Editing my post cause I thought I was replying to someone else, sorry, same basic principle holds true though.
Hi David,
I know that there are really no set in stone rules when it comes to diabetes and that everyone is different, however, part of my reason for posting what I did is maybe some who think they are type 2 are really type 1
With you not having insulin resistance, which is a hallmark of type 2, could you be type 1, not type 2? A lot of adults are mistakenly diagnosed as type 2 when if fact they are type 1
@Gina@Stang777 Sorry to be so heady but this community is so very smart. I am pretty good at keeping it very simpleā¦ 8))
In a nutshell some people believe that type 2 diabetes is caused by loss of a certain cell called the beta cell in the pancreas. The beta cells produce insulin While that is true, other organs contribute to the the development of type 2 diabetes.
Itās important for people with type 2 diabetes to know that. Organs such as the liver, skeletal muscle (skeletal muscle is regular old body muscle) and body fat also known as adipose tissue contribute to the development of type 2 diabetes.
(Side point. Did you know that muscle is a storage site for glucose? That is why it is such an important organ).
The liver produces sugar/glucose when body is in a fasting state (while we sleep) and sometimes it produces so much glucose, metformin is not enough. BTW, chemicals from metformin target the liver to help control the amount of glucose it delivers to the blood. When metformin isnāt sufficiently effective, some physicians recommend a long-acting insulin also called basal insulin to help remove some of glucose from the blood so when the individual wakes up, their fasting blood glucose is within a normal range.
Diabetes is a complicated disease. Itās one of the reason why there are so many drugs manufactured to help manage it.
Now, letās not forget that the cells that make insulin in the pancreas are still progressively being destroyed, so two organs (pancreas and the liver ,for this sake of this explanation) contribute to the development of type 2 diabetes.
I think we have a lot of uncertainty about the ācausesā of type 2 diabetes. In truth we mostly never talk about the āetiologyā (causes) of T2 because we just donāt understand the causes. We know risk factors, but those are not causes. From what I have read, Genome Wide Association Studies (GWAS) can explain up to 80% of the risk of T2. Williams Textbook of Endocrinology is a good source of what is currently taught in endocrinology about this topic. There is certainly lots of research going on about physiological role of things like the role of Free Fatty Acids (FFAs) in the development of T2, but there is no good understanding of the process. Unfortunately there is a great deal of misunderstanding both in society and in the medical profession about the concepts behind āassociation,ā ārisk,ā and ācause.ā Obesity is associated with diabetes, we have not proven that it ācausesā diabetes.
When people do talk about how to classify (i.e. ātypingā) type 2 diabetes they donāt revert to ācausesā like in autoimmune T1, instead the often revert to talking about classes of defects that are present. That is why I consider the work of DeFronzo and Schwarz important.
In practice today diabetes diagnosis is just āmessed up.ā Type 2 is a huge heterogeneous bin that really just means ādiabetes of unknown cause.ā If you have abnormal blood sugars your doctor can diagnose you as having T2 with 90% accuracy, a far higher accuracy then their diagnostic performance in general. If you have a specific form of diabetes (like autoimmune T1 or MODY) and you are lucky your doctor will give you additional tests and you may get a specific diagnosis. If you donāt test positive for any specific type of diabetes then you have Type 2 diabetes which is a ādiagnosis of exclusion.ā There isnāt any test for Type 2.
Yes many people have insulin resistance, but as DeFronzo has noted that by the time you are diagnosed with full blown T2 you have already lost 80% of your beta cell function. And I have come to believe that pre-diabetes is just diabetes. And we really have to face up to pre-diabetes being truly abnormal glucose regulation and it warrants being considered to be an actual disease state.
ps. Since my c-peptide is now 0.4 mg/dl my doctor has at times started classifying me as ideopathic T1 but I test negative for autoimmune T1 as do some non trivial number of people who carry the T1 diagnosis.
pps. The reason that basal insulin helps fasting blood sugars is not because of increased glucose uptake it is because insulin suppresses gluconeogenesis (much more powerfully than metformin).
@Brian_BSC just trying to keep it simple for the masses. 8)) Perhaps when I am at the AADE Convention this year we can discuss this face to face? Feeling really bummed that I put the etiology word out there because it seems like it destroyed the context. Oh well 8((.
Iām sorry for the length diatribe, I hope you didnāt take it as a criticism. I have some sensitivities about things. I donāt like the way that everyone leaps to the conclusion that lifestyle causes diabetes. And I have a suffered a bit of incompetence and mistreatment at the hands of the medical establishment (as have others here). So I am at times aggressive about getting things right. And while there are many people here with a wide range of understanding and background in diabetes it is important to understand that there is a wisdom of crowds here. There are literally millions of years of experience of people living with diabetes. And for many of us having diabetes has driven us to learn about the condition.
I would love to meet you at AADE but I have not decided whether I can really afford either the time or the cost to attend.
Iām so sorry. Iām sure if I saw you I would remember. I attended ADA, AADE, FFL, Innovation Summit, Unconference as well as all my work conferences. My mind turns to jello with the thousands I met. Iām sorry. I do hope to meet you āagain.ā
I get asked that question a lot. No chance. I managed to keep my A1c in the sixes for 16 years using just a sulfonylurea. If I were T1 Iād be dead now.
Thank you Jojeegirl for explaining. The more I read the easier it is to understand. I read almost all of the subjects last night and got stopped on my comments as I made too many on my very first day on the site.
