Overview of Diagnosis
What Is Mold Illness?
Mold illness is not an allergy. It is inflammation within the body which is caused by an immune system that has gone haywire. The term "mold illness" is a subcategory of biotoxin illness, called Chronic Inflammatory Response Syndrome (CIRS). The proper definition of CIRS is:
an accute and chronic, systemic inflammatory response syndrome acquired following exposure to the interior environment of a water-damaged building with resident toxigenic organisms, including, but not limited to fungi, bacteria, actinomycetes and mycobacteria as well as inflammagens such as endotoxins, beta glucans, hemolysins, proteinases, mannans, c-type lectins and possibly spirocyclic drimanes, plus volatile ogranic compounds.
Symptoms
If you are experiencing several of these symptoms, you could be suffering from mold illness. Take the Online Screening Test to determine your probability of having this illness.
♦Fatigue ♦Weakness ♦Aches ♦Muscle Cramps ♦Unusual Pain ♦Ice Pick Pain ♦Headache ♦Light Sensitivity ♦Red Eyes ♦Blurred Vision ♦Tearing ♦Sinus Problems ♦Cough ♦Shortness of Breath ♦Abdominal Pain ♦Diarrhea ♦Joint Pain ♦Morning Stiffness ♦Memory Issues ♦Focus/Concentration Issues ♦Word Recollection Issues ♦Decreased Learning of New Knowledge ♦Confusion ♦Disorientation ♦Skin Sensitivity ♦Mood Swings ♦Appetite Swings ♦Sweats (especially night sweats) ♦Temperature Regulation or Dysregulation Problems ♦Excessive Thirst ♦Increased Urination ♦Static Shocks ♦Numbness ♦Tingling ♦Vertigo ♦Metallic Taste ♦Tremors
This illness affects multiple systems in the body, which causes the patient to exhibit multiple symptoms.
How Did I Get Sick?
This illness happens after exposure to the interior environment of a Water-Damaged Building (WDB). There are many ways buildings become home to a toxic mix of microbes, fragments of microbes, and harmful chemicals. Buildings can host fungi, bacteria, mycobacteria, and actinomycetes as a result of construction defects like inappropriate ventilation; faulty construction of crawl spaces or inadequate building design; flat roofs or fake stucco cladding without adequate caulking; incomplete basements exposed to saturated ground water conditions; or not correcting water leaks.
Since 1998, Dr. Shoemaker has treated over 6,000 patients with an illness caused by exposure to these conditions. Each patient has a syndrome that is readily identified by blood tests performed in standard medical labs all over the country. These illnesses reflect a growing societal problem: dangerous buildings. Inhaling these dangerous inflammagens is what makes people sick.
We live in the Era of Dangerous Buildings, so the likelihood that you won't ever be exposed to dangerous buildings is quite low.
What Happens in the Body?
Many patients don't "look that bad." But that person is struggling with an illness that causes them to lose their quality of life. These patients didn't know that their genes made them prime targets for an assault by their own innate immune systems. Because of exposure to the interior environment of a Water-Damaged Building (WDB), these patients have an innate immune response that is going haywire.
At the core of why one person becomes ill from this exposure and another doesn't is because of their genetic susceptibility (or predisposition) - what is built into their DNA. Every person's innate immune system is personal and genetically coded - thus, it works differently for each of us. When the body is faced with a foreign substance, it immediately begins to process that substance - determine if it is good or bad, a friend or a foe. If the body determines the substance is a foe, it will develop antibodies to bind these substances, called antigens. Normally then, the next time a non-mold susceptible person walks into a WDB, his antibodies will target the antigen and clear it out fast.
However, there is an occurence of specific genes in about 25% of the population that cause this process of building antibodies to the substances in the WDB to fail. Think of a computer operating system full or errors. In these people, the antigens stay in the body, and our own defenses bombard our body and cause inflammation in the body to go wild. What you now have is a shell of a person who is defenseless against new exposures and is suffering daily from inflammation. The inate immune system doesn't recognize these toxic organisms and goes nuts in the body.
It is a vicious cycle - the foreign antigens (substances) stay in the body, causing the immune system to constantly fight back. This causes so much inflammation in the body that it leads to chronic illness, and the occurrence of the many symptoms listed above. Our entire being suffers from friendly fire from our own innate immune system.
What to look for?
The laboratory tests that are ordered are blood tests done in labs around the world, and paid for by insurance companies. These tests hold the secrets of survival. The names may be foreign to you, but since they are the things that hold the secrets to Surviving Mold, meet them today and perhaps know them as friends tomorrow. You don't need to be an expert to read further, but you should not turn away from learning more. Take the time to learn the language of mold illness and this site will try to make things as understandable as possible. No one says learning is easy, but that doesn't mean you can skip the learning process when it's your illness. Knowledge is power.
HLA DR - Your Genes
Human Leukocyte Antigens (HLAs), are found on the surface of nearly every cell in the human body. They help the immune system tell the difference between body tissue and foreign substances.
The immune response genes are found on chromosome six. Patients could have two alleles, copies of genes (for each gene, one allele is inherited from a person's father, and the other is inherited from a person's mother), out of approximately 10 possible, as part of their genotype. Based on Dr. Shoemaker's data, in normal populations compared to international registries of gene frequencies of HLA DR, we know the frequency of mold illness-susceptible patients approximates 24% of the normally distributed population. Almost a quarter of the normal population is genetically susceptible to chronic mold illness. Three quarters isn't.
DRB1 | DQ | DRB3 | DRB4 | DRB5 | |
Multisusceptible | 4 | 3 | 53 | ||
11/12 | 3 | 52B | |||
14 | 5 | 53B | |||
Mold Susceptible | 7 | 2/3 | 53 | ||
13 | 6 | 52A, B, C | |||
17 | 2 | 52A | |||
18* | 4 | 52A | |||
Borrelia, post Lyme Syndrome | 15 | 6 | 51 | ||
16 | 5 | 51 | |||
Dinoflagellates | 4 | 7/8 | 53 | ||
Multiple Antibiotic Resistant Staph Epidermis (MARCoNS) | 11 | 7 | 52B | ||
No recognized significance | 8 | 3, 4, 6 | |||
Low-risk Mold | 7 | 9 | 53 | ||
12 | 7 | 52B | |||
9 | 9 | 53 | |||
C4a
Normal Range: 0-2830 ng/ml
C4a has become the inflammatory marker of greatest significance looking at innate immune responses in those with exposure to WDB.
The complement system is a group of proteins that move freely through your bloodstream. The proteins work with your immune system and play a role in the development of inflammation.
Each complement activates inflammatory responses, with spillover of effect from the innate immune response to acquired immune response and hematologic parameters.
These short-lived products are re-manufactured rapidly, such that an initial rise of plasma levels is seen within 12 hours of exposure to biotoxins, and sustained elevation is seen until definitive therapy is initiated.
TGF Beta-1 - Transforming Growth Factor Beta-1
Normal Range: <2380 pg/ml
TGF Beta-1 is a protein that has important regulatory effects throughout innate immune pathways. This protein helps control the growth and division (proliferation) of cells, the process by which cells mature to carry out specific functions (differentiation), cell movement (motility), and the self-destruction of cells (apoptosis). The TGF Beta-1 protein is found throughout the body and plays a role in development before birth, the formation of blood vessels, the regulation of muscle tissue and body fat development, wound healing, and immune system function (especially regulatory T-cells).
TGF Beta-1 can impair T-regulatory cell function, which in turn contributes to the activation of autoimmunity, yet TGF Beta-1 also plays a role in suppressing autoimmunity(!). TGF Beta-1 has become important in the exploding incidences of childhood asthma, raising the tantalizing issue of remodeling due to biotoxin exposure. The EPA says that 21% of all new cases of asthma are due to exposure to Water Damaged Buildings. If an individual develops wheezing after exposure to a water damaged building, look for remodeling to be the cause. Remodeling means "something" happens that the airway changes to be more reactive and in need of medications to reduce wheezing. Neurologic, autoimmune and many other systemmic problems also are found with high TGF Beta-1.
MSH - Melanocyte Stimulating Hormone
Normal Range: 35-81 pg/mL
Alpha melanocyte stimulating hormone (MSH) has multiple anti-inflammatory and neurohormonal regulatory functions, exerting regulatory control on peripheral cytokine release, as well as on both anterior and posterior pituitary function.
In mold illness, MSH will be too low in over 95% of patients. This means increased susceptibility to mold illness, ongoing fatigue, pain, hormone abnormalities, mood swings, and much more. MSH is a hormone, called a regulatory neuropeptide, and it controls many other hormones, inflammation pathways, and basic defenses against invading microbes. Without MSH, bad things happen; chronic sleep disorders with non-restful sleep develop, and endorphin production is reduced, so chronic pain follows.
In mold illness, MSH will be too low in over 95% of patients. This means increased susceptibility to mold illness, ongoing fatigue, pain, hormone abnormalities, mood swings, and much more. MSH is a hormone, called a regulatory neuropeptide, and it controls many other hormones, inflammation pathways, and basic defenses against invading microbes. Without MSH, bad things happen; chronic sleep disorders with non-restful sleep develop, and endorphin production is reduced, so chronic pain follows.
VIP - Vasoactive Intestinal Polypeptide
Normal Range: 23-63 pg/mL
Vasoactive intestinal polypeptide (VIP) is a neuroregulatory hormone with receptors in the hypothalamus. This hormone/cytokine regulates peripheral cytokine responses, pulmonary artery pressures, and inflammatory responses throughout the body.
Low VIP levels are present in mold illness patients. This leads to unusual shortness of breath, especially in exercise. To date, every multiple chemical sensitivity patient Shoemaker has seen (over 500) have had low VIP. VIP plays a role similar to MSH in regulating inflammatory responses.
With respect to the digestive system, VIP seems to induce smooth muscle relaxation (lower esophageal sphincter, stomach, gallbladder), stimulate secretion of water into pancreatic juice and bile, and cause inhibition of gastric acid secretion and absorption from the intestinal lumen, which can lead to chronic, watery diarrhea.
VIP replacement, when used according to a strictly administered protocol, has proven to be fabulously effective in returning chronically fatigued patients back to a normal life. Do not use VIP if you are exposed to mold (with ERMI values greater than 2); if you fail a VCS test; or if you have a MARCoNS present in your nose.
MMP-9
Normal Range: 85-332 ng/mL
Matrix metallopeptidase 9 (MMP-9) is an enzyme that in humans, is encoded by the MMP9 gene. Proteins of the MMP9 family are involved in the breakdown of extracellular matrix in normal physiological processes, such as embryonic development, reproduction, and tissue remodeling, as well as in disease processes.
It has been implicated in pathogenesis COPD by destruction of lung elastin, in rheumatoid arthritis, astherosclerosis, cardiomyopathy, and abdominal aortic aneurysm.
MMP-9 delivers inflammatory elements of of blood into subintimal spaces, where further delivery into solid organs (brain, lung, muscle, peripheral nerve and joint) is initiated.
Leptin
Normal Range: Male: 0.5-13.8 ng/mL; Female: 1.1-27.5 ng/mL
Leptin turns on how tightly the body holds onto fatty acids. When Leptin is high, one holds onto fatty acids and stores them in fat. This leads to rapid weight gain, and because of the high Leptin, standard approches to weight loss like eating less and exercising more will fail. The inflammatory responses that causes Leptin levels to rise lead to patients who are chronically tired, in chronic pain, and forever overweight.
ADH/Osmolality
Normal Range: ADH - 1.0-13.3 pg/ml; Osmolality - 280-300 mosmol
Antidiuretic hormone (ADH), or vasopressin, is a substance produced naturally by the hypothalamus and released by the pituitary gland. The hormone controls the amount of water your body removes.
Osmolality is a test that measures the concentration of all chemical particles found in the fluid part of the blood.
Symptoms associated with dysregulation of ADH include dehydration, frequent urination, with urine showing low specific gravity; excessive thirst and sensitivity to static electrical shocks; as well as edema and rapid weight gain due to fluid retention during initial correction of ADH deficits.
ACTH/Cortisol
Normal Range: ACTH - 8-37 pg/mL; Cortisol - a.m. 4.3-22.4 / p.m. 3.1-16.7 ug/dL
ACTH is a hormone released from the anterior pituitary gland in the brain. Cortisol is a steroid hormone produced by the adrenal cortex, which is the outer part of the adrenal gland. The adrenal glands are located on top of both kidneys.
Early in the illness, as MSH begins to fall, high ACTH is associated with few symptoms; a marked increase in symptoms is associated with a fall in ACTH. Finding simultaneous high cortisol and high ACTH may prompt consideration of screening tumors, but the reality is that the dysregulation usually corrects with therapy.
ACLA IgA/IgG/IgM
Normal Range: IgA - 0-12; IgG 0-10; IgM 0-9
Anticardiolipins (ACLA) are autoantibodies. Antibodies are proteins in the blood that the body produces to fight off foreign agents. Antibodies do this by creating an immunity against unfamiliar microorganisms. Autoantibodies are antibodies that are directed against one's self. They interfere with the normal function of blood vessels and react with proteins in the blood that are bound to phospholipid, a type of fat molecule that is a part of the normal cell membrane.
IgA, IgM, and IgG are autoantibodies often identified in collagen vascular diseases such a lupus and scleroderma, and are often called anti-phospholipids.
An increased risk of spontaneous fetal loss in the first trimester of pregnancy is not uncommonly seen in women with the presence of these autoantibodies. They are found in over 33% of children with biotoxin-associated illnesses.
AGA IgA/IgG
Normal Range: 0-19
Antigliadin (AGA) antibodies are produced in response to gliadin, a small protein that is part of gluten, biologically active of wheat, barley and rye. These antibodies were thought at one time to be specific for Celiac Disease.
Within 30 minutes of ingestion of gliadin, for those with antigliadin antibodies, there will be an inflammatory response. This inflammatory response can provide many symptoms, including some that mimic attention deficit disorder. We all know that some kids are labeled as having ADHD because of their abnormal behavior seen within 30 minutes of eating a cupcake. It is not the sugar in the icing, it is the gluten in the cake. Antigliadin antibodies are found in over 58% of children with biotoxin-associated illness.
VEGF
Normal Range: 31-86 pg/mL
Vascular endothelial growth factor (VEGF) is a substance made by cells that stimulates new blood vessel formation and increases blood flow in the capillary beds. VEGF is a polypeptide. Deficiency of VEGF is quite common and is a serious problem in biotoxin illness patients that must be corrected. If you don’t have blood flow, cells begin starve and don’t work properly.
Please note: Parts of this page include proprietary information belonging to survivingmold.com, surviving mold, llc. It has been reposted here with express consent from surviving mold, llc.
Source: http://www.survivingmold.com/diagnosis