Inflammation and Psychosis

Jill Littrell, PhD

A report by Bloomfield et al. in the January 2016 issue of American Journal of Psychiatry demonstrated that psychosis is associated with increased inflammatory activity in the brain.  What the researchers did was to inject a marker, [11C]PBR28, which binds to activated white blood cells (microglia) in the brain and then can be seen on a brain scan.  (None of the subjects had been treated with antipsychotic medications.)  Bloomfield et al. showed that in persons who are at high risk for the development of psychosis and in those in whom psychosis had emerged, there was a greater degree of binding of the marker indicating more activated microglia in the brain.  Moreover, Bloomfield et al. noted that degree of binding (degree of microglia activation) was correlated with the level of symptoms.

Regardless of how readers of this website view the physiological basis for hearing voices, psychiatrists clearly do assume a physiological basis for hearing voices.  A consensus is emerging in the psychiatric literature that the fast spiking GABA interneuron and the NMDA receptors on these fast spiking GABA interneurons form the basis for psychosis.  Current issues of American Journal of Psychiatry and JAMA Psychiatry typically contain 4-6 articles per issue on either the NMDA receptors or the fast-spiking GABA interneurons.  The Bloomfield et al. report fits in well with this larger literature pointing the finger at dysfunction in fast spiking GABA interneurons as the culprit in causing hallucinations and cognitive impairment.  (This story is reviewed in chapter 6 in Neuroscience for Psychologists and Other Mental Health Professionals.)

There is a strong connection between the NMDA receptors, fast-spiking GABA interneurons and inflammation.  Inflammation negatively impacts fast spiking GABA interneurons.  Oxidative stress, a component of inflammation, also impairs the function of NMDA receptors which are the drive on the fast spiking GABA interneurons (Sorce, Schiavone, Tucci et al., 2010; Sullivan & O’Donnell, 2012).  Brain inflammation also fits well with the observation that many persons with psychosis relapse when they incur infections in other parts of the body which than can raise inflammatory factors in brain (see Brian Miller, 2016).

Many posts on this website have cited studies linking stressful life events as a causal factor in the emergence of psychosis.  What science requires is a mechanism connecting psychological stressors with functional changes that drive behavior.  The whole field of psychoneuroimmunology has as its major premise that stress/trauma induce brain inflammation.  Numerous studies have established a connection between psychological stress and inflammatory hormones in brain. Stressful life experiences can increase oxidative stress.  Recent studies connect psychosis with inflammation in the brain.  Thus, the studies provide a mechanism for how trauma can increase the emergence of psychosis (Cabungcal, Steullet et al., 2013; Jing et al., 2013).

With the emerging consensus, at least in psychiatric circles, that the fast-spiking GABA interneurons are key in creating psychosis and the acknowledged disabling effect of inflammation on the fast-spiking GABA interneurons, it is important to ask how current treatments impact inflammation.

The Impact of Antipsychotic Drugs on Brain Inflammation:  A recent study by Cotel et al.  showed that taken over the long-term, antipsychotics induce inflammation in the brain.  The Cotel finding contradicts some of the studies cited by Bloomfield et al.  Bloomfield et al. (2016) cited two studies using microglia cells in a petri dish which showed that antipsychotics tamed activation of these cells (Bian et al., 2008; Kato et al., 2008).  Bloomfield et al. also cited a study by Zhu et al. (2014) in live rats which showed that when a molecule of the wall of a bacterium (lipopolysaccharide) is injected into the brain of a rat and subsequently the rat is given a 14 day administration of an antipsychotic the brain’s inflammatory response to the provocation is attenuated.  Bloomfield et al. did not cite the study by Cotel et al. The Cotel et al. study showed the opposite of what the studies cited by Bloomfield et al. showed.  Arguably, the Cotel et al. study is more relevant to the question of how antipsychotic drugs influence inflammation in the brain.  Cotel et al. administered antipsychotics for 8 weeks, much longer than in the other studies.  Moreover, Cotel et al. did not use another activator of an inflammatory response (as was done in the other studies).  Cotel et al. only examined the impact of the antipsychotics in brains which were not exposed to another inflammatory provocation. The Cotel et al. study demonstrated that antipsychotics create brain inflammation.

The Cotel et al. study is important because it might offer an explanation/mechanism for how antipsychotics shrink cortex.  Readers of this website probably remember the Ho et al. (2011) that showed that persons treated for several years with antipsychotics demonstrate a sizable reduction in cortex volumes.  Studies in monkeys, none of whom were schizophrenic, confirmed that treatment with antipsychotics causes brain shrinkage (Dorph-Petersen et al., 2005).  Inflammation, caused by long term use of antipsychotics, may be the proximal cause of brain shrinkage.

The Search for Alternatives to Antipsychotics:   There is a literature on using anti-inflammatories to treat psychosis.  In fact, in a study of children at high risk of converting to psychosis, omega-3s (which are anti-inflammatory) was the only treatment that prevented the emergence of frank psychosis with 27.5% becoming psychotic in the control group versus 4.9% in the omega-3 group at the 12 month follow-up (Amminger et al., 2010).  There is also a literature attesting to the beneficial effects of anti-inflammatories on psychosis.  The anti-inflammatories have included aspirin, minocycline, statins, N-acetylcysteine, and the COX-2 inhibitor, celecoxib (Keller et al., 2013; Sommer et al., 2014).  Sommer et al. concluded that aspirin, estrogen, and N-acetyl-cysteine showed the best effects.  Additionally, social support can also reduce systemic inflammation.

Unfortunately, there are only a few studies in which anti-inflammatory interventions were used as the sole treatment for early psychosis.  In line with Robert Whitaker’s response to Allen Frances yesterday, with everyone acknowledging the need for greater concern for those with psychosis, perhaps we all can join forces to demand more clinical trials of anti-inflammatories as the sole treatment for early psychosis.  Anti-inflammatories such as aspirin and N-acetyl-cysteine have relatively benign side effects.  Hopefully, in the future, we’ll have drug trials of anti-inflammatories as the sole pharmacological treatment along with attention to an anti-inflammatory diet and Soteria Project support.  (There is little reason to believe that any chemical anti-inflammatory can eclipse the impact of an inflammatory diet.)  Perhaps the future will offer a better way.

Readers on this website may object to any notion that biology influences human behavior.  At risk of offending this audience, I present the findings in these studies because they demonstrate the folly of antipsychotics even for those who believe in physiological explanations for hearing voices.  Since doctors probably won’t ever give up their prescription pads, perhaps they can be coaxed into gentler drugs to prescribe.  I think that for those who are involuntarily committed to the psychiatric hospital, telling the doctor to prescribe “this” instead of “that” and backing up the demand with a study published in a legitimate journal might hold some weight.  Even without additional studies, I think the review articles cited here legitimize a request to try an anti=inflammatory first. If asking for a legitimate alternative does not influence the doctor, it might influence a judge.  In fact, most states have informed consent laws which mandate that physicians discuss all the options available for treating a given condition so that the patient can choose which option they prefer.  Perhaps demanding that physicians become acquainted with their own literature might offer a way to proceed.

* * * * *


Amminger, G. P., Schafer, M. R., Papageorgiou, K. et al. (2010).  Long-chain omega-3 fatty acids for indicated prevention of psychotic disorders:  a randomized, placebo-control trial.  Archives of General Psychiatry, 67, 146-154.

Bian, Q., Kato, T., Monji, A. et al. (2008).  The effect of atypical antipsychotics, perospirone, ziprasidone, and quetiapine on microglia activation induced by interferon-gamma.  Progress in Neuropsychophamacology and Biological Psychiatry, 32, 42-48.

Bloomfield, P. S., Selvaraj, S., Veronese, M., Rizzo, G., Bertoldo, A., Owen, D. R., Bloomfield, M.A.P., Bonoldi, I., Kalk, N., Turkheimer, F., McGuire, P., de Paola, V., & Howes, O. D.  (2016).  Microglia activity in people at ultra high risk of psychosis and in schizophrenia:  An [11C]PBR28 PET brain imaging study.  American Journal of Psychiatry, 173 (1), 44-52.

Cabungcal, J-H., Steullet, P., Morishita, H., Kraftsik, R., Cuenod, M., Hensch, T. K., & Do, K. Q.  (2013).  Perineuronal nets protect fast-spiking interneurons against oxidative stress.  Proceedings of the National Academy of Sciences, 110(22), 9130-9135.

Chaudhry, I. B. Hallak, J., Husain, N.  (2012).  Minocycline benefits negative symptoms in early schizophrenia: a randomized double-blind placebo controlled clinical trial in patients on standard treatment.  Journal of Psychopharmacology, 26, 1185-1193.

Cotel, M-C., Lenartowicz, E. M., Natesan, S., Modo, M. M., Cooper, J. D., Willaims, S. C. R., Kapur, S., &  Vernon, A. C.  (2015).  Microglia activation in the rat brain following chronic antipsychotic treatment at clinically relevant doses.  European Neuropsychopharmacology,

Dorph-Petersen, K. A., Pierri, J. N., Perel, J. M., Sun, Z., Sampson, A. R., & Lewis, D. A.  (2005).  The influence of chronic exposure to anti-psychotic medications on brain size before and after tissue fixation:  A comparison of haloperiodol and olanzapine in macaque monkeys.  Neuropsychopharmacology, 30 (9), 1649-1661.

Ho, B. C., Andreasen, N. C., Ziebell, S., Pierson, R., & Magnotta, V.  (2011).  Long-term antipsychotic treatment and brain volumes:  a longitudinal study of first-episode schizophrenia.  Archives of General Psychiatry, 68(2), 128-137.

Jiang, Z., Rompala, G. R., Zhang, S., Cowell, R. M., & Nakazawa, K.  (2013).  Social isolation exacerbates schizophrenia-like phenotypes via oxidative stress in cortical interneurons.  Biological Psychiatry, 73 (10), 1024-1034.

Kato, T., Mizoguchi, Y., Monji, A.  et al. (2008).  Inhibitory effects of aripiprazole on interferon-γ-induced microglia activation via intracellular Ca2+ regulation in vitro.  Journal of Neurochemistry, 106, 815-825.

Keller, W. R., Kum, L. M., Wehring, H. J., Koola, M. M., Buchanan, R. W., & Kelly, D. L.  (2013).  A review of anti-inflammatory agents for symptoms of schizophrenia.  Journal of Psychopharmacology, 27 (4), 337-342.

Kirkpatrick, N., & Miller, B. J.  (2013).  Inflammation and schizophrenia.  Schizophrenia Bulletin, 39 (6), 1174-1179.

Littrell, J.  (2015).  Neuroscience for Psychologists and Other Mental Health Professionals:  Promoting Well-Being and Treating Mental Illness.  New York: Springer.

Miller, B. J.  (2016, January 7).  Adjunctive monoclonal antibody immunotherapy in schizophrenia.  Psychiatric Times.

Miller, B. J., Graham, K. L., Bodenheimer, C. M., Culpepper, N. H., Waller, J. L., & Buckley, P. F.  (2013).  A prevalence study of urinary tract infections in acute relapse of schizophrenia.  Journal of Clinical Psychiatry, 74(3), 271-277.

Mṻller, N., Riedel, M., Scheppach, C.  et al. (2002).  Beneficial antipsychotic effects of celecoxib add-on therapy compared to risperidone alone in schizophrenia.  American Journal of Psychiatry, 159, 1029-1034.

Sorce, S., Schiavone, S., Tucci, P., Colaianna, M., Jaquet, V., Cuomo, V., Dubois-Dauphin, M., Trabace, L., & Krause, K-H. (2010).  The NADPH oxidase NOX2 controls glutamate release: a novel mechanism involved in psychosis like ketamine responses.  Journal of Neuroscience, 30(34), 11317-11325.

Sommer, I. E., van Westrhenen, R., Begemann, M. J., de Witte, L. D., Leucht, S., & Kahn, R. S.  (2014).  Efficacy of anti-inflammatory agents to improve symptoms in patients with schizophrenia: an update.  Schizophrenia Bulletin, 40 (1), 181-191.

Sommer, I. E., de Witte, L., Begemann, M., & Kahn, R. S.  (2012). Nonsteroidal anti-inflammatory drugs in schizophrenia:  ready for practice or a good start?  Journal of Clinical Psychiatry, 73(4), 414-419.

Sorce, S., Schiavone, S., Tucci, P., (2010).  The NADPH oxidase NOX2 controls glutamate release:  a novel mechanism involved in psychosis-like ketamine response.  Journal of Neuroscience, 30, 11317-11325.

Sullivan, E. M., & O’Donnell, P.  (2012). Inhibitory interneurons, oxidative stress, and schizophrenia.  Schizophrenia Bulletin, 38 (3), 373-376.

Zhou, F., Zheng, Y., Ding, Y.Q. et al. (2014).  Minocycline and risperidone prevent microglia activation and rescue behavioral deficits induced by neonatal intrahippocampal injection of lipopolysaccharide in rats.  PLoS One, 2014, 9:e93966


  1. prescription pads? you mean jails?
    Once in the jail that isn’t a jail (because those in authority call it a hospital), what is the warden and guards to do with upset prisoners? They have to drug them/give them “medicine”.
    You have to tell someone what they are doing wrong, you can’t just put them in prison and give them magical chemicals.
    “Nothing good or productive can come from such a confrontation.”

    “Involuntary mental hospitalization and the insanity defense should be seen for what they are: symmetrical symbols of psychiatric power. In the one case, the psychiatrist “accuses” the innocent; in the other, he “excuses” the guilty.”Szasz

  2. Jill,

    I have some well-intended critiques of this paper:

    Regarding this, “psychiatrists clearly do assume a physiological basis for hearing voices” – what exactly does this mean? Are you trying to say that psychiatrists clearly assume that biology causes the phenomenon of hearing voices? Or do you mean that they think that biology may play some role in causing voices along with other factors? Or do you mean that they think biology is the template/substrate through which environmental factors cause psychotic symptoms?

    In the Oxford dictionary, “Basis” is defined as:

    1) the underlying support or foundation for an idea, argument, or process:

    2) the system or principles according to which an activity or process is carried on:

    3)the justification for or reasoning behind something:

    So basis is a quite general world with several meanings – which of these is it?

    Regarding this, “With the emerging consensus, at least in psychiatric circles, that the fast-spiking GABA interneurons are key in creating psychosis”…

    What does this really mean? Is there really any evidence that GABA interneurons cause psychosis? I don’t think so. At best this literature is correlational, from what I’ve read. The possibility remains that stress, trauma, fear of environmental events, isolation, etc. could be causing the GABA interneurons to spike and thus generating psychotic symptoms. Thus psychiatrists could be repeating their classic error of assuming that biology is causing a phenomenon when in fact an earlier cause is expressing itself through biology.

    Secondly, psychosis is just a general word referring to a wide variety of anomalous or unusual experience. It should be admitted that psychotic states are not a known disease process and that they vary greatly between individuals and do not represent one entity. In this regard, the pseudoscientific position of nondoctors (psychiatrists) is weakened.

    Regarding this, “perhaps we all can join forces to demand more clinical trials of anti-inflammatories as the sole treatment for early psychosis.”

    Perhaps not. Your article also said, “social support can also reduce systemic inflammation.” So if that is the case (and it obviously is from a common sense standpoint), then I’d vote for limited research money to be put toward studying psychotherapy and family approaches for psychosis. Anti-inflammatories will likely become another profit center for drug companies with patients treated as ill objects needing to be given the pills for life… let’s get real about how this would be used. It just plays in to the unproven disease model.

    At best, these anti-inflammatory drugs are 5-10 years away, and at best they will have a small effect on reducing people’s stress, in my estimation. Pills are not an adequate substitute for addressing stress holistically through complicated psychological-relational-environmental factors – in my opinion the environment-individual interaction reveals the primary causes of voice-hearing experience. To make a big difference, pills would have to act as if they were a complete holding environment / external person comforting the individual. If only it were that easy. Pills also play into the myth that there is some easy way to control or neutralize psychotic experience, that it is a disease needing to be controlled, and that psychotic experience doesn’t represent something valuable to explore and understand.

    Ok enough.

    • Chiming in to applaud this excellent articulation of an almost mystical process:

      “What does this really mean? Is there really any evidence that GABA interneurons cause psychosis? I don’t think so. At best this literature is correlational, from what I’ve read. The possibility remains that stress, trauma, fear of environmental events, isolation, etc. could be causing the GABA interneurons to spike and thus generating psychotic symptoms. Thus psychiatrists could be repeating their classic error of assuming that biology is causing a phenomenon when in fact an earlier cause is expressing itself through biology. ”

      Sure to hear contradictory personal anecdotes– and I mean no disrespect to anyone’s self reflective analysis of their personal experience with “psychosis”—BUT, almost three decades of emersion in the setting where “psychosis” becomes a “disease/disorder”– or rather on a locked psych ward, I have to agree 100% with BPDs conclusion– Contrasting inpatient *torture* with community encounters– open space and open dialogue, there is no doubting the subtle interplays that reveal keys to individual’s who are struggling to create a reasonable narrative from a terrifying inner break from their own capacity to reason.

      Everything that makes us feel uncomfortable in our own skin– from psychical pain to terror, effects and is reflected in our behavior– signaling others, whether we intend to or not, to intervene or run away from us. The *signals* sent by these reactions makes all the difference.

      I can’t help taking a risk here and commenting on an aspect of cognitive dissonance that clinches the anti-psychiatry stance. It is the mere presence of someone sending signals that reflect the *seasoned* psych clinician’s adherence to *assess this aberrant behavior and employ a treatment* that creates the *patient* they want to.need to *treat*. Want to make an existential crisis into *florid psychosis*? All you have to do is transport the person in crisis to the location of the nearest psychiatrist/psychiatric clinician– .

      There! I said it. I cannot find anything BUT error in the very foundation of psychiatry– and hope to finish my *blog post* soon that provides the historical evidence to back that up–.

      It’s one thing to sell an interesting theory— and call it science, then *medical science*–Quite another to chronically misinterpret the scientific evidence of failed experiments — but then, these salesmen were not men of science to begin with–

      Anyway, good show, BPD !! Seems to be getting easier to debunk psychiatric jargon once it is noted that the linear thinking process only goes one way– in the same direction!! You have made a tremendous contribution to this body of literature 🙂

  3. This is my brand of medicine. It considers the science (as fluid and evolving) and looks at all treatments as options. My experience with psychosis/iatrogenic illness was unsavory to say the least, but my life came back into alignment with a combination of talk therapy, and medication, and sunlight, and food and sleep and an open mind to solutions. I don’t discount the research that points to trauma/life events as a cause for psychosis (or non-consensus reality as part of the spectrum of human experience) because I’ve seen it play out. But for me, endless talk therapy and soul searching turned up no trauma, and the onset of my psychosis appeared before stressful life events, substance use or psychiatric medication. None of us should shoehorn our experiences into any model or theory, but if that model or theory offers a tool that helps, I’m going for it.

  4. I bet none of the psychiatrists heard of cerebral allergies, reactions to foods and inhalants that produce psychiatric symptoms. They were first investigated by Theron Randolph, MD, an allergist, about 60 years ago, probably why you’ll never hear about them in mainstream psychiatry. Basic treatment for them also involves fasting; without drug involvement, certain to put them on the Forbidden List with nutrient therapies.

  5. Thank you for this article. I agree that there are various physiological markers associated with increased inflammatory activity in the brain. But we should not forget that mental activity such as rumination, worry, etc., RESULT IN changes in the brain. In other words, more activated microglia in the brain (and other physiological changes) are CAUSED by such mental activity. Also, if issues like hearing voices were entirely caused by physiological events (that just happen to suddenly take place in the brain), then we would not be able to explain how such problems go away with practises such as mindfulness training and various psychological interventions. I think clinical studies are needed to assess how mind-related interventions bring about changes in all these brain chemicals that are listed in this article (changes in functioning of fast spiking GABA interneurons, deactivation of microglia in the brain, etc.).

  6. Thanks Jill for your research on this topic. The possibility of new treatments for psychosis fills me with hope. Our son has been suffering from psychosis for many years and he is one of the ones for whom no psychological interventions or anti-psychotics have helped. I will talk with his psychiatrist about the possibility of trying anti-inflammatories. Thank you very much!

    • Hi madincanada,
      When your son was first diagnosed, did the doctor use check lists to diagnose him or use objective tests (i.e., blood tests)?
      Psychological interventions take time to work. Often, people get over these things even if you don’t do anything (see: When circumstances change in life, when he develops new interests, etc., things can change in most unexpected ways. But if he is given a label as being “mentally ill”, then this normalization would not happen, because the label itself causes him a lot of worry and mental proliferation (thinking that he is somewhat different from others, etc.), making him not engage in life. When this happens, all this mental proliferation brings about changes in the brain (epigenetic and neuroplastic changes) that maybe detectable in blood tests. Then when various drugs are given as treatment (on a trial and error basis), things can get so much worse. At least this is my perspective.

      • I don’t think they did any blood tests. He was very psychotic when he first came in contact with the mental health system and began using many different meds. He did not really get much worse but not any better either. Seven years of talk therapy with several different doctors has not yielded any results either. That is why I keep hoping for new treatments.

        • Hi madincanada:
          Despite decades of research, scientists have not been able to find any structural or other brain differences between patients who first show up with “mental illness” and healthy individuals. This is why doctors use subjective criteria to diagnose patients – they do not have any objective tests like blood tests. Yet, they give drugs (that the drug companies come up with) in a trial and error fashion.
          So, what happens is, when a person is labeled as “mentally ill” (and are often told that these “are long-term conditions”), for the patient, having a label itself can lead to a great deal of worry – thinking that one is mentally ill permanently, ‘doomed for life’, ‘why me’, etc. This will lead to excessive mental proliferation, worry, rumination, etc., and could in turn aggravate their situation (many psychological studies have clearly shown that rumination, worry, etc., lead to mental illness). A label can also increase stigma, affecting how others treat the person, further aggravating the whole situation. All this mental proliferation, worry, rumination, would also gradually result in adverse structural changes in the brain (via epigenetic and neuroplastic changes in the brain – there are so many studies that support this). Additionally, making matters worse, the drugs affect the brain in non-beneficial ways and you probably know that they also have really bad side effects. Then the person is really “mentally ill.”
          I personally suggest giving ‘mindfulness’ a try (I am telling this by having personally benefited immensely from this practise, and also know others who have benefited) – although it would have been better if he had started it much earlier in his treatment. You as the mother (dealing with all what your son is going through) can even benefit from participating in an 8-week MBSR program (one weekly class for 8 weeks). The skills you learn may even indirectly help your son.
          I wish you and your son the very best in your journey to recovery…

          • He is currently trying cognitive behavioral therapy, along with more drugs and vitamins. I don’t know if this is similar to mindfulness training. Since he is an adult, I don’t have much control over what he tries, but I can suggest it to him. Thank you.

    • madincanada,
      Has your son ever tried classical homeopathy? In all the work my son has done, I overlooked homeopathy, erroneously thinking at first that seeing a homeopath was sort of equivalent to seeing a nutritionist or orthomolecular doctor. I couldn’t have been more off base. It’s interesting that MIA has not yet featured a blog post on what classical homeopathy can do for “mental” illness. I’m blown away by what I’ve seen so far.

      • Thank you Rossa. I can suggest it to him, however, since he is an adult, there is only so much I can do. He is currently being treated by a psychiatrist who is not very interested in alternatives. He has tried vitamins and special diets in the past, but with little success. How is homeopathy different from nutritional and orthomolecular treatments?

        • Madincanada, there is a big difference between homeopathy and say, orthomolecular (nutrient) therapy. Homeopathy is “a system of complementary medicine in which ailments are treated by minute doses of natural substances that in larger amounts would produce symptoms of the ailment.” It’s cheap, and time limited. And profound.

          MIA author Jennifer Bahr writes: “Trying homeopathy was like a Hail Mary – if it didn’t work out I would be no worse off than I already was. In retrospect, I should probably write a letter to thank that short-sighted psychiatrist for giving me so little hope I would try something I didn’t believe in because homeopathy ended up being the most profound medicine I have ever used. Homeopathy gave me relief from depressions and brought me out of manias quickly and without negatively impacting my cognition or sense of self. To this day, I use it with my patients as a cornerstone of their treatment and see the same results for them that I saw for myself.”

          I highly recommend that your son check out Amy Lansky’s book, Impossible Cure: The Promise of Homeopathy. If you want more information you can e-mail me through my blog or through my Facebook account.

  7. As I see it, studying and treating the brain to promote mental wellbeing is like studying all the biochemical pathways that are involved in wasting of skeletal muscles and strategizing how it can be manipulated with biochemicals with the hope of normalizing it (ignoring the fact that physical exercise can bring about this change naturally).
    Also in other organs in the body (organs like the liver, spleen, etc.) biological abnormalities are extremely rare. What I do not understand is, when it comes to the brain, everything is explained away as a biological abnormality that needs to be treated with a drug!

  8. In the state “hospital” where I work there is no such thing as informed consent. Requests on the part of “patients” for an alternative to the antipsychotics is totally ignored and never given any consideration. The judges in the court that is connected to this hospital are not swayed by any such requests since they take their direction and cues from the psychiatrists who testify that the “patients” need to be held in the “hospital” for at least 45 days so that they can be treated with antipsychotics. Once in a great while there is an informed patient who mentions specific studies that support other methods of “treatment” but once again the psychiatrists totally ignore the person as if they’ve never said a word. It’s pretty amazing.

    I think that you’re too optimistic about how requests will be dealt with.

    • Jill’s paper (link reference above) conforms your concerns about the response by the establishment- prescribers of antipsychotics as first line, bee line, for all time remedies for unproven diagnoses…

      She writes with a sensitivity for the plight of a social worker in a therapist role, who cannot recommend or denounce pharmaceutical agents–but can educate and refer clients to *alternative* therapies.

      My real issue with her paper, is that though it is bulging scientific language and data, it is lacking a crucial piece of this puzzle.

      Every study she sites references people diagnosed with schizophrenia, which is– regardless of validity or reliability as a diagnosis, is in and of itself a very intense experience accompanied by severe anxiety that correlates with the cultural understanding of the life sentence that most people regard as part of the treatment package. Now, how is it possible to attribute changes in *the brain* – exclusively to *the disorder*??

      The fact that this is not addressed or suggested speaks volumes. Is this truly *scientific investigation*– or is it cognitive dissonance as a premorbid state?

      However critical I mean to be, I am certainly not disparaging the development of non-drug treatments– What I continue to question is the damaging effects of encounters with the psychiatry driven mental health system– Seems you can’t even rightly study the effects of this paradigm when your subjects are altered the moment the clinician introduces herself. No slight intended toward Jill, but I have wondered if this is part of the long range business plan of contemporary psychiatrists–. Creating their revenue, one traumatized, drugged person at a time…

      • Katie: Regarding your last sentence, I do not think psychiatrists do these things intentionally. They have been deeply conditioned (when they were in medical school, by established professors) to think that all “mental disorders” are neurological conditions, and these “disorders” need to be treated by treating the brain, by targeting neurotransmitters, using drugs, etc. They cling to this concept as the truth, without ever questioning it. The belief is so deep that they do not wish to even consider any alternative explanations – yet they occasionally say that the mind is not understood by science. This is a pathetic state that affects the whole of humanity.
        Perhaps MIA should specifically target/educate budding scientists and psychiatrists in universities and schools!

        • Thanks for offering another explanation, @Nancy99. I wish I could agree, but observing and interfacing with psychiatrists in training at two major academic medical centers, I have noted more emphasis on authoritative posturing and DSM use than study of “the brain”–. I have yet to meet a psychiatrist who could perform, much less interpret a neurological exam– Say “neuro exam” to a psychiatrist, she will likely answer.. “Alert and oriented to person,p lace and time or “times three”. She couldn’t tell you how many cranial nerves we have, let alone how to Test them and what constitutes a positive sign– etc. I know that many people believe that psychiatrists have a full grasp of what is known about the brain—sorry to disappoint you. Brain+behavior= drug is about the extent of their neurological expertise. The simplistic way psychiatrists are taught about the neurotransmitter systems is very similar to a luncheon talk given by a pharma rep.- Short and sweet.

          If you are curious about how deep their knowledge of “neurological disorders” runs, ask a psychiatrist which neurological disorder is indicated by this positive neurological sign:

          Myers’s sign or glabellar tap sign. –or glabellar reflex

          Where is the glabella located?

          Hint: patient cannot resist blinking her eyes when area between nose and eyebrows is lightly tapped.

          There is indeed a belief system that psychiatrists seem to master quite readily, that develops in a condition/response atmosphere–,but it in no way resembles what is commonly referred to as education, study or mastery of a specific function of human physiology.

          Agree that I cannot attribute to malice that which can also be explained as ignorance.

          Without skepticism, an open mind and curiosity, there is no science . Rigid adherence to unproven beliefs is more like religion than science.

  9. Hi, Jill.

    Thank you for an interesting article on the biology of psychosis, and I believe you are on the right
    track here, but I have one issue. I apologize in advance if my comment is insulting.

    Isn’t attacking inflammation a little bit like taking Tylenol for a headache? I’ve heard (I think
    his name was Doctor Ash?) that inflammation is the body’s way of healing. In my opinion, giving pills like aspirin and such might interfere with the body’s natural ability to fight whatever is diseased about the body(through the process of inflammation which the body uses to heal itself). Instead (sorry I’m not a doctor, but I have opinions), I think the best way to attack inflammation
    is to get at its source (i.e. cause).

    Perhaps an anti-inflammatory diet isn’t really anti-inflammatory at all, rather it is actually healing the source of the problem (and therefore the body has no need to inflame itself anymore), but I think drugs such as aspirin might just prevent the body from healing itself (via inflammation, based on Doctor Ash’s opinion).

    It’s interesting that you said anti-psychotics create inflammation. That might mean that the body is
    compensating for something that harms it (which would mean anti-psychotics). Most of us know that
    already, but it’s good to hear.