Laboratories Used by Appalachian Wellness Ctr.

by Oct 14, 2018



EnviroBiomics doesn’t test PEOPLE, it tests BUILDINGS.  Using a special test kit containing vinyl gloves and a Swiffer-type cloth, house dust that has been collecting for a longer than usual period of time (I like the top of door frames & picture frames) is collected according to the instructions in the envelope provided to you at your visit with Appalachian Wellness Ctr.   These tests are incredibly sophisticated.  They analyze house dust, determine the DNA types present in the house dust and then are able to figure out how much of each species of DNA is present providing a toxicity risk score for the building.

EnviroBiomics provides 2 specific types of tests.  It’s up to you to choose which of these two tests you want to do.

The Health Effects Roster of Type Specific Formers of Mycotoxins and Inflammagens – 2nd Version (HERTSMI2) looks at 5 commonly toxic mold species.  This is a less expensive test.

The Environmental Relative Moldiness Index (ERMI) looks at 26 toxic mold species.

It’s up to you to decide which test you want to order, both are adequate to do.

It’s important to remember that you should not only test your home, but any other building you spend significant amounts of time in and/or are suspicious of (even brief exposures in a building that is highly toxic/dangerous will prevent your recovery).

Remember, the FIRST RULE of treatment is to ELIMINATE exposure!

There are other thoughts regarding this test as well.  Ideally, the best way to assess a building for mold is with evaluation by an experienced Indoor Environmental Professional (IEP) who is familiar with the standards needed.  Most IEP’s are trained to the standards of the Environmental Protection Agency (EPA).

Standards  for mold-certified inspectors are much more complex.  Scott Armour is one of those folks.  He has his own views on this:

“My opinion is that if these lab reports, which are usually for sampling done DIY, create panic and instill fear, they are NOT valuable to the health community – you, me, anyone and everyone.


I agree the use of “red” scoring adds confusion also – is red bad?
the interpretation is, of course, based on the the original EPA description and use of the score, as well as the Shoemaker statements about ERMI and HERTSMI and health (per Shoemaker himself, but not replicated elsewhere).
As I explain, the “danger” Shoemaker applied to the condition is VERY limited – based on the factors of his study.
So some explanations are in order for both ERMI and HERTSMI:
In some ERMI lab reports, the red/yellow/green is simply based on the quartile cutoffs of ERMI score, here is what i provide to my clients – and anyone who needs clarification on ERMI:
“When looking at the graph of the ERMI scores, the colors are simply quartiles of the data – this means, green is the 25% of homes with an ERMI score under negative 4 (these are the lowest scoring homes). Yellow range is the middle 50% of scores (between -4 and 6), and red is the last 25% of homes, which had an ERMI score above 6 (the highest scoring homes). The numbers do not correlate to any quantification such as species or amount of mold growth, or water damage, or illness. The EPA research did not follow up on any of its findings or methods – it was a one time study …” – unpublished but widely distributed, by J.Scott Armour, 2016.
The HERTSMI is a bit different, it uses a logic flow chart mechanism, where four conditions MUST be met – which is because that is how Shoemaker arrived at this conclusion that above 15 is dangerous”. in other words, if a study is based on 4 conditions, then you can only interpolate to those same conditions unless you explicitly make assumptions that the new “real world” differences (variables) will actually not create differences in outcome (i.e., conclusion).
He said, IF a patient is diagnosed with CIRS (per his criteria), AND has genetic predisposition (using the HLA criteria), AND the doc intended to treat with cholestyramine, AND the HERTSMI score was above 15, THEN the patient was unlikely to show improvement.
Thats it. The relationship for lower HERTSMI scores was not strong and hence not even reliably predictable with regard to patient outcome – in other words, it didnt really matter what the HERSMI score was. 
THIS IS WHY sampling doesnt matter in nearly all cases – because the range of HERTSMI scores is actually all encompasssing of actual mold growth conditions – if you have mold growth, remove and clean the area. and if necy , clean all ambient dust in occupied high touch area and surfaces. Move on. Dont waste time and money on ERMI/HERTSMI/qPCR.”
Scott Armour, M.S.
Armour Applied Science, LLC
216-225-5237 phone and text

Humidity can also be a problem.

Every little bit helps. 
In wet/damp basement situations, if humidity can’t get low (e.g., 45-50), then the act of lowering (using the dehu to continually pull some water from one location to the device) will help slow/stop growth, even if room is “around” 70, such as this case.
Also, the little bit of air movement (aka ventilation) from the device will also help, since airflow over wet/damp surfaces will slow/prevent growth.
The biological reason for these changes in growth are because as the surface dries, or the air vapor is lowering, the actual point of growth will not have the optimal amount of available water – so, e.g., the wall “leaks”, paint fails because brick is wet, and efflorescence appears, but the mold won’t grow because the very top surface is undergoing evaporation, or the vapor in thin layer of air flowing over it is not sufficient. This is not 100%, nor universal, but it occurs more often than not – so the drying process does improve the overall condition (i.e., it’s better tomorrow than yesterday!)
Direction of the device output, and location of the input will make a difference also.
The output is warm,dry, and will quickly pick up vapor, and will aid evaporation of wet/damp surfaces. So tell them to point the output toward the wettest wall corner if possible. Or, put the device in that corner also.
If you put the device in the “middle” of the space, with output going to the wettest corner/surface, then you might get lucky and create a circulation pattern that pushes dry air toward the wet area, and that newly “wet” air will move back to the device to be dried again. (this is not ez, and for most people it’s only somewhat intuitive).
In the meantime, if this person is a DIY, they should make some attempt to clean visible mold off of surfaces (walls, ceilings) and discard visibly moldy contents – in situation with chronic high humidity in a basement, inevitably there will be contents, objects, furniture with a surface haze of mold (typically white to light green and yellow, sometimes light brown). This often is thought to be housedust, or construction dust like drywall.
Scott Armour, M.S.
Armour Applied Science, LLC
216-225-5237 phone and text
Genova Diagnostics

Genova Diagnostics

Genova Diagnostics provides a variety of labs from heavy metal testing to hormone testing.  This is widely considered a lab for integrative/alternative practitioners.  

Great Plains Labs

 Great Plains Laboratory

The most frequent tests we order from GPL are;

Urine Mycotoxin test

Determines exposure to toxic mold/fungi by analyzing for those toxins in the urine.

Mycotoxins are some of the most prevalent toxins in the environment.  Mycotoxins are metabolites produced by fungi like mold, which can infest buildings, vehicles, and foodstuffs.   A majority of mycotoxin exposures are through food ingestion or airborne exposure.  In the European Union, 20% of all grains harvested have been found to be contaminated with mycotoxins.  Unfortunately, mycotoxins are resistant to heat and many processing procedures.

Fungi are able to grow on almost any surface, especially if the environment is warm and wet.  Inner wall materials of buildings, wall paper, fiber glass insulation, ceiling tiles, and gypsum support are all good surfaces for fungi to colonize.  These fungi then release mycotoxins into the environment causing symptoms of many different chronic diseases.  Diseases and symptoms linked to mycotoxin exposure include fever, pneumonia-like symptoms, heart disease, rheumatic disease, asthma, sinusitis, cancer, memory loss, vision loss, chronic fatigue, skin rashes, depression, ADHD, anxiety, and liver damage.  With our new MycoTOX Profile, we can identify mycotoxin exposures and make recommendations for detoxification treatments that have been effective.


  • MycoTOX screens for eleven different mycotoxins, from 40 species of mold, in one urine sample.
  • MycoTOX is the most comprehensive and competitively priced mycotoxin test available.
  • MycoTOX uses the power of advanced mass spectrometry (MS/MS), which is necessary to detect lower levels of these fungal toxins. This test is optimal for follow up testing to ensure that detoxification therapies have been successful.
  • MycoTOX pairs perfectly with the Organic Acids Test (OAT), GPL-TOX (Toxic Non-Metal Chemical Profile), Phospholipase A2 Activity Test, and the Glyphosate Test. This gives you comprehensive testing to assess exposure to common environmental toxins and the damage that can be caused by this exposure, all at a great value, and all from one urine sample.



Aflatoxin M1 (AFM1) is the main metabolite of aflatoxin B1, which is a mycotoxin produced by the mold species Aspergillus. Aflatoxins are some of the most carcinogenic substances in the environment.  Aflatoxin susceptibility is dependent on multiple different factors such as age, sex, and diet.  Aflatoxin can be found in beans, corn, rice, tree nuts, wheat, milk, eggs, and meat.  In cases of lung aspergilloma, aflatoxin has been found in human tissue specimens. Aflatoxin can cause liver damage, cancer, mental impairment, abdominal pain, hemorrhaging, coma, and death.  Aflatoxin has been shown to inhibit leucocyte proliferation.  Clinical signs of aflatoxicosis are non-pruritic macular rash, headache, gastrointestinal dysfunction (often extreme), lower extremity edema, anemia, and jaundice.  The toxicity of Aflatoxin is increased in the presence of Ochratoxin and Zearalenone.


Ochratoxin A (OTA) is a nephrotoxic, immunotoxic, and carcinogenic mycotoxin.  This chemical is produced by molds in the Aspergillus and Penicillium families.  Exposure is primarily through contaminated foods such as cereals, grape juices, dairy, spices, wine, dried vine fruit, and coffee.  Exposure to OTA can also come from inhalation exposure in water-damaged buildings.  OTA can lead to kidney disease and adverse neurological effects.  Studies have shown that OTA can cause significant oxidative damage to multiple brain regions and the kidneys.  Dopamine levels in the brain of mice have been shown to be decreased after exposure to OTA.


Sterigmatocystin (STG) is a mycotoxin that is closely related to aflatoxin.  STG is produced from several species of mold such as Aspergillus, Penicillium, and Bipolaris. It is considered to be carcinogenic, particularly in the cells of the GI tract and liver.  STG has been found in the dust from damp carpets.  It is also a contaminant of many foods including grains, corn, bread, cheese, spices, coffee beans, soybeans, pistachio nuts, and animal feed. In cases of lung aspergilloma, STG has been found in human tissue specimens.  The toxicity of STG affects the liver, kidneys, and immune system.  Tumors have been found in the lungs of rodents that were exposed to STG.  Oxidative stress becomes measurably elevated during STG exposure, which causes a depletion of antioxidants such as glutathione, particularly in the liver.


Roridin E is a macrocyclic trichothecene produced by the mold species Fusarium, Myrothecium, and Stachybotrys (i.e. black mold).  Trichothecenes are frequently found in buildings with water damage but can also be found in contaminated grain.  This is a very toxic compound, which inhibits protein biosynthesis by preventing peptidyl transferase activity. Trichothecenes are considered extremely toxic and have been used as biological warfare agents.  Even low levels of exposure to macrocyclic trichothecenes can cause severe neurological damage, immunosuppression, endocrine disruption, cardiovascular problems, and gastrointestinal distress.


 Verrucarin A (VRA) is a macrocyclic trichothecene mycotoxin produced from Stachybotrys, Fusarium, and Myrothecium. Trichothecenes are frequently found in buildings with water damage but can also be found in contaminated grain. VRA is a small, amphipathic molecule that can move passively across cell membranes.  The primary tissues affected by VRA are intestinal and gastric mucosa, bone marrow, and spleen.  VRA causes damage to human cells by inhibiting protein and DNA synthesis, disrupting mitochondrial functions, and by producing oxidative stress (due to generation of free radicals).  Exposure to VRA can cause immunological problems, vomiting, skin dermatitis, and hemorrhagic lesions.


Enniatin B1 is a fungal metabolite categorized as cyclohexa depsipeptides toxin produced by the fungus Fusarium. This strain of fungus is one of the most common cereal contaminants.  Grains in many different countries have recently been contaminated with high levels of enniatin.  The toxic effects of enniatin are caused by the inhibition of the acyl-CoA cholesterol acyltransferase, depolarization of mitochondria, and inhibition of osteoclastic bone resorption.  Enniatin has antibiotic properties and chronic exposure may lead to weight loss, fatigue, and liver disease. 


Zearalenone (ZEA) is a mycotoxin that is produced by the mold species Fusarium, and has been shown to be hepatotoxic,  haematotoxic, immunotoxic, and genotoxic.  ZEA is commonly found in several foods in the US, Europe, Asia, and Africa including wheat, barley, rice, and maize.  ZEA has estrogenic activity and exposure to ZEA can lead to reproductive changes.  ZEA’s estrogenic activity is higher than that of other non-steroidal isoflavones (compounds that have estrogen-like effects) such as soy and clover.  ZEA exposure can result in thymus atrophy and alter spleen lymphocyte production as well as impaired lymphocyte immune response, which leads to patients being susceptible to disease. 


Gliotoxin (GTX) is produced by the mold genus Aspergillus.  Aspergillus spreads in the environment by releasing conidia which are capable of infiltrating the small alveolar airways of individuals.  In order to evade the body’s defenses Aspergillus releases Gliotoxin to inhibit the immune system.  One of the targets of Gliotoxin is PtdIns (3,4,5) P3.  This results in the downregulation of phagocytic immune defense, which can lead to the exacerbation of polymicrobial infections.  Gliotoxin impairs the activation of T-cells and induces apoptosis in monocytes and in monocyte-derived dendritic cells.  These impairments can lead to multiple neurological syndromes.


Mycophenolic Acid (MPA) is produced by the Penicillium fungus.  MPA is an immunosuppressant which inhibits the proliferation of B and T lymphocytes.  MPA exposure can increase the risk of opportunistic infections such as Clostridia and Candida. MPA is associated with miscarriage and congenital malformations when the woman is exposed in pregnancy.  


Dihydrocitrinone is a metabolite of Citrinin (CTN), which is a mycotoxin that is produced by the mold species Aspergillus, Penicillium, and Monascus.  CTN exposure can lead to nephropathy, because of its ability to increase permeability of mitochondrial membranes in the kidneys.  The three most common exposure routes are through ingestion, inhalation, and skin contact.  CTN has been shown to be carcinogenic in rat studies.  Multiple studies have linked CTN exposure to a suppression of the immune response.  


Chaetoglobosin A (CHA) is produced by the mold Chaetomium globosum (CG).   CG is commonly found in homes that have experienced water damage.   Up to 49% of water-damaged buildings have been found to have CG.  CHA is highly toxic, even at minimal doses.  CHA disrupts cellular division and movement.  Most exposure to CG is through the mycotoxins because the spores tend not to aerosolize.  Exposure to CHA has been linked to neuronal damage, peritonitis, and cutaneous lesions.

*These markers are expected (not guaranteed) to be available as part of the test by November 1, 2018.




Aspergillus is the most prevalent mold group in the environment.  It has caused billions of dollars of in damage to crops and livestock.  Two of the most common Aspergillus mycotoxins are aflatoxin and ochratoxin.  The main target of these toxins is the liver.  These toxins have been found in all major cereal crops including peanuts, corn, cotton, millet, rice, sorghum, sunflower seeds, wheat, and a variety of spices.  Theyare also found in eggs, milk, and meat from animals fed contaminated grains.  Diseases caused by Aspergillus are called aspergillosis.  The most common route of infection is through the respiratory system.  Aspergillus can cause severe asthma when the mold colonizes the lung, forming a granulomatous disease.


There are over 200 species of Penicillium that have been discovered.  Penicillium chrysogenum is the most common of these species.  It is often found in indoor environments and is responsible for many allergic reactions.  Penicillium is also a known contaminant in many different food items.  Many different types of citrus fruits can become contaminated with Penicillium, but it can also contaminate seeds and grains.  One reason that Penicillium is such a common infestation is because of its ability to thrive in low humidity.  In the home, Penicillium can be found in wallpaper, carpet, furniture, and fiberglass insulation.  The most common mycotoxin produced by Penicillium is ochratoxin (OTA).  Ochratoxin is nephrotoxic, which means that it damages the kidneys.  It is also carcinogenic.


Stachybotrys is a greenish-black mold.  This mold can grow on materials with high cellulose and low nitrogen content such as gypsum board, paper, fiberboard, and ceiling tiles.  Stachybotrys is known for its production of the highly toxic macrocyclic trichothecene mycotoxins.  Two of the more common mycotoxins produced by Stachybotrys are roridin E and verrucarin.  In addition to these mycotoxins, the fungus produces nine phenylspirodrimanes, as well as cyclosporine, which are potent immunosuppressors. These immunosupressors along with the mycotoxin trichothecenes may be responsible for the high toxicity of Stachybotrys.


Fusarium’s major mycotoxins are zearalenone (ZEN) and fumonisin.  Fusarium fungi grow best in temperate climate conditions.  They require lower temperatures for growth than Aspergillus. Fusarium grows worldwide on many different types of grains including corn and wheat.  Exposure to mycotoxins from Fusarium can lead to both acute and chronic effects.  These symptoms can include abdominal distress, malaise, diarrhea, emesis, and death.  ZEN possesses estrogenic effects and has been implicated in reproductive disorders.


If you or a patient has done a MycoTOX Profile and the results show moderate to high levels of mycotoxins there are things you can do to help the body eliminate the toxins and prevent future exposures.  The first step is to eliminate or reduce exposure to mold.  The majority of exposures result from contaminated food, skin contact, and inhalation of spore-borne toxins, which is often caused by water-damaged buildings.  Inhalation of spore-borne toxins can be limited by detecting and eliminating damp and moldy environments, both indoor and outdoor.

Mold can enter homes through open windows, vents, doorways, and heating and air conditioning systems.  Mold grows well on organic products such as paper, wood, cardboard, and ceiling tiles.  Mold can also grow on insulation, drywall, wallpaper, carpet, fabric, and upholstery.  Mold can be controlled by cleaning and drying after water intrusion; having proper ventilation for showers, laundry, and cooking areas; making sure that windows, roofs, and pipes are free of leaks; and by controlling humidity levels.  After moisture problems are alleviated it is recommended that mold removal be performed by a licensed contractor.  Attempts to remove mold may cause mold spores to scatter and spread to other areas.  In addition, treating mold without proper ventilation could result in health problems caused by the release of mycotoxins from the mold spores.  

Treatment for mold exposure should include fluid support to prevent dehydration.  The drug Oltipraz can increase glutathione conjugation of mold toxins while inhibiting the toxic effect of P450 oxidation, reducing liver toxicity and promoting safer elimination.  A diet of carrots, parsnips, celery, and parsley may reduce the carcinogenic effects of mold. Bentonite clay and zeolite clay are reported to reduce the absorption of mold found in food. Supplementation with chlorophyllin, zinc, A, E, C, NAC, rosmarinic acid, and liposomal glutathione alone or in combination have been shown to mitigate the oxidative effects of mold

Organic Acid Test 

Organic acids are chemical compounds excreted in the urine of mammals that are products of metabolism. Metabolism is the sum of chemical reactions in living beings by which the body builds new molecules and breaks down molecules to eliminate waste products and produce energy. Organic acids are organic compounds that are acidic. Organic acids are substances in which carbon and hydrogen are always present but which may also contain the elements of oxygen, nitrogen, sulfur, and phosphorus as well.

The names of most organic acids contain the suffix –ic, followed by the word “acid” such as lactic acid. Every organic acid has one or more conjugate bases named with the suffix –ate. Thus, the conjugate base of lactic acid is lactate. Many times, the name of the organic acid and its conjugate base(s) are used interchangeably when discussing physiology and biochemistry, such as lactate or lactic acid. The most common chemical groups associated with organic acids are carboxylic acids which are present in the conjugate base form at neutral pH, 7.0, the pH of the inside of most living cells. Organic acids with one carboxylic acid have one conjugate base while some organic acids may have two or three carboxylic acids and two or three conjugate bases.


Almost all organic acids used for human testing are measured by a combination of gas or liquid chromatography linked with mass spectrometry. Organic acids are most commonly analyzed in urine because they are not extensively reabsorbed in the kidney tubules after glomerular filtration.  Thus, organic acids in urine are often present at 100 times their concentration in the blood serum and thus are more readily detected in urine.  This is why organic acids are rarely tested in blood or serum. The number of organic acids found in urine is enormous.  Over 1,000 different organic acids have been detected in urine since this kind of testing started.


Many genetic disorders are caused by the production of an inefficient enzyme that reacts at a slower than usual rate, resulting in an accumulation of a metabolic intermediate.  More than 50 phenotypically different organic acidemias are now known since the oldest known disease, isovaleric aci­demia, was described in 1966.  An organic acid is any compound that generates protons at the prevailing pH of human blood.  Although some organic acidemias result in lowered blood pH, other organic acidemias are associated with organic acids that are relatively weak and do not typically cause acidosis.  Organic acidemias are disorders of intermediary metabolism that lead to the accumulation of toxic compounds that derange multiple intracellular biochemical pathways including glucose catabolism (glycolysis), glucose synthesis (gluconeogenesis), amino acid and ammonia metabolism, purine and pyrimidine metabolism, and fat metabolism.  The accumulation of an organic acid in cells and fluids (plasma, cerebrospinal fluid, or urine) leads to a disease called organic acidemia or organic aciduria.

Clinical presentations of organic acidemias vary widely and may include failure to thrive, mental and/or developmen­tal retardation, hypo- or hyperglycemia, encephalopathy, lethargy, hyperactivity, seizures, dermatitis, dysmorphic facial features, microcephaly, macrocephaly, anemia and/or immune deficiency with frequent infections, ketosis and/or lactic acidosis, hearing, speech, or visual impairment, peripheral neuropathy, sudden cardiorespiratory arrest, nau­sea and coma.  Many organic acidemias are associated with slight to marked increases in plasma ammonia.  Some organic acidemias may be chronic and present in the first few days of life. In others, such as medium chain acyl dehydrogenase deficiency, a child might appear completely normal until a potentially fatal episode of cardiorespiratory arrest.

Many other non-genetic factors can also alter human metabolism. Toxic amounts of the drug acetaminophen and other toxic chemicals can use up a key molecule, glutathione, that helps the body detoxify, leading to the overproduction of the organic acid pyroglutamic acid. Tumors of the adrenal gland called pheochromacytomas can cause the overproduction of the neurotransmitter epinephrine, resulting in marked increases in its metabolite, vanillylmandelic acid (VMA). Genetic diseases of the mitochondria, the cell’s energy source, as well as toxic chemicals that disrupt mitochondrial function cause elevation of succinic acid.  Succinic acid is a key intermediate of both the Kreb’s cycle and the electron transport chain that generates adenosine triphosphate (ATP), the currency for most of the body’s energy transactions.

A number of organic acids directly or indirectly indicate deficiencies of critical vitamins such as vitamin B12, pantothenic acid, biotin, and others. One of the most important uses of the organic acids test is as an indicator of dysbiosis, an abnormal overgrowth of yeast and bacteria in the intestinal tract. Some of these bacterial byproducts from the intestine enter the blood stream and may alter the metabolism of neurotransmitters such as dopamine.

The Organic Acids Test (OAT) offers a comprehensive metabolic snapshot of a patient’s overall health with over 70 markers.  It provides an accurate evaluation of intestinal yeast and bacteria.  Abnormally high levels of these microorganisms can cause or worsen behavior disorders, hyperactivity, movement disorders, fatigue and immune function. Many people with chronic illnesses and neurological disorders often excrete several abnormal organic acids in their urine. The cause of these high levels could include oral antibiotic use, high sugar diets, immune deficiencies, acquired infections, as well as genetic factors.

Our Organic Acids Test also includes markers for vitamin and mineral levels, oxidative stress, neurotransmitter levels, and is the only OAT to include markers for oxalates, which are highly correlated with many chronic illnesses.

If abnormalities are detected using the OAT, treatments can include supplements, such as vitamins and antioxidants, or dietary modification. Upon treatment, patients and practitioners have reported significant improvement such as decreased fatigue, regular bowel function, increased energy and alertness, increased concentration, improved verbal skills, less hyperactivity, and decreased abdominal pain. The OAT is strongly recommended as the initial screening test.

Toxic non-Metal Profile

Every day, we are exposed to hundreds of toxic chemicals through products like pharmaceuticals, pesticides, packaged foods, household products, and environmental pollution.  As we have become more exposed to chemical-laden products and to toxic chemicals in food, air, and water, we have been confronted with an accelerating rate of chronic illnesses like cancer, heart disease, chronic fatigue syndrome, chemical sensitivity, autism spectrum disorders, ADD/AD(H)D, autoimmune disorders, Parkinson’s disease, and Alzheimer’s disease.

Because exposure to environmental pollutants has been linked to many chronic diseases, The Great Plains Laboratory has created GPL-TOX, a toxic non-metal chemical profile that screens for the presence of 172 different toxic chemicals including organophosphate pesticides, phthalates, benzene, xylene, vinyl chloride, pyrethroid insecticides, acrylamide, perchlorate, diphenyl phosphate, ethylene oxide, acrylonitrile, and more.  This profile also includes Tiglylglycine (TG), a marker for mitochondrial disorders resulting from mutations of mitochondrial DNA.  These mutations can be caused by exposure to toxic chemicals, infections, inflammation, and nutritional deficiencies.


  • GPL-TOX screens for 172 different environmental pollutants using 18 different metabolites, all from a single urine sample.
  • GPL-TOX uses the power of advanced mass spectrometry (MS/MS), which is necessary to detect lower levels of certain genetic, mitochondrial, and toxic chemical markers that conventional mass spectrometry often misses.
  • GPL-TOX also includes Tiglylglycine, a marker for mitochondrial damage, which is often seen in chronic toxic chemical exposure.
  • GPL-TOX pairs perfectly with our Organic Acids Test (OAT) and our Glyphosate Test in the Enviro-TOX Panel.  This panel offers you comprehensive testing to assess exposure to common environmental toxins and the damage that can be caused by this exposure, all at a great value, and all from one urine sample.
  • William Shaw, Ph.D., Director of The Great Plains Laboratory is board-certified in both clinical chemistry and toxicology by the American Board of Clinical Chemistry.


Perhaps the most widespread group of toxic chemicals found in our environment. Phthalates are commonly found in after shave lotions, aspirin, cosmetics, detergents, foods microwaved with plastic covers, oral pharmaceutical drugs, intravenous products prepared in plastic bags, hair sprays, insecticides, insect repellents, nail polish, nail polish remover, skin care products, adhesives, explosives, lacquer, janitorial products, perfumes, paper coatings, printing inks, safety glass, and varnishes. Phthalates have been implicated in reproductive damage, depressed leukocyte function, and cancer. Phthalates have also been found to impede blood coagulation, lower testosterone, and alter sexual development in children. Low levels of phthalates can feminize the male brain of the fetus, while high levels can hyper-masculinize the developing male brain.

Vinyl Chloride
Vinyl chloride is an intermediate in the synthesis of several commercial chemicals, including polyvinyl chloride (PVC). Exposure to vinyl chloride may cause central nervous system depression, nausea, headache, dizziness, liver damage, degenerative bone changes, thrombocytopenia, enlargement of the spleen, and death.

Benzene is an organic solvent that is widespread in the environment. Benzene is a by-product of all sources of combustion, including cigarette smoke, and is released by outgassing from synthetic materials, and is a pollutant released by numerous industrial processes. Benzene is an extremely toxic chemical that is mutagenic and carcinogenic. High exposures to benzene cause symptoms of nausea, vomiting, dizziness, lack of coordination, central nervous system depression, and death. It can also cause hematological abnormalities.

Pyrethrins are widely used as insecticides. Exposure during pregnancy doubles the likelihood of autism. Pyrethrins may affect neurological development, disrupt hormones, induce cancer, and suppress the immune system.

Xylenes (dimethylbenzenes) are solvents found not only in common products such as paints, lacquers, pesticides, cleaning fluids, fuel and exhaust fumes, but also in perfumes and insect repellents. Xylenes are oxidized in the liver and bound to glycine before eliminated in urine. High xylene levels may be due to the use of certain perfumes and insect repellents. High exposures to xylene create an increase in oxidative stress, causing symptoms such as nausea, vomiting, dizziness, central nervous system depression, and death. Occupational exposure is often found in pathology laboratories where xylene is used for tissue processing.

Styrene is used in the manufacturing of plastics, in building materials, and is found in car exhaust fumes. Polystyrene and its copolymers are widely used as food-packaging materials. The ability of styrene monomer to leach from polystyrene packaging to food has been reported. Occupational exposure due to inhalation of large amounts of styrene adversely impacts the central nervous system, causes concentration problems, muscle weakness, tiredness and nausea, and irritates the mucous membranes of the eyes, nose, and throat.

Organophosphates are one of the most toxic groups of substances used throughout the world. They are often used as biochemical weapons and terrorist agents, but are most commonly used in pesticide formulations. Organophospates are inhibitors of cholinesterase enzymes, leading to overstimulation of nerve cells, causing sweating, salivation, diarrhea, abnormal behavior, including aggression and depression. Children exposed to organophosphates have more than twice the risk of developing pervasive developmental disorder (PDD), an autism spectrum disorder. A study done in the San Francisco Bay area found that in California agricultural areas, children born to mothers living within 500 meters of fields where organochlorine pesticides were used were more than 6 times more likely to develop autism than children whose mothers did not live near such fields. ASD risk increased with the poundage of organochlorines applied and decreased with distance from field sites. Maternal organophosphate exposure has been associated with various adverse outcomes including having shorter pregnancies and children with impaired reflexes.

MTBE and ETBE are gasoline additives used to improve octane ratings. Exposure to these compounds is most likely due to groundwater contamination, and inhalation or skin exposure to gasoline or its vapors and exhaust fumes. MTBE has been demonstrated to cause hepatic, kidney, and central nervous system toxicity, peripheral neurotoxicity, and cancer in animals. Since the metabolites of these compounds are the same, ETBE may be similarly toxic.

2, 4-Dicholorophenoxyacetic (2,4-D)
A very common herbicide that was a part of Agent Orange, used by the United States during the Vietnam War to increase visibility for war planes, by destroying plant undergrowth and crops. It is most commonly used in agriculture on genetically modified foods, and as a weed killer for lawns. Exposure to 2, 4-D via skin or oral ingestion is associated with neuritis, weakness, nausea, abdominal pain, headache, dizziness, peripheral neuropathy, stupor, seizures, brain damage, and impaired reflexes. 2, 4-D is a known endocrine disruptor, and can block hormone distribution and cause glandular breakdown.

Diphenyl Phosphate
This is a metabolite of the organophosphate flame retardant triphenyl phosphate (TPHP), which is used in plastics, electronic equipment, nail polish, and resins.  TPHP can cause endocrine disruption.  Studies have also linked TPHP to reproductive and developmental problems.

Acrylamide can polymerize to form polyacrylamide.  Polyacrylamide is used in many industrial processes such as plastics, food packaging, cosmetics, nail polish, dyes, and treatment of drinking water.  Food and cigarette smoke are also two major sources of exposure.  Acrylamide has been found in foods like potato chips, French fries, and many others such as asparagus, potatoes, legumes, nuts, seeds, beef, eggs, and fish.  Asparagine, which is found in these foods can produce acrylamide when cooked at high temperature in the presence of sugars.  High levels of acrylamide can elevate a patient’s risk of cancer.  In addition, acrylamide is known to cause neurological damage.

This chemical is used in the production of rocket fuel, missiles, fireworks, flares, explosives, fertilizers, and bleach.  Studies show that perchlorate is often found in water supplies.  Many food sources are also contaminated with perchlorate.  Perchlorate can disrupt the thyroid’s ability to produce hormones.  The EPA has also labeled perchlorate a likely human carcinogen.  Patients that are high in perchlorate can use a reverse osmosis water treatment system to remove the chemical from their water supply.

1,3 Butadiene
This is a chemical made from the processing of petroleum.  It is often a colorless gas with a mild gasoline-like odor.  Most of this chemical is used in the production of synthetic rubber.  1,3 Butadiene is a known carcinogen and has been linked to increased risk of cardiovascular disease.  Individuals that come into contact with rubber, such as car tires, could absorb 1,3 Butadiene through the skin.  The increased use of old tires in the production of crumb rubber playgrounds and athletic fields is quite troubling because children and athletes may be exposed to toxic chemicals this way.

Propylene Oxide
This chemical is used in the production of plastics and is used as a fumigant.   Propylene oxide is used to make polyester resins for textile and construction industries.  It is also used in the preparation of lubricants, surfactants, and oil demulsifiers.  It has also been used as a food additive, an herbicide, a microbicide, an insecticide, a fungicide, and a miticide.  Propylene oxide is a probable human carcinogen.

1-Bromopropane (1-BP)
1-Bromopropane is an organic solvent used for metal cleaning, foam gluing, and dry cleaning.  Studies have shown that 1-BP is a neurotoxin as well as a reproductive toxin.  Research indicates that exposure to 1-BP can cause sensory and motor deficits.  Chronic exposure can lead to decreased cognitive function and impairment of the central nervous system.  Acute exposure can lead to headaches.

Ethylene Oxide
Ethylene oxide is used in many different industries including agrochemicals detergents, pharmaceuticals, and personal care products.  Ethylene oxide is also used as a sterilizing agent on rubber, plastics, and electronics.  Chronic exposure to ethylene oxide has been determined to be mutagenic to humans.  Multiple agencies have reported it as a carcinogen.  Studies of people exposed to ethylene oxide show an increased incidence of breast cancer and leukemia.  Caution is needed with ethylene oxide because it is odorless at toxic levels.

Acrylonitrile is a colorless liquid with a pungent odor.  It is used in the production of acrylic fibers, resins, and rubber.  Use of any of these products could lead to exposure to acrylonitrile.  Smoking tobacco and cigarettes is another potential exposure.  Exposure to acrylonitrile can lead to headaches, nausea, dizziness, fatigue, and chest pains.  The European Union has classified acrylonitrile as a carcinogen.


  • Alzheimer’s Disease
  • Amyotrophic Lacteroclerosis (ALS)
  • Anorexia Nervosa
  • Anxiety Disorder
  • Apraxia
  • Arthritis
  • Asthma
  • Attention deficit (ADD)
  • Attention deficit with hyperactivity (ADHD)
  • Autism
  • Autoimmune disorders
  • Bipolar disorder
  • Cancer
  • Cerebral palsy
  • Chronic fatigue syndrome
  • Crohn’s disease
  • Depression
  • Developmental disorder
  • Down Syndrome
  • Epilepsy
  • Failure to thrive
  • Fibromyalgia
  • Genetic diseases
  • Irritable bowel syndrome
  • Learning disability
  • Mitochondria disorder
  • Multiple sclerosis
  • Obsessive compulsive disorder (OCD)
  • Occupational exposures
  • Parkinson’s disease
  • Peripheral neuropathy
  • Schizophrenia
  • Seizure disorders
  • Systemic lupus erythematosus
  • Tic disorders
  • Tourette syndrome
  • Ulcerative colitis


The GPL-TOX profile tests for Tiglylglycine (TG), one of the most specific markers for mitochondrial disorders resulting from mutations of mitochondrial DNA. These mutations can result from exposure to toxic chemicals, infections, inflammation, and nutritional deficiencies. Mitochondria are important in all cells in the body, but are especially important to organs that utilize large amounts of energy, such as the muscles, heart, and brain. The mitochondria also have several other important functions in the cell, including steroid synthesis, calcium regulation, free radical production, and the induction of apoptosis or programmed cell death, all of which are involved in the pathogenesis of numerous disorders. The marker used in the GPL-TOX profile indicates mitochondrial dysfunction by monitoring a metabolite that is elevated in mitochondrial deficiency of cofactors such as NAD+, flavin-containing coenzymes, and Coenzyme Q10. Disorders associated with mitochondrial dysfunction include autism, Parkinson’s disease, and cancer.


2-Methylhippuric Acid (2MHA), 3-Methylhippuric Acid (3MHA), 4-Methylhippuric Acid (4MHA)
These are metabolites of xylenes, solvents found in paints, lacquers, cleaning agents, pesticides, and gasoline. Exposure to xylenes generates methylhippuric acid isomers. Avoid/reduce exposure to these substances.

N-acetyl phenyl cysteine (NAP)
NAP is a metabolite of benzene. Benzene is a solvent that is widespread in the environment. It is found in cigarette smoke and gasoline, and is a byproduct of all types of combustion, including motor vehicle exhaust. Treatment consists of removing sources of exposure.

Phenylglyoxylic Acid (PGO)
Exposure to environmental styrene may slightly increase phenylglyoxylic and mandelic acid. Reduce exposure by eliminating the use of plastic and styrofoam containers for cooking, reheating, eating or drinking. Elimination of styrene can be accelerated by supplementing with glutathione and N-acetyl cysteine (NAC).

2-Hydroxyisobutyric Acid (2HIB)
2-Hydroxyisobutyric acid is formed endogenously as a product of branched-chain amino acid degradation and ketogenesis. This compound is also the major metabolite of gasoline octane enhancers such as MTBE and ETBE. Elevated levels indicate environmental exposure and very high values have been reported in genetic disorders.

Monoethyl Phthalate (MEP)
MEP from diethyl phthalate is the most abundant phthalate metabolite found in urine. Diethyl phthalate is used in plastic products. Elevated values indicate exposure from various possible sources. Elimination of phthalates may be accelerated by sauna treatment.

Dimethylphosphate (DMP) & Diethylphosphate (DEP)
DMP and DEP are major metabolites of many organophosphate pesticides. Reduce exposure by eating organic foods and avoiding use of pesticides in your home or garden. Living near agricultural areas or golf courses and areas regularly sprayed with pesticides will increase exposure. Elimination of organophosphates can be accelerated by sauna treatment.

3-Phenoxybenzoic Acid (3PBA)
3-Phenoxybenzoic acid is a metabolite of pyrethroid insecticides. Elimination can be accelerated by sauna treatment.

2,4-Dichlorophenoxyacetic Acid (2,4-D)
2,4-D was an ingredient in Agent Orange, and is most commonly used in agriculture of genetically modified foods, and as a weed killer for lawns. Reduce exposure by eating organic foods and avoiding use of pesticides in your home or garden.

Tiglylglycine (TG)
TG is a marker for mitochondrial dysfunction. Mutations of mitochondria DNA may result from exposure to toxic chemicals, infections, inflammation, and nutritional deficiencies.

NAE is a metabolite of acrylamide, which is detoxified through a two-step process.  First acrylamide is metabolized by the cytochrome P450s.  Second it is conjugated to glutathione in order to make it more water soluble.  Acrylamide is used in many industrial processes such as plastics, food packaging, cosmetics, nail polish, dyes, and treatment of drinking water.  High levels of acrylamide can elevate a patient’s risk of cancer and cause neurological damage.  Supplementation with glutathione can assist in the elimination of this compound.

Diphenyl Phosphate
This is a metabolite of the organophosphate flame retardant triphenyl phosphate (TPHP), which is used in plastics, electronic equipment, nail polish, and resins.  TPHP can cause endocrine disruption.  Studies have also linked TPHP to reproductive and developmental problems.

Perchlorate is used in the production of rocket fuel, missiles, fireworks, flares, explosives, fertilizers, and bleach.  Studies show that perchlorate is often found to contaminate water supplies and food sources.  It can disrupt the thyroid’s ability to produce hormones.  The EPA has also labeled perchlorate a likely human carcinogen.  Patients that are high in perchlorate can use a reverse osmosis water treatment system to remove perchlorate.

N-Acetyl (3,4-Dihydroxybutyl) Cysteine (NABD)
NADB is a metabolite of 1,3 butadiene, which is evident of exposure to synthetic rubber such as tires.  1,3 butadiene is a known carcinogen and has been linked to increased risk of cardiovascular disease.  Individuals that come into contact with rubber, such as car tires, could absorb 1,3 butadiene through the skin.

N-Acetyl (2,Hydroxypropl) Cysteine (NAHP)
NAHP is a metabolite of propylene oxide which is used in the production of plastics and as a fumigant.  It is also used in the preparation of lubricants, surfactants, and oil demulsifiers and as a food additive, an herbicide, a microbicide, an insecticide, a fungicide, and a miticide.  Propylene oxide is a probable human carcinogen.

N-Acetyl (Propyl) Cysteine (NAPR)
NAPR is a metabolite of 1-bromopropane.  Chronic exposure can lead to decreased cognitive function and impairment of the central nervous system.  Acute exposure can lead to headaches.

2-Hydroxyethyl Mercapturic Acid (HEMA)
HEMA is a metabolite of ethylene oxide, which is used in the production of agrochemicals, detergents, pharmaceuticals, and personal care products.  Chronic exposure to ethylene oxide has been determined to be mutagenic to humans.    HEMA is also a metabolite of vinyl chloride and halopropane, which are used in many commercial chemical processes such as foam glueing, dry cleaning, and in the production of solvents.  Supplementation with glutathione should assist in the detoxification process of these chemicals.

N-Acetyl (2-Cyanoethyl) Cysteine (NACE)
NACE is a metabolite of acrylonitrile, which is used in the production of acrylic fibers, resins, and rubber.  Acrylonitrile is metabolized by the cytochrome P450s and then conjugated to glutathione.  Supplementation with glutathione should assist in the detoxification of acrylonitrile.


If you or a patient has had a GPL-TOX profile and/or a Glyphosate test run and found moderate-high levels of any compounds, there are things you can do to help your body eliminate the toxins and to prevent future exposures.  The first steps to reducing the amount of toxins presently in the body are to switch to eating only organic food and drinking water that has common toxins, including pesticides filtered out.  Most conventional food crops are exposed to larger and larger doses of pesticides and herbicides, and by switching to organic you will prevent exposure to hundreds of these toxicants.  Many of these chemicals have also contaminated our water supplies.  Installing a high-quality water filtration system in the home that eliminates them is important to do and there are several options available.

The next step to avoiding future exposures is to change the products you use on a daily basis – from food and beverage containers to beauty and cleaning products.  Instead of using plastic water bottles and food containers, switch to glass or metal.  Never microwave food in plastic or styrofoam containers and do not drink hot beverages from plastic or styrofoam cups.  Make sure your shampoo, soaps, lotions, and other beauty products are free of phthalates.  Use cleaning products made from natural ingredients or make your own at home.

To eliminate toxins from the body, we highly recommend exercise and the use of saunas, especially infrared sauna therapy to rid many chemicals through sweat.  Infrared sauna is superior to conventional sauna because it reaches deeper into the body,  increasing the circulation in the blood vessels, and causing the body to start to releasing many of the chemicals stored in body fat.

There are two supplements that are particularly useful in helping the body detoxify.  The first is glutathione, or its precursor N-acetyl cysteine.  Glutathione is one of the most common molecules used by the body to eliminate toxic chemicals.  If you are constantly exposed to toxicants your stores of glutathione could be depleted.  The second supplement is vitamin B3 (niacin).  Some may not enjoy the flushing that can happen when taking niacin, however, this flushing is from the blood vessels dilating, which is useful in the detoxification process.  If sensitive to the flushing, start with the lowest recommended dose and work up from there.

Phospholipase A2 test

The Great Plains Laboratory, Inc. is excited about our recently developed phospholipase A2 (PLA2) test that measures the activity of PLA2 in urine. We are the only commercial lab currently offering PLA2 level measurement as a urine test. PLA2 is elevated in a wide range of inflammation-related disorders and is considered a good marker for increased risk of developing or worsening of inflammatory conditions. PLA2 levels can easily be sampled along with the organic acid test (full or microbial), offering a powerful new combination of clinical insights.

Bee stings and venomous snake bites cause immediate inflammation, resulting in pain and swelling. The enzyme in venom that triggers this immune response is phospholipase A2. This enzyme is also present in human tissue. During infection, PLA2 activates a cascade that results in the destruction of the cell membranes of invading microbes. The products of the PLA2 reaction responsible for eliminating these organisms, lysolecithins and free fatty acids, are powerful detergents that damage cell membranes, denature proteins, and disrupt their function. However, this killing mechanism comes at a cost to the human host. Lysolecithin products are involved in the pain response and cause hemolysis of erythrocytes. The most common free fatty acid produced by PLA2is arachidonic acid, which can increase the production of powerful mediators of inflammation: prostaglandins, leukotrienes, and thromboxanes, collectively called eicosanoids. Release of these mediators initiates the pain, swelling, and other unpleasant symptoms we experience as part of an inflammatory response.

Excess PLA2 not only causes local damage, but can be transported by the blood vessels to other parts of the body, causing widespread tissue damage. Normal amounts of PLA2 are involved in remodeling cell membranes and changing cell architecture, but sustained release of PLA2 and the resulting inflammation is implicated in the development of chronic conditions including multiple sclerosis, cardiovascular disease, rheumatoid arthritis, gastrointestinal disorders, allergies, and neuropsychiatric disorders.


A large dose of PLA2 is delivered in venom from snakes, spiders, and bees (experienced as pain and stinging) and is responsible for much of the toxicity of these venoms. Microorganisms such as Candida albicans and certain Clostridia species produce PLA2, which increases the ability of the microorganism to infect the host. This same enzyme is produced in the body as a response to invading microorganisms and foreign proteins such as allergens, particularly house dust and cats. Physical trauma may also cause significant increases in PLA2, contributing to tissue damage and brain injury.

Phospholipase A2 is in fact a family of enzymes that are categorized by location and function. They have strong antibacterial and antiviral properties as part of the innate immune system, but also participate in many other biochemical processes that include cell signaling, cell proliferation and differentiation, cell migration and apoptosis, and modulation of inflammatory response. PLA2 is not only released in tissues and cells of the immune system, it is also produced by the pancreas and released into the small intestine following a fatty meal, to assist in the digestion and absorption of phospholipids. Additionally, PLA2 is expressed in neuronal tissue and is involved in the degranulation process that releases neurotransmitters from neurons. Research efforts have focused on the role that derangement of normal PLA2 activity plays in the etiology of many chronic illnesses. The specific roles, interactions, and interdependencies of PLA2 have been a major area of interest as it relates to chronic inflammatory conditions, cardiovascular disease, and cancer.


Research has implicated PLA2 in the pathophysiology of neurodegenerative diseases such as multiple sclerosis (MS) and Alzheimer’s disease (AD). Multiple sclerosis involves both antigen-specific mechanisms and components of the innate immune system that result in inflammatory response. Elevated PLA2 activity was found to be ongoing among MS patients, with the highest levels measured in patients with progressive disease. In the development of Alzheimer’s disease, the abnormal PLA2 levels appear to be related to oxidative signaling pathways involving NADPH oxidase and production of ROS species that lead to impairment and destruction of neurons and inflammation of glial cells.

Inflammation is the hallmark of rheumatoid arthritis (RA), a joint-destructive autoimmune disease. PLA2 is found in synovial fluid of RA-affected individuals and in the cartilage of RA patients as compared to cartilage from osteoarthritic and normal individuals.

Measurement of PLA2 is emerging as an important tool for evaluating the chance of cardiovascular disease (CVD), including future stroke, myocardial infarction, heart failure, and other vascular events. PLA2 appears to be more specific than hsCRP for CVD risk and may also have a pivotal role as a mediator of cardiovascular pathology. In atherosclerosis, PLA2 not only activates macrophages and formation of foam cells, but it also hydrolyzes LDL and HDL, spawning increased numbers of pro-atherogenic small LDL particles, and impairing anti-atherogenic HDL. PLA2 activity may even precipitate bleeding from atherosclerotic plaques.

PLA2 is expressed normally in pancreatic, gall bladder, and GI epithelial cells, but is significantly increased in inflammatory gastrointestinal disorders. In ulcerative colitis and Crohn’s disease, all intestinal cell types increase expression of PLA2, which increases gut permeability and may actually contribute to infectivity.


Elevations of PLA2 have been found in gastrointestinal cancers including colonic adenomas and carcinomas and pancreatic ductogenic carcinomas, among others. Patients with lung tumors positive for PLA2 had a greatly increased tumor growth rate and a markedly reduced survival rate. Patients with lung cancer also had higher plasma levels of PLA2 than patients with benign nodules. A similar pattern has been observed in prostate cancer, although metastatic tumors expressed lower PLA2 than primary tumors. As PLA2 releases arachidonic acid and other fatty acids from cell membranes, they initiate downstream production of tumor-promoting eicosanoids. In cancer, the spread of tumor cells from a primary tumor to the secondary sites within the body is a complicated process involving cell proliferation and migration, degradation of basement membranes, invasion, adhesion, and angiogenesis. Continued research on PLA2 expression in cancer will certainly reveal valuable new insights.


Glucocorticoids such as the natural hormone cortisol and pharmaceutical agents such as dexamethasone inhibit the production of phospholipase, decreasing harm caused by the enzyme but also decreasing the benefits of the enzyme in killing harmful microorganisms. Thus, excess glucocorticoids can reduce inflammation in a patient with tuberculosis while reducing the effects of PLA2 against the bacteria resulting in spread of the illness. Lithium at pharmacological doses, carbamazepine, and the antimalarial drug chloroquine are all PLA2 inhibitors. Vitamin E is also an inhibitor of PLA2. In addition, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) (belonging to the omega-3 class of fatty acids) inhibit PLA2.

Cytidine 5-diphospho-choline (CDP-choline), a precursor in the formation of phospholipids, is a potent inhibitor of PLA2 that has been used as a nutritional supplement at doses ranging from 500-4000 mg per day in the treatment of patients with a variety of disorders including Parkinson’s disease, memory disorders, vascular cognitive impairment, vascular dementia, senile dementia, schizophrenia, Alzheimer’s disease (especially effective in those with the epsilon-4 apolipoprotein E genotype), head trauma, and ischemic stroke. A trial in patients with Alzheimer’s disease indicated that citicoline (1,000 mg/day) is well tolerated and improves cognitive performance, cerebral blood perfusion, and the brain bioelectrical activity pattern. No side effects were noticed at the lower doses of CDP-choline and only some mild gastrointestinal symptoms were found using higher doses. No abnormal blood chemistry or hematology values were found after the use of CDP-choline.


Because PLA2 is a relatively small enzyme (about 14 KD), it is able to be excreted in urine. 10 mL of the first morning urine before food or drink is suggested for testing. There are no dietary restrictions. This test is convenient to include with the organic acids test. Since chelating agents might interfere with the test, they should not be used for at least 48 hours prior to testing.


  • Multiple sclerosis
  • Rheumatoid arthritis
  • Crohn’s disease
  • Pancreatitis
  • Ulcerative colitis
  • Allergies
  • Cardiovascular disease including atherosclerosi
  • Neurodegenerative diseases
  • Schizophrenia
  • Bipolar depression, subtype with psychosis
  • Candida infection
  • Sepsis
  • Long term depression
  • Asthma
  • Chronic obstructive pulmonary disease (COPD)

Glyphosate test 

Glyphosate is the world’s most widely produced herbicide and is the primary toxic chemical in Roundup™, as well as in many other herbicides. In addition, it is a broad-spectrum herbicide that is used in more than 700 different products from agriculture and forestry to home use. Glyphosate was introduced in the 1970s to kill weeds by targeting the enzymes that produce the amino acids tyrosine, tryptophan, and phenylalanine. The enzymes of many bacteria are also susceptible to inhibition by this chemical, thus altering the flora of many animals. Usage of glyphosate has since amplified, after the introduction of genetically modified (GMO) glyphosate-resistant crops that can grow well in the presence of this chemical in soil. In addition, toxicity of the surfactant commonly mixed with glyphosate, polyoxyethyleneamine (POEA), is greater than the toxicity of glyphosate alone (1). In addition, in 2014 Enlist Duo™, a herbicide product which contains a 2,4-dichlorophenoxyacetic acid (2,4-D) salt and glyphosate, was approved for use in Canada and the U.S. for use on genetically modified soybeans and genetically modified maize, both of which were modified to be resistant to both 2,4-D and glyphosate. 2,4-D has many toxic effects of its own and can be measured in the GPL-TOX test.

The Great Plains Laboratory, Inc. offers a urine test for glyphosate and we are also now testing water samples.

Recent studies have discovered glyphosate exposure to be a cause of many chronic health problems. It can enter the body by direct absorption through the skin, by eating foods treated with glyphosate, or by drinking water contaminated with glyphosate. A recent study (2) stated that a coherent body of evidence indicates that glyphosate could be toxic below the regulatory lowest observed adverse effect level for chronic toxic effects, and that it has teratogenic, tumorigenic and hepatorenal effects that can be explained by endocrine disruption and oxidative stress, causing metabolic alterations, depending on dose and exposure time. The World Health Organization International Agency for Research on Cancer published a summary in March 2015 that classified glyphosate as a probable carcinogen in humans (3). Possible cancers linked to glyphosate exposure include non-Hodgkin lymphoma, renal tubule carcinoma, pancreatic islet-cell adenoma, and skin tumors. Studies have also indicated that glyphosate disrupts the microbiome in the intestine, causing a decrease in the ratio of beneficial to harmful bacteria (4). Thus, highly pathogenic bacteria such as Salmonella entritidis, Salmonellagallinarum, Salmonella typhimurium, Clostridium perfringens, and Clostridium botulinum are highly resistant to glyphosate but most beneficial bacteria such as Enterococcus faecalis, Enterococcus faecium, Bacillus badius, Bifidobacterium adolescentis, and Lactobacillus spp. were found to be moderately to highly susceptible. The relationship between the microbiome of the intestine and overall human health is still unclear, but current research indicates that disruption of the microbiome could cause diseases such as metabolic disorder, diabetes, depression, autism, cardiovascular disease, and autoimmune disease.

Treatment of glyphosate toxicity should be centered on determining the route of introduction and avoiding future exposure. Eating non-GMO (genetically modified organism) foods and drinking reverse osmosis water are two of the best ways to avoid glyphosate. A recent study showed that people eating organic food had considerably lower concentrations of glyphosate in the urine (2). Drinking extra water may also be beneficial since glyphosate is water soluble. More than 90% of corn and soy used are now of the GMO type. In addition, non-GMO wheat is commonly treated with glyphosate as a drying procedure. Glyphosate is somewhat volatile and a high percentage of rain samples contained glyphosate (2).

Another study found that glyphosate accumulated in bones. Considering the strong chelating ability of glyphosate for calcium, accumulation in bones is not surprising. Other results showed that glyphosate is detectable in intestine, liver, muscle, spleen and kidney tissue (5). A 54-year-old man who accidentally sprayed himself with glyphosate developed disseminated skin lesions six hours after the accident (6). One month later, he developed a symmetrical parkinsonian syndrome.

The chelating ability of glyphosate also extends to toxic metals (7). The high incidence of kidney disease of unknown etiology (renal tubular nephropathy) has reached epidemic proportions among young male farm workers in sub-regions of the Pacific coasts of the Central American countries of El Salvador, Nicaragua, Costa Rica, India, and Sri Lanka (8). The researchers propose that glyphosate forms stable chelates with a variety of toxic metals that are then ingested in the food and water or in the case of rice paddy workers, may be absorbed through the skin. These glyphosate-heavy metal chelates reach the kidney where the toxic metals damage the kidney. These authors propose that these chelates accumulate in hard water and clay soils and persist for years, compared to much shorter periods of persistence for non-chelated glyphosate. Furthermore, these chelates may not be detected by common analytical chemistry methods which can only detect free glyphosate, thus dramatically reducing estimates of glyphosate persistence in the environment when metals are high (for example, in clay soil or hard water).

High correlations exist between glyphosate usage and numerous chronic illnesses, including autism, which is shown in the figure on the first page (9). Other disease incidences with high correlations include hypertension, stroke, diabetes , obesity, lipoprotein metabolism disorder , Alzheimer’s, senile dementia, Parkinson’s, multiple sclerosis, inflammatory bowel disease, intestinal infections, end stage renal disease, acute kidney failure, cancers of the thyroid, liver, bladder, pancreas, kidney, and myeloid leukemia (9). Correlations are not causations, yet they raise concern over the use of a chemical to which all life on earth appears to be exposed.




LabCorp is the lab that we use the most.  When dealing with Chronic Inflammatory Response Syndrome (CIRS), there are many labs that most physicians have never heard of–as well as a lot of tests that are commonly known by other practitioners.

Initial CIRS Profile;

  • Trans. Growth Fact. beta 1*
  • Antidiuretic Hormone Profile
  • Cortisol
  • ACTH, Plasma
  • Melanocyte Stimulating Hormone
  • Osmolality
  • TestT+E2+TestF+DHEA
  • Complement C4a
  • HNK1 (CD57) Panel
  • Plasminogen Act Inhibitor-1
  • Lipase
  • Vitamin D, 25-Hydroxy
  • HLA DRB1,3,4,5,DQB1 (IR)
  • TSH+T3+T4F
  • Lipid Panel
  • Urinalysis, Routine
  • CMP14+CBC/D/Plt
  • CK
  • Sedimentation Rate-Westergren
  • Ferritin
  • Iron and TIBC
  • Leptin
  • Magnesium
  • Phosphorus
  • CD4
  • T-Cell Activation, CD8 Subsets
  • CMP14
  • ImmuKnow (R)
  • MMP-9 (Matrix metalloprot.-9)

We need to formulate a broad “differential diagnosis”; this is a list of all of the various things that may be wrong with you, causing your symptoms.  Numerous labs are required to “rule out” these various illnesses that we’re thinking may be causing your problems.   LabCorp is covered by all insurance plans, unfortunately, not all of the other labs are covered by insurance.

Mast Cell Activation Syndrome Profile;

  • Heparin Anti-Xa
  • N-Methylhistamine, Urine
  • Histamine Determination, Blood
  • Tryptase
  • Prostaglandins: D2, S
  • HCV NAA Qualitative (rfx Geno)

Whenever possible, we try to concentrate on using labs that ARE covered by your insurance carrier.




Who should be tested?

Neurotransmitter testing may be applicable to both male and female patients. Expression of the following symptoms can indicate neurotransmitter imbalances. Review of the neurotransmitter test menu will help determine which test should be ordered.

  • Depressed mood
  • Anxiety
  • Adrenal dysfunction
  • Fatigue
  • Poor sleep
  • Loss of mental focus, or cognitive fog
  • ADD and ADHD
  • Addiction or dependency
  • Loss of appetite control
  • Compulsive behavior
  • Cravings
  • Low libido
  • Sexual dysfunction

Adrenal hormones, sex hormones, and neurotransmitters are functionally interrelated. Changes in sex hormones and adrenal hormones can lead to neurotransmitter imbalances. In turn, neurotransmitter imbalances can affect hormone function. Including neurotransmitters with hormone panels provides a more comprehensive view of the body’s functional neuroendocrine status, this interrelationship, and the associated factors that may be contributing to symptoms.

Which Neurotransmitters are tested?

Labrix provides testing of urine amino acids that are used to create neurotransmitters.  They can provide results to help with refractory mental health disorders, helping to guide the clinician to more effective medications to treat the issues at hand.

SEROTONIN is a key neurotransmitter that is involved in the regulation of sleep, appetite and aggression. Serotonin imbalance is a common contributor to mood problems, and pharmacologic agents that alter serotonin levels are among the most commonly used class of drugs prescribed for anxiety and depression.

High stress, insufficient nutrients, fluctuating hormones and the use of stimulant medications or caffeine can all contribute to the depletion of serotonin over time. When serotonin is out of range, depression, anxiety, worry, obsessive thoughts and behaviors, carbohydrate cravings, PMS, difficulty with pain control, and sleep cycle disturbances can result.

GABA is the major inhibitory neurotransmitter found in the CNS and, as such, is important for balancing excitatory action of other neurotransmitters. High levels of GABA may be a result of excitatory overload, or a compensatory mechanism to balance the surplus excitatory neurotransmitter activity. These high levels result in a ‘calming’ action that may contribute to sluggish energy, feelings of sedation, and foggy thinking. Low GABA levels are associated with dysregulation of the adrenal stress response. Without the inhibiting function of GABA, impulsive behaviors are often poorly controlled, contributing to a range of anxious and/or reactive symptoms that extend from poor impulse control to seizure disorders. Alcohol as well as benzodiazepine drugs act on GABA receptors and imitate the effects of GABA. Though these substances don’t cause an increase in GABA levels, understanding their mechanism can give us additional insight into the effects of GABA.

DOPAMINE is largely responsible for regulating the pleasure reward pathway, memory and motor control. Its function creates both inhibitory and excitatory action depending on the dopaminergic receptor it binds to. Memory issues are common with both elevations and depressions in dopamine levels. Caffeine and other stimulants, such as medications for ADD/ADHD, often improve focus by increasing dopamine release, although continual stimulation of this release can deplete dopamine over time.

Common symptoms associated with low dopamine levels include loss of motor control, cravings, compulsions, loss of satisfaction and addictive behaviors including: drug and alcohol use, smoking cigarettes, gambling, and overeating. These actions often result from an unconscious attempt to self-medicate, looking for the satisfaction that is not occurring naturally in the body.

Elevated dopamine levels may contribute to hyperactivity or anxiety and have been observed in patients with schizophrenia. High dopamine may also be related to autism, mood swings, psychosis and attention disorders. L-DOPA is a precursor to dopamine, and is used therapeutically for low dopamine conditions such as Parkinson’s disease. These medications can cause elevations in dopamine.

NOREPINEPHRINE, also called noradrenaline, is an excitatory neurotransmitter produced in the CNS, as well as a stress hormone produced in the adrenal medulla. Norepinephrine is involved in a wide variety of actions including attention, focus, regulating heart rate, affecting blood flow, and suppressing inflammation. Involved in arousal, it prepares the body for action by relaying messages in the sympathetic nervous system as part of the autonomic nervous system’s fight-or-flight response. High levels of norepinephrine are often linked to anxiety, stress, elevated blood pressure, and hyperactivity, whereas low levels are associated with lack of energy, focus, and motivation.

EPINEPHRINE, often better known as adrenaline, is synthesized from norepinephrine in both the CNS and the adrenal medulla. Much like norepinephrine, this excitatory neurotransmitter helps regulate muscle contraction, heart rate, glycogen breakdown, blood pressure and more, and is heavily involved in a stress response. Elevated levels of epinephrine are often associated with hyperactivity, ADHD, anxiety, sleep issues, and low adrenal function. Over time, chronic stress and stimulation can deplete epinephrine stores leading to difficulty concentrating, fatigue, depression, insufficient cortisol production, chronic stress, poor recovery from illness, dizziness and more.

GLUTAMATE is an excitatory neurotransmitter and is considered to be the most abundant neurotransmitter in the nervous system. Glutamate is involved in most aspects of normal brain function including cognition, memory and learning, although high levels of glutamate can cause excitotoxicity, a process where nerve cells are damaged by excessive stimulation. Elevated glutamate levels are commonly associated with panic attacks, anxiety, difficulty concentrating, OCD and depression, whereas low glutamate levels may result in agitation, memory loss, sleeplessness, low energy levels and depression.

GLYCINE is inhibitory and plays dual roles as both a neurotransmitter and an amino acid that serves as a building block of proteins. Glycine improves sleep quality, calms aggression, and serves as an anti-inflammatory agent. Glycine has been shown to boost mental performance and memory. Elevated glycine levels may be associated with compromised cognitive processing. Low levels of glycine may contribute to poor sleep, poor cognitive function, and issues with memory.

HISTAMINE is an excitatory neurotransmitter involved in the sleep/wake cycle and inflammatory response. Histamine plays a dual role in the body as both a neurotransmitter and immunomodulator increasing metabolism, promoting wakefulness, attention, circadian rhythms, learning, and memory. Elevated levels may be associated with allergy-like symptoms, gastro-intestinal concerns, and inflammation. Elevated histamine can interfere with sleep, contributing to insomnia. Low histamine may affect digestion and appetite control, learning, memory, and mood, and may result in drowsiness.

PEA (PHENETHYLAMINE) promotes energy, elevates mood, regulates attention and aggression, and serves as a biomarker for ADHD. Elevated PEA may contribute to anxiety, with very high levels having amphetamine-like effects. Elevated PEA levels may be associated with higher cortisol levels. Low PEA may be associated with ADHD, depression, Parkinson’s disease and bipolar disorder.


Microbiology Dx

MicrobiologyDx performs the API-Staph testing that lets us know if you have an occult sinus infection with Multiple Antibiotic Resistant Coagulase Negative Staph (MARCoNS).  This is a germ that creates a biofilm (mucus or “slime” layer) deep in the sinuses.  This biofilm shields the germ from the medications that we would use to treat the infection–so the infection is more difficult to treat.  If the test is positive for infection, it’s essential that we do a follow-up test to ensure we’ve killed all of the germs causing the infection.  Any surviving germs will prevent healing from Chronic Inflammatory Response Syndrome (CIRS).

Complete elimination of MARCoNS is essential because the germ lowers levels of  α-Melanocyte Stimulating Hormone (MSH), a key part of the “Neuro-Endocrine” link between the brain and the endocrine (hormone) system.  Lowered MSH is the root cause for the symptoms of CIRS as shown on the Bio-Toxin Pathway.  These levels won’t return to normal if MARCoNS is not eliminated completely.

Quest Labs

Quest Laboratories Is the other major lab that we use for our routine CIRS panels.


This lab is also covered by insurance companies universally


RealTime Labs

RealTime Labs;

Urine Mycotoxin Testing;

Testing for mold/mycotoxins in humans is a simple and usually noninvasive procedure. In most cases, only a urine sample is required. Testing can also be done on nasal secretions, sputum or tissue biopsy collected by a physician. Patients must be referred to RealTime Labs by a physician or healthcare professional. If mold or mycotoxins are found to be present, the ordering healthcare professional is notified by our Medical Director.

The RealTime Labs mycotoxin test detects 16 different mycotoxins, including 9 macrocyclic trichothecenes. Testing is done using competitive ELISA, a very sensitive detection method using antibodies prepared against mycotoxins. In fact, RealTime Labs was recently granted a U.S. patent for its macrocyclic trichothecene test.

All mycotoxin testing results are displayed in an easy-to-understand numeric format, showing detection levels in ppb as standardized by the FDA, WHO, CDC and Food Industry for clinical use. Results also tell if the test was positive, negative or equivocal, along with ranges of detection for each.

Mycotoxins are well documented for their toxic effects on the human cell, causing a number of problems in normal cell function and association with a wide variety of clinical symptoms and diseases as shown below.

Kidney Toxicity
Immune Suppression
Chronic Fatigue Syndrome
Acute Pulmonary Hemorrhage
Aplastic Anemia
Birth Defects


Ochratoxin A
Aflatoxin B1
Aflatoxin B2
Aflatoxin G1
Aflatoxin G2
Satratoxin G
Satratoxin H
Isosatratoxin F
Roridin A
Roridin E
Roridin H
Roridin L-2
Verrucarin A
Verrucarin J
Chaetoglobosin A


Sanesco Health

Sanesco Health Labs;

Neurotransmitter & Hormone Precursor Analysis;

Provides testing for the urine amino acid precursors for;


ϒ-Amino Butyric (Butyrate) Acid (GABA)


DiHydroEpiAndosterone Sulfate (DHEA-s)




Glutamate/Glutamic acid

Visual Contrast Test

 Visual Contrast Testing is another test frequently used for our CIRS patients.   

This test can be done on your home computer.  It was designed by the US Air Force and measures acquired, reversible mitochondrial problems in the rod cells, the black & white receptors of the retina, the film in the back of the eyeball. 

It takes about 10 minutes to do this test on your home computer and results are available immediately upon completion.

When you do this test, please EMail your results to Dr. Oenbrink  at