The 2015 DGA committee has released a 571 page document which is meant to inform the next dietary guidelines.[1] Changes are that % fat vs carbohydrate is no longer prescribed and cholesterol is no longer subject to a limit.
However, the old limit of 10% energy from saturated fat remains in place. Low fat or no fat dairy is the only dairy you're allowed. Meat? However poor or aged you may be, you should eat less of it. Although consumption of added sugars and refined grains is of concern, it always takes secondary place to the established evils of saturated fat and sodium.
Most of the document is dreadfully written and repetitively displays a circular logic. The healthy diet pattern (there are three of these, but they are interchangeable) is healthy (because it outperforms, slightly, a dummy version of the SAD diet); the healthy diet pattern avoids certain foods; ergo, these foods are not part of a healthy diet (even though they weren't an important part of the dummy SAD diet either).
Thus the verdict is repeated many, many times, and the prosecution does its summing up, and only then is the evidence presented. I'm familiar with this evidence. It's presented dishonestly.
The analysis pretends to be applying a truncated version of the Bradford Hill criteria. There's a good summary of these criteria and examples of their application here. There are 9 criteria and the first two are Strength of the Association and Consistency.
"Strong and consistent evidence from RCTs and statistical modeling in prospective cohort studies shows that replacing SFA with PUFA reduces the risk of CVD events and coronary mortality.
For every 1 percent of energy intake from SFA replaced with PUFA, incidence of CHD is reduced by 2 to 3 percent."
For every 1 percent of energy intake from SFA replaced with PUFA, incidence of CHD is reduced by 2 to 3 percent."
Part D. Chapter 6. page 16. (p451 doc)
Problem #1 - The evidence is not strong; in the meta-analysis by Dariush Mozaffarian et al., which is a meta-analysis supportive of substitution with PUFA, the average reduction in coronary mortality for 5% substitution was 0.80.[2]
Nowhere does the correlation attain the strength that Bradford Hill asked for, a factor of two or greater.
When the correlation is closest to one, as here, it can only be called weak. In fact it is even weaker than that, because the effect in primary prevention is not significant.
Nowhere does the correlation attain the strength that Bradford Hill asked for, a factor of two or greater.
When the correlation is closest to one, as here, it can only be called weak. In fact it is even weaker than that, because the effect in primary prevention is not significant.
Emphasizing the benefits of replacement of saturated with polyunsaturated fats, Mozaffarian et al., 2010 found in a MA of 8 trials (13,614 participants with 1,042 CHD events) that modifying fat reduced the risk of myocardial infarction or coronary heart disease death (combined) by 19 percent (RR = 0.81; 95% CI = 0.70 to 0.95; p = 0.008), corresponding to 10 percent reduced CHD risk (RR = 0.90; 95% CI = 0.83 to 0.97) for each 5 percent energy of increased PUFA. This magnitude of effect is similar to that observed in the Cochrane MA. In secondary analyses restricted to CHD mortality events, the pooled RR was 0.80 (95% CI = 0.65 to 0.98). In subgroup analyses, the RR was greater in magnitude in the four trials in primary prevention populations but non-significant (24 percent reduction in CHD events) compared to a significant reduction of 16 percent in the four trials of secondary prevention populations.
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| From Ramsden et al. BMJ 2013 |
Problem #2 - The evidence is not consistent, because there is more coronary mortality in some PUFA substitution studies, less in others, and no difference in others again.
You cannot use meta-studies as evidence of consistency!
The DGA committee also draw on the Harvard et al. meta-analysis by Farvid et al.[3]|
You cannot use meta-studies as evidence of consistency!
The DGA committee also draw on the Harvard et al. meta-analysis by Farvid et al.[3]|
Consistent with the benefits of replacing SFA with PUFA for prevention of CHD shown in other studies, Farvid et al., 2014 conducted an SR and MA of prospective cohort studies of dietary linoleic acid (LA), which included 13 studies with 310,602 individuals and 12,479 total CHD events (5,882 CHD deaths). Farvid et al. found dietary LA intake is inversely associated with CHD risk in a dose-response manner: when comparing the highest to the lowest category of intake, LA was associated with a 15 percent lower risk of CHD events (pooled RR = 0.85; 95% CI = 0.78 to 0.92; I²=35.5%) and a 21% lower risk of CHD deaths (pooled RR = 0.79; 95% CI = 0.71 to 0.89; I²=0.0%). A 5 percent of energy increment in LA intake replacing energy from SFA intake was associated with a 9 percent lower risk of CHD events (RR = 0.91; 95% CI = 0.86 to 0.96) and a 13 percent lower risk of CHD deaths (RR = 0.87; 95% CI = 0.82 to 0.94).
Once again, the word "consistent" is abused. Individual studies are not consistent, and this is a meta-analysis (which is supposed to include all the relevant studies) so the concept of consistency does not apply. In what sense is an average consistent?
However an even larger deception is taking place in this selective quotation from Farvid et al., because that paper also concludes that a 5 percent of energy increment in LA intake replacing energy from carbohydrate intake is associated with similar benefits as replacing SFA.
Every meta-analysis that tells you that there is no benefit from replacing SFA with CHO, but a benefit from replacing SFA with PUFA, is saying the same thing, but Farvid et al. finally spelled it out.
9 cohort studies evaluating substitution of LA for carbohydrate showed that substituting 5% energy intake from LA for carbohydrates lowered risk by about 10%. A slightly lower risk benefit was seen for substitution of LA for SFA.This systematic review and meta-analysis suggests that risk of CHD decreases with higher dietary LA intake, when replacing either carbohydrate or saturated fat.
Once again, the word "consistent" is abused. Individual studies are not consistent, and this is a meta-analysis (which is supposed to include all the relevant studies) so the concept of consistency does not apply. In what sense is an average consistent?
However an even larger deception is taking place in this selective quotation from Farvid et al., because that paper also concludes that a 5 percent of energy increment in LA intake replacing energy from carbohydrate intake is associated with similar benefits as replacing SFA.
Every meta-analysis that tells you that there is no benefit from replacing SFA with CHO, but a benefit from replacing SFA with PUFA, is saying the same thing, but Farvid et al. finally spelled it out.
9 cohort studies evaluating substitution of LA for carbohydrate showed that substituting 5% energy intake from LA for carbohydrates lowered risk by about 10%. A slightly lower risk benefit was seen for substitution of LA for SFA.This systematic review and meta-analysis suggests that risk of CHD decreases with higher dietary LA intake, when replacing either carbohydrate or saturated fat.
As a third criticism, how plausible is this claim - "for every 1 percent of energy intake from SFA replaced with PUFA, incidence of CHD is reduced by 2 to 3 percent"? With no safe upper limit set or implied.
For every 1 percent? Is the reduction the same for the 1st% and the 20th%?* And what of the observation that higher PUFA % intakes (like lower SFA % intakes) tend to be reported by those under-reporting calories? Is the correlation the same for absolute intakes (grams/day)?
The graphic from Farvid et al. above shows that there is less data above 6-7% LA and correlations become less reliable. As Ancel Keys would have predicted - dietary intake of LA above 7% is not a usual part of natural human diets, and the range of intakes in the 7 Countries study was 3-7%.
We are still in the "weak" range of correlation, meaning there could always be another explanation for what we are seeing. And we do not have all the data. The countries of the former Soviet Union have very low SFA intakes (6-7%) and very high LA intakes (unknown, but sunflower oil is the main cooking fat), and these countries have some of the highest rates of CHD mortality in the world. If we had reliable cohort data from these countries, what then?
And what of the elephant in the room of PUFA celebration - the lack of any association with all-cause, age-adjusted mortality? If PUFA substitution prevents CHD deaths, and CHD deaths are a major part of all deaths, then PUFA substitution should reduce all deaths. If it doesn't, then either the reduction in CHD mortality is illusory, or PUFA (or something associated with it) is causing more death from other causes. It doesn't.[4] Well there is a small, non-significant reduction, and the theory is that if this were multiplied to infinity by more and more studies it would attain significance and be interpreted as saving thousands of lives. As long as the new studies didn't come from parts of the world like Azerbaijan and, well, most of the rest of the world. But that the idea that a tiny association magnified means anything in a world of uncertainty, unreliability, and alternative explanations (known and hidden confounders) is nothing but clutching at straws.
The graphic from Farvid et al. above shows that there is less data above 6-7% LA and correlations become less reliable. As Ancel Keys would have predicted - dietary intake of LA above 7% is not a usual part of natural human diets, and the range of intakes in the 7 Countries study was 3-7%.
We are still in the "weak" range of correlation, meaning there could always be another explanation for what we are seeing. And we do not have all the data. The countries of the former Soviet Union have very low SFA intakes (6-7%) and very high LA intakes (unknown, but sunflower oil is the main cooking fat), and these countries have some of the highest rates of CHD mortality in the world. If we had reliable cohort data from these countries, what then?
And what of the elephant in the room of PUFA celebration - the lack of any association with all-cause, age-adjusted mortality? If PUFA substitution prevents CHD deaths, and CHD deaths are a major part of all deaths, then PUFA substitution should reduce all deaths. If it doesn't, then either the reduction in CHD mortality is illusory, or PUFA (or something associated with it) is causing more death from other causes. It doesn't.[4] Well there is a small, non-significant reduction, and the theory is that if this were multiplied to infinity by more and more studies it would attain significance and be interpreted as saving thousands of lives. As long as the new studies didn't come from parts of the world like Azerbaijan and, well, most of the rest of the world. But that the idea that a tiny association magnified means anything in a world of uncertainty, unreliability, and alternative explanations (known and hidden confounders) is nothing but clutching at straws.
Has all this effort and expense and messing with peoples' lives only had the result of sweeping the problem of CHD under the carpet of death from other causes?
I know anecdotal evidence has low admissibility, but all evidence is evidence of something. All over the internet and print media people will tell you that eating a lot less carbohydrate and more fat, sometimes more saturated fat, has improved their lives and their health. Doctors are saying this about their patients too.
Where are the blogs where people rave about how replacing butter with margarine has fixed their health problems? Millions of people take statins - where are the stories from statin users about the improvements to their lives? You will find more negative stories from statin users online. You might find stories of improved cholesterol, but where is the increased vitality and reversal of obesity and type 2 diabetes? Oh, wait.
You might conclude from this that any association between improvements in cholesterol and improvements in health is not necessarily a linear or temporal one. There is perhaps stronger evidence for the idea that improvements in health are temporally associated with improvements in cholesterol.
The DGAC are a bunch of brainy people, familiar with the evidence (some of them anyway), presenting a summary of this evidence to non-specialists - the Secretaries of the U.S. Department of Health and Human Services (HHS) and the U.S. Department of Agriculture (USDA).
How honest is their case?They present the observational evidence as being stronger than it is, and they suppress an important finding of this evidence which would contradict their saturated fat recommendation.
After all, if 7% PUFA is where the benefit lies (which is endlessly debateable and certainly not a case I'd personally want to make, especially in light of the all-cause mortality association), who eating either a standard American diet or one of the healthy "Healthy" DGA diets doesn't have a few % CHO to spare? And in that case, if you're willing to trade some sugar for some nuts, then where is the evidence against SFA? The observational evidence, weak though it was in terms of consistency and strength of association, just flew out the window.
Bye bye.
*Appendix 1
Walter Willet of Harvard put his name to this study, about a decline in CHD mortality in Eastern Europe where rapeseed oil has been substituted for sunflower oil.[5] Sunflower oil is about 44-75% PUFA, as LA, rapeseed oil supplies 15-30% PUFA, 15-20% as LA.[6, 7] This is evidence for the hypothesis that restricting PUFA or LA reduces CHD mortality.
Consistency.
[1] Scientific Report of the 2015 Dietary Guidelines Advisory Committee link
[2] Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. Mozaffarian D, Micha R, Wallace S. PLoS Med. 2010 Mar 23;7(3):e1000252. doi: 10.1371/journal.pmed.1000252.
[3] Dietary linoleic acid and risk of coronary heart disease: a systematic review and meta-analysis of prospective cohort studies. Farvid MS, Ding M, Pan A. et al. Circulation. 2014 Oct 28;130(18):1568-78. doi: 10.1161/CIRCULATIONAHA.114.010236. Epub 2014 Aug 26.
[4] Chewing the saturated fat: should we or shouldn’t we? Thornley S, Henderson G, Schofield G. NZMJ 23 May 2014, Vol 127 No 1394; ISSN 1175 8716
[5] Rapid declines in coronary heart disease mortality in Eastern Europe are associated with increased consumption of oils rich in alpha-linolenic acid. Zatonski W1, Campos H, Willett W. Eur J Epidemiol. 2008;23(1):3-10. Epub 2007 Oct 23.
[6] http://www.chempro.in/fattyacid.htm
[7] Chemical composition and stability of rapeseed oil produced from various cultivars grown in Lithuania. Dainora Gruzdienė, Edita Anelauskaitė.
http://www.icef11.org/content/papers/epf/EPF278.pdf