An autoimmune disease is a condition arising from an abnormal immune response to a normal body part. There are at least 80 types of autoimmune diseases. Nearly any body part can be involved. (1)



Although the symptoms for autoimmune diseases vary, common ones include:Depression FatigueFeverGeneral malaise (feeling ill)Muscle aches Inflammation is the classic sign of an autoimmune disease; it often causes redness, heat, pain, and swelling. Symptoms can come and go


For conventional medicine,  cause is generally unknown (2) Some autoimmune diseases such as lupus run in families, and certain cases may be triggered by infections or other environmental factors.[1] Some common diseases that are generally considered autoimmune include celiac disease, diabetes mellitus type 1, Graves’ disease, inflammatory bowel disease, multiple sclerosis, psoriasis, rheumatoid arthritis, and systemic lupus erythematosus.[1][4] The diagnosis can be difficult to determine.[1]


To gain a deeper understanding of a person’s autoimmune disease, we measure a full range of autoimmune and inflammatory markers, as well as the presence of allergens, toxins, mold, and heavy metals. These analyses may include the following: Glucose and insulin tolerance tests Gastrointestinal evaluations Blood tests (to identify markers for post-translation protein modification) Adrenal tests, including saliva tests for cortisol levels In addition, we may measure interleukins (IL6, IL10, and IL12), chemical messengers that help to mediate acute systemic immune responses. tests to detect secondary indicators of thyroid disease, including procedures to identify bacterial overgrowth in the gut and tests to measure autonomic nervous system effects.

examining all of the body’s systems and how they interact, including the gut, the brain, and inflammatory markers. By looking at their effects on other body systems and on biomarkers, we can see the downstream effects that are often missed by conventional testing.

We look deeper to diagnose each person as an individual, instead of relying on routine tests that identify conditions based on values determined by the population range. We get to know every patient; we recognize that the longer a problem persists, the less likely that a blood test will reveal it.


Treatment depends on the type and severity of the condition.[1] Nonsteroidal anti-inflammatory drugs (NSAIDs) and immunosuppressants are often used.[1] Intravenous Immunoglobulin may also occasionally be used.[2] While treatment usually improves symptoms they do not typically cure the disease.[1] 

Our treatments clear toxins and damaged proteins from the body. They prevent damage to healthy proteins and reduce both inflammation and free-radical damage. We prescribe therapies that support the gastrointestinal tract and recalibrate immune system functioning at the disease site, including the following:

•Restoration of the microbiome

•Natural anti-inflammatory compounds


•Targeted probiotics

•Ultraviolet blood irradiation (UVBI)

•IV nutrient therapy

•Ozone therapy

•Homeopathic immunomodulators



Cryptic determinants/molecular sequestration

Although it is possible for a potential autoantigen to be geographically sequestered in an immune privileged site within the body (e.g. the eye), mechanisms exist to express even these antigens in a tolerogenic fashion to the immune system. However, it is impossible to induce tolerance (immune unresponsiveness) to all aspects of an autoantigen. This is because under normal physiologic conditions some regions of a self-antigen are not expressed at a sufficient level to induce tolerance. These poorly displayed areas of an antigen are called “cryptic determinants.” The immune system maintains a high-affinity repertoire to the cryptic self because the presentation of these determinants was insufficient to induce strong tolerance.[13]

Molecular mimicry

The concept of molecular mimicry describes a situation in which a foreign antigen can initiate an immune response in which a T or B cell component cross-recognizes self. The cross reactive immune response is responsible for the autoimmune disease state.[14] Cross-reactive immune responses to self were first described for antibodies.

Altered glycan theory

According to this theory the effector function of the immune response is mediated by the glycans (polysaccharides) displayed by the cells and humoral components of the immune system. Individuals with autoimmunity have alterations in their glycosylation profile such that a proinflammatory immune response is favored. It is further hypothesized that individual autoimmune diseases will have unique glycan signatures.[15]

Hygiene hypothesis

According to the hygiene hypothesis, high levels of cleanliness expose children to fewer antigens than in the past, causing their immune systems to become overactive and more likely to misidentify own tissues as foreign, resulting in autoimmune conditions such as asthma.[16]


The first estimate of US prevalence for autoimmune diseases as a group was published in 1997 by Jacobson, et al. They reported US prevalence to be around 9 million, applying prevalence estimates for 24 diseases to a US population of 279 million.[17] Jacobson’s work was updated by Hayter & Cook in 2012.[18] This study used Witebsky’s postulates, as revised by Rose & Bona,[19] to extend the list to 81 diseases and estimated overall cumulative US prevalence for the 81 autoimmune diseases at 5.0%, with 3.0% for males and 7.1% for females. The estimated community prevalence, which takes into account the observation that many people have more than one autoimmune disease, was 4.5% overall, with 2.7% for males and 6.4% for females.[18]


In both autoimmune and inflammatory diseases, the condition arises through aberrant reactions of the human adaptive or innate immune systems. In autoimmunity, the patient’s immune system is activated against the body’s own proteins. In chronic inflammatory diseases, neutrophils and other leukocytes are constitutively recruited by cytokines and chemokines, leading to tissue damage.

Mitigation of inflammation by activation of anti-inflammatory genes and the suppression of inflammatory genes in immune cells is a promising therapeutic approach.[20][21][22] There is a body of evidence that once the production of autoantibodies has been initialized, autoantibodies have the capacity to maintain their own production.[23]

Stem cell transplantation is being studied and has shown promising results in certain cases.[24]





Approximately 50 million Americans have autoimmune disease, according to the American Autoimmune Related Diseases Association. More than 80 different conditions—including rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, Graves’ disease, and Hashimoto’s disease, fall under this umbrella, and some have similar symptoms. While these diseases are generally viewed as separate conditions by other Immunologists, they share common causes.

As the body’s primary defense against disease and infection, the immune system is integrally connected to all other biological systems. As a result, cross-reaction can wreak havoc throughout the body, causing chronic systemic inflammation (CSI). This condition further exhausts the immune system and leads to greater dysfunction.

Rather than classifying a patient’s symptoms as fitting a specific condition, we strive to identify the underlying causes of inflammation and autoimmunity. This deeper perspective acknowledges the interconnected causes of diseases, as well as the body’s ability to return to wholeness. By treating these fundamental issues, we relieve patients’ suffering and allow them to experience long-term healing.


While the causes of autoimmune disease are not fully known, many triggers have been identified. In some cases, microorganisms, such as bacteria or viruses, spark changes in the immune system. Other triggers may include environmental factors, pharmaceuticals, or chemical irritants. Intestinal permeability and food sensitivities can also play a large role. Immune attacks may even result from mistaken identity; foreign matter can sometimes look similar to healthy cells, creating a type of confusion in which both become targets.

A person’s genetic makeup also seems to affect his or her susceptibility to developing an autoimmune disease. Many

About 24 million (7%) people in the United States are affected by an autoimmune disease.[1][3] Women are more commonly affected than men.[1] Often they start during adulthood.[1] The first autoimmune diseases were described in the early 1900s.[5]

of these conditions are believed to be passed on from parents to children.



Reference and Precision Notes

(  ) Traditionally it was believed that the immune system was unable to react against the body’s own tissues, a concept described by the German immunologist Paul Ehrlich as “horror autotoxicus”. In 1904 this theory was challenged by the discovery of a substance in the serum of patients with paroxysmal cold hemoglobinuria that reacted with red blood cells.[25]




(1). ”Autoimmune diseases fact sheet”. OWH. 16 July 2012. Archived

(2) Borgelt, Laura Marie (2010). Women’s Health Across the Lifespan: A Pharmacotherapeutic Approach. ASHP. p. 579. ISBN 9781585281947Archived from the original on 2017-09-08.




2^ Jump up to:
a b Katz, U; Shoenfeld, Y; Zandman-Goddard, G (2011). “Update on intravenous immunoglobulins (IVIg) mechanisms of action and off- label use in autoimmune diseases”. Current pharmaceutical design. 17 (29): 3166–75. doi:10.2174/138161211798157540. PMID 21864262.

3^ Jump up to:
a b c d Borgelt, Laura Marie (2010). Women’s Health Across the Lifespan: A Pharmacotherapeutic Approach. ASHP. p. 579. ISBN 9781585281947. Archived from the original on 2017-09-08.

4 Jump up
Reinhard Hohlfeld, Klaus Dornmair, Edgar Mein, Hartmut Weker, The search for the target antigens of multiple sclerosis, part 1: autoreactive CD4+ T lymphocytes as pathogenic effectors and therapeutic targets. The Lancet, Neurology, Volume 15, Issue 2, February 2016, Pages 198-209,

5 Jump up
Paniker, Ananthanarayan And (169). Ananthanarayan and Paniker’s Textbook of Microbiology. 2005: Orient Blackswan. ISBN 9788125028086. Archived from the original on 2017-09-08.

6 Jump up
Witebsky E, Rose NR, Terplan K, Paine JR, Egan RW (1957). “Chronic thyroiditis and autoimmunization”. J. Am. Med. Assoc. 164 (13): 1439–47. doi:10.1001/jama.1957.02980130015004. PMID 13448890.

7 Jump up
Rose NR, Bona C (September 1993). “Defining criteria for autoimmune diseases (Witebsky’s postulates revisited)”. Immunol. Today. 14 (9): 426–30. doi:10.1016/0167-5699(93)90244-F. PMID 8216719.

8 Jump up
“Autoimmune disorders: MedlinePlus Medical Encyclopedia”. Archived from the original on 2016-01-12. Retrieved 2016-01-21.

9 Jump up
Walsh, SJ; Rau, LM (September 2000). “Autoimmune diseases: a leading cause of death among young and middle-aged women in the United States”. American Journal of Public Health. 90 (9): 1463–6. doi:10.2105/ajph.90.9.1463. PMC 1447637pastedGraphic.png. PMID 10983209.

10 Jump up
“MedlinePlus medical encyclopedia – autoimmune disorders”. National Institutes of Health. 16 July 2014. Archived from the original on 5 January 2015. Retrieved 21 December 2014.

11 Jump up
Cotsapas C, Hafler DA (2013). “Immune-mediated disease genetics: the shared basis of pathogenesis”. Trends in Immunology. 34 (1): 22–6. doi:10.1016/ PMID 23031829.

12 Jump up
Harrison’s Principles of Internal Medicine: Volumes 1 and 2, 18th Edition (18 ed.). McGraw-Hill Professional. 2011-08-11. ISBN 9780071748896. Archived from the original on 2016-05-29.

13 Jump up
Gammon G, Sercarz E (1989). “How some T cells escape tolerance induction”. Nature. 342: 6246. doi:10.1038/342183a0. PMID 2478888.

14 Jump up
Wucherpfennig KW, Strominger JL (1995). “Molecular mimicry in T cell-mediated autoimmunity: viral peptides activate human T cell clones specific for myelin basic protein”. Cell. 80 (5): 695–705. doi:10.1016/0092-8674(95)90348-8. PMID 7534214.

15 Jump up
Maverakis E, Kim K, Shimoda M, Gershwin M, Patel F, Wilken R, Raychaudhuri S, Ruhaak LR, Lebrilla CB (2015). “Glycans in the immune system and The Altered Glycan Theory of Autoimmunity”. J Autoimmun. 57 (6): 1–13. doi:10.1016/j.jaut.2014.12.002. PMC 4340844pastedGraphic.png. PMID 25578468.

16 Jump up
Rook, Graham A. W. (17 November 2011). “Hygiene Hypothesis and Autoimmune Diseases”. Clinical Reviews in Allergy & Immunology. 42 (1): 5–15. doi:10.1007/s12016-011-8285-8. PMID 22090147.

17 Jump up
Jacobson, DL; Gange, SJ; Rose, NR; Graham, NM (September 1997). “Epidemiology and estimated population burden of selected autoimmune diseases in the United States”. Clinical immunology and immunopathology. 84 (3): 223–43. doi:10.1006/clin.1997.4412. PMID 9281381.

18^ Jump up to:
a b Hayter, SM; Cook, MC (August 2012). “Updated assessment of the prevalence, spectrum and case definition of autoimmune disease”. Autoimmunity reviews. 11 (10): 754–65. doi:10.1016/j.autrev.2012.02.001. PMID 22387972.

19 Jump up
Rose, NR; Bona, C (September 1993). “Defining criteria for autoimmune diseases (Witebsky’s postulates revisited)”. Immunology Today. 14 (9): 426–30. doi:10.1016/0167-5699(93)90244-F. PMID 8216719.

20 Jump up
Mukundan L, Odegaard JI, Morel CR, Heredia JE, Mwangi JW, Ricardo-Gonzalez RR, Goh YP, Eagle AR, Dunn SE, et al. (Nov 2009). “PPAR-delta senses and orchestrates clearance of apoptotic cells to promote tolerance”. Nat Med. 15 (11): 1266–72. doi:10.1038/nm.2048. PMC 2783696pastedGraphic.png. PMID 19838202.

21 Jump up
Roszer T, Menéndez-Gutiérrez MP, Lefterova MI, Alameda D, Núñez V, Lazar MA, Fischer T, Ricote M (Jan 2011). “Autoimmune kidney disease and impaired engulfment of apoptotic cells in mice with macrophage peroxisome proliferator-activated receptor gamma or retinoid X receptor alpha deficiency”. J Immunol. 186 (1): 621–31. doi:10.4049/jimmunol.1002230. PMID 21135166.

22 Jump up
Singh RP, Waldron RT, Hahn BH (2012). “Genes, tolerance and systemic autoimmunity”. Autoimmunity Reviews. 11 (9): 664–9. doi:10.1016/j.autrev.2011.11.017. PMC 3306516pastedGraphic.png. PMID 22155015.

23 Jump up
Böhm I (2003). “Disruption of the cytoskeleton after apoptosis induction by autoantibodies”. Autoimmunity. 36 (3): 183–9. PMID 12911286.

24 Jump up
Swart, JF; Delemarre, EM; van Wijk, F; Boelens, JJ; Kuball, J; van Laar, JM; Wulffraat, NM (April 2017). “Haematopoietic stem cell transplantation for autoimmune diseases”. Nature reviews. Rheumatology. 13 (4): 244–256. PMID 28228650.

25 Jump up
Moticka, Edward J. (2013). Historical perspective on evidence-based immunology. Elsevier Science Publishing. p. 300. ISBN 9780123983817.

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