Monday, March 3, 2014

The Diet Heart Hypothesis: Part 4

Summary
 
People who support the diet heart hypothesis (DHH)* may use the Hooper, et al meta-analysis or the Mozaffarian, et al meta-analysis as evidence to replace SFA with PUFA, even though both meta-analyses found no benefit for total mortality.  After looking at the trials included in the meta-analyses, I found that those that were better controlled didn’t support the DHH**, and in fact suggested some harm, particularly for women.  Whereas the trials that supported the DHH were quite multifactorial in favour of the experimental group
 
The meta-analyses were only able to find some benefit (CHD events in Hooper, et al and CHD events and CHD mortality in Mozaffarian, et al) by including trials that were poorly controlled – trials that not only replaced SFA with PUFA, but also either altered the high PUFA diet in other ways and/or had other confounding variables that favoured the experimental group.  The Mozaffarian, et al was particularly guilty of this as they included three favourable trials that were multifactorial and also excluded two unfavourable trials for poor reasons
 
* Replace SFA with PUFA to lower LDL-C to reduce risk of CVD
 
** The only benefit was in a non-blinded trial that found a decrease in possible + probable angina (not very persuasive)
 
 
Some Possible Objections
 
The vegetable oils and margarine in the 60s-90s were often high in trans fats, therefore the trials were unbalanced in favour of the control group
 
The investigators generally took a lot of care to reduce the amount of trans fats in the experimental group by restricting hydrogenated oils and/or junk food, and by using soft margarines rather than common margarines.  But let’s say for the sake of argument that the experimental groups had some trans fats in their seed oils/margarine.  Then that might just balance out the restriction of hydrogenated oils and/or junk food that was present in all trials (except MCS because I don’t know), which leaves us with the same four trials that were better controlled: Rose, MRC, Sydney and MCS
 
Clinical trials are difficult to design and execute so we shouldn’t rely on them for answers.  Instead we should rely on observational studies, which prove/suggest replacing SFA with PUFA reduces CHD.
 
Yes, trials are hard, but if you don’t do them properly, then why do them at all?  What is the point of trials like the ACC, Oslo, FMHS and STARS?  You can’t even say which variables worked, which were unnecessarily and which were harmful.  All you can say is that the results are interesting and the variables need to be tested individually in further trials.  One of the earliest lessons in high school science is how important it is to test one variable at a time, so why didn't the researchers do that.
 
It’s really quite bad, if people want to know whether they should eat butter or margarine and whether to cook with animal fats or seed oils a trial should have just looked at that (one group butter and animal fats, the other group margarine and seed oils), nothing else.
 
As for observational studies or trials with blood lipids as the end-point, you shouldn’t rely on them for dietary guidelines or for establishing causality.  There are instances where things that appear favourable in observational studies and things that lower cholesterol or improve the total:HDL-C ratio have been found to have no effect or an adverse effect in RCTs (see these links)
 
The precautionary principle suggests that because LDL-C is associated with CVD and SFA increases LDL-C while PUFA decreases LDL-C we should replace SFA with PUFA
 
If anything the precautionary principle should be used against replacing SFA with PUFA.  After all the consumption of refined vegetable (seed) oils is very recent (~ 100 years), which is incidentally when deaths from CVD started climbing.  There is also a lack of long term data on the safety of high (~ 10%) PUFA diets (what Mozaffarian, et al and others suggest), and based on the studies Chris Masterjohn discusses here: as linoleic acid builds up in adipose tissue, vegetable oils seem to increase vitamin E depletion and consequently impair health*
 
* This may also counter the potential argument that the trials weren’t able to show benefit because they didn’t last long enough.  Besides that, some of the multifactorial trials found benefit and some of the better controlled found harm quite quickly (within ~ 5 years)

4 comments:

  1. Mozaffarian et al. redeemed themselves with what I think is the best-designed fat-related diet study ever.
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3056495/

    Independent verification of reported intakes, and diagnosed disease as an endpoint.
    With a very strong OR at the end, only slightly weakened on repetition in 2013.

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    1. That one seems to be quite a step above the average observational study. I find it more interesting when observational studies find a particular food/nutrient is beneficial when the food/nutrient is part of a less healthy diet/lifestyle pattern (and vice versa). Perhaps this will bring them to a puzzling conclusion, that dairy fat is bad for CVD but good for T2D.

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  2. The public health specialists here in New Zealand, who hate SFA "because PUFA/ because energy-dense", are open to the idea that dairy fat may be protective in CVD, or at least not harmful. They love referring to Guyenet's review, actually, and highlighted the margaric acid part of Chowdhury when they were debunking the rest.
    This hasn't led them to revise their inclusion of dairy fat in their anti-SFA guidelines just yet, but it is nonetheless promising.

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    1. It's pretty similar with the Australian Dietary Guidelines. They don't have any evidence against full fat dairy and in fact some to support it, but still recommend low fat because of SFA and energy density.

      The energy density argument doesn't make much sense. Full fat milk and fatty meats generally aren't as energy dense as grains, mature legumes, nuts or seeds, but the guidelines have no problem with those things being the staples of our diet (not that I care, it's just inconsistent). Also butter is actually less energy dense than other oils

      My impression of the logic in the guidelines was: 'we don't have solid evidence that SFA causes CVD, but SFA increases LDL-C' and 'calories determine weight regardless of macronutrient, but fat is more energy dense per gram, therefore high fat diets and fatty foods have a higher energy density' (it's a leap, with of course the implicit assumption that energy density matters a lot)

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