Sunday, November 2, 2008

This is an article about a study on type II diabetes treatment with a vegan diet. Neal Barnard of the Physicians Committee for Responsible Medicine was involved. The vegan diet improved blood glucose control and HBA1C levels when compared to the American Diabetic Association Diet.

There's also a 'cure' for diabetes video going the rounds, which has even found it's way deep into carnivore territory.

The video's about a raw vegan program, and makes more spectacular claims than the PCRM study--PCRM is talking improved blood glucose control, while Gabriel Cousens and others are talking cure--actual reversal of type II diabetes.

If you poke around on some raw vegan sites, you'll find some people with spectacular results.

Increased energy, spectacular weight loss, control of bipolar disorders. The list goes on and on.

Lots of good things to say about this diet, even if you don't necessarily buy into the explanation of the benefits given by those who enjoy them. Detox? I don't really follow you. Enzymes? The usual answer in carnivore (or just cooked food) circles seems to be that enzymes from the diet are broken down into amino acids in the stomach, and do the consumer no good as enzymes. But we release enzymes in our saliva, don't we? So it must be possible to benefit from enzymes, pre-stomach. And if dietary enzymes don't do anything, are just broken down into their component amino acids, then why are there studies that show benefits from consuming the pineapple derived enzyme, bromelain?

These people are eating food that belongs in the human diet, even if it's often lower in protein than most would consider desirable. Some of them may have serious honey or agave nectar habits, but I get the impression, mostly, from the blogosphere, that it is more common for raw whole foods to be the focus, whether fatty or carby, precluding most refined sugars from the diet.

There's another, non-vegan cure for Type II diabetes. It goes like this; feed mice or rats a choline-deficient diet. The rodents get fatty liver disease; excess buildup of triglycerides in the liver. This decreases free fatty acids in the liver. Free fatty acids encourage glucogenesis; which makes sense. When glucose is high, fat cells tend to synthesize glycerol, which acts sort of like a lynchpin to keep fatty acids in the cell. Glucose gets low, and less glycerol is synthesized, so that the breakdown of triglycerides predominates over synthesis; so that free fatty acids serve as a signal that glucose levels are low.

I got a lot of that from Wikipedia; I think most of it still stands, although I think that the increase in blood glucose from high free fatty acids in the liver is probably because of increased glycogen breakdown, because of a post Michael Eades did a while back about a colleague who traced glucogenesis in the liver and found that before finding it's way into the general circulation, newly formed glucose was formed into glycogen. I wonder if that's true of fats, too--are they first stored as triglycerides in the liver, before being released packaged as VLDL? Since there's such a thing as fatty liver disease, I guess that's probably true. If glucose isn't the proper endpoint, I guess we should probably just call it glycogenesis as well. So this must not just be a problem of glucose synthesis, but of glycogen breakdown, as well.

This also explains why rodents with visceral fat removed fail to get type 2 diabetes, even when genetically susceptible or when fed a diet that would normally give them type 2 (high fructose, for example.) And why it works also in humans, although they can't go to the extremes they go to with animals. Visceral fat is kind of close to the liver, and enjoys more blood flow than most fat tissue. It's a ready source of free fatty acids, and thus a steady source of encouragement to the liver to push blood sugar up.

Back to the mice; they get fatty liver from the choline-deficient diet. But no type 2 diabetes. Hooray.

Here's an interesting study that ties into this choline, fatty liver thing;

Mice that are fed a diet that is both choline and methionine free (and high in sugar) enjoy some curious therapeutic benefits; increased metabolism, weight loss (largely fat), increased fatty acid oxidation, and of course a nice fatty liver.

Not to put too fine a point on this, but it wouldn't be too hard to design a vegan diet that was low in both methionine and choline, would it? (Please don't start an online fat-loss clinic called fattyliverkins. Seriously.)

What we need isn't a diet that keeps visceral fat and liver fat from breaking down; we need something that reverses and prevents its excess accumulation.

Saturated fat protects against fatty liver disease, especially that caused by alcohol. Polyunsaturated fats don't, so you could imagine studies where saturated fat worsened blood sugar control when compared to polyunsaturated fat.

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