Rapeseed oil for weight loss (2) and butter for obesity round one

This is the next paper. These people are good. Really good. There is almost nothing amateurish in this paper:

A highly saturated fat-rich diet is more obesogenic than diets with lower saturated fat content

and here is the graph which sums it up

I'm not saying these people aren't stacking the deck and I'm not for a moment suggesting that they understand anything about obesity. But they deliver in spades to support the current (anti saturated fat) narrative.

I'm going to speculate from here onwards about how they managed it.

The above graph did not materialise out of thin air.

They made their own foods in their own lab. For the high fat diet they "chose" 67% of calories as fat, For the low fat period they "chose" 27% of energy as fat.

Why?

Because, obviously, markedly different values would not have generated the above graph. They could, and I suspect they did, formulate almost any diet macro ratio they wanted to. It's called a pilot study and and I think you should seriously consider that they did one, and kept quiet about it.

Very few people using a rodent diet induced obesity model would consider 27% of calories from fat to be low in fat. Their chow was ~11% of calories as fat and very low in PUFA (Diet 5075, which included beef tallow as a partial fat source. It's not made anymore but you can guess it resembles 5001 but with less PUFA. Probably. But who knows?). My presumption for butter is that medium and short chain fatty acids are, by the Protons hypothesis, insulin sensitising. At low dose rates they are largely diverted from gut to liver and never reach peripheral adipocytes. So they are not obesogenic. They increase hepatic insulin sensitivity which lowers the penetration of both glucose and insulin to the systemic circulation and, certainly in the case of MCT oil, are slimming. My guess is that much less than 27% of calories in the "low fat" period would have produced active weight loss. So you simply do not use less than 27% of calories as fat from butter, if you want obesity in your model. 

If you supply enough insulin sensitising shorter chain fatty acids that they penetrate past the liver to peripheral adipocytes they will continue to work their insulin sensitising effect but this time on adipocytes rather than hepatocytes. With enhanced adipocyte insulin signalling there is enhanced fat gain. This appears to be optimal at 67% of calories from butter. Much more than 67% would tend towards ketogenically low levels of insulin exposure and the insulin sensitising effect would become irrelevant. Again, a guess, but much over or under 67% would have generated less obesity. It's a model, it's designed to make a point.

In the canola oil arm the high fat diet provide ~20% of calories as LA, verging on an uncoupling dose rate. In addition to this there are 10% of calories as ALA, a significantly better activator of UCP1 and UCP2 than LA. This is clearly a factor in the high fat group and there are oddities on the graph and elsewhere in the paper which do suggest that this is the case. Another post.

What would have happened if they had lowered the canola oil to a real low fat level, say 4% of calories from PUFA? LA at under 4% of energy is not usually obesogenic, though it should tend that way via the Protons F:N ratio, absenting uncoupling effects. Some fat storage is beneficial. And ALA would accentuate this effect, so long as levels were high enough for the Protons effect to occur but low enough to avoid uncoupling effects. So very low dose canola oil might well be obesogenic and was sensibly avoided.

You don't write your experimental protocol until you are damned sure it is going to deliver. The required result here is to show that "saturated" fat rich diets are obesogenic and "PUFA" rich diets are not.

They succeeded. As I say, they are good. Here's the start of their discussion:

"The present study tested canola, lard, and butter, respectively, low, moderate, and rich sources of SFA, widely consumed in the human diet, in an animal model of dietary obesity. As predicted, results confirmed the hypothesis that an SFA-rich diet is more obesogenic than diets with lower SFA content."

They obtained the result they predicted. Probably by dint of a lot of hard work.

Peter