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

Saturday, November 13, 2010

Abrupt Type 2 Diabetes Onset and 1st Phase Insulin Response

I've titled this "Abrupt Type 2 Diabetes Onset" because I'm am coming to believe that very different types of diabetics have this and that it involves, not the beta cells themselves, but a mechanism or loop that the  beta cells are in that has failed.

How I've come to this conclusion is personal. By sheer luck, I fell across a method of reactivating my 1st phase insulin response. You basically have two responses that come from your pancreas, basal and 1st phase. The basal is the constant but low flow of insulin that occurs all the time in your body. The 1st phase is a modifier of this basic level of insulin to account for changes in the amount of blood sugar that occurs with things like eating, exercise and stress. I use to think of it as a big wave of insulin that suddenly flowed in to your blood stream to counter act potentially high blood sugars caused by something like eating a fast acting carbohydrate. It can and will do this but mostly it's active like a computerized glucose monitoring system counter acting small spikes in the system due to the actions of other things going on in the body.

It should be noted that I'm talking about spikes not drops in blood sugar. Drops aren't the problem usually. (There is reactive hypoglycemia but I view it more as part of a failed mechanism.) Your body is set up to strongly defend against hypoglycemia. This can kill you in a day while hyperglycemia make take years. There are a series of systems and hormones that interact to assure that the body has enough glucose. The one which is counter to those is insulin.

At any rate, I've found a way to get that first phase back and conversely, I've found how to lose this 1st phase. In the last month, I've gotten to the point where I have been able to more or less switch it off and on and notice when it is working. I've even dropped all medications. My typical blood sugar profile kept me at about 110 with spikes of 40 to 50 points higher after meals. This is even with eating a largely low carb diet. Now my typical profile keeps me in the 90's with spikes never above 130 and generally about 20 points above my basal rate. It should be noted this is without insulin, exercise or supplements. (I'm trying to keep down the confounding variables. Ned Kock is big on this!)

One thing this has shown me is that the beta cells are there. They aren't dying off or sick. I'll have a 1st phase for a few days, make an adjustment and then I won't have a 1st phase. I'm thinking that this is very much an abrupt type 2 onset thing.

Type 2 is traditionally thought of as slow onset with continually rising blood sugars over many years. With us, insulin failure occurs quickly but on the converse side insulin recovery occurs quickly as well. I've read where various methods were used to assess beta cell function or mass and it was found to be intact.

I produce insulin but not a 1st phase so my constant dribble of insulin is not enough to keep down my blood sugars without additional insulin. Guess where my blood sugar average is usually, without medications? 134. This is about an A1c of 6.3 which is pretty standard for a Ketosis Prone type 2 diabetic.  This A1c and its implications were discussed in a few posts back. Here.

All this and more lead me to believe that this isn't a problem of beta cells desensitizing but of a failure of a control loop that the beta cells respond to by releasing 1st phase insulin. By saying "control loop", I am talking about a circuit. Think of it as a lightbulb and switch. If this switch is controlled by a sensor for certain amount of darkness then when it gets too dark, the switch is activated and the light comes on. There might be a sensor for lack of movement in area where the light is. If no motion is detected, the switch is deactivated and the light goes off. There is nothing wrong with the light, it's fine. Its behavior, however, is being controlled through the sensors that activate or deactivate the switch.

What my intuition is telling me, that at least in those with "abrupt type 2 diabetes onset", the circuit isn't working and what breaks it down are hyperglycemic episodes which effect one or more components which are part of the loop that operates in the 1st phase circuit. These components could be anywhere. They could function as an aggregate or there could be just one component which is effected by hyperglycemia. What seems clear is that the message isn't getting through.

I bring up hyperglycemia because all I have to do to shut down the 1st phase is to initiate a high glycemic environment which is too high for my 1st phase to cover, typically for me, this is a tub of popcorn at my local cinema. (If you're going to do something bad, you should at least enjoy it.) My blood sugars will stay below 160 then they will soar above 200 and stay there for 4 or five hours. After that, no more 1st phase and higher blood sugars till I make the adjustment.

You are probably wonder what this adjustment is. I should say it is relatively safe but there are potential side effects and frankly I don't want people starting to take stuff with little or no understanding what they're undertaking. I'm going to keep this under wraps for a while.

What I'd love to know is what chemicals or hormones or whatever breaks down in a high glucose environment? Some where, at least for us, that is where the answer lies I believe. Part 2