ADA calls this idiopathic T1 diabetes. This is what I have. It’s interesting that there is no real forum here for this type because it is estimated that 50% of the diabetes in African Americans is of this type. It’s probably close to a third of all people of color who have diabetes. Here’s a link.
I’m hoping that some people out there will come out and tell me about their experiences. Diabetes is weird but this baby takes the cake. I show negative for GAD and Islet antibodies. My BMI is 22. My HDL is 75 and my trigs are 65. All my numbers are normal or better even my C-peptides are better than 1.5. Put a few carbs in me, however and it is spike city.
My readings and my endo tells me this is hereditary. I couldn’t know this because, in my family, we tend to die young. It’s a type of MODY but it seems to stay under the radar then BOOM - you die of colon cancer, heart attack or stroke.
One of things important to know about this diabetes is that it will go into a type of remission where diet and exercise will control it. I got my A1c down to 5.2 but I was on Actos which was very bad in terms of side effects. Now that I’m off it, I can see my numbers going up. One thing I do know about this is that glucosetoxicity is a problem with its attendant IR. My hope was to get my bs’s down and to the remission stage. It hasn’t happened and I know that I’m moving back up to higher numbers.
I know there are a lot of my type out there but what works for LADA, T1’s and T2’s is really applicable. What I don’t know is 'what is applicable." and what will get this thing to move down back to its remission range. Hey, I know that I’m going to be diabetic for the rest of my life but Ketosis Prone Diabetics are known to be able to move back to near normal and stay there with diet and exercise. I need to hit this spot and I want to hear from all the people that have found there way back to near normal blood sugars.
I question if there are more types of diabetes than commonly believed. Reading how many people are misdiagnosed merely between T1 & T2 there must be more people who may have your type, but haven’t received the correct diagnosis. You must have a good endo to have recognized it.
Would Symlin be an option? Since your C-peptide is good, perhaps this would be effective since T2s on insulin & T1s have been helped with Symlin. There’s good Symlin info here to search. Is your endo against very small doses of rapid acting nsulin for meals to control the spikes? Is your morning fasting good?
Very interesting Information, Michael. I am Type 1 for 42 years, African-American. I am very concerned abiout the pandemic of diabeters-related early death and destruction I see in The African -American community… Could it be due to misdiagnoses and under-treatment and education? I have met African-Americans, like you, who are thin, athletic, diagnosed as Type 2, then they wither away within about 7-10 years of diagnoses, all the while following the treatment protocols. that they have been given. I hope you can talk to others who have experienced what you are going through…, and that you can your medical team come up with a . plan that works for you as an individual.
My endo is very good. We talked about Symlin but I have a BMI of 22 and I take in a lot of calories. Symlin would bring down my appetite as well. We went to Starlix because it would just do a mild, short reducing of spikes. The problem is that I went off Actos at the same time and my basal numbers are moving up even if you count in my DP. This is a long process and our typical approach is to try something small and keep moving up until I get the results I’m looking for.
Could it be due to misdiagnoses and under-treatment and education? I have met African-Americans, like you, who are thin, athletic, diagnosed as Type 2, then they wither away within about 7-10 years of diagnoses
Misdiagnoses - I don’t see how Black people or any people of color are going to get good diagnoses when most Docs haven’t even been informed of this condition. ADA lists it as T1b, that’s it. The good thing is that this presents with such horrendous DKA that it forces medicos initially to do proper procedures such as immediately prescribing insulin. The hypos that begin to occur after that force them to reduce the insulin and eventually they wind up on oral meds. There it rests because no one seems to know enough about to do anything more.
Treatment and education - Most Black T2s are Ketosis Prone T2s but I bet you’ve never heard of it and you’ve been diabetic for 42 years. I had never heard of it either and I’m 57 and know plenty of diabetics. This type has an intense multi-tissue IR component. I’ve seen that we maybe 30% more insulin resistant then other T2s. People like this can’t handle “fructose” at all because it is processed in the liver. It, very simply, is a poison for a KPD T2.
I have friends that have been told by their CDE’s that they need to take in, at least 150g of carbs a day. It really can’t be done without weight gain. High carbs give you higher insulin requirements and more fat deposition with more IR. This thing just keeps spiraling downward.
The last thing to go on a KPD T2 is their fasting rate, their diabetes would be apparent 10 years earlier with a glucose tolerance test.
Good to know this. I have a similar pattern. One things that I dont know is if I DKA. I was too busy trying to stay alive at the ICU with a 1000 bg. When I finally normalized I was never told what exactly happened and I DKA. I always find it amazing how many endos never tell you what you are. You have a good endo. I did not know there was type 1 and type 2 until years later after diagnosis.
I used to be on lantus and humalog for about a year and today I am on metformin. It took a lot of testing to get under normal range. I test after every piece of food I eat and then figure out the impact on bg’s. With this i manage to take less meds. I had my a1c down to 6.1 with this method. I started hitting numbers in the 80s and 90s but I would get the feeling of lows under those numbers that I tended to over correct. I just found out about the rule of 15 now and I try to correct based on that instead of shoving food and soda to bring numbers back up to get rid of the feeling.
So to get normal for me requires a lot of excercise, modified diet, and constant checking to correct highs with excercise.
take care if you have any other questions feel free to contact me directly
One things that I dont know is if I DKA. I was too busy trying to stay alive at the ICU with a 1000 bg.
DKA isn’t generally diagnosed on just bg but I’m willing to bet since you were in ICU you had a severe DKA event. If DKA occurs in type 2 diabetics, their condition is called “ketosis-prone type 2 diabetes”.[7] The exact mechanism for this phenomenon is unclear, but it appears that very high levels of glucose suppress the release of insulin from the pancreas through “glucotoxicity”, leading to levels that are insufficient to suppress ketogenesis.[1] Furthermore, insulin resistance may be so severe that ketogenesis cannot be suppressed
So to get normal for me requires a lot of excercise, modified diet, and constant checking to correct highs with excercise.
I use to get close to 5000 miles a year of cycling done but it didn’t stop this. I believe that exercise helps the IR issues of muscles but doesn’t do a whole bunch for the fat and liver issues. My point is that we need to know more about why we are so much more IR. I’m thin so obviously my fat cells are responding pretty good and I get plenty of exercise so my biggest IR issue is with my liver. How do I reduce the IR of my liver?
Multitissue Insulin Resistance Despite Near-Normoglycemic Remission in Africans With Ketosis-Prone Diabetes
Michael, U R right I had never heard of KPD Type2. Unfortunately, I have heard of msoe African-American persons ( who presentned in DKA upon diagnoses in the emergancy with blood sugars in the 800-900 range. they werer started on insuoin for a short time, then gradually went to oral meds. I do not know what diet and exerfise protocols that they were recommended to follow. I do know that they did recover from the DKA, but in the foloowing weeks and months off of insulin, were having trouble getting good A1c’s and many became sick and weak.
Your endo sounds like a good doctor… Does he have any suggestions on how to deal with Insulin resistance and the liver/ Do you take a long-acting basal does of Lantus or Levemir?
I was hoping that Symlin would have the effect of improving IR since people on insulin take less when using Symlin. You certainly don’t need it for appetite suppression. But, I wonder if its other attributes would be worth trying it as long as you forced yourself to eat enough to maintain your weight. Symlin can cause hypos in people injecting insulin, so that’s something to be concerned with.
A very perplexing & extremely frustrating condition. The liver IR is awful. Would it be helpful to consult with a liver specialist?
Did Starlix help?
I’ve yet to meet a CDE or dietician who didn’t push 150-180+ carbs per day. I was told 45-60 carbs per meal, plus 1-2 15 carb snacks. I think that’s a prescription for diabetes disaster. It was for me.
Wish I could remember where I recently read a great article about T2 oral meds. The reseachers, an atypical group, questioned the effectiveness of T2 drugs. They felt these drugs burned out the pancreas by forcing more insulin production. Their recommendation was low doses of insulin.
I do not know what diet and exerfise protocols that they were recommended to follow. I do know that they did recover from the DKA, but in the foloowing weeks and months off of insulin, were having trouble getting good A1c’s and many became sick and weak.
More than likely they were told to do the high carb diet not recognizing how sensitive KPD’s are to carbs due to this IR problem. If they were obese this just makes it worse. Exercise is always good but this is a metabolic problem. These people are starving on a cellular level. If an animal is starving it slows down its activity and metabolic rate, people are no different.
As for me my endo did give me Levemir. He wanted me to go on insulin immediately but my low carbing and the Actos brought my bs down so fast that I never had a chance to go insulin. My A1c went from 9.9 to 5.8 in 3 months. Here is the problem as I see it. KPDs have a pancreas that is fully capable of providing insulin but due to glucose toxicity has largely shutdown. KPDs are very sensitive to glucose toxicity. If that toxicity drops then insulin suddenly becomes available. Most of the KPDs have to come off insulin due to hypos. Now, I’m at an A1c of 5.2. Would you want to give me insulin knowing that, the very fact of giving it to me would turn off more of the glucose toxicity, I could very quickly begin to produce a lot more of my own?
My endo is smart but he knows this stuff on a theoretical level. I’m a paradox to him and he wants to be cautious. I’m taking Starlix to address post prandial spikes and we are just seeing where this takes us.
I’m guessing that I take in about 2500 to 3000 calories a day but in the time my endo has seen me I’ve lost 15 lbs. He looked at me cross eyed when I brought up Symlin. “You’ll vanish”, he said. He calls all medications “poisons” and since I’m at a A1c of 5.2 he figures we have time.
A very perplexing & extremely frustrating condition. The liver IR is awful. Would it be helpful to consult with a liver specialist?
One of the reasons I started this post was to find people who have this condition with the hopes that they would have fell across various solutions. My friend is a liver and kidney specialist and the problem is there is no protocol for this. KPDs though plentiful don’t even know what they have and research is still only at the point of defining the problem.
The jury is still out on Starlix. It is very weak and I’ve only recently started. I’m seeing some results but since it works on the pancreas I have to wonder is it going to deplete my beta cells. I’m at sea here and I’m just going to have to take is slow.
Yeah, there is this whole thing about resting the pancreas. I don’t know if that counts in my case. I don’t have a first phase function for insulin but I seem to have plenty going on for the basal. Part of first phase is the shut down on glucogenesis from the liver. If the liver is showing IR then it’s not going to respond when bs is rising but continue to put out glucose into the blood stream. If the pancreas is IR as well then it won’t put out that burst of initial insulin that blunts bs rise.
Looks like to me there might be way too much resting going on in my body already.
