13 research outputs found

    Sitting Time and Body Mass Index in Diabetics and Pre-Diabetics Willing to Participate in a Lifestyle Intervention

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    This cross-sectional study examined the relationship between Body Mass Index (BMI), total sitting time and total physical activity time in a generally overweight or obese population of type 2 diabetics or pre-diabetics willing to participate in a lifestyle intervention [n = 221, 55.1% male, mean age (SD) 62.0 (9.9), mean BMI (SD) 31.4 (5.0)]. In addition, we aimed to identify demographic and psychosocial associates of the motivation to become more physically active. The measurement instrument was a self-report questionnaire. Results showed that total sitting time was more closely related to BMI than total physical activity time. Subjects with a higher weight status were more sedentary, but they were also more motivated to be physically active. On the other hand, their self-efficacy to be physically active was lower than subjects with a lower weight status. Lifestyle interventions to decrease the risk of obesity and type 2 diabetes should aim not only at increasing total physical activity time, but also at reducing the total sitting time. Despite generally high levels of motivation among these obese participants, intervention designers and intermediaries should be aware of their low level of self-efficacy towards being physically active

    Acute effects of caffeine and cigarette smoking on ventricular long-axis function in healthy subjects

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    <p>Abstract</p> <p>Background</p> <p>Few data exist regarding the direct effects of caffeine and smoking on cardiac function. We sought to explore the acute effects of caffeine assumption, cigarette smoking, or both on left ventricular (LV) and right ventricular (RV) function in a population of young normal subjects.</p> <p>Methods</p> <p>Forty-five healthy subjects aged 25 ± 2 years underwent echocardiography. Fifteen of them were non-smokers and habitual coffee consumers (group 1), 15 were smokers and not habitual coffee consumers (group 2), and 15 were smokers and habitual coffee consumers (group 3). Peak systolic (S<sub>a</sub>), early diastolic E<sub>a</sub>, and late diastolic (A<sub>a</sub>) velocity of mitral annulus were measured by pulsed Tissue Doppler, and left atrioventricular plane displacement was determined by M-mode. Tricuspid annular velocities and systolic excursion (TAPSE) were also determined. Measurements were performed at baseline and after oral assumption of caffeine 100 mg in group 1, one cigarette smoking in group 2, and both in group 3.</p> <p>Results</p> <p>No changes in ventricular function were observed in group 1 after caffeine administration. In group 2, cigarette smoking yielded an acute increase in mitral A<sub>a </sub>(+12.1%, p = 0.0026), tricuspid S<sub>a </sub>(+9.8%, p = 0.012) and TAPSE (+7.9%, p = 0.017), and a decrease in the mitral E<sub>a</sub>/A<sub>a </sub>ratio (-8.5%, p = 0.0084). Sequential caffeine assumption and cigarette smoking in group 3 was associated with an acute increase in mitral A<sub>a </sub>(+13.0%, p = 0.015) and tricuspid A<sub>a </sub>(+11.6%, p < 0.0001) and a reduction in mitral E<sub>a</sub>/A<sub>a </sub>ratio (-8.5%, p = 0.0084) tricuspid E<sub>a </sub>(-6.6%, p = 0.048) and tricuspid E<sub>a</sub>/A<sub>a </sub>ratio (-9.6%, p = 0.0003). In a two-way ANOVA model controlling for hemodynamic confounding factors, changes in the overall population remained significant for mitral A<sub>a </sub>and E<sub>a</sub>/A<sub>a </sub>ratio, and for tricuspid A<sub>a </sub>and E<sub>a</sub>/A<sub>a </sub>ratio.</p> <p>Conclusion</p> <p>In young healthy subjects, one cigarette smoking is associated to an acute impairment in LV diastolic function and a hyperdynamic RV systolic response. Caffeine assumption alone does not exert any acute effect on ventricular long-axis function, but potentiates the negative effect of cigarette smoking by abolishing RV supernormal response and leading to a simultaneous impairment in both LV and RV diastolic function.</p

    A Nested Case-Control Study of Intrauterine Exposure to Persistent Organochlorine Pollutants in Relation to Risk of Type 1 Diabetes

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    BACKGROUND: The incidence of type 1 diabetes in Europe is increasing at a rate of about 3% per year and there is also an increasing incidence throughout the world. Type 1 diabetes is a complex disease caused by multiple genetic and environmental factors. Persistent organochlorine pollutants (POPs) have been suggested as a triggering factor for developing childhood type 1 diabetes. The aim of this case-control study was to assess possible impacts of in utero exposure to POPs on type 1 diabetes. METHODOLOGY/ PRINCIPAL FINDINGS: The study was performed as a case-control study within a biobank in Malmö, a city located in the Southern part of Sweden. The study included 150 cases (children who had their diagnosis mostly before 18 years of age) and 150 controls, matched for gender and day of birth. 2,2',4,4',5,5'-hexachlorobiphenyl (PCB-153) and the major DDT metabolite 1,1-dichloro-2,2-bis (p-chlorophenyl)-ethylene (p,p'-DDE) were used as a biomarkers for POP exposure. When comparing the quartile with the highest maternal serum concentrations of PCB-153 with the other quartiles, an odds ratio (OR) of 0.73 (95% confidence interval [CI] 0.42, 1.27) was obtained. Similar results was obtained for p,p'-DDE (OR 0.56, 95% CI 0.29, 1.08). CONCLUSIONS: The hypothesis that in utero exposure to POPs will trigger the risk for developing type 1 diabetes was not supported by the results. The risk estimates did, although not statistically significant, go in the opposite direction. However, it is not reasonable to believe that exposure to POPs should protect against type 1 diabetes
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