What is multiple sclerosis?
Multiple sclerosis (MS) occurs when the immune system attacks the central nervous system, which consists of the brain, spinal cord, and optic nerves. Some doctors believe MS is an autoimmune disease but others disagree because the specific target of the immune attack in MS has not yet been identified. Therefore, MS is known as an immune-mediated disease rather than an autoimmune disease.
Each nerve fibre consists of an axon and a myelin sheath, which is the fatty substance that surrounds and protects the axon. Myelin serves as insulation and aids efficient nerve fibre conduction.
In MS both the myelin and axon are damaged and scar tissue forms (sclerosis). As a result, nerve impulses travelling to and from the brain and spinal cord are distorted or interrupted. The location of the scarring determines symptoms, which vary greatly from patient to patient, because of the extensive nature of the central nervous system.
MS is a chronic condition, involving interplay between genetic and environmental factors that results in episodic and usually progressive demyel¬ination of nerve fibres of the central nervous system. In severe cases, progress can result in permanent axonal and neuronal death and severe neurological disability.
The incidence of MS varies with geographic latitude, occurring at greater frequency in northern European countries than in those closer to the tropics. Peculiarly, there also appears to be a residential time period for susceptibility, as northern European residents who emigrate to tropical countries before the age of 15 years exhibit a reduced prevalence of the disease compared with their home countries, whereas beyond 15 years of age, migration to tropical countries appears to confer no protective benefit.
Thus, it is hypothesised that genetic susceptibility to an environmental factor under¬lies the pathogenesis of this disease, triggering Th1 dominant autoimmune activity that operates via myelin-reactive T-cells, resulting in chronic cell-mediated toxicity, inflammatory and hypersensitivity reactions.
The time course and progression of MS varies considerably, from mild, episodic and non-progressive disease to persistent and rapidly progressive degeneration with severe neurological disability. However, neuronal degeneration usually advances to progressive disability and, long term, are resistant to medical therapy. Steroid therapy and interferon treatment may reduce the frequency and severity of demyelination episodes in acute episodes.
Conventional medical treatment for multiple sclerosis
Since multiple sclerosis (MS) was first identified the disease has been the subject of much research worldwide. While much has been learnt about the disease process, the exact cause remains unknown and no cure has been found. MS is not directly hereditary, although genetic susceptibility plays a part in its development.
Medical treatment can’t cure MS, but treatments are available that can modify the course of the disease. These treatments may help to reduce relapses, relieve symptoms, and improve day-to-day functioning.
In the absence of a definitive cure and as new drugs become available, the decision to treat or not treat MS, and how to treat, is becoming increasingly complex. Treatment with medication must be tailored to the individual’s MS type and stage. A person who has relapsed just once each year is treated differently to a person with highly active disease.
Immunomodulating drugs aim to prevent disability by modifying the immune system response. Trials show success in modifying the severity of the disease by reducing inflammatory injury to the central nervous system.
A number of first-line disease-modifying treatments have been shown to reduce relapse rates and disease progress in the short-term. Depending on the dosage, immunomodulating drugs, such as interferon beta 1b (betaferon), interferon beta 1a (Rebif, Avonex, Cinnovex) and glatiramer acetate, are injected each week, every few days, or daily.
Interferon beta-1a and beta-1s are antiviral agents that fight tumours, but are also effective in treating and controlling MS. Glatiramer acetate may reduce progression of disability by acting as a decoy for the immune system.
If these drugs don’t work then monthly IV infusion of natalizumab or oral finglomod might be prescribed. Natalizumab reduces the ability of inflammatory immune cells to attach to and pass through the intestinal wall and blood–brain barrier. Natalizumab is usually prescribed when a person has a high level of disease activity.
Mitozantrone, an anthracenedione antineoplastic agent, may be prescribed for more aggressive cases of MS, in particular if natalizumab is not well tolerated.
Fingolimod absorbs lymphocytes in lymph nodes, which prevents lymphocytes from contributing to an autoimmune reaction.
The majority of people with multiple sclerosis have mild, slow progressive symptoms and do not become severely disabled.
Nutritional medicine treatment for multiple sclerosis
Dietary-nutrient prescription is dependent on a thorough assessment of the patient’s individual nutritional status, genetic susceptibility, specific nutrient requirements, and social and environmental habitat.
Following careful assessment, synthesis and prescription of a dietary and nutrient supplement program should proceed systematically, correcting for disturbances of a number of contributing factors.
Optimisation of digestive capacity should be diligent because of the known relationship between maldigestion, bowel dysbiosis, and immune system activation. This is particularly important in view of the reported benefit of proteolytic enzyme therapy in improving the clinical condition and reducing disease progression in MS patients.
Saturated fat consumption and excessive carbohydrate intake have been associated with increased prevalence of MS. Adherence to a low-fat diet is reported to benefit clinical symptoms and retard disease progression, while non-adherence resulted in disease activation.
Essential fatty acid balance
Both omega-3 and omega-6 fatty acid supplementation is reported to retard disease progression and reduce the frequency and severity of episodes. Doses need to be quite high and used in conjunction with a diet low in saturated fat diet. Essential fatty acid balance suppresses immune system activity and cytokine production, which promote inflammation.
As is the case with all immune-mediated chronic disease conditions, adequate antioxidant capacity should be ensured, with particular emphasis placed on glutathione and selenium status, particularly in the presence of suspected mercury exposure.
Gut flora imbalance
Normalisation of bowel dysbiosis (glut flora imbalance) is important with respect to reducing gut-associated lymphoid tissue (GALT) activation and hepatic chemical load.
Specific disease treatment
Perhaps the most specific therapy is to identify the presence of mercury toxicity, followed by the removal of dental and tissue mercury if detected. Additional supplements of selenium, calcium and zinc will help to displace tissue mercury, while thiol-containing nutrients and ascorbate may facilitate mercury chelation and removal. In addition, specific nutrients docu¬mented to enhance axonal regeneration may confer additional benefit.
Liver detoxification problems
Though no specific research is available, the known increased levels of oxidative damage that derives from autoimmune and hyperactive immune disease, particularly as documented in Parkinson’s disease and Alzheimer’s disease, suggests that hepatic detoxi¬fication pathways require assessment, and need to be corrected if found to be compromised.
Again, no specific research relating to MS is available, apart from the immunosuppressive benefit associated with corticosteroid therapy. However, if anabolic steroid hormone levels (DHEA, pregnenolone, and testosterone) are compromised on appropriate testing, then judicious supplementation to improve anabolic protein synthesis is a logical corollary.
Enhanced brain serotonin status, with supplements of 5-hydroxytryptophan (check Mel added 5-) or L-tryptophan, may reduce hypothalamic-pituitary dysfunction, which is associated with MS-induced depression and stress, and is reportedly beneficial in alleviating mood disturbance and cerebellar ataxia.