Comments on: Saturated Fat is Bad – If You’re a Mouse!

By: Steve Parker, M.D.

Steve Parker, M.D. — Tue, 15 Dec 2009 14:56:17 +0000

I hadn’t heard of aortic-augmentation index before.

For those who don’t click on the link: a UK study seemed to show increased arterial stiffness in overweight people on a low-carb (20% carb) weight-loss diet compared to a low-fat (20% fat) weight-loss diet.

At least they weren’t studying mice.

The issue bears watching.

By: isaac

isaac — Mon, 14 Dec 2009 15:51:37 +0000

Had you seen this study?

http://www.theheart.org/article/1033837.do

I’m not familiar with the aortic agumentation index so I can’t really judge the quality of the outcome.

By: isaac

isaac — Fri, 11 Dec 2009 18:16:29 +0000

To expand a bit, the whole point of the low carb diet is to lower A1C levels which are known to be a strong risk factor for mortality, not to necessarily improve lipoprotein profiles (though it may have some effect on that, whether beneficial or not is still up for debate). It’s to reduce heart disease by reducing diabetes. The ApoE model doesn’t even begin to address that question because they don’t even get hyperinsulinemic, much less develop elevated A1C levels. It looks at high protein and high fat in the context of lipid levels when they’re at superphysiological levels, cholesterol especially. It completely removes the diabetes aspect and looks at lipids in a highly artificial model of dubious relation to the human condition. To me, it’s asking a question using the wrong tool.

By: Steve Parker, M.D.

Steve Parker, M.D. — Fri, 11 Dec 2009 15:09:32 +0000

Thanks for the input, Isaac.

-Steve

By: isaac

isaac — Fri, 11 Dec 2009 03:33:13 +0000

That study is a joke. Having worked with ApoE and LDLr mice for over a decade, where do I even begin? This study was clearly not done by anyone with a physiology background nor a good grasp of disease etiology and it amazes me that it made to NEJM for a review article.
1 – ApoE are not a good model for obesity. They don’t get that obese, nor do they reliably develop insulin resistance.
2 – ApoE mice are impaired in the clearance of VLDL/chylomicron remnant particles. Why in the world would one choose them to look at the effects of dietary lipids when altering macronutrient levels? I don’t have access to PNAS anymore. Did they even bother to measure food consumption or look at the lipoprotein profile?
3 – ApoE plaques look nothing like a human plaque at mid/later stage. No plaque rupture and no thrombotic events in these guys despite the similarities of initial plaque formation.
4 – Overall, they are very poor models for human dyslipidemia (all VLDL/little LDL, no CETP, very high LDL clearance, etc). Case in point, statins do NOT work in this model but ezetimibe DOES. Kinda the opposite in humans. I could continue but that last point should drive it home.