naturopathydigest.com -- Critical Research

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Critical Research

Critical Research is a regular feature in Naturopathy Digest. Each month, we provide abstracts from studies published in the top peer-reviewed journals; each abstract includes the complete citation and an online link to the journal. Whenever possible, this link directs you to a page where you can order the full text of the study, if desired.

This Month's Featured Abstract

Effect of intensive versus standard lipid-lowering treatment with atorvastatin on the progression of calcified coronary atherosclerosis over 12 months.

Axel Schmermund, MD; Stephan Achenbach, MD; Thomas Budde, MD; et al.

Background: Recent clinical trials have suggested that intensive versus standard lipid-lowering therapy provides for additional benefit. Electron-beam computed tomography provides the opportunity to quantify the progression of coronary artery calcification (CAC) in serial measurements.
Methods and Results: In a multicenter, randomized, double-blind trial, 471 patients (age 61-8 years) who had no history of coronary artery disease and no evidence of high-grade coronary stenoses (>50% diameter reduction) were randomized if they had >2 cardiovascular risk factors and moderate calcified coronary atherosclerosis as evidenced by a CAC score >30. Patients were assigned to receive 80 mg or 10 mg of atorvastatin per day over 12 months. Progression of CAC volume scores could be analyzed in 366 patients. After pretreatment with 10 mg of atorvastatin for four weeks, 12 months of study medication reduced LDL cholesterol from 106�22 to 87�33 mg/dL in the group randomized to receive 80 mg of atorvastatin (P<0.001), whereas levels remained stable in the group randomized to receive 10 mg (108�23 at baseline, 109�28 mg/dL at the end of the study, P=NS). The mean progression of CAC volume scores, corrected for the baseline CAC volume score, was 27% (95% CI 20.8% to 33.1%) in the 80 mg atorvastatin group and 25% (95% CI 19.1% to 30.8%) in the 10 mg atorvastatin group (P=0.65). CAC progression showed no relationship with on-treatment LDL cholesterol levels.
Conclusions: We did not observe a relationship between on-treatment LDL cholesterol levels and the progression of calcified coronary atherosclerosis. Over a period of 12 months, intensive atorvastatin therapy was unable to attenuate CAC progression compared with standard atorvastatin therapy. The possibility remains that the time window was too short to demonstrate an effect.
Source: Circulation 2006;113:427-437.

Safety of St. John's Wort extract compared to synthetic antidepressants.

V. Schulz

The clinical efficacy of some standardized St. John's Wort extracts (SWEs) such as WS® 5570, WS® 5572 or LI 160 in the treatment of mild, moderate and severe major depression has been demonstrated in 38 controlled clinical trials and two recent meta-analyses. Sixteen post-marketing surveillance studies with such preparations, based on a total of 34,804 patients, recorded an incidence of adverse events (AEs) among patients between 0% and 6%. Of these studies, the four large-scale surveillance studies with a total of 14,245 patients recorded a rate of AEs ranging from 0.1% to 2.4% and a dropout rate due to AEs of 0.1% to 0.9%. This is at least tenfold lower than that recorded with synthetic antidepressants. AEs associated with SWE treatment were mild and transient in nearly all cases. As with synthetic antidepressants, pharmacokinetic interactions may occur occasionally as a result of activity changes of drug-metabolising and drug-transporting proteins, especially CYP 3A4 and P-gp. Risks to the patient are not caused by SWE but by drugs with a narrow therapeutic range. Consequently, SWE preparations should not be taken concurrently with other antidepressants, with coumarin-type anticoagulants, the immunosuppressants cyclosporine and tacrolimus, protease and reverse transcriptase inhibitors used in anti-HIV treatment or with certain antineoplastic agents. However, such cases are extremely rare and, with medical supervision, easily avoided. In conclusion, the safety of SWE must be considered more favourable than that of synthetic antidepressants.
Source: Phytomedicine, Feb. 3, 2006;13(3): 199-204 (access the journal by title).

Gestational glucose tolerance and risk of type 2 diabetes in young Pima Indian offspring.

Paul W. Franks, Helen C. Looker, Sayuko Kobes, et al.

The in utero environment is a powerful risk factor for type 2 diabetes in offspring, but little is known about the risk conveyed by nondiabetic gestational glucose levels. This issue was explored in 911 nondiabetic Pima Indian mothers and 1,436 of their children. Associations were assessed in multivariate models between maternal third-trimester glucose tolerance and indexes of body composition and glycemic control in their children. At parturition, the mothers' ages ranged from 14 to 43 years. Offspring were studied at age 0-39 years. An SD (1.3 mmol/l) of maternal glucose was associated with 56 g higher birth weight (P = 0.0002). This effect persisted when only offspring of normal glucose tolerant mothers were examined (57 g, P < 0.0001). In Cox proportional hazards models, the adjusted hazard rate ratio for offspring risk of diabetes per SD maternal glucose was 1.6 (95% CI 1.3-2.0, P < 0.0001). When only offspring of normal glucose tolerant mothers were examined, the risk was reduced but remained significant (1.3 [1.04-1.71], P = 0.026). In conclusion, maternal glycemia during pregnancy is associated with increased birth weight and risk of diabetes in Pima Indian offspring, even when mothers are normal glucose tolerant during pregnancy. Thus, prevention of offspring type 2 diabetes may require strategies that focus on improving gestational glucose tolerance even within the normal range.
Source: Diabetes 2006;55:460-465.

Seizure-induced changes in mitochondrial redox status.

Li-Ping Liang and Manisha Patel

The aim of this study was to determine seizure-induced oxidative stress by measuring hippocampal glutathione (GSH) and glutathione disulfide (GSSG) levels in tissue and mitochondria. Kainate-induced status epilepticus (SE) in rats resulted in a time-dependent decrease of GSH/GSSG ratios in both hippocampal tissue and mitochondria. However, changes in GSH/GSSG ratios were more dramatic in the mitochondrial fractions compared to hippocampal tissue. This was accompanied by a mild increase in glutathione peroxidase activity and a decrease in glutathione reductase activity in hippocampal tissue and mitochondria, respectively. Since coenzyme A (CoASH) and its disulfide with GSH (CoASSG) are primarily compartmentalized within mitochondria, their measurement in tissue was undertaken to overcome problems associated with GSH/GSSG measurement following subcellular fractionation. Hippocampal tissue CoASH/CoASSG ratios were decreased following kainate-induced SE, the time course and magnitude of change paralleling mitochondrial GSH/GSSG levels. Cysteine, a rate-limiting precursor of glutathione, was decreased following kainate administration in both hippocampal tissue and mitochondrial fractions. Together, these changes in altered redox status provide further evidence for seizure-induced mitochondrial oxidative stress.
Source: Free Radical Biology and Medicine, January 2006;40(2):316-322 (access the journal by title).