Schizophrenia is a relatively uncommon brain disorder that affects approximately 1% of the population. This severe and disabling neurological disorder can affect anyone at any age, but most cases develop between the ages of 16 and 30. Schizophrenia treatment is usually in the form of therapy in combination with medication. Most pharmacological research now focuses on regulating neurotransmitters and hence there is interest in the role of certain fatty acids, which support neurotransmitter pathways and cell signalling and are naturally anti-inflammatory.
Schizophrenia is still relatively misunderstood and hard to diagnose, with matters made worse by the slow progression of the condition. Schizophrenia affects a person’s thoughts, perspectives and behaviours and presents as a range of symptoms grouped into three categories.
Positive symptoms refer to thoughts, behaviours and perceptions experienced by someone with schizophrenia that are not normally experienced by the general population. These symptoms and their severity vary considerably and can come and go over long periods. Positive symptoms experienced include abnormal thoughts, such as delusions and hallucinations.
Negative symptoms are the absence of thoughts, perceptions, or behaviours that are ordinarily present in people in the general population. These symptoms can include withdrawn behaviour, lack of interest in people and things, poor attention and speech as well as long periods of being totally motionless.
General symptoms of schizophrenia that can affect all sufferers include the inability to think clearly, control emotions, make decisions and relate to others. Many schizophrenics experience significantly altered senses, meaning their ability to interpret and respond correctly to situations is affected. This may result in a strong inability to communicate. This can also affect their self-perception and many sufferers may experience dramatic changes in emotion, movements and behaviour.
The cause of schizophrenia is not yet known and it appears to occur from a combination of factors. Both genetics and environmental factors (such as diet) appear to play a role in the development of schizophrenia and there is evidence to suggest it is more prevalent within families, supporting a genetic susceptibility.
Changes to the way we process fatty acids, the individual fat molecules that make up our cell membranes, have been found in schizophrenia and there is strong evidence to suggest that replacing the specific fats affected is an effective way to reduce and manage symptoms.
Immune factors, specifically inflammation regulation, appear to play a strong role in the development of schizophrenia. Infections during pregnancy, as well as high inflammatory signals later in life that alter neurotransmitter function and therefore brain function, can increase risk of schizophrenic disorders.
Diet plays an important role in brain function, with specific fats being essential for brain structure and communication between cells, whilst glucose is important for supplying energy to the cells. A balanced diet that is rich in long-chain omega-3 fats found in oily fish, together with adequate amounts of carbohydrate, is important for reducing the severity of schizophrenia symptoms.
Blood sugar control should be a high priority for dietary choices, as sweet foods and refined carbohydrates can worsen many of the behavioural and attention-related symptoms seen in schizophrenics. Basing diets on low-glycaemic load foods and eating lots of good quality fats and proteins is important to reduce fluctuations in blood sugar, which can negatively influence symptoms. To protect the brain from oxidative damage, diets should also be rich in colourful vegetables and seasonal local fruits to provide high levels of nutrients and antioxidants.
Research shows that prenatal nutritional deficiency is a risk factor for schizophrenia and related disorders. Homocysteine elevation in the third trimester of pregnancy seems to be a particularly strong predictor of schizophrenia in offspring and is a marker of low B-vitamin status. Homocysteine levels are an important indicator that your methylation cycle (a biochemical process involved in hundreds of chemical processes in the body, including control of gene function) is functioning properly. High homocysteine levels are linked to increased risk of mental health conditions, including schizophrenia. Vitamins B6, B12 and folic acid are important for efficient recycling of homocysteine into the protein building blocks, amino acids and antioxidants essential for health, thus low levels of these vitamins contribute to high homocysteine levels. Recent studies have found that, in comparison to healthy controls, schizophrenics have lower folate (the form of folic acid found in the body) and vitamin B12 levels. Low vitamin D status, both in pregnancy and early life, has also been linked to increased schizophrenia risk.
“Recent studies have found that, in comparison to healthy controls, schizophrenics have lower folate and vitamin B12 levels.”
Numerous studies looking at large groups of the population have found that schizophrenia (along with many other mental disorders including depression and bipolar disorder) is associated with reduced consumption of foods rich in long-chain omega fats, also known as polyunsaturated fatty acids (PUFAs), and a reduced ability of the cells to absorb and utilise these fats.
Anyone seeking natural remedies for schizophrenia should start first with polyunsaturated fatty acids (PUFAs). These are a type of fat, which form the building blocks of phospholipids, the main structural components of all of our cell membranes including cells that make up the brain and nerve fibres. Low intake and poor metabolism of these fats is associated with disorders of the brain and its function – a finding confirmed in schizophrenia.
One of the roles of omega-3 fats or PUFAs is in regulating neurotransmitter function, the chemicals essential to the communication of messages between brain cells. Given the importance of having the right levels of PUFAs in the brain, studies using fatty acid supplements have been carried out to see if this would benefit schizophrenic sufferers. Results have shown that amounts of the omega-3 fats EPA and DHA within the supplement is critical to the efficacy of the treatment. Many studies show that unless the supplement contains EPA omega-3 alone, it is unlikely to significantly improve schizophrenia symptoms and so standard fish oils are not effective because these nearly always contain EPA and DHA together and in low amounts.
Professor Basant K. Puri, a leading psychiatrist and medical researcher based at Imperial College, London, found that supplementing with EPA-only fish oil reversed the abnormalities in fatty acid metabolism associated with schizophrenia and this resulted in a dramatic and sustained clinical improvement in both positive and negative symptoms. Brain scan studies also carried out by Professor Puri and colleagues found a strong link between the size of specific brain structures (the lateral ventricle) and symptoms of psychotic illness. They found that schizophrenics’ ventricles were often enlarged due to increased ‘spaces’ in this area of the brain, which represents a reduction in “grey matter” or brain tissue. Professor Puri showed in one case that EPA supplementation was able to reduce the size of the ventricle spaces and thus increase brain tissue density.
“It is through restoring EPA levels and subsequently reducing inflammation to regulate neurotransmitters that EPA offers relief from the symptoms of schizophrenia.
Another way in which EPA specifically is important in the management of schizophrenia is through its ability to control and reduce the level of inflammation occurring in the body. Inflammatory chemicals called cytokines are known to degrade neurotransmitters and reduce their availability in the very areas of the nerve fibres where they are needed to transmit messages around the body, allowing us to interpret and respond to our surroundings and process emotions. High levels of inflammation can thus directly affect and even cause symptoms of schizophrenia; it is through restoring EPA levels and subsequently reducing inflammation to regulate neurotransmitters that EPA offers strong therapeutic potential as a schizophrenia treatment.
Ahmad Saedisomeolia, Mahmoud Djalali, Ali Malekshahi Moghadam, Ozra Ramezankhani, Laya Najmi (2011) Folate and vitamin B12 status in schizophrenic patients J Res Med Sci. Mar 16(Suppl1): S437–S441.
Anna M. et al. (2013) Inflammatory Cytokines and Neurological and Neurocognitive Alterations in the Course of Schizophrenia Fineberg, Biological Psychiatry, Volume 73 , Issue 10 , 951-966).
Emsley R, Myburgh C, Oosthuizen P & van Rensburg SJ. (2002) Randomized, placebo-controlled study of ethyl-eicosapentaenoic acid as supplemental treatment in schizophrenia. American Journal of Psychiatry 159:1596-8.
Hamlyn J, Duhig M, McGrath J, Scott J. (2013) Modifiable risk factors for schizophrenia and autism – Shared risk factors impacting on brain development. Neurobiology of Disease. 53:3-9.
Peet M. (2003) Eicosapentaenoic acid in the treatment of schizophrenia and depression: rationale and preliminary double-blind clinical trial results. Prostaglandins, Leukotrienes & Essential Fatty Acids 69:477-85.
Puri BK, Richardson AJ, Horrobin DF, Easton T, Saeed N, Oatridge A, Hajnal JV & Bydder GM. (2000) Eicosapentaenoic acid treatment in schizophrenia associated with symptom remission, normalisation of blood fatty acids, reduced neuronal membrane phospholipid turnover and structural brain changes. International Journal of Clinical Practice 54:57-63.
Puri BK. (2006) High-resolution magnetic resonance imaging sinc-interpolation-based subvoxel registration and semi-automated quantitative lateral ventricular morphology employing threshold computation and binary image creation in the study of fatty acid interventions in schizophrenia, depression, chronic fatigue syndrome and Huntington’s disease. International Review of Psychiatry 18:149-54. Review.
Richardson AJ, Easton T & Puri BK. (2000) Red cell and plasma fatty acid changes accompanying symptom remission in a patient with schizophrenia treated with eicosapentaenoic acid. European Neuropsychopharmacology 10:189-93.
Richardson AJ, Easton T, Gruzelier JH & Puri BK. (1999) Laterality changes accompanying symptom remission in schizophrenia following treatment with eicosapentaenoic acid. International Journal of Psychophysiology 34:333-9.
Richardson, AJ. (2003) The role of omega-3 fatty acids in behaviour, cognition and mood. Scandinavian Journal of Nutrition 47:92-98.
Richardson AJ, Easton T & Puri BK. (2000) Red cell and plasma fatty acid changes accompanying symptom remission in a patient with schizophrenia treated with eicosapentaenoic acid. European Neurophyschopharmacology 10:189-93.
Vita A, Dieci M, Silenzi C, Tenconi F, Giobbio G & Invernizzi G. (2000) Cerebral ventricular enlargement as a generalized feature of schizophrenia: a distribution analysis on 502 subjects, Schizophrenia Research 44:25-34.
Yao JK, Magan S, Sonel AF, Gurklis JA, Sanders R & Reddy RD. (2004) Effects of omega-3 fatty acid on platelet serotonin responsivety in patients with schizophrenia. Prostaglandins Leukotrienes and Essential Fatty Acids 71:171-6.