Anyway, the first thing to do with a paper like this is to check whether the authors cited Nielsen's 2006 case report of a human being having their diabetic renal failure halted and partially reversed. I mean, this might be relevant...
They didn't.
The Swedish group simply fixed a patient without a mouse model in sight. They got ignored for their temerity. Shocking to fix a human without the death of a single leptin deficient mouse, but there you go. And it's not so hard to do either............
As a complete aside:
It turned out to be interesting to go back and see where the mouse folks were coming from. They cited this paper.
Here is part of figure 6, the line to follow is the open triangles.
Up to day 84 a high fat diet was fed. As happens so often, the high fat diet is 31.7% sucrose/maltodextrin by weight and (gasp) 20.7% lard.
From day 84 onwards these lazy, greedy porkers of mice were switched to a diet which was 47.5% lard and, utter horror, 19.95% butter. Of course this is not really a high fat diet as it has no sucrose or maltodextrin...
Look at the weight drop to below (ns) that of the mice fed crapinabag throughout........
Obviously this must be the satiating effect of protein, so often cited by idiots as the reason for weight loss of LC diets. Except it's not, the ketogenic mice had the lowest protein intake, 9.5% by weight cf 24% in the crapinabag and HF diets. That is very low in protein.
Here are the actual diets in Table 1:
A far more plausible explanation is that ketosis induces dissatisfaction in these mice concerning their body image due to their obese state so they then started to cut calories and go to the gym every night. Duh.
Now please don't make me put up the fasting insulin levels. Aw, okay, you twisted my arm.
Edit: I noticed that these are the FED insulin levels, we don't get fasting levels in the paper...
No comment.
Peter
