There is value in treating elevated levels of diabetes distress: the clinical impact of targeted interventions in adults with Type 1 diabetes.

AIM: To compare the effect of targeted interventions to reduce high diabetes distress among adults with Type 1 diabetes with a comparison sample of similar but untreated individuals, and to document the stability of untreated diabetes distress over time. METHODS: A total of 51 adults with Type 1 diabetes with elevated baseline diabetes distress (distress score ≥ 2.0) and HbA1c levels (≥ 58 mmol/mol) were identified from a longitudinal, non-intervention study, and compared with a similar sample of 51 participants in an intervention study. Both groups completed the T1-DDS diabetes distress questionnaire at baseline and 9 months. RESULTS: Large and significant reductions in diabetes distress scores were recorded in the intervention group (mean ± sd change = -0.6 ± 0.6), while minimal change was found in the non-intervention group (-0.2 ± 0.6, group effect P = 0.002; effect size d = 0.67). Additional analyses using the established minimal clinically important difference for the T1-DDS showed that diabetes distress increased significantly (minimal clinically important difference ≥ 1) or persisted at high levels for 51% of participants in the non-intervention group, compared with 23.5% in the intervention group. CONCLUSION: Our results showed that targeted interventions led to dramatic reductions in diabetes distress compared with a lack of treatment. We also conclude that elevated diabetes distress, when left unaddressed, does not resolve over time and often remains chronic. (Clinical Trials Registry no.: NCT02175732).

Increased ratio of quinolinic acid to kynurenic acid in cerebrospinal fluid of D retrovirus-infected rhesus macaques: relationship to clinical and viral status.

Increased concentrations of excitotoxin quinolinic acid in cerebrospinal fluid (CSF) are associated with infection with the human immunodeficiency virus (HIV-1) and have been implicated in the pathogenesis of the acquired immune deficiency syndrome (AIDS) dementia complex. In the present study, inoculation of macaques with D/1/California, an immunosuppressive serotype 1 type D retrovirus, was associated with acute and chronic increases in CSF and serum quinolinic acid concentrations in macaques that had developed SAIDS, a simian disease analogous to AIDS in humans--particularly macaques with demonstrable opportunistic infections. Kynurenic acid, an antagonist of excitatory amino acid receptors as well as the excitotoxic effects of quinolinic acid, was also increased in the CSF of SAIDS macaques, but to a significantly lesser degree than was quinolinic acid (kynurenic acid, 1.8-fold; quinolinic acid, 15.6-fold). CSF quinolinic acid, but not kynurenic acid, was also increased in viremic macaques with SAIDS-related complex (2.4-fold) and asymptomatic virus positive carriers (3.4-fold). Macaques that had recovered from D/1/California infection and were antibody positive and virus negative had normal CSF quinolinic acid and kynurenic acid concentrations. Increased activity of indoleamine-2,3-dioxygenase, the first enzyme of the kynurenine pathway, was indicated in the macaques with SAIDS by reduced serum L-tryptophan and elevated serum L-kynurenine concentrations. Macaques infected with D/1/California may provide a primate model for investigation of the mechanisms involved in increases in CSF quinolinic acid in retrovirus and other infectious diseases, including HIV-1. It remains to be determined whether the increased CSF quinolinic acid concentrations and the increased ratio of quinolinic acid to kynurenic acid have neurological significance or are a useful "marker" of infection.