Barker's Type 2 Ketosis Prone Diabetes / Atypical Diabetes T1b/ Flatbush Diabetes

Thinking about: Western technology, food and the health of people of color and world food production and trade.

2011-09-06T02:20:00.006-04:00

I've added, what I think, is an important addition to this post. If you've read this already just skip to the bottom.

Guess whose back? Me! I've finished my latest assignment so it's back to KPD or abrupt type 2 diabetes; however you wish to look at it.

I was working down in Southwest Detroit (One of the few multicultural areas there.) and I was looking at many of the people walking around and many of them were heavy. The thing about this area is that it isn't a "food desert" there are plenty of stores with many types of produce. This is also a working class area so most people do work that requires a certain amount of physical effort. Yet the story remains the same, way too much weight and with all the problems that this portends.

One of the things that helped to keep this in mind was looking at the stats on this blog while I was away. This blog in particular seemed to be getting a lot of those hits. I tried to address this issue further while I was away with this blog. Now I want to go back again and try to put this all a little more together.

In the last thirty years diabetes appears to be surging both in the US and around the world and it seems to affect people of color disproportionately.

You should look at this graph very carefully. Something happened after 1990. One of them is probably a statistical fluke having to do with the change in what is considered diabetic or the fact that the US baby boomer population is entering its mature years but you would expect for that to flatten out eventually. It hasn't.

Here's another fact to consider. Diabetes is a chronic disease that develops overtime. How long this period of time is varies. Even in the case of Abrupt onset T2, there appears to be a long lag before our type of diabetes becomes full blown. You can view that here. My point is that viewing the take off point of diabetes isn't enough. We have to look at the preceding years and what might have occurred in them, if we wish to see some turning point.

The time frame we're looking at is about 30 to 40 years and frankly there are plenty of changes that have occurred in this time that could be correlated with this sudden take off in diabetes. This is diabetes, however, and the dog that hunts best here, at least for me, is diet.

I've talked about the contamination of traditional foods before. Here. You could look at this post as an expansion of that post. My point was that due to economics the constituents of foods around the world are being replaced with cheaper products that I think are problematic.

First up: wheat. Wheat has been around for years. It was first domesticated around the Fertile Crescent and this wheat is Emmer. Later on with get Eichorn wheat and a host of other varieties. Wheat has been bred and bred through out the years for all types of qualities. It has become one of the central characters in the diseases of civilization. Take a normal healthy society of humans and introduce them to flour and problems tend to arise. Denise Minger on her blog statistically demonstrates a strong correlation between wheat and cardiovascular disease. What should be even more worrying is that 99% of all wheat is of one kind, the dwarf wheat variety. Many people have pointed to this variety as having toxic properties especially as relates to blood sugars. Anecdotally, I've read where people have tried Eikhorn wheat and found no big jump in blood sugars.

My standard answer to any ketosis prone diabetic is to give up wheat. It really doesn't matter what their symtoms are. I say, "Give up wheat." and if they do they always feel better after a month. It makes me appear as if I know what I talking about.The truth of the matter is the giving up of wheat seems to always ease physical problems. Give it a try.

What this has to do with traditional foods is the fact that, due to global trade, a cheaply produced product is easily substituted for a more traditional product that tends to be more expensive. The more plentiful that cheap product is; the more likely it will be used as a substitute. Dwarf Wheat became the dominant variety starting in the late 70's. Unless that traditional food is tightly regulated such as Fasso wheat in Italy, it is more than likely Dwarf Wheat. More Dwarf Wheat If you look at our chart, it was just in time for our diabetes epidemic.

On to seed oils. These have been around since the start of agriculture but except for a few cases like olive oil they could not be produced in great quantity until we had the industrial techniques to do so. These are what we call vegetable oils.

Here's some nice charts.

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So what are these graphs about? This is about fats particularly polyunsaturated fats. These typically come from seeds that are processed to get the oil out of them. The fats obtained from seeds tends to be mostly Omega -6's. The body uses Omega-6's and Omega-3's as building blocks. The problem is that the body doesn't distinguish between the two. This really wasn't necessary because in nature they would generally be found in roughly a 1 to 1 ratio. Thanks to modern technology, this has changed. The consumption of seed oils has continues to climb so much so that the ratio is now guessed to be between 10:1 to 25:1. Well what of it?

As noted before, the body does not distinguish much between these two fatty acids. If the body is taking in 6's when it should be taking in 3's then the building blocks for a healthy body are wrong. It sets up a situation of chronic inflammation. This is from Wikipedia.

Some medical research suggests that excessive levels of certain n−6 fatty acids, relative to certain n−3 (Omega-3) fatty acids, may increase the probability of a number of diseases.^[1]^[2]^[3]

Modern Western diets typically have ratios of n−6 to n−3 in excess of 10 to 1, some as high as 30 to 1. The optimal ratio is thought to be 4 to 1 or lower.^[4]^[5]

Excess n−6 fats interfere with the health benefits of n−3 fats, in part because they compete for the same rate-limiting enzymes. A high proportion of n−6 to n−3 fat in the diet shifts the physiological state in the tissues toward the pathogenesis of many diseases: prothrombotic, proinflammatory and proconstrictive.^[6]

Chronic excessive production of n−6 eicosanoids is associated with heart attacks, thrombotic stroke, arrhythmia, arthritis, osteoporosis, inflammation, mood disorders, obesity, and cancer.

Here's a listing of the Omega 6 amounts in some of the most used seed oils.

Most of these oils are not bought by people for consumption. They, for the most part, are used in the preparation of foods because they are cheap. Just imagine if your traditional food now made with flour from Dwarf Wheat is cooked in Soy oil.

I was going to throw sugar in this overlong post but if you don't know about that then nothing I'm going to say here is going to change things. I will say this that once again cost is driving cheap substitutes like high fructose corn syrup into more and more foods.

Look back up at the graphs. Look at the times. Does it seem as if we are doing something in our diets that have led to our present problems?

Now back to the problems of people of color and this quiet but possibly toxic mix that has invaded their foods. If we once again look at a graph of the A1c's of KPD's we see a long running period of elevated A1c's.

Normal A1c's should be around 5. These hover at about 6.3 month after month before taking off. I suggest that what we're seeing is inflammation caused by dietary components that over time essentially

damage our bodies. I'm thinking that these elevated numbers are due to a low level hyperglycemia that is a reaction to chronic infection. In this case, I once again bring up the hypothalamus which is an active part of this system and is susceptible to malfunction due to high blood sugar.

Remember, we are already prone to problems with dealing with carbohydrates, if you throw some fructose in there and cause the liver problems then you can be well on your way to DKA even with a traditional diet.

We are looking at economics possibly overwhelming good sense. Cheap food additives produced thousands of miles away are quietly replacing the traditional healthy foods. I would say simply eat whole foods but under what conditions was this food raised?You should be reading labels on anything that is manufactured but do you know what you're seeing. Did you know that the "emulsifiers" you now see on labels is more than likely a transfat? Once again I make my usual plea. Get a meter and test the foods that you and your family eats.

This is an addendum to this post. I started thinking that the key to much of what I have said is food production and the trade in food products. A little research found me this graph.

http://maps.grida.no/go/graphic/trends-in-world-agricultural-exports

Once again I ask you to look back at the graph of the growth of diabetes. The growth of trade takes off at about 1986. Ten years later in about 1996 diabetes takes off as well and both increase rapidly from there to the present. I don't see this being explained by ideas of food palatability though there is certainly some of that there, nor do I see genetics or behavior explaining this either. Food has not got that much better tasting. Certainly genetics hasn't changed that much and I doubt we have become less industrious in the entire world in the last forty years. This last graph suggests to me that we have done something in the production of our foods that is metabolically traumatic. I well know that correlation is not causation but there seems to be something here and all I can do is nibble around the edges. This calls for a better mind than mine or more specifically some one like a Ned Kock who could possibly tease out what might be going on here.

One could say that this is simply the usual "diseases of civilization" but one has to answer the question "Why does this occur now?".

I'm at Michigan State University, where some of the best agricultural scientists in the world do their work and though I'm not at liberty to divulge any specifics, world food production is about to seriously take off in the next 10 years. The tests that I have seen suggests we could see a doubling to quadrupling of food production. In other words, an end to famine. More food is good but what if the food isn't?

Chinese study on Ketosis Prone T2 Diabetes

2011-08-04T19:00:00.000-04:00

This is for our Chinese KPD's. Here's a study presently recruiting KPD's in China. Chinese KPT2D Trial One of it's big novel features is that it's recruiting both lean and obese KPD's. This isn't one of those studies showing that KPDM exists in a given population. They quite clearly know it exists. This study is meant to try and understand it.

This is one of the things I've been waiting for. Most of the research on KPD research has been done in the US and Europe even the studies done in African have mostly been carried out by Europeans. What I've been waiting for is for the third world to start picking up the research and expanding it. This is, after all, a growing problem in their countries.

Here it is buried in both bad science and a majority culture which largely ignores it. I talk to Blacks, Hispanics and Native Americans and all of them get this big surprised face when I talk about a diabetes that is prominent in peoples of color in the US.

I am especially perturbed by the advice given them by their local medical people. These people have no idea about this and so treat it just like a regular type 2, type 1 or LADA. This is probably one of the reasons DKA's have doubled in the last thirty years in the US.

Good for you China and let's hope the rest of the world gets going too.

Caution on NSAIDS

2011-04-18T19:03:00.001-04:00

I've pointed out a NSAID as the drug I was using to effect my 1st phase insulin response but anyone who is thinking about trying this should be aware of the risks involved. Beyond the usual issues of stomach and intestinal distress, there are other issues. You can read about many of them here. Jenny's Blood Sugar 101

One thing that she doesn't cover is that NSAIDs are NOT recommended for those who are G6PD deficient because of the chance of hemolytic anemia. If you've been reading this blog you should know that KPD's have a very high rate of this deficiency. So I do urge caution in their use.

How I got normal blood sugars for 60 cents a week

2011-04-11T20:49:00.002-04:00

Being that I'm still on assignment, I've decided to let you in on the experiment that I did on myself to try to understand the nature of Ketosis Prone Type 2 diabetes or as I call it Abrupt onset type 2 diabetes.

Okay, a bit of a review. Ketosis prone type 2 diabetes is an abrupt onset type 2 diabetes though highly prevalent in people of color it can and does pop up in any group. The fact is that KPDM is actually a subset of this form of diabetes. I know LADA's that have gone DKA. There is a real question in my mind whether Abrupt onset T2 (AOT2) is a type of diabetes or simply a mechanism through which diabetes is expressed.

At any rate, this is a diabetes that comes on very strong because the body simply quits producing insulin. It is therefore classified as a type 1 diabetes, T1b. It comes out of nowhere. In 6 months time a person can go from near normal blood sugars to DKA. I talk about this process in these posts. Relapse

It has also been shown to vanish just as quickly, if handled correctly. In the space of a year, a person can go from near normal blood sugars to close to death from DKA and then back again. This not a regular diabetes and so far has failed serious classification. It is so fantastical that most people don't know it exists, even those most susceptible to it such as people of Latin, African and Asian descent.

I, however, got lucky. About six months ago, I found myself with a revived 1st phase insulin response. I wasn't content with this. I had to find out what happened and how this could be and I kept experimenting until I not only found it but was able to manipulate it. I could turn it off and on with a simple manipulation. You can read about this process through this link, This is a dialogue on diabetesforums where I talk about this experiment

Here are some of the citations that I dug up to back up what I believed to be the cause of my suddenly restored 1st phase insulin response.
Non-steroidal anti-inflammatory drugs increase insulin release from beta-cells by inhibiting atp-sensitive potassium channel

EFFECT OF NAPROXEN ON GLUCOSE METABOLISM AND TOLBUTAMIDE KINETICS AND DYNAMICS IN MATURITY ONSET DIABETICS

Effect of selective cyclooxygenase-2 (COX-2) inhibitor treatment on glucose-stimulated insulin secretion in C57BL/6 mice

Use of Salsalate to Target Inflammation in the Treatment of Insulin Resistance and Type 2 Diabetes

Targeting INflammation using SALsalate for Type 2 Diabetes.

Potential Role of Salicylates in Type 2 Diabetes

This got me to thinking about KPDM and its quick rise and fall which you can read here. Here

Now you know. It was a NSAID called Sodium Naproxen taken as needed. The net cost was about 60 cents. More when I have the time.

Roux-en-Y gastric bypass

2011-04-07T17:32:00.003-04:00

I, in no way, endorse this procedure but it does have some bearing on Abrupt T2. It was orignally thought that much of the gains from this surgery was due to the limiting of / and types of food that people could eat once this surgery was performed. The citation below, however, shows that, in this case, there are far ranging effects on the hypothalamus that suddenly take effect. These effects proceed weight loss and involve the whole series of hormones that influence metabolism.

My point for Abrupt T2 is that this shows that the hypothalamus is a higher order mechanism that can certainly effect, if not control, the whole insulin cycle. Once again, there is no change in the underlying beta cell structure. The change isn't there but higher up.

http://journals.lww.com/annalsofsurgery/Abstract/2004/08000/The_Early_Effect_of_the_Roux_en_Y_Gastric_Bypass.7.aspx

Facebook Page for Abrupt Onset Type 2 Diabetes

2011-04-07T16:55:00.001-04:00

People have suggested that I put up a Facebook page so that people can easily comment and add information.

Okay, I've done this and I'll be adding more in the future. Hopefully, while I'm off on this project, this will keep the dialogue going.

Abrupt Onset Type 2 Diabetes

Obviously, I just got this set up before I went off on my latest assignment. I really didn't know what it was going to be but now I think I'm getting it. I don't have time to seriously go through scientific papers at this moment. I still am thinking about things and interesting citations still come across my desk. What I plan to use facebook for are these clues about Abrupt Onset that keep arising.

This will give me a chance to talk about and hopefully get feed back on ideas that you might find interesting.

Who gets KPD T2? Everybody!

2011-04-07T16:42:00.001-04:00

I've decided to keep updating this with citations as they come in.

Thai
Indian

Peruvian

Bangladeshi

Turkish

Hispanics have higher rate of KPD
http://care.diabetesjournals.org/content/26/8/2485.1.full.pdf

Adult-Onset Atypical (Type 1) Diabetes: Additional Insights And Differences With Type 1a Diabetes In A European Mediterranean Population. Http://Www.Ncbi.Nlm.Nih.Gov/Pubmed/15111529

Severe diabetes in remission: a Singapore's perspective - Malay
http://www.ncbi.nlm.nih.gov/pubmed/11817290?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews&logdbfrom=pub

Clinical characteristics of Korean patients with new-onset diabetes presenting with diabetic ketoacidosis.http://www.ncbi.nlm.nih.gov/pubmed/19477546

Ketosis-onset diabetes in Tunisian adults: immunological markers and β-cell function

http://www.emro.who.int/publications/emhj/1601/article12.htm

High Frequency of Type 1B (Idiopathic) Diabetes in North Indian Children With Recent-Onset Diabeteshttp://care.diabetesjournals.org/content/26/9/2697.1.full

[HETEROGENEITY OF TYPE 1 DIABETES MELLITUS] - Brazilian

http://www.ncbi.nlm.nih.gov.proxy1.cl.msu.edu/pubmed/18438531
A Subtype of Markedly Abrupt Onset With Absolute Insulin Deficiency in Idiopathic Type 1 Diabetes in Japanese Children

http://care.diabetesjournals.org/content/25/12/2353.2.full

South Asian version of flatbush diabetes mellitus- A case report and review article
http://www.acadjourn.org/IJMMS/abstracts/abstracts/abstracts2009/Sept/Khan%20and%20%20Akram.htm

Ketoacidosis in Apache Indians with non-insulin-dependent diabetes mellitus
http://www.ncbi.nlm.nih.gov/pubmed/9382666

Cetoacidosis diabética:una complicación frecuente de la diabetes tipo 2 en hispanoamericanos
http://www.sediabetes.org/resources/revista/00011519archivoarticulo.pdf

The Occurrence of Diabetic Ketoacidosis in Type 2 Diabetic Chinese Adults
http://www.tsim.org.tw/journal/jour10-6/P10_230.PDF

Characteristics of Caucasian type 2 diabetic patients during ketoacidosis and at follow-up
http://www.ncbi.nlm.nih.gov/pubmed/10842773

The prevalence of ketosis-prone type 2 diabetes is not known, but observational studies suggest that this type of diabetes accounts for a substantial number of patients with diabetic ketoacidosis. In the United States, the prevalence has been estimated to be between 20% and 50% in African-American and Hispanic patients with new diagnoses of diabetic ketoacidosis . In addition to ethnicity, clinical features predictive of future near-normoglycemic remission are obesity and a family history of type 2 diabetes. Among 154 consecutive African-American patients admitted to the hospital with diabetic ketoacidosis, we observed that obesity was present in 29% and that the prevalence of obesity was higher among those with newly diagnosed diabetes (56%). More than 80% of patients have a family history of type 2 diabetes. The mean body mass index at presentation in African-American patients with ketosis-prone type 2 diabetes has ranged between 28 kg/m2 to 37 kg/m2 . A high rate of obesity is also reported in Hispanic and Chinese persons and in sub-Saharan black African immigrants to Europe. Obesity in persons with diabetic ketoacidosis from minority ethnic groups is more common than in white persons, in whom the rate of obesity is less than 20%.

Balasubramanyan and colleagues reviewed the clinical profiles of 141 adults admitted to the hospital with diabetic ketoacidosis. At presentation, 39% of patients were considered to have type 1 diabetes, 53% were considered to have type 2 diabetes, and 8% were not classified.Twenty-eight percent of patients had newly diagnosed diabetes, 93% of whom were reassessed at least 2 years after their initial episode of diabetic ketoacidosis and were considered to have type 2 diabetes. More recently, Pin˜ero-Pilon˜a and Raskin reported that the incidence of this type of diabetes among persons with new-onset diabetes with diabetic ketoacidosis was approximately 60%. In agreement with the U.S. experience, African studies have reported that 42% to 64% of patients with diabetic ketoacidosis initially treated with insulin therapy do not have classic type 1 diabetes and may experience prolonged remission. The prevalence of ketosis-prone type 2 diabetes seems to be lower in Asian and white persons and may represent fewer than 10% of cases of diabetic ketoacidosis.

Narrative Review: Ketosis-Prone Type 2 Diabetes Mellitus
http://www.annals.org/content/144/5/350.abstract

The extent of the prevalence of this syndrome really isn't known. As far as I know, there is no ready test for KPD T2. What we have is hospital admittance records for DKA. The numbers quoted for Mexican and African Americans is about 60% of all the DKA cases. What this means in terms of the general Mexican and African American population is in question but you have to recognize that for every case where it is bad enough to cause hospitalization there has to be many multiples of it in existence.

Mike

Contamination of traditional foods

2011-02-06T18:35:00.000-05:00

I'm still off on assignment but this subject came up and I thought that it would be good to drop a brief note on it.

We tend to think that if we stick to traditional foods that we can expect to be safe from problems with blood sugar. What needs to be recognized is that traditional foods were typically raised by the consumer or the farmer was near to the consumer. Preparations were carried out by the person eating the food.

The modern world is different, however. You might very well be eating a traditional diet but what are its constituents? Is that wheat the traditional wheat which was used in the preparation of that bread? How was it prepared? This is important. Traditional preparation will do nothing to offset problems of diet, if the underlying food is problematic.

If you look at our "diabetes epidemic", you will note how much it has taken off in peoples of color across the world in the last few decades. I suspect that some of the reason has to do with newer varieties being substituted for old traditional foods. I know I keep harping on this but the only way to truly know is to test your blood. Don't be complacent. The world isn't very dietarily safe for you or me.

Please make the fight

2010-12-28T01:32:00.000-05:00

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

Thinking about the nature of Abrupt Onset Type 2 diabetes

2010-12-19T17:00:00.001-05:00

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

2010-11-18T17:05:00.004-05:00

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

2010-11-13T17:22:00.001-05:00

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

Downloadable Scientific Ketosis Prone Type 2 Diabetes powerpoint presentation

2010-10-21T22:50:00.004-04:00

KPD 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.

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

A1c, glycation problems and DKA

2010-10-04T01:37:00.004-04:00

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	Prevalence (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		N/A	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	N/A	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: www.nhlbi.nih.gov/health/dci/Diseases/Sca/SCA_All.html. Posted May 2007. Accessed June 27, 2007.

² National Human Genome Research Institute, NIH. Learning about sickle cell disease. Available at: www.genome.gov/10001219. 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.

http://diabetes.niddk.nih.gov/dm/pubs/hemovari-A1C/

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

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.

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

2010-09-19T20:45:00.007-04:00

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.

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

2010-09-09T16:46:00.002-04:00

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

The A1c tipping point

2010-08-27T16:52:00.004-04:00

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

http://diabetes.diabetesjournals.org/content/53/3/645.full.pdf

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.*
OR
2. FPG 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.*
OR
3. Two-hour plasma glucose 200 mg/dl (11.1 mmol/l) during an OGTT.

Standards of Medical Care in Diabetes—2010

http://care.diabetesjournals.org/content/33/Supplement_1/S11.full.pdf+html

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.

Increased weight and insulin resistance revisited

2010-08-24T19:55:00.001-04:00

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.

Multi-Tissue resistance in KPD's

2010-08-23T18:00:00.001-04:00

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
SIMEON-PIERRE CHOUKEM, MD, EUGENE SOBNGWI, MD, PHD, LILA-SABRINA FETITA, MD, PHILIPPE BOUDOU, PHD, ERIC DE KERVILER, MD, YVES BOIRIE, MD, PHD, ISABELLE HAINAULT, PHD, PATRICK VEXIAU, MD, FRANCK MAUVAIS-JARVIS, MD, PHD, FABIEN CALVO, MD, PHD, JEAN-FRANC¸ OIS GAUTIER, MD, PHD
DIABETES CARE, VOLUME 31, NUMBER 12, DECEMBER 2008
http://care.diabetesjournals.org/content/31/12/2332.full

Table 2—

Metabolic parameters and indexes of insulin action

	KPD	Control subjects	P
Fasting plasma glucose (mmol/l)	6.3 ± 0.2	4.9 ± 0.1	<0.001
Fasting plasma insulin (μU/ml)	9.4 ± 1.9	6.7 ± 1.0	0.33
Insulinogenic index (mU/mmol)	4.6 ± 0.9	21.3 ± 5.4	0.001
HOMA-IR	3.1 ± 0.6	1.1 ± 0.2	0.005
SSPI₁ (μU/ml)	20.9 ± 3.3	17.4 ± 1.2	0.82
SSPI₂ (μU/ml)	189.6 ± 20.5	181.5 ± 14.8	0.89
TGD (mg · kg⁻¹ · min⁻¹)	7.5 ± 0.8	10.5 ± 0.9	0.018
TGD × insulinogenic index	28.1 ± 4.0	193.3 ± 46.1	<0.001
bEGP (mg · kg⁻¹ · min⁻¹)	4.0 ± 0.3	3.0 ± 0.1	0.001
rEGP₁ (mg · kg⁻¹ · min⁻¹)	1.6 ± 0.2	0.6 ± 0.1	0.004
bEGP × FPI (mg · kg⁻¹ · min⁻¹ · mU · l⁻¹)	35.9 ± 7.2	20.7 ± 3.6	0.04
rEGP₁ × SSPI₁ (mg · kg⁻¹ · min⁻¹ · mU · l⁻¹)	33.2 ± 7.2	10.9 ± 2.8	0.006
rEGP₂ × SSPI₂ (mg · kg⁻¹ · min⁻¹ · mU · l⁻¹)	50.3 ± 22.1	0	0.007
Fasting NEFA (μmol/l)	1,936.7 ± 161.4	1,230.0 ± 174.1	0.002
SSNEFA₁ (μmol/l)	706.6 ± 96.5	381.6 ± 55.9	0.015
SSNEFA₂ (μmol/l)	187.8 ± 27.7	116.1 ± 11.2	0.05
Fasting IR_NEFA (10³ · μmol · mU · l⁻²)	17.7 ± 3.2	8.0 ± 1.7	0.009
IR_NEFA1 (10³ · μmol · mU · l⁻²)	17.4 ± 4.6	6.9 ± 1.4	0.05
IR_NEFA2 (10³ · μmol · mU · l⁻²)	40.2 ± 9.2	21.2 ± 2.6	0.06

Data are means ± SE. SSNEFA, steady-state nonesterified fatty acid; IR_NEFA, 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

http://www.ncbi.nlm.nih.gov/pubmed/16176205

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.
Emerging Epidemic of Type 2 Diabetes in Youth, but once
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?

The Provoking Event of Ketosis Prone T2 Diabetes

2010-06-26T02:38:00.000-04:00

I am not a scientist but I've been wandering around the marshes of KPD ever since I was diagnosed and, I believe, the answer to what provokes KPD is actually quite prosaic. Researchers have been looking at viruses, stress and other things because they have not come up with something that pushes off the KPD diabetic crisis. I'm willing to bet that this provoking factor hasn't been discovered because the researchers are looking too hard. The simplest explanation is diet. Too much carbs in too short of a time done over and over in a few days is what does it. To be more specific, I think, if anyone would look, they would find that KPD's before DKA slacked their thirst with high glycemic products such as juice and soda. This would be enough to push them over the edge.

Increased weight and Insulin resistance lead to improved glycemic control

2010-06-26T01:31:00.003-04:00

Somebody needs to explain this to me. This, once again, deals with Ketosis Prone Type 2 Diabetes but I don't care. This seems to go against everything that I know about being T2. This is from two of the seminal papers on Ketosis Prone Type 2 Diabetes so it isn't junk science. I went back and read these papers because I was researching what was meant by "near-normoglycemic remission". This data caught my eye and when I looked at other papers, I found confirmation.

Ketosis Prone T2 Diabetics are known for the fact that they can suddenly go into acute insulin failure and essentially become T1's, some will even stay T1's, with no autoimmune factors. The others will recover their beta functioning incredibly fast, we are talking weeks, if given insulin therapy. Even though their IR hasn't receded on bit, they will still proceed to stabilize their blood sugars at or near normal levels. Many, can and do, require only diet and exercise regimens. This is weird enough but this next part is inexplicable to me.

Weight does not really play a part in KPD. There are just as many thin KPD's as obese ones.They both are prone to DKA just as much. The recovery, however, is something different. The KPD's who recover fastest and have the lowest A1c's tend to be the ones who put on weight. Weight gain is the best predictor of near-normoglycemic remission. If we follow the logic, these are people who gain glycemic control by increasing their insulin resistance. How? This makes no sense. The thin ones don't do as well as those who put on weight. It gets better. Those with metabolic syndrome actually do better than those without metabolic syndrome. I can not wrap my head around this. Here are some of the quotes from these papers

We also noted significant weight gain associated with improvement of glycemic control, regardless of what therapy was used. Insulin-treated patients gained more weight than individuals on other therapies.

Our study also indicates that weight-gain is a good clinical marker of improved glycemic control, regardless of what therapy is used.

There was a significant correlation between changes in HbA1c and weight changes (r 5 0.45, P , 0.001, n 5 54) in both treatment groups. Patients with greater improvement in HbA1c had greater weight gain. Weight gain after initiation of diabetes treatment was 6.6 6 12.5 kg, regardless of what therapy was used. However, 17 patients continued to lose weight during the years of follow-up. These patients had a follow-up HbA1c of 11.4 6 3.5%. Of the patients that lost weight during the study, 5 were on insulin and 12 were on diet and/or oral agent therapy (7 on diet therapy alone, 2 on glyburide/metformin, 2 on glyburide alone, and 1 on glyburide/troglitazone combination). In the 37 patients who gained weight, HbA1c was 8.0 6 2.5% at follow-up. Of the patients that gained weight, 28 were on insulin and 9 were on oral agents or diet. The patients in the insulin-therapy group that gained weight had a significantly lower HbA1c than the patients in the diet and/or oral agent group that gained weight (P 5 0.01; difference of 2.6%, 95% CI 0.83– 4.4%). There was also a significant difference of 3.4% in HbA1c in patients that gained weight (regardless of therapy) compared with those that lost weight during the observational period (P , 0.0001, 1.7–5.1%). The patients on insulin therapy had a mean weight gain of 11.0 6 11.2 kg (P , 0.0001, 6.6 –18.5kg) versus non–insulin-treated patients.

Other than weight gain, there was no difference in diabetes-related complications between treatment groups in this short study period.

Idiopathic Type 1 Diabetes in Dallas, Texas A 5-year experience

Antonio Piñero-Piloña, MD,

Patrick Litonjua, MD,

Larissa Aviles-Santa, MD and

Philip Raskin MD

DIABETES CARE, VOLUME 24, NUMBER 6, JUNE 2001

In conclusion, over 40% of patients in a multi-ethnic cohort of indigent patients with ketosis-prone diabetes have the MetS. These patients have better glycemic control, higher h-cell functional reserve, and a greater likelihood of following a noninsulin-dependent course, than do those who do not have the MetS.

The glycemic control at baseline was very poor in both groups’ mean Hba1c of 13%; it significantly improved in both groups, but it was significantly better in the +MetS group. Improved glycemic control has been well described in ketosis-prone Type 2 diabetes mellitus
(Balasubramanyam et al., 1999; Banerji et al., 1994; Maldonado et al., 2003; Umpierrez et al., 1999).
Preserved h-cell function is a feature of ketosis-prone Type 2 diabetes (Balasubramanyam et al., 1999; Banerji et al., 1994; Maldonado et al., 2003; Umpierrez et al., 1999). In both groups, the h-cell function was lower on presentation and improved significantly in both groups at 6 and 12 months of follow-up. Based on the C-peptide, C-peptide-to-glucose ratio, and C-peptide response to glucagon stimulation, the +MetS group had significantly higher h-cell functional reserve both at presentation and during follow-up. Autoantibodies against the h-cell were more frequently present in the MetS group.

Presence of the metabolic syndrome distinguishes patients with ketosis-prone diabetes who have a Type 2 diabetic phenotype
Max E. Otinianoa, Ashok Balasubramanyama,b, Mario Maldonadoa,b,
Journal of Diabetes and Its Complications 19 (2005) 313– 318

Don't think that this is some weird or isolated diabetes, a conservative estimate puts the number to be, at least, 1 million diabetics in this country alone, twice as high would be more realistic. Still this doesn't make much sense.

Mike

It took me a couple of months but here is my answer to this post.

KP T2 on Oprah Audition

2010-06-22T14:59:00.000-04:00

I guess this is my 3 minutes of fame. Whatever happened to the "15 mins"? I'm a diabetic so you gotta figure I would get screwed out of the other 12 minutes. Oh,well. Here's me talking about a special type of diabetes. If you like it vote and pass the link on.

http://myown.oprah.com/audition/index.html?request=video_details&am...

Thinking out loud about how prevalent is KPD T2?

2010-06-14T17:09:00.004-04:00

Tip of the Iceberg
"It is our view that KPD patients (especially those with A forms of KPD) represent only the “tip of the iceberg”; below the surface is likely to be a much larger pool of patients who have early or primary -cell defects in development, expansion in the face of insulin resistance, regeneration in response to injury, or insulin secretion."
Syndromes of Ketosis-Prone Diabetes Mellitus
Ashok Balasubramanyam, Ramaswami Nalini, Christiane S. Hampe, and Mario Maldonado

"Idiopathic type 1diabetes is highly common in major cities whose populations include large numbers of African-Americans."
Idiopathic Type 1 Diabetes in Dallas, Texas -ANTONIO PI ˜NERO-PILO ˜NA, MD, PATRICK LITONJUA, MD LARISSA AVILES-SANTA, MD PHILIP RASKIN, MD

One of the things I keep trying to figure out the prevalence of KPD in the diabetic community. I'm obviously getting no help from the medical community, in this regard. Since we have not championed our cause, medicine has been allowed to shrug and let things go on as they are. All I can do is take the few hints out there and make a supposition.

In various papers I have quoted, the concensus is that 60% of new diabetic emergency admissions are Ketosis Prone T2. The rest of the cases can be attributable to poor diabetic management, T1 admissions and stress related type things, such as illness.

I must state here again the basic rule of our secret diabetes. "Ketosis Prone Type 2 Diabetes can not be distinguished from either Type 1 or Type 2." What does this mean? It means that all or most of those admittances could have been KPD. KPD is recognized due to its acute onset and then restoration of some semblance of beta cell functioning. This is to say that it has been allowed to be known only by its consequences. There is a car crash. It is noted as such but no cause exists or is considered. This is pretty much where we are now.
What we have been getting is the car crash equivalent of stating that all side crashes are KPD and the others are T1 and T2. They are being distinguished by no real criteria except result. It means nothing in terms of actual cause. Where can we go from here? I think we can go anywhere we wish.

What we can say about its prevalence, at least in terms of Blacks and Latinos, is that it represents 10% of diabetics. This is a guess made by researchers based on hospital admissions. This is the car crash equivalent of saying that the problem only exists when there are accidents. All driver error and equipment malfunctions cause accidents. If there is no accidents then those things did not occur. Basing prevalence on acute incidences, strongly under counts all things that don't reach that level of acuteness.

Where would I put the number for prevalence? Since there is no test, the best I can go from is my experience with Black diabetics. Most of the people I know, had symptoms and went to their doctors and were diagnosed as T2. These symptoms typically involved the usual thirst, excessive urination, tiredness, blurred vision and tingling in the feet. This onset could have been due to a undiagnosed T2's pancreas finally giving out or it could have been the beginnings of KPD onset.

After a bit more thought and research on this, I realized that DKA is the extreme situation of Ketosis Prone Type 2 Diabetics. Obviously, there's going to be a greater number as we move away from the extremes and more towards the mean. If I took 3 standard deviations, I might have got this up to 30% of Black and Hispanic type 2 diabetics. This would have given me at least 2 million KPD's in this country alone!

I've decided that a goodly percent were actually KPD. Most hadn't been diagnosed as even prediabetic. The fasting blood sugar isn't generally going to pick up most KPD's. One of the hallmarks of KPD is the sense that it came out of nowhere. Their fasting blood sugars, like mine, were typically near or above 300 with spikes passed 400 when diagnosed. Now, even without weight loss, their sugars are near normal, controlled mostly by diet and exercise with a little Met.

These are going to be my KPD's. They didn't reach acuteness and maybe never would have. These would be mild KPD's. What would prevalence be now? Well over 25%. This would put the overall number into the millions.

Most would argue that I've played a little fast and loose here. My point is that, we don't know. I could be wrong and I would love for somebody to do the research and prove me wrong. People should know if they have a time bomb ticking inside them.

Weaning Type 1’s from insulin

2010-04-29T02:03:00.001-04:00

This seems to be a burning topic that I thought I’d answered in my previous post but because of Halle Berry and YouTube videos like “Raw for thirty days”, I must revisit the topic.

What does it mean to “wean” anybody from insulin? It means to withdraw it from their system, take it away from them. People, none of us can live without insulin! The body isn’t accepting any substitutes, either. Those who have been “weaned” from taking insulin obviously have working beta cells which produce insulin. If they did not, it would probably be over pretty quickly.

The claim for this “weaning” then is based on the reanimation of dead beta cells through various techniques. Now what makes this plausible are the testimonies of many individuals who were diagnosed as T1 and then found themselves able, through the use of (name your technique), to become insulin independent. These people are adamant. They were DKA, might have even gone into a coma. They were thoroughly dependent upon insulin injections, for maybe years and now they don’t need it.

Unlike some, I’m not going to call them liars, I will even vouch for their experience but I want to examine this rationally.

The very first thing to note is that they were diagnosed and told they were T1 because of severe hypoglycemia, DKA, weight loss and maybe or maybe not the presence of antibodies. They were given the ADA diet of 200 to 300 grams of carbs a day, with most of the carbs coming from healthy grains and stuff like that.

They believed the diagnosis, as anyone would, but they, just like most of us experimented with their situations. The major thing that they all found was “Bernsteins’ law of small numbers”. If carbs are reduced then the insulin adjustment can be reduced as well. This simply means a change in diet. If the carbs are going down something else must be replacing them. If you now throw in some sort of physical regimen then you’ve got something going. This is a type of “weaning” but reducing the insulin need isn’t the same as producing insulin. How does that happen? It doesn’t. You either have it or you don’t. But a person might object saying that they didn’t produce hardly any insulin before and now they don’t need it and this has gone on longer than any honeymoon on record.

The key to this is diagnosis. At the point of diagnosis, they were given the T1 designation, because there isn’t another. What if there were? Well, there is, the problem is there is no way to distinguish a T1 from a Ketosis Prone T2 Diabetic at diagnosis. It is only after months and with a c-peptide test can they be told apart. This is because, for whatever reason, a KP T2 can regenerate their beta cells once glucose levels return to normal even in the face of testing positive for antibodies.

The other key is the ADA diet. This diet is high in carbohydrates and KPD’s have a 20% higher deficiency G6PD then even regular T2 diabetics. This is a significant disadvantage in handling carbs. High carb intake will keep them from regenerating beta cells and they will effectively stay T1. A KPD T2 is the only known diabetic that can go from a T1 status (no beta cell functioning, no insulin) to a T2 status.

Anytime there is a claim of “weaning “ a T1 from insulin, it should be viewed in this light. A person who makes that claim must know of KPD T2 and must demonstrate that the T1 they have “cured” is not, in fact, a KPD T2. Guess what, they can’t because there is no real test but time

Magnesium

2010-04-28T22:42:00.000-04:00

Once again, this is addressed to KPD's and also to a wider population. This is about magnesium so it's a continuation of the previous Vitamin D topic since it's needed for the proper action of Vitamin D.

Magnesium is an essential mineral that's slowly disappearing from the modern diet, as industrial agriculture and industrial food processing increasingly dominate our food choices. One of the many things it's necessary for in mammals is proper insulin sensitivity and glucose control. A loss of glucose control due to insulin resistance can eventually lead to diabetes and all its complications.

Magnesium status is associated with insulin sensitivity (2, 3), and a low magnesium intake predicts the development of type II diabetes in most studies (4, 5) but not all (6). Magnesium supplements largely prevent diabetes in a rat model* (7). Interestingly, excess blood glucose and insulin themselves seem to reduce magnesium status, possibly creating a vicious cycle.
http://wholehealthsource.blogspot.com/2010/02/magnesium-and-insulin-sensitivity.html
Stephan Guyenet

Oral Magnesium Supplementation Improves Insulin Sensitivity and Metabolic Control in Type 2 Diabetic Subjects

http://care.diabetesjournals.org/content/26/4/1147.long

Most Americans are considered to be deficient in magnesium. This is a mineral and we get it by eating plants or animals that have taken it up. The point Stephan is making is that our industrial system of agriculture isn't replacing essential minerals therefore they are falling as a percent of our diet.

Now if that weren't bad enough, we also have the problem of malabsorption. This means that our bodies are being blocked from taking up these nutrients even when they are present. The chief villain here are grains with the gold star for bad news and all around trouble maker going to wheat. Not only do they drive up blood sugar but they all contain Phytic Acid. This chemical binds to minerals and keeps them from being absorbed into the body. We've been told about the rich nutrients in grains but what we haven't been told is that it hardly makes a difference if the grains block the absorption of these nutrients. This is about magnesium but there are a whole bunch of essential metals that are blocked by this particular chemical. Our buddy, wheat, is particularly good at this. You may as well get this straight, almost every problem I will talk about will implicate wheat as a villain in some way. Wheat and wheat products should be avoided whether you are diabetic or not.

The recommended minimum dosage of magnesium is 350 mg. Here's a list of foods which are magnesium rich. http://www.whfoods.com/genpage.php?tname=nutrient&dbid=75 I would caution you about seeds and beans though. Beans have phytic acid and seeds tend to harbor Omega 6. They won't get you there anyway. Take the supplement on this one. Magnesium Oxide gets absorbed the worst but it's cheap so something is better than nothing.

Caution. Magnesium tends to have a laxative effect so if things start to loosen up, you should go down in dosage until the problem goes away.

Thinking out loud: The month of diagnosis

2010-04-24T00:17:00.002-04:00

I spend an inordinate amount of time reading blogs and scientific literature. This gives me a great deal to think about but I find that many of these thoughts can't be moved to completion because there are too many uncertainties. Instead of keeping all this stuff fermenting in my head, I've decided to share it with others. Okay, this is a nice way of saying I'm dumping but I did say it nicely.

I would love to know this piece of information. When people go DKA, are the months that it occurs in random or do they group? I ask this because I still wonder about the Vit D link to diabetes in general and KPD in particular. Does it show a seasonal effect? I am betting that it would be during the winter months that DKA goes up. You could say that this would buttress my idea of Vit D implication but actually it doesn't. We tend to exercise a lot less in the winter months because of the danger and inconvenience. Blood sugars are often offset by exercise.

I started going bad in March basically because I wasn't out riding much. I doubt, if I lived in a warmer clime, that I would have ever found out I was diabetic until it was far too late. March, now that I think about it, would still be an interesting month. If we start at November as the time of, more or less, enforced sloth then by February a person should start to feel pretty bad from high blood sugars. This is passed the holidays, when gluttony would have pushed the glucose toxicity through the roof. The glucose toxicity would have pared back much of the pancreases functioning and the highs would be continuing and mounting. By February or March, the crap should have been hitting the fan.

Fessing up to diabetes miracle cures.

2010-04-07T20:39:00.001-04:00

The previous post posits the idea that Ketosis Prone Diabetes might be at the center of a breakthrough in curing diabetes. This would be a good thing since, it's my guess that we are also at the center of a whole bunch of "miracle cures" for diabetes.

Why am I pointing to KPD's as the bad guys here? I mean don't we pet animals? Aren't we nice to children? Yeah, all the above but I didn't say we aren't nice, I said that we are the bad guys. You just have to look at what we are and it all becomes clear. We are the essence of mystery, magic, tragedy, conquest and redemption. In other words, we are Hollywood, big time.

The first thing is our air of mystery. We are so mysterious that we don't even know about ourselves. Imagine a superhero with secret powers who doesn't know it because he has to know the secret word or situation to invoke his powers. Well, he doesn't know about his secret power because no one has ever told him such a power exists and the secret word or situation are kind of locked up in never never land. So he goes about his ordinary life doing ordinary things without a hint of the secret locked inside of him.

Okay, so we've got mystery here. Now we go for the magic. The KPD wanders through life until for some reason, maybe it was a pizza party or a triple double banana chocolate split, the magic happens. The blood sugar goes through the roof. A nurse asks him in Emergency, "How long have you been a diabetic?" Diabetic? He answers, "Ten seconds". Anyway, out of nowhere, magically, the KPD becomes a diabetic. He doesn't get to be the guy who has to give up the donuts. He gets the death sentence. He's a Type 1! A week ago he was just Joe Schmoo, now he's on death row.

This is, at least, the greater publics perception of being T1: bland foods, needles and then your body parts start getting hacked off. They don't know some of the party beast T1's we know but before we were anointed with the "Big D", we pretty much had the same view.

Life's over. It's just a matter of time. There's the brave fight in intensive care and he battles his way through only to find himself, stabbing his fingers daily, sticking needles in his body and chasing wild blood sugars around as he tries to keep up with the ADA rule of eating 300 g of carbs a day.

Then it happens, some how some where, he hears of a cure. It involves eating meat, or protein, or raw vegetables, could be anything. The point is that he starts working this new system and his need for insulin goes down and continues to go down till eventually he doesn't need to take insulin. His A1c is normal. His FBG's are fantastic and the Lipid profile is to die for. The diabetes is cured!

There you have it, all the Hollywood drama you could want and with a happy ending. I mean it's all there. Type 1 takes the cure and within 30 days, he's off insulin and living a normal life.

I love a good story but let's look under the hood here. Most KPD's are very sudden onset, most of them don't show diabetic FBG's six months before winding up in ER. If they are thin, like me, they are going to be diagnosed as T1 and standard practice for DKA is a insulin regimen. If they continue eating the "healthy food pyramid", which is low fat and high carb, they will continue to have to take insulin. Once the problem of diet is solved. They will have both more energy and lower blood sugars and as a consequence will lose weight and be more active. TADA! The miracle of a diabetic cure.

Of course, the real trick is knowing the secret word. Ketosis Prone Type 2 Diabetes.

Mike

Ketosis Prone T2 Diabetes, the key to finding a diabetes cure?

2010-04-07T01:33:00.001-04:00

A interesting piece of information fell across my path today and I'd like to share it.

Some Cells in Pancreas Can Spontaneously Change Into Insulin-Producing Cells, Diabetes Researchers Show

You can find this here.

This paper purports to look at possible cures for Type 1 diabetes but what was done seems very close to what happens to a KPD during sudden onset of DKA.

Researcher engineered mice to respond to a toxin that would destroy 99% of their beta cells inducing a sudden onset of DKA because these mice had essentially no beta cells left.What they found is that the pancreas would, without any further manipulations, grow new beta cells by using the alpha cells. If the mice were kept on insulin this process would continue until the pancreas would once again return to full functioning and the mice would no longer have diabetes.

Does this sound like anyone you know: sudden onset DKA, intensive insulin therapy and a return to near normal glycemic levels independent of insulin?

This gets better. Because of this blog, I have come in contact with quite a few KPD's, and (I might have mentioned this some where else in this blog) I've noted that many KPD's return to having very normal type numbers, hardly ever going over 100. What has seemed to be the case is that the ones who had DKA seemed to have better numbers than those who caught the process early, like me.

The researchers found that the destruction of beta cells had to exceed 95% to get the significant rebound back to glycemic normalcy.

People, we might have caught the break we have been looking for. Researchers are looking at this experiment as a significant breakthrough in the understanding of diabetes but this was done in mice. Typically, mice studies, if they ever prove out, take years before the lessons learned result in any type of treatment. Here we might very well have the process that they are looking at as the key to solving diabetes.

Vitamin D and why

2010-04-03T01:04:00.004-04:00

This concerns much more than KPD's. What if I told you I could reduce your risk of colon cancer by 60% and your chance of heart attack by 30%? What if I threw into the mix, just for the heck of it, reductions in insulin resistance, improved beta cell function and defense against osteoporosis? I bet you would start to like me even though you know that whatever I'm going to tell you will probably involve 40 miles of bad road. What if I told you that you didn't have to do anything but take a pill, once a day? Guess what, it's all true and the little genie that's going to pull this off "Vitamin D". Hey, I can feel the love already.

First you need to look at this chart. Vitamin D incidence prevention

What you see are some of the problems that Vitamin D is involved in.You also see the level that's needed in your body to get these effects. The level needed is 60. Now the bad part, if you are like most people you are probably around 25. Here's the problem, you get Vit D from the sun and most of us don't get enough good sunlight to get a healthy dosage. The fact is that is we live in a temperate zone on the planet, the angle of the sun striking our skin does not allow us to get enough Vit D. If you're dark skinned, you are seriously screwed.

I live in Michigan and it is known that if you live above Atlanta, Georgia there is no way to get enough sunshine in the winter months. Fair skin helps here. Sunlight hitting fair skin rapidly creates Vit D. Fair skin is a necessity in the north or south temperate regions. This is because the colder temps force people to cover up to preserve body temperature. This means the sun has less surface on which Vit D can be created. Being pale is an advantage here. Being dark, however, means that you will almost never get the needed Vit D, if you live in a cold climate.

This isn't a problem. You can go out and buy Vitamin D at your local drug store and make sure it's Vitamin D3 and not D2. Get the 2000 IU version, take two little pills a day and you should at least get up to 30 or 40. If you're, like me, dark skinned then taking 4 pills a day would get you up to 70 or 80. Who knows, this could change your luck.

Mike

PS If you continue to eat wheat, you might need a lot more since wheat, for whatever reason, tends to be antagonistic to Vitamin D.

Reduced plasma half-life of radio-labelled 25-hydroxyvitamin D3 in subjects receiving a high-fibre diet.

http://www.ncbi.nlm.nih.gov/pubmed/6299329?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Grocery Shopping or starvation amongst plenty

2010-03-18T01:11:00.001-04:00

Before diabetes, I could hang out in a grocery store for hours because I love to eat. Now, I'm in and out in about thirty minutes and that's a weeks worth up shopping. I use to wander the aisles savoring the possibilities with all the possible combinations. There was just so so much and decisions that excluded one thing or another almost seemed punitive.
I've obviously had a change of heart. Now I roll in the store and for the most part all I see are piles of sugar. I grab my green veggies and never even look at the fruits - sugar. The bread section is next and I wouldn't even bother to go through here if the deli wasn't on the other side instead I cruise through healthy breads - sugar, multiwheat breads - sugar, organic, fresh baked bread - sugar, flatbread - sugar, unleavened bread - sugar, spelt wheat bread - sugar. It's packaged in different ways, with different claims on them with various shapes but all I'm seeing are piles of white sugar sitting there.
They didn't always look this way but I've got a meter now and it colors my world. Once the meter has marked a food "sugar", it turns white and granular and I back away from it like its a nasty beast temporarily slumbering. I slink passed the now deadly pasta, rice, and noodles and give a fond but fleeting glance at the couscous as it sits seductively in its box.
Okay, that's bad but at least, it's expected. What really kills me is that I can't even buy dressing without finding sugar in it. The truth is about the only thing they don't add sugar to, that I know for sure, is toilet paper. If you know different please keep it to yourself. Life is hard enough as it is

G6PD - something else you haven't heard of

2010-03-10T20:38:00.002-05:00

What is G6PD and why should a KPD care? Well, it's another one of your problems and it may be the reason why KPD's should be wary of carbohydrates.

G6PD is an enzyme that helps in the breakdown of carbohydrates. If it isn't present then certain pathways that deal with glucose metabolism aren't activated. There's a lot more to it but the short form is that glucose is a bad actor and this helps keep it contained. You more than likely are deficient here. This shouldn't be a great surprise since this is the most common deficiency in humans.

G6PD deficiency: its role in the high prevalence of hypertension and diabetes mellitus

http://www.ncbi.nlm.nih.gov/pubmed/11763298

Currently, there are 200 million people worldwide with red cell x-linked chromosome defects who, with the persistent ingestion of refined carbohydrates, are at greater risk of developing hypertension or diabetes mellitus...

What has been found is that KPD's are far more likely to have G6PD deficiency than other diabetics. You could view it as a marker for KPD.

High Prevalence of Glucose-6-Phosphate Dehydrogenase Deficiency without Gene Mutation Suggests a Novel Genetic Mechanism Predisposing to Ketosis-Prone Diabetes http://jcem.endojournals.org/cgi/content/abstract/90/8/4446

The prevalence of G6PD deficiency was higher in KPDthan in T2DM and controls (42.3%; 16.9%; 16.4%; P = 0.01). InKPD, but not in T2DM, insulin deficiency was proportional tothe decreased G6PD activity (r = 0.33; P = 0.04).

42% to 17% that's big. What I find interesting is that insulin deficiency was proportionate to decreased G6PD activity. The other really important part is that, for the most part, there was NO gene mutations beyond regular type 2's controls. So we are looking at a difference of about 20% that comes from some where but it isn't genetic.This, however, was done on a West African population so it could be a bit skewed.

If you took the time to read this post, you really should read this other post which puts it all in context for this type of diabetes. Here

Being type 1 then type 2 only part of the story or deadly, common and dangerous

2010-03-06T13:21:00.000-05:00

There are 4 classifications of KPD's. We are classified by antibodies and beta cell functioning (c-peptide).

The majority of us are Antibody negative and Beta cell positive (c-pep >.9) ..... A-B+

The others are: Antibody positive and Beta cell positive ......A+B+

Antibody positive and Beta cell negative ......A+B-

Antibody negative and Beta cell negative ......A-B-

You can see how wild this gets LADA's would be part of the A+ groups and a type 1's would be part of the B- groups. Type 2's are the B+ groups. You can understand why someone with poor to no insulin secretion might go DKA but how do you explain DKA with normal insulin secretion?

The really ugly part is that this tends to be newly diagnosed and sadly the DKA can return quickly.

Yep, deadly and common and most of you who have it, have no idea of your danger.

The Four Types of Ketosis Prone Type 2 Diabetics

2010-02-20T01:21:00.000-05:00

There are four types of KPD T2's
.Ketosis-prone diabetes: dissection of a heterogeneous syndrome using an immunogenetic and beta-cell functional classification, prospective analysis, and clinical outcomes

It is classified by antibodies and pancreatic capacity. This seems obscure but it isn't very hard.Analysis of clinical, phenotypic, and genotypic data derivedfrom this prospective characterization of multiethnic, heterogeneous,ketosis-prone diabetic patients indicates the presence of novelforms of ß-cell dysfunction as well as a classificationscheme to categorize these patients. We propose four groupsbased on two important features commonly used to distinguishtype 1 and type 2 diabetes: presence or absence of biologicalmarkers of ß-cell autoimmunity, and presence or completeabsence of ß-cell functional reserve. This is notmeant to be rigid classification, but rather a hypothesis-testingscheme to differentiate etiologically and clinically distinctforms of ketosis-prone diabetic syndromes, and thus to uncovernovel forms of ß-cell dysfunction. The distinctivepathogenetic features and diagnostic implications of the fourAß groups are discussed individually below.

A+ß- group
Patients in this group, with significantly low ß-cellfunctional reserve together with circulating ß-cellautoantibodies, are likely identical with the well-defined formof autoimmune type 1 diabetes. They had early onset diabetesand were generally lean. African-American patients predominatedin this group. The results of the HLA analysis supported thecontention that these patients have typical autoimmune type1 diabetes. Irrespective of ethnicity, certain HLA allelic variantsare found in high frequency in persons with autoimmune type1 diabetes (19, 24, 25, 26, 27, 28, 29, 30,31). The proportionof patients with the type 1 diabetes susceptibility HLA allelesDQB1*02 and DQA*03 was significantly higher in the A+ß-group than in the three other groups, including the phenotypicallysimilar A-ß- group. Furthermore, no A+ß-patients were positive for the protective HLA alleles DRB1*15and DQB1*0602 (19, 32, 33, 34, 35, 36). All patients in thisgroup required multiple daily insulin injections to avoid ketosis12 months after the episode of DKA, and a significant proportionhad recurrence of DKA during this period despite close monitoringby the study team.
A-ß- group
Patients in this group are likely to have diverse pathogenicmechanisms leading to ketosis-prone diabetes, including potentiallynovel forms of nonautoimmune ß-cell failure. Therewere numerous similarities in clinical characteristics and ß-cellfunctional reserve between the A+ß- and A-ß-groups (Table 2 and Figs. 2–4 ). At first glance, the differencebetween these two groups appeared to lie solely in their autoantibodystatus. However, HLA analysis revealed that there were alsomajor differences between these two groups in genetic susceptibilityto ß-cell autoimmunity. The frequencies of one classII allele (DQB1*02), which is strongly associated with autoimmunetype 1 diabetes susceptibility (24, 29, 32, 37), and of another(DQA*03), which is in linkage disequilibrium with the strongsusceptibility alleles DQB1*0302 and DQB1*0301, were low inthe A-ß- group compared with the A+ß- group(Fig. 4). These features make it likely that the A-ß-group consists primarily of persons with nonautoimmune mechanismsof ß-cell injury, rather than persons with autoimmunetype 1 diabetes whose circulating autoantibody levels have declinedover time to undetectable levels (38). No A+ß- patientswere positive for the protective allele DQB*0602 (33, 35, 39),whereas 9% of A-ß- patients possessed this allele.(There were no statistically significant group differences inthe frequency of DQB*0602, however, probably because of thesmall sample sizes as well as the relatively low prevalenceof the DQB*0602 allele in the general population (40). A-ß-patients also were more likely to have first-degree relativeswith type 2 diabetes. The current classification scheme of theExpert Committee on the Diagnosis and Classification of DiabetesMellitus (41) would tend to place patients in the A-ß-group into the clinical category of idiopathic type 1 diabetes,a category that begs further definition, as provided by thecriteria presented here.
A+ß+ group
Some patients in this group may represent a variant of whatseveral reports of European cohorts have termed antibody-positivetype 2 diabetes (42, 43, 44) or latent autoimmune diabetes ofadults (45, 46). However, others in the A+ß+ grouplikely represent a more aggressive form of late-onset autoimmunetype 1 diabetes than described in these reports. DQB1*02 maybe a marker for the more aggressive subset of A+ß+,because the six A+ß+ patients with DQB1*02 had highermean HbA_1c (8.6 ± 2.5%) than those without DQB1*02 (6.5± 0.6%) after 12 months of close management (P = 0.05).Furthermore, five of the six patients with DQB1*02 still requireinsulin treatment to avoid ketosis after 12 months of follow-up,whereas insulin has been discontinued safely in four of thefive A+ß+ patients who lack this allele (P = 0.03).Although analysis of a larger cohort of A+ß+ patientsis needed to confirm this suggestive trend, this combinationof class II HLA and autoantibody markers may represent an importantdiagnostic opportunity to identify A+ß+ patients destinedto have a more aggressive course. Because the presence of boththe genetic markers and autoantibodies should precede the onsetof clinical manifestations, it may be possible to identify suchpatients before their ß-cells are irreversibly destroyed(47).
A-ß+ group
This is the largest group of ketosis-prone patients, comprisingthe greatest number with new-onset diabetes. The frequenciesof the autoimmune type 1 diabetes susceptibility HLA allelesDQB1*02 and DQA*03 are low in this group. A-ß+ patientsappear clinically heterogeneous, with a wide range of BMI (Table2). A-ß+ patients have achieved good glycemic controlwithin 6 months of follow-up, and half have been able to discontinueinsulin treatment.
The causes of severe, acute ß-cell dysfunction leadingto DKA are likely to be diverse in this group. Half the A-ß+patients have new-onset diabetes, without a notable precipitatingfactor for DKA. The mean HbA_1c of this subgroup at presentationwith DKA was 13.9 ± 2.2, indicating a relatively longperiod of undetected and untreated hyperglycemia. It is possiblethat the cause of acute ß-cell failure in these patientswas glucotoxicity (48, 49, 50) or lipotoxicity (51), which reversedwith excellent control of glycemia after the episode of DKA.The sustained, preserved ß-cell functional reserveand glycemic improvement in these patients argue against thelikelihood that they have a form of type 1 diabetes with thepoorly defined honeymoon period (52). In fact, all A-ß+patients have now been evaluated for more than 1 yr, and onethird for more than 2 yr, and they continue to maintain uniformlyexcellent glycemic control (mean HbA_1c 7.0%) with adequatefasting levels of C-peptide (1.25 nmol/liter).The subset of A-ß+ patients with previously diagnoseddiabetes may comprise patients with long-standing forms of type2 diabetes with progressive ß-cell failure (53, 54)of such causes as ß-cell apoptosis (55), islet cellamyloid (56), or iron infiltration (57).
Three previous studies have measured islet cell autoantibodiesand ß-cell function in subsets of African-Americanpatients presenting with DKA (5, 6, 7). The patients describedin these studies (e.g. those with "Flatbush diabetes") wouldfit into our two ß+ groups. Consistent with our ß+group data, the mean age at diagnosis of these African-Americancohorts was in the fifth decade, the mean BMI was high, onlya minority had ß-cell autoantibodies, and glycemiccontrol improved markedly after intensive treatment. These similaritiesadd support to the concept of the A-ß+ group as manifestinga distinct form of ketosis-prone diabetes, but our data extendthe expression of this syndrome to patients of Hispanic, Caucasian,and Asian ethnicity.
HLA genotyping was particularly helpful in distinguishing autoimmune-associatedfrom probable nonautoimmune-associated forms of ß-celldysfunction within the class of patients with low ß-cellfunctional reserve (i.e. in distinguishing the A+ß-and A-ß- syndromes). In the initial analysis, theclass II alleles selected were those known to be strongly associatedwith autoimmune type 1 diabetes in multiple ethnic groups, e.g.the positively associated DQB1*02 and DQB1*0302 (22, 24, 27,58, 59, 60, 61, 62, 63) and the negatively associated DQB1*0602(19, 23, 32, 33,35, 39). In the pair-wise comparison, therewas a clear difference in the relative frequencies of DQB1*02:high in the A+ß- group (72%) and low in the A-ß-group (26%). The frequency of DQB1*0302 showed a trend in thesame direction, but did not attain significance after Bonferroniadjustment (which may not be necessary, because the associationbetween this allele and autoimmune type 1 diabetes is well established).The protective allele DQB1*0602 (64) was absent in all patientsin the A+ß- group, but present in 9% of A-ß-patients. DQB1*0602 is a low-frequency allele in the generalpopulation of Caucasian-Americans (5–13%) and African-Americans(4–15%) (40), hence a larger sample of patients wouldbe necessary to have the power to detect group differences inits frequency. Interestingly, DQA*03, an allele not frequentlyreported to be associated per se with autoimmune type 1 diabetessusceptibility, also distinguished the A+ß- group(89%) from the A-ß- group (44%). DQA*03 is known tobe in linkage disequilibrium with the strong susceptibilityalleles DQB1*0302 and DQB1*0301, hence its frequency distributionis likely to represent a real difference in susceptibility toautoimmunity between the A+ß- and A-ß- groups.
The absence of features of autoimmune diabetes or HLA-associatedsusceptibility to autoimmune diabetes in the A- groups raisesthe possibility that they could include persons with geneticcauses of ß-cell dysfunction, such as syndromes ofmaturity onset diabetes of youth (MODY) or mitochondrial transferRNA mutations. The MODY syndromes are characterized by Mendeliandominant inheritance due to monogenic mutations (65). Althoughthere are at present no reported cases of subjects with documentedMODY gene mutations presenting with ketoacidosis, this is certainlya possibility. Sixty-four (86%) of the patients in our A- cohorthave a family history of type 2 diabetes, 45 of these with apotentially dominant mode of transmission. Screening of theextended pedigrees for linkage to the currently known MODY genesis ongoing. Diabetes associated with mitochondrial gene mutationsalso involves defects in glucose-stimulated insulin secretion(66). However, the absence of evidence for maternal transmissionof diabetes and other typical features (e.g. deafness, neurologicdisorders, cardiac or renal failure) make it unlikely that anyof our patients harbor known mitochondrial gene mutations.
Imagawa et al. (67) have described a cohort of lean Japanesesubjects who developed new-onset, fulminant ß-cellfailure of apparently nonautoimmune cause after a relativelyshort period of hyperglycemia (HbA_1c < 8%). Our two A- groupsdo not appear to include such patients, inasmuch as all of ourA- patients, including those who were of new onset, had significantlyhigher HbA_1c levels, a less fulminant course, greater BMI andhigher frequency of first-degree relatives with diabetes. Furthermore,it is not clear that the Japanese patients were truly nonautoimmune,because they possessed HLA haplotypes (DRB1, DQA1, DQB1 0405,0303,0401,or DQB1 0901,0302,0303, or 0802,0401,0302) known to be associatedwith autoimmune type 1 diabetes (68, 69, 70).
The clinical course of the two ß- groups highlightsthe critical importance of ß-cell functional reservein achieving effective glycemic control. Although both ß-groups experienced significant (3%) decreases in HbA_1c and markeddeclines in the rate of hospital readmissions for DKA as a resultof the study intervention, their chronic glycemic status remainedquite poor. Other factors, such as lack of compliance with insulintreatment, could also have played a role in this outcome. Wedid not systematically record treatment compliance, but it iswell-known that treatment noncompliance is particularly severeand glycemic control is especially difficult to achieve in type1 diabetic patients in indigent, minority-ethnic, urban settingsin the United States (42, 43, 44).
In conclusion, we have used a heterogeneous, multiethnic cohortto demonstrate that patients presenting with DKA comprise atleast four distinct diabetic syndromes that are separable byautoantibody status, HLA genotype, and quantitative assessmentof ß-cell function. Novel, nonautoimmune causes resultingin variable degrees of ß-cell dysfunction are likelyto underlie the A-ß+ and A-ß- syndromes.Detailed genotypic and phenotypic characterization studies ofpatients in these categories are ongoing, in the hope that theywill specify the etiologic bases of the syndromes revealed bythe present analysis. The current data are also of clinicalrelevance to the evaluation and prognosis of patients with ketosis-pronediabetes. ß-Cell functional reserve at the time ofDKA is the strongest indicator of future metabolic control,but GAD and IA-2 autoantibody status and class II HLA allelotypescan assist in classifying ketosis-prone patients and improvingprediction of clinical outcomes.

Syndromes of Ketosis-Prone Diabetes Mellitus

http://edrv.endojournals.org/cgi/content/full/29/3/292
Ketosis-prone diabetes (KPD) is a widespread, emerging, heterogeneoussyndrome characterized by patients who present with diabeticketoacidosis or unprovoked ketosis but do not necessarily havethe typical phenotype of autoimmune type 1 diabetes. Multiple,severe forms of β-cell dysfunction appear to underlie thepathophysiology of KPD. Until recently, the syndrome has lackedan accurate, clinically relevant and etiologically useful classificationscheme. We have utilized a large, longitudinally followed, heterogeneous,multiethnic cohort of KPD patients to identify four clinicallyand pathophysiologically distinct subgroups that are separableby the presence or absence of β-cell autoimmunity and thepresence or absence of β-cell functional reserve. The resulting"Aβ" classification system of KPD has proven to be highlyaccurate and predictive of such clinically important outcomesas glycemic control and insulin dependence, as well as an aidto biochemical and molecular investigations into novel causesof β-cell dysfunction

IV. Classification of KPD

Top Abstract I. Introduction II. Case Reports III. History of KPDIV. Classification of KPD V. Natural History and...VI. Pathophysiology of KPD...VII. Management of KPD VIII. Conclusion and Prospects References

To date, attempts to differentiate patients with KPD into clinicallydistinct and relevant subgroups have resulted in four differentclassification schemes: the ADA classification, a BMI-basedsystem, a modified ADA classification, and the Aβ system.
The first is contained within the ADA’s most recent classificationof diabetes in general (15) and has been adopted by investigatorsat the University of Texas Southwestern Medical School (Dallas,TX). All patients who experience DKA are defined as having type1 diabetes, and among this group those who lack autoantibodiesare referred to as "idiopathic type 1" or "type 1b." Strictlyinterpreted, the ADA scheme would define patients with bothtype 1a and type 1b diabetes as insulin dependent, because itdoes not mention possible reversion to insulin independencein either category; however, the Dallas group considers patientswith type 1b to behave more like patients with type 2 diabetes,with some becoming insulin-independent. A second scheme is thatdeveloped by investigators at Emory University (Atlanta, GA)who separate KPD patients into lean or obese (9). "Lean KPD"patients are those with clinical characteristics of type 1 diabeteswith low β-cell function, whereas "obese KPD" patientsare those with clinical characteristics of type 2 diabetes withsome preservation of β-cell function. A modification ofthe ADA scheme is used by investigators at the University ofParis who divide KPD patients into three groups (20). Patientswith β-cell autoantibodies are classified as type 1a justas in the ADA scheme, whereas those who lack autoantibodiesare distinguished retroactively, based on long-term insulindependence, into "KPD insulin-dependent" (KPD-ID) and "KPD non-insulindependent" (KPD-NID). Both type 1a and KPD-ID patients haveclinical characteristics of type 1 diabetes with poor β-cellfunction, whereas subjects with KPD-NID have clinical characteristicsof type 2 diabetes with preserved β-cell function for aprolonged duration.
Our collaborative group at Baylor College of Medicine and theUniversity of Washington has used a classification system thatdistinguishes four KPD subgroups based on the presence or absenceof autoantibodies and the presence or absence of β-cellfunctional reserve (Aβ classification) (1). The four subgroupsare: A+β– (patients with autoantibodies and absentβ-cell function); A+β+ (those with autoantibodiesbut preserved β-cell functional reserve); A–β–(those without autoantibodies but absent β-cell function);and A–β+ (those without autoantibodies and preservedβ-cell functional reserve). A+β– and A–β–patients are immunologically and genetically distinct from eachother but share clinical characteristics of type 1 diabeteswith very low β-cell function, whereas A+β+ and A–β+patients are immunologically and genetically distinct from eachother but share clinical characteristics of type 2 diabeteswith preserved β-cell functional reserve (Fig. 1and

There will be a test on this later so please read up.

Mike

The obesity epidemic or what's up with all the fat people.

2010-02-14T19:41:00.002-05:00

Most likely, if you're reading this, you're diabetic and you're overweight. You might have tried diets and lost a little bit or a lot but you probably gained it back and have pretty much learned to live with it. This isn't all that unusual unfortunately. We are in an unprecedented epidemic of obesity with rising diabetes.

The usual prescription is for more exercise and cutting the calories. The basic prescription has at its base the biblical idea of gluttony and sloth. If you are fat, you feel shame. I'm going to row against the tide on this one with something called "common sense".

I will start with the single principle that all humans are animals and that the basic principles of being a living being applies to all living beings. The idea I wish to bring forth from here has to do with eating and this idea is this: animals eat because they are hungry and they stop eating when they are not.

Now you could bring up various animal experiments about fat mice and rats and how they will eat long after they are so fat that they can't stand and other bizarre displays but I didn't mention obesity. I only said that:animals eat because they are hungry and they stop eating when they are not. I didn't mention obesity because I don't think it's relevant to the discussion. Obesity, I have come to believe, is a symptom and not a cause.

If obesity is not a cause but a symptom, what's the cause? Hunger! Yep, hunger. I'm putting forth the proposition that we are in the midst of famine.

My youngest boy is exhibit A. He was a poor college student who went to school in his hometown so he was able to scrounge food from family and friends. His typical procedure was to arrive for dinner and then try to eat - forever. He would sit and eat until he was full and then, not knowing where his next meal was coming from, would continue to try and put food away. It was horrible to watch. He would slowly chew with a mild revulsion on his face then swallow. No matter how hard he tried, he could never seem to get beyond a few fork fulls before he had to give up.

This isn't news. Eating after you're full is very hard and the thought of doing it over and over again makes you feel green. Try it. You can't do it. But you might say that you've seen people overeat all the time. Once again, stick with the idea. I didn't say people don't overeat. I said that it is nearly impossible to eat, if you aren't hungry.

I am exhibit B. For the last thirty years, I have been a bike rider. What ever I had to do, I would try to do it on a bike. I would put somewhere between four thousand and five thousand miles a year on a bike. I ate carbs like crazy in order to do this because carbo loading was the thing to do when you were putting in a lot of physical exertion. My reputation for absolute gluttony is based on this. I was never fat but I could eat plate after plate of food. I ate until my stomach was full and then ate some more but I remained hungry. This was my life. I couldn't stop eating because I was famished.

You can't diet, if you're hungry. It will only make you hungrier. You can't excercise when you're hungry because your body cuts back on motion. You can, however, grow fat because there really isn't a connection between appetite and obesity.

I hear the experts talk about empty calories, large portions and too many snacks but rats, no matter the density or type of calories, would stop eating. Hunger is basic and at a level far below regard.

Stole this from Peter of HyperLipid

Here

Now I'll say it again: we eat because we are hungry not out of some lascivious need. What we are seeing now is hunger, one that isn't slacked by eating. Something has gone wrong with our diet and we are now hungry at a level that causes us to eat in search of a satiation which we can't achieve.

Mike

Western Diet Implicated in African American Diabetes

2010-02-04T00:53:00.000-05:00

PUT THE SODA DOWN, NOW!

Okay, now that I've got your attention, I want to tell you why. Diabetes has a very large footprint in the African American community and researchers have been looking for the reason why. Here I have a novel paper that says that it is genetic and that we are the victims of the FDA food pyramid. To put it concisely, people of African descent have a problem with processing carbohydrates at a genetic level. This may very well be the cause of a good deal of the metabolic problems noted in African Americans.

Stable Patterns of Gene Expression Regulating Carbohydrate Metabolism Determined by Geographic Ancestry

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0008183#pone.0008183-Lindquist1

Individuals of African descent in the United States suffer disproportionately from diseases with a metabolic etiology (obesity, metabolic syndrome, and diabetes), and from the pathological consequences of these disorders (hypertension and cardiovascular disease)...

...Differences in expression of several carbohydrate metabolism genes suggest both genetic and transcriptional mechanisms contribute to these patterns and may play a role in exacerbating the disproportionate levels of obesity, diabetes, and cardiovascular disease observed in Americans with African ancestry.

The KPD's I've spoken to all have lamented their problems with post prandial spikes. This specifically refers to the hour after a person has taken their first bite of a meal. This blood sugar should never go over 140. A normal blood sugar doesn't and there is a very good reason why. Research has shown this is the point where damage begins to occur throughout the body.

This link is to "Blood Sugar 101": http://www.phlaunt.com/diabetes/14045678.php . It is run by Janet (Jenny) Ruel and any time you spend there will be profitable if you're really interested in the ins and outs of diabetes.

If you have a genetic problem handling carbohydrates and have the added problem of being Ketosis Prone this combination will eventually move you into hyperglycemia and / or DKA. The eating of carbs will force your blood sugar up which will create glucostoxicity. This is glucose poisoning. Beta cells in the pancreases of KPD's are very sensitive to this and will slowly shutdown. The more carbs ingested the worse the condition will come and god help you, if you drink soda or juice to try to slack your thirst because they are almost pure carbs and filled with High Porn Corn.

The truth is there is almost no average American meal that will not push your blood sugar beyond the 140 mark. I can't handle better than 20 grams of carbs at any setting and those carbs need to be very complex to keep me from spiking my blood sugar. Even the supposedly healthy diet is problematic here. Whole grains, potatoes, brown rice, apples, bananas, oranges and pastas are just a few things that I have to avoid.

This doesn't match what you would get from a dietitian but you have to recognize that most of the research has been done on Europeans and the minority communities have not been factored into this. Some might claim this is racism but it more neglect than anything. We, much like the LADA and MODY community, must look after ourselves here. I've got one more piece of the puzzle that I want to put out and then I can really lay this out in a logical fashion.

Mike

Ketosis Prone diabetes as a MODY

2010-02-03T23:47:00.000-05:00

It has been one of my conclusions that KPD is a type of MODY which shows up unannounced and then works its wickedness undetected for years. The italics are mine.

Endocrinol Metab Clin North Am. 1999 Dec;28(4):765-85.

Monogenic diabetes mellitus in youth. The MODY syndromes.

Winter WE, Nakamura M, House DV.

Department of Pathology, Immunology, University of Florida College of Medicine, Gainesville, USA. winter.pathology@mail.health.ufl.edu

Maturity onset diabetes of the young is characterized by early onset diabetes inherited in an autosomal dominant pattern. Classic MODY occurs predominantly in Caucasians and presents before age 25, is nonketotic, and is generally not insulin-requiring. Less than 5% of cases of childhood diabetes in Caucasians are caused by MODY. ADM is a subtype of MODY that occurs in approximately 10% of African-Americans with youth onset diabetes. In contrast to MODY in Caucasians, ADM presents clinically as acute onset diabetes often associated with weight loss, ketosis, and even diabetic ketoacidosis. Approximately 50% of patients with ADM are obese. Therefore, based strictly on clinical grounds, at onset, ADM cannot be distinguished from type 1 diabetes. Months to years following diagnosis, a non-insulin-dependent clinical course develops in patients with ADM that is clearly different from type 1 diabetes. Mutations in five genes can cause MODY. These genes encode hepatocyte nuclear factor-4 alpha (HNF-4 alpha, MODY1), glucokinase (MODY2), hepatocyte nuclear factor-1 alpha (HNF-1 alpha, MODY3), insulin promoter factor-1 (IPF-1, MODY4), and hepatocyte nuclear factor-1 beta (HNF-1 beta, MODY5). These monogenic forms of MODY have been used as model systems to investigate the inheritance and pathophysiology of type 2 diabetes. Clinicians, should be able to diagnose MODY. Type 1 diabetes, the most common form of diabetes in Caucasians, is always insulin-requiring for control and survival, whereas patients with MODY do not usually require long-term insulin for survival. Diagnostic confusion can lead to inappropriate management and patient expectations. Primary care physicians must be alert to avoid therapeutic confusion when patients with ADM enter into the non-insulin-dependent stage. An approach to the diagnosis of childhood diabetes is offered in Table 4. The majority of youth onset diabetes remains type 1; however, the frequency of type 2 diabetes is rising in obese children and adolescents and especially in obese minority youth. The diagnosis of MODY can be made through a careful review of the patient's clinical course, severity of hyperglycemia, and family history. The identification of islet autoantibodies is confirmatory evidence of autoimmune (type 1) diabetes. Because testing for MODY mutations is expensive and is performed at a select number of research laboratories only, routine molecular genetic studies to search for the various MODY mutations should be limited to research investigations. In the future, the availability of gene chip technology may allow rapid screening of mitochondrial and MODY mutations.

Winters is one of the original investigators of KPD and has written extensively on it.

Ketosis Prone Type 2 diabetes in Black People

2010-01-25T16:07:00.000-05:00

This one of the best pieces on KPD T2 in Black peoples.

Diabetes in African Americans - M C Marshall Jr

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1743410/pdf/v081p00734.pdf

Atypical diabetes may constitute 10% of African American diabetic youth and is

quite similar to the atypical diabetes in African American adults (vida infra). Unlike classic type 1 diabetes or MODY, 50% of African American youth with atypical diabetes are obese. Also unlike type 1 diabetes, these patients lack islet cell autoantibodies and have a subsequent clinical course that is similar to type 2 diabetes. However, unlike typical type 2 diabetes, atypical diabetes generally presents acutely, often with weight loss and ketosis.

ATYPICAL DIABETES

A review of diabetes in the African American community would not be complete without a discussion of the ‘‘atypical’’ diabetes that has been described in this population. African Americans with type 2 diabetes have been found to have two distinctive atypical features. The first is that adult African American diabetics may present with classic signs and symptoms of DKA and thus look like type 1 diabetic patients. However, unlike type 1 diabetic patients:

(1) these patients have no autoimmune markers of type 1 diabetes;
(2) they are often obese;
(3) there is evidence of insulin resistance; and
(4) most importantly, after intensive therapy, spontaneous remission is the rule, with restoration of b cell
function within months and maintenance of normoglycaemia with oral agents or only dietary treatment.

These patients have impaired insulin secretion when admitted with DKA, but their subsequent clinical course is typical of type 2 diabetes. Recurrence of DKA is infrequent. Among those patients who remain insulin-requiring, recurrence of DKA is most often caused by non-compliance with insulin therapy. The other unique feature of diabetes in African Americans is that spontaneous remission is also seen among patients who are not ketotic. When adult African Americans with newly diagnosed type 2 diabetes receive an average of three months of intensive, multidisciplinary therapy, 30%–40% of these patients will go into remission—that is, they will achieve normoglycaemia without pharmacological therapy. Those who remit have a significantly greater return of b cell function. However, there are no clinical characteristics that can differentiate those who will remit from those who will not. There is evidence that these atypical features are also present in African American children and adolescents with type 2 diabetes. It bears remembering that the African American diabetic patient who is initially controlled with insulin need not necessarily remain on insulin therapy, and the African American diabetic patient who is initially controlled with oral agents need not necessarily remain on pharmacological therapy.

Mike

2010-01-25T03:07:00.000-05:00

Remission

Even if my fondest wishes are met.

I can't go back.

I will have caged a tiger but there will always be that tiger and I will never let it out.

Vigilance is my defense and having seen the destruction of this beast,

I can never consider myself safe.

There is a type of remission but having seen its cold yellow eyes, I think not.

I can not ever go back.

My innocence is lost in that regard but is that so bad?

I have played carelessly in a dangerous place and been mauled.

Now I know this place and wish to forever avoid it.

I have lost my ignorance but why would I wish to reclaim it whilst a tiger paces near by.

Carbohydrates and diabetes

2010-01-25T02:16:00.000-05:00

I didn't know about the civil war until I became diabetic. No, not the war of northern aggression, I mean the one between diabetics and the American Diabetic Association. It has several aspects but the one I'm concerned with now is ADA carbohydrate recommendations.

They recommend a high carbohydrate - low fat diet. The problem is most diabetics can't handle carbs. It makes your blood sugar shoot up. The ADA response was to promote medications that would keep the blood sugar down even while you were pushing it up with carbs. Their recommendation comes to about 200 grams of carbs a day. I can't handle more than 20 at any given meal but I'm a KPD and we are very poor handlers of carbs. This is something I'm going to show you later but for now we'll just stick with carbs and anyones diet.

This link is to Gary Taubes, who, if you know any physics, ripped the heart out of "cold fusion". He is probably the most respected science writer in the English language. He has reluctantly become the point man in the diabetic's war with the ADA. He has challenged the accepted dogma with clear good science and, if there is a god, will probably get the Nobel Prize for Medicine some day. The book that this talk is based on is called: Good Calories, Bad Calories. The book is rough but worthwhile sledding and should be force fed to all diabetics as soon as they are diagnosed.

I believe he's correct but I think it is more important that all diabetics learn to trust their meters, even if the meters can have a 20% error rate. I ate to my meter and found that virtually everything I was told by my well intending diabetes educator was wrong. I believed my meter and followed it to a Low Carb - High Fat diet. My triglycerides dropped by 100, my HDL's rose fifty percent and my A1c dropped to 5.2. I had to resist all that I was told to get there. It was in my search to find some scientific backing for my results that I fell across Mr. Taubes. He got everything that I was looking for. Listen for yourself - http://video.google.com/videoplay?docid=4362041487661765149#

Mike

High Fructose Corn Syrup or Hard Corn Porn

2010-01-25T02:04:00.001-05:00

This is a link that anyone should see but especially diabetics. It is Robert Lustig, a highly respected endocrinologist researcher. http://www.youtube.com/watch?v=dBnniua6-oM

His idea is that HFCS is a poison and should be eliminated from all ingestion. The video can be a bit much. He gets pretty technical and specific but it is probably the best 70 minutes you're going to spend.

Mike

Diabetes - The gift that keeps on giving

2010-01-23T16:50:00.000-05:00

I'm on the Diabetes Forum and I would recommend this site to anyone, especially those who are new to diabetes. There is a intro section to the forum and inevitably the person will be distraught with a sense that their life is over.

As far as I know, Ketosis-Prone Type 2 is a silent killer. It lives quietly in the background unraveling your life thread by thread. You might have slightly high blood pressure, be a bit overweight, have a bit of cholesterol, virtually nothing that the average American doesn't have. What you don't know is that the life that you were planning is not going to happen. The children and the grandchildren are not going to part of your life. Those magic moments that you look towards ain't going to happen. You are traveling a different road and you won't know it until you're staring from a hospital bed watching your destination recede.

That is unless, of course, you get diabetes. This is me. I was tooling along pretty good even with the thought that I come from a short-lived family. Nearly sixty and headed to seventy, I thought I was doing everything right and I would get through. Diabetes changed that.

Everything that I thought was the case was wrong. I needed a serious change in diet, one that reduced my dearly loved carbohydrates. I needed to see what my blood sugar was doing so that I could control it. I needed to have my eyes opened so that I would learn more about my metabolism and how I existed in the world. Things were going on beneath my notice but no more. I'm a diabetic and the blinders are off.

I've got a chance now for those moments. My life, that I surely would have lost shortly, now is on the road that I envisioned. I get to do something that people in my family rarely do. I get to be old. Who do I have to thank for this: Diabetes, the gift that keeps on giving.

Mike

Guest at the funeral or the three D's

2010-01-19T11:41:00.000-05:00

I am 57 and I am going to a family reunion in August of 2010. If you came with me one thing that you would notice is the lack of old people. There will be a few but "few" is the operative word here. You see we don't tend to live beyond the age of seventy.

My aunt Dimple, who passed away a few years back, when she reached seventy one you would have thought she had won the lottery. She was calling all around blathering to anyone who would listen how she had made it.

In my family, we die of stroke, colon cancer and heart attack. What I like to call the three Deaths or three D's, for short. I always wondered why my family was so snake bit then I became diabetic. You would think this wouldn't be such a big surprise, after all I am Black and over fifty. But you would be very wrong. I'm a life long cyclist. I'm very fit. From the neck down, I could pass for a twenty year old. There is almost nothing about me that says, " type 2 diabetes", but I am.

It gets weirder. I am not only a type 2 diabetic but I'm prone to ketosis just as if I were a type 1. If my blood sugars get high my pancreas will simply shutdown and without insulin I could easily die from ketoacidosis much the same as any type 1 would.

This gets even better. If given insulin, overtime my pancreas will recover and I will begin producing enough insulin of my own and go back to being a type 2. The American Diabetes Association has two big classifications for diabetics, there is none insulin dependent and insulin dependent, which we call Type 2 and Type 1. I get to be both depending on which way my metabolic winds are blowing.

The more I learned about Ketosis Prone Diabetes, the more I began to reflect on certain aspects of my life and my family's. Like I said, I'm an avid cyclist and on average I would put 3000 to 4000 miles on the road in any given year. Cyclist get very use to listening to what is going on with their bodies. As we ride our bikes, we have to monitor ourselves and provide food and water at critical moments or we lose all of our energy. This habit of self-monitoring got me to a doctor before my situation got bad. I just didn't feel right.

I had the signs of ketosis: great thirst, tiredness, aching muscles and blurred vision but I didn't see those as important because, ever since my twenties, I've always had those. I would drink until my stomach hurt but I would still be thirsty. I long sense learned to push passed any tiredness or stiffness that I felt and since I've got terrible vision anyway, a little blurriness was no big deal.

Now that I'm diabetic, I look back and see that these things have been with me for awhile. One of the big keys for me was that these symptoms are the symptoms of winter. I'm from Detroit and I still live in Michigan. Michigan weather has been described as 9 months of winter and 3 months of bad sledding. Typically, I would get forced off the bike from late November into early March. During this time, I always lost weight and the previously mentioned symptoms would come marching back. Basically, I felt terrible during the winter months. I solved this problem by becoming a year round cyclist. The diabetes came on strong when I attempted to do a project at home last year and hardly got on the bike.

Here is the last piece of the puzzle. My diabetes is characterized by itching. Suddenly, I get itchy all over my body, if my blood sugar goes above 150. Now that I use a meter, I know that the itching occurs, not when my blood sugar is high, but when it returns to normal. I felt this itching years ago. Like most cyclist, I tend to load up on carbs before a ride to have energy. Carbs, however, drives up blood sugar and I carb loaded like mad before I rode. Always during the ride just when I started breaking a serious sweat, I would get this brief moment where I would feel intense itchy all over but I would ride through it. Strenuous exercise brings blood sugars down. This suggests to me that I've been diabetic since my twenties but due to all the exercise, it never showed itself.

This is where the light comes on. The only way I could be diabetic at that age was because it was inherited. What if my whole family, like me, carried this time bomb in our genes? It would work like this somewhere in young adulthood (When I first started feeling these effects.)our blood sugar begins to move outside of normal range, not much but enough to get us up past the 140 mark where damage is known to occur. I've already mentioned that high blood sugars causes the pancreas to shutdown in KP T2s. The initial part of that shutdown is always the first phase insulin response.

The body has two insulin phases. The first phase occurs when you eat and your blood sugar began to rise. The liver constantly puts glucose into the blood but when you eat something it shuts down and insulin is supplied to blunt the sharp rise in blood sugar. The second phase is the insulin supplied by the pancreas during the daily routine matching the supply of glucose being put forth by the liver.

What if, over time, this first phase slowly began to shutdown? Blood sugars would rise but the second phase over hours would slowly bring it back to normal. The problem with this is that the time above 140 is the point in which damage occurs and the pancreas loses more and more ability to respond. Eventually, a deadly spiral upwards would begin to occur. The more the blood sugar rose, the less the pancreas would respond and so on. Imagine if this process took place over 20 to 40 years. Damage would be occurring across the body. It would feed the formation of cancers and the inflammation of the circulatory system. You would expect to see deaths from heart attacks, strokes and colon cancer which has shown itself to be attuned to fluctuating blood sugars. Guess whose family dies in its forties, fifties and sixties from stroke, heart attacks and cancer?

This, I believe, is the guest at the funeral whose shadow falls across the coffin.

Michael

In the begining

2010-01-14T11:16:00.000-05:00

http://www.annals.org/content/144/5/350.full.pdf+html

I've not done this before so you will just have to bear with me. I'll try to have scientific citations and I will also try to explain them to the best of my understanding.

Here's a common story.

You're about fifty years old and you've been working in the back yard. It's been pretty hot so you've been drinking iced tea. Over the last week, you've been kind of drinking to much tea and having to go to the bathroom at night so you've been trying to cut back but you have been thirsty.

You come back into house and stand in the kitchen munching on a few teacakes. You're thirsty, got to go to the bathroom and you're a bit woozy. You wait a little bit, probably a bit of blood pressure. Suddenly, your wife pulls you into a chair and calls your name. You snap out of it. You're nauseous, weak and you're having a hard time catching your breath. 911 is called and the next thing you know you're in a hospital with all kinds of tubes running out of you and they're telling you you're diabetic and you're in ketoacidosis.

Diabetes? You were at the doctor's office six months ago for your checkup but you're blood sugar was fine. I mean, were having some problems with being stiff and tired but, let's face it, fifty means a certain amount of aches and pains.

A couple of days later you're home and are taking blood sugar readings and giving yourself insulin shots. You have to admit you're feeling better and your blood sugars are going down. The surprise is that they keep going down and now after only a month or so from joining the diabetic masses you are introduced to a new term - hypos.

The same dose of insulin that brought you down to normal is now taking you to low blood sugars. This is just great. You almost go into a coma from not having insulin and now you almost go into a coma from having too much. The docs tell you to keep reducing the insulin till finally they have to take you off insulin completely. They give you Metaformin and tell you to watch your diet and get some exercise and off you go.

Two months ago, you were a regular joe then you became a type 1 diabetic. Another month later, you're off insulin and now you're a type 2 diabetic. What nexts, type 3?

Welcome to the world of Ketosis Prone Diabetes! Pull up a chair, sit down because we have a lot to talk about.

Mike

Ketosis Prone diabetes

2010-01-13T20:07:00.001-05:00

I'm starting this blog because I see almost no information on this syndrome. It is estimated that more than half of all new onset DKA cases of African Americans with diabetes are of this type. To make matters worse, this is the type of diabetes that is fairly prevalent in ALL peoples of color.

Barker's Type 2 Ketosis Prone Diabetes / Atypical Diabetes T1b/ Flatbush Diabetes

Thinking about: Western technology, food and the health of people of color and world food production and trade.

Chinese study on Ketosis Prone T2 Diabetes

Caution on NSAIDS

How I got normal blood sugars for 60 cents a week

Roux-en-Y gastric bypass

Facebook Page for Abrupt Onset Type 2 Diabetes

Who gets KPD T2? Everybody!

Contamination of traditional foods

Please make the fight

Thinking about the nature of Abrupt Onset Type 2 diabetes

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

Abrupt Type 2 Diabetes Onset and 1st Phase Insulin Response

Downloadable Scientific Ketosis Prone Type 2 Diabetes powerpoint presentation

A1c, glycation problems and DKA

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

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

The A1c tipping point

Increased weight and insulin resistance revisited

Multi-Tissue resistance in KPD's

The Provoking Event of Ketosis Prone T2 Diabetes

Increased weight and Insulin resistance lead to improved glycemic control

KP T2 on Oprah Audition

Thinking out loud about how prevalent is KPD T2?

Weaning Type 1’s from insulin

Magnesium

Oral Magnesium Supplementation Improves Insulin Sensitivity and Metabolic Control in Type 2 Diabetic Subjects

Thinking out loud: The month of diagnosis

Fessing up to diabetes miracle cures.

Ketosis Prone T2 Diabetes, the key to finding a diabetes cure?

Some Cells in Pancreas Can Spontaneously Change Into Insulin-Producing Cells, Diabetes Researchers Show

You can find this here.

Vitamin D and why

Reduced plasma half-life of radio-labelled 25-hydroxyvitamin D3 in subjects receiving a high-fibre diet.

Grocery Shopping or starvation amongst plenty

G6PD - something else you haven't heard of

G6PD deficiency: its role in the high prevalence of hypertension and diabetes mellitus

http://www.ncbi.nlm.nih.gov/pubmed/11763298

High Prevalence of Glucose-6-Phosphate Dehydrogenase Deficiency without Gene Mutation Suggests a Novel Genetic Mechanism Predisposing to Ketosis-Prone Diabetes http://jcem.endojournals.org/cgi/content/abstract/90/8/4446

The prevalence of G6PD deficiency was higher in KPD than in T2DM and controls (42.3%; 16.9%; 16.4%; P = 0.01). In KPD, but not in T2DM, insulin deficiency was proportional to the decreased G6PD activity (r = 0.33; P = 0.04).

Being type 1 then type 2 only part of the story or deadly, common and dangerous

The Four Types of Ketosis Prone Type 2 Diabetics

Syndromes of Ketosis-Prone Diabetes Mellitus

The obesity epidemic or what's up with all the fat people.

Western Diet Implicated in African American Diabetes

Stable Patterns of Gene Expression Regulating Carbohydrate Metabolism Determined by Geographic Ancestry

Ketosis Prone diabetes as a MODY

Monogenic diabetes mellitus in youth. The MODY syndromes.

Ketosis Prone Type 2 diabetes in Black People

Carbohydrates and diabetes

High Fructose Corn Syrup or Hard Corn Porn

Diabetes - The gift that keeps on giving

Guest at the funeral or the three D's

In the begining

Ketosis Prone diabetes

The prevalence of G6PD deficiency was higher in KPDthan in T2DM and controls (42.3%; 16.9%; 16.4%; P = 0.01). InKPD, but not in T2DM, insulin deficiency was proportional tothe decreased G6PD activity (r = 0.33; P = 0.04).