Guest guest Posted September 24, 2004 Report Share Posted September 24, 2004 Harmful Brain Effects of Interferons Dr. Mercola's Comment: Dr. Blaylock, a board-certified neurosurgeon and author of the highly recommended books _Health and Nutrition Secrets That Can Save your Life_ (http://www.amazon.com/exec/obidos/ASIN/0929173422/optimalwellnessc) and _Natural Strategies for Cancer Patients_ (http://www.amazon.com/exec/obidos/ASIN/0758202210/optimalwellnessc) , contributed this outstanding article about interferons, which are used widely for the treatment of multiple sclerosis (MS), hepatitis, cancer and more. If you, or someone you know, are taking these drugs, this article will help you decide if the benefits outweigh the many risks. ____________________________________ By L. Blaylock, M.D. _http://www.russellblaylockmd.com/_ (http://www.russellblaylockmd.com/) Interferons are used in clinical medicine for a number of medical conditions including: * A wide range of cancers * Chronic hepatitis * Multiple sclerosis * Chronic granulomatous disease * AIDS-related disorders Rarely considered are the effects of large doses of this immune cytokine on brain function. For example, the conventional treatment of chronic hepatitis is interferon-alpha-2b. Despite poor results in controlling the disease and the existence of safer, more effective natural treatments, physicians continue to use this toxic treatment. Of major concern are the neurologic effects of the treatment. Acute Problems It is known that interferons have two patterns of injury to the brain. One is acute and occurs within hours of treatment, often lasting for the first one to three weeks of the treatment. This usually includes fever, chills, headache and fatigue. Chronic Problems This is followed by a chronic phase in which more serious injuries to the nervous system result. Chronic symptoms can include malaise, lethargy, somnolence, headaches, low-grade fevers, anorexia (loss of appetite) and more serious symptoms such as psychomotor symptoms, cognitive problems, psychiatric behaviors and even delirium and coma. Brain Toxicity The severity of symptoms depends on the dose of the interferon and manner of administering the medication. Continuous infusion of high-dose interferons is associated with more severe neurologic problems. It is known that chronic brain toxicities occur at all doses but more so after doses higher than 18 million to 20 million units a day. Most common is severe fatigue. Even lower doses have been associated with a lack of drive and disinterest in participating in normal activities, a process called psychomotor retardation. This occurs in anywhere from 47 percent to 80 percent of patients. Changes in the ability to think clearly (cognitive changes) are frequently seen in patients treated with as little as 9 million units of interferon per week. The difficulty with thinking reaches a peak at one to three months. This can include a decreased attention span, difficulty concentrating, defective short-term memory and mental clouding. Studies have described frequent periods of silence and vacant staring, occurring even in mid-sentence. Objective testing for recall and cognitive function have shown an incidence of 17 percent to 50 percent in patients receiving standard doses of interferons. Most of these cognitive difficulties do improve, yet there are reports of persistent impairments lasting up to two years following cessation of treatment. In some patients the effect is so severe on the brain that patients sleep up to 20 hours a day and during waking periods experience disorientation and confusion. Speech difficulties (expressive dysphasia) and problems with balance have also been reported. On rare instances, these neurological effects have progressed to a demented state. Hallucinations have also been reported. It is important to appreciate that the patients in the first two categories to be described had no previous psychiatric history. Renault and co-workers, who examined many of these patients, divided the neurobehavioral effects into three syndromes: organic personality syndrome, organic affective syndrome and delirium effects. Patients with organic personality syndrome frequently experience uncontrollable overreaction to minor frustrations, are very irritable and have a short temper. Depression Common Those with the organic affective syndrome often describe feelings of depression and hopelessness. They cry easily and have difficulty interacting socially with others. Patients experiencing delirium have a clouding of their thinking, have short-term memory problems and have frequent mood changes. Many become severely agitated, abusive, withdrawn and may exhibit suicidal thoughts, delusions of being persecuted and phobias. Patients having delirium symptoms often had co-existing liver disease, history of psychiatric disorder or previous brain injury. Severe Reactions in Cancer Treatment The most severe effects have been seen in patients treated for cancers. In these patients death due to encephalopathy (widespread brain injury) and associated seizures have been described. This may be a result of combined toxicities of radiation, chemotherapy and interferon. Interferon-gamma is less toxic than the alpha or beta-interferons. With higher doses one can see chronic neurotoxicities, which can include dizziness, slowed thinking, confusion, crying spells, and even symptoms resembling Parkinson's disease. How Interferon Ruins Your Brain The mechanism of this injury to the brain appears to involve the brain's special immune cell called the microglia. Normally, these cells remain dormant in the brain. That is, they are sleeping. Microglia cells can be activated by numerous factors, including mercury, aluminum, iron, overvaccination, and brain trauma, strokes, infections (viruses, bacteria, rickettsia) and cytokines such as interferons. Once activated, microglia can move about the brain secreting very toxic compounds, which include two excitotoxins (glutamate and quinolinic acid). These excitotoxins dramatically increase free radical generation in the brain as well as oxidation of lipids (called lipid peroxidation). These radicals damage synaptic connections, interfere with neurotransmitters and can even kill neurons. In addition, these activated microglia generate other toxic compounds such as prostaglandins (PGE2), which increase brain inflammation. If the microglia activation is short lived, the damage to the brain is minimal and recovery takes place. Yet, should the activation continue, which would occur with high-dose and long-term use of interferons, the damage could be substantial and irreversible. Protecting the brain with high-dose and varied antioxidants as well as certain metabolic stimulants can substantially reduce this damage. Certain nutrients, such as malate, pyruvate, DHA, ascorbate, magnesium and methylcobalamin inhibit excitotoxicity. Physicians Frequently Miss Side Effects Physicians often ignore patient complaints of neurological difficulties during interferon treatments, assuming they are benign and reversible. As stated in the beginning, natural alternatives have been shown to be much more effective and dramatically safer than interferon treatments. ____________________________________ Related Articles: _MS Drugs 'a Waste of Money'_ (http://www.mercola.com/2003/mar/5/ms_drugs.htm) _Hepatitis Drug Interferon Linked to Depression_ (http://www.mercola.com/2002/dec/21/interferon.htm) _Amazing Recovery From Multiple Sclerosis_ (http://www.mercola.com/2003/oct/11/ms_success.htm) _Is Glutamine Supplementation Helpful or Harmful?_ (http://www.mercola.com/2004/may/1/glutamine.htm) _Is it Hepatitis C or Iron Toxicity?_ (http://www.mercola.com/2003/apr/2/iron.htm) _Modified Interferon Reported to be Effective Against Hepatitis C_ (http://www.mercola.com/2000/dec/17/hepatitis_c.htm) ____________________________________ References: Turowski RC, Triozzi PL. Central Nervous System Toxicities of Cytokine Therapy. In, Plotnikoff NP, et al (eds): Cytokines: Stress and Immunity. CRC Press, Boca Raton,1998. pp 93-114. F, et al. Neuropsychiatric manifestations of human leukocyte interferon therapy in patients with cancer. JAMA 252: 938, 1984. Iaffaiolo RV, et al. Neurotxic effects of long-term treatment with low-dose ab interferon. Current Therapy Research 48: 403, 1990. Meyers CA, et al. Persistent neurotoxicity of systemically administered interferon-a Neurology 41: 672, 1991. Renault PF, et al. Psychiatrc complications of long-term interferon-a therapy. Arch Internal Medicine 147: 1577, 1987. Kurzock R, et al. Phase I study if IV administrated recombinant g interferon in cancer patients. Cancer Treatment Reports 70: 1357, 1986. Blaylock RL. Chronic Microglial activation and excitotoxicity secondary to excessive immune stimulation: Possible factors in Gulf War Syndrome and autism. Journal of American Physicians and Surgeons. 9: 46-51, 2004. Thyroid autoimmunity disorders during interferon beta-1b treatment in patients with multiple sclerosis: review and case report] [Article in German] Lange-Asschenfeldt C, Boor S, Kahaly GJ, Thomke F. Klinik und Poliklinik fur Neurologie, Klinikum, Johannes-Gutenberg-Universitat, Mainz, lange@... Occurrence of thyroid autoimmunity and dysfunction following interferon alpha treatment of viral hepatitis and other diseases are known adverse effects and have been ascribed to the cytokine's general immunomodulatory and -activating properties. However, in spite of its extensive application, there have been few reports of such incidents during interferon beta (IFN-beta-1a/b) therapy, which is considered the standard treatment of relapsing-remitting multiple sclerosis (MS), and prospective studies have been published only recently. Here we present the case of a 38-year-old woman with Graves' disease including massive thyroid-associated ophthalmopathy appearing de novo following IFN-beta-1b therapy for MS. A literature search revealed an 11% (5% clinically overt) overall incidence of de novo thyroid dysfunction in IFN-beta-treated MS patients, mostly autoimmune hyperthyroidism. (Large-scale comparative studies for IFN-beta-1a are not available at present). Specific treatment but not necessarily discontinuation of IFN-beta-1b therapy was required in most cases. Female gender, pre-existing thyroid autoimmunity, and family history of thyroid disorders are presumable risk factors for thyroid dysfunction de novo during IFN-beta-1b treatment. PMID: 15257382 [PubMed - in process] ____________________________________ Jeff el _http://www.msprotocols.netfirms.com/_ (http://www.msprotocols.netfirms.com/) _http://www.msprotocols.netfirms.com/Getting%20Started.htm_ (http://www.msprotocols.netfirms.com/Getting%20Started.htm) Quote Link to comment Share on other sites More sharing options...
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