Title: Nutrition, Brain Function And Chronic Fatigue Syndrome
Key words: psychoneuroimmunology, mind, immune system, Epstein-Barr virus, chronic fatigue syndrome, hypocortisolism, food intolerance, allergies, intestinal permeability, gut dysbiosis, opiod excess, gluten, casein, pineal gland, sulphate metabolism, cytokines, nitric oxide, glucose intolerance, antioxidants
Date: May 2001
Category: Specific conditions
Author: Kate Neil (NS3)
Nutrition, Brain Function And Chronic Fatigue Syndrome
Psychoneuroimmunology (PNI) addresses the influence of the cognitive images of the mind on the central nervous system (CNS) and consequent interactions with the immune system1.
There is increasing evidence to link chronic Epstein-Barr virus (EBV) infections with fatigue syndromes2,3,4. A normally functioning immune system keeps this virus in check5.
CFS sufferers have a mild hypocortisolism, which is associated with cognition and behavioural problems6,7. Researchers have proposed that CFS is a disease of the hypothalamic-pituitary-adrenal axis8. Cortisol deficiency may lead to an impaired immune response7.
Evidence indicates that some CFS patients suffer food intolerances and allergies 9. Increased intestinal permeability allows an excess of incompletely digested protein molecules into the blood-stream potentiating allergic responses in sensitive individuals10. Research by Bland and others found patients to have abnormal liver detoxification pathways and abnormal gut permeability11. Both patient symptoms and laboratory test results significantly improved over a 10 week period incorporating a strategy of: avoiding food allergens, stimulating repair of the intestinal linings, supporting liver detox pathways with specific nutrients, and using a hypoallergenic rice protein formula11.
Gut dysbiosis1,12, overgrowth of Candida albicans2112 and parasitic infections1,13 are implicated in CFS. Administration of antibiotics, immune suppressants, EBV or cytomegalovirus, enable this organism to proliferate, which would usually be kept in check by a normal immune system and other bowel bacteria12. Parasitic, yeast, bacterial infections, maldigestion, food allergies and intolerances can predispose towards increased intestinal permeability13. Hyperpermeability of the intestinal barrier may play a primary role in the aetiology of many systemic disorders10.
ME/CFS is implicated in the opioid-excess theory, which hypothesises that the incomplete breakdown and excessive absorption of peptides with opioid activity (gluten and casein), across an abnormally porous gut membrane, causes disruption to biochemical and neuroregulatory processes14. Opioids have been found to play a major role in the extensive bi-directional signalling between the brain, endocrine and immune systems. The opioid theory provides a holistic understanding of opioid-induced changes that affect stress responses, the peripheral, autonomic and CNS, the immune system, pineal gland, sleep, circadian and diurnal rhythms15.
Disordered sulphate metabolism has also been shown in CFS15. Inefficient activity of sulphite oxidase could give rise to high levels of sulphites, which are neurotoxic16,. This enzyme detoxifies cyanide ions. Cyanide ions inhibit oxidative phosphorylation and cellular oxidation reducing ATP supplies (in vivo) leading to cell damage and death16. This enzyme is also inhibited by cytokines, particularly TNF-alpha, indicating an inflammatory response17. Viral induced illness can are also implicated in uncoupling of oxidative phosphorylation due to increased cytokine production1.
Reduced sulphation is associated with poor digestive processes, increased intestinal permeability16 colonisation of Candida albicans and poor detoxification17. Current research suggests that a relationship may exist between impaired detoxifying pathways and symptomatology, and that toxic exposure may influence CFS11.
CFS sufferers have increased production of nitric oxide leading to excess formation of peroxynitrite1. The ‘lipid’ brain is most vulnerable to peroxynitrite attack, particularly mitochondrial membranes, which are less able to recover from oxidative stress1. Excessive release of nitric oxide in the CNS stimulates NMDA receptor activity leading to excessive stimulation and neurotoxicity1. Activation of poly adenosine 5 diphosphoribose synthetase, due to gut dysbioisis and toxic overload can also overstimualte NMDA receptors and induce neurotoxicity1. Glucose intolerance occurs in a subset of CFS sufferers1. Preventing low blood glucose is vital as the brain is highly glucose dependent1.
Using an integrative approach is the only sensible approach to treat PNI disorders such as CFS1. Gut/brain/endocrine/immune interactions appear common. Screening for imbalances in these systems can provide the most appropriate nutritional strategy for the individual.
Nutritional strategies include: the 4R approach to gut function, hypoallergenic diets, antioxidant therapy, hepatic support, hormone replacement, glucose regulation, correction of nutrient deficiencies oral/intravenous, amino therapy, herbal formulations for brain function, stress reduction, immune support (1,3-beta-glucan, Kutapressin, Immunoglobulins – intramuscular/intravenous1 and acetyl-l-carnitine18.
Dr Ian Hyams, MSc lecture, Surrey University, July 2000
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Nutritional Support for Chronic Fatigue Syndrome (CFS) Scott Rigden MD, Functional Medicine Adjunctive, The Institute for Functional Medicine