Thinking about the nature of Abrupt Onset Type 2 diabetes

This is still a continuation of the “Abrupt onset t2 series”. You can read those Here. This is one of my “thinking about” pieces and this means a lot of speculation. I have to do this because the research is so spare for this. We do have the research on “ketosis Prone Type 2” diabetes but this syndrome is a lot bigger than that. Most people don’t reach ketoacidosis, I didn’t, even though I was definitely headed that way.

We are talking here about a severe metabolic derangement that comes on swiftly. This is different than just heading towards DKA. It is the parts of our metabolic system losing the ability to act in concert. Glugagon from the alpha cells causes the liver to produce glucose to respond to falling blood sugars. How long and when this happens will produce various effects depending on what the beta cells are doing with insulin. We would get a range of effects here. If insulin is high, blood sugar might rise only slightly, if at all. If insulin is high but glucagon is low, reactive hypoglycemia would occur. These systems are meant to match each other, when we have diabetes, they don't.

The term “metabolic derangement” is used because we aren’t talking about systems that have deteriorated due to autoimmune attack or toxicity. I’m talking of systems that are operational, meaning they’re functional capacity is not diminished. What is lost is the correct timing of the systems behavior.

Why would I make this statement given all the research on type 2 diabetes? One word, “speed”. Glucose toxicity or Glucose desensitization are long drawn out processes that are thought to take years to take effect. Sudden onset t2 is abrupt. It takes less than 6 months to go from near normal to fulminant and about the same time to return to near normal.  

The experiments that I’ve been performing on myself have been occurring in the space of a few weeks. This isn’t enough time for cellular failure or regeneration in any body system. This suggests that the underlying systems of blood sugar metabolism are intact but that the triggers that allow the timely interactions that give us normal blood sugars aren’t functioning correctly.

Now I’ll even go further out on a limb. The body has many more systems to prevent hypoglycemia than hyperglycemia. The obvious reason is that hypos can kill you in a day: hyperglycemia may take years. Given this, my guess, is that there is a failsafe set into the operation of insulin, in particular, the 1^st phase of insulin. This first phase is essentially a dump of a large amount of insulin to offset blood sugar spikes from pushing blood sugar over the magic 140 barrier.

Now, as a thought experiment, think of a drug injected into a person that suppresses some signal that's essential for the alpha cells, liver and beta cells to cooperate to maintain blood sugars. Probably the first thing you would see would be spikes and reactive hypos. The spikes would be due to both glucagon and the liver. The liver would be putting out glycogen while glucagon suppressed insulin: this would be hyperglycemia. If the glucagon and liver stop then suddenly the person would go low, reactive hypoglycemia. This might go on for awhile but eventually something in the body would have to react to the lows and essentially shutdown part of the insulin production. I say "have to" because too much insulin will kill you very quickly and continuous hypos have been shown to increase mortality.

There has to be some sort of failsafe in the body to prevent this. Cutting off all insulin would be deadly as well but the beta cells have two phases; one is slow and steady and the other puts out large amounts of insulin in a short time. It would have to suppress the first phase. What we do know about type 2 is that early stages typically involve reactive hypos then the loss of 1^st phase insulin. The later phase involves the steady rising flow of insulin to keep bringing blood sugars back in line. This is an interesting supposition but what I’ve shown is that hyperglycemia suppresses my 1^st phase.

Here we go to a little control system theory. I am an Operations and Maintenance guy for industrial wastewater processes. (By the way, I’ll be going off to a project for a couple of months. This means and end to experimentation for awhile and it will slow down, if not stop, my blogging till I get done. This is another reason to try to get this post out.) I work with systems that sense conditions then send commands to various systems to keep the process in balance. Typically, systems will be nested in larger systems. Troubleshooting such systems will involve me looking at a system which isn’t functioning and testing it to see if it’s okay. If that system is fine then I move up to higher control systems to see how they are affecting the system that isn’t functioning.

What this has to do with hypoglycemia and hyperglycemia is that, if, as I’ve come to believe, the insulin system is intact, then the problem is higher up. My experiments tell me it must be involved in glucose metabolism, susceptible to the med I’ve been using, affected by hyperglycemia and interestingly enough by insulin. Why insulin? All the papers that I’ve read on KPD say that insulin performs better than any med in bringing people back to near normal blood sugars.

My candidate for this system is the hypothalamus. Here’s a paper which talks about the importance of the hypothalamus is the secretion of insulin from the beta cells. Pancreatic neuronal melanocortin-4 receptor modulates serum insulin levels independent of leptin receptor  

This talks of a hormone secreted by the hypothalamus which is part of blood sugar control but is suppressed by hyperglycemia. Role of orexin in the regulation of glucose homeostasis

This one shows the effects of hyperglycemia on the hypothalamus and suggest that these effects are reversible. Hyperglycemia impairs glucose and insulin regulation of nitric oxide

Here’s a paper detailing the relationship of the hypothalamus to the production of glucose by the liver. CNS Regulation of Glucose Homeostasis

This paper, though ostensibly about brain cholesterol, does talk about the curative effect of insulin on the hypothalamus. Diabetes and insulin in regulation of brain cholesterol metabolism.

A well known fact of diabetes is that the loss of 1^st phase insulin is an early occurrence. What occurs because of this is hyperglycemia since a basal can’t catch up with the initial spike from food. A person will endure hours of blood sugars above 140. Now, I’m willing to go to the idea of beta cell toxicity due to continuously high blood sugars. I’m thinking that what we have is a mix.

This may explain the fact that, at least, half of KPD’s do not come back to remission. The damage done over time may well have reduced the amount of beta cells that are available for insulin secretion. This might explain the sudden onset as well. We have two processes, one which suppresses beta functioning, while the other is the dying off of cells due to hyperglycemia. A tipping point is going to be reached at a certain point.

What does all this mean in terms of dealing with this type of diabetes? The first thing always will be the fact that this isn’t a good set-up for carbohydrate metabolism. This is a deranged metabolism. A metabolism that has virtually no control over the liver will have serious problems with eating carbs. It doesn’t take much to spike me or many of the people I know with this. Glucose is already being added to the blood. Basal insulin is being secreted to try to match this. If you throw a significant source of glucose on top of this then you are going to be hyperglycemic. Diet, you see, is a must.

What we really need is more research and we won’t get that until we begin to get the word out on this. I’m doing my part, are you?

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 1^st 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 1^st phase insulin response more clearly, I know what disrupts it. 170 is considered by the ADA as prediabetes. It isn’t. My 1^st phase is gone at that point. Indeed, as I’ve come to consider, the reaching of that point means that my 1^st 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 1^st 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 1^st 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

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