I've got at least one more post in this series directly relating to the neuropathy study to which concerns over BG levels over 140 mg/dL and nerve damage can be traced.
This post is actually going to be rather short. In the study, they found that half of those with neuropathy were diagnosed with IGT having a BG level over 140 mg/dL at the 2 hr mark on an OGTT. An additional 18% were diabetic and 32% normoglycemic. So the incidence of IGT was roughly three times as prevalent in this neuropathic population as in the general population. Further, the IGT group had more painful sensory symptoms than the normoglycemic group. But here's the thing:
As summarized in Fig. 1 [at right], our results indicate that OGTT is more sensitive in detecting abnormalities of glucose handling than either FPG or HbA1c. Only 4 of 105 patients had IFG, whereas 36 of 72 patients had IGT. Diagnosis of more than half of patients with frank diabetes by ADA criteria would have been missed if HbA1c or FPG alone was used for screening. These results mirror large prospective studies in which results of OGTT in older patients are often consistent with diabetes but normal FPG, and asymptomatic patients with IGT have normal HbA1c. Use of HbA1c for screening purposes is discouraged by the 1997 ADA guidelines. We suggest that measurement of HbA1c using typical thresholds is inappropriate when evaluating the cause of neuropathy.
Now, the average age of participants in this study was 65, and remember they were suffering from neuropathy of unknown cause. Fully two-thirds would be diagnosed with impaired glucose metabolism by the OGTT, but as the plots show, almost none of these would be diagnosed by measures of fasting glucose metabolism or longer-term glycation. This flies in the face of what Taubes, TWICHOOB's and countless others tell us, which is that repeated glucose spikes, and postprandial levels remaining elevated results in hyperglycemia and/or chronic hyperinsulinemia. Again, these folks had no clue what their BG responses were for who knows how many years. While they developed neuropathy (next post) it does not appear to be by the commonly accepted (and scare-mongered) mechanism of glycation damage. Furthermore, the postprandial spikes and higher AUC's do not appear to be related to fasting gluconeogenic glucose production. Hepatic insulin sensitivity appears to be intact then as well.
What could be going on here? My bet is are on insulin insufficiency. In T2 diabetes there is often basal hyperinsulinemia but an inability of the beta cell to mount the appropriate acute insulin spike in response to a glucose challenge. In the next post I'll put together these results here with some papers looking into neuropathy in different types of diabetes, etc. I think there's some interesting conclusions that may be drawn here.