install theme
neuromorphogenesis: Folate and vitamin B12 reduce disabling schizophrenia symptoms in some patients Adding the dietary supplements folate and vitamin B12 to treatment with antipsychotic medication improved a core symptom component of schizophrenia in a study of more than 100 patients. The study focused on negative symptoms of schizophrenia – which include apathy, social withdrawal, and a lack of emotional expressiveness. While the level of improvement across all participants was modest, results were more significant in individuals carrying specific variants in genes involved with folate metabolism. The report from a team based at Massachusetts General Hospital (MGH) will appear in the journal JAMA Psychiatry (formerly Archives of General Psychiatry) and has been issued online. “The symptoms of schizophrenia are complex, and antipsychotic medications provide no relief for some of the most disabling parts of the illness. These include negative symptoms, which can be particularly devastating,” says Joshua Roffman, MD, MMSc, of the MGH Department of Psychiatry, corresponding author of the JAMA Psychiatry paper. “Our finding that folate plus vitamin B12 supplementation can improve negative symptoms opens a new potential avenue for treatment of schizophrenia. Because treatment effects differed based on which genetic variants were present in each participant, the results also support a personalized medical approach to treating schizophrenia.” An essential nutrient, folate (or folic acid) is required for the synthesis of DNA and neurotransmitters and plays a role in the control of gene expression. Adequate folate intake during pregnancy can reduce the risk of birth defects – in particular neural tube defects – and studies have suggested that folate deficiency during pregnancy significantly increases the risk of schizophrenia among offspring. Earlier research by members of the MGH-based team associated low blood folate levels with more severe negative symptoms among patients with schizophrenia. The current study was designed specifically to investigate whether supplementation with folate and B12 – which can magnify the effects of folate – reduced negative symptoms of schizophrenia. A 2011 pilot study found symptom improvement only among patients carrying a variant in a folate-pathway gene called MTHFR that reduced the gene’s activity. To get a clearer picture of folate’s effect on negative symptoms, the current study enrolled 140 patients with schizophrenia at community mental health centers in Boston, Rochester, N.Y., and Grand Rapids, Mich. Participants were all taking antipsychotic medications – which have been shown to alleviate positive symptoms, such as hallucinations and delusions, but not negative symptoms – and were randomized to receive daily doses of either folate and vitamin B12 or a placebo for 16 weeks. Every two weeks their medical and psychiatric status was evaluated, using standard symptom assessment tools along with measurements of blood levels of folate and homocysteine, an amino acid that tends to rise when folate levels drop. Nutritional information was compiled to account for differences in dietary intake of the nutrients. Participants’ blood samples were analyzed to determine the variants they carried of MTHFR and three other folate-pathway genes previously associated with the severity of negative symptoms of schizophrenia. Among all 140 participants in the study protocol, those receiving folate and vitamin B12 showed improvement in negative symptoms, but the degree of improvement was not statistically significant compared with the placebo group. But when the analysis accounted for the variants in the genes of interest, intake of the two nutrients did provide significant improvement in negative symptoms, chiefly reflecting the effects of specific variants in MTHFR and in a gene called FOLH1. Variants in the other two genes studied did not appear to have an effect on treatment outcome. While a low-functioning variant in FOLH1 had been associated with more severe negative symptoms in previous research, in this study it was the high-functioning FOLH1 variant that predicted a better treatment outcome. Measurement of participants’ blood folate levels throughout the study provided an explanation for this unexpected finding. Those with the low-functioning FOLH1 variant started the trial with substantially lower folate levels, suggesting a problem with folate absorption. Although supplementation enabled their blood folate levels to eventually catch up with those of participants with the high-functioning variant, it was probably too late to produce symptom improvement during the 16-week trial period. “For participants who did show a benefit, it took the full 16 weeks of treatment for that benefit to appear,” Roffman explains. “While we don’t know why this is the case, changes in gene expression – which take time – are a likely explanation. Folate plays a critical role in DNA methylation, which regulates gene expression, so it’s plausible that its effects on negative symptoms act through gene expression changes. Participants with the low-functioning FOLH1 variant might eventually show a benefit of folate supplementation if treated for a longer period of time, but that needs to be investigated in future studies.” He adds that, while the benefits of supplementation for the overall group were modest, the lack of effective treatment for negative symptoms and the safety of folate and vitamin B12 supplementation support the need for larger-scale trials. In addition, the impact of genotype on this study’s results suggests the need to investigate the role of folate pathway variants in conditions such as dementia and cardiovascular disease, in which low folate appears to increase risk but supplementation trials have had inconclusive results. “We are now conducting a clinical trial of 1-methylfolate, which bypasses some of these folate-pathway enzymes and might have greater efficiency among individuals with low-functioning variants,” explains Roffman, an assistant professor of Psychiatry at Harvard Medical School. “Understanding more about the basic neural mechanisms of folate in patients with schizophrenia could help us generate more targeted and effective interventions to reduce and possibly even prevent symptoms.”
furples: (by gsamie)
thewildewood: -source
ferfuxsake: Canada, Medicine Lake by simon.auchterlonie on Flickr.
ayustar: DSC02519 by oktay_calisir on Flickr.
crookedindifference: A Sagittarius Triplet
laboratoryequipment: Losing Weight While Younger is Better for the HeartIn a study of the impact of weight loss on reversing heart damage from obesity, Johns Hopkins researchers found that poor heart function in young obese mice can be reversed when the animals lose weight from a low-calorie diet. However, older mice, who had been obese for a longer period of time, did not regain better heart function after they were on the same low-calorie diet.“Our research indicates that the longer mice are obese, the greater the risk that their heart damage is irreversible,” says Majd AlGhatrif, the first author of the study and an assistant professor of medicine at the Johns Hopkins Univ. School of Medicine.Read more: http://www.laboratoryequipment.com/news/2013/03/losing-weight-while-younger-better-heart
petrich0rr: (*)
opticoverload: Milky Way in Gran Paradiso National Park (By Edoardo Brotto)
neuromorphogenesis: Doctoring Yourself? Proceed With Caution When you self-diagnose, you are essentially assuming that you know the subtleties that diagnosis constitutes. This can be very dangerous, as people who assume that they can surmise what is going on with themselves may miss the nuances of diagnosis. For example, people with mood swings often think that they have manic-depressive illness or bipolar disorder. However, mood swings are a symptom that can be a part of many different clinical scenarios: borderline personality disorder and major depression being two examples of other diagnoses. The clinician can help you discern whether you swing from normal to down or down to up, and by considering how long the mood swings last, the clinician can make the appropriate diagnosis. Here, the danger is that you may misdirect the clinician or even yourself. One of the greatest dangers of self diagnosis in psychological syndromes, is that you may miss a medical disease that masquerades as a psychiatric syndrome. Thus, if you have panic disorder, you may miss the diagnosis of hyperthyroidism or an irregular heart beat. Even more serious is the fact that some brain tumors may present with changes in personality or psychosis or even depression. If you assume you have depression and treat it with an over-the-counter preparation, you may completely miss a medical syndrome. Even if you do not want conventional treatment for depression, you may want conventional treatment for a brain tumor. Self-diagnosis also undermines the role of the doctor-which is not the best way to start the relationship. While doctors are generally very enthusiastic about getting packaged information, it would help if you actually trusted your doctor. If your doctor is someone whom you cannot trust, then think again about why you see this doctor. Your doctor should respect your opinion, but the discussion should be an active one. If you doubt the doctor’s diagnosis, tell him or her that you do and say why. This is much better than silently diagnosing your own syndrome. Then there is the fact that we can know and see ourselves, but sometimes, we need a mirror to see ourselves more clearly. The doctor is that mirror. By self-diagnosing, you may be missing something that you cannot see. For example, you may be overwhelmed by anxiety and think that you have an anxiety disorder. The anxiety disorder may be covering up a major depressive disorder. Approximately 2/3 of people who present to outpatient clinics with anxiety have depression as well. In general, when two or more syndromes occur in the same person, we call this comorbidity. When people self-diagnose, they often miss the comorbidity that exists. Another danger of self diagnosis is that you may think that there is more wrong with you than there actually is. For example, if you had insomnia, inattention and depression, you may believe that you have a sleep disorder, ADD and major depression. However, major depression can account for all of these symptoms. Thus, you may make things worse by worrying more as well. Self-diagnosis is also a problem when you are in a state of denial about your symptoms. You may think that you have generalized body aches that started when your mood got worse, but a doctor may elect to do an EKG for chest pain that reveals possible coronary artery disease. You may have been trying to avoid the chest pain or you may have minimized this. Lastly, there are certain syndromes that may not seem like problems to you even though they are very disruptive to your life. For example, with delusional disorder people do not think that they are delusional and because they are not overtly psychotic, they may not think to report paranoid symptoms that add up to delusional disorder. Also, many personality disorders are not spontaneously reported since they are usually problematic to other people. ns on the patient. For this reason, while reading is helpful and informative, it is always best to discuss your impressions with a doctor before you decide on the treatment you want.
TOP