The accepted knowledge is that Diabetes destroys gradually over years. Ketosis Prone Type 2 diabetes is an acute form of type 2. This type 2 can reach fasting blood sugars of 300 or higher in months. This blog brings together all the documentation that I could find in the world and my speculation of what it means for KPD’s in specific and diabetics in general. I ask you to leave your stories about what happened to you so that we can all gain a better understanding of what we are dealing with.
Tuesday, December 28, 2010
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.
Sunday, December 19, 2010
There has to be some sort of failsafe in the body to prevent this. Cutting off all insulin would be deadly as well but the beta cells have two phases; one is slow and steady and the other puts out large amounts of insulin in a short time. It would have to suppress the first phase. What we do know about type 2 is that early stages typically involve reactive hypos then the loss of 1st phase insulin. The later phase involves the steady rising flow of insulin to keep bringing blood sugars back in line. This is an interesting supposition but what I’ve shown is that hyperglycemia suppresses my 1st phase.
Thursday, November 18, 2010
Saturday, November 13, 2010
How I've come to this conclusion is personal. By sheer luck, I fell across a method of reactivating my 1st phase insulin response. You basically have two responses that come from your pancreas, basal and 1st phase. The basal is the constant but low flow of insulin that occurs all the time in your body. The 1st phase is a modifier of this basic level of insulin to account for changes in the amount of blood sugar that occurs with things like eating, exercise and stress. I use to think of it as a big wave of insulin that suddenly flowed in to your blood stream to counter act potentially high blood sugars caused by something like eating a fast acting carbohydrate. It can and will do this but mostly it's active like a computerized glucose monitoring system counter acting small spikes in the system due to the actions of other things going on in the body.
It should be noted that I'm talking about spikes not drops in blood sugar. Drops aren't the problem usually. (There is reactive hypoglycemia but I view it more as part of a failed mechanism.) Your body is set up to strongly defend against hypoglycemia. This can kill you in a day while hyperglycemia make take years. There are a series of systems and hormones that interact to assure that the body has enough glucose. The one which is counter to those is insulin.
At any rate, I've found a way to get that first phase back and conversely, I've found how to lose this 1st phase. In the last month, I've gotten to the point where I have been able to more or less switch it off and on and notice when it is working. I've even dropped all medications. My typical blood sugar profile kept me at about 110 with spikes of 40 to 50 points higher after meals. This is even with eating a largely low carb diet. Now my typical profile keeps me in the 90's with spikes never above 130 and generally about 20 points above my basal rate. It should be noted this is without insulin, exercise or supplements. (I'm trying to keep down the confounding variables. Ned Kock is big on this!)
One thing this has shown me is that the beta cells are there. They aren't dying off or sick. I'll have a 1st phase for a few days, make an adjustment and then I won't have a 1st phase. I'm thinking that this is very much an abrupt type 2 onset thing.
Type 2 is traditionally thought of as slow onset with continually rising blood sugars over many years. With us, insulin failure occurs quickly but on the converse side insulin recovery occurs quickly as well. I've read where various methods were used to assess beta cell function or mass and it was found to be intact.
I produce insulin but not a 1st phase so my constant dribble of insulin is not enough to keep down my blood sugars without additional insulin. Guess where my blood sugar average is usually, without medications? 134. This is about an A1c of 6.3 which is pretty standard for a Ketosis Prone type 2 diabetic. This A1c and its implications were discussed in a few posts back. Here.
All this and more lead me to believe that this isn't a problem of beta cells desensitizing but of a failure of a control loop that the beta cells respond to by releasing 1st phase insulin. By saying "control loop", I am talking about a circuit. Think of it as a lightbulb and switch. If this switch is controlled by a sensor for certain amount of darkness then when it gets too dark, the switch is activated and the light comes on. There might be a sensor for lack of movement in area where the light is. If no motion is detected, the switch is deactivated and the light goes off. There is nothing wrong with the light, it's fine. Its behavior, however, is being controlled through the sensors that activate or deactivate the switch.
What my intuition is telling me, that at least in those with "abrupt type 2 diabetes onset", the circuit isn't working and what breaks it down are hyperglycemic episodes which effect one or more components which are part of the loop that operates in the 1st phase circuit. These components could be anywhere. They could function as an aggregate or there could be just one component which is effected by hyperglycemia. What seems clear is that the message isn't getting through.
I bring up hyperglycemia because all I have to do to shut down the 1st phase is to initiate a high glycemic environment which is too high for my 1st phase to cover, typically for me, this is a tub of popcorn at my local cinema. (If you're going to do something bad, you should at least enjoy it.) My blood sugars will stay below 160 then they will soar above 200 and stay there for 4 or five hours. After that, no more 1st phase and higher blood sugars till I make the adjustment.
You are probably wonder what this adjustment is. I should say it is relatively safe but there are potential side effects and frankly I don't want people starting to take stuff with little or no understanding what they're undertaking. I'm going to keep this under wraps for a while.
What I'd love to know is what chemicals or hormones or whatever breaks down in a high glucose environment? Some where, at least for us, that is where the answer lies I believe. Part 2
Thursday, October 21, 2010
Guillermo E. Umpierrez, Dawn Smiley, and Abbas E. Kitabchi
There is no news for you KPD fans in this presentation. This was done in 2006. This blog has a lot more current information and speculation on that information. This, however, represents the best thoughts of the current researchers at that time and these people have undisputed credentials. Whether people have heard of Ketosis Prone Type 2 diabetes or disbelieve its existence becomes moot because of this document. Here you have a complete presentation telling all about it. I post this in that light. You can simply download it and give it to family and friends.
I found this presentation on the web and these are some of the chief writers and researchers of Ketosis Prone Type 2 diabetes. It seems to be a presentation in China and might be a bit dated but it is very thorough.
I spend a good bit of time introducing people to this subject and so I started to develop a presentation on it. Low and behold, this pops up!
You no longer have to go through the long discussions. This power point will do nicely. This would be a good thing to pass around, post or show to your diabetes educators. Who knows, it might make a difference.
Ketosis Prone Type 2 Scientific Presentation
PS If some one can translate the characters in this document, chime in.
Monday, October 4, 2010
Table 1. Common Hemoglobinopathies: Populations Affected, Prevalence, and Outcomes
Hemoglobin (Hb) Variant
(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)
Also found in East India, the Mediterranean, and the Middle East
About one in 12 African Americans has sickle cell
About one in 100 Hispanic Americans/Latinos has sickle cell
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)
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
HbE trait (also called HbAE): asymptomatic
HbE disease (also called HbEE disease): mild hemolytic anemia, microcytosis, and mild enlargement of the spleen
Hemoglobin SC (HbSC)
African Americans and people of West African descent
Also found in East India, the Mediterranean, and the Middle East
HbSC disease (also called sickle-hemoglobin C disease): mild hemolytic anemia and moderate enlargement of the spleen; may have blocking of blood vessels as in sickle cell anemia but milder symptoms
Hemoglobin F (HbF) elevated
Occurs in patients with hereditary persistence of fetal hemoglobin, sickle cell anemia, severe anemias, leukemia, and other conditions
About 1.5 percent have more than 2 percent HbF but some groups may have concentrations as high as 12 percent 3
Those with elevated HbF and sickle cell anemia may have a milder form of sickle cell anemia
Sunday, September 19, 2010
Thursday, September 9, 2010
What does this tell us about KPD's and weight? I keep hearing and seeing ads telling parents to make sure their children are active and eating right. This is the answer to childhood obesity, exercise and diet. Okay, I am a fan of both sloth and gluttony, I tend to be good at them, but I have to admit there's nothing wrong with having children out there physically engaging the world without a candy bar in their mouths.
KPD is showing us something, however. What do you say to a person who is a thin diabetic? You obviously can't ask him or her to go on a diet nor would you put them on exercise schedule to help burn calories. We don't give the same advice to the thin KPD simply because it doesn't make obvious sense. They are thin. We give it to the heavy ones because they are fat. It's still the same condition with the same underlying causes. It gets expressed differently but the numbers between fat and thin are pretty much the same. I'm saying this because, I believe we have to look deeper than this. There is something going here and the range of body types it effects doesn't seem to point at behavior.
The people of sub-Saharan Africa have a much bigger problem with Ketosis Prone Diabetes but this tends to be more in urban environments. There hasn't been a study but I would hazard a guess that you could draw a trendline representing length of urbanization of KPDs and their families and find quite a correlation.
Another thing to note is it tends to cluster in people of color, not that whites don't get it, they do, but the prevalence is far higher in people of color. Now I'm pretty sure you don't want to say that all these people of color are lazy and eat too much. Besides, how could that be true if a good many of them are thin?
I believe that most of this is a response to diet. It is, after all, about metabolism. Its higher rate of prevalence in urban areas suggests that it has something to do with the moving from traditional diets to more modern diets. It would be logical to point out that there are many things that go with urbanization that could just as readily be pointed as a cause. This is true but I would say that this exists worldwide in varied modern environments so I would have to ask: how many things could this be? To tell the truth, I don't know nor does anybody else. What I do know is purely anecdotal and the KPD's I've talked to have had to change their diets significantly to hold their blood sugars down with diet and exercise, those on insulin, generally, have not.
This difference in insulin using KPD's and non-insulin using KPD's suggest that some element of diet is effecting blood sugars. Think of it as some sort of intolerance. What is it? I really can't know. I list a bunch of blogs I follow that are all about nutrition because I'm trying to find out.
I ate a very healthy diet before I was diagnosed but now I find I can't eat that same diet without a significant rise in blood sugar. Would I say that, simply because I can't eat it, no one should? No. What I will say is that KPD is different and pretending that it isn't does not work. We can not assume what is healthy. We must verify.
I've just read the usual recommendations of the ADA and others about what is healthy to eat but does it include KPD? I think not. If these foods are fine there is really only one way to know and that's to test the blood sugar. I see all these recommendations about what to eat but, one size does not fit all and this is especially true of KPD. What should be recommended is that all families get a meter and test what their food is actually doing to them. If there is a significant intolerance, blood sugar will exceed 140. If this was the recommendation of the USDA there would be far fewer DKA events in this country. It would also provide important data about what is safe and what is not about a whole range of products.
To repeat, there is something in the KPD diet, that may not effect others but which is probably poisonous to KPDs. We can't identify who is KPD but if people were checking their blood sugars and correlating it with what they ate, the KPDs that are out there, who aren't diagnosed, could see this truck coming
Friday, August 27, 2010
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.
This is a study that tracks KPD's over ten years and compares them to regular Type 2's and Ketosis Prone Type 1's. This study is out of Paris done on emigrants who come mostly from Sub-Saharan Africa. I have talked or corresponded with people who question the relevance of this research to them because they aren't remotely African or descended from Africans. As I said before, this syndrome has been documented almost every. The research is very spare and I've had to cobble data from all over the world. I suggest that beggars can't be choosy. My position is that anything that says anything about KPD is relevant to all KPD's irrespective of color or origin.
ADA Criteria for the diagnosis of diabetes
1. A1C 6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.*
2. FPG 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.*
3. Two-hour plasma glucose 200 mg/dl (11.1 mmol/l) during an OGTT.
That being said, let's get on with it. Above I have copied the ADA guidelines for diabetes diagnosis. It's important to keep these numbers in mind. It is especially important because, as I've said, most docs have no idea about how this works so you need to look out after your needs or those you know.
Buried in the KPD paper is a graph that describes the path that relapse takes in KPD's. Though it describes relapse, I am looking at it as just the course which KPD's take before their blood sugars go awry. What is my evidence for this. Well, there is one thing but I'll get to that later. Of course, A KPD, by definition, has already been diagnosed so it very definitely pertains to those.
What they found was that the course before relapse could be predicted by A1c over a years time. I tried to get this but it wouldn't copy. You can find it on page 650. Here's what they had to say.
The median duration between the development of hyperglycemia (HbA1c 6.3%) and the onset of a ketotic relapse was 12 months (95% CI, 6–21, Kaplan-Meier). During this period, the insulin secretory reserve, measured before the onset of hyperglycemia and during readmission for relapse, dramatically deteriorated ( C-peptide, 2.88 0.21 vs. 0.19 0.08 ng/ml; P 0.05). There was no precipitating illness other than hyperglycemia. The increase in HbA1c 6.3% was associated with an increased risk of ketotic relapse with an HR of 38 (95% CI, 5–286; P 0.0004). Thus, hyperglycemia preceded and was strongly associated with
the subsequent development of an insulin-deficient, ketotic relapse.
The chart is pretty clear. It tracks the A1c for 40 months. The A1c stays steady at around 6.3% and at about 12 months before relapse takes a slight jog up. At 6 months, it takes another jog up to about 6.6 %. From this point on, the curve becomes steep.
What you can see is that below 6.3% blood sugars remained steady. Above that number events go bad very quickly. The 6.3% averages out to a blood sugar of 134. The first jog up appears to be about 6.5%, which averages to daily blood sugar of 140. This 140 is not a random number. It is thought to be the point at which blood sugars become damaging and bring on long term complications.
My thought on this as occurring before the first episode is from some reading, which I can't find, that said it was frequent, that previous to diagnosis, a KPD would have a normal or near normal blood sugars 6 months before. This graph shows something similar. We have no idea what causes this catastrophe but the fact that its beginnings sit at this critical juncture seems to suggest that something gets broken here. What you have to recognize is that this is for people who've already broke down then gone into remission, so whatever got broken got fixed once the blood sugars were brought down.
Now look at the ADA guidelines. They've tightened them up but look how close they are to the KPD danger point. This guideline is really for T2's. Would you give this as a guideline for KPD's knowing that they can crash very quickly? If you are a KPD should you feel safe with these guidelines?
If you showed up at a doc with these numbers, the ADA recommends that the physician should inform you that you're prediabetic and that maybe you should start making adjustments with diet and exercise. You would be asked to return in 6 months for a checkup to see how things were going. This wouldn't be a problem for a Type 2 because onset isn't abrupt and acute but for a KPD these numbers should be sending off all types of alarms because in 6 months you could very well be hospitalized or at worse, dead.
Until there is a diagnostic test for KPD, we will continue to windup in emergency. For those who already know what they are; keep and eye on your blood sugars because, unlike a T2, whose numbers trend steadily, you can go off the rails very quickly.
Tuesday, August 24, 2010
I am now going to put forth an idea that popped into my head after reading a post by Ned Kock over at Health Correlator. Here What got my attention were people who were heavy but were more insulin sensitive then their control group. What was even better: once they received medication they began to lose weight but became more insulin resistant with a rise in blood sugar.
Insulin Resistance is very much at the heart of obesity and thinness as far as I can see but it is also one of the central aspects of Ketosis Prone Type 2 diabetes. Pal Jabekk speaks of the fact that insulin resistance is a body wide behavior. I agree given insulin's importance in energy metabolism obviously everything has critical involvement with it. This doesn't, however, mean that insulin is used at the same rate through out the body all the time. At any given moment, there will always be some systems that are more or less resistant.
This brings me back to the puzzle of KPD weight gain while at the same time reaching near normal blood sugars. First of all KPD's are infamous in the fact that weight is not an issue. Just as many KPD's are thin as obese. Some have separated this along the lines of those who lack sufficient insulin so that they become thin and those who have plenty so they become fat.
When the DKA or severe ketosis event occurs KPD's, who recover, are shown to have a low normal reading of C-peptides. The cut off that has been cited is .9. In six months, it is common for this to go back into the normal range and higher. It is also known that KPD's recover near normal blood sugars even though their measurable IR isn't reduced one jot. It should be noted, as well, that the best blood sugars tend to go to the heavier KPD's and not the thin ones.
Given that the IR is still high, the C-pep is normal or above and the blood sugars have normalized, we have to assume that there is relatively enough insulin present. What is the difference between thin and obese?
Now the leap of faith. It has to be relative insulin sensitivity issues. We can see with a thin person that insulin is putting relatively more energy in other systems besides fat. What those systems are we really don't know. What we can tell, however, is those systems on the whole are more sensitive to insulin than fat. Likewise, if the person is putting on weight then their adipose is relatively more sensitive to insulin than other body systems.
Now my thinking about the KPD's gaining weight with better A1c's. I believe fat works better for glucose storage then muscle or other systems. You can look at obesity as the body's way to reacting to high amounts of glucose. This is why I believe there are so many heavy people. Obviously, the body is sending glucose everywhere but the fat cells seem to get more. If we make this about controlling blood sugar then the fat cells become like the catch basin for the extra glucose in the system.
A thin KPD is relatively more insulin resistant in the fat cells, and this is why I say fat works better, sending glucose to other systems with fat lower down on the list doesn't normalize blood sugars as well as those who can send it to fat. So thin KPD's are typically not going to have blood sugars as good as heavier KPD's. This would also say that thin KPD's are more at risk of relapse to DKA then heavier KPD's. I would also add that this probably isn't how normal people work but we have broken metabolisms. Our livers are pretty much blind to insulin.
Monday, August 23, 2010
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
|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 IRNEFA (103 · μmol · mU · l−2)||17.7 ± 3.2||8.0 ± 1.7||0.009|
|IRNEFA1 (103 · μmol · mU · l−2)||17.4 ± 4.6||6.9 ± 1.4||0.05|
|IRNEFA2 (103 · μmol · mU · l−2)||40.2 ± 9.2||21.2 ± 2.6||0.06|
If you look at these numbers and toss in glucose toxicity, you can get an idea of why we go DKA quickly.
Despite an increasing number of reports of ketoacidosis in populations with Type 2 diabetes mellitus, the pathophysiology of the ketoacidosis in these patients is unclear. We therefore tested the roles of three possible mechanisms: elevated stress hormones, increased free fatty acids (FFA), and suppressed insulin secretion.
Conclusions At the time of hospital presentation, the predominant mechanism for ketosis in KPDM2 is likely to be greater insulinopenia.
Pathophysiology of ketoacidosis in Type 2 diabetes mellitus
P. Linfoot , C. Bergstrom and E. Ipp Diabetic Medicine Volume 22 Issue 10, Pages 1414 - 1419
The question I have is: when did this start? Is this part and parcel of our lives as youths? Have we always been KPD and it took bad diet to get us here. There is plenty of documentation that this is present in the young.
again more research needs to be done.
Purely from an anecdotal perspective, looking back at my childhood and viewing my present day symptoms, I would say they were present then. The problem is we really don't know what KPD is. It is described by its most dramatic symptom, which is its acute presentation. What is going on before that? Is it the same syndrome in children? How insidious is it? What is the continuum of its behavior?