The accepted knowledge is that Diabetes destroys gradually over years. Ketosis Prone Type 2 diabetes is an acute form of type 2. This type 2 can reach fasting blood sugars of 300 or higher in months. This blog brings together all the documentation that I could find in the world and my speculation of what it means for KPD’s in specific and diabetics in general. I ask you to leave your stories about what happened to you so that we can all gain a better understanding of what we are dealing with.

Thursday, November 18, 2010

Abrupt Type 2 Diabetes Onset and 1st Phase Insulin Response - pt 2

Part 3This is a further discussion on the previous post. Here. I was my own lab rat and I managed to turn off and on my 1st phase insulin response. It's nice to get good numbers but this isn't what this was about. For one thing, the nature of diabetes is such that no short term answer is adequate. I monkeyed around for a couple of months and managed to find a method that allowed me to manipulate some of my insulin response. I locked down everything: little or no exercise, no supplements, no change in diet, no medications. What you have to wonder about is the sustainability of what I'm doing and I've serious questions about that.

What’s kept me at it was that, for the first time, I got a glimpse of this diabetes and how its behavior fits with all that I've read. It clearly pointed out a few issues which I wish to discuss.

Prediabetes is diabetes

In 1997 and 2003, the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus recognized an intermediate group of individuals whose glucose levels, although not meeting criteria for diabetes, are nevertheless too high to be considered normal. This group was defined as having impaired fasting glucose (IFG) (FPG levels of 100 mg/dL [5.6 mmol/L] to 125 mg/dL [6.9 mmol/L]) or impaired glucose tolerance (IGT) (2-h OGTT values of 140 mg/dL [7.8 mmol/L] to 199 mg/dL [11.0 mmol/L]).

It takes me only one hyperglycemic event to lose my 1st phase. I really want to emphasize this. One big postprandial excursion (after meal blood sugar rise over 170) was all it took to set my blood sugar’s 40 pts higher. As Ned, my statistical guru, might say, “I’m a small data set”. But I am a data set and, as far as I know, the only one around because of the paucity of research on KPD. You should read this with that limitation in mind.

This could be because I’ve already got a broken metabolism. It is entirely possible that it might take a significant amount of times to move into mild diabetes. I want to talk about the discreet steps that my blood sugars take for a moment. I find myself with the same numbers. One step puts me at 115, the other 135 and another at around 170. After 170 though, all bets seem to be off. This 170 is near the take off point for KPD’s that was talked about in a previous post. Here It could be that there are a series of stopping points from normal blood sugars to bad blood sugars. The increment may only be 5 pts for each 500 postprandial excursions. No matter what the amount of times or the increments of increase in blood sugars, the important thing to notice is the outcome is controlled by repeated hyperglycemia. This hyperglycemia, I assume, feeds off itself. The higher it goes, the higher it will continue to go.

Because I can see my 1st phase insulin response more clearly, I know what disrupts it. 170 is considered by the ADA as prediabetes. It isn’t. My 1st phase is gone at that point. Indeed, as I’ve come to consider, the reaching of that point means that my 1st phase has failed.  Part of my pancreatic function is now missing. This is diabetes. There is nothing “pre” about it.

Healthy Foods are bad for you.

Remember, our issues are no matter to the ADA. The rules that they apply and promulgate have almost nothing to do with us. This means that you have to forget about the dietary rules that are being put out there for diabetics. Maybe they work for some of them but they don’t work for us and we should be very careful about following them. I tried to address this in a previous post. Here 

I can not keep a 1st phase insulin response by eating so called “healthy foods”. For me, there can be no such thing as a healthy grain because they stop my first phase much the same as sugar. How about “healthy fruit”? I can handle some berries but the larger fruits are a no no. In order to sustain this first phase, I have to largely consist on fats, which are saturated, and protein. Almost all my carbs come from green vegetables.

There is an increasing epidemic of diabetes around the world. Well meaning people are moving across the globe preaching about “healthy diets”. Unfortunately, they aren’t for anyone subject to acute onset type 2 diabetes. This is why I have said that a meter is your best friend. Diabetes educators will tell you what you should eat, even though, most have never heard of any type of acute onset type 2 diabetes, most would probably even dispute that such a thing occurs. You can’t take their advice on diet. You shouldn’t even take my advice on diet. Take your meter’s advice on diet.

With a low carb diet and this simple medication, I am effecting a change of nearly a percentage point in A1c at a cost of about 20 cents a week. No drug company can make such a claim and, as far as I know, there is no diabetic regimen that can match this. My intuition is that this will only truly work on us. We are prone to a malfunctioning but an essentially intact insulin system. I couldn’t get these results, if this were not true. This is, as far as I’m concerned, the missing piece of the puzzle.

If you look at the literature it assumes that we have lost beta cells much like regular type 2’s and that we would be subject to the same progressive failure as they are. My experiences tell me this idea is a fallacy. I went through fasting blood sugars of nearly 300, for god knows how long, and no meds were able to bring back my numbers to truly normal, save insulin. Suddenly, I’ve been able to produce normal numbers in a way that should be easily replicable. Upon further reflection, it could be said that I’ve lost a good deal of beta cell function due to probably years of high blood sugars and that all I’ve done is successfully bring fully on line whatever function was left.
Even if this isn’t a workable regimen, it should at least get things pointed in the right direction and hopefully get us the type of patient management that we have been so far lacking.

I am still experimenting with my 1st phase and in the months and weeks ahead I hope to communicate to you my experiences and intuitions about what is happening. In the meantime, think about my experience with hyperglycemia and its immediate effects on beta cell functioning and be very careful about what you eat. Part 3

2 comments:

  1. Have you noticed the comments about HbA1c on the WholeHealthSource blog? It seems that it becomes a less accurate marker for people on low-carb diets, not going as low as the actual blood sugar should take it. The discussion suggests that the erythrocyte turnover is lower on a low-carb diet, thereby inflating the HbA1c number. The fructosamine seems to be somewhat more accurate, although a more short term marker.

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  2. Hi David
    Thanks for commenting. I didn't read about this on Stephan's blog. Jenny Ruhl, who else, got me on to this because her A1c stays at 5.7, yet her blood sugars are better than normal. I think Stephan has something similar.

    The assumption of the A1c test is a certain lifespan for a blood cell, generally 90 days. If the cells last longer the glycation will be higher, shorter and the glycation will be lower.

    Here's a good one: low carbers tend to have high fasting blood sugars. You can read about it on Hyperlipid.
    http://high-fat-nutrition.blogspot.com/2007/10/physiological-insulin-resistance.html

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