I just wanted to say that it is my opinion that Type 1 is very special as compared to Type 2 (I’m T2). It deserves its own exclusive website. I’m seeing that most new postings are about Type 1, as they should be, but they are off-topic for me. That’s why I’ve unsubscribed to FUD updates. I guess I must admit that I no longer need much support (except for vision problems), as my A1c is 5.5 on a ketogenic diet and no meds. My best wishes to everyone.
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TuD has a “Beyond Type2” website I believe that may be more useful to you!
Sounds right to turn off notifications. I turned them off ages ago myself but for a different reason. I read all posts already anyway!
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Slightly off topic for the topic but relevant here; how did you get where you are today?
Most of my family by marriage are T2, most have high HbA1c, but my wife only “qualified” recently when her HbA1c managed to get over 6.5.
Despite that late, for her family, onset it was clear that something was going on, not necessarily “wrong” but certainly suspicious. Fingersticks would show high and sometimes low BG after a meal; hardly unknown for non-Ds but slightly worrying because the effects were detectable to her. Eventually we got her a CGM; you guys, the keto crowd, made that possible! I could just buy it on Amazon. She had clear, unambiguously clear, failure in her post-prandial insulin response. The docs, well, nada, then metformin; whatever.
That’s our story. But what happened with you? Someone decided you were a diabetic and now you are not (because the breakpoint is an HbA1c of 6.5)!
I just saw an article on a study that was finding that postprandial BG tracking was more important than just fBG and HbA1c. I wasn’t able to read the actual paper, but it calls into question current diagnostic criteria.
Long before I was diagnosed, I had 2 symptoms. All my life I had reactive hypoglycemia. I know that by looking back. The other was probably postprandial hyperglycemia after lunch. When I am hyperglycemic I have both cognitive slowing and reduced physical coordination. I suspect that all my life before diagnosis I had poor glucose regulation.
My diagnose came about because of a sudden blurring of vision. My ophthalmologist told me to get my BG tested. My fBG was very high400+mg/dl and my HbA1c was 14.5%.
I was lucky that my heath care providers (Scott and White) had a very good system of education and therapy. First I was prescribed a sulfonylurea. These drugs increase insulin sensitivity and stimulate the Beta cells to secrete more insulin. Secretagogue is the term used.
I determined to be ultra compliant on diet, drugs and exercise. After 6 months I started having hypos and my doc weaned me of the drug. This worked for 10 years, and then I learned that T2DM is progressive.
In my opinion a person that ever had glucose regulatory issues, including reactive hypoglycemia, prediabetes or T2DM are always at risk of it progressing even though HbA1c is below the diagnostic criteria.
So fast forward about 24 years from my 1st progression. I have been on MDI and currently a pump for about 6-7 years. I still eat a carb reduced diet, exercise every day and take metformin as well. My last HbA1c was 5.6%.
When I was in my 10 year honeymoon period my HbA1c was in the range of 5.0% to 5.4%.
The cause of the progression is the same as the cause - inherited abnormal resistance of skeletal, liver and fat cells to accept the attachment of insulin when the cells are in need of fuel, glucose.
This causes the Beta cells to secrete higher and higher amounts of insulin in response to elevated BG levels. At some point this does not keep BG in the normal range. This would be prediabetes. Eventually the Beta cells die from over work.
This is were I am. My C-Peptide is low enough to be diagnosed as T1DM, but of course my cells just wore out, not destroyed by the immune system.
Back to @DavidSpector While the causes and therapies of our diseases are different, we all face the possibilities of severe diabetic complications. And there are those who have T1 autoimmune DM compounded with inherited insulin resistance, formally called double diabetes.
Not the paper but on the same subject
https://journals.sagepub.com/doi/full/10.1177/11795514251370507
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