Schizophrenia | Food for the Brain Foundation

What is Schizophrenia 

Schizophrenia is a progressive psychiatric disorder, which commonly emerges during adolescence and affects over 20 million people across the globe. It is characterised by an array of severe psychological symptoms, which may include:

  • An inability to distinguish between what is real and unreal
  • Hallucinations and delusions, and related muddled thoughts
  • Social avoidance and paranoia
  • Poor personal hygiene
  • Loss of interest in activities 

Schizophrenia is still a highly stigmatised mental health condition, and there exists a great deal of misinformation and misunderstanding. It is important to remember that schizophrenia does not cause an individual to become violent or dangerous, or to have a split personality (NHS, 2021).  

Causes of Schizophrenia

The exact aetiology of Schizophrenia remains unknown. However, the following has been identified as potential factors:

  • activation in the immune system of the mother prenatally or advanced paternal age at time of conception
  • perinatal hypoxia (as in hypoxic ischaemic encephalopathy) and other pregnancy and perinatal complications
  • use of recreational drugs, such as cannabis, during adolescence
  • Lifestyle and environmental factors, such as stress, trauma or living in a polluted city (Schmidt and Mirnic, 2015). 

Moreover, disruptions in various body systems have been identified as playing a role in the presentation of the disease. Elucidated below are several pathophysiological mechanisms and biological systems which have been implicated in the pathogenesis of schizophrenia.

Disruptions of Telomere Biology

Individuals with schizophrenia have been demonstrated to have shorter telomere length, a marker of biological aging. One potential explanatory mechanism for this is that individuals with schizophrenia may have genetic variants for the TERT (telomerase reverse transcriptase) gene, which encodes telomerase, the enzyme responsible for maintaining telomere length integrity (Rao et al., 2016). Further proposed mechanisms for shortened telomere length in schizophrenia are via processes of inflammation, chronic stress and oxidative stress (Corfidir et al., 2021).

Microbiota Gut-Brain-Axis Disruption

Tight Junction Modulators

Zonulin associated with tight junction permeability for endothelial cells, in the intestinal barrier, and claudin-5 and -12, associated with tight junction permeability in  the blood brain barrier,, (BBB), have both been implicated in schizophrenia  (Greene, Hanley and Campbell, 2019; Fasano, 2012). Zonulin levels may rise in response to heavy alcohol consumption (Patel et al., 2015), smoking (Malickova et al., 2017), as well as exposure to gluten, indicating increased intestinal permeability (Fasano, 2012). Claudin-5 levels have been observed to decrease following exposure to high levels of glucose, and the heavy metal, lead (Pb), resulting in increased permeability of the BBB (Jia et al., 2013). Furthermore,  the aforementioned TERT gene has extra-telomeric functions, and impairment of the gene as a result of oxidative stress, a hallmark of schizophrenia, results in the downregulation of proteasome 26S activity (Im et al., 2017). Impaired activity of proteasome 26S reduces degradation of occludins and zonulin, which in turn decreases transepithelial resistance and contributes to intestinal and BBB permeability (Andersen et al., 2010; Im et al., 2017).

Microbiota Composition

Imbalances in the gut microbiota and subsequent dysfunction via the gut-brain axis has been suggested to be a key consideration for schizophrenia. This may result in increased neuronal and synaptic damage, as a result of increased inflammation and  neurotoxin synthesis (Yuan et al., 2019).  Dominance of particular strains of gut bacteria have also been observed to be associated with disease onset of schizophrenia and related symptoms. Age of onset of the disease has been associated with dominance of Cyanobacteria in the gut microbiota, and increased levels of Lactobacillus phage phiadh have also been observed in patients with schizophrenia (Kraeuter, 2020). 

The following strains have been identified as being dominant in the gut microbiome of individuals with schizophrenia: 

  • Succinivibrio
  • Megasphaera
  • Collinsella
  •  Clostridium
  •  Klebsiella 
  • Methanobrevibacter (Shen et al., 2018). 

However, levels of  the following observed to be reduced in the gut microbiome of individuals with schizophrenia:

  • Blautia
  • Coprococcus
  • Roseburia  (Shen et al., 2018)

Disrupted Neurotransmitter Synthesis and Functioning

Until recently, research has focused primarily on a dopamine hypothesis, which proposes that aberrant functioning of this neurotransmitter plays a key role in the pathophysiology of schizophrenia. However, presently research has expanded to propose an integrated theory of complex interplay, involving  disrupted functioning of the dopaminergic, glutamatergic, serotonergic, and gamma-aminobutyric acid (GABA) signaling systems (Yang and Tsai, 2017).


Dysfunctional activation and function of serotonin has been suggested to play a role in the pathology of schizophrenia. Serotonin is involved in the brain in social behaviour, mood and sensory modulation, executive functioning, communication between brain cells, and is also vital for sleep, appetite regulation and digestion.  Reduced availability of serotonin has been suggested to result in increased incidence of cognitive fragmentation, which impacts on the brain’s ability to filter out irrelevant information and manage sensory overload (Patrick and Ames, 2015). 

Insufficiency of serotonin has also been linked to increased aggression and self injurious behaviour.  The serotonin-derived metabolite, 5-hydroxy-indole acetic acid (5- HIAA), as derived from the cerebrospinal fluid, is considered a biomarker for reduced serotonin levels in the brain.  Another consideration for individuals with schizophrenia may be genetic variants on the gene TPH2, along with other serotonin modulating genes.  Some genetic variations of this gene may affect the biosynthesis of serotonin. And therefore contribute to the pathophysiology of the disease via mechanisms of defective and insufficient serotonin synthesis (Patrick and Ames, 2015).  


Dopamine hyperactivation has also been implicated in the pathogenesis of schizophrenia (Kraeuter, 2020). Increased synthesis of dopamine, particularly in response to stress, has been observed in individuals with the disease, and this has been correlated with altered cortical and cognitive functioning. Furthermore, (Howes et al., 2017). Altered hippocampal activity, as observed in schizophrenia, is also thought to be correlated with increased levels of dopamine (Kraeuter, 2020).


Impaired glutamate neurotransmission has also been hypothesised to be involved in schizophrenia pathology (Kraeuter, 2020), particularly via N-methyl-d-aspartate receptor (NMDAR) functioning due to disrupted circuitry in the brain (Uno and Coyle, 2019).  


RELN, NRG1/ErbB4, and BDNF are all involved in the establishment of circulatory GABA signalling. It has been theorised that alterations to these processes during gestational brain development may be involved in the aetiology of schizophrenia, due to impaired GABA signalling (Egerton et al., 2017). GABA levels have also been observed to be lower in individuals with schizophrenia compared with individuals without the disease (p = 0.02) (Kumar, Vajawat and Rao, 2021).  

Impaired Glucose Metabolism

Impaired glucose metabolism and insulin resistance has been implicated in schizophrenia, as imbalanced glucose levels have been observed in the cerebrospinal fluid of patients diagnosed with the disease (Roosterman and Cottrell, 2021). Additionally, schizophrenia has been associated with an increased risk of type II diabetes development, glucose intolerance, and elevated fasting blood glucose and insulin levels have been observed clinically in presentations of the disease  (Pillinger et al., 2017). Hyperglycaemia causes cortisol synthesis to be increased, which impacts on the regulation of adipose tissue accumulation and storage and may also affect appetite control and energy intake balance, as these functions are glucocorticoid-regulated bodily functions (Epel et al., 2001).  

One potential mechanism for the involvement of impaired glucose metabolism in schizophrenia pathology is via disruption of mTOR mitochondrial pathway (Bryll et al., 2020).  Consumption of sugar and processed foods leads to hyperglycaemia, which impairs pancreatic beta cells’ ability to regulate blood glucose and insulin. Hyperglycaemia induced oxidative stress activates the JNK pathway, which initiates apoptosis of pancreatic beta cells, causing insulin insufficiency and impaired glucose tolerance (Bachar et al., 2009). Hyperglycaemia also stimulates mTORC1 and induces oxidative stress in mitochondria. Disruption of the mTOR pathway increases β- and γ-secretases, which alter APP metabolism (Cai et al., 2015). Activation of the mTOR and JNK pathways also impairs hTERT, which may increase degeneration in the brain (Cai et al., 2015). This is because hTERT has been hypothesised to be neuroprotective, because it localises within mitochondria and protects neurons from oxidative stress, DNA damage and neuronal apoptosis (Miwa and Saretzki, 2016).

Nutrition and Schizophrenia

Nutritional psychiatry is an emerging field of research, which investigates the role of nutrients in brain health and their salience and potential application to psychiatric disorders (Sarris et al., 2015). 

The following factors have been identified as pertinent nutritional interventions to address in Schizophrenia. 

Ketogenic diet 

A ketogenic diet, which is lower in carbohydrates and higher in protein / fats,  may improve clinical presentations of schizophrenia through reducing metabolic symptoms. Furthermore, in animal models of schizophrenia, a ketogenic diet has been observed to significantly ameliorate the disease. However, further research is required to explore this in human models (Sarnyai, Kraeuter, Palmer , 2019).  Further evidence has suggested that  ketogenic diets may be beneficial in schizophrenia, due to exerting positive effects of hypometabolism, neurotransmitter imbalances, oxidative stress and inflammation (Norwitz, Dalai, Palmer, 2020). Glucose levels were observed to be reduced as a result of a ketogenic diet, and therefore this diet may be useful for improving symptoms of impaired glucose metabolism in the disease. Moreover, cognitive and memory disturbances have been observed to be improved following implementation of a ketogenic diet (Bostock, Kirby and Taylor, 2017). Adopting a ketogenic diet may also be useful for increasing tryptophan, which may in turn help to increase levels of serotonin. 


Depletion of the essential amino acid, tryptophan, is a highly merited consideration for schizophrenia, due to the role of tryptophan in the synthesis of serotonin.  Impact of tryptophan deficiency, and subsequent serotonin insufficiency, can be observed via adverse effects on the prefrontal cortex of the brain, in terms of reduced impulse control and impaired decision making. Furthermore, tryptophan insufficiency has been associated with overactivation of the ventral striatum, which is a part of the brain involved in short term decision making, and underactivation of the dorsal striatum, which is involved in long term decision making. However, supplementation of tryptophan has been observed to rectify this imbalance (Patrick and Ames, 2015).    

Gut Health


Prebiotics may increase the expression of gut hormones such as peptide tyrosine tyrosine, glucagon-like peptide 1 and leptin, which may increase satiety, whilst decreasing levels of hunger hormones, such as ghrelin (Kao, Burnet and Lennox, 2018). Prebiotics may therefore be useful for addressing metabolic symptoms in schizophrenia, such as impaired glucose metabolism.

Cruciferous and sulphurous vegetables, such as broccoli, leeks, onions and garlic, are sources of prebiotic fibres, such as inulin (Swennen, Courtin and Delcour, 2006).

Inulin specifically has been shown to reduce circulating levels of Zonulin, which may help to support intestinal barrier integrity, reduce levels of ghrelin and increase the production of short chain fatty acids (SCFAs), such as butyrate, propionate and acetate (Swennin, Courtin and Delcour, 2006). SCFAs are integral for the balance of gut microbiota. Butyrate may help to regulate glucose and energy homeostasis and help prevent gut dysbiosis through beta-oxidation (De Vadder et al., 2014; Byndloss et al., 2016). Propionate is transported to the liver, where it has been observed to be involved in the regulation of gluconeogenesis and satiety signalling, as it interacts with fatty acid receptors in the gut (De Vadder et al., 2014). Acetate is transferred to peripheral tissues, where it is involved in cholesterol metabolism, lipogenesis and regulation of appetite (Frost et al., 2014). 


Gut microbiota are essential for the synthesis of neurotransmitters. Lactobacillus and  Bifidobacteria are involved in the production of  Gamma aminobutyrate (GABA), and Bacillus spp is important for the synthesis of dopamine. Candida albicans, Escherichia, Streptococci, and Enterococci spp are all involved in the synthesis of serotonin (Grover et al., 2019). 

Consuming fermented foods such as kimchi, sauerkraut and kefir and taking a broad spectrum probiotic may be beneficial for increasing the strains of different bacteria in the gut microbiota. 

Gluten Elimination Diet

Research looking at a sample of participants who had schizophrenia or had not been diagnosed with the disorder, observed that there was a higher incidence of gluten intolerance in individuals diagnosed with schizophrenia, compared with those without the diagnosis (Jackson et al., 2014). Therefore asking one’s physician for a coeliac test is important, to rule out coeliac’s disease. However, it should be noted if the test is negative, an individual may still be non coeliac gluten sensitive and therefore adopting a gluten free diet may be beneficial.

Omega 3

Omega-3 supplementation may impact on dopamine and glutamate transmission, oxidative stress, inflammation, myelination, and neurotransmission pathways. Omega-3 has been linked to improved symptoms in those experiencing a schizophrenic episode (Frajerman et al., 2021). Moreover,  A randomized placebo-controlled trial was conducted over 26 weeks to study whether omega-3 fatty acids would have an effect on symptom severity in first episode schizophrenic patients. 71 patients were assigned either a placebo of olive oil or 2.2g/day of omega-3 supplement. Severity of symptoms were measured using the positive and negative syndrome scale (PANNSS). A 50% improvement in symptom severity was recorded more frequently in the omega-3 group compared to the placebo group. Significant improvements were found in depressive symptoms, the level of functioning and clinical global impression when patients were supplemented.

These findings suggest that a 6-month intervention of omega-3 supplementation may be able to decrease symptom severity in first episode schizophrenia patients (Pawełczyk et al., 2016).

Vitamins and Minerals

B Vitamins

Folate, Vitamin B6 and Vitamin B12 have all been suggested to be key considerations for schizophrenia, due to their essential function in methylation and the lower serum levels commonly observed clinically in patients with schizophrenia (Wang et al. 2016). Methylation is a vital biochemical process used by the body to module the expression of genes. When there is a deficiency of folate, B6 and B12, homocysteine levels can build up, as these vitamins metabolise homocysteine into cysteine. When homocysteine levels accumulate, this can cause an excessive build up, or hyperhomocysteinaemia, to occur. Hyperhomocysteinaemia impairs the integrity of the blood-brain-barrier (BBB) and causes neurodegeneration, and has been implicated in the pathophysiology of schizophrenia (Kalani et al., 2014; Teasdale et al., 2020). 

Vitamin D

Study was conducted to understand whether vitamin D supplementation, especially sunlight exposure, would have an impact on negative symptoms of those with schizophrenia. 52 patients took part in the study and had their serum 25 OH Vitamin D levels were then measured to understand their current vitamin D level in the blood. The severity of symptoms was measured using the scale for the assessment of negative symptoms (SANS). The mean SANS score was statistically significantly lower after replacement of vitamin D, the total attention score was also significantly improved. The study concluded that addressing vitamin D deficiency in schizophrenic patients can improve symptoms of schizophrenia (Neriman et al., 2021).


A study was conducted to identify whether low blood iron levels could be related to severity of schizophrenia symptoms. This study was conducted on 121 patients during their first episode of schizophrenia disorder. Symptoms were measured using the positive and negative syndrome scale (PANSS), and iron deficiency was defined as a serum ferritin less than 20ng/ml. The study found patients with iron deficiency were significantly more likely to have more prominent negative symptoms, and patients with more negative symptoms had significantly lower serum ferritin (iron) levels than their counterparts. This study highlights a possibility for further investigation as to whether iron supplementation could be used as an intervention (Kim et al., 2018).

Note: Any nutritional interventions should be implemented only under the supervision of a GP and psychiatrist and with the support of a qualified nutritional professional.


  1. Charlson FJ, Ferrari AJ, Santomauro DF, et al. Global Epidemiology and Burden of Schizophrenia: Findings From the Global Burden of Disease Study 2016. Schizophr Bull. 2018;44(6):1195-1203. doi:10.1093/schbul/sby058
  2. Sarris, J., Logan, A. C., Akbaraly, T. N., Amminger, G. P., Balanzá-Martínez, V., Freeman, M. P., Hibbeln, J., Matsuoka, Y., Mischoulon, D., Mizoue, T., Nanri, A., Nishi, D., Ramsey, D., Rucklidge, J. J., Sanchez-Villegas, A., Scholey, A., Su, K. P., Jacka, F. N., & International Society for Nutritional Psychiatry Research (2015). Nutritional medicine as mainstream in psychiatry. The lancet. Psychiatry, 2(3), 271–274.
  3. Kalani, A., Kamat, P. K., Givvimani, S., Brown, K., Metreveli, N., Tyagi, S. C., & Tyagi, N. (2014). Nutri-epigenetics ameliorates blood-brain barrier damage and neurodegeneration in hyperhomocysteinemia: role of folic acid. Journal of molecular neuroscience : MN, 52(2), 202–215.
  4. Frajerman A, Scoriels L, Kebir O, Chaumette B. Shared Biological Pathways between Antipsychotics and Omega-3 Fatty Acids: A Key Feature for Schizophrenia Preventive Treatment? Int J Mol Sci. 2021 Jun 26;22(13):6881. doi: 10.3390/ijms22136881. PMID: 34206945; PMCID: PMC8269187.
  5. Pawełczyk T, Grancow-Grabka M, Kotlicka-Antczak M, Trafalska E, Pawełczyk A. A randomized controlled study of the efficacy of six-month supplementation with concentrated fish oil rich in omega-3 polyunsaturated fatty acids in first episode schizophrenia. J Psychiatr Res. 2016 Feb;73:34-44. doi: 10.1016/j.jpsychires.2015.11.013. 
  6.     Fasano, A, 2012. Intestinal Permeability and its Regulation by Zonulin: Diagnostic and Therapeutic Implications. Clinical Gastroenterology and Hepatology, 10 (10), pp 1096 – 1100. Available at: <> [Accessed 13 September 2018] 
  7. Grover S, Patil A, Kaur A, Garg G. Probiotics: A Potential Immunotherapeutic Approach for the Treatment of Schizophrenia. J Pharm Bioallied Sci. 2019;11(4):321-327. doi:10.4103/jpbs.JPBS_47_19
  8.  Patel, S, Behara, R, Swanson, G, Forsyth, C, Voight, R, Keshavarzian, A, 2015. Alcohol and the Intestine. Biomolecules, 5(4), pp 2573 – 2588. <
  9. Malickova, K, Francova, I, Lukas, M, 2017. Fecal zonulin is elevated in Crohn’s disease and in cigarette smokers. Practical Laboratory Medicine, 9, pp 39 -44.> 
  10. Kao, A. C., Burnet, P., & Lennox, B. R. (2018). Can prebiotics assist in the management of cognition and weight gain in schizophrenia?. Psychoneuroendocrinology, 95, 179–185. 
  11. Patrick, R. P., & Ames, B. N. (2015). Vitamin D and the omega-3 fatty acids control serotonin synthesis and action, part 2: relevance for ADHD, bipolar disorder, schizophrenia, and impulsive behavior. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 29(6), 2207–2222.
  12. Sarnyai, Z., Kraeuter, A. K., & Palmer, C. M. (2019). Ketogenic diet for schizophrenia: clinical implication. Current opinion in psychiatry, 32(5), 394–401.
  13. Norwitz, N. G., Dalai, S. S., & Palmer, C. M. (2020). Ketogenic diet as a metabolic treatment for mental illness. Current opinion in endocrinology, diabetes, and obesity, 27(5), 269–274.
  14. Greene, C., Hanley, N., & Campbell, M. (2019). Claudin-5: gatekeeper of neurological function. Fluids and barriers of the CNS, 16(1), 3.
  15. Uno, Y., & Coyle, J. T. (2019). Glutamate hypothesis in schizophrenia. Psychiatry and clinical neurosciences, 73(5), 204–215.
  16. Jackson J, Eaton W, Cascella N, et al. Gluten sensitivity and relationship to psychiatric symptoms in people with schizophrenia. Schizophr Res. 2014;159(2-3):539-542. doi:10.1016/j.schres.2014.09.023
  17. Jia, W., Lu, R., Martin, T. A., & Jiang, W. G. (2014). The role of claudin-5 in blood-brain barrier (BBB) and brain metastases (review). Molecular medicine reports, 9(3), 779–785.
  18. Yuan et al., 2019. The gut microbiota promotes the pathogenesis of schizophrenia via multiple pathways. Biochemical and Biophysical Research Communications. 512(2), pp 373-380.
  19. Kraeuter AK, Phillips R, Sarnyai Z. The Gut Microbiome in Psychosis From Mice to Men: A Systematic Review of Preclinical and Clinical Studies. Front Psychiatry. 2020;11:799. Published 2020 Aug 11. doi:10.3389/fpsyt.2020.00799
  20. Shen, Y., Xu, J., Li, Z., Huang, Y., Yuan, Y., Wang, J., Zhang, M., Hu, S., & Liang, Y. (2018). Analysis of gut microbiota diversity and auxiliary diagnosis as a biomarker in patients with schizophrenia: A cross-sectional study. Schizophrenia research, 197, 470–477.
  21. Rao, S., Ye, N., Hu, H., Shen, Y., & Xu, Q. (2016). Variants in TERT influencing telomere length are associated with paranoid schizophrenia risk. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 171B(3), 317–324.
  22. Corfdir, C., Pignon, B., Szöke, A., & Schürhoff, F. (2021). Érosion prématurée des télomères et schizophrénies : synthèse et hypothèses [Accelerated telomere erosion in schizophrenia: A literature review]. L’Encephale, 47(4), 369–375.
  23. Swennen, K., Courtin, C. M., & Delcour, J. A. (2006). Non-digestible oligosaccharides with prebiotic properties. Critical reviews in food science and nutrition, 46(6), 459–471.
  24. Yang, A. C., & Tsai, S. J. (2017). New Targets for Schizophrenia Treatment beyond the Dopamine Hypothesis. International journal of molecular sciences, 18(8), 1689.
  25. Frost, G., Sleeth, M. L., Sahuri-Arisoylu, M., Lizarbe, B., Cerdan, S., Brody, L., Anastasovska, J., Ghourab, S., Hankir, M., Zhang, S., Carling, D., Swann, J. R., Gibson, G., Viardot, A., Morrison, D., Louise Thomas, E., & Bell, J. D. (2014). The short-chain fatty acid acetate reduces appetite via a central homeostatic mechanism. Nature communications, 5, 3611.
  26. Howes, O. D., McCutcheon, R., Owen, M. J., & Murray, R. M. (2017). The Role of Genes, Stress, and Dopamine in the Development of Schizophrenia. Biological psychiatry, 81(1), 9–20.
  27. Bryll, A., Skrzypek, J., Krzyściak, W., Szelągowska, M., Śmierciak, N., Kozicz, T., & Popiela, T. (2020). Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia. Biomolecules, 10(3), 384.
  28. De Vadder, F., Kovatcheva-Datchary, P., Goncalves, D., Vinera, J., Zitoun, C., Duchampt, A., Bäckhed, F., & Mithieux, G. (2014). Microbiota-generated metabolites promote metabolic benefits via gut-brain neural circuits. Cell, 156(1-2), 84–96.
  29. Kumar, V., Vajawat, B., & Rao, N. P. (2021). Frontal GABA in schizophrenia: A meta-analysis of 1H-MRS studies. The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry, 22(1), 1–13.
  30. Bostock EC, Kirkby KC, Taylor BV. The Current Status of the Ketogenic Diet in Psychiatry. Front Psychiatry. 2017;8:43. Published 2017 Mar 20. doi:10.3389/fpsyt.2017.00043
  31. Byndloss, M. X., Olsan, E. E., Rivera-Chávez, F., Tiffany, C. R., Cevallos, S. A., Lokken, K. L., Torres, T. P., Byndloss, A. J., Faber, F., Gao, Y., Litvak, Y., Lopez, C. A., Xu, G., Napoli, E., Giulivi, C., Tsolis, R. M., Revzin, A., Lebrilla, C. B., & Bäumler, A. J. (2017). Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. Science (New York, N.Y.), 357(6351), 570–575.
  32. Pillinger, T., Beck, K., Gobjila, C., Donocik, J. G., Jauhar, S., & Howes, O. D. (2017). Impaired Glucose Homeostasis in First-Episode Schizophrenia: A Systematic Review and Meta-analysis. JAMA psychiatry, 74(3), 261–269.
  33. Frajerman A, Scoriels L, Kebir O, Chaumette B. Shared Biological Pathways between Antipsychotics and Omega-3 Fatty Acids: A Key Feature for Schizophrenia Preventive Treatment? Int J Mol Sci. 2021 Jun 26;22(13):6881. doi: 10.3390/ijms22136881. PMID: 34206945; PMCID: PMC8269187.
  34. Schmidt MJ, Mirnics K. Neurodevelopment, GABA system dysfunction, and schizophrenia. Neuropsychopharmacology. 2015;40(1):190-206. doi:10.1038/npp.2014.95
  35. Kim SW, Stewart R, Park WY, Jhon M, Lee JY, Kim SY, Kim JM, Amminger P, Chung YC, Yoon JS. Latent iron deficiency as a marker of negative symptoms in patients with first-episode schizophrenia spectrum disorder. Nutrients. 2018 Nov;10(11):1707.
  36. Neriman A, Hakan Y, Ozge U. The psychotropic effect of vitamin D supplementation on schizophrenia symptoms. BMC psychiatry. 2021 Dec;21(1):1-0.
  37. Pawełczyk T, Grancow-Grabka M, Kotlicka-Antczak M, Trafalska E, Pawełczyk A. A randomized controlled study of the efficacy of six-month supplementation with concentrated fish oil rich in omega-3 polyunsaturated fatty acids in first episode schizophrenia. J Psychiatr Res. 2016 Feb;73:34-44. doi: 10.1016/j.jpsychires.2015.11.013. Epub 2015 Nov 25. PMID: 26679763.
  38. Roosterman, D., & Cottrell, G. S. (2021). The two-cell model of glucose metabolism: a hypothesis of schizophrenia. Molecular psychiatry, 26(6), 1738–1747.