The Academy of Nutrition and
Dietetics (AND) recently responded to the Dietary Guidelines Advisory Committee’s
(DGAC) scientific report. In their
response, the AND praised the DGAC in general and for removing cholesterol from
a ‘nutrient of concern’ and mentioned the problems related to population wide
recommendations to lower salt and the limitations related to SFA and CHD. They instead recommend that carbohydrate should
be replaced by PUFA. This is certainly a
more defensible position from the evidence in observational studies and is
likely to translate to better health outcomes if added sugars and refined
starches are the carbohydrates that are being replaced* [1]
I imagine some people will
challenge the recommendation to replace carbohydrate with PUFA, arguing that
‘not all carbohydrates are equal’ or that ‘there are good carbs and bad carbs’,
because this is exactly what happened when studies were published showing no
difference in CHD between carbohydrate and SFA.
Yet this argument very rarely gets applied to SFA, PUFA or other
nutrients
In a previous post I suggested
that the current RCTs aren’t very good and that a valid and fair test of
replacing SFA with PUFA could help resolve any remaining debate (blog).
But what does this look like in
practice? In the table below I have 6
different hypothetical scenarios of RCTs to test whether carbohydrate (CHO),
SFA, MUFA or PUFA are healthier, and the likely winner in the right column
(don’t get too caught up with the examples, that’s not the point)
CHO
|
SFA
|
MUFA
|
PUFA
|
Winner
|
|
Scenario 1
|
White rice
|
Butter
|
Olive oil
|
Corn oil
|
?
|
Scenario 2
|
Fruit
|
Butter
|
Olive oil
|
Corn oil
|
CHO
|
Scenario 3
|
White rice
|
Cheese
|
Olive oil
|
Corn oil
|
SFA
|
Scenario 4
|
White rice
|
Butter
|
Avocado
|
Corn oil
|
MUFA
|
Scenario 5
|
White rice
|
Butter
|
Olive oil
|
Nuts
|
PUFA
|
Scenario 6
|
Fruit
|
Cheese
|
Avocado
|
Nuts
|
?
|
These scenarios remind me of
the debate whether chronic (not postprandial) SFA intake impairs endothelial
function. There were two trials: one
which concluded SFA impair endothelial function, but half the intervention was
not a fair comparison for the SFA group (butter vs. almonds vs. walnuts vs.
sultanas), so it’s hardly surprising it did worse [2]; and the
other trial which had a fairer comparison and concluded SFA don’t impair
endothelial function [3]
(blog)
The diet heart trials were
mainly in scenario 1**. The meat, full
fat dairy and added fats in the control group were replaced by filled meats,
filled milk/cheeses and vegetable oils in the experimental group. This aspect of the trials is a fair
comparison, as the other nutrient/chemical differences between the fat sources
is relatively minor (vitamin A, butyrate and CLA vs. vitamin E and phytochemicals
that make it through processing). However,
it could be argued that it wasn’t valid comparison because we should base our
diet on whole foods and shouldn’t have much added fat anyway (which was where
most of the replacement occurred) (which I kind of agree with)
Alternatively, let’s say to improve
validity we would by conduct a clinical trial with one group having extra
cheese and another group having extra nuts to test the relative effects SFA and
PUFA have on CHD (scenario 6). We are
certainly comparing cheese with nuts, at least in the context of the background
diet and lifestyle, but are we really comparing SFA with PUFA? Surely the sum of all the other nutrients and
other chemicals in cheese and nuts has a far more meaningful impact on CHD than
any potential effect of SFA or PUFA (though I doubt either has much effect
within reasonable limits). In this
example it’s quite likely that the other nutrients/chemicals in cheese or nuts
will bias the results in favour of one of the groups, therefore not making it a
fair comparison.
This presents a dilemma for
nutrition research of this kind. If we
have a hypothesis that replacing SFA with PUFA reduces CHD, then a clinical
trial replacing butter with margarine could be accused as having poor validity,
while a trial comparing cheese with nuts could be accused as not being a fair
comparison. Either way, the trial has questionable
generalisability to other whole foods (due to the unique mix of other
nutrients/chemicals in the whole food likely having a greater effect than SFA
or PUFA)
Perhaps the solution here is:
(1) to simply base our diets on whole, minimally proceed foods, which in almost
all cases are superior to refined foods; and (2) for nutrition research and
recommendations to be based on food rather than nutrients. This simplicity is also likely to improve
adherence (ego depletion
and decision fatigue
(blog))
and circumvent the processed food industry who can capitalise on reformulating
and marketing products to meet the ‘nutrient of the month’
* The response also discusses
the limitations of ‘eating patterns’, which is a very important part of the
response that I think has been quite underappreciated
** Excluding differences in
TFA intake (all of them), reducing baked goods/junk food as a means to reduce
SFA intake (RCOT, MRCT, DART), multifactorial diet interventions (ODHS, STARS),
vitamin E deficient control groups (LAVAT) and differences in cardiotoxic
medication (FMHS)
If you excluded rapidly absorbed carbs and sugar, you'd find that nothing in the whole food category was harmful.
ReplyDeleteAre you suggesting that fruit and high GI root vegetables are harmful?
DeleteHere's a good example of what you mean - it is, I think, the first ever low fat diet trial, by Lester Morrison in 1951.
ReplyDeleteIt significantly restricts fat, cholesterol, calories, and refined carbohydrates.
https://www.dropbox.com/s/ekn8emrvpca9d7g/morrison1951.pdf?dl=0
https://www.dropbox.com/s/rwa4411pkpapkaq/morrison1960.pdf?dl=0
Of note is the baseline weight of these patients - 75 Kg for men, 64 Kg for women, which dropped by 8-9 Kg over the trial. Which, unless they were midgets, is a simple trip across the "normal" weight range today!
You might have some idea how many calories, and how much carbohydrate, the controls were likely eating in Los Angeles in 1951.
It seems to me that much of the CHO in the test group's diet was fibre. 3 teaspoons of sugar was allowed at breakfast.
Lester Morrison can't have been satisfied with the low-fat diet, because he went to experiment with chondroitin sulfate A for secondary prevention and got even better results than these.
https://www.dropbox.com/s/17vsix1d1qbctft/morrison1973.pdf?dl=0
This is plausible, if you think that the glycocalyx of the coronary vasculature might be important in CHD etiology. Morrison certainly did a great deal of animal experimental groundwork to support his later hypothesis. I wonder what the modern view of this is. It fits in with a paleo prescription that includes connective tissue and bone broth, sources of CSA.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1915585/
From the text it seems like the calorie target was 1500 and 1200 for those with high cholesterol. Which makes sense because 75/64 kg is generally not overweight. I agree, it looks like almost all the carbohydrate was fruit, veg and whole grains. Fibre intake could have been 25-35g, which is much higher than the (current) US average of ~15g
DeleteIf you thought fat and cholesterol were 'the' cause of atherosclerosis, then surely that almost no fat no cholesterol diet should have achieved more. Not to mention the difficultly in getting people to adhere to that kind of diet and calorie restriction
That endothelial glycocalyx review is interesting. The response to retention hypothesis never sat comfortably with me; surely the endothelium would protect itself from penetrating LDL particles. This is probably one the factors behind paradoxes whereby metabolically people with high LDL-P show no signs of atherosclerosis