Wednesday, October 20, 2010

Long-term Effects of a Lifestyle Intervention on Weight and Cardiovascular Risk Factors in Individuals With Type 2 Diabetes Mellitus

Intensive lifestyle intervention bagi penderita diabetes tipe 2 dalam jangka panjang dapat menurunkan berat badan, memperbaiki tingkat fitness, memperbaiki kontrol glikemik, dan menurunkan risiko kardiovaskuler

Arch Intern Med 170(17):1566-1575, 27 September 2010 © 2010 to the American Medical Association
Long-term Effects of a Lifestyle Intervention on Weight and Cardiovascular Risk Factors in Individuals With Type 2 Diabetes Mellitus-Four- Year Results of the Look AHEAD Trial. The Look AHEAD Research Group.

Background  Lifestyle interventions produce short-term improvements in glycemia and cardiovascular disease (CVD) riskfactors in individuals with type 2 diabetes mellitus, but no long-term data are available. We examined the effects of lifestyle intervention on changes in weight, fitness, and CVD risk factors during a 4-year study.
Methods  The Look AHEAD (Action for Health in Diabetes) trial is a multicenter randomized clinical trial comparing theeffects of an intensive lifestyle intervention (ILI) and diabetes support and education (DSE; the control group) on the incidence of major CVD events in 5145 overweight or obese individuals (59.5% female; mean age, 58.7 years) with type 2 diabetes mellitus. More than 93% of participants provided outcomes data at each annual assessment.
Results  Averaged across 4 years, ILI participants had a greater percentage of weight loss than DSE participants (–6.15% vs –0.88%; P < .001) and greater improvements in treadmill fitness (12.74% vs 1.96%; P < .001), hemoglobin A1clevel (–0.36% vs –0.09%; P < .001), systolic (–5.33 vs –2.97 mm Hg; P < .001) and diastolic (–2.92 vs –2.48 mm Hg;P = .01) blood pressure, and levels of high-density lipoprotein cholesterol (3.67 vs 1.97 mg/dL; P < .001) and triglycerides (–25.56 vs –19.75 mg/dL; P < .001). Reductions in low-density lipoprotein cholesterol levels were greater in DSE than ILI participants (–11.27 vs –12.84 mg/dL; P = .009) owing to greater use of medications to lower lipid levels in the DSE group. At 4 years, ILI participants maintained greater improvements than DSE participants in weight, fitness, hemoglobin A1c levels, systolic blood pressure, and high-density lipoprotein cholesterol levels.
Conclusions  Intensive lifestyle intervention can produce sustained weight loss and improvements in fitness, glycemiccontrol, and CVD risk factors in individuals with type 2 diabetes. Whether these differences in risk factors translate to reduction in CVD events will ultimately be addressed by the Look AHEAD trial.

Friday, October 15, 2010

Alcohol and Acute Ischemic Stroke Onset

Sehabis minum alkohol risiko stroke meningkat.

 
Stroke. 2010;41:1845.© 2010 American Heart Association, Inc.

Original Contributions;Clinical Science

Alcohol and Acute Ischemic Stroke Onset
The Stroke Onset Study
Elizabeth Mostofsky, MPH; Mary R. Burger, MD; Gottfried Schlaug, MD, PhD; Kenneth J. Mukamal, MD, MPH;Wayne D. Rosamond, PhD Murray A. Mittleman, MD, DrPH

From the Cardiovascular Epidemiology Research Unit (E.M., K.J.M., M.A.M.), Department of Medicine, Department of Neurology (G.S.), and the Division of General Medicine & Primary Care (K.J.M.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Mass; the Department of Epidemiology (E.M., M.A.M.), Harvard School of Public Health, Boston, Mass.; Cincinnati Children's Hospital Medical Center Heart Institute (M.R.B.), Cincinnati, Ohio; and the Department of Epidemiology (W.D.R.), University of North Carolina School of Public Health, Chapel Hill, NC.
Abstract
Background and Purpose— Previous research suggests that regular heavy alcohol consumption increases the risk for ischemic stroke, whereas frequent light to moderate alcohol intake may decrease the risk. However, the risk of ischemic stroke associated with transient exposure to alcohol remains unclear. In this study, we used a case–crossover approach to test the hypothesis that alcohol consumption affects the acute risk of ischemic stroke, to determine the length of time between alcohol intake and the onset of symptoms (induction time), and to examine whether the risk varies by the type of alcohol.
Methods— In this multicenter study, we interviewed 390 patients (209 men, 181 women) between January 2001 and November 2006 (median 3 days after stroke). Alcohol consumption in the hour before stroke symptoms was compared with its expected frequency based on the usual frequency of alcohol consumption over the prior year.
Results— Of the 390 patients, 248 (64%) reported alcohol consumption in the prior year, 104 within 24 hours and 14 within 1 hour of stroke onset. The relative risk of stroke in the hour after consuming alcohol was 2.3 (95% CI, 1.4 to 4.0; P=0.002). The relative risks were similar for different types of alcoholicbeverages and when the sample was restricted to those who were not simultaneously exposed to other potential triggers.
Conclusions— The risk of stroke onset is transiently elevated in the hour after alcohol ingestion.

Monday, October 11, 2010

Homocysteine-Lowering by B Vitamins Slows the Rate of Accelerated Brain Atrophy in Mild Cognitive Impairment

Suplemen vitamin B6, B12 dan asam folat akan menurunkan kadar homosistein. Penurunan kadar homosistein akan memperlambat atrofi otak, sehingga menjaga fungsi kognitif pada usia lanjut. Apakah suplemen ini dapat juga mencegah Alzheimer?

Homocysteine-Lowering by B Vitamins Slows the Rate of Accelerated Brain Atrophy in Mild Cognitive Impairment: A Randomized Controlled Trial
A. David Smith, Stephen M. Smith, Celeste A. de Jager1, Philippa Whitbread, Carole Johnston, Grzegorz Agacinski, Abderrahim Oulhaj, Kevin M. Bradley, Robin Jacoby, Helga Refsum
Background
An increased rate of brain atrophy is often observed in older subjects, in particular those who suffer from cognitive decline. Homocysteine is a risk factor for brain atrophy, cognitive impairment and dementia. Plasma concentrations of homocysteine can be lowered by dietary administration of B vitamins.
Objective
To determine whether supplementation with B vitamins that lower levels of plasma total homocysteine can slow the rate of brain atrophy in subjects with mild cognitive impairment in a randomised controlled trial (VITACOG, ISRCTN 94410159).
Methods and Findings
Single-center, randomized, double-blind controlled trial of high-dose folic acid, vitamins B6 and B12in 271 individuals (of 646 screened) over 70 y old with mild cognitive impairment. A subset (187) volunteered to have cranial MRI scans at the start and finish of the study. Participants were randomly assigned to two groups of equal size, one treated with folic acid (0.8 mg/d), vitamin B12(0.5 mg/d) and vitamin B6 (20 mg/d), the other with placebo; treatment was for 24 months. The main outcome measure was the change in the rate of atrophy of the whole brain assessed by serial volumetric MRI scans.
Results
A total of 168 participants (85 in active treatment group; 83 receiving placebo) completed the MRI section of the trial. The mean rate of brain atrophy per year was 0.76% [95% CI, 0.63–0.90] in the active treatment group and 1.08% [0.94–1.22] in the placebo group (P = 0.001). The treatment response was related to baseline homocysteine levels: the rate of atrophy in participants with homocysteine >13 µmol/L was 53% lower in the active treatment group (P = 0.001). A greater rate of atrophy was associated with a lower final cognitive test scores. There was no difference in serious adverse events according to treatment category.
Conclusions and Significance
The accelerated rate of brain atrophy in elderly with mild cognitive impairment can be slowed by treatment with homocysteine-lowering B vitamins. Sixteen percent of those over 70 y old have mild cognitive impairment and half of these develop Alzheimer's disease. Since accelerated brain atrophy is a characteristic of subjects with mild cognitive impairment who convert to Alzheimer's disease, trials are needed to see if the same treatment will delay the development of Alzheimer's disease.