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.

Saturday, June 26, 2010

The Provoking Event of Ketosis Prone T2 Diabetes

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

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.

  • Antonio Piñero-Piloña, MD

  • Patrick Litonjua, MD

  • Larissa Aviles-Santa, MD and  

  • Philip Raskin MD


    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.


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

    Tuesday, June 22, 2010

    KP T2 on Oprah Audition

     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.

    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.