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.