Religion, Spirituality, and Health: The Research and Clinical Implications.

Religion, spirituality, and health: the research and clinical implications.

ISRN Psychiatry. 2012; 2012: 278730
Koenig HG

This paper provides a concise but comprehensive review of research on religion/spirituality (R/S) and both mental health and physical health. It is based on a systematic review of original data-based quantitative research published in peer-reviewed journals between 1872 and 2010, including a few seminal articles published since 2010. First, I provide a brief historical background to set the stage. Then I review research on R/S and mental health, examining relationships with both positive and negative mental health outcomes, where positive outcomes include well-being, happiness, hope, optimism, and gratefulness, and negative outcomes involve depression, suicide, anxiety, psychosis, substance abuse, delinquency/crime, marital instability, and personality traits (positive and negative). I then explain how and why R/S might influence mental health. Next, I review research on R/S and health behaviors such as physical activity, cigarette smoking, diet, and sexual practices, followed by a review of relationships between R/S and heart disease, hypertension, cerebrovascular disease, Alzheimer’s disease and dementia, immune functions, endocrine functions, cancer, overall mortality, physical disability, pain, and somatic symptoms. I then present a theoretical model explaining how R/S might influence physical health. Finally, I discuss what health professionals should do in light of these research findings and make recommendations in this regard. HubMed – depression


High-flux hemodialysis and levocarnitine in the treatment of severe valproic Acid intoxication.

Case Rep Emerg Med. 2013; 2013: 526469
Temel V, Arikan M, Temel G

Valproic acid (VPA) intoxication incidence is increasing, because of the use of VPA in psychiatric disorders. The most common finding of VPA intoxication is central nervous system depression which leads to coma and respiratory depression. Pancreatitis, hyperammonemia, metabolic, and bone marrow failure (thrombocytopenia and leukopenia) have also been described. Treatment is mainly supportive. We present the case of an 18-year-old female patient, who made an attempt to autolysis with VPA. Our patient’s VPA plasma level was very high (924? ? g/mL), confirming that it was a severe intoxication. Our treatment including levocarnitine (50?mg/kg per day for 3 days), and high-flux hemodialysis was performed for four hours. The patient’s hemodynamic status and mental function improved in conjunction with the acute reduction in VPA concentrations. Her subsequent hospital course was complicated by transient thrombocytopenia and levocarnitine induced hypophosphatemia. By day 6, the patient’s laboratory values had completely normalized, and she was transferred to an inpatient psychiatric facility for continuing therapy. HubMed – depression


Trans-10, cis 12-Conjugated Linoleic Acid-Induced Milk Fat Depression Is Associated with Inhibition of PPAR? Signaling and Inflammation in Murine Mammary Tissue.

J Lipids. 2013; 2013: 890343
Kadegowda AK, Khan MJ, Piperova LS, Teter BB, Rodriguez-Zas SL, Erdman RA, Loor JJ

Exogenous trans-10, cis-12-CLA (CLA) reduces lipid synthesis in murine adipose and mammary (MG) tissues. However, genomewide alterations in MG and liver (LIV) associated with dietary CLA during lactation remain unknown. We fed mice (n = 5/diet) control or control?+?trans-10, cis-12-CLA (37?mg/day) between d 6 and d 10 postpartum. The 35,302 annotated murine exonic evidence-based oligo (MEEBO) microarray and quantitative RT-PCR were used for transcript profiling. Milk fat concentration was 44% lower on d 10 versus d 6 due to CLA. The CLA diet resulted in differential expression of 1,496 genes. Bioinformatics analyses underscored that a major effect of CLA on MG encompassed alterations in cellular signaling pathways and phospholipid species biosynthesis. Dietary CLA induced genes related to ER stress (Xbp1), apoptosis (Bcl2), and inflammation (Orm1, Saa2, and Cp). It also induced marked inhibition of PPAR ? signaling, including downregulation of Pparg and Srebf1 and several lipogenic target genes (Scd, Fasn, and Gpam). In LIV, CLA induced hepatic steatosis probably through perturbations in the mitochondrial functions and induction of ER stress. Overall, results from this study underscored the role of PPAR ? signaling on mammary lipogenic target regulation. The proinflammatory effect due to CLA could be related to inhibition of PPAR ? signaling. HubMed – depression



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