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Mellor D.D.,University of Hull | Kilpatrick E.S.,Chemical Pathology | Beckett S.,Sporomex
Diabetic Medicine

Aim To examine the effects of chocolate on lipid profiles, weight and glycaemic control in individuals with Type 2 diabetes.Methods Twelve individuals with Type 2 diabetes on stable medication were enrolled in a randomized, placebo-controlled double-blind crossover study. Subjects were randomized to 45 g chocolate with or without a high polyphenol content for 8-weeks and then crossed over after a 4-week washout period. Changes in weight, glycaemic control, lipid profile and high-sensitivity C-reactive protein were measured at the beginning and at the end of each intervention.Results HDL cholesterol increased significantly with high polyphenol chocolate (1.16 ± 0.08 vs. 1.26 ± 0.08 mmol/l, P = 0.05) with a decrease in the total cholesterol: HDL ratio (4.4 ± 0.4 vs. 4.1 ± 0.4 mmol/l, P = 0.04). No changes were seen with the low polyphenol chocolate in any parameters. Over the course of 16 weeks of daily chocolate consumption neither weight nor glycaemic control altered from baseline.Conclusion High polyphenol chocolate is effective in improving the atherosclerotic cholesterol profile in patients with diabetes by increasing HDL cholesterol and improving the cholesterol:HDL ratio without affecting weight, inflammatory markers, insulin resistance or glycaemic control. © 2010 The Authors. Diabetic Medicine © 2010 Diabetes UK. Source

Martin S.A.,University of Adelaide | Atlantis E.,University of Western Sydney | Lange K.,University of Adelaide | Taylor A.W.,University of Adelaide | And 2 more authors.
Journal of Sexual Medicine

Introduction: The progress and determinants of sexual dysfunction in middle-aged and elderly men remain unclear. Aim: To describe the incidence or remission and biopsychosocial predictors of erectile dysfunction (ED) and low sexual desire (SD). Main Outcome Measures: Erectile function (International Index of Erectile Function) and sexual desire (Sexual Desire Inventory 2) were assessed at follow-up. Sociodemographic, lifestyle, and health-related factors were examined in multivariate models of ED and low SD. Methods: Data were collected from 810 randomly selected men residing in northern and western Adelaide, Australia, and aged 35-80 years at baseline, who made clinic visits 5 years apart. Results: At baseline, 23.2% (n=123) of men had ED. ED incidence and remission were observed in 31.7% (n=179) and 29.0% (n=71) of eligible men, respectively. At baseline, 19.2% (n=165) had low solitary sexual desire, and 6.0% (n=50) had low dyadic sexual desire; incidence of low sexual desire occurred in 17.6% (n=83) (solitary) and 8.3% (n=51) (dyadic), while remission occurred in 15.4% (n=68) (solitary) and 22.6% (n=40) (dyadic) of men. In the final regression models, predictors of incident ED were higher age, lower income, higher abdominal fat mass, low alcohol intake, higher risk of obstructive sleep apnea (OSA) risk, voiding lower urinary tract symptoms (LUTS), depression, and diabetes. Predictors of ED remission were lower age, current employment, and absence of voiding LUTS, angina, diabetes, and dyslipidemia. Predictors of low dyadic SD incidence included higher age, never having been married, widowhood, being unemployed, being retired, insufficient physical activity, and low alcohol intake. Predictors of low dyadic SD remission were being married, not being widowed, higher income, lower abdominal fat mass, lower OSA risk, and higher plasma testosterone. Predictors of low solitary SD included never having been married, being unemployed, low alcohol intake, lower testosterone, storage LUTS, and hypertension. Predictors of low solitary SD remission were being married, being employed, higher income, higher physical activity, moderate alcohol intake, and depression. Conclusions: Sexual dysfunction in aging men is a dynamic disorder whose incidence and remission are predicted by a range of modifiable risk factors. © 2014 International Society for Sexual Medicine. Source

Anderson P.H.,University of South Australia | Lam N.N.,Chemical Pathology | Turner A.G.,University of South Australia | Davey R.A.,University of Melbourne | And 3 more authors.
Journal of Steroid Biochemistry and Molecular Biology

A current controversial question related to vitamin D supplementation is what level of serum 25- hydroxyvitamin D3 (25(OH)D3) is required to reduce the incidence of osteoporotic fractures. The reasoning behind vitamin D supplementation has been mostly derived from the role of vitamin D to promote intestinal calcium absorption and reduce bone resorption. While minimum 25(OH)D3 levels of 20 nmol/L are required for sufficient intestinal calcium absorption to prevent osteomalacia, the mechanistic details of how higher 25(OH)D3 levels, well beyond that required for optimal calcium absorption, are able to prevent fractures and increase bone mineral density is unclear. Substantial evidence has arisen over the past decade that conversion of 25(OH)D3 to 1,25(OH)2D3 via the 1-alpha hydroxylase (CYP27B1) enzyme in osteoblasts, osteocytes, chondrocytes and osteoclasts regulates processes such as cell proliferation, maturation and mineralization as well as bone resorption, which are all dependent on the presence the of the vitamin D receptor (VDR). We and others have also shown that increased vitamin D activity in mature osteoblasts by increasing levels of VDR or CYP27B1 leads to improved bone mineral volume using two separate transgenic mouse models. While questions remain regarding activities of vitamin D in bone to influence the anabolic and catabolic processes, the biological importance of vitamin D activity within the bone is unquestioned. However, a clearer understanding of the varied mechanisms by which vitamin D directly and indirectly influences mineral bone status are required to support evidence-based recommendations for vitamin D supplementation to reduce the risk of fractures. Copyright © 2012 Published by Elsevier Ltd. All rights reserved. Source

Punyadeera C.,University of Queensland | Dimeski G.,Chemical Pathology | Kostner K.,Materials Hospital | Beyerlein P.,Wildau University of Applied Sciences | Cooper-White J.,University of Queensland
Journal of Immunological Methods

Background: Cardiovascular disease is the leading cause of death in the world. Human C-reactive protein (CRP) has been used in the risk assessment of coronary events. Human saliva mirrors the body's health and well-being and is non-invasive, easy to collect and ideal for third world countries as well as for large patient screening. The aim was to establish a saliva CRP reference range and to demonstrate the clinical utility of salivary CRP levels in assessing the coronary events in a primary health care setting. Methods: We have used a homogeneous bead based assay to detect CRP levels in human saliva. We have developed a rapid 15. min (vs 90. min), sequential, one-step assay to detect CRP in saliva. Saliva was collected from healthy volunteers (n = 55, ages 20-70. years) as well as from cardiac patients (n = 28, ages 43-86. years). Results: The assay incubation time was optimised from 90. min to 15. min and generated a positive correlation (n = 29, range 10-2189. pg/mL, r2 = 0.94; Passing Bablok slope 0.885, Intercept 0, p > 0.10), meaning we could decrease the incubation time and produce equivalent results with confidence. The mean CRP level in the saliva of healthy human volunteers was 285. pg/mL and in cardiac patients was 1680. pg/mL (p < 0.01). Analysis of CRP concentrations in paired serum and saliva samples from cardiac patients gave a positive correlation (r2 = 0.84, p < 0.001) and the salivary CRP concentration capable of distinguishing healthy from diseased patients. Conclusions: The results suggest that this minimally invasive, rapid and sensitive assay will be useful in large patient screening studies for risk assessment of coronary events. © 2011 Elsevier B.V. Source

Tormey W.P.,Chemical Pathology | Tormey W.P.,University of Ulster
Medicine, Science and the Law

A 37-year-old, one-pack-per-day tobacco smoker collapsed and died at home. At autopsy, he had an occluded left anterior descending coronary artery. δ9-Tetrahydrocannabinol-carboxylic acid was found in his urine but no cannabinoids were detected in his blood. Misadventure was the inquest verdict on the basis of the urinary cannabis, with acute myocardial infarction as the primary cause and cannabis as the secondary cause of death. Such a conclusion is a misinterpretation of the evidence when the time duration for cannabis as a trigger for myocardial infarction is at most two hours. The absence of cannabis in the blood likely places the time since inhalation at more than two hours. The role of tobacco smoking as a trigger was ignored. Cotinine, the biochemical marker of tobacco smoke, should be added to the standard toxicological screen in the guidelines on autopsy practice of the Royal College of Pathologists. Source

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