High-intensity interval training for reducing blood pressure: a randomized trial vs. moderate-intensity continuous training in males with overweight or obesity

The optimal exercise-training characteristics for reducing blood pressure (BP) are unclear. We investigated the effects of 6-weeks of high-intensity interval training (HIIT) or moderate-intensity continuous training (MICT) on BP and aortic stiffness in males with overweight or obesity. Twenty-eight participants (18–45 years; BMI: 25–35 kg/m2) performed stationary cycling three times per week for 6 weeks. Participants were randomly allocated (unblinded) to work-matched HIIT (N = 16; 10 × 1-min intervals at 90–100% peak workload) or MICT (N = 12; 30 min at 65–75% peak heart rate). Central (aortic) and peripheral (brachial) BP and aortic stiffness was assessed before and after training. There were no significant group × time interactions for any BP measure (all p > 0.21). HIIT induced moderate reductions in central (systolic/diastolic ∆: −4.6/−3.5 mmHg, effect size d = −0.51/−0.40) and peripheral BP (−5.2/−4 mmHg, d = −0.45/−0.47). MICT induced moderate reductions in diastolic BP only (peripheral: −3.4 mmHg, d = −0.57; central: −3 mmHg, d = −0.50). The magnitude of improvement in BP was strongly negatively correlated with baseline BP (r = −0.66 to −0.78), with stronger correlations observed for HIIT (r = −0.73 to −0.88) compared with MICT (r = −0.43 to −0.61). HIIT was effective for reducing BP (~3–5 mmHg) in the overweight to obese cohort. Exercise training induced positive changes in central (aortic) BP. The BP-lowering effects of exercise training are more prominent in those with higher baseline BP, with stronger correlation in HIIT than MICT

The effect of high-intensity interval training and moderate-intensity continuous training on aerobic fitness and body composition in males with overweight or obesity: A randomized trial

The optimal exercise training characteristics for improving body composition in individuals with obesity are not clear. This study assessed the effects of 6-weeks of high-intensity interval training (HIIT) or moderate-intensity continuous training (MICT) on aerobic fitness and body composition in males with overweight or obesity. Twenty-eight participants (18–45 years; BMI: 25–35 kg/m2) performed stationary cycling 3 times per week for 6 weeks. Participants were randomly allocated to work-matched HIIT (N = 16) (10 × 1-min intervals at ~90% peak heart rate) or MICT (N = 12) (30 min at 65–75% peak heart rate). Maximal aerobic capacity (VO2peak) and body composition were assessed before and after 6-week training. Both HIIT and MICT induced moderate increases in aerobic fitness (Δ% VO2peak: HIIT 9 ± 8%, ES = 0.42; MICT: 7 ± 13%, ES = 0.32) and work capacity (Δ% peak workload: HIIT 13 ± 10%, ES = 0.69: MICT 17 ± 15%, ES = 0.76), but these changes did not differ significantly between the groups (all p > 0.16). The effects of HIIT or MICT on body composition outcomes were negligible to small across whole-body and all regional-specific sites (all effect sizes ES = −0.19 to 0.38) and did not differ significantly between the groups (all p > 0.21). Short-term (6-weeks) cycling training did not improve body composition in males with overweight or obesity. Improvements in aerobic fitness were comparable between work-matched HIIT and MICT

Modeling the cost of influenza: the impact of missing costs of unreported complications and sick leave

Background Estimating the economic impact of influenza is complicated because the disease may have non-specific symptoms, and many patients with influenza are registered with other diagnoses. Furthermore, in some countries like Norway, employees can be on paid sick leave for a specified number of days without a doctor's certificate ("self-reported sick leave") and these sick leaves are not registered. Both problems result in gaps in the existing literature: costs associated with influenza-related illness and self-reported sick leave are rarely included. The aim of this study was to improve estimates of total influenza-related health-care costs and productivity losses by estimating these missing costs. Methods Using Norwegian data, the weekly numbers of influenza-attributable hospital admissions and certified sick leaves registered with other diagnoses were estimated from influenza-like illness surveillance data using quasi-Poisson regression. The number of self-reported sick leaves was estimated using a Monte-Carlo simulation model of illness recovery curves based on the number of certified sick leaves. A probabilistic sensitivity analysis was conducted on the economic outcomes. Results During the 1998/99 through 2005/06 influenza seasons, the models estimated an annual average of 2700 excess influenza-associated hospitalizations in Norway, of which 16% were registered as influenza, 51% as pneumonia and 33% were registered with other diagnoses. The direct cost of seasonal influenza totaled US$22 million annually, including costs of pharmaceuticals and outpatient services. The annual average number of working days lost was predicted at 793 000, resulting in an estimated productivity loss of US$231 million. Self-reported sick leave accounted for approximately one-third of the total indirect cost. During a pandemic, the total cost could rise to over US$800 million. Conclusions Influenza places a considerable burden on patients and society with indirect costs greatly exceeding direct costs. The cost of influenza-attributable complications and the cost of self-reported sick leave represent a considerable part of the economic burden of influenza

Rates and predictors of risk of stroke and its subtypes in diabetes: a prospective observational study

Background Small vessel disease is reported to be a more common cause of ischaemic stroke in people with diabetes than in others. However, population based studies have shown no difference between those with and those without diabetes in the subtypes of stroke. We determined the rates and predictors of risk of stroke and its subtypes in the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial. Methods 9795 patients aged 50–75 years with type 2 diabetes were followed up for a median of 5 years. Annual rates were derived by the Kaplan–Meier method and independent predictors of risk by Cox proportional hazards regression analyses. Results The annual rate of stroke was 6.7 per 1000 person years; 82% were ischaemic and caused by small artery disease (36%), large artery disease (17%) and embolism from the heart (13%); 10% were haemorrhagic. Among the strongest baseline predictors of ischaemic or unknown stroke were age (60–65 years, HR 1.98; >65 years, HR 2.35) and a history of stroke or transient ischaemic attack (TIA) (HR 2.06). Other independent baseline predictors were male sex, smoking, history of hypertension, ischaemic heart disease, nephropathy, systolic blood pressure and blood low density lipoprotein (LDL) cholesterol, HbA1c and fibrinogen. A history of peripheral vascular disease, low high density lipoprotein, age and history of hypertension were associated with large artery ischaemic stroke. A history of diabetic retinopathy, LDL cholesterol, male sex, systolic blood pressure, smoking, diabetes duration and a history of stroke or TIA were associated with small artery ischaemic stroke. Conclusions Older people with a history of stroke were at highest risk of stroke, but the prognosis and prognostic factors of subtypes were heterogeneous. The results will help clinicians quantify the absolute risk of stroke and its subtypes for typical diabetes patients.FIELD trial sponsored by Laboratoires Fournier SA, Dijon, France (part of Abbott

Pathway to the PiezoElectronic Transduction Logic Device

The information age challenges computer technology to process an exponentially increasing computational load on a limited energy budget - a requirement that demands an exponential reduction in energy per operation. In digital logic circuits, the switching energy of present FET devices is intimately connected with the switching voltage, and can no longer be lowered sufficiently, limiting the ability of current technology to address the challenge. Quantum computing offers a leap forward in capability, but a clear advantage requires algorithms presently developed for only a small set of applications. Therefore, a new, general purpose, classical technology based on a different paradigm is needed to meet the ever increasing demand for data processing.Comment: in Nano Letters (2015

Associations with sight-threatening diabetic macular oedema among Indigenous adults with type 2 diabetes attending an Indigenous primary care clinic in remote Australia: a Centre of Research Excellence in Diabetic Retinopathy and Telehealth Eye and Associated Medical Services Network study

Objective To identify factors associated with sight-threatening diabetic macular oedema (STDM) in Indigenous Australians attending an Indigenous primary care clinic in remote Australia. Methods and analysis A cross-sectional study design of retinopathy screening data and routinely-collected clinical data among 236 adult Indigenous participants with type 2 diabetes (35.6% men) set in one Indigenous primary care clinic in remote Australia. The primary outcome variable was STDM assessed from retinal images. Results Age (median (range)) was 48 (21–86) years, and known diabetes duration (median (range)) was 8.0 (0–24) years. Prevalence of STDM was high (14.8%) and similar in men and women. STDM was associated with longer diabetes duration (11.7 vs 7.9 years, respectively; p300 mg/mmol) (20.6 vs 5.7%, respectively; p=0.014) and chronic kidney disease (25.7 vs 12.2%, respectively; p=0.035). Some clinical factors differed by sex: anaemia was more prevalent in women. A higher proportion of men were smokers, prescribed statins and had increased albuminuria. Men had higher blood pressure, but lower glycated Haemoglobin A1c (HbA1c) levels and body mass index, than women. Conclusion STDM prevalence was high and similar in men and women. Markers of renal impairment and longer diabetes duration were associated with STDM in this Indigenous primary care population. Embedded teleretinal screening, known diabetes duration-based risk stratification and targeted interventions may lower the prevalence of STDM in remote Indigenous primary care services.Trial registration number Australia and New Zealand Clinical Trials Register: ACTRN 12616000370404.Laima Brazioni, Anthony Keech, Christopher Ryan, Alex Brown, David O'Neal, John Boffa, Sven-Erik Bursell, Alicia Jenkin

Effects of fenofibrate on renal function in patients with type 2 diabetes mellitus: the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) Study

Abstract Aims/hypothesis Fenofibrate caused an acute, sustained plasma creatinine increase in the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) and Action to Control Cardiovascular Risk in Diabetes (ACCORD) studies. We assessed fenofibrate’s renal effects in a FIELD washout sub-study. Methods Type 2 diabetic patients (n=9795) aged 50 to 75 years were randomly assigned to fenofibrate (n=4895) or placebo (n=4900) for 5 years, after 6 weeks fenofibrate run-in. Albuminuria (urinary albumin:creatinine ratio) measured at baseline, year 2 and close-out) and estimated GFR, measured 4 to 6 monthly according to the Modification of Diet in Renal Disease study, were pre-specified endpoints. Plasma creatinine was re-measured 8 weeks after treatment cessation at close-out (washout sub-study, n=661). Analysis was by intention-to-treat. Results During fenofibrate run-in, plasma creatinine increased by 10.0 µmol/l (p<0.001), but quickly reversed on placebo assignment. It remained higher on fenofibrate than on placebo, but the chronic rise was slower (1.62 µmol/l vs 1.89 µmol/l annually, p=0.01), with less estimated GFR loss (1.19 vs 2.03 ml min−1 1.73 m−2 annually, p<0.001). After washout, estimated GFR had fallen less from baseline on fenofibrate (1.9 ml min−1 1.73 m−2, p=0.065) than on placebo (6.9 ml min−1 1.73 m−2, p<0.001), sparing 5.0 ml min−1 1.73 m−2 (95% CI 2.3-7.7, p<0.001). Greater preservation of estimated GFR with fenofibrate was observed during greater reduction over the active run-in period (pre-randomisation) of triacylglycerol (n=186 vs 170) and baseline hypertriacylglycerolaemia (n=89 vs 80) alone, or combined with low HDL-cholesterol (n=71 vs 60). Fenofibrate reduced urine albumin concentrations and hence albumin:creatinine ratio by 24% vs 12% (p<0.001; mean difference 14% [95% CI 9-18]; p<0.001), with 14% less progression and 18% more albuminuria regression (p<0.001) than in participants on placebo. End-stage renal event frequency was similar (n=21 vs 26, p=0.48). Conclusions/interpretation Fenofibrate reduced albuminuria and slowed estimated GFR loss over 5 years, despite initially and reversibly increasing plasma creatinine. Fenofibrate may delay albuminuria and GFR impairment in type 2 diabetes patients. Confirmatory studies are merited. Trial registration: ISRCTN64783481 Funding: The study was funded by grants from Laboratoires Fournier, Dijon, France (now part of Solvay and Abbott Pharmaceuticals) and the NHMRC of Australia.Laboratoires Fournier, Dijon, France (now part of Solvay and Abbott Pharmaceuticals

Lack of effect of lowering LDL cholesterol on cancer: meta-analysis of individual data from 175,000 people in 27 randomised trials of statin therapy

&lt;p&gt;Background: Statin therapy reduces the risk of occlusive vascular events, but uncertainty remains about potential effects on cancer. We sought to provide a detailed assessment of any effects on cancer of lowering LDL cholesterol (LDL-C) with a statin using individual patient records from 175,000 patients in 27 large-scale statin trials.&lt;/p&gt; &lt;p&gt;Methods and Findings: Individual records of 134,537 participants in 22 randomised trials of statin versus control (median duration 4.8 years) and 39,612 participants in 5 trials of more intensive versus less intensive statin therapy (median duration 5.1 years) were obtained. Reducing LDL-C with a statin for about 5 years had no effect on newly diagnosed cancer or on death from such cancers in either the trials of statin versus control (cancer incidence: 3755 [1.4% per year [py]] versus 3738 [1.4% py], RR 1.00 [95% CI 0.96-1.05]; cancer mortality: 1365 [0.5% py] versus 1358 [0.5% py], RR 1.00 [95% CI 0.93–1.08]) or in the trials of more versus less statin (cancer incidence: 1466 [1.6% py] vs 1472 [1.6% py], RR 1.00 [95% CI 0.93–1.07]; cancer mortality: 447 [0.5% py] versus 481 [0.5% py], RR 0.93 [95% CI 0.82–1.06]). Moreover, there was no evidence of any effect of reducing LDL-C with statin therapy on cancer incidence or mortality at any of 23 individual categories of sites, with increasing years of treatment, for any individual statin, or in any given subgroup. In particular, among individuals with low baseline LDL-C (&#60;2 mmol/L), there was no evidence that further LDL-C reduction (from about 1.7 to 1.3 mmol/L) increased cancer risk (381 [1.6% py] versus 408 [1.7% py]; RR 0.92 [99% CI 0.76–1.10]).&lt;/p&gt; &lt;p&gt;Conclusions: In 27 randomised trials, a median of five years of statin therapy had no effect on the incidence of, or mortality from, any type of cancer (or the aggregate of all cancer).&lt;/p&gt