[ Nutrition ]

Elevated hemoglobin A1c as a possible indicator of diabetes mellitus and diabetic ketoacidosis in schizophrenia

I have always had pretty good control over my diabetes. Mean +/- SD serum glucose levels were higher in HD and PD patients relative to non-nephropathy controls (HD 169.7 +/- 62 mg/dL, PD 168.6 +/- 66 mg/dL, controls 146.1 +/- 66 mg/dL; p = 0.03 HD vs controls, p = 0.13 PD vs controls). The aldose reductase inhibitor, sorbinil, which is reported to normalize the impaired NCV associated with experimental diabetes, was used as a positive control. Flurbiprofen treatment of ND rats replicated many of the biochemical and physiological abnormalities of EDN, i.e., reduced motor nerve conduction velocity (MNCV), total and endoneurial nerve blood flow (NBF), Na,K-ATPase activity, and myo-inositol (MI) and taurine content. I was seeing really high post meal spikes. I was 25 years old when I saw my first A1c under 8.5%. The mean changes in HbA(1c) were not statistically significant in either the resistance training (-0.16%; 95% CI, -0.46% to 0.15%; P = .32) or the aerobic (-0.24%; 95% CI, -0.55% to 0.07%; P = .14) groups compared with the control group.

Greater than 200 mg/dL means diabetes. Of the 11 patients with diabetes presenting as diabetic ketoacidosis, the mean HbA1c level at admission was 13.3% +/- 1.9% (10.4%-16.9%). The past 2 weeks I have started substituting the cheap alpha lipoic acid for the r-alpha lipoic acid with some relief. The EIP denied benefits for the diabetes educational training session concluding that the state health plan expressly excluded diabetes educational training and that the state statute that mandated coverage for diabetes educational programs in certain insurance policies did not apply to the state health plan.

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