The accepted knowledge is that Diabetes destroys gradually over years. Ketosis Prone Type 2 diabetes is an acute form of type 2. This type 2 can reach fasting blood sugars of 300 or higher in months. This blog brings together all the documentation that I could find in the world and my speculation of what it means for KPD’s in specific and diabetics in general. I ask you to leave your stories about what happened to you so that we can all gain a better understanding of what we are dealing with.

Thursday, October 21, 2010

Downloadable Scientific Ketosis Prone Type 2 Diabetes powerpoint presentation

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

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

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

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

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

Ketosis Prone Type 2 Scientific Presentation  

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

Monday, October 4, 2010

A1c, glycation problems and DKA

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

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

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

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

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

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

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

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

DKA’s Admissions per year

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

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

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