28-05-2016 12:52 AM
28-05-2016 12:52 AM
30-05-2016 05:22 PM
30-05-2016 05:22 PM
Thanks Tawney.
Unfortunately,this isn't groundbreaking as Research studies as early as the 1960s have shown links between immune dysregulation
30-05-2016 05:30 PM
30-05-2016 05:30 PM
and certain mental illnesses.
What usually happens is there will be a press release and then it's pretty much forgotten about the next day and nothing changes for patients clinically.
I hope the same won't happen for this Newspaper story.
The reality is that most Psychiatrists don't know the Immune System connection and are trained to believe that Psychiatric symptoms are caused by "non organic causes".
If patients try to raise this with them they will often be labelled as having Health anxiety/Neuroticim for looking at health articles online/using "Dr Google".
At the same time,Immunologists don't want to treat patients with Psychiatric symptoms and believe those patients should be treated in the realm of Psychiatry and they often discriminate against them and disbelieve that their Mental symptoms could be immunologically related.
so what good really are articles like these I left there can be a huge cultural shift in the attitude of doctors
30-05-2016 05:33 PM
30-05-2016 05:33 PM
30-05-2016 05:34 PM
30-05-2016 05:34 PM
Typo:"I left" should say "unless"
30-05-2016 05:41 PM
30-05-2016 05:41 PM
30-05-2016 07:05 PM
30-05-2016 07:05 PM
Hi @ivana
I like that you have included a link to a scholarly peer reviewed article, much more credible than some of the things in print.
Also, just thought i'd let you know the 2nd link you have provided, medscape only allows members to view this article.
30-05-2016 07:57 PM
30-05-2016 07:57 PM
Sorry @Former-Member,
I should clarify my "what good really are articles like these" was directed towards the media outlets and not towards you.I thinks its great you posted and shared this information on Sane Forums.
30-05-2016 08:06 PM
30-05-2016 08:06 PM
Hi @-karma,
Sorry about that.The below is a copy-past of the first page of the Medscape article.
Literature Review
A review of the literature was done using the Cochrane Database. Databases searched included MEDLINE, PubMed, EMBASE, and EMBASE reviews. The search terms were autoantibody, autoimmunity, immune dysfunction, and schizophrenia. Both investigators reviewed the search results. Published studies were included in this review if they reported on objective measurements or health outcomes in patients diagnosed as having schizophrenia; extracted information included the study design, the immunologic basis for the findings, the characteristics of the study population, and the main outcome measure. One hundred eighteen articles met the inclusion criteria. Three tertiary references and one conference proceedings were also included.
Heredity and Pedigree Studies
Evidence of an association between schizophrenia and a wide range of autoimmune disorders emerged from an evaluation of data from Danish national registries on patients diagnosed with schizophrenia (n = 7704) and their parents.[3] Nine autoimmune disorders were more prevalent among the patients with schizophrenia relative to matched comparison subjects without schizophrenia (incidence rate ratios [IRRs] for the nine disorders ranged from 1.5 to 12.9). Twelve autoimmune diseases were more common among the parents of patients with schizophrenia (calculated IRRs for the disorders ranged from 1.3 to 3.8) than among the comparison parent population. Overall, the results indicated that "having a history of any autoimmune disease was associated with a 45% increase in risk for schizophrenia" (IRR, 1.45; 95% confidence interval [CI], 1.25–1.68), the investigators reported. They speculated that the human leukocyte antigen (HLA) system may play a role in the development of schizophrenia either because of direct involvement of HLAs or because of the proximity of the loci for auto-immune disorders and schizophrenia in the HLA regions. Interestingly, the study found that rheumatoid arthritis (RA) was neither more nor less common among the patients with schizophrenia than among the comparison subjects; other research has suggested an association between RA and schizophrenia, but the evidence on this topic is inconsistent.[3–5]
Wright et al.[6] found that patients with schizophrenia who had a first-degree relative with schizophrenia were significantly more likely to have a first-degree relative with an auto-immune disease (p = 0.0003). Other research, however, has found no correlation between schizophrenia and severe immune system compromise or HIV infection.[7]
Some etiologic studies have called into question the hypothesis that schizophrenia might be the result of neurotransmitter-receptor abnormalities, suggesting that schizophrenia might instead be the product of a different etiology that also results in neurotransmitter abnormalities.[8–12] However, other research has suggested an association between schizophrenia and a number of neuroanatomical abnormalities, including changes in brain function (impaired stimulus response activation), electrical activity abnormalities, neurochemical abnormalities, and "neuronal disorganization."[13]
Steen and associates[14] conducted a meta-analysis of studies of magnetic resonance imaging (MRI) findings in adult patients with first-episode schizophrenia. The results suggested that compared with healthy controls, the patients with schizophrenia had reduced average whole-brain volume (21 studies, p < 0.0001), reduced hippocampal volume (10 studies, p < 0.0001), and increased ventricular volume (11 studies, p < 0.0001); the limitations of MRI technology were acknowledged. Neuropathologic changes have been noted among patients with schizophrenia, suggesting that the disorder may contribute to neuronal disorganization in cortical and limbic regions of the brain.[10,13] Reported neurobiological differences between patients with schizophrenia and family members may be a result of genetic differences or in utero insults (e.g., maternal infection, maternal immune system activation) or may involve neurodevelopmental abnormalities secondary to insults after birth, including immune system activation during development.
Prenatal and perinatal environmental factors linked to an increased risk of schizophrenia include maternally mediated variables (infections, nutritional deficiencies, severe stress, obstetric and perinatal complications), more advanced paternal age, and the season of birth.[15–18] Several of these environmental risk factors suggest immune system dysfunction or autoimmunity as a possible etiology
Immunogenicity Studies
The immune system has two main components: innate immunity and adaptive immunity. Innate immunity involves a rapid-response system composed of physical defense systems (e.g., skin, mucus) and specific immune cells, including monocytes, macrophages, neutrophils, mast cells, eosinophils, natural killer cells, and dendritic cells, all of which attack or process the invading pathogen (antigen) in some way, including the production of chemokines, inflammatory cytokines, and antimicrobial peptides.[23–25] This antigen processing leads to the activation of adaptive immunity, which involves a response to specific antigens that provides long-term immunity.[26,27] In addition, the immune system uses major histocompatibility complex (MHC) molecules to determine what is "self" and "nonself."
Cytokines are soluble factors secreted by both components of the immune system and have a wide range of effects on immune system function.[23] Some cytokines are pro-inflammatory, enhancing the body's ability to fight a foreign pathogen; some are antiinflammatory, keeping the immune system response proportionate to the need, shutting down the immune response when it is no longer needed, and preventing the immune system from responding to self, or benign, pathogens.
The immune system may malfunction in numerous ways.[24] There may be genetic or environmental alterations of normal self molecules that make them more antigenic, allowing T cells to recognize them as antigens. The body may recognize molecules from pathogens that are very similar to human molecules (molecular mimicry) and produce antibodies that recognize both the pathogen and the similar self molecule to which it is usually tolerant.
Inflammatory Cytokines
Th1 cytokines, such as interferon (INF)-γ and IL-2, stimulate cell-mediated immunity and are usually considered proinflammatory. Th2 cytokines, such as IL-4, stimulate humoral immunity.[52] Some studies have documented an increase in Th2 activity in schizophrenia, with a concomitant decrease in Th1 activity.[52,53] In a study involving 100 inpatients, Avgustin et al.[52] found increases in both Th1 and Th2 activities in patients experiencing acute exacerbations of schizophrenia compared with healthy controls, with a "relative predominance of Th2 immunity." Patients in this study (n = 100) met Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision (DSM-IV-TR) criteria for schizophrenia,[54] had a mean age of 38 years, were hospitalized for an acute exacerbation of psychosis, and had received antipsychotic medication for at least three weeks; controls (n = 34) were matched by age and sex. Exclusion criteria for both patients and controls included acute or chronic infection or inflammatory responses, other chronic illnesses known to change immune function, any neurological disorder, and alcohol or drug abuse. In vitro secretion of INF-γ by peripheral blood mononuclear cells differed significantly between patients and controls (p = 0.037), as did the secretion of IL-4 (p < 0.001). The ratio of INF-γ (proinflammatory) to IL-4 (antiinflammatory) cytokines was 1022 in patients with schizophrenia and 1432 in controls (p = 0.005).[
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