No I don't think I match the profile for T2 - I only found out because my son participates in the ALSPAC study and they started to investigate parents and up popped high fasting BS. It could be another type but in view of my age and not on any medication, not cost-effective to investigate further. I did see an endocinologist who was pretty convinced it would be Glucokinase but it isn't. It was suggested it could be T1 but apparently it would have progressed more quickly. My GP says it doesn't matter as Metformin would be first resort in any event. I would like to know what type but does it matter?
It seems to matter. Eg, a defect in the HNF1A gene (this is 'MODY 3') involves a secretory defect only. The experts say that the only appropriate medical treatments for MODY 3 are insulin or drugs which stimulate the secretion of insulin. MODY 3 can be mild for years, during which time you can postpone insulin. The secretagogues are cheaper and there are no needles. 10% of MODY 3 is diagnosed after age 40.
With MODY 2, the GCK gene mutation, the fasting glucose is prediabetic for life (below 7.0), and the postmeal value is the same as normal people's (under about 7.8). A postmeal value of 13 makes GCK MODY unlikely.
There is slow onset autoimmune diabetes, which is known as LADA. The healthcare system is overburdened. LADA is commonly misdiagnosed as T2, and when metformin doesn't work, the patient might get a referral to a specialist, who might think to test for LADA. You must test for two antibodies, not one: GADA and ZnT8A. But ask for IA-2A and IAA to be included.
Has your fasting plasma insulin been measured? This test is cheap, and it's hard to estimate the value of insulin resistance without fasting insulin. A commonly used index of IR is HOMA-IR, a normalized number: insulin * glucose / 22.5. [22.5 if glucose is in mmol/l and insulin is in uIU, 'u' is the Greek letter mu.] The value of 1.0 is a good, but not excellent value. The HOMA-IR threshold for declaring insulin resistance is, I forget, 1.8 or 2.2. If the HOMA-IR is below the threshold, I would wonder what metformin could do for me.
Other strong indicators there is (pre-)diabetes of the insulin resistance type are chronically rising blood pressure, trigs exceeding about 1.7, being fat, and falling HDL. If there is none of these, or just one, it would be hard to argue there is T2.
I am sceptical of the view that treats metformin as the aspirin of diabetes, good for everybody. In either type of autoimmune diabetes, loss of insulin production is the only cause. Metformin doesn't promote production or secretion or insulin. It tweaks various tissues so that blood glucose will fall. However, if you do not have insulin resistance, then metformin is treating a problem you don't have, the glucose won't fall much, and the doctor will be masking the progression of the beta cell failure. Diet and exercise are healthier stopgaps than metformin.
For most people with dysglycaemia, there are really only two MODY's to consider: HNF1A and HNF4A. The other MODY's are exceedingly rare or the symptoms are severe. The mutation in HNF1A is five times more frequent than mutation in HNF4A. Researchers recommend to test for the latter only after a test for the former comes out negative.