If you have 8 of the 13 symptom clusters and fail the vision test, you are a strong candidate for bloodwork.

The CIRS bloodwork will provide your genetic haplotype to see if you have one (or more) genes that make you more susceptible to chronic inflammation. If you’ve ever been diagnosed with mold, Lyme or MS, you may want to get tested.

NOTE: You only need to test for your haplotype once.  For future testing for improvements, you will only need to test a few markers. (e.g., MMP-9, MSH, TGF-Beta 1, etc.)

The following markers will be tested and an overall synthesis of your bloodwork will be provided. Follow-up support will also be provided via email.

HLA DR1/3/4/5, DQ Intermediate Resolution (167120)

• HLA antigens may be correlated with certain disease states or other clinical conditions. It can also be used for screening of transplant candidates and potential donors, transfusion of specifically compatible blood products, and other areas. Researchers have identified hundreds of different versions (alleles) of the HLA-DRB1 gene, each of which is given a particular number such as HLA-DRB1*04:01.
• Note: In his FAQ’s, Dr. Ritchie Shoemaker says, “In assessment of the DRB-1 1-5 over the years (together with its related haplotypes of 10-5 and 103-5, and 1-3 and 1-4) the only variable that reaches statistical significance we have seen is a reduced level of MSH in cases compared to other cases and then to controls.”
• Up to 5% with a Benign haplotype may still get CIRS from mold but will recovery more easily. There are a total of 54 known haplotypes – see page 716 in the book “Surviving Mold”. Alternatively, upon completion of the Biotoxin Test, you’ll be shown the 54 haplotypes.

Human Transforming Growth Factor beta 1 (TGF-b1) (821342)

• Elevated TGF beta-1 indicates an over-active immune response and is a key marker for severity in CIRS. It can change regulatory T cells into pathologic T cells, which then drive further inflammation.
• It also may cause tissue remodeling in multiple tissues in the body. Lowering TGF Beta-1 is critically important due to the potential for long term tissue changes due to the remodeling capacity of this cytokine

Melanocyte-Stimulating Hormone (MSH) (010421)

• Release of this neuroregulatory hormone is controlled by leptin in the pituitary. With biotoxin illness, disruption of the leptin receptor due to an increase in cytokines causes a drop in MSH, a master controller of many functions in the body.
• Low levels of MSH lead to dysregulation of multiple processes causing:
  • Problems with sleep patterns and melatonin, leading to disturbed sleep
  • Problems with salt and water balance through interaction with ADH/AVP and serum osmolality, leading to increased thirst and urination, palpitations and POTS
  • Dysregulation of the immune system with increased inflammatory cytokines, T cell abnormalities, and increase in autoimmunity.
  • Increased pain due to decreased endorphin production
  • Issues with increased gut permeability
  • Reduction in androgens/low testosterone
  • Colonization of the nose with MARCoNS
  • Weight gain unresponsive to changes in diet and exercise

Complement C4a (004330)

• Activation of the complement system plays an important role in our natural ability to ward off infection and in the pathogenesis of infection and inflammation.^1-6 Anaphylatoxins produced as the result of complement activation play a role in a number of infectious and inflammatory conditions including sepsis, ischemia-reperfusion injury, immune complex diseases, and hypersensitivity diseases like asthma.¹ Anaphylatoxins are also thought to be important in the pathogenesis of allergy, autoimmunity, neurodegenerative diseases, and cancer.^2,3
• Complement activation can occur through three separate mechanisms. The first mechanism to be discovered, referred to as the classical complement cascade, is activated by antigen-antibody complexes.^4-6 This was the basis for the name of this system as they serve to “complement” humoral immunity. Alternatively, the complement cascade can be activated directly by contact with bacterial cell surface molecules, including lipopolysaccharide from gram-negative outer membranes, teichoic acid from gram-positive cell walls, zymosan from fungal and yeast cell walls, and some parasite surface molecules. Recently, a third activation mechanism has been characterized in which mannose-binding lectin synthesized by the liver in response to inflammatory macrophage cytokines stimulates the activation of complement.
• Complement cascade activation results in the formation of complement split products C₃a, C₄a, and C₅a.⁴ These proteins, referred to as anaphylatoxins, facilitate the phagocytosis of immune complexes, viral particles, toxic cell debris and apoptotic corpses. Anaphylatoxins promote an inflammatory response by binding to complement receptors on granulocytes and macrophages.² Anaphylatoxins also bind to receptors on mast cells, which trigger the release of histamine, increasing blood vessel permeability and smooth muscle contraction.⁶ They control the local inflammatory response through activation of leukocytes and stimulating their chemotaxis to the site of infection.⁴
• Complement C₄a levels can become increased in any condition associated with inflammation.^2,3 Normal human pregnancy is associated with evidence of complement activation, with an increase in concentrations of the anaphylatoxins C₃a, C₄a, and C₅a in the maternal circulation.⁷ Levels of anaphylatoxins C₃a and C₄a have also been found to be elevated in patients with antiphospholipid syndrome relative to healthy controls.⁸ Ingram and associates have shown that levels of C₄a are increased in patients with multiple sclerosis, especially during relapse.⁹
• Complement activation split products are present only in trace amounts in normal plasma in vivo.¹⁰ It is crucial that samples be collected and stored properly in order to avoid in vitro activation.¹⁰ Blood must be drawn directly into tubes containing EDTA at a final concentration of at least 10 mM.¹⁰ Citrate and heparin do not block complement activation efficiently and should not be used.¹⁰ The addition of nafamostat mesilate (Futhan, FUT-175) further reduces in vitro complement activation.¹¹

MMP-9 (Matrix Metalloproteinase-9) (500124)