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.

Tuesday, December 28, 2010

Please make the fight

I have to go back to work, and I wish to say this before I sign off. I wrote this blog because I saw unnecessary suffering, I come from a family  that  died  young because of this accursed diabetes. The peoples who have read this blog span the world and know that we are in the grips of something horrible that has not been given name or face in the world. I see you from all corners of the globe. This is a real thing. The science is there but the recognition is not. People are dying and suffering due to this. I can't do this alone. Others must step forth and push this agenda.

I come from slaves in the US. We suffered lynchings and burnings because we believed that there was something right that had to be pursued. I was brought up to make the fight for justice and this is was this blog has been for me. It is dedicated to my family who died young from heart attacks, strokes and cancer. It is based on the belief that this did not have to happen and that it can be stopped, if I would make the fight.

In this blog, I have not only brought forth the information about this diabetes but also put myself on the line by actively experimenting on myself to show that this is a special type of diabetes. I can't do it alone. You, out there, have to push this issue in China, Indonesia, Brazil, Turkey, Africa. It is up to us to make this known and get proper care for our brothers and sisters.

I've made the fight. Please, make the fight as well. Nothing will get better without our efforts. No more funerals, no more amputations without the understanding of what we face. This is what I ask. This is what making the fight is about. The information is here. What is needed is the will to push it and challenge all the thoughts on diabetes that endangers us.

Take this information and, please, make the fight.

Mike Barker

Sunday, December 19, 2010

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 1st 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 1st 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 1st 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 1st 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?

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

Thursday, October 21, 2010

Downloadable Scientific Ketosis Prone Type 2 Diabetes powerpoint presentation

Guillermo E. Umpierrez, Dawn Smiley, and Abbas E. Kitabchi

There is no news for you KPD fans in this presentation. This was done in 2006. This blog has a lot more current information and speculation on that information. This, however, represents the best thoughts of the current researchers at that time and these people have undisputed credentials. Whether people have heard of Ketosis Prone Type 2 diabetes or disbelieve its existence becomes moot because of this document. Here you have a complete presentation telling all about it. I post this in that light. You can simply download it and give it to family and friends.

I found this presentation on the web and these are some of the chief writers and researchers of Ketosis Prone Type 2 diabetes. It seems to be a presentation in China and might be a bit dated but it is very thorough.

I spend a good bit of time introducing people to this subject and so I started to develop  a presentation on it. Low and behold, this pops up!

You no longer have to go through the long discussions. This power point will do nicely. This would be a good thing to pass around, post or show to your diabetes educators. Who knows, it might make a difference.

Ketosis Prone Type 2 Scientific Presentation  

PS If some one can translate the characters in this document, chime in.

Monday, October 4, 2010

A1c, glycation problems and DKA

This might be a bit of a mess but I wanted to get this information out and I figure I can clean it up a bit later.
You might have noted that I keep adding on to the ethnic KPD list. You might have also noticed the strong representation of people of color in this list. It is tempting to think that there is some aspect of melanin involved in KPD but I seriously doubt it. I tend to see color as an indicator of certain things. The first thing it indicates is global location. Fairer people tend to live in more temperate climes. Darker skinned people tend to be located in more tropical regions.

What is it about those regions. One thing is parasites and malaria. It is known that genetic tests tend to show that people with protection against malaria also seem to have higher rates of kpd. I won’t go into the genetics but typically the same genes tend to be cited and they all tend to give an advantage in handling malaria. Here’s a listing of G6PD deficiency.

Table 1. Common Hemoglobinopathies: Populations Affected, Prevalence, and Outcomes
Hemoglobin (Hb) Variant
Populations Affected
(in the United States unless otherwise noted)
Outcome with One Abnormal Gene and One Normal Gene (Heterozygous State)
Outcome with Two Abnormal Genes (Homozygous State)
Hemoglobin S (HbS)
African Americans
Hispanic Americans/Latinos
Also found in East India, the Mediterranean, and the Middle East
About one in 12 African Americans has sickle cell
trait 1
About one in 100 Hispanic Americans/Latinos has sickle cell
trait 2
Sickle cell anemia occurs in one of every 500 African American births 1
Sickle cell anemia occurs in one of every 1,000 to 1,400 Hispanic American/Latino births 1
Sickle cell trait (also called HbAS): usually asymptomatic
Sickle cell anemia (also called HbSS disease): sickled red blood cells that interfere with circulation and decrease life span of red blood cells; can result in hemolytic, splenic sequestration, and aplastic crises and multiple complications
Hemoglobin C (HbC)
African Americans
People of West African descent
About 2.3 percent of African Americans have HbC trait 3
HbC trait (also called HbAC): asymptomatic
HbC disease (also called HbCC disease): mild hemolytic anemia, mild to moderate enlargement of the spleen
Hemoglobin E (HbE)
Asian Americans, especially those of Southeast Asian descent
Common in Cambodia, Indonesia, Laos, Malaysia, Thailand, and Vietnam. Also seen in southern China, India, the Philippines, and Turkey
Prevalence of HbE may be 30 percent in Southeast
Asia 3
HbE trait (also called HbAE): asymptomatic
HbE disease (also called HbEE disease): mild hemolytic anemia, microcytosis, and mild enlargement of the spleen
Hemoglobin SC (HbSC)
African Americans and people of West African descent
Also found in East India, the Mediterranean, and the Middle East

HbSC disease (also called sickle-hemoglobin C disease): mild hemolytic anemia and moderate enlargement of the spleen; may have blocking of blood vessels as in sickle cell anemia but milder symptoms
Hemoglobin F (HbF) elevated
Occurs in patients with hereditary persistence of fetal hemoglobin, sickle cell anemia, severe anemias, leukemia, and other conditions
About 1.5 percent have more than 2 percent HbF but some groups may have concentrations as high as 12 percent 3
Those with elevated HbF and sickle cell anemia may have a milder form of sickle cell anemia
1 National Heart, Lung, and Blood Institute, NIH. Sickle cell anemia. Available at: Posted May 2007. Accessed June 27, 2007.
2 National Human Genome Research Institute, NIH. Learning about sickle cell disease. Available at: Posted February 2007. Accessed July 3, 2007.
3 Bry L, Chen PC, Sacks DB. Effects of hemoglobin variants and chemically modified derivatives on assays for glycohemoglobin. Clinical Chemistry. 2001;47(2):153–163.

Unless you are totally blind, you will recognize that all this information matches up with who gets KPD. It also matches up with Malaria.

Now the reason for bringing this up is about the tendency of these issues to affect the A1c. They can cause an over estimation of A1c but most typically they will cause and under reading for A1c. This is because the A1c is a measure of glycation. (basically carmelized blood cells)This measure, however, assumes that the average blood cell will be around for 90 days. What if the cell has a shorter life as it tends to have with these two issues? The number for glycation is going to be lower simply because the blood cell hasn’t been around long enough to get glycated as much. The A1c will appear to be lower.

I have already written about the ADA, diabetes and the danger to KPD’s. This needs to be tossed in. We are in serious trouble with the ADA guidelines since they sit right at the point of DKA for us but what if the test is off? We shouldn’t be anywhere near an A1c of 6.3 for safety sake. The A1c number could be 5.8 but, in truth, we could be at 6.5, which is trouble.

Here is what that trouble means. It means a continual rise in DKA admissions to hospitals with all the attendant costs. As has been noted before, there isn’t any real way to separate out KPD’s from Type 2’s but the suspicion is that greater than 50% of new onset DKA admissions are KPD’s and for all we know a good many of the Type 2’s are KPD, as well.

DKA’s Admissions per year

Graph showing Number (in Thousands) of Hospital Discharges with Diabetic Ketoacidosis as First-Listed Diagnosis, United States, 1980-2005. Links for data figures, sources, methodology and data limitations, and detailed tables follow this figure.

This graph shows a doubling of admissions in the last 25 years, basically 60,000 more than 25 years ago and it is rising. KPD’s are probably a little better than half this number. If you add the blood glycation problem with the ADA recommendations you can see how this might be the case.

Things aren’t getting any better for us and they won't get better anytime soon because they are now going to make the A1c the diagnostic tool for diabetes. For us, this is a really really bad idea.

Sunday, September 19, 2010

Thinking about: A1c Relapse Progression and the Insidious Nature of KPD

These are the graphs from Ketosis-Prone Type 2 Diabetes in Patients of Sub-Saharan African Origin. These graphs especially C & D  are too important not to be seen.

This is my recreation of C for clearer viewing.

Let's recap.
Ketosis Prone Diabetes is known for sudden onset without a precipitating factor. I posted this Here
The A1c at which the diabetes stayed controlled is about 6.3. This is in the previous post.  Here
Spontaneous Remission is the norm where there are no antibodies present. This is posted everywhere on this site.

What we have is a type 1 like syndrome that shows up out of seemingly nowhere then vanishes, leaving a type 2 diabetic, who can maintain blood sugars with diet and exercise.

My speculation is that the KPD syndrome is insidious. I have speculated in other posts using anecdotal evidence that this is the case but it occurs to me that there is enough here to do better.

The graph is important because what we need to wonder about is: what is a KPD before DKA?  This graph puts the regular blood sugars at about 6.3 A1c or 134. Jenny Ruhl's "Blood Sugar 101"  talks about dangerous blood sugars and, the short of it is, that blood sugars above 140 cause damage. She details other blood sugar levels that are considered safe but are bad as well. If you're new to diabetes I strongly advise you to read this site, carefully.

No one's blood sugar is steady. It goes up and down during the day and an A1c is best viewed as an average of blood sugars over a 3 month period. Actually, it's a measure of glycation of blood cells but seeing it as an average will do just fine for my purposes.

As I said, no ones blood sugars are steady and the more metabolic damage you have, the more they tend to fluctuate. Now, for whatever reason, KPD's tend to have great big fluctuations. This means that at 134 KPDs are going to spend considerable time above the dangerous 140. In fact it is so close to 140 as to almost be the same thing. KPDs have another trick that most other diabetics don't seem to have and that's remission. Rather than continue on a path of gradual rise, they can and do drop back to near normal. This would essentially reset their diabetes and they would, once again be back to a gradual rise.

What I'm saying is that the flat portion of this graph represents both the tendency to fluctuate wildly and the tendency to balance this with a fall back into remission. A KPD would get in trouble if the numbers stayed significantly above 140 but even then, if intensive insulin therapy were applied blood sugars once brought down would go back into a range where things would balance.

There is a problem here. Over time, continuous damage would be occurring. It would be small each time but the cumulative effect over decades would cause serious damage body-wide.

If we run this all back, we could start with a normal blood sugar but with a tendency to get large fluctuations from certain types of foods. Whatever the mechanism is for remission would keep pulling blood sugars down but over time they would rise as more and more damage was being done metabolically and to other body systems. The abrupt onset would occur when this remission mechanism itself broke down. Maybe it has a limited range to work in and the KPDs that go DKA have a functionally smaller range.

Okay, this is speculation. There are many ways this could be playing out, all I've done is outline one possible scenario. What isn't speculative is the nearness of normoglycemia to the line of danger and how quickly this takes off.

Once again we visit the ADA guidelines.

ADA Criteria for the diagnosis of diabetes
1. A1C 6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.*
2. FPG 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.*
3. Two-hour plasma glucose 200 mg/dl (11.1 mmol/l) during an OGTT. 

It isn't said but if the FBG (fasting plasma glucose) is below 126 most medical people will not go to the other tests. Even if they did, the next test would be an A1c and a KPD would pass there as well. The OGTT (oral glucose tolerance test) would catch it but it isn't done if the first two don't give indicators.

Years of damage with an attendant rise in mortality would occur because all those numbers sit in the danger zone for KPD's and the graph shows that DKA could easily be around the corner.

If you're reading this, you're probably KPD. You should recognize that it has a strong genetic component so if you've got family members they are likely to have it or some component of it. This is where I diverge from all the diabetic advice on diet. Screw looking at or adjusting diet. You don't know what precipitates KPD. The only thing that is known is that the blood sugar numbers represented by the "prediabetes" ADA recommendations are, in fact, the launching point for a serious diabetic emergency.

I said that the OGTT would more than likely have shown diabetes but this test tends not to be performed. You can do something similar with a meter, a couple of bowls of breakfast cereal and a glass of juice. Just test someone an hour after they took their first bite of breakfast and see if their numbers are above 160. I think that would catch a lot but since we really don't know what the bad actor in the food is, wisdom dictates testing the blood sugar with all types of food. What puts the blood sugar above 160 should always be avoided because whether you're a KPD or not, damage occurs to the body above that number diabetic or not.

Thursday, September 9, 2010

Thinking about: Eating. Maybe one size does not fit all

Though most of the testing of KPD's tends to involve obese participants, it should be noted that many KPD's  are not only not obese, they are lean. Typically, when I look at papers where the participants aren't chosen, the lean members comprise a quarter to a third. Even in childhood DKA episodes, the obese number about fifty percent.

What does this tell us about KPD's and weight? I keep hearing and seeing ads telling parents to make sure their children are active and eating right. This is the answer to childhood obesity, exercise and diet. Okay, I am a fan of both sloth and gluttony, I tend to be good at them, but I have to admit there's nothing wrong with having children out there physically engaging the world without a candy bar in their mouths.

KPD is showing us something, however. What do you say to a person who is a thin diabetic? You obviously can't ask him or her to go on a diet nor would you put them on exercise schedule to help burn calories. We don't give the same advice to the thin KPD simply because it doesn't make obvious sense. They are thin. We give it to the heavy ones because they are fat. It's still the same condition with the same underlying causes. It gets expressed differently but the numbers between fat and thin are pretty much the same. I'm saying this because, I believe we have to look deeper than this. There is something going here and the range of body types it effects doesn't seem to point at behavior.

The people of sub-Saharan Africa have a much bigger problem with Ketosis Prone Diabetes but this tends to be more in urban environments. There hasn't been a study but I would hazard a guess that you could draw a trendline representing length of urbanization of KPDs and their families and find quite a correlation.

Another thing to note is it tends to cluster in people of color, not that whites don't get it, they do, but the prevalence is far higher in people of color. Now I'm pretty sure you don't want to say that all these people of color are lazy and eat too much. Besides, how could that be true if a good many of them are thin?

I believe that most of this is a response to diet. It is, after all, about metabolism. Its higher rate of prevalence in urban areas suggests that it has something to do with the moving from traditional diets to more modern diets. It would be logical to point out that there are many things that go with urbanization that could just as readily be pointed as a cause. This is true but I would say that this exists worldwide in varied modern environments so I would have to ask: how many things could this be? To tell the truth, I don't know nor does anybody else. What I do know is purely anecdotal and the KPD's I've talked to have had to change their diets significantly to hold their blood sugars down with diet and exercise, those on insulin, generally, have not.

This difference in insulin using KPD's and non-insulin using KPD's suggest that some element of diet is effecting blood sugars. Think of it as some sort of intolerance. What is it? I really can't know. I list a bunch of blogs I follow that are all about nutrition because I'm trying to find out.

I ate a very healthy diet before I was diagnosed but now I find I can't eat that same diet without a significant rise in blood sugar. Would I say that, simply because I can't eat it, no one should? No. What I will say is that KPD is different and pretending that it isn't does not work. We can not assume what is healthy. We must verify.

I've just read the usual recommendations of the ADA and others about what is healthy to eat but does it include KPD? I think not. If these foods are fine there is really only one way to know and that's to test the blood sugar. I see all these recommendations about what to eat but, one size does not fit all and this is especially true of KPD. What should be recommended is that all families get a meter and test what their food is actually doing to them. If there is a significant intolerance, blood sugar will exceed 140. If this was the recommendation of the USDA there would be far fewer DKA events in this country. It would also provide important data about what is safe and what is not about a whole range of products.

To repeat, there is something in the KPD diet, that may not effect others but which is probably poisonous to KPDs. We can't identify who is KPD but if people were checking their blood sugars and correlating it with what they ate, the KPDs that are out there, who aren't diagnosed, could see this truck coming

Friday, August 27, 2010

The A1c tipping point

Whilst looking for correlations on some other things, I fell across this important information that didn't make an impression on me then but it certainly does now. I guess it shows that it's a good practice to go back with the new ideas that you've gained and look at the data again.

Even though, by my estimates, there are millions of Ketosis Prone Diabetics out there, we remain the "mystery meat" of diabetics. There is very little research about its genesis. There is no way to identify a KPD before a diabetic emergency occurs. In fact, as far as I know, very few people are diagnosed as KPD even after they have had an extreme glycemic event and recovered. We don't even know what the numbers are for KPD. I tend to believe that an A1c greater than 10 with spikes above 300 is a good indicator, especially if the fasting blood sugar was less than 140 in the previous year. That thinking and two bucks might get you a cup of coffee.

We aren't high on anybody's list of things to do. So, I think it's important to glean what facts I can from whatever data is out there to help people deal with KPD. This brings up this little fact. It has to do with the tipping point or when does KPD go from being just a type of diabetes to something that can be deadly.

Ketosis-Prone Type 2 Diabetes in Patients of Sub-Saharan African Origin
Clinical Pathophysiology and Natural History of -Cell Dysfunction and Insulin Resistance

Franck Mauvais-Jarvis,1 Eugene Sobngwi,1 Raphae¨ l Porcher,2 Jean-Pierre Riveline,3
Jean-Philippe Kevorkian,4 Christian Vaisse,5 Guillaume Charpentier,3 Pierre-Jean Guillausseau,4
Patrick Vexiau,1 and Jean-Francois Gautier1

This is a study that tracks KPD's over ten years and compares them to regular Type 2's and Ketosis Prone Type 1's. This study is out of Paris done on emigrants who come mostly from Sub-Saharan Africa. I have talked or corresponded with people who question the relevance of this research to them because they aren't remotely African or descended from Africans. As I said before, this syndrome has been documented almost every. The research is very spare and I've had to cobble data from all over the world. I suggest that beggars can't be choosy. My position is that anything that says anything about KPD is relevant to all KPD's  irrespective of color or origin.

ADA Criteria for the diagnosis of diabetes
1. A1C 6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.*
2. FPG 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.*
3. Two-hour plasma glucose 200 mg/dl (11.1 mmol/l) during an OGTT.

Standards of Medical Care in Diabetes—2010

That being said, let's get on with it. Above I have copied the ADA guidelines for diabetes diagnosis. It's important to keep these numbers in mind. It is especially important because, as I've said, most docs have no idea about how this works so you need to look out after your needs or those you know.

Buried in the KPD paper is a graph that describes the path that relapse takes in KPD's. Though it describes relapse, I am looking at it as just the course which KPD's take before their blood sugars go awry. What is my evidence for this. Well, there is one thing but I'll get to that later. Of course, A KPD, by definition, has already been diagnosed so it very definitely pertains to those.

What they found was that the course before relapse could be predicted by A1c over a years time.  I tried to get this but it wouldn't copy. You can find it on page 650. Here's what they had to say.

The median duration between the development of hyperglycemia (HbA1c 6.3%) and the onset of a ketotic relapse was 12 months (95% CI, 6–21, Kaplan-Meier). During this period, the insulin secretory reserve, measured before the onset of hyperglycemia and during readmission for relapse, dramatically deteriorated ( C-peptide, 2.88 0.21 vs. 0.19 0.08 ng/ml; P 0.05). There was no precipitating illness other than hyperglycemia. The increase in HbA1c 6.3% was associated with an increased risk of ketotic relapse with an HR of 38 (95% CI, 5–286; P 0.0004). Thus, hyperglycemia preceded and was strongly associated with
the subsequent development of an insulin-deficient, ketotic relapse.

The chart is pretty clear. It tracks the A1c for 40 months. The A1c stays steady at around 6.3% and at about 12 months before relapse takes a slight jog up. At 6 months, it takes another jog up to about 6.6 %. From this point on, the curve becomes steep.

What you can see is that below 6.3% blood sugars remained steady. Above that number events go bad very quickly. The 6.3% averages out to a blood sugar of 134. The first jog up appears to be about 6.5%, which averages to daily blood sugar of 140. This 140 is not a random number. It is thought to be the point at which blood sugars become damaging and bring on long term complications.

My thought on this as occurring before the first episode is from some reading, which I can't find, that said it was frequent, that previous to diagnosis, a KPD would have a normal or near normal blood sugars 6 months before. This graph shows something similar. We have no idea what causes this catastrophe but the fact that its beginnings sit at this critical juncture seems to suggest that something gets broken here. What you have to recognize is that this is for people who've already broke down then gone into remission, so whatever got broken got fixed once the blood sugars were brought down.

Now look at the ADA guidelines. They've tightened them up but look how close they are to the KPD danger point. This guideline is really for T2's. Would you give this as a guideline for KPD's knowing that they can crash very quickly? If you are a KPD should you feel safe with these guidelines?

If you showed up at a doc with these numbers, the ADA recommends that the physician should inform you that you're prediabetic and that maybe you should start making adjustments with diet and exercise. You would be asked to return in 6 months for a checkup to see how things were going. This wouldn't be a problem for a Type 2 because onset isn't abrupt and acute but for a KPD these numbers should be sending off all types of alarms because in 6 months you could very well be hospitalized or at worse, dead.

Until there is a diagnostic test for KPD, we will continue to windup in emergency. For those who already know what they are; keep and eye on your blood sugars because, unlike a T2, whose numbers trend steadily, you can go off the rails very quickly.

Tuesday, August 24, 2010

Increased weight and insulin resistance revisited

This relates to a baffling previous post.Here This was puzzling because it involved KPD diabetics gaining weight after a DKA event and becoming normoglycemic. I've discussed remission in KPD's before and though the mechanism isn't well understood, it is known to be common enough to be considered a part of the KPD syndrome. No, what upset the apple cart here was that thin KPD's did not do as well as the ones who gained weight. This seems counter to all the advice about weight loss that is given to diabetics. Almost the first thing a doctor will say to a patient is to lose weight. If a KPD followed this advice their blood sugars would rise and lowering blood sugars is central tenet of all things diabetic. What the heck is going on here?

I am now going to put forth an idea that popped into my head after reading a post by Ned Kock over at Health Correlator. Here What got my attention were people who were heavy but were more insulin sensitive then their control group. What was even better: once they received medication they began to lose weight but became more insulin resistant with a rise in blood sugar.

Insulin Resistance is very much at the heart of obesity and thinness as far as I can see but it is also one of the central aspects of Ketosis Prone Type 2 diabetes. Pal Jabekk speaks of the fact that insulin resistance is a body wide behavior. I agree given insulin's importance in energy metabolism obviously everything has critical involvement with it. This doesn't, however, mean that insulin is used at the same rate through out the body all the time. At any given moment, there will always be some systems that are more or less resistant.

This brings me back to the puzzle of KPD weight gain while at the same time reaching near normal blood sugars. First of all KPD's are infamous in the fact that weight is not an issue. Just as many KPD's are thin as obese. Some have separated this along the lines of those who lack sufficient insulin so that they become thin and those who have plenty so they become fat.

When the DKA or severe ketosis event occurs KPD's, who recover, are shown to have a low normal reading of C-peptides. The cut off that has been cited is .9. In six months, it is common for this to go back into the normal range and higher. It is also known that KPD's recover near normal blood sugars even though their measurable IR isn't reduced one jot. It should be noted, as well, that the best blood sugars tend to go to the heavier KPD's and not the thin ones.

Given that the IR is still high, the  C-pep is normal or above and the blood sugars have normalized, we have to assume that there is relatively enough insulin present. What is the difference between thin and obese?

Now the leap of faith. It has to be relative insulin sensitivity issues. We can see with a thin person that insulin is putting relatively more energy in other systems besides fat. What those systems are we really don't know. What we can tell, however, is those systems on the whole are more sensitive to insulin than fat. Likewise, if the person is putting on weight then their adipose is relatively more sensitive to insulin than other body systems.

Now my thinking about the KPD's gaining weight with better A1c's. I believe fat works better for glucose storage then muscle or other systems. You can look at obesity as the body's way to reacting to high amounts of glucose. This is why I believe there are so many heavy people. Obviously, the body is sending glucose everywhere but the fat cells seem to get more. If we make this about controlling blood sugar then the fat cells become like the catch basin for the extra glucose in the system.

A thin KPD is relatively more insulin resistant in the fat cells, and this is why I say fat works better, sending glucose to other systems with fat lower down on the list doesn't normalize blood sugars as well as those who can send it to fat. So thin KPD's are typically not going to have blood sugars as good as heavier KPD's. This would also say that thin KPD's are more at risk of relapse to DKA then heavier KPD's. I would also add that this probably isn't how normal people work but we have broken metabolisms. Our livers are pretty much blind to insulin.

Monday, August 23, 2010

Multi-Tissue resistance in KPD's

I've been away doing research and other things but now I'm back.

KPD's don't have enough insulin therefore the body hovers at a high bg level. I originally was going to write another piece about the oddness of KPD and weight gain and then obtaining acceptable levels of blood sugar but I thought I had published this piece.  Sorry, I'm doing it now.

It has been noted that insulin resistance is a big part of being Type 2. This is why many Type 2's have high insulin numbers because the pancreas has to put out more insulin to overcome this resistance. KPD is Type 2, at least most of the time. What they have found to be different about KPD's is that all systems in the body seem to have relatively high insulin resistance.

This is the first investigation of diabetic patients in a metabolic state close to normoglycemia without insulin treatment. The multiorgan insulin resistance observed in near-normoglycemia suggests that these defects are primary rather than secondary to the diabetic state.
Multitissue Insulin Resistance Despite Near-Normoglycemic Remission in Africans With Ketosis-Prone Diabetes
Table 2—
Metabolic parameters and indexes of insulin action
KPDControl subjectsP
Fasting plasma glucose (mmol/l)6.3 ± 0.24.9 ± 0.1<0.001
Fasting plasma insulin (μU/ml)9.4 ± 1.96.7 ± 1.00.33
Insulinogenic index (mU/mmol)4.6 ± 0.921.3 ± 5.40.001
HOMA-IR3.1 ± 0.61.1 ± 0.20.005
SSPI1 (μU/ml)20.9 ± 3.317.4 ± 1.20.82
SSPI2 (μU/ml)189.6 ± 20.5181.5 ± 14.80.89
TGD (mg · kg−1 · min−1)7.5 ± 0.810.5 ± 0.90.018
TGD × insulinogenic index28.1 ± 4.0193.3 ± 46.1<0.001
bEGP (mg · kg−1 · min−1)4.0 ± 0.33.0 ± 0.10.001
rEGP1 (mg · kg−1 · min−1)1.6 ± 0.20.6 ± 0.10.004
bEGP × FPI (mg · kg−1 · min−1 · mU · l−1)35.9 ± 7.220.7 ± 3.60.04
rEGP1 × SSPI1 (mg · kg−1 · min−1 · mU · l−1)33.2 ± 7.210.9 ± 2.80.006
rEGP2 × SSPI2 (mg · kg−1 · min−1 · mU · l−1)50.3 ± 22.100.007
Fasting NEFA (μmol/l)1,936.7 ± 161.41,230.0 ± 174.10.002
SSNEFA1 (μmol/l)706.6 ± 96.5381.6 ± 55.90.015
SSNEFA2 (μmol/l)187.8 ± 27.7116.1 ± 11.20.05
Fasting IRNEFA (103 · μmol · mU · l−2)17.7 ± 3.28.0 ± 1.70.009
IRNEFA1 (103 · μmol · mU · l−2)17.4 ± 4.66.9 ± 1.40.05
IRNEFA2 (103 · μmol · mU · l−2)40.2 ± 9.221.2 ± 2.60.06

  • Data are means ± SE. SSNEFA, steady-state nonesterified fatty acid; IRNEFA, insulin resistance index to NEFA disappearance (1 and 2denote the last 20 min of the first and second steps of the glucose clamp, respectively).
I'm not going to go through all these numbers but they are meant to represent calculated indexes of insulin resistance. It would have been nice, if the comparison had been made to regular Type 2's. It would have been great, if they could have tested this before people went DKA but, as you know, there is no way to distinguish KPD before it occurs. It suffices to say that, metabolically, we aren't the most normal group on the planet.
If you look at these numbers and toss in glucose toxicity, you can get an idea of why we go DKA quickly. 

Despite an increasing number of reports of ketoacidosis in populations with Type 2 diabetes mellitus, the pathophysiology of the ketoacidosis in these patients is unclear. We therefore tested the roles of three possible mechanisms: elevated stress hormones, increased free fatty acids (FFA), and suppressed insulin secretion.
Conclusions  At the time of hospital presentation, the predominant mechanism for ketosis in KPDM2 is likely to be greater insulinopenia.

Pathophysiology of ketoacidosis in Type 2 diabetes mellitus
P. Linfoot C. Bergstrom and E. Ipp    Diabetic Medicine   Volume 22 Issue 10, Pages 1414 - 1419

The question I have is: when did this start? Is this part and parcel of our lives as youths? Have we always been KPD and it took bad diet to get us here. There is plenty of documentation that this is present in the young. 
again more research needs to be done.

Purely from an anecdotal perspective, looking back at my childhood and viewing my present day symptoms, I would say they were present then. The problem is we really don't know what KPD is. It is described by its most dramatic symptom, which is its acute presentation. What is going on before that? Is it the same syndrome in children? How insidious is it? What is the continuum of its behavior?