It's all very well to test the metabolic effects of high-fat diets in RCTs. There are usually beneficial results in type 2 diabetes, but compliance is limited. The trial isn't showing what the diet does, but what effect the advice has on people who may be more or less indifferent to it. In fact, it's amazing these trials produce the positive results they do.
A metabolic ward study involves subjects who follow the diet because they have nothing else to eat; all variables such as exercise are kept constant. Because you don''t get huge numbers volunteering for these studies, and the cost is high because of the round-the-clock supervision and testing, the crossover method is normally used. Half the subjects eat the test diet, the other half the control, then they switch over. Results from the end of each period in both groups are averaged.
This is a 1988 study authored by Abhimanyu Garg, Roger Unger and 3 colleagues.
Comparison of a high-carbohydrate diet with a high-monounsaturated-fat diet in patients with non-insulin-dependent diabetes mellitus.
Thanks to Ivor Cummings, I have the full-text pdf, and it's very interesting.
The other dietary variables are well controlled for.
The types of fatty acids, if that makes any difference, are also well-matched between diets (low fat diet used corn and palm oils, high fat diet used olive oil, so neither was high omega-3).
The results are fascinating (this is the average from the last week of each period, days 21-28).
Who knew that a urinary glucose output of 142 mg/day was normal on a high-carbohydrate diet in subjects with "non-insulin dependent diabetes mellitus treated with insulin" - to disappear completely on a diet with 50% of calories from olive oil?
Oh, and the base line? That was after a week on the diet recommended by the ADA in 1988, which was the lead-in diet.
What about lipids? They improved too:
What's especially interesting aboout these lipid results is the comparison between this study (second phase T2D) and Garg and Unger's 1992 study of the same diets in mild (first phase) T2D. In mild T2D, a high MUFA diet improved lipids but did not influence insulin sensitivity. This seems consistent with high-carb/high-calorie diets and hyperinsulinaemia in those prone to diabetes driving lipotoxicity, when then produces the phase 2 phenomenon of hyperglycaemia plus hyperlipidaemia by altering the ratio of alpha- to beta- cell sensitivity and activity. Dietary carbohydrate drives fat which drives endogenous glucose.
The authors of the 1988 paper sum up thus:
Abhimanyu Garg has authored this convenient review of all the studies using a high-MUFA diet for Type 2 NIDDM.
It includes this classic line:
Of course what we lack is a comparative series of studies with high SFA diets, or indeed diets in the normal range of mixed SFA, MUFA and PUFA. Does the type of fat matter if carbohydrate is low enough? Quite possibly not, at least for the majority. Is 35% carbohydrate low enough to see the full benefit of a high-fat diet? Maybe not, but the results, after only 28 days, were impressive enough.