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.

Monday, June 14, 2010

Thinking out loud about how prevalent is KPD T2?

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."

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.

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