Schizophrenia – Keeping It Real

 “A spontaneous recovery from schizophrenia…is so rare…that when it occurs psychiatrists routinely question the validity of the original diagnosis”A Beautiful Mind

It’s sad when you realize how much is actually known about the metabolic or biochemical issues behind the symptoms of schizophrenia, and how little of it ever makes its way into treatment. And it’s not like the standard approach has ever been that successful.

“Psychosocial stress is included in most etiologic models of schizophrenia…The biological effects of stress are mediated by the hypothalamic-pituitary-adrenal (HPA) axis, which governs the release of steroids, including cortisol.” (Corcoran C, et al., 2003)

“…communication between the nervous, endocrine, and immune systems…plays an essential role in modulating the adequate response of the hypothalamic–pituitary–adrenal (HPA) axis to the stimulatory influence of cytokines and stress-related mediators…studies have shown that the interface between these complex systems is impaired in schizophrenia…Elevations in cortisol were associated with increase in both IL-2 and IL-6 in [schizophrenia]…” (Zhang XY, et al., 2005)

Officially, when it comes to diagnosing schizophrenia, no symptom is seen as definitive, and a so called ‘psychotic pathology’ of delusions, hallucinations or disorganized speech is considered central.

Cases get further assessed on the basis of arbitrary judgements, regarding social or occupational functioning, expected levels of academic achievement, interpersonal relations, and self-care.

Schizophrenia is popularly understood to be a distinct and unique, largely genetically driven disease, which relies upon a variety of ‘anti-psychotic’ medications for treatment, with limited improvement potential. It all sounds a bit contradictory, and not very promising.

From a metabolic perspective however, a potentially more practical and illuminating way to view the symptoms of schizophrenia, is to see them as existing somewhere along a spectrum of stress exposure, and the effects that stress can have upon brain and overall system function.

“The role of stress in precipitating psychotic episodes in schizophrenia…has long been acknowledged…Current neurodevelopmental models of psychosis implicate early dysfunction in biological systems regulating hypothalamic-pituitary-adrenal axis and immune function…” (Green MJ, et al., 2014)

“…increased activity of cortisol metabolism in patients with bipolar disorder and schizophrenia compared to healthy controls…is involved in the pathophysiology and stress vulnerability in these severe mental disorders.” (Steen NE, et al., 2011)

“…psychotic disorders are associated with elevated baseline and challenge-induced HPA activity…and…agents that augment stress hormone (cortisol) release exacerbate psychotic symptoms.” (Walker E, et al., 2008)

When you think about schizophrenia in terms of the function of metabolism (and the symptoms of interference which result from stress), just the mention of the HPA axis and high cortisol can be enough to make light bulbs go off in your head, inspiring a multitude of possible treatment ideas. But first you might need to do a little detective work.

Some of the signs of schizophrenia are said to include: an inability to enjoy regular activities; low energy; lack of motivation or interest in socializing; a flat voice; inability to make friends and social isolation in general; slow thinking; poor concentration and memory; difficulty understanding or expressing thoughts; and poor sleep. All potential symptoms of stress, and metabolic suppression.

The more distinct and extreme ‘psychotic manifestations’ associated with schizophrenia, are often identified based on vague, inconsistent judgements regarding what is and isn’t deemed ‘normal’ behavior and thought, with many possible metabolic explanations for their existence being ignored.

A good place to start is to look at the relationship between high stress and thyroid dysfunction. What if the provision of an abundance of energy in the face of stress, is able to support thyroid performance, enable proper cellular function, and protect against schizophrenia?

“Thyroid disorders are highly prevalent in patients with schizophrenia. Changes in the levels of thyroid hormones cause the occurrence of psychiatric disorders and affect the response to treatment.” (Telo S, et al., 2016)

“The clinical presentations of thyroid hormone deficiency are diverse, complicated, and often overlooked… Psychiatric presentations include cognitive dysfunction, affective disorders, and psychosis…Since psychiatric complaints may be one of the earliest manifestations of hypothyroidism, they are often misdiagnosed as functional psychiatric disorders…” (Heinrich TW, et al., 2003)

“Abnormal thyroid hormonal status was observed in 29.3 per cent patients with schizophrenia-spectrum disorders in our study. This was comparable with that reported in a similar study in a hospital sample in South-East Asia which showed that 36.4 per cent of patients with schizophrenia had thyroid dysfunction.” (Radhakrishnan R, et al., 2013)

Insufficient energy availability when stress is high, impacts upon HPA axis function, increasing cortisol, and this can create conditions that are known to promote the things that interfere with thyroid energy metabolism, causing symptoms associated with schizophrenia.

“Increasing evidence suggests that within those at risk for psychosis, higher levels of cortisol is associated with…psychotic symptoms…the onset of psychosis is characterized by HPA axis hyperactivity, as supported by findings of high cortisol levels…” (Borges S, et al., 2013)

“Dysfunction in energy metabolism is one of the most consistent scientific findings associated with these disorders…The presence of metabolic alterations related to energy pathways have been recurrently implied as one of the physiological features of SCZ [schizophrenia]…” (Zuccoli GS, et al., 2017)

The idea is to find the metabolic, biochemical links in the chain leading to worsening symptoms, and then use that information to build a holistic therapeutic response, so that you can work on improving overall function of metabolism from as many angles as possible.

Symptoms of schizophrenia can worsen a great deal (and fluctuate significantly) over time, so there is every reason to believe that an awareness of the different measures of metabolism connected to worsening symptoms (and knowledge regarding different stressors that have a negative impact) will be able to make a big difference in relation to disease progression.

Stress wastes glycogen stores leading to an increase in cortisol, and this promotes other biochemical changes associated with HPA axis dysfunction and schizophrenia. Rising levels of the stress substances are encouraged by a hypo-metabolic state, together with increased free fatty acid release, often polyunsaturated. These factors combined can cause a downward spiraling vicious circle of stress and metabolic suppression.

The breakdown products of the polyunsaturated fats (PUFAs) promote ‘oxidative stress’, inflammation and mitochondrial dysfunction, all of which are associated with thyroid energy production issues, and are known to be involved in the development of schizophrenia.

“Oxidative stress is a part of the pathology in schizophrenia and appears as a promising field to develop new therapeutic strategies. Considerable attention has been focused on the determination of biomarkers of lipid peroxidation in schizophrenia. PUFAs peroxidation is a chain reaction with a large number of intermediates and end point molecules.” (Bošković M, et al., 2011)

“The vulnerability-stress-inflammation model may help to explain the role of inflammation in schizophrenia because stress can increase pro-inflammatory cytokines and may even contribute to a chronic pro-inflammatory state…the benefit of anti-inflammatory medications found in some studies…provide further support for the role of inflammation in this debilitating disease…” (Müller N. et al., 2018)

“Mitochondrial deficit, altered redox balance and chronic low-grade inflammation are evident in schizophrenia. It is hypothesized that oxidative/nitrosative stress responses due to mitochondrial dysfunctions might activate immuno-inflammatory pathways and subsequently lead to neuroprogressive changes in schizophrenia…” (Rajasekaran A, et al., 2015)

“Mitochondria are key players in the generation and regulation of cellular bioenergetics, producing the majority of adenosine triphosphate [ATP] molecules by the oxidative phosphorylation system (OXPHOS)…One consistent pathological finding implicated in SCZ is abnormal brain energy metabolism…Mitochondria…portray various deficits in SCZ…malfunctioning of the OXPHOS, source of ATP production…main driving force of various mitochondrial-related cellular functions.” (Bergman O, et al., 2016)

An under active metabolism resulting from stress, tends to go hand in hand with a sluggish, irritated and inflamed digestive system. Intestinal interference plays a significant part in the advancement of metabolic issues, including the disorders of the mind.

When digestion is slow, bacteria can grow in number and move further up the intestine promoting an increase in the release of bacterial toxins such as endotoxin. Endotoxin is involved in the promotion of inflammation and elevation of numerous stress substances associated with schizophrenia and other mood related issues.

“Neuropsychiatric disorders (e.g., autism, schizophrenia) are partially characterized by social cognitive deficits, including impairments in the ability to perceive others’ emotional states…endotoxin-induced inflammation led to significant decreases in performance…” (Moieni M, et al., 2015)

“Endotoxin…caused a profound transient physiological response with dose-related…increases in plasma interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-α and IL-1 receptor antagonist (IL-1ra), salivary and plasma cortisol, and plasma norepinephrine. These changes were accompanied by dose-related decreased mood and increased anxiety levels…there is growing experimental and clinical evidence implicating systemic inflammation to be involved in the pathophysiology of neuropsychiatric diseases such as depression and schizophrenia…” (Grigoleit JS, et al., 2011)

Endotoxin promotes serotonin, estrogen and nitric oxide, and all of these things can interfere with mitochondria, reduce intestinal barrier function, and lead to an increase in absorption of toxins into the main system. This results in greater circulation of stress substances (including estrogen and cortisol), worsening inflammation, and further disruption of thyroid systems, impacting on the brain, encouraging symptoms of schizophrenia.

“Nitric oxide (NO) has been proposed to act as an intracellular messenger in the brain and its overproduction is associated with schizophrenia…data show that the iNOS inhibitor…may be efficacious in attenuating memory impairments often observed in schizophrenia patients.” (Lafioniatis A, et al., 2016)

“Because the considerable evidence base showing that alterations of activity of NO are active in pathogenesis of schizophrenia, recent attempts have been undertaken to develop the therapy correcting disturbances of the synthesis and release of nitric oxide. Minocycline, semisynthetic tetracycline of the second generation, inhibiting enzyme iNOS and preventing development of microglial inflammatory process has been quite well studied.” (Nasyrova RF, et al., 2015)

“Chronic widespread stress-induced serotonergic overdrive in the cerebral cortex in schizophrenia…is the basic cause of the disease….Disruption of glutamate signalling by serotonergic overdrive leads to neuronal hypometabolism and ultimately synaptic atrophy and grey matter loss according to principles of brain plasticity.” (Eggers AE, et al., 2013)

Metabolic suppression resulting from stress, intensifies the bacteria promoting effects of hard to digest foods (like beans, grains, legumes, and other starchy and fibrous things), increasing the quantity of inflammatory substances which pass through the intestine, placing a greater load upon the liver.

Stress has more impact upon metabolic function when the liver is damaged, and this can then suppress thyroid metabolism even further. The provision of enough protein, sugar and certain vitamins and minerals, play a crucial role in liver function, as well as protection from metabolic dysfunction and schizophrenia progression.

“…certain vitamins and minerals may be effective for improving symptomatic outcomes of schizophrenia, by restoring nutritional deficits, reducing oxidative stress, or modulating neurological pathways….vitamin B supplementation…reduced psychiatric symptoms significantly more than control conditions…” (Firth J, et al., 2017)

“Average vitamin D values were deficient for FEP [first episode psychosis] patients, especially those 22 with a final diagnosis of schizophrenia.” (Salavert J, et al., 2017)

Continuously running down glycogen stores can mean that the stress substances become chronically high, and this is an important factor implicated in the progression of schizophrenia and other brain and mood related disorders and metabolic illness in general.

Chronic or acute stress and persistently low glycogen stores, lead to an increase in the release of the polyunsaturated free fatty acids, directly promoting inflammation, and impeding thyroid energy systems, promoting blood sugar dysregulation and insulin resistance. It is probably not a coincidence that schizophrenia and diabetes often go together.

“It has been reported in the earlier literature that many patients with psychoses had abnormalities in glucose metabolism as revealed by glucose tolerance testing…the schizophrenic population appears to have…a 2–3-fold increased risk for…diabetes…Because glucose is essential for energy metabolism in neurons, any change in…levels in brain…may have significant clinical implications.” (Dwyer DS, et al., 2001)

“Schizophrenia is associated with increased risk for type 2 diabetes mellitus, resulting in elevated cardiovascular risk and limited life expectancy, translated into a weighted average of 14.5 years of potential life lost and an overall weighted average life expectancy of 64.7 years. The exact prevalence of type 2 diabetes among people with schizophrenia…ranges 2-5fold higher than in the general population…” (Mamakou V, et al., 2018)

Stress, blood sugar dysregulation and high levels of PUFAs in the blood, promote further increases in cortisol and adrenaline, interfering with sleep, energy provision, cellular regeneration and optimal brain function.

“Previous studies have indicated that schizophrenia is linked to abnormal lipid metabolism. Free fatty acids (FFAs) in peripheral blood can reflect the status of lipid metabolism in human body…Monounsaturated fatty acids (MUFAs) and ω-6 polyunsaturated fatty acids (ω-6 PUFAs) were significantly increased in SCZs [schizophrenia] compared with HCs [healthy controls]…” (Yang X, et al., 2017)

Too much exposure to PUFAs can feed a vicious circle of serotonin, estrogen and nitric oxide dominance, fueling systemic inflammation and exacerbating many symptoms which are biologically connected to the development of schizophrenia.

“In agreement with previous findings, we show that the schizophrenia group exhibits significantly higher levels of MDA [malondialdehyde, breakdown product of PUFA] and NO [nitric oxide]…” (Gonzalez-Liencres C, et al., 2014)

One thing impacts upon another, and so rising stress substance exposure, lack of sugar, and excessive circulation of PUFAs, can promote dysregulation in almost every biological system, creating the potential for a gradually worsening degree of symptom seriousness, and yet the same information can be utilized for prevention or treatment.

“Deregulations of the pituitary-TH axis continue to be of interest given the interaction between the pituitary-thyroid axis and the dopaminergic, serotonergic, glutamatergic, and GABAergic systems, together with relationships with myelination and proinflammatory response, which are strongly implicated in schizophrenia.” (Santos NC, et al., 2012)

Sugar avoidance in combination with stress, excess PUFAs and exposure to endotoxin, interfere with pregnenolone production and can lead to an estrogen dominant (progesterone or testosterone deficient) state, similar to those seen post menopause as well as in breast cancer.

Although it is popular to suggest (as a means to explaining increased occurrence of schizophrenia in men) that estrogen is protective, this is contradicted by the fact that schizophrenia in women is associated with an increased risk of breast cancer and is more common post menopause, where tissue levels of estrogen are significantly increased, and progesterone is reduced. High testosterone has been shown to have protective effects against schizophrenia in men. Some other conditions which happen more regularly with schizophrenia, and are connected to estrogen dominance, include MS and epilepsy.

Another possible explanation for higher rates of schizophrenia in men, is the fact that women are better protected from iron accumulation pre-menopause. Interaction between accumulated iron, PUFAs and endotoxin, has been shown to promote iron dysregulation, and iron issues are involved in inflammation and oxidative stress, and have been demonstrated to play a role in the development of diseases like cancer and diabetes, as well as brain disorders including schizophrenia.

If you look at changing levels of individual stress hormones, as well as inflammation or thyroid dysfunction, as though they were all unrelated (genetically predetermined) issues, it’s easy to think then, that there isn’t that much known about the development or potential treatment of schizophrenia, and often co-occurring diseases such as cancer and diabetes.

“High levels of pro-inflammatory substances such as cytokines have been described in the blood and cerebrospinal fluid of schizophrenia patients…stress may increase pro-inflammatory cytokines and…contribute to a lasting pro-inflammatory state…” (Müller N, et al., 2015)

“Typical alterations of dopaminergic, serotonergic, noradrenergic, and glutamatergic neurotransmission described in schizophrenia have….been found in low-level neuroinflammation and consequently may be key factors in the generation of schizophrenia symptoms.” (Müller N. 2018)

If you are unaware of the potential impact of excessive exposure to PUFAs, and ongoing sugar restriction (and other nutritional factors), on all of the above conditions and on stress and metabolic function in general, it’s easy to disregard diet as a powerful causative or preventative element.

It’s not surprising that official dietary guidelines are unhelpful (at best), and sadly the ‘healthy diet’ paradigm is almost never questioned by practitioners, but rather it tends to be obediently and blindly recommended.

The ubiquitous nature of anti-sugar and salt, pro-PUFAs propaganda, means that the power of real nutrition as a means to fueling metabolism and protecting against stress, is no longer harnessed therapeutically.

Popularly prescribed anti-psychotic medications, whilst sometimes working at least for a while to suppress the so called ‘positive symptoms’ of schizophrenia, have been shown to gradually worsen metabolic function and lead to the progression of many symptoms often considered unrelated or irrelevant.

“Treatment with the new atypical antipsychotics has a much lower risk of movement disorders; however, weight gain, hyperglycemia, and diabetes are emerging as significant side effects.” (Dwyer DS, et al., 2001)

Some other known ‘side-effects’ of the anti-psychotic medications include movement disorders, heart problems, sexual dysfunction, suicidal depression and suicide. It has been suggested that failure to stay on these medications (because of their unpleasant effects) explains poor treatment success rates. Or it could be that they damage overall metabolic function, explaining lack of long term success.

I’m not a doctor or a scientist, and I’m no expert on the subject of schizophrenia. I don’t believe that we have the power to fix every health issue, but it seems to me that there is a lot that is known that can help people who are suffering from schizophrenia, and if I’m able to know a bit about it, then what exactly am I missing here? Perhaps healing is not the priority.

The first generation anti-histamine cyproheptadine (Periactin), is one example of a drug which has been shown over time to safely and effectively treat symptoms of schizophrenia. It has anti-serotonergic, anti-estrogenic, anti-cortisol, pro-metabolic effects, protects against the substances of stress and inflammation (including endotoxin, nitric oxide and PUFAs) and is generally thyroid supportive and stress protective.

“We conclude that cyproheptadine 16 mg/day is as effective as propranolol for the treatment of acute NIA [neuroleptic-induced akathisia]. The antiakathisic effect of cyproheptadine may be mostly attributable to its serotonin antagonistic activity.” (Fischel T, et al., 2001)

Other pro-metabolism, anti-stress things which have been shown to improve symptoms of schizophrenia include glycine, pregnenolone, progesterone, DHEA, thyroid hormone, the anti-histamine famotidine, aspirin, theanine, lysine, methylene blue, and certain antibiotics.

“The beneficial effects of short-term glycine administration in chronic schizophrenic subjects have been shown to persist after discontinuation for at least 8 weeks…” (Woods SW, et al., 2013)

“Treatment with…pregnenolone significantly decreased negative symptoms in patients with schizophrenia or schizoaffective disorder…and elevations in pregnenolone…post-treatment…were correlated with cognitive improvements.” (Marx CE, et al., 2011)

“Pregnenolone and L-Theanine have shown ameliorative effects on various schizophrenia symptoms…” (Kardashev A, et al., 2018)

The therapeutic application of red light, as well as techniques which look at the relationship between eye function, vestibular issues, and nervous system performance, have potential in relation to brain function and mood issues.

“The brain suffers from many different disorders…traumatic events…degenerative diseases…and psychiatric disorders…There is some evidence that all these seemingly diverse conditions can be beneficially affected by applying light to the head.” (Hamblin MR. 2016)

“…visual abnormalities in children in the general population are more strongly associated with the later development of schizophrenia than any other form of sensory impairment…Given this, and the fact that vision is the most studied and best understood function in neuroscience, why is vision such an understudied area in schizophrenia research?” (Silverstein S, et al., 2015)

A metabolism enhancing diet, removing PUFAs and limiting difficult to digest starches and fibers, whilst including sufficient protein from milk, cheese and gelatin, and plenty of sugar from sweet ripe fruits, fruit juice and white sugar, is one possible approach to protecting against symptoms of schizophrenia.

Relapses into psychosis are commonly blamed on ‘genetics’, on brain defects, or on a failure to adhere to drug therapy regimens. What tends to be disregarded, are the effects of changes in levels of exposure to biological stress in general (including dietary stress), and the cumulative damage from long-term exposure to numerous metabolically suppressive and harmful things.

See More Here

Neuropsychopharmacology. 2005 Aug;30(8):1532-8. Cortisol and Cytokines in Chronic and Treatment-Resistant Patients with Schizophrenia: Association with Psychopathology and Response to Antipsychotics. Zhang XY, Zhou DF, Cao LY, Wu GY, Shen YC.

Dis Nerv Syst. 1976 Feb;37(2):98-103. Glucose-insulin metabolism in chronic schizophrenia. Brambilla F, Guastalla A, Guerrini A, Riggi F, Rovere C, Zanoboni A, Zanoboni-Muciaccia W.

Cell Biochem Funct. 2002 Jun;20(2):171-5. Lipid peroxidation and antioxidant enzyme levels in patients with schizophrenia and bipolar disorder. Kuloglu M, Ustundag B, Atmaca M, Canatan H, Tezcan AE, Cinkilinc N.

Maturitas. 2012 Jun;72(2):117-20. Treating schizophrenia at the time of menopause. Seeman MV.

J Clin Psychiatry. 2011. Increased systemic cortisol metabolism in patients with schizophrenia and bipolar disorder: a mechanism for increased stress vulnerability? Steen NE, et al.

Biol Psychiatry. 2000. Cognitive functioning, cortisol release, and symptom severity in patients with schizophrenia. Walder DJ, et al.

Prim Care Companion J Clin Psychiatry. 2003 Dec;5(6):260-266. Hypothyroidism Presenting as Psychosis: Myxedema Madness Revisited. Heinrich TW, Grahm G.

Annu Rev Clin Psychol. 2008;4:189-216. Stress and the hypothalamic pituitary adrenal axis in the developmental course of schizophrenia. Walker E, Mittal V, Tessner K.

Transl Psychiatry. 2017 Aug 22;7(8):e1215. Reduction of plasma glutathione in psychosis associated with schizophrenia and bipolar disorder in translational psychiatry. Nucifora LG, Tanaka T, Hayes LN, Kim M, Lee BJ, Matsuda T, Nucifora FC Jr, Sedlak T, Mojtabai R, Eaton W, Sawa A.

Schizophr Bull. 2016 Sep;42(5):1290-302. Chronic Peripheral Inflammation is Associated With Cognitive Impairment in Schizophrenia: Results From the Multicentric FACE-SZ Dataset. Bulzacka E, Boyer L, Schürhoff F, Godin O, Berna F, Brunel L, Andrianarisoa M, Aouizerate B, Capdevielle D, Chéreau-Boudet I, Chesnoy-Servanin G, Danion JM, Dubertret C, Dubreucq J, Faget C, Gabayet F, Le Gloahec T, Llorca PM, Mallet J, Misdrahi D, Rey R, Richieri R, Passerieux C, Roux P, Yazbek H, Leboyer M, Fond G;

J Psychopharmacol. 2004. The relationship of sex hormones and cortisol with cognitive functioning in Schizophrenia. Halari R, et al.

Mol Psychiatry. 2013 Jan;18(1):67-78. Potential metabolite markers of schizophrenia. Yang J, Chen T, Sun L, Zhao Z, Qi X, Zhou K, Cao Y, Wang X, Qiu Y, Su M, Zhao A, Wang P, Yang P, Wu J, Feng G, He L, Jia W, Wan C.

Schizophr Bull. 2003;29(4):671-92. Review. The stress cascade and schizophrenia: etiology and onset. Corcoran C, Walker E, Huot R, Mittal V, Tessner K, Kestler L, Malaspina D.

Front Neurosci. 2015 May 19;9:177. Secondary psychosis induced by metabolic disorders. Bonnot O, Herrera PM, Tordjman S, Walterfang M.

J Clin Psychopharmacol. 2016 Dec;36(6):580-587. Antipsychotic Response Worsens With Postmenopausal Duration in Women With Schizophrenia. González-Rodríguez A, Catalán R, Penadés R, Ruiz Cortés V, Torra M, Seeman MV, Bernardo M.

Biol Psychiatry. 2013 Sep 15;74(6):400-9. Meta-Analysis of Oxidative Stress in Schizophrenia. Flatow J, Buckley P, Miller BJ.

Psychiatry Res. 1997 Oct 31;75(3):131-44. Cerebral glucose metabolism in childhood onset schizophrenia. Jacobsen LK, Hamburger SD, Van Horn JD, Vaituzis AC, McKenna K, Frazier JA, Gordon CT, Lenane MC, Rapoport JL, Zametkin AJ.

N Engl J Med. 1955 May 5;252(18):756-9. Recurrent Psychosis Associated with Liver Disease and Elevated Blood Ammonia. HAVENS LL, CHILD CG.

Am J Psychiatry. 1998 Mar;155(3):325-36. Schizophrenia-like psychosis and epilepsy: the status of the association. Sachdev P.

Mult Scler Relat Disord. 2017 Feb;12:9-14. The varieties of psychosis in multiple sclerosis: A systematic review of cases. Camara-Lemarroy CR, Ibarra-Yruegas BE, Rodriguez-Gutierrez R, Berrios-Morales I, Ionete C, Riskind P.

J Nerv Ment Dis. 1989 Jun;177(6):351-8. Serum thyroxine levels in schizophrenic and affective disorder diagnostic subgroups. Mason JW, Kennedy JL, Kosten TR, Giller EL Jr.

J Clin Pharm Ther. 1999. Cyproheptadine in treatment of chronic schizophrenia: a double-blind, placebo-controlled study. Akhondzadeh S, et al.

PLoS One. 2012;7(12):e51455. Pregnenolone Rescues Schizophrenia-Like Behavior in Dopamine Transporter Knockout Mice. Wong P, Chang CC, Marx CE, Caron MG, Wetsel WC, Zhang X.

Psychoneuroendocrinology. 2013 May;38(5):603-11. A systematic review of the activity of the hypothalamic–pituitary–adrenal axis in first episode psychosis. Borges S, Gayer-Anderson C, Mondelli V.

J Neuroinflammation. 2017 Sep 4;14(1):179. Bridging Autism Spectrum Disorders and Schizophrenia through inflammation and biomarkers – pre-clinical and clinical investigations. Prata J, Santos SG, Almeida MI, Coelho R, Barbosa MA.

Schizophr Res. 2002. Effects of the 5HT antagonist cyproheptadine on neuropsychological function in chronic schizophrenia. Chaudhry IB, et al.

Schizophr Res. 2018 Jun;196:35-38. The role of estradiol in schizophrenia diagnosis and symptoms in postmenopausal women. Searles S, Makarewicz JA, Dumas JA.

Behav Brain Res. 2010 May 1;209(1):59-65. Progesterone reduces hyperactivity of female and male dopamine transporter knockout mice. Frye CA, Sora I.

Br J Psychiatry. 2017 Jul;211(1):7-13. Cancer mortality in patients with schizophrenia: systematic review and meta-analysis. Zhuo C, Tao R, Jiang R, Lin X, Shao M.

J Clin Psychopharmacol. 1994 Dec;14(6):424-5. Cyproheptadine in treatment-resistant chronic schizophrenics with prior negative response to fluoxetine. Bacher NM, Sanzone MM, Kaup B.

PLoS One. 2013 Oct 31;8(10):e77496. Testosterone Is Inversely Related to Brain Activity during Emotional Inhibition in Schizophrenia. Vercammen A, Skilleter AJ, Lenroot R, Catts SV, Weickert CS, Weickert TW.

Transl Psychiatry. 2017 Jul 25;7(7):e1176. Serum fatty acid patterns in patients with schizophrenia: a targeted metabonomics study. Yang X, Sun L, Zhao A, Hu X, Qing Y, Jiang J, Yang C, Xu T, Wang P, Liu J, Zhang J, He L, Jia W, Wan C.

JAMA Psychiatry. 2018 Apr 1;75(4):363-369. Association of Schizophrenia With the Risk of Breast Cancer Incidence: A Meta-analysis. Zhuo C, Triplett PT.

West Indian Med J. 2016 Mar 15;65(2):312-315. Thyroid Hormone Levels in Chronic Schizophrenic Patients: Association with Psychopathology. Telo S, Bilgic S, Karabulut N.

Curr Diab Rep. 2016 Feb;16(2):16. Diabetes and Schizophrenia. Suvisaari J, Keinänen J, Eskelinen S, Mantere O.

Psychol Med. 2017 Apr;47(6):1030-1040. The relationship between cognitive impairment in schizophrenia and metabolic syndrome: a systematic review and meta-analysis. Bora E, Akdede BB, Alptekin K.

Neurosci Biobehav Rev. 2015 Jan;48:10-21. Mitochondrial dysfunction in schizophrenia: pathways, mechanisms and implications. Rajasekaran A, Venkatasubramanian G, Berk M, Debnath M.

Indian J Med Res. 2013 Dec;138(6):888-93. Thyroid dysfunction in major psychiatric disorders in a hospital based sample. Radhakrishnan R, Calvin S, Singh JK, Thomas B, Srinivasan K.

J Clin Psychopharmacol. 2001. Cyproheptadine versus propranolol for the treatment of acute neuroleptic-induced akathisia: a comparative double-blind study. Fischel T, et al.

Psychiatriki. 2018 Jan-Mar;29(1):64-73. Schizophrenia and type 2 diabetes mellitus. Mamakou V, Thanopoulou A, Gonidakis F, Tentolouris N, Kontaxakis V.

Mol Psychiatry. 2016 Nov;21(11):1599-1607. Brain iron accumulation affects myelin-related molecular systems implicated in a rare neurogenetic disease family with neuropsychiatric features. Heidari M, Johnstone DM, Bassett B, Graham RM, Chua AC, House MJ, Collingwood JF, Bettencourt C, Houlden H, Ryten M, Olynyk JK, Trinder D, Milward EA.

Schizophr Res. 2017 Sep;187:3-10. Mitochondrial multifaceted dysfunction in schizophrenia; complex I as a possible pathological target. Ben-Shachar D.

PLoS One. 2011;6(12):e28330. Dose-Dependent Effects of Endotoxin on Neurobehavioral Functions in Humans. Grigoleit JS, Kullmann JS, Wolf OT, Hammes F, Wegner A, Jablonowski S, Engler H, Gizewski E, Oberbeck R, Schedlowski M.

Schizophr Res. 2009 Oct;114(1-3):6-16. Schizophrenia and breast cancer incidence: a systematic review of clinical studies. Bushe CJ, Bradley AJ, Wildgust HJ, Hodgson RE.

Mol Psychiatry. 2004 Jul;9(7):684-97, 643. Mitochondrial dysfunction in schizophrenia: evidence for compromised brain metabolism and oxidative stress. Prabakaran S, Swatton JE, Ryan MM, Huffaker SJ, Huang JT, Griffin JL, Wayland M, Freeman T, Dudbridge F, Lilley KS, Karp NA, Hester S, Tkachev D, Mimmack ML, Yolken RH, Webster MJ, Torrey EF, Bahn S.

J Clin Psychiatry. 2010 May;71(5):520-7. Adjuvant aspirin therapy reduces symptoms of schizophrenia spectrum disorders: results from a randomized, double-blind, placebo-controlled trial. Laan W, Grobbee DE, Selten JP, Heijnen CJ, Kahn RS, Burger H.

Neurochem Res. 2014 Jul;39(7):1245-53. Level of Thyroid-Stimulating Hormone (TSH) in Patients with Acute Schizophrenia, Unipolar Depression or Bipolar Disorder. Wysokiński A, Kłoszewska I.

Innov Clin Neurosci. 2015 Sep-Oct;12(9-10):18-24. The Effect of Carnitine Supplementation on Hyperammonemia and Carnitine Deficiency Treated with Valproic Acid in a Psychiatric Setting. Nakamura M, Nagamine T.

J Thyroid Res. 2012;2012:569147. Revisiting Thyroid Hormones in Schizophrenia. Santos NC, Costa P, Ruano D, Macedo A, Soares MJ, Valente J, Pereira AT, Azevedo MH, Palha JA.

Int Clin Psychopharmacol. 1995. Cyproheptadine augmentation of haloperidol in chronic schizophrenic patients: a double-blind placebo-controlled study. Lee HS, et al.

Biopsychosoc Med. 2017 Jul 5;11:19. Association between the blood concentrations of ammonia and carnitine/amino acid of schizophrenic patients treated with valproic acid. Ando M, Amayasu H, Itai T, Yoshida H.

Psychoneuroendocrinology. 2014. Morning cortisol levels in schizophrenia and bipolar disorder: a meta-analysis. Girshkin L, et al.

Indian J Clin Biochem. 2004 Jul;19(2):114-8. Superoxide dismutase and catalase activities and their correlation with malondialdehyde in schizophrenic patients. Rukmini MS, D’Souza B, D’Souza V.

European Neuropsychopharmacology 23(2):S457-S458 October 2013 P.3.d.001 The effects of adjuvant treatment with L-triiodothyronine (T3) on acute schizophrenia treatment with risperidone. Steiblienė Vesta, Bunevicius Robertas, Mickuvienė Narseta,Savickas Arūnas

Med Hypotheses. 2013 Jun;80(6):791-4. A serotonin hypothesis of schizophrenia. Eggers AE.

J Clin Psychopharmacol. 1995 Feb;15(1 Suppl 1):2S-3S. The role of serotonin in schizophrenia and the place of serotonin-dopamine antagonist antipsychotics. Meltzer HY.

Thyroid Res Pract [serial online] 2016 [cited 2019 Aug 7];13:63-6. Serum thyroid stimulating hormone levels and suicidal tendency in patients with first-episode schizophrenia: An exploratory study. Amresh Shrivastava, Vidya Jadhav, Sagar Karia, Nilesh Shah, Avinash De Sousa

Indian J Psychiatry. 2017 Oct-Dec;59(4):478-482. Serum cholesterol and Suicide in first episode psychosis: A preliminary study. Shrivastava A, Johnston M, Campbell R, De Sousa A, Shah N.

J Steroid Biochem Mol Biol. 2003 Sep;86(3-5):225-30. Review. Sources of estrogen and their importance. Simpson ER.

Mol Psychiatry. 2014 Dec;19(12):1252-7. Genomics of schizophrenia: time to consider the gut microbiome? Dinan TG, Borre YE, Cryan JF.

BMJ 2016; 352 Refugee migration and risk of schizophrenia and other non-affective psychoses: cohort study of 1.3 million people in Sweden. na-Clara Hollander, postdoctoral researcher, Henrik Dal, statistician2, Glyn Lewis, professor of psychiatric epidemiology, Cecilia Magnusson, professor of public health epidemiology, James B Kirkbride, Sir Henry Dale fellow, Christina Da

Front Physiol. 2015 May 11;6:139. Role of nitric oxide and related molecules in schizophrenia pathogenesis: biochemical, genetic and clinical aspects. Nasyrova RF, Ivashchenko DV, Ivanov MV, Neznanov NG.

J Clin Endocrinol Metab. 2014 Dec;99(12):E2661-7. Breast Adipose Tissue Estrogen Metabolism in Postmenopausal Women With or Without Breast Cancer Breast Adipose Tissue Estrogen Metabolism in Postmenopausal Women With or Without Breast Cancer. Savolainen-Peltonen H, Vihma V, Leidenius M, Wang F, Turpeinen U, Hämäläinen E, Tikkanen MJ, Mikkola TS.

Front Neurosci. 2017 Sep 7;11:493. The Energy Metabolism Dysfunction in Psychiatric Disorders Postmortem Brains: Focus on Proteomic Evidence. Zuccoli GS, Saia-Cereda VM, Nascimento JM, Martins-de-Souza D.

Scientific Reportsvolume 8, Article number: 6216 (2018). Mitochondrial function in individuals at clinical high risk for psychosis. Tania Da Silva, Abbie Wu, Isabelle Laksono, Ivana Prce, Margaret Maheandiran, Michael Kiang, Ana C. Andreazza & Romina Mizrahi.

J Psychopharmacol. 2012 May;26(5 Suppl):33-41. The metabolic syndrome in schizophrenia: is inflammation a contributing cause? Leonard BE, Schwarz M, Myint AM.

Prog Neuropsychopharmacol Biol Psychiatry. 2012 Oct 1;39(1):170-4. Triiodothyronine may be possibly associated with better cognitive function and less extrapyramidal symptoms in chronic schizophrenia. Ichioka S, Terao T, Hoaki N, Matsushita T, Hoaki T.

Front Psychol. 2015 Feb 5;6:41. Vision in schizophrenia: why it matters. Silverstein S, Keane BP, Blake R, Giersch A, Green M, Kéri S.

J Med Case Rep. 2015 Nov 17;9:264. Acute psychosis as an initial manifestation of hypothyroidism: a case report. Ueno S, Tsuboi S, Fujimaki M, Eguchi H, Machida Y, Hattori N, Miwa H.

Behav Brain Res. 2016 Aug 1;309:14-21. Effects of the inducible nitric oxide synthase inhibitor aminoguanidine in two different rat models of schizophrenia. Lafioniatis A, Orfanidou MA, Papadopoulou ES, Pitsikas N.

NPJ Schizophr. 2016 May 4;2:16018. Candida albicans exposures, sex specificity and cognitive deficits in schizophrenia and bipolar disorder. Severance EG, Gressitt KL, Stallings CR, Katsafanas E, Schweinfurth LA, Savage CL, Adamos MB, Sweeney KM, Origoni AE, Khushalani S, Leweke FM, Dickerson FB, Yolken RH.

Brain Behav Immun. 2015 Aug;48:132-8. Inflammation impairs social cognitive processing: a randomized controlled trial of endotoxin. Moieni M, Irwin MR, Jevtic I, Breen EC, Eisenberger NI.

Eur Neuropsychopharmacol. 2013 Aug;23(8):931-40. Glycine treatment of the risk syndrome for psychosis: Report of two pilot studies✩. Woods SW, Walsh BC, Hawkins KA, Miller TJ, Saksa JR, D’Souza DC, Pearlson GD, Javitt DC, McGlashan TH, Krystal JH.

Acta Psychiatr Scand. 2009 Oct;120(4):274-80. Prevalence of metabolic syndrome among patients with schizophrenia or schizoaffective disorder in Taiwan. Huang MC, Lu ML, Tsai CJ, Chen PY, Chiu CC, Jian DL, Lin KM, Chen CH.

Arch Gen Psychiatry. 1999 Jan;56(1):29-36. Efficacy of high-dose glycine in the treatment of enduring negative symptoms of schizophrenia. Heresco-Levy U, Javitt DC, Ermilov M, Mordel C, Silipo G, Lichtenstein M.

Klinik Psikofarmakoloji Bülteni-Bulletin of Clinical Psychopharmacology 2016 Volume 23, 2013 – Issue 4 A role for bioenergetic abnormalities in the pathophysiology of schizophrenia. Dost Öngür , PhD. , M.D. (Associate Professor of Psychiatry).

BBA Clin. 2016 Oct 1;6:113-124. eCollection 2016 Dec. Review. Shining light on the head: Photobiomodulation for brain disorders. Hamblin MR.

Neurophotonics. 2016 Jul;3(3):031404. Review of transcranial photobiomodulation for major depressive disorder: targeting brain metabolism, inflammation, oxidative stress, and neurogenesis. Cassano P, Petrie SR, Hamblin MR, Henderson TA, Iosifescu DV.

Psychoneuroendocrinology. 2018 May;91:226-234. Prevalence and correlates of low-grade systemic inflammation in adult psychiatric inpatients: An electronic health record-based study. Osimo EF, Cardinal RN, Jones PB, Khandaker GM.

Psychoneuroendocrinology. 2016 Sep;71:102-9. Executive functioning and diabetes: The role of anxious arousal and inflammation. Murdock KW, LeRoy AS, Lacourt TE, Duke DC, Heijnen CJ, Fagundes CP.

Can J Psychiatry. 2016 Aug;61(8):457-69. Mitochondrial Oxidative Phosphorylation System (OXPHOS) Deficits in Schizophrenia. Bergman O, Ben-Shachar D.

PLoS Biol. 2010 Jun 8;8(6):e1000393. Dysregulation of the Norepinephrine Transporter Sustains Cortical Hypodopaminergia and Schizophrenia-Like Behaviors in Neuronal Rictor Null Mice. Siuta MA, Robertson SD, Kocalis H, Saunders C, Gresch PJ, Khatri V, Shiota C, Kennedy JP, Lindsley CW, Daws LC, Polley DB, Veenstra-Vanderweele J, Stanwood GD, Magnuson MA, Niswender KD, Galli A.

Ann Clin Psychiatry. 2001 Jun;13(2):103-13. Review. Glucose Metabolism in Relation to Schizophrenia and Antipsychotic Drug Treatment. Dwyer DS, Bradley RJ, Kablinger AS, Freeman AM 3rd.

Schizophr Res. 2001 Mar 1;48(1):125-36. Evidence for a mitochondrial oxidative phosphorylation defect in brains from patients with schizophrenia. Maurer I, Zierz S, Möller H.

Psychiatry J. 2015;2015:352979. Near-Infrared Transcranial Radiation for Major Depressive Disorder: Proof of Concept Study. Cassano P, Cusin C, Mischoulon D, Hamblin MR, De Taboada L, Pisoni A, Chang T, Yeung A, Ionescu DF, Petrie SR, Nierenberg AA, Fava M, Iosifescu DV.

Schizophr Bull. 2014 Sep;40(5):1022-9. Clonidine Normalizes Levels of P50 Gating in Patients With Schizophrenia on Stable Medication. Oranje B, Glenthøj BY.

J Pineal Res. 2000 Aug;29(1):48-53. Effect of clonidine on plasma ACTH, cortisol and melatonin in children. Muñóz-Hoyos A, Fernández-García JM, Molina-Carballo A, Macías M, Escames G, Ruiz-Cosano C, Acuña-Castroviejo D.

Neuroscience. 2011 Sep 15;191:78-90. Pregnenolone as a novel therapeutic candidate in schizophrenia: emerging preclinical and clinical evidence. Marx CE, Bradford DW, Hamer RM, Naylor JC, Allen TB, Lieberman JA, Strauss JL, Kilts JD.

Psychiatry and Clinical Psychopharmacology 2016 Volume 27, 2017 – Issue 1. Oxidative metabolism may be associated with negative symptoms in schizophrenia. Mehmet Gunes, Abdurrahman Altindag, Mahmut Bulut, Suleyman Demir, Aslihan Okan Ibiloglu, Mehmet Cemal Kaya, Abdullah.

Clin Schizophr Relat Psychoses. Winter 2017;10(4):201-210. Adjunctive Pregnenolone Ameliorates the Cognitive Deficits in Recent-Onset Schizophrenia: An 8-Week, Randomized, Double-Blind, Placebo-Controlled Trial. Kreinin A, Bawakny N, Ritsner MS.

PLoS One. 2012;7(12):e51455. Pregnenolone Rescues Schizophrenia-Like Behavior in Dopamine Transporter Knockout Mice. Wong P, Chang CC, Marx CE, Caron MG, Wetsel WC, Zhang X.

Case Rep Psychiatry. 2015;2015:678040. Levothyroxine Augmentation in Clozapine Resistant Schizophrenia: A Case Report and Review. Seddigh R, Azarnik S, Keshavarz-Akhlaghi AA.

Psychol Med. 2017 Jul;47(9):1515-1527. The effects of vitamin and mineral supplementation on symptoms of schizophrenia: a systematic review and meta-analysis. Firth J, Stubbs B, Sarris J, Rosenbaum S, Teasdale S, Berk M, Yung AR.

Schizophr Res. 2017 Sep;187:1-2. Role of mitochondria and energy metabolism in schizophrenia and psychotic disorders. Konradi C, Öngür D.

Mol Psychiatry. 2010 Sep;15(9):877, 896-904. Sex differences in corticotropin-releasing factor receptor signaling and trafficking: potential role in female vulnerability to stress-related psychopathology. Bangasser DA, Curtis A, Reyes BA, Bethea TT, Parastatidis I, Ischiropoulos H, Van Bockstaele EJ, Valentino RJ.

Horm Mol Biol Clin Investig. 2011 May 1;6(2):227-30. Altered levels of circulating GABAergic 5α/β-reduced pregnane and androstane steroids in schizophrenic men. Bicikova M, Hill M, Ripova D, Mohr P.

J Nerv Ment Dis. 2017 May;205(5):409-412. Association Between Vitamin D Status and Schizophrenia: A First Psychotic Episode Study. Salavert J, Grados D, Ramiro N, Carrión MI, Fadeuilhe C, Palma F, López L, Erra A, Ramírez N.

Clin Schizophr Relat Psychoses. Spring 2018;12(1):31-41. Add-on Pregnenolone with L-Theanine to Antipsychotic Therapy Relieves Negative and Anxiety Symptoms of Schizophrenia: An 8-week, randomized, double-blind, placebo-controlled trial. Kardashev A, Ratner Y, Ritsner MS.

European PsychiatryVolume 41, Supplement, April 2017, Page S802. Brain metabolic abnormalities in schizophrenia patients. M.Amorim, A.Moreira, A.Marques, T.Summavielle.

Nutrients. 2016 Jan 19;8(1). pii: E53. Anti-Stress, Behavioural and Magnetoencephalography Effects of an l-Theanine-Based Nutrient Drink: A Randomised, Double-Blind, Placebo-Controlled, Crossover Trial. White DJ, de Klerk S, Woods W, Gondalia S, Noonan C, Scholey AB.

J Biomed Opt. 2015 May;20(5):57006. Ammonia and ethylene biomarkers in the respiration of the people with schizophrenia using photoacoustic spectroscopy. Popa C, Petrus M, Bratu AM.

Trends Psychiatry Psychother. 2012 Sep;34(3):121-8. The “selfish brain” hypothesis for metabolic abnormalities in bipolar disorder and schizophrenia. Mansur RB, Brietzke E.

BMC Psychiatry. 2014 Sep 24;14:268. Oxidative stress in schizophrenia: a case–control study on the effects on social cognition and neurocognition. Gonzalez-Liencres C, Tas C, Brown EC, Erdin S, Onur E, Cubukcoglu Z, Aydemir O, Esen-Danaci A, Brüne M.

Psychiatry Res. 1998 Apr 10;82(1):25-35. GABA and brain abnormalities in schizophrenia. van Kammen DP, Petty F, Kelley ME, Kramer GL, Barry EJ, Yao JK, Gurklis JA, Peters JL.

Translational Psychiatry volume 6, page e949 (2016). Evidence for impaired glucose metabolism in the striatum, obtained postmortem, from some subjects with schizophrenia. B Dean, N Thomas, E Scarr & M Udawela

Genome Biol. 2008;9(8):R124. Metabolic changes in schizophrenia and human brain evolution. Khaitovich P, Lockstone HE, Wayland MT, Tsang TM, Jayatilaka SD, Guo AJ, Zhou J, Somel M, Harris LW, Holmes E, Pääbo S, Bahn S.

J Clin Psychopharmacol. 2013 Aug;33(4):472-8. A randomized clinical trial of histamine 2 receptor antagonism in treatment-resistant schizophrenia. Meskanen K, Ekelund H, Laitinen J, Neuvonen PJ, Haukka J, Panula P, Ekelund J.

Antioxid Redox Signal. 2011 Oct 1;15(7):2067-79. The role of energy metabolism dysfunction and oxidative stress in schizophrenia revealed by proteomics. Martins-de-Souza D, Harris LW, Guest PC, Bahn S.

BMC Med. 2011 Apr 18;9:40. L-lysine as adjunctive treatment in patients with schizophrenia: a single-blinded, randomized, cross-over pilot study. Wass C, Klamer D, Katsarogiannis E, Pålsson E, Svensson L, Fejgin K, Bogren IB, Engel JA, Rembeck B.

Neuropsychiatr Dis Treat. 2014 Jun 17;10:1103-11. Profile of minocycline and its potential in the treatment of schizophrenia. Zhang L, Zhao J.

IOP Conference Series: Earth and Environmental Science, 2018 Volume 125, Number 1 Exploring the link between inflammation and mental disorders. E Effendy

Schizophr Bull. 2018 Aug 20;44(5):973-982. Inflammation in Schizophrenia: Pathogenetic Aspects and Therapeutic Considerations. Müller N.

Transl Psychiatry. 2016 Aug 16;6:e871. Altered brain arginine metabolism in schizophrenia. Liu P, Jing Y, Collie ND, Dean B, Bilkey DK, Zhang H.

Front Neurosci. 2015 Oct 21;9:372. The role of inflammation in schizophrenia. Müller N, Weidinger E, Leitner B, Schwarz MJ.

Mol Psychiatry. 2016 Aug;21(8):1090-8. Elevated peripheral cytokines characterize a subgroup of people with schizophrenia displaying poor verbal fluency and reduced Broca’s area volume. Fillman SG, Weickert TW, Lenroot RK, Catts SV, Bruggemann JM, Catts VS, Weickert CS.

Lik Sprava. 1997 Jan-Feb;(1):61-5. Russian. Microhemodynamics and energy metabolism in schizophrenia patients. Kut’ko II, Frolov VM, Rachkauskas GS, Pavlenko VV, Petrunia AM.

Curr Neuropharmacol. 2011 Jun;9(2):301-12. Oxidative Stress in Schizophrenia. Bošković M, Vovk T, Kores Plesničar B, Grabnar I.

J Clin Psychopharmacol. 2003 Dec;23(6):601-40. Review. GABA and schizophrenia: a review of basic science and clinical studies. Wassef A, Baker J, Kochan LD.

Neurosci Biobehav Rev. 2015 Aug;55:612-26. Inflammation in schizophrenia: A question of balance. Leza JC, García-Bueno B, Bioque M, Arango C, Parellada M, Do K, O’Donnell P, Bernardo M.

Curr Top Behav Neurosci. 2014;18:217-35. Stress, schizophrenia and bipolar disorder. Green MJ, Girshkin L, Teroganova N, Quidé Y.

Cochrane Systematic Review – Intervention – Protocol Version published: 10 March 2016. Acetylsalicylic acid (aspirin) for schizophrenia. Tracey Roberts, Farhad Shokraneh, Selin Nur.

Neurosci Biobehav Rev. 2011 Jan;35(3):878-93. Oxidative Stress in Schizophrenia: An Integrated Approach. Bitanihirwe BK, Woo TU.

Transl Psychiatry. 2017 Feb 7;7(2):e1024. Inflammation and the neural diathesis-stress hypothesis of schizophrenia: a reconceptualization. Howes OD, McCutcheon R.

Shanghai Arch Psychiatry. 2017 Oct 25;29(5):277-286. Abnormal Concentration of GABA and Glutamate in The Prefrontal Cortex in Schizophrenia.-An in Vivo 1H-MRS Study. Chen T, Wang Y, Zhang J, Wang Z, Xu J, Li Y, Yang Z, Liu D.

Pharmacol Biochem Behav. 2014 Sep;124:361-6. Effects of aspirin on immobile behavior and endocrine and immune changes in the forced swimming test: comparison to fluoxetine and imipramine. Guan XT, Shao F, Xie X, Chen L, Wang W.

J Neuroinflammation. 2008 May 13;5:15. Minocycline attenuates lipopolysaccharide (LPS)-induced neuroinflammation, sickness behavior, and anhedonia. Henry CJ, Huang Y, Wynne A, Hanke M, Himler J, Bailey MT, Sheridan JF, Godbout JP.

J Neuroinflammation. 2017 Sep 18;14(1):188. Using blood cytokine measures to define high inflammatory biotype of schizophrenia and schizoaffective disorder. Boerrigter D, Weickert TW, Lenroot R, O’Donnell M, Galletly C, Liu D, Burgess M, Cadiz R, Jacomb I, Catts VS, Fillman SG, Weickert CS.

Neuroimage Clin. 2014 Oct 15;6:398-407. GABA and glutamate in schizophrenia: A 7 T 1H-MRS study. Marsman A, Mandl RC, Klomp DW, Bohlken MM, Boer VO, Andreychenko A, Cahn W, Kahn RS, Luijten PR, Hulshoff Pol HE.

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