Thought I would continue this since the moderator guy decided to close the last topic.
on a note from what i have read if you have had schizophrenia for over 10 years your chances of this helping are very low. it has potential for effectiveness if you start during the first acute episode.
its kinda like , why do some people react horribly on ssri’s and other people it works great etc… its all just a trial and error balancing game
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I thought I would post a couple things relating to why niacin has a possiblity to help and isnt just a load of crap.
sometimes i get a little uneasy and think people on here may think im just trying to pedal nonsense and that i dont even have mental issue etc… but it really does work for me. so even if just 1 person can get benefit from this info thats fantastic.
no need to reply.
E Messamore,
Schizophrenia research , May 2012
Sensitivity to the skin flush effect of niacin is reduced in a portion of patients with schizophrenia. Though this peripheral physiological abnormality has been widely replicated, its relevance to neuropsychiatric manifestations of the illness has been unclear. The goal of this study was to determine if the niacin response abnormality in schizophrenia is associated with functional impairment.Following psychiatric assessment, a Global Assessment of Functioning (GAF) score was assigned to each of 40 volunteers with schizophrenia. For each subject, the blood flow responses to several concentrations of topical methylnicotinate were recorded. Blood flow was measured objectively, using laser Doppler flowmetry. From the dose-response data, EC(50) values were derived. GAF scores were assigned without knowledge of the participants' niacin response data.There was a significant negative correlation between GAF scores and EC(50) values for methylnicotinate (Pearson r=-0.42; p=0.007).Reduced niacin sensitivity is associated with greater functional impairment among patients with schizophrenia. These findings raise the possibility that a subset of schizophrenia patients possesses a biochemical abnormality that reduces niacin sensitivity in the skin and contributes to functional impairment from the disease.
CL Miller and JR Dulay,
Brain research bulletin , Sep 2008 05
The pathway for de novo synthesis of the suite of niacin congeners, the kynurenine pathway, has been shown to be upregulated in prior studies of postmortem brain tissue from individuals with schizophrenia. The cause of the upregulation is unknown, but one factor may be a defect in feedback regulation via receptors responsive to niacin. A high-affinity and low-affinity receptor for niacin have been identified, HM74A and HM74, respectively. We used RT-QPCR and Western blots to quantify expression of HM74A and HM74 receptors in brain tissue obtained postmortem from patients with schizophrenia (N=12) or bipolar disorder (N=14) and from normal controls (N=14). Although the protein for the HM74 receptor was unchanged, the protein for HM74A was significantly decreased in the schizophrenia group, both when normalized to GAPDH protein or to HM74 as an internal control for degradation and gel-loading error (0.56-fold+/-0.36, p=0.016 and 0.58-fold+/-0.19 the mean control value, p=0.001, respectively). In contrast, the transcript for HM74A was significantly increased, revealing a striking dysregulation between gene transcription and final protein product. No significant differences in HM74A were found for the bipolar group relative to controls. These results are consistent with the blunted niacin flush response reported for individuals with schizophrenia and may be relevant to different rates of comorbid disease.