Counting on commitment; the quality of primary care-led diabetes management in a system with minimal incentives

Background

The aim of the present study was to assess the performance of three primary care-led initiatives providing structured care to patients with Type 2 diabetes in Ireland, a country with minimal incentives to promote the quality of care.

Methods

Data, from three primary care initiatives, were available for 3010 adult patients with Type 2 diabetes. Results were benchmarked against the national guidelines for the management of Type 2 diabetes in the community and results from the National Diabetes Audit (NDA) for England (2008/2009) and the Scottish Diabetes Survey (2009).

Results

The recording of clinical processes of care was similar to results in the UK however the recording of lifestyle factors was markedly lower. Recording of HbA1c, blood pressure and lipids exceeded 85%. Recording of retinopathy screening (71%) was also comparable to England (77%) and Scotland (90%). Only 63% of patients had smoking status recorded compared to 99% in Scotland while 70% had BMI recorded compared to 89% in England. A similar proportion of patients in this initiative and the UK achieved clinical targets. Thirty-five percent of patients achieved a target HbA1c of < 6.5% (< 48 mmol/mol) compared to 25% in England. Applying the NICE target for blood pressure (≤ 140/80 mmHg), 54% of patients reached this target comparable to 60% in England. Slightly less patients were categorised as obese (> 30 kg/m²) in Ireland (50%, n = 1060) compared to Scotland (54%).

Conclusions

This study has demonstrated what can be achieved by proactive and interested health professionals in the absence of national infrastructure to support high quality diabetes care. The quality of primary care-led diabetes management in the three initiatives studied appears broadly consistent with results from the UK with the exception of recording lifestyle factors. The challenge facing health systems is to establish quality assurance a responsibility for all health care professionals rather than the subject of special interest for a few.

     

Skeletal muscle apoptotic response to physical activity: potential mechanisms for protection

Apoptosis is a highly conserved type of cell death that plays a critical role in tissue homeostasis and disease-associated processes. Skeletal muscle is unique with respect to apoptotic processes, given its multinucleated morphology and its apoptosis-associated differences related to muscle and (or) fiber type as well as mitochondrial content and (or) subtype. Elevated apoptotic signaling has been reported in skeletal muscle during aging, stress-induced states, and disease; a phenomenon that plays a role in muscle dysfunction, degradation, and atrophy. Exercise is a strong physiological stimulus that can influence a number of extracellular and intracellular signaling pathways, which may directly or indirectly influence apoptotic processes in skeletal muscle. In general, acute strenuous and eccentric exercise are associated with a proapoptotic phenotype and increased DNA fragmentation (a hallmark of apoptosis), whereas regular exercise training or activity is associated with an antiapoptotic environment and reduced DNA fragmentation in skeletal muscle. Interestingly, the protective effect of regular activity on skeletal muscle apoptotic processes has been observed in healthy, aged, stress-induced, and diseased rodent models. Several mechanisms for this protective response have been proposed, including altered anti- and proapoptotic protein expression, increased mitochondrial biogenesis and improved mitochondrial function, and reduced reactive oxygen species generation and (or) enhanced antioxidant status. Given the current literature, we propose that regular physical activity may represent an effective strategy to decrease apoptotic signaling, and possibly muscle wasting and dysfunction, during aging and disease.     

Explained and unexplained racial and regional inequality in obesity prevalence in the United States

ABSTRACT

Objective: There are substantial racial and regional disparities in obesity prevalence in the United States. This study partitioned the mean Body Mass Index (BMI) and obesity prevalence rate gaps between non-Hispanic blacks and non-Hispanic whites into the portion attributable to observable obesity risk factors and the remaining portion attributable to unobservable factors at the national and the state levels in the United States (U.S.) in 2010.

Design: This study used a simulated micro-population dataset combining common information from the Behavioral Risk Factor Surveillance System and the U.S. Census data to obtain a reliable, large sample representing the adult populations at the national and state levels. It then applied a reweighting decomposition method to decompose the black-white mean BMI and obesity prevalence disparities at the national and state levels into the portion attributable to the differences in distribution of observable obesity risk factors and the remaining portion unexplainable with risk factors.

Results: We found that the observable differences in distribution of known obesity risk factors explain 18.5% of the mean BMI difference and 20.6% of obesity prevalence disparities between non-Hispanic blacks and non-Hispanic whites. There were substantial variations in how much the differences in distribution of known obesity risk factors can explain black-white gaps in mean BMI (?67.7% to 833.6%) and obesity prevalence (?278.5% to 340.3%) at the state level.

Conclusion: The results from this study demonstrate that known obesity risk factors explain a small proportion of the racial, ethnic and between-state disparities in obesity prevalence in the United States. Future etiologic studies are required to further understand the causal factors underlying obesity and racial, ethnic and geographic disparities.