Sunday, March 30, 2014

Low Fat and CHD

I originally didn’t think about writing on low fat and CHD because I didn’t see the point.  After all, throughout the literature and the dietary guidelines there was no suggestion that low fat diets would reduce the risk of CHD.  But then I don’t subscribe to pop science, where calories make you fat, protein damages your kidneys, fat clogs your arteries, carbs give you diabetes and everything causes cancer.  For most people fat (of any kind) still remains the villain in CHD. 

Remember that the three main lines of evidence against saturated fat were: 

1.      Observational studies
2.      Clinical trials measuring blood lipids
3.      Clinical trials measuring end-points (events and mortality) 

I’m going to briefly go through each of these as they relate to low fat and CHD 

Observational Studies 

The Australian National Heart Foundation’s ‘Summary of evidence. Dietary fats and dietary cholesterol for cardiovascular health’ (2009) cites a review by Mozaffarian as evidence for “there is no direct relationship between total fat intake and the incidence of CHD”. 

The Australian Heart Foundation later use a meta-analysis of cohort studies by Jakobson, et al as evidence against saturated fat.  The Jakobson, et al meta-analysis found that replacing SFA with PUFA was associated with less CHD events and death, but replacing SFA with MUFA or carbohydrate had no effect* [1]. 

Another meta-analysis of cohort studies by Skeaff & Miller found that intake of total fat wasn’t significantly associated with CHD events or CHD mortality [2]. 

And finally, there’s also the well-known meta-analysis of cohort studies by Siri-Tarino, et al, which found “no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD” [3] 

* So if you’re going to debate the National Heart Foundation I don’t think you should spend much time arguing against low fat diets, because they will simply say that they don’t recommend a low fat diet, which is exactly what they did on Catalyst.  I would rather argue that (1) it’s unwise to make recommendations from observational studies and clinical trials measuring blood lipids; and (2) the better controlled fat modification trials don’t support the DHH and suggest some harm.  If you want to argue that they are recommending a low fat diet (because it seems most people challenging mainstream advice are pro-low carb), please define what ‘low fat’ means (I’ll be providing my take in a future post), otherwise it’s going to be one of those pointless ‘yes you are, no I’m not’ type of debate 

Clinical Trials Measuring Blood Lipids 

Two meta-analyses of clinical trials found that replacing fat with carbohydrate increases the total cholesterol to HDL-C ratio* [4] [5], which is perhaps the best CHD risk factor based on blood lipids [6]
* Only palmitic acid and artificial TFA increased the ratio, but the fats in food are comprised of many different fatty acids so even fat sources high in palmitic acid and/or artificial TFA like butter, shortening and palm oil reduce the total cholesterol to HDL-C ratio relative to carbohydrate 

** They also found replacing fat with carbohydrate increased triglycerides [4] [5] 

Clinical Trials Measuring End-Points (Events and Mortality) 

But we shouldn’t dismiss low fat diets based on findings of observational studies and their effect on blood lipids.  Just as it’s wrong to use observational studies to ‘prove’ there is an effect, it’s also wrong to use them to ‘prove’ there isn’t one either 

To my knowledge, there are two main meta-analyses looking at low fat (fat reduction) and CHD: the same Hooper, et al meta-analysis and the meta-analysis by Skeaff & Miller (who also did one for the fat modification trials*).  The results of the meta-analyses are in the table below: 

CHD Events
CHD Mortality
Total Mortality
Hooper, et al
0.97 (0.87, 1.08)
0.96 (0.82, 1.13)
0.97 (0.90, 1.04)
Skeaff & Miller
0.93 (0.84, 1.04)
1.00 (0.80, 1.24)
0.98 (0.90, 1.06)

Skeaff & Miller only included a trial by Ball, et al and the Women’s Health Initiative (WHI), while Hooper, et al included several others that were either very small (only a few events or deaths in each group), for cancer (mostly breast cancer and one bowel cancer) and one (the DO IT trial) that looks more like a fish oil trial.  So I’m only going to do Ball, et al and the WHI. 

This won’t limit me (or Skeaff & Miller) that much.  The WHI was a huge trial, lasting 8.1 years with 46,558 participants.  Consequently the WHI has well over 50% of the weighting in statistical analyses, which is probably a main reason why the results of the two meta-analyses are so similar, even though Hooper, et al included several other trials 

* They included Rose (but only compared olive oil to corn oil), LA Vets, MRC, Oslo, Finnish, DART and STARS and found for: CHD events RR = 0.83 (0.69, 1.00), p = 0.073; CHD mortality RR = 0.84 (0.62, 1.12), p = 0.335; and total mortality RR = 0.88 (0.76, 1.02), p = 0.005.  The somewhat positive result isn’t surprising considering their poor trial selection (pretty much as bad as Mozaffarian, et al) 

** My main objection to the fat modification trials was that the trials changed a lot more than SFA and PUFA intakes.  Some accidental changes would be expected when you make a dietary change.  For example: you would expect the control group (higher SFA) to have a higher vitamin A and cholesterol intake and the experimental group (higher PUFA) to have a higher vitamin E intake.  Other changes, like the amount of hydrogenated oil and junk food, is not expected and makes for a poorly controlled trial.  In the fat reduction trials you would expect the low fat diet would have more accidental changes, like increasing intake of vegetables, fruit and grains, as a function of increasing carbohydrate intake 


Despite the dogma that ‘fat will clog your arteries’, low fat diets wouldn’t be expected to reduce CHD based on both observational studies and their effect on blood lipids.  Also, low fat diets haven’t been found to reduce CHD events, CHD mortality or total mortality in clinical trials.

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