Development of a multi-component lifestyle intervention for preventing type 2 diabetes and cardiovascular risk factors in adults with intellectual disabilities.

Background: We report on the development of the 'STOP Diabetes' education programme, a multi-component lifestyle behaviour change intervention for the prevention of type 2 diabetes and cardiovascular risk factors in adults with intellectual disabilities (ID). Methods: We combined qualitative stakeholder interviews with evidence reviews to develop the intervention, guided by the MRC Framework and informed by intervention mapping and two existing diabetes prevention programmes. We conducted two pilot cycles drawing on additional stakeholder interviews to inform and refine the intervention. Results: The STOP Diabetes education programme employed a theoretical framework, using sound learning and behavioural principles and concrete kinaesthetic methods, to provide the grounding for innovative games and activities to promote health behaviour change in adults with ID. Qualitative data also suggested that two educators and one support person delivering a programme of one carer session followed by seven 2.5-h sessions over 7 weeks was acceptable to service users, carers and educators and appeared to benefit the participants. Conclusions: The STOP Diabetes education programme was successfully developed and is suitable for a definitive randomized controlled trial.

Pilot feasibility study examining a structured self-management diabetes education programme, DESMOND-ID, targeting HbA1c in adults with intellectual disabilities.

AIM: To report on the outcomes of a pilot feasibility study of a structured self-management diabetes education programme targeting HbA1c . METHODS: We conducted a two-arm, individually randomized, pilot superiority trial for adults with intellectual disability and Type 2 diabetes mellitus. A total of 66 adults with disabilities across the UK met the eligibility criteria. Of these, 39 agreed to participate and were randomly assigned to either the DESMOND-ID programme (n = 19) or a control group (n = 20). The programme consisted of seven weekly educational sessions. The primary outcome was HbA1c level, and secondary outcomes included BMI, diabetes illness perceptions, severity of diabetes, quality of life, and attendance rates. RESULTS: This study found that the DESMOND-ID programme was feasible to deliver. With reasonable adjustments, the participants could be recruited successfully, and could provide consent, complete the outcome measures, be randomized to the groups and attend most of the sessions, with minimal loss to follow-up. The fixed-effects model, the interaction between occasion (time) and condition, showed statistically significant results (0.05 level) for HbA1c ; however, the CI was large. CONCLUSION: This is the first published study to adapt and pilot a national structured self-management diabetes education programme for adults with intellectual disability. This study shows it is possible to identify, recruit, consent and randomize adults with intellectual disabilities to an intervention or control group. Internationally, the results of this pilot are promising, demonstrating that a multi-session education programme is acceptable and feasible to deliver. Its effectiveness should be further tested in an adequately powered trial.

Increasing capacity to deliver diabetes self-management education: results of the DESMOND lay educator non-randomized controlled equivalence trial.

AIM: To develop and test a format of delivery of diabetes self-management education by paired professional and lay educators. METHODS: We conducted an equivalence trial with non-randomized participant allocation to a Diabetes Education and Self Management for Ongoing and Newly Diagnosed Type 2 diabetes (DESMOND) course, delivered in the standard format by two trained healthcare professional educators (to the control group) or by one trained lay educator and one professional educator (to the intervention group). A total of 260 people with Type 2 diabetes diagnosed within the previous 12 months were referred for self-management education as part of routine care and attended either a control or intervention format DESMOND course. The primary outcome measure was change in illness coherence score (derived from the Diabetes Illness Perception Questionnaire-Revised) between baseline and 4 months after attending education sessions. Secondary outcome measures included change in HbA1c level. The trial was conducted in four primary care organizations across England and Scotland. RESULTS: The 95% CI for the between-group difference in positive change in coherence scores was within the pre-set limits of equivalence (difference = 0.22, 95% CI 1.07 to 1.52). Equivalent changes related to secondary outcome measures were also observed, including equivalent reductions in HbA1c levels. CONCLUSION: Diabetes education delivered jointly by a trained lay person and a healthcare professional educator with the same educator role can provide equivalent patient benefits. This could provide a method that increases capacity, maintains quality and is cost-effective, while increasing access to self-management education.

TGF-beta 1 uses distinct mechanisms to inhibit IFN-gamma expression in CD4+ T cells at priming and at recall: differential involvement of Stat4 and T-bet.

TGF-beta1 plays a critical role in restraining pathogenic Th1 autoimmune responses in vivo, but the mechanisms that mediate TGF-beta1's suppressive effects on CD4(+) T cell expression of IFN-gamma expression remain incompletely understood. To evaluate mechanisms by which TGF-beta1 inhibits IFN-gamma expression in CD4(+) T cells, we primed naive wild-type murine BALB/c CD4(+) T cells in vitro under Th1 development conditions in the presence or the absence of added TGF-beta1. We found that the presence of TGF-beta1 during priming of CD4(+) T cells suppressed both IFN-gamma expression during priming as well as the development of Th1 effector cells expressing IFN-gamma at a recall stimulation. TGF-beta1 inhibited the development of IFN-gamma-expressing cells in a dose-dependent fashion and in the absence of APC, indicating that TGF-beta1 can inhibit Th1 development by acting directly on the CD4(+) T cell. During priming, TGF-beta1 strongly inhibited the expression of both T-bet (T box expressed in T cells) and Stat4. We evaluated the importance of these two molecules in the suppression of IFN-gamma expression at the two phases of Th1 responses. Enforced expression of T-bet by retrovirus prevented TGF-beta1's inhibition of Th1 development, but did not prevent TGF-beta1's inhibition of IFN-gamma expression at priming. Conversely, enforced expression of Stat4 partly prevented TGF-beta1's inhibition of IFN-gamma expression during priming, but did not prevent TGF-beta1's inhibition of Th1 development. These data show that TGF-beta1 uses distinct mechanisms to inhibit IFN-gamma expression in CD4(+) T cells at priming and at recall.