Monday, June 23, 2008

Diabetes in Sweden update

Just an update from Nielson and Joensson, original comment here. Happened on it while chasing assorted lipoprotein numbers for another post.

HbA1c below 5% without meds is possible through diet. I wouldn't describe these people as cured, a pizza a week would have them in trouble, but with HbA1c this low I'd not be worrying about CVD too much.

"Of the total of 10 controls, who have switched diet, 2 persons after a weight reduction of 20 kg each are free of all signs of diabetes after 3 and 2 years respectively i.e. HbA1c below 5.0%, fasting blood glucose below 5.0 mmol/l and free of any blood glucose lowering medication"

Second comment is that, even with successful weight loss and diabetes imporvement, carb creep is real and hard to avoid.

"After 22 months 2 patients had resumed insulin treatment following an increase of carbohydrates."

I know that rye crisp bread was a feature of this diet. I wonder what would have happened in the complete absence of gluten? Or whether the problems of removing this potentially addictive carbohydrate source would just have sabotaged the initial compliance?



gunther gatherer said...

Hi Peter. This is unrelated but I am dying to understand more about resistant starches and their benefits vis-a-vis gut bacteria and metabolism.

Can you please explain how they work, how you use them in your diet (I notice you eat a fair amount of chips and potato) and what they do on a biochemical level?

I simply can't find unbiased info on this anywhere.


gunther gatherer said...

Hi again. Sorry if I wasn't too clear above. What I'm asking is are resistant starches good for you or bad?

Are you and JK recommending the potato as your main starch because it turns to sugar quickly, has little fructose and not much fiber, or because it's more practical for loading up with fat?

Given the above, don't you get a bit "stopped up" in your bowels eating like that over the long term?

Thanks again,

ItsTheWooo said...

My HbA1C is never below 5... I've had it measured twice and the first time it was 5.4 and the second it was 5.1. In fact, the blood test when it came up 5.4, my fructosamine was 255, which implies a very high average 2 week blood sugar (fructosamine 255 = a1c 5.9!)

I'm thin and eat 60 carbs/day and I don't eat a lot of calories... I'm not diabetic.
In fact, my a1c was worse when I was eating less calories and was underweight, presumably because glucose control was not as good as a result of the stress and low leptin (which would make sense, because I felt my blood sugar was all screwy and was always getting hypoglycemia back then, in spite of eating less calories and not more carbs).

Even when I was strict ketogenic dieting and eating low calorie (while actively losing weight) my fructosamine was 204, which translates into an a1c of about 5. This should have been the best possible glucose control - I was not underweight, I was actively losing weight, and I was eating ketogenic. Even then, my a1c was only 5.

I should also mention that I do have blood glucose abnormalities - I have extremely brittle sugar (very unstable) but am almost always fasting hypoglycemia, 59-69 range.
Considering my experiences as a non-diabetic, I can't imagine how it is realistic for a diabetic to get their a1c under 5, and have that be worth it (i.e. not loading themselves up with excessive drugs or starving constantly).

Gyan said...

I got this thru Plant Poisons blog

The central problem in the most common form of Type 2 Diabetes mellitus and the Metabolic Syndrome is the infiltration of the islets of Langerhans in the pancreas with amyloid. This disrupts the islet architecture, causing the alpha cells to lose touch with their companion beta cells, which in turn has the effect of causing them to secrete glucagon inappropriately and in relatively large amounts regardless of the blood sugar level.

When glucagon is secreted in large quantities, regardless of the blood sugar level, the liver is stimulated to secrete inappropriate amounts of glucose into the blood of the resting person. This raises the blood sugar level, which stimulates the beta cells in the islets to secrete insulin

Could you interpret it as I dont understand it well but is he saying sensible?

ItsTheWooo said...

gyan - basically what he's saying is:

"Because of a certain kind of protein plaque in the pancreas, the person with diabete makes too much blood sugar-making hormone."

(Personally, I don't know if it is appropriate to view amyloidosis as the point of origin defect in hyperglycemia from the liver. It was my understanding that amyloidosis is a RESULT of hyperinsulinemia, because insulin degrading enzyme also prevents amyloidosis. If hyperinsulinemia already exists, that means glucose from the liver and diet is / was already abnormally regulated.

"When insulin, a well characterized substrate of IDE [insulin degrading enzyme], was added to the in vitro degradation assay, removal of AICD [a precursor to amyloid] was efficiently blocked."

Peter said...


The body probably uses cross talk between cells to control everything. The pancreas has beta cells which secrete insulin when glucose levels are too high. It also contains alpha cells which secrete glucagon when glucose levels are too low. The cells are right next door to each other. As well as both types of cell monitoring glucose it seems as if the glucagon secreting cells look at the local amount of insulin being secreted and use this as a signal to moderate their glucagon secretion. There is no point in trying to raise blood sugar levels with glucagon when the body is producing lots of insulin due to a recent meal intake. It's probably a fine tuning mechanism which can be over ridden by catastrophic changes in glucose. The beta amyloid is debris which blocks this fine tuning mechanism and results in over secretion of glucagon which raises blood glucose inappropriately.

This looks to be a failsafe mechanism. If you have a problem with your blood glucose control it's better high than low. An hour of hyperglycaemia is survivable. An hour with a glucose of 0.5mmol/l may not be. Fail to high glucose. Fail to diabetes rather than acute death... Hee hee, could the ADA be correct? Only joking!

Personally I feel it is probably a significant effect but not primary. Hyperglycaemic failure of the vagus nerve supply to the liver (and probably the pancreas too) may well have similar effects on blood glucose but are not primary.

These are probably reasons why LC side steps type 2 diabetes but doesn't cure. Also why it works well for most but not all.

Beta amyloid is also a feature (probably significant) of the damage in the brain in excitotoxin diseases (Parkinsons, ALS, Alzheimers) and I doubt very much whether it is primary there either.