Eating Through The Myths: Food, Health and Happiness - Taylor, Prof. R., Berlin, 28-Sep-12
EDIT: The link above needs Flash. If Flash isn't available, see YouTube video below.
Salient points:
1) It's a chronic calorie excess (of carbohydrates and/or fats) that causes problems.
2) Motivation, motivation, motivation!
3) Both diet and exercise are important. See Move More: Solutions to problems.
4) You can't outrun your fork. See The 5th Myth of Modern Day Dieting: You Can Outrun Your Fork.
5) Underlying Insulin Resistance needs to be addressed. See Insulin Resistance: Solutions to problems.
See also Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol, and Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause (PDF).
For more information on Prof. Taylor's work, see Reversing Type 2 Diabetes.
EDIT: Long-term results are now in. See Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. The full study is behind a pay-wall, but here are a couple of Figures from it.
86% of participants who completed all 3 phases of the trial maintained over 15kg of weight loss and achieved remission from diabetes. Participants who dropped-out at various points achieved less weight loss at the 1 year point and achieved a lower % of remission. It's not easy for people who are consuming 15% fewer kcals/day of healthy foods to maintain motivation when they're constantly being bombarded by persuasive marketing encouraging them to eat yummy Food Products.
If beta cells have been irreversibly damaged and the above approach doesn't work, improved glycaemic control can be achieved using a LCHF diet.
11 comments:
"You can't outrun your fork."
Brilliant!
Welcome to the mad-house! You're now in my whitelist, so future comments will appear immediately.
Thanks, Nigel. Refreshing to see a post which shows diabetes involves too many calories of all types. It is a disorder of fat metabolism, not just carbs. Americans value quantity over quality + convenience. It's a lethal combo.
You might notice that hyperinsulinaemia storing fat is central to Prof Taylor's mechanism. People clear liver fat on VLCKDs. And reverse diabetes. This has been tested many times. There is more than one way to achieve the same results. Fasting works for people who are impatient and motivated. Carbohydrate restriction works for people who are patient and motivated.
There is nothing in the Newcastle theory inconsistent with LCHF or Paleo approaches to diabetes, nothing about those approaches that precludes also fasting.
Hyperinsulinaemia is caused by excessive fat and/or carbohydrate intake, relative to expenditure. With the Western Diet, it's usually both (SSB's provide excessive sugar).
Prof Taylor's diet is a PSMF, which is a mostly-protein, low-fat, low-carb ketogenic diet. This results in the fastest rate of liver depletion. The extremely low food intake may be hard for some people to bear (according to the lecture, the subjects seemed to bear it with no problems as it gave them rapid results).
Adding fat to such a diet would increase the energy intake and reduce the rate of liver emptying. It still works, but takes longer to deplete the liver. For some people, a bit more fat might be necessary to make the diet tolerable.
That sounds right. There is also the possibility that some people arrived at DM2 after a lifetime of counterproductive dieting and need to stimulate BMR up. But I suspect most people's BMR is fairly resistant to fasting if there is stored energy. It is perhaps not-overweight people obsessively restricting calories at most risk of disturbing BMR and gaining weight that way.
VLCKD might be a good way to approach a fast if the idea of eating 600cals appals. It won't seem so daunting to someone who has already survived without carbs.
PSMF VLCKD's are great for rapidly depleting things that need to be depleted. It's when there's no further need for depletion and it's time to add something that we don't agree.
You would add just fat, to bring intake up to expenditure and stay in ketosis.
I would add carbs and fat to bring intake up to expenditure and come out of ketosis. The resulting diet would be LC, but it wouldn't be ketogenic. I'm not convinced by the discussions on Peter's blog about the non-atherogenicity of VLCVHFKD's.
Personally I would follow Atkins and add carbs back to some level of efficiency or comfort, erring however on the side of fat (i.e. under 140g carbs). Unless or until there were some reason to stay in ketosis. Or unless the individual enjoys being in ketosis.
George--that's how I read it too. That while a chronic positive calorie balance [from any and all macronutrients] plus the presence of muscle IR were the necessary foundation for developing Type2, they were still insufficient. That the additional factor required--indeed sine qua non--for liver fat accumulation was de novo lipogenesis from "excess" carbs, because the critical driver was the accompanying hyperinulinemia:
"SUPERIMPOSED upon a positive caloric balance, the extent of portal vein hyperinsulinemia determines how rapidly conversion of excess sugars to fatty acid occurs in the liver...Conversely, in Type1 diabetes the relatively low insulin concentration in the portal vein (as a consequence of insulin injection into subcutaneous tissue) is associated with SUBNORMAL LIVER FAT CONTENT." [Taylor (2013) Type 2 diabetes: Etiology and Reversability. Diabetes Care]
My emphasis.
Taylor then listed several options--hypocaloric diet, physical activity, thiazolidinedione use--"each of which REDUCES INSULIN SECRETION AND DECREASES LIVER FAT CONTENT." [my emphasis].
For some reason, he forgot to mention another insulin-reducing option: a low-carb diet.
Agree completely Nige. George Blackburn (& associates) finding in 1973 that the feeding of ONLY a complete protein in quantities of 1.0 to 1.5g/kg/day could reduce or spare the loss of tissue protein was an important discovery. He called such a diet a "modified fast." [Blackburn, GL et al. Peripheral intravenous feeding with isotonic amino acid solutions. Am Jrnl Surg (1973) 25:4477-454]
What I was getting at is: Just as this protein sparing modified fast could provide the "benefits" of starvation but without having to catabolize bodily tissues, in a similar fashion a low-carb diet provides the [insulin-reducing] benefits of a PSMF but without having to endure the hunger of a modified fast.
Catastophic weight loss works most rapidly to decrease liver fat, but must not be necessary since Prof Taylor includes physical exercise as an insulin-reducing option that will decrease liver fat.
By decreasing insulin secretion, a low-carb diet should decrease liver fat content just as Prof Taylor's version of a PSMF does--albeit more slowly. And I wonder why Prof Taylor didn't say so.
You could email him and ask.
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