Tuesday, March 25, 2014

Some Criticisms of the Paleolithic Diet Trials

There are a number of potential criticisms of the Paleo diet trials that I want to address 

Define Paleo 

Paleo is poorly defined 

Paleo critics are quite hypocritical on this point.  On the one hand they want a unified definition, but criticise it for being inflexible and say stuff like: ‘you can’t promote The Paleo diet because the diets of hunter-gatherers varied by geography and season and sometimes by a great deal’ and “chucking the many different hunter–gather diets into a blender to come up with some kind of quintessential smoothie is a little ridiculous”. 

Never mind that the Paleo community acknowledges the diversity of hunter-gatherer diets.  I also don’t understand the last objection.  If we draw a made up Venn diagram (below) to symbolise the differences between HG diets, then there are going to be many areas of common ground.  What’s so bad about finding value in the common ground?
 

What Paleo Diet? 

The Paleo diet used in the trials is very different to the Paleo diet that is being promoted 

I agree, but I don’t think it’s so black or white.  If people could only promote the exact diet people adhered to in clinical trials we would have a lot of half-assed diets and a lot of recommendations that lack evidence to support them, such as SFA and salt restriction in the Paleo trials. 

There are some people who describe the Paleo diets in the trials as something they’re not, and then use them as evidence to support their position.  That’s clearly dishonest and wrong.  But I can’t see the harm in using these studies to say: 

‘The Paleo diet (which contained A, but not/restricted/reduced B, with emphasis on C) used in these trials was more successful at doing X than the Mediterranean/Diabetes (whatever) diet (which contained D, but not/restricted/reduced E, with emphasis on F).  Since there were many differences between the two diets, it’s very difficult to know for sure which particular difference(s) was/were responsible for the difference(s) between the groups.  The Paleo diet used in the trials is similar to, but also different from the diet that I recommend.  Here are my reasons for how the diet I recommend differs from the Paleo diet in the trials… 

Obviously that won’t fit in a tweet 

For example: one of the main points of this objection is that the Paleo diet in the trials is low in SFA, but as it’s more commonly promoted, the Paleo diet doesn’t have restrictions on SFA.  So it would be dishonest and wrong to use these trials as evidence that SFA is ok (obviously), but there shouldn’t be a problem with using other sources of evidence (the fat modification trials) as support for SFA being ok.  As long as they acknowledge that cholesterol levels in the Paleo group would have been slightly higher if the SFA content was higher 

* Just in case you’re not aware here are some of the differences.  The Paleo diet used in the trials is a lot more consistent than the various incarnations of Paleo as it’s more commonly promoted, so the last column depends a lot on who you’re talking to (especially regarding macronutrients, dairy, fruit and starch).  Many popular versions of Paleo also include some variation of things like cured meats, fermented foods, some dark chocolate, other parts of the animal and ‘Paleo’ junk food (which should be an oxymoron) 

 
The Paleo Diet in the Trials
The Paleo Diet as it’s more Commonly Promoted
Macronutrients
High protein, moderate fat, moderate carb.  Low SFA, high MUFA and PUFA
Moderate-high protein, high fat, low carb.  High SFA and MUFA, low PUFA
Ad Libitum Foods
Lean meats, fruit, vegetables
Fatty meat, non-starchy vegetables, eggs, fats (mostly animal fats, olive oil and coconut oil)
Moderate Amounts Of
Eggs, potatoes, nuts, olive/canola oil
Dairy, fruit, starchy vegetables, salt
Restrict
Grains, legumes, dairy, refined sugar, salt
Grains (except white rice), legumes, refined sugar

The Trials Aren’t Well Controlled 

There are many differences between the two diets in the Paleo diet trials, so we don’t know what effect each variable has 

I completely agree.  My main complaint against the fat modification trials was that the experimental groups did more than just replace SFA with PUFA.  They were all advised to restrict TFA, many of them were advised to eat less junk food (baked goods, ice cream) and some were also advised to eat more whole foods (fruits, vegetables, etc).  So how could you say the differences in outcomes were due to fat modification rather than something else that was altered? 

Same thing is true in the Paleo trials where the Paleo diet tends to be: 

·         Higher in fruit, vegetables and meat, but lower in grains and dairy
·         Higher in protein, but lower in calories, carbohydrate and saturated fat 

If there’s a difference in outcomes between the groups we don’t know which of these factors was responsible.  Sometimes studies try to answer this by doing correlations, but I don’t think they are that useful.  Often they will really just be a marker of compliance, not only to grains/dairy/etc, but also to things like junk food and perhaps even exercise and other lifestyle factors. 

The bottom line is that the trials aren’t designed to say whether grains are bad.  Hopefully there will be a trial with a similar design to DART (multiple groups, each with a different combination of diet advice) to better test individual components and perhaps even examine whether there are any interactions 

Compliance 

Compliance was poor in the most recent trial, so you can’t really compare the diets 

I agree to some extent.  Metabolic wards and the more community based trials have their advantages and disadvantages.  Metabolic wards are better for measuring the actual diet (construct validity), while free living trials are better at measuring what will happen in real life (external validity).  You may have come up with the best diet, but in practice will people stick to it*?  If people find it too difficult to stick to the diet, then chances are that’s a problem of the diet. 

The recent Paleo trial had poor compliance in both groups.  I’m not sure if the level of compliance was better/worse than in other trials, but it was pretty bad and would have affected the results quite a bit.  Just to focus on the Paleo diet, the diet used is fairly difficult to adhere to (no grains and dairy is the main thing, but also lean meats and restricting salt**).  Perhaps the adherence, and then consequently the result would have been more favourable if some of the restrictions (like lean meats, low salt, low SFA and no cream and butter) were lifted.  Particularly those without much evidence to support them like low salt and low SFA (so lean meats). 

I imagine one of the main difficulties for dieticians is giving sufficient unpalatable advice to be effective, but not too much to be sustainable, and all of which depends on the person and their needs. 

* This is the issue with calorie restriction for weight loss.  Of course it works, but it’s very difficult to stick to long term. 

** I’m not counting legumes because people don’t eat much of them and don’t have the same desire for them as bread, pasta, baked goods, milk, cheese, butter, ice cream, etc. 

*** This isn’t only an issue for Paleo, but rather an issue for all dietary advice, whether it’s a particular diet, national dietary guidelines, etc.
 
Finally, there's also the issue of the trials only measuring stuff like weight and biomarkers, but not disease endpoints, which is a function of them being small and short

3 comments:

  1. "I imagine one of the main difficulties for dieticians is giving sufficient unpalatable advice to be effective, but not too much to be sustainable, and all of which depends on the person and their needs."

    Or as I put it, in somewhat Foucaultian terms, "the tension between the proscriptive and the permissive", which is the core weakness in all diets, less so with the few lucky enough to be both delicious and effective. Which is where Paleo and LCHF do have an edge over the competition.

    I found out some interesting stuff about lipids the other day:
    trans fats increase cholesterol synthesis and elevate serum cholesterol pool (LDL)
    linoleic acid increases cholesterol synthesis, depletes serum cholesterol pool, elevates tissue cholesterol pool.
    palmitic acid does not increase cholesterol synthesis or tissue cholesterol pool.
    Hence the lipid lowering effect of linoleic acid is at the expense of tissue accumulation and overall increase in cholesterol. Excess cholesterol is probably more toxic in living cells than it is in lipid droplets.
    In some cases high cholesterol may be showing tissue saturation; but this could happen as easily, maybe more, with low cholesterol. It all depends on factors that lipid tests can't measure.
    Statins may be most useful in people with excessive linoleic acid (or trans fat) intake. They definitely have their place in the "tissue cholesterol accumulation" hypothesis.
    http://www.jci.org/articles/view/16452

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    Replies
    1. That's a concise way of putting it. One of reasons I like Perfect Health Diet is the Jaminets emphasised that the diet should be satisfying and delicious. Like exercise, there's often too much of a 'no pain, no gain' mentality with diet as well.

      Looks interesting and seems kind of related to something Chris Masterjohn said:

      "Maybe cholesterol linoleate can accumulate in the liver for 13 days without adverse effects, but what happens over the long term when cholesterol esters progressively accumulate in that organ? Can that go on forever?"
      http://blog.cholesterol-and-health.com/2009/01/total-to-hdl-cholesterol-ratio-what.html

      Who knows, perhaps the anti-inflammatory effect of statins comes from lowering free cholesterol in cells?

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    2. Yes, that's what it looks like to me. Possibly, in the cells of people who've consumed too much margarine and vege oil for too long.
      Especially, I think, if the diet also supplies much cholesterol; I think linoleic acid creates a condition where the liver doesn't respond to dietary cholesterol by turning down cholesterol synthesis.

      it would specifically protect against apoptosis of those cells, which might account for some reduction in mortality of free cholesterol was the problem. But there are many types of cells that don't have LDL receptors, these could be adversely affected by statins.

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