US and UK dietary advice on fats “should not have been introduced” Part 2
Evidence from prospective cohort studies did not support the introduction of dietary fat guidelines in 1977 and 1983: A systematic review
When this paper was published in February 2015, Public Health England conceded astonishingly quickly that there was no randomised controlled trial (RCT) evidence to justify dietary fat recommendations at the time they were introduced (1977 US/1983 UK).
However, they continued to dig holes with the following assertions:
1) Ah yes – but this review “looks at the results of just six relatively short-term randomised controlled trials (RCTs), whose limitations are acknowledged by the authors”;
2) Ah yes – but we know that that “saturated fat consumption influences cholesterol levels and increases the risk of cardiovascular disease” (quotations from the PHE letter to the journal, BMJ Open Heart);
3) Ah yes – but the RCT evidence available today is overwhelming;
4) Ah yes – but the epidemiological evidence at the time was strong.
1) Is so funny. That was our conclusion – as set out here. Our two dramatic findings were 1) there was no evidence to support restrictions on total or saturated fat and 2) not even 2,500 sick men had even been studied to come to this conclusion.
Don’t criticise us for pointing out that guidelines had been introduced for hundreds of millions of Brits and Americans, when they were not even justified following studies of a few sick men! That’s your limitation – not ours!
2) Good try – but read the Open Heart paper again. One of the significant findings was that 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 coronary heart disease (CHD) or all-cause mortality.
The Open Heart paper published in February 2015 found no evidence for the dietary fat/blood cholesterol/heart disease HYPOTHESIS.
3) Professor Julien Baker, Dr James J DiNicolantonio, Professor Bruce Davies and I are waiting on a follow-up paper, which has been in submission since January 2016. This was the natural follow-up paper to last February’s paper – it reviews the pool of RCT evidence available today. Guess what – it provides no retrospective support for the dietary fat guidelines. Watch this space for the full results…
4) A paper has been published today, 30 June 2016 reviewing the epidemiological evidence available to the dietary guidelines committees in 1977 (US) and 1983 (UK) respectively. The abstract is here. The key findings are as follows:
Dietary fat recommendations were introduced by the US Select Committee on Nutrition and Human needs in 1977 and the UK National Advisory Committee on Nutritional Education in 1983. The two specific recommendations were 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 intended to address mortality from coronary heart disease (CHD).
The most comprehensive population study undertaken at the time was the Seven Countries Study. 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. Keys acknowledged that epidemiological studies could reveal relationships, not causation.
This BJSM paper is the first to review the epidemiological evidence available to the dietary committees.
The paper documents the systematic review that was undertaken to identify and examine all prospective cohort studies available to the dietary committees. A meta-analysis was not possible as suitable data were not available.
Two studies were available to the US committee, meeting in 1977: The Western Electric Study;[5 6] and The Seven Countries Study. Four further studies were available to the UK committee: The Puerto Rico Heart Health Program;[7-9] The Framingham Heart Study;[7 10] The Honolulu Heart Program;[7 11 12] and a study conducted in London and the South East.
While the RCT evidence of the day had exclusively studied men with existing heart disease, the prospective cohort studies also exclusively studied men, but this time mostly without existing heart disease. The one exception was The Seven Countries Study, which included men with previous heart disease. This gave one of the major findings: “The death rate from CHD for those with, and without previous myocardial infarction was 20.9% and 1.0% respectively.” i.e. one of the major causes of heart disease is heart disease!
None of the six cohort studies examined either of the introduced dietary guidelines: a total fat consumption of 30%, or a saturated fat consumption of 10%, of energy intake.
None of the six studies found any significant relationship between CHD deaths and total dietary fat intake.
One of the six studies, The Seven Countries Study, found a statistically significant relationship between CHD deaths and saturated dietary fat intake. The Seven Countries Study also reported that smoking, activity levels/exercise and weight played no part in CHD. Importance was assigned to a study for its saturated fat finding, which contradicted contemporary evidence about smoking, activity and weight.[14-16]
Some interesting and statistically significant relationships were found by the cohort studies:
– Four of the studies (Puerto Rico, Framingham, Honolulu and the London bus and bank study) found a significant relationship between higher calorie intake and lower incidence of CHD.
– The Framingham and Honolulu studies found a significant relationship between higher alcohol intake and lower incidence of CHD!
– The London and Honolulu studies found a significant relationship between higher starch/cereal intake and lower incidence of CHD.
Affluence and/or activity levels could have been confounding variables in these findings.
One study alone, The Seven Countries Study, found support for the diet-heart hypothesis. This study suffered the most serious limitations: first of selection bias and second of not comparing the development of CHD against non development of CHD in each cohort. Rather it was an inter country comparison, comparing the development of CHD in one cohort/country with the development of CHD in another cohort/country, which therefore introduced many other confounders.
Five of the studies made no mention of dietary fat in their conclusions. The Western Electric Study concluded: “No relation was encountered between body weight, mean blood sugar levels, lipoprotein lipase levels, or diet (other than coffee), and the development of coronary heart disease” (p30). Morris et al identified healthy and unhealthy patterns of behaviour: “Meanwhile, a pattern of healthy living may have been identified: high energy intake and expenditure, high intake of cereal fibre, no cigarettes, with relatively little proneness to heart attack; and another behaviour pattern, of low energy intake and physical inactivity, low intake of cereal fibre, smoking cigarettes-carrying a relatively high risk” (p.1313). The 1981 publication combining the Framingham, Honolulu and Puerto Rico cohorts summarised the findings of the three studies together: “In conclusion, men who developed MI or died of CHD consumed significantly fewer calories (but weighed more) and consumed less alcohol than average” (p.514).
Some correlation coefficients reported by Keys were strong: median serum cholesterol and saturated fat as a percentage of calories r = 0.89 (p.I-170); median serum cholesterol and CHD deaths and infarctions (data for CHD deaths alone were not presented) per 100 people r = 0.76 (p.I-172); CHD deaths and infarctions and saturated fat as a percentage of calories: r = 0.84 (p.I-174); and CHD deaths and infarctions and total fat as a percentage of calories r = 0.40 (p.I-173).
These correlation coefficients established strong relationships between the component parts of the diet-heart hypothesis, using saturated, not total, dietary fat and using CHD deaths and infarctions. However, strong correlations were found with CHD and other factors, as different as animal protein and television sets, with Gross Domestic Product and living standards suggested as the confounding and possibly causal variables.[18 19]
I found the strongest correlation of all with latitude, as presented in my 2010 book “The Obesity Epidemic: What caused it? How can we stop it?” The correlation coefficient for CHD deaths and latitude of the cohort was 0.93. The correlation coefficient for CHD deaths and latitude of the country was 0.96.
The latitude finding offers an alternative explanation for the observed relationship with cholesterol and CHD. Vitamin D is made when sunshine synthesises cholesterol in skin membranes. In cohorts further away from the equator, cholesterol is less able to be turned into vitamin D. Population mean serum cholesterol levels are higher and concomitantly population mean vitamin D levels are lower. Higher CHD could be associated with lower vitamin D, with cholesterol a marker, not a maker, of heart disease.
Harcombe et al reported that the dietary fat guidelines were not supported by RCT evidence available at the time of their introduction. This systematic review finds that the prospective cohort study evidence available at the time did not support the introduced dietary guidelines. Both reviews reported serious limitations with the availability of primary prevention, both-sex, studies, which are the ones most likely to have generalisability for whole populations.
1. Select Committee on Nutrition and Human Needs. Dietary goals for the United States. First ed. Washington: U.S. Govt. Print. Off., February 1977.
2. National Advisory Committee on Nutritional Education (NACNE). A discussion paper on proposals for nutritional guidelines for health education in Britain. London: The Health Education Council, 1983.
3. Keys A. Coronary heart disease in seven countries I. The study program and objectives. Circulation 1970;41(I-1-I-8) doi: 10.1161/01.CIR.41.4S1.I-1[published Online First: Epub Date]|.
4. Keys A. Coronary heart disease in seven countries Summary. Circulation 1970;41(I-186-I-195) doi: 10.1161/01.CIR.41.4S1.I-186 [published Online First: Epub Date]|.
5. Paul O, Lepper MH, Phelan WH, et al. A Longitudinal Study of Coronary Heart Disease. Circulation 1963;28(1):20-31 doi: 10.1161/01.cir.28.1.20[published Online First: Epub Date]|.
6. Shekelle RB, Shryock AM, Paul O, et al. Diet, Serum Cholesterol, and Death from Coronary Heart Disease. New England Journal of Medicine 1981;304(2):65-70 doi: doi:10.1056/NEJM198101083040201[published Online First: Epub Date]|.
7. Gordon T, Kagan A, Garcia-Palmieri M, et al. Diet and its relation to coronary heart disease and death in three populations. Circulation 1981;63(3):500-15 doi: 10.1161/01.cir.63.3.500[published Online First: Epub Date]|.
8. Garcia-Palmieri MR, Feliberti M, Costas R, Jr., et al. An epidemiological study on coronary heart disease in Puerto Rico: The Puerto Rico Heart Health Program. Bol. Asoc. Med. P. R. 1969;61(6):174-9
9. Garcia-Palmieri MR, Tillotson J, Cordero E, et al. Nutrient intake and serum lipids in urban and rural Puerto Rican men. The American journal of clinical nutrition 1977;30(12):2092-100
10. Gordon T, Kannel WB. The Framingham Massachusetts Study twenty years later. In: Kessler I, Levin M, eds. The Community as an Epidemiologic Laboratory; A Casebook of Community Studies. Baltimore: Johns Hopkins Press, 1970:123-46.
11. Kagan A, Harris BR, Winkelstein W, Jr., et al. Epidemiologic studies of coronary heart disease and stroke in Japanese men living in Japan, Hawaii and California: demographic, physical, dietary and biochemical characteristics. J. Chronic Dis. 1974;27(7-8):345-64
12. Yano K, Rhoads GG, Kagan A, Tillotson J. Dietary intake and the risk of coronary heart disease in Japanese men living in Hawaii. The American journal of clinical nutrition 1978;31(7):1270-9
13. Morris JN, Marr JW, Clayton DG. Diet and heart: a postscript. BMJ 1977;2(6098):1307-14 doi: 10.1136/bmj.2.6098.1307[published Online First: Epub Date]|.
14. Dawber TR. Summary of recent literature regarding cigarette smoking and coronary heart disease. Circulation 1960;22:164-6
15. Kannel WB. Habitual level of physical activity and risk of coronary heart disease: the Framingham study. Can. Med. Assoc. J. 1967;96(12):811-2
16. Morris JN, Crawford MD. Coronary Heart Disease and Physical Activity of Work. BMJ 1958;2(5111):1485-96
17. Keys A. Coronary heart disease in seven countries XVII. The Diet Circulation 1970;41(I-162-I-183) doi: 10.1161/01.CIR.41.4S1.I-162[published Online First: Epub Date]|.
18. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease; a methodologic note. N. Y. State J. Med. 1957;57(14):2343-54
19. Yudkin J. Diet and coronary thrombosis: Hypothesis and fact. The Lancet 1957;270(6987):155-62
20. Gillie O. Sunlight robbery: a critique of public health policy on vitamin D in the UK. Molecular nutrition & food research 2010;54(8):1148-63 doi: 10.1002/mnfr.200900589[published Online First: Epub Date]|.
21. Scragg R. Seasonality of cardiovascular disease mortality and the possible protective effect of ultra-violet radiation. Int J Epidemiol 1981;10(4):337-41
22. Harcombe Z, Baker JS, Cooper SM, 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. Open Heart 2015;2(1) doi: 10.1136/openhrt-2014-000196.
21 thoughts on “US and UK dietary advice on fats “should not have been introduced” Part 2”
I was planning to email you this somewhat long comment, but couldn’t find an address (which I assume is deliberate, given the amount of non-constructive mail you’d probably receive). Anyhow…
I’d like to thank you for your blog; I’ve been reading it for about twelve months now, and it’s been a breath of fresh air to hear someone else (both more eloquent and more qualified than myself) discuss the flaws of the lipid hypothesis. The fact that I share your opinion puts me a difficult position, as I work as a doctor (third year resident) in an Australian hospital, where the lipid hypothesis is considered gospel. Despite this, I cannot bring myself to list “hypercholesterolaemia” or, worse still, “dyslipidaemia” under a patient’s past medical history.
This incongruity between my opinions and those of the medical profession at large is likely to become even more problematic for me next year, when I commence my training as a general practitioner. I will certainly never find it necessary to measure a patient’s serum cholesterol level, but I have no doubt that some of my patients will request that I do so. And I shudder to think of the damning accusations that might be levelled at me by cardiologists who consult on my patients, demanding to know why I have not yet started Mr. Smith on a statin, or why I have not advised Mrs. Brown to eat less fat. Sadly, I have already resigned myself to the reality that I will be forced to abide by guidelines that run contrary not only to my own personal opinions, but also to common sense.
I like to think that I will live to see the downfall of the lipid hypothesis, but considering how recalcitrant the medical profession is being, even in the face of overwhelming evidence, I’m not sure that I will. What frightens me the most is the irreparable damage that will be inflicted upon the profession’s reputation when the hypothesis finally does meet its end, opening up every other medical recommendation to accusation and ridicule. After all, if we lied about heart disease, who’s to say that we didn’t also lie about the link between smoking and lung disease, or vaccination and autism?
Still, I hope you’ll continue the crusade, and please know that some of us who are contributing to the perpetuation of the lipid hypothesis are doing so against our better judgement.
Keep up the good work, Jason! We need more GPs like you. You are probably already aware of people like Dr Malcolm Kendrick and Dr Joanne McCormack here in the U.K. who continue GP work. And I have personally come across some great GPs who think for themselves. It’s good to read the comments of doctors like you. Bon courage!
I don’t know if you saw this report on a Harvard study, which was mentioned in “The Guardian” on July 6.
These big studies apparently well conducted are difficult for the layman to understand and criticise! Whats your take on it?
Eating more saturated fats raises risk of early death, says US study
It’s yet another association study. Here’s one saying something different just a few days earlier http://edition.cnn.com/2016/07/01/health/butter-health-study/
Here’s another saying the veg oil consumers had a higher risk of death than the butter eaters – from just over a month ago http://www.telegraph.co.uk/wellbeing/health-advice/why-butter-is-no-longer-the-bad-guy/
Association studies should largely be ignored. They should be used to observe exactly what the name suggests – associations. They should be of the Bradford Hill level of evidence (e.g. differences should be two fold – not 8%!) Then randomised controlled trials need to be undertaken to test observations made. e.g. we observe people who wear red socks die more often from heart disease. We’ll do a large trial of healthy men and women for a long period of time and make half of them wear red socks and leave the other half unchanged and see if the red sock people die more from heart disease.
The RCTs have been done in this field (http://openheart.bmj.com/content/2/1/e000196.full.pdf+html) and show no evidence to support any fat claim. As Prof Tim Noakes said yesterday on twitter: “If assoc studies found something real, RCTs would confirm. Have not. Why doesn’t @HarvardHealth admit?”
Best wishes – Zoe
I see the papers are faithfully reporting the latest “Anti Butter” fightback!
They won’t give up.
Professor Tim Noakes nailed it on twitter yesterday when he said “If assoc studies found something real, RCTs would confirm. Have not. Why doesn’t @HarvardHealth admit?”
Best wishes – Zoe
Hello, I wanted to explain the 3,500 calorie misunderstanding. In order to gain 1 pound, you need to consume 3,500 calories more than your normal diet, without changing your workout routine. That 1 pound isn’t necessarily all fat either. This is what is being referred to on the Mayo clinic site. What you are actually pointing out is the amount of energy/kcal (kilo calorie) in 1 gram of fat when it is consumed as part of a meal – this is 8.8kcal, or rounded to the nearest whole number as 9 kcal. Proteins & carbs are 4kcal/gram, and alcohol is about 7 kcal/gram. The 3,500 calories consumed to gain a pound would obviously not be all fat, as I doubt anyone could stomach (no pun intended) such a meal. This of course is a guideline as metabolism, activity levels, age, and gender all have a component in this equation. If someone is trying to lose weight, reducing their caloric intake and increasing activity levels helps. They just need to remember when losing weight, fat, water, and lean muscle, all respond to a weight loss routine – so 1 pound of weight lost does not equal 1 pound of fat loss. I hope this helps.
Sorry but the 3,500 calorie myth is just that – a myth. You may find these interesting:
Best wishes – Zoe
Perhaps, if you haven’t already, you should read some of Atwaters original work on this. They were not convinced that the c in c out was entirely relevant to the metabolism of the human body. One thing they did seem to deduce was that carbohydrate showed the most correlation to metabolism. As for alcohol it has been my experience that the human body treats it as a poison and excretes it any way it can. Breath pee etc etc. You cannot put on weight by drinking alcohol. You can put on weight by drinking beer which is bread in a glass that has a bit of alcohol in it. I can elaborate on this but not now. The final issue with the c in c out theory is that people forget that you don’t just eat to bag calories. There is the small matter of nutrient density which I’m sure Zoe will be more that happy to explain. C in c out is a paradigm that is in great need of overhaul if not ditching all together.
How much do you actually believe that “Higher CHD could be associated with lower vitamin D”? I read a book advocating getting more sun, and I try to do so when I can. However, a lot of the supporting evidence in the book was epi, which we know proves correlation but not causation. In fact, I could disprove some of the assertions by using the same data.
I’ve got my bets on Malcolm Kendrick’s theory (if he ever gets around to wrapping it up ;-). It seems to make the most sense to me. (But so does “fat has 9 calories per gram and therefore is more fattening than carbs at 4 calories per gram” and “fiber protects you from cancer”, and both of those have been proven to be wrong in my opinion.)
I’m also loving Dr Malc’s series! He is a fan of sun and vitamin D (click on this https://drmalcolmkendrick.org/?s=vitamin+D
or search vitamin d on his site)
I do think there is at least an association. One of the few 600 page books I read was Dr David Grimes Vitamin D and Cholesterol (all about CHD really).
Best wishes – Zoe
Another point Kendrick makes, which I haven’t often seen elsewhere, is the effect of sun on NO levels. A double whammy.
“fat has 9 calories per gram and therefore is more fattening than carbs at 4 calories per gram”
Only makes sense if they’re metabolised the same way and require the same amount of energy to metabolise. Which isn’t the case. They’re metabolised by different pathways and used by the body differently. So it really is a case of apples and oranges (or bananas and bacon).
I think this comes from the mechanical model of biology which regards food as fuel, from which follows the assumption that the body can run on either fat or carbs as “fuel”. Now because you can run a steam engine on wood or coal, it doesn’t mean the two are interchangeable. The same applies to foods.
The thing that I find most amusing though is the idea that meat is bad for us. Why would something that’s essentially identical to what we’re made of be toxic?
I should give you site access – redirect some emails too?! We certainly think alike ;-)
Best wishes – Zoe
LOL! I’m a rank amateur in this. I just read a lot and think critically.
But I’m happy to help :)
Couldn’t agree more. The human body is not a calorific bomb. There is something in the nutrient density connection. I run a small hotel. We serve a variety of options one of which is eggs, bacon, sausage ( high quality 90% + meat) and that delicacy of delicacies Black Pudding, all made by a local butcher. I never cease to be amazed at the number of people who think that are ‘sinning’ by eating a decent breakfast. It goes to show how ingrained the low fat high carb myth has inveigled itself into the worlds psyche. I do my best to steer people in a different direction, only problem is that we have fair proportion of our guests who are taking statin medicine they don’t remember the conversation; sad but true.
Black pudding! Where can I sign up?
I don’t usually eat breakfast — intermittent fasting works quite well for me. But at weekends I’ll often eat “breakfast” for lunch.
I have a friend who calls himself a pig doctor (he cures pigs) his home-cured bacon and black pudding are wonderful!
Oh, the Hugh Mannity of it all…..lol,
Bill, if they don’t want to eat it then all the more for me and my buddy Hugh
Sounds like my kind of hotel! It must be frustrating for you. I feel sad that so many people I see battling weight and/or diabetes are being misled into believing that a breakfast of cereal with skimmed milk and a glass of orange juice is the saintly route.
Thanks. I also enjoyed your comments on fats, and much else, in the Cape Town lecture—which Jimmy Moore has just posted as a podcast.
By the way, I think the comment the lady made to you about oysters probably goes back to the work of Stephen Cunnane of the Département de médecine, Université de Sherbrooke in Canada, and was made with specific reference to brain chemistry. The relevant tables have been popularised by Jack Kruse but were originally published here:
What Cunnane did was to remark that the most significant thing about human beings is their brain capacity, linking that to evolutionary data on encephalisation. Accordingly, he took a basket of ten “brain selective nutrients” (Fe, Se, I, Zn, etc.) and measured how much of each of a whole range of foods one would have to eat to get sufficient of each nutrient to support the human brain. If you do that, then Shellfish comes out on top by a fair way. (I can’t recall if DHA is in that basket, but there’s an important nutrient from the brain’s point of view!) From this point of view, fish is next best, and some types of offal from land animals are the best after that.
So the pointing to oysters is based not on nutrients in general, but specifically on those that are needed to support a large brain, since that’s what’s most important from the point of view of human evolution—and flourishing.
Hi Michael – many thanks for this – I love learning! I might get an opportunity to slip that one in to a talk one day. I’ll say a fan of Jimmy’s told me if I do :-)
Very best wishes – Zoe