A nifty study of a personal genome was published in the journal Cell last week. What makes it fascinating is that the subject of the study apparently developed type 2 diabetes during the study and the researchers were able to follow its progress.
During the course of the study, the subject had a couple of viral infections, and after the second infection, his blood glucose (BG) levels, which were normal at the beginning of the study, started rising. Because of this, the researchers started monitoring his BG levels and A1c more often than before.
The subject had nonfasting BG levels below 100 mg/dL when the study began, and after the second viral infection, they went up to about 150 and he was diagnosed with diabetes. At this point, his hemoglobin A1c was 6.4. According to the article, the man then changed his lifestyle, and by the end of the study, his BG levels were below 100 again, and his A1c was 4.7.
Unfortunately, because the focus of the study was on the genes, although the article says that most BG measurements were "at a fixed time after a constant meal," they don't reveal what the time or meal were. A BG of 150 mg/dL at 60 minutes after a carby meal wouldn't be very unusual in a nondiabetic, especially during or after an infection. A BG of 150 2 hours after a noncarby meal would.
The final A1c of 4.7 is interesting because it agrees with Dr. Richard K Bernstein's assertion that really normal A1cs are in the 4s, not just below 6.
You can see a graph of the BG results in the full article.
According to the popular press article, "with dramatic changes in diet, exercise and a regular low dose of aspirin, his glucose levels dropped back down." Unfortunately, they didn't say what the dramatic changes in diet consisted of. Presumably the aspirin was because he showed signs of inflammation after the infection.
The genetic analysis showed that the man was at high risk for type 2 diabetes, but the article in Cell said there was no evidence of insulin resistance when his BG levels were rising. Type 2 diabetes is currently defined by insulin resistance, so it's not clear why he was given that diagnosis except that he was at risk for the disease and was still producing insulin. The man had no anti-GAD or anti-islet antibodies, which suggests that he didn't have early type 1 diabetes, although it's always possible that antibodies could show up later.
The man had a body mass index (BMI) of 24 at the beginning of the study and reduced that to 22 by the end of the study, which is consistent with type 2 caused by being slightly overweight. But then why no insulin resistance?
It's unlikely that he had MODY as the more common MODY genes are known and should have been picked up by the detailed genetic analysis.
Maybe non-type 2, non-type 1 would have been a better diagnosis.