as related to autoimmunity. In my practice, infections are a common root cause of autoimmune conditions, and when we ad- dress these infections patients’ autoimmune conditions begin to improve signifi cantly.
There is a scientifi c term called mo- lecular mimicry that has been associated with autoimmune conditions and shown to be a leading mechanism to induce autoim- munity due to parasites, bacteria, viruses, mycotoxins, metals and chemicals. It has long been linked to autoimmune disease but only most recently has gained atten- tion. Molecular mimicry can trigger an immune response against what is called autoantigens. An autoantigen is a protein that is recognized by the immune system for people with autoimmune disease. A person can obtain an infection, like Epstein Barr virus, Strep or Mycoplasma, that has antigens that look similar to the person’s antigens. This resemblance of antigens by bacteria or viruses can activate T cells and thereby become autoreactive. This con- tinual series of events can begin to create what is a called a loss of self-tolerance and serve as initiating factor for autoimmune conditions. Many people have multiple infections and exposures over their life- time. It is important to continue to create and maintain a healthy lifestyle through diet, exercise, sleep and supplementation, if needed, to allow your body to get rid of them in a timely basis. Persistent infections that are not managed well can increase the possibility of initiating autoimmunity.
Let’s outline some examples of autoim- mune conditions that have been connected to some infections. For the past 60 years, proposed mechanisms of etiology for multiple sclerosis (MS) link MS to persistent viral infections. Close to two dozen viruses have been found in the brains of patients with MS including ones like herpes, and retrovirus. Neurological lyme disease mim- ics many MS symptoms (e.g. headaches, stiff neck, memory and ability to process information, fatigue, coordination chal- lenges) and can act to trigger MS.
Epstein Barr Virus (EBV) or herpesvirus 4, affects a majority of the population at large, over 90%. Research links its connec- tion to systemic autoimmunity; particularly for conditions like lupus (SLE). Studies have shown patients with lupus having higher titers of EBV antibodies as compared to the healthy population. EBV causes T cells to produce more pro-infl ammatory mediators (i.e. cytokines) for systemic autoimmunity. Studies have shown EBV antigen-1 having similar autoantigens in lupus which could possibly enable disease pathogenesis.
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