HOMA Wrong on IR and Insulin Deficiency. Early Type 2s have Insulin Deficiency NOT Just IR.

Buried in this month's issue of the journal Diabetes is a study that, properly understood, suggests that most of what doctors "know" about Type 2 diabetes is wrong.

The study is titled β-Cell Dysfunction in Subjects With Impaired Glucose Tolerance and Early Type 2 Diabetes: Comparison of Surrogate Markers With First-Phase Insulin Secretion From an Intravenous Glucose Tolerance Test.

To understand why this study is important, you have to know that for decades scientists have evaluated insulin resistance using something called HOMA or homeostasis model assessment. HOMA is nothing more than a formula that computes insulin resistance from fasting C-peptide, fasting insulin and blood sugar. If you have had a fasting insulin or C-peptide test, you can compute your own HOMA using the Oxford University HOMA calculator.

What the scientists did in this latest study was something blindingly simple. They hooked up people who had been recently diagnosed with pre-diabetes or diabetes to an intravenous glucose tolerance test and measured their insulin and preinsulin levels. Then then compared what they found with the HOMA calculations.

What they found was "HOMA-B markedly underestimated the magnitude of the β-cell defect across declining glucose tolerance." They went on to conclude, "Subjects with IGT and early-stage, asymptomatic type 2 diabetic patients have more pronounced β-cell defects than previously estimated from epidemiological studies using homeostasis model assessment."

What this means in plain English is that contrary to what you have been reading for decades, prediabetes and early Type 2 diabetes are NOT primarily caused by insulin resistance. Instead, this study found these people had an unexpectedly high deree of insulin deficiency which was NOT apparent when they calculated HOMA using the cheap fasting tests.

This should be a shocker, but like most of the truly important research about Type 2 diabetes it probably won't even get noticed because no drug company is going to talk it up at the big ADA dog and pony show this week. Instead the medical news will be full of reports of how wonderful Drug A is and how all people with Type 2 should be taking Drug B--even if Drug B only lowers A1c from 7.5% to 7.0% and costs $200 a month.

The finding that people with pre-diabetes already show insulin secretion defects points to several things.

1. It emphasizes that there are genetic defects involved in blood sugar deterioration that have nothing to do with overeating or obesity. No one has ever found anything that connected overeating with the failure of beta cells to secrete properly.

2. It calls into question huge amounts of diabetes research done over the past decades because the HOMA formula has been used almost universally to determine if people had IR or beta cell deficiency. This study suggests that the HOMA result is wrong and so any research about insulin resistance based on HOMA is wrong. That's almost ALL large group research.

3. It makes it all the more clear why people with early diabetes diagnoses should consider a trial of insulin when lowering insulin resistance with diet or drugs like metformin does not give normal blood sugars. If your beta cells can't produce insulin, you need insulin. End of story.

4. It makes me wonder how much of the IR that doctors believe to be the sole cause of Type 2 diabetes is actually being caused by abnormally high blood sugars. it is possible that IR increases dramatically when blood sugars go over a much lower threshold than previously believed. Possibly as low as 130 mg/dl. If so, much of the IR found in Type 2 diabetes may be caused by high blood sugars caused by insulin deficiency. If that isn't a mind blower, what is?

Now mind you many people with Type 2 diabetes do have insulin resistance that is independent of their blood sugars. But they also may have decades of functioning with higher than normal blood sugars due to insulin deficiency. What the impact of that on their metabolisms may have been is unknown.

But one thing is for sure, this is a major blow to the idea that type 2 is caused by insulin resistance caused by obesity and that people with Type 2 secrete higher than normal levels of insulin which their body can't use. That belief came from studies based on HOMA calculations, but this study that measured the actual insulin secreted found that simply wasn't true.

P.S. My own HOMA calculation showed that I was twice as insulin resistant as normal. However, when I started to inject insulin I learned that I have normal insulin sensitivity in that one unit of insulin lowers my blood sugar the same amount that it would for a normal person. I use about 1/10 the total daily dose of insulin that an insulin resistant person my size would use. I thought that this discrepancy was because I have an oddball form of diabetes. But it is more likely that it is an example of just how badly this HOMA formula works for people whose fasting blood sugar has not yet reached the 200 mg/dl level which was typical of the population in which the formula was first computed.