and journal articles, challenging current dietary advice, since March 2013.
The papers are listed in reverse chronological order and I’ll try to keep this updated. Please post a comment with those I’ve missed and I’ll update.
February 9th 2015: Harcombe et al. “Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis.” BMJ Open Heart. 2015.
February 1st 2015: Nathalie Genevieve Puaschitz et al. “Dietary Intake of Saturated Fat Is Not Associated with Risk of Coronary Events or Mortality in Patients with Established Coronary Artery Disease.” The Journal of Nutrition. (Many thanks to Ted Hutchinson for this one).
November 24th 2014: Sean C Lucan and James J DiNicolantonio: “How calorie-focused thinking about obesity and related diseases may mislead and harm public health. An alternative.” Public Health Nutrition. 2014.
November 21st 2014: Brittanie M. Volk, Laura J. Kunces, Daniel J. Freidenreich, et al. “Effects of Step-Wise Increases in Dietary Carbohydrate on Circulating Saturated Fatty Acids and Palmitoleic Acid in Adults with Metabolic Syndrome”. PLoS One 2014.
November 17th 2014: Malhotra A, Maruthappu M, Stephenson T. “Healthy eating: an NHS priority A sure way to improve health outcomes for NHS staff and the public.” Postgrad Med J 2014.
October 8th 2014: Lamarche, B., and Couture, P. “It is time to revisit current dietary recommendations for saturated fat.” Applied Physiology, Nutrition, and Metabolism. pp.1-3. 2014 (Many thanks to Gaby in comments for this one).
September 2014: Bazzano LA, Hu T, Reynolds K, et al. “Effects of Low-Carbohydrate and Low-Fat Diets A Randomized Trial”. Ann Intern Med 2014; 161(5): 309-18.2
August 2014: Harcombe Z, Baker J. “Plant Sterols lower cholesterol, but increase risk for Coronary Heart Disease.” Online J Biol Sci 2014; 14(3): 167-9.
June 2014: Feinman RD, Pogozelski WK, Astrup A, et al. “Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base.” Nutrition (Burbank, Los Angeles County, Calif) 2014.
April 2014: Schwingshackl L, Hoffmann G. “Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression“. BMJ Open 2014; 4(4).
April 2014: Hansen A. “Swedish health advisory body says too much carbohydrate, not fat, leads to obesity“. BMJ 2013; 347.
March 2014: Chowdhury R, Warnakula S, Kunutsor S, et al. “Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis“. Ann Intern Med 2014; 160(6): 398-406.
March 2014: Georgina E. Crichton and Ala’a Alkerwi. “Whole-fat dairy food intake is inversely associated with obesity prevalence: findings from the Observation of Cardiovascular Risk Factors in Luxembourg study.” Nutrition Research. (Many thanks to Evonne in comments for this one).
February 2014: Ravnskov U, DiNicolantonio JJ, Harcombe Z, Kummerow FA, Okuyama H, Worm N. “The Questionable Benefits of Exchanging Saturated Fat With Polyunsaturated Fat.” Mayo Clinic proceedings Mayo Clinic 2014. (Viewable here thanks to Dr Michael Eades)
January 2014: DiNicolantonio JJ. “The cardiometabolic consequences of replacing saturated fats with carbohydrates or Ω-6 polyunsaturated fats: Do the dietary guidelines have it wrong?” Open Heart 2014; 1(1).
December 2013: Schwingshackl L, Hoffmann G. “Comparison of effects of long-term low-fat vs high-fat diets on blood lipid levels in overweight or obese patients: a systematic review and meta-analysis”. Journal of the Academy of Nutrition and Dietetics 2013; 113(12): 1640-61.
October 2013: Malhotra A. “Saturated fat is not the major issue”. BMJ 2013; 347.
May 2013: Malhotra A. “The dietary advice on added sugar needs emergency surgery“. BMJ 2013; 346.
May 2013: Glen D.Lawrence: “Dietary Fats and Health: Dietary Recommendations in the Context of Scientific Evidence.” Advances in Nutrition. 2013.
March 2013: Z. Harcombe, J. Baker, B. Davies. “Food for Thought: Have We Been Giving the Wrong Dietary Advice?” Food and Nutrition Sciences 2013; 4(3): 240-4. (This is the second most popular paper for the journal Food & Nutrition Sciences, confirming the interest in progressive, rather than conventional, thinking.)
And, of course, none of these should have been necessary as Uffe Ravnskov ended the debate in May 2010 in this book - viewable here.
If I told you that a private company had instructed me to remove this video, I would expect you to be shocked. What do you think about the same private company instructing me to stop saying this: “the calorie theory and conventional weight loss advice is wrong” and this: “weight gain and loss also depends far more on carbs consumed, than calories, or fat, consumed“? Appalled? Outraged?
That’s exactly what has happened, over the past year. The private company is the Advertising Standards Authority.
* You probably think that the Advertising Standards Authority (ASA) is an official body. You would be wrong. It is a self-appointed, self-regulated, upholder of the opinions of another non-official, self-appointed, self-regulated body: the Committees of Advertising Practice (CAP).
* CAP make up ‘the Codes of Advertising Practice”; the ASA apply them. Think of CAP and the ASA like Simon and Louis in the X Factor, only not as entertaining: Simon makes up the rules, Louis follows them.
They are two sides of the same coin; partners in crime. One has a red web site; the other has a blue web site – look how similar they are. Well, they do live at the same address: Mid City Place, 71 High Holborn, London, WC1V 6QT. They even publish a shared annual report.
* Both bodies use the tag line “Legal, decent, honest, truthful.” These are not legal bodies, (as in set up by law) let alone decent, honest or truthful. These two organisations are more misleading per se than any misleading advert I have seen. The most misleading thing is that they lead you to believe they are official bodies. They aren’t. They write to you as if they have legal powers. They don’t. You can’t even lodge a complaint about them being misleading because they are accountable to no one.
* CAP/ASA decided in 2010 that they will extend their self appointed remit to the internet. As someone who does not place adverts and does not allow adverts on any of my web sites, I would not expect to have anything to do with either body. CAP and the ASA have different views. They have decreed that, if you are connected to ‘a product’ in any way e.g. author of a book, web pages that they decide are connected with that book shall be deemed adverts.
* CAP have opinions. They have opinions on things you may not even think warrant an opinion. They have opinions on global warming, fat burning, the calorie theory, current dietary advice, cholesterol, stripograms (yes, really!) and religious organisations, just as examples.
* In my world of diet, health and nutrition, CAP believe that the current dietary advice is correct. They believe the calorie theory. They believe that Flora gunge is good for the heart and that cholesterol is bad. They have no evidence for any of this – but they are a self-appointed regulator, so they do whatever they like.
* A troll writes to the ASA and complains that you say things on your web site like “the calorie theory and conventional weight loss advice is wrong“. The ASA then writes to you saying:
i) We have decreed that your web page is an advert;
ii) You are in breach of the CAP code; and
iii) You must stop saying things that CAP don’t like, or we will put you on our naughty boys’ list.
Hence – we are now on the naughty boys’ list. Or, as Dr Malcolm Kendrick says, we now have a badge of honour!
This blog is about censorship. This blog is about one unofficial body trying to silence any views that are different to the opinions of their partner unofficial body, which you can assume to be conventional. It’s also about the scum levels that troll cowards are stooping to, to try to silence progressive thinking.
We asked CAP for evidence for their codes. The full exchange can be seen here. The bottom line is that CAP have no evidence for their opinions, against which they are judging us and in the field in which they are demanding evidence from us.
I wrote to the ASA chair, Rt Hon Lord Smith of Finsbury, and the CAP chair, James Best, and asked them four questions:
1) What gives the ASA/CAP (you are two parts of the same) the right to try to censor free speech?
2) Who gave the ASA/CAP the power to police any debate on the internet (including, but not limited to, health, nutrition, climate change etc) upon which CAP holds an opinion for the ASA to enforce?
3) How do you justify demanding evidence from me when a) you have none of your own (in my area of expertise anyway – see Appendix) and b) when the ASA are not able to consider our evidence because it differs from CAP’s opinions?
4) What will you do about this case, now and ongoing, given that I will not remove content from the World Wide Web, which challenges the status quo, just because CAP holds a conventional view?
I have not yet received a reply from CAP. The ASA chair did not deign to reply, but the head of casework replied on his behalf. Her response was as follows:
1) “Marketers have a right to express their opinions freely so long as they do so in line with the rules set out in the CAP code.”
i.e. you can freely express your opinions so long as they are the same as CAP’s. CAP holds conventional opinions and thus any non-conventional views are not allowed.
2) “Our authority to regulate marketing materials derives from an agreement from Government through which the ASA is designated as the ‘established’ means for administering the Consumer Protection from Unfair Trading Practice Regulations 2008 (the CPRs), which prohibit unfair, misleading or aggressive marketing to consumers.”
This is misleading. It implies that the ASA have been appointed by the Government to regulate adverts, which they have not. All that they have is access to the Office of Fair Trading (now abolished, by the way), which everyone else in the UK also has. They have no government authority to impose their opinions across the internet and to silence debate.
3) “It is not for the ASA to disprove a claim that a marketer has made and we are entitled to base our rules on generally accepted public health advice in the interest of consumer protection.”
i.e. we don’t have to provide evidence. We don’t have to disprove your evidence. We “are entitled” to rely on conventional thinking and insist on any non-conventional views being removed.
4) “If you refuse to comply with the advertising code following an ‘Upheld’ ASA adjudication, our Compliance team has a range of sanctions that include posting your name on our wall of non-compliant advertisers.”
i.e. if you do not allow yourself to be censored, we will put you on our naughty boys list.
That’s censorship and bullying and all sorts of other contemptible behaviour.
Logic & futility – you cannot win
To use one of our examples, a troll objected to this video “as it implied that conventional weight loss advice was wrong.” You bet it does!
The ASA decreed that the video is an advert for the book The Obesity Epidemic: What caused it? How can we stop it? That’s tenuous enough – but go with it. They then say that you’re not allowed to imply that conventional weight loss advice is wrong (because CAP have decreed that it is right) and therefore you must remove your ‘advert’ a.k.a. the video. Yes – seriously folks – George Orwell was way more prophetic than he/we realised.
If my site contained details of a book that reflected CAP’s opinions, there would be no issue. The Simon and Louis, Yin and Yang, of CAP and the ASA would not be trying to censor me. The ‘but for’ is therefore my content, not the notion that I am ‘advertising a book’.
To use another of our examples: This is a direct quotation from ASA correspondence:
“The claim “In no way is the body as simplistic as energy in = energy out – and, therefore, we do not need to put less energy in and/or try to get more energy out. We need to eat better, not to eat less” in ad (e) [ZH – that’s a web page] and comparison in ad (g) [ZH – that’s the video] misleadingly implied that conventional weight loss advice was wrong.” Again – you bet it does!
The ASA have decreed that this is i) in breach of CAP’s opinions (sorry – the CAP code) and ii) misleading. We pointed out to the ASA that – IF the web pages are adverts (and we have never accepted this – they are my editorial content) then we have two options:
i) Write conventional nonsense, which makes CAP happy, but then site visitors would be misled because the book is anything but conventional; or
ii) NOT mislead visitors and make site content clear that I do NOT subscribe to conventional wisdom, but then CAP would put you on the naughty boys list.
You cannot win in the ASA/CAP world of Alice in Wonderland.
The bottom line
We shared the attempt to elicit evidence from CAP with the ASA and asked a specific question:
“Please can you let us know how the ASA can review evidence submitted, in a “legal, decent, honest and truthful”, way when you exist to impose the opinions of CAP and the evidence submitted is counter to the opinions of CAP?”
The ASA replied back “As you are aware, it is the role of CAP to write, and review as necessary, the rules and it is the ASA’s role to apply them. Whilst I have noted your comments, because the ASA simply apply those rules I would not be able to consider as part of the investigation the evidence base or validity of those rules.”
And there you have it ladies and gentlemen. CAP admit they have no evidence. The ASA admit they have no choice but to administer the opinions of CAP. If someone complains to the Alternative-view Silencing Agency about you, don’t waste a second of your time submitting evidence. It makes not one iota of difference. Knowing this – you may like to choose your response more appropriately. From now on, ours will be “to ignore”.
“Freedom is the right to tell people what they do not want to hear.” George Orwell.
p.s. I always like to check conflicts of interest. To quote the ASA: “The ASA is funded by advertisers through an arm’s length arrangement that guarantees the ASA’s independence”. Ha ha. Check out P35 of the 2013 Annual Report, Unilever had 3 of the top 6 most complained about adverts. None were upheld by the Alternative-view Silencing Agency. Don’t bite the hand that feeds eh!?
The Royal Society for Public Health (RSPH) published a press release on 31st October 2014 calling on the drinks industry and the newly appointed EU Health Commissioner to introduce calorie labelling for alcoholic drinks. The RSPH claimed that there was strong public backing for this to happen and a general lack of awareness among consumers about the calorie content of alcoholic drinks.
The RSPH commissioned a polling company, Populus, who interviewed a random sample of 2,117 British adults, online, between 10-12th October 2014. The results were as follows (Please note – the press release claims “two thirds of the public”/”over 80% of the public”, but claims can only be made on behalf of those interviewed – not the Great British public):
– Two thirds (67%) of those interviewed supported the addition of calorie labels on packaging of alcohol drinks (we don’t know how this was positioned in the survey);
– Over 80% of those interviewed didn’t know, or guessed incorrectly, the calorie content of a large glass of wine (we don’t know what margin for error was allowed);
– Almost 9% didn’t know, or incorrectly estimated, the calories in a pint of lager (ditto).
(As an aside, this blog, by the RSPH chair said that 80% of 500 people “didn’t know the calorie content of their favourite tipple”. 2,117 or 500? How many people were interviewed?)
The European Commission is due to make a decision by December 2014, about extending nutrition labelling (including calorie labelling) on alcohol. (Alcoholic drinks are currently not recognised as food and are therefore exempt from food labelling.)
The Chief Executive of RSPH, Shirley Cramer CBE, was quoted in the press release as saying:
“Calorie labelling has been successfully introduced for a wide range of food products and there is now a clear public appetite for this information to be extended to alcohol to help individuals make informed choices. With 2 in 3 adults overweight or obese and given that adults who drink get approximately 10 percent of their calories from alcohol, this move could make a major difference to waistlines of the nation.”
I’m familiar with the UK Family Food Survey, so the “10 percent of their calories from alcohol” didn’t sound right. (Check the 2012 document – Table 24.4, page 18 – and you can see that alcohol accounts for 58 calories out of 1,990 – 2.9% of calorie intake.)
I emailed the communications manager to ask for the source of the 10% claim and she replied by return to say that it was from p17 of this. Start on p16 and notice that averages (means) for all adults (or in a couple of cases children) are reported for: fruit and vegetables; oily fish; all energy; total fat; saturated fat; transfats; Non Milk Extrinsic Sugars; non-starch polysaccharides; vitamins and minerals. Only one intake is reported differently. Alcohol is not reported as a mean intake of all adults, but as an average of those who drank alcohol in a four-day recording period: “58% of adults aged 19 to 64 years and 52% of adults aged 65 years and over consumed alcohol during the four-day recording period. Adults aged 19 to 64 years who consumed alcohol during the four-day recording period obtained 9% of energy intake from alcohol; older adult consumers obtained 7%.”
That’s how Cramer manipulated the figures to make the ‘prize’ of alcohol calorie reduction look larger than it is. Even then, 7 and 9% became “approximately 10%.” This is disingenuous.
Alcohol and calories
As followers of this blog/recipients of this newsletter will know, there are fundamental issues with calories in general: thermodynamics not being about calories or weight; the calorie theory being unsourced and unproven, etc. There are additional issues with alcohol calories…
The assignment of calories to different foodstuffs is generally credited to Wilbur Atwater (1844-1907) and Max Rubner (1854-1932). Their work around the turn of the 19th-20th century developed the first calorimeter and this enabled them to estimate that carbohydrate, protein and fat had approximately 4.1, 4.1 and 9.3 calories per gram respectively.[i] (Rubner recorded the calorific value for olive oil as 9.4, so even his 9.3 was an average of four fats reviewed. This has never been a precise science).
Atwater was concerned about helping American working men to fuel their physical labour and he discovered that alcohol had approximately 7 calories per gram. This was much to the joy of the liquor industry, giving rationale for alcohol consumption for its calorie value. It’s ironic that, just over 100 years later, the powers-that-be are trying to curtail alcohol consumption for its calorie value.
Those who know about the thermic effect of nutrients and the work of Jequier,[ii] Feinman and Fine,[iii] know that macronutrient calories behave very differently within the human body. Alcohol calories even more so. The body sees alcohol as a toxin and wants to get rid of it. Some is got rid of as acetic acid. (When you drink, you wee – yes?) Alcohol digestion takes place mostly in the liver and the kidneys, not in the digestive system – big clue there. So alcohol calories don’t count in the same way as sugary drink calories. Those RSPH pictures claiming a glass of wine = a slice of pizza – also disingenuous.
Arguably, given that alcohol calories are not properly digested – the more Brits drink and the less they eat, the slimmer they will be!
Calorie labelling and choices
Let’s be honest – what is really going on here is that the Royal Society for Public Health is trying to stop people drinking alcohol. Frightening people with health scares hasn’t worked, so they are now trying the calorie angle to see if this will curb drinking instead. And it might. Women especially are more calorie aware/obsessed than men and may choose a lower calorie drink. But this won’t necessarily lower alcohol – which is the end in mind, is it not?
The RSPH web site accompanying the press release has a picture of a Pina Colada (scroll down), claiming that it has 450 cals. It has 2 units of alcohol. On the same web page, I can see that I could have 2.5 x 250ml glasses of wine with a total of 8.2 units of alcohol for the same 450 calories. The law of unintended consequences could take effect here. On the RSPH’s own video here (bottom one) a woman says she won’t drink less – she may choose lower calorie alcohol options.
Alcohol and weight
You can download the RSPH’s position paper on alcohol here.
Here is the paragraph on alcohol and weight in the position paper:
“There is evidence that heavy drinkers (drinking four or more drinks per day) are at a greater risk of obesity than moderate or non-drinkers. The odds of being overweight or obese are also significantly higher among binge drinkers than among those who consume the same amount of alcohol over multiple sessions. (Ref 14) Weight gain from drinking alcohol is also greater in individuals who are already overweight or obese and there are individual differences in the impact of alcohol consumption on weight. (Ref 15) Drinkers dependent on alcohol, however, due to the propensity to substitute alcohol for meals, may experience weight loss (Ref 16).”
Ref 14 can be seen in full here. This is the results section of the abstract:
“Current drinkers had lower odds of obesity (Adjusted odds ratio = 0.73, 95% CI: 0.55, 0.97) as compared to non-drinkers. The odds of overweight and obesity were significantly greater among binge drinkers and those consuming four or more drinks/day. However, those who reported drinking one or two drinks per day had 0.46 (95% CI: 0.34, 0.62) and 0.59 (95% CI: 0.41, 0.86) times the odds of obesity, respectively. Similarly, the odds of obesity were significantly lower among those who reported drinking frequently and consuming less than five drinks per week.”
Did you get that? Current drinkers had lower odds of obesity. Those drinking one or two drinks per day had approximately half the incidence of obesity compared to non drinkers. The odds of obesity were significantly lower for the frequent drinkers. Look at Table 2 in the paper to see that you do not want to be a non drinker, or even in the first quartile of drinking days per year. Those in the second, third and highest quartiles of drinking days all had a significantly lower incidence of obesity. The average drinks per week data shows that you want to be having more than 15 drinks a week (a drink was counted as a 12oz beer or 4oz wine), rather than 10-14 drinks a week. Although the only statistically significant findings on the drinks per week section was those drinking up to 5 drinks a week had significantly lower levels of obesity than teetotalers.
The only finding in favour of alcohol intake and obesity was the one quoted by the RSPH position paper. This is disingenuous.
Ref 15 (abstract) can be seen here. The paper title is: “Is alcohol consumption a risk factor for weight gain and obesity” and it opens by noting “Epidemiologic data showed a positive, negative, or no relationship between alcohol intake and body weight.” Again – only the circumstance in favour of the RSPH’s anti-alcohol position has been cited: “Weight gain from drinking alcohol is also greater in individuals who are already overweight or obese.”
What about those not overweight or obese? You can either buy the paper ($54) or assume that – had there been any more ammunition from this paper, the RSPH would have used it.
Ref 16 doesn’t try to offer evidence for an association between weight and alcohol intake – other than an inverse one. It admits that very heavy drinkers tend to drink rather than eat and therefore tend to experience weight loss. This is further evidence for the notion that replacing food calories with drink calories could actually aid weight loss. (I think it would, but I am not advising it as an overall health strategy).
And that’s it. So we don’t actually have evidence presented by the RSPH for the implication that reducing alcohol consumption will reduce calories will reduce weight. It’s all just inferred. So what is the evidence for alcohol and weight?
Here is where you should do yourself a favour and get this fab little read from amazon. Tony Edwards has gone through reams of evidence on alcohol and all important conditions, from weight to heart disease and cancer to diabetes, so that you don’t have to. There were a couple of summary articles at the time of publication. Try this or this.
In Chapter 7 of his book, Edwards runs through the major studies reviewing alcohol and weight over the past 25 years: Wang et al 2010 studied 19,220 women, their drinking habits and weight for almost 13 years. Approximately 9,000 gained significant weight over the study. The study concluded: “Compared with non-drinkers, initially normal-weight women that consumed light-to-moderate amount of alcohol experienced smaller weight gain and lower risk of becoming overweight and/or obese during 12.9 years of follow-up.”
Then there’s the findings of a 5-6 year long Danish study, involving 43,500 people, where daily drinkers had the smallest waistlines. Then there’s the 8 year long University College London study of nearly 50,000 women, which showed that women who drank 30 grams of alcohol daily were less likely to put on weight than teetotalers. Then there’s the 10 year study, of 7,000 US adults, showing that drinker gained less weight than non drinkers. And so on.
Please note that this is all still association, not causation; relative, not absolute risk. Nonsense on top of nonsense therefore but not even the underlying association is supporting the RSPH position.
Don’t forget in all of this that the unit guidelines were plucked from thin air. Although Richard Smith wasn’t popular with the Royal College of Physicians for saying so.
Has the RSPH proven that calorie labelling on alcohol would reduce alcohol consumption? No.
Has the RSPH proven that alcohol and weight are even positively associated? No.
Has the RSPH proven that labels would have any impact on any health condition that alcohol is claimed to be associated with? No.
There’s just been a lot of insinuation, inference and disingenuity. And a lot of media hot air. Talking of hot air…
Here’s a final thought for you…
Coal apparently has 7,000 calories (kcal) per kg. That’s 7 kcal per gram – the same as alcohol. Do you think that a gram of coal would make you fat?! Well then…
[i] Max Rubner, “Zeitschrift fur Biologie,” Festschrift zu Voit, (1901).
[ii] Eric Jequier, “Pathways to Obesity”, International Journal of Obesity, (2002).
[iii] Richard Feinman and Eugene Fine, “A calorie is a calorie violates the second law of thermodynamics”, Nutritional Journal, (2004).
Michael Mosley was back on our screens last week (15 October 2014). I do like MM. I like his bedside manner. I like his preparedness to self-experiment and he’s becoming more and more aligned with the real foodie way of thinking, as shown with his confession on exercise here and on fat here.
However, he and the other doctors on Trust me I’m a doctor (TMIAD), are being badly let down by whoever is advising them on nutrition. Doctors receive barely a few hours of training in nutrition, despite Hippocrates’ advice “Let food be thy medicine and medicine be thy food.”
The carb experiment
Dr Chris van Tulleken, one of the twins who did the Horizon fat vs. sugar experiment in January 2014, is one of the TMIAD presenters. He took part in a ‘ground-breaking’ experiment, in an Italian restaurant, with the positioning statement: “starchy foods, like potatoes and pasta, have lots of calories but can you make these goods better for you?”
The study lead was Dr Denise Robertson from the University of Surrey. The 10 participants were given 100g (cooked weight) of pasta (with a tomato based sauce), 3 days in succession. On day one the pasta was hot, just cooked; on day two the pasta was cold, having been chilled overnight; and on day three they had the chilled pasta re-heated. This is a good experiment design, as the same subjects are used for all three interventions thus minimising any impact of different people responding differently to the same circumstances. The participants took their own blood samples every 15 minutes for the 2 hours following the pasta consumption.
Robertson’s hypothesis was that cooking the pasta differently would “reduce its calories.”
Tulleken narrated: “starchy foods like this are very quickly broken down into sugars … high sugars, and the resulting insulin, are unhealthy and they may make you feel hungry soon after a meal. And that’s the problem with refined sweet sugars, but it’s also true for things like pasta, potatoes, white rice and white bread.”
A graph was shown of the rise in blood glucose levels after eating first the freshly cooked pasta.
The average fasting blood glucose level is 5.6 mmol/L, but the normal range is wide and most people fall into a fasting blood glucose range of 3.3-7.7 mmol/L. The starting average blood glucose level for the group of 10 was 4.6 mmol/L (reading from the graph on the TV as accurately as possible). The peak blood glucose level occurred after 30 minutes – 6.6 mmol/l. At 120 minutes, the mean blood glucose levels were 5.3 mmol/L.
The chilled pasta peaked at about 6.4 mmol/L and the peak was slightly later than the freshly cooked pasta. However, the graph shown on the programme put the fresh pasta and chilled pasta alongside each other. I don’t know about you, but I found the difference between the green and blue lines completely underwhelming.
Robertson explained what had happened as follows: “We know that when a starch, such as potato or pasta, is cooked in water and then it’s allowed to cool, you’re changing the structure of that starch. You’re changing it in such a way, it becomes resistant to the normal enzymes that we have within our bodies. And, because the enzymes don’t work on it, it releases less glucose and so you get a lower glucose response.”
Tulleken clarifies “So it’s good for you because you get a lower blood sugar.”
Robertson: “You do and it’s now called resistant starch. And resistant starch, because you’re not digesting it will move down your intestine; it will end up in your large bowel and it becomes part of your dietary fibre.”
It got a bit more interesting when the two-day-old chilled pasta was re-heated. The graph for this one led Tulleken to exclaim: “astonishingly, it reduces the rise in glucose by another 50% making it even healthier.” You can see the second graph below
The blood glucose peak for the re-heated pasta is 5.7 mmol/L. The 50% is a relative claim, using the 4.6 mmol/L starting blood glucose level and is highly misleading. The red line is more different from the green line than the blue line is, but it’s not ground-breaking and here is why…
The programme could have produced a flat line – none of the ‘bad’ rise in glucose, sugar peak and insulin production by either 1) giving the subjects meat or fish or 2) giving them the pasta packaging to eat!
What this experiment has done is to make food less digestible so that it doesn’t produce the physiological changes that occur when the body registers that we have eaten food. The ultimate indigestible substance would be the cardboard box from which the pasta came. “But that would be stupid – it has no nutrients“, I hear you cry and you would hit the nail on the head. This experiment seems to completely disregard the reason why we eat. We eat food because we need nutrients to survive: essential fats; complete proteins; vitamins and minerals. This experiment is celebrating indigestibility – the pointlessness of eating something.
White pasta has little enough nutrition to start with. When it has been boiled once, chilled in a fridge overnight, left for another day and then re-boiled – how many nutrients do you think survived? I don’t know. I can tell you what it had after it was first cooked. And then compare it to the meat or fish that the participants could have enjoyed in the same Italian restaurant:
|(All per 100g of cooked product)
|Calories per 100g
|TOTAL (Ash makes up remainder)
|A (3000 IU)
|B1 (1.2 mg)
|B2 (1.3 mg)
|B3 (16 mg)
|B5 (5 mg)
|B6 (1.7 mg)
|Folate (400 mcg)
|B12 (2.4 mcg)
|C (90 mg)
|D (600 IU)
|E (15 mg)
|K (120 mcg)
|Calcium (1000-1200 mg)
|Magnesium (420 mg)
|Phosphorus (700 mg)
|Potassium (4,700 mg)
|Sodium (1,500 mg)
|Copper (0.9 mg)
|Iron (18 mg)
|Manganese (2.3 mg)
|Selenium (55 mcg)
|Zinc (11 mg)
As you can see from the table, the pasta has no essential fats, no complete protein and is pretty pointless for vitamins and minerals – manganese being an unimpressive exception. And this was before it was chilled, left and re-heated – no doubt destroying more of these paltry nutrients. The essence of this part of the programme was that a researcher managed to reduce the nutritional content of pasta by making it less digestible and this was considered a good thing?!
The really interesting points from this experiment are:
1) It shows how deeply and completely ingrained the belief is that we should be basing our meals on starchy foods. At no point did a nutritional scientist (Robertson) or a doctor (Tulleken) – both very bright people no doubt – question the wisdom of eating starchy carbohydrates in the first place. Especially in the context of the discussion about blood glucose and insulin response being desirable to avoid.
2) It was a fun admission that a calorie is not a calorie. Those who think that there is only one law of thermodynamics (and even this one doesn’t say energy in = energy out) will be beyond distressed trying to work out where the missing calories have gone.
Those who know that the second law, entropy, must be taken into account will enjoy the example of what entropy is all about – calories being lost and calorie being used in making available energy.
Those who really understand thermodynamics will know that it says nothing whatsoever about weight anyway – it is entirely about the movement of heat – and therefore it says no more about 100g of pasta than it says about 100g on the bathroom scales.
3) It was a wonderful admission, from a doctor, that starch is sugar. The starch that our government tells us to eat is sugar.
And those were the real lessons from the experiment.
The fat investigation
Later on in the programme, Mosley addressed the nutritional issue that led to the advice that we should eat more carbohydrate – the demonisation of fat. Mosley explained that he grew up in the 1960s when “medics declared war on saturated fat.” He shared that this had led to an increase in consumption of margarine and then we realised that the trans fats in spreads “are fantastically bad for the heart and they are being phased out“. Mosley described this as an example of “a public health campaign which had an unfortunate consequence.” But – Mosley set out to ask – how bad was the original advice on saturated fat?
In the introduction to this part of the programme, Mosley made all the errors that can be made in relation to fat in just a few words: “Saturated fatty acids, as they are technically known, are found in animal fats… and also in some vegetable oils, like palm and coconut, while other oils such as olive and sunflower contain polyunsaturated fatty acids.”
1) Saturated fatty acids are found in every single food that contains fat – not just animal foods – there are no exceptions.
2) Saturated fatty acids are found in all vegetable oils – not just palm and coconut – there are no exceptions.
3) Oils, such as olive and sunflower, and palm and coconut, do contain polyunsaturated fatty acids. They also contain saturated fatty acids and monounsaturated fatty acids because all foods with fat contain all three fats – there are no exceptions.
Mosley then sets off to try to answer the question” Does saturated fat really increase the risk of heart disease, as is widely believed?” But what hope does he have when he doesn’t even know what saturated fat is?!
Mosley interviews Professor Kay-Tee Khaw, from the Department of Public Health at Cambridge University, who was part of the study group that did a systematic review of 49 observational studies and 27 Randomised Controlled Trials (RCTs) with the conclusion “Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”
Professor Christian Drevon, from the Department of Nutrition at Oslo University, was the BBCs classic counter-balance interview. He still thinks that “saturated fat in the diet is one of the major risk factors for Coronary Heart Disease“. This is where Mosley’s ignorance didn’t help, as he wasn’t armed with the right questions to challenge Drevon, who should have been asked: What is saturated fat? How can we obtain the essential fats, complete protein, vitamins and minerals that we need to survive without eating saturated fat? (and quite a lot of it) Why do you tell people to favour vegetable fats over animal fats when a tablespoon of olive oil has nearly three times the total fat and twice thee saturated fat of a 100g pork chop? And so on…
From a lack of basic understanding, it was perhaps not surprising that Mosley’s announced that his personal conclusion on saturated fat is: “These days I do eat butter and drink milk, but it’s not an excuse to pour down double cream because, whatever it’s doing to your heart, fat is very rich in calories.” Where the heck did calories come in?!
Trust me I’m a doctor?
I did enjoy the programme. The evidence for acupuncture having a visible effect under MRI, but without the mechanism being known, was honest and interesting. The paralysed patient being able to stand and move his limbs again was utterly inspirational and hugely significant for spinal cord injuries. The vitamin D study was interesting – mostly for the fact that less than half of a group of office workers had adequate vitamin D levels – more so than the discovery that sun, vitamin supplements or oily fish would work equally well and quickly at restoring those levels. There was much of value in the programme. However, it sadly showed that, when it comes to nutritional science, you may not want to trust your doctor.