MycoTOX

Lyme, Mold and Mycotoxins: Strategies for Navigating Complex Illness

Darin Ingels, ND

SUmmary:

In the full presentation Lyme, Mold, and Mycotoxins: strategies for Navigating Complex Illness, Darin Ingels, ND, discusses the origin of Lyme Disease, how Lyme is spread, different ways to test for Lyme Disease and treat those affected by Lyme Disease.

Lyme Disease (LD) is among the more difficult of chronic syndromes – difficult to define, to diagnose and to treat. Since the mysterious outbreak of juvenile rheumatoid arthritis in the 1970s in Lyme, Connecticut, was first connected to microbial Borrelia burgdorferi spread by ticks, the understanding of these conditions has increased as Lyme itself has spread through the US and Europe.

Several species of ticks are expanding their range. The spread includes Canada, although Canada drastically underreports Lyme cases. Dr. Ingels provides considerable detail on Borrelia variants with maps documenting its relentless advance during the last few decades. He mentions that US variants have a stronger T-1 pro-inflammatory response, while European variants have a strong T-17 pro-inflammatory response.

Making identification of Lyme more difficult is the slow replication of Borrelia species (days instead of hours) and the organism’s ability to change shapes. The production of antibodies by Lyme sufferers isn’t dependable either. Many patients are entirely seronegative.

Laboratories often do not test for the full extent of the antibodies that have been associated with Lyme. The well-known bull’s-eye rash resulting from a tick bite is only present in 70% of patients according to the CDC, but other sources say 40%, and many Lyme sufferers have no recollection of a tick bite.

Symptoms are vague and overlap with other infectious and autoimmune conditions, which further confounds the problem of Lyme diagnosis. In children, confounding is even higher and symptoms include PANS and OCD.  Also, diseases such as tularemia may present similarly to Lyme.

Dr. Ingels points out that the CDC criteria for Lyme Disease was designed for surveillance purposes and do not necessarily reflect active infection with Borrelia species. The official diagnosis of Lyme Disease is a clinical diagnosis (signs and symptoms). The CDC warns against diagnosis of asymptomatic individuals, although it is possible to carry the microbes without symptoms. CDC-approved testing includes ELISA and Western blot: these are 40-year-old criteria.

ILADS (the International Lyme and Associated Disease Society) has more complex criteria for diagnosis of Lyme (LD) and coinfections. Their LD assessment approach includes a symptom questionnaire and suggested labs include hormones (thyroid, adrenal), nutritional (Vitamin D, minerals, amino acids), and immune markers as well as microbial coinfections. However, different laboratory tests may report markers for different microbial strains.

Dr. Ingels then segues into the involvement of mold as a major confounder of Lyme diagnosis. Mycotoxin toxic effects (mycotoxicosis) often overlap with Lyme Disease effects, and the damage both can do to the terrain also allows them to persist in a patient and contribute to ongoing oxidative stress and cell damage.

Fixing the terrain begins with – no surprise – healing the gut. Dr. Ingels offers the standard anti-inflammatory supplements such as probiotics and glutamine, and goes on to provide detailed diet guidance, emphasizing alkaline foods. The next step is to treat active infections, preferably with herbal supplements rather than antibiotics. He recommends several lesser-known herbal products for Lyme. Steps to reduce stress, improve sleep, and remove mold from the body and the environment are also presented. Treatment protocols should be tailored to each patient: “the best binder is the one your patient will take and tolerate’. Since sensitive mitochondria suffer “collateral damage” from these chronic conditions, Dr. Ingels winds up the lecture with mitochondria support supplements and detoxification strategies.

Order a Test or
Open an Account

GPL improves health treatment outcomes for chronic illnesses by providing the most accurate, reliable, and comprehensive biomedical analyses available.

Identifying and Treating Mold Toxin Induced Illness with MycoTOX Profile

SUMMARY:

In this presentation, James Neuenschwander, M.D., reviews some tell-tale signs of mold illness. He discusses the mechanisms by which mold toxins make patients ill and how a MycoTOX Profile helps identify these factors. Dr. Neuenschwander also provides practical protocols to remove patient barriers to healing of those suffering from mold or chronic illnesses.  

Before outlining a practical approach to treating mold illness patients, James Neuenschwander, M.D. provides a step-by-step description of the cellular response to toxins. The health information we consume frequently refers to “toxins” and “toxicity” without explaining how cellular processes are altered by toxic compounds. These cellular responses to toxins can manifest as the myriad and often baffling symptoms that chronic patients report.

He begins with the cell danger response (CDR), which triggers a cascade of cellular responses that may result in recycling of organelles or end in apoptosis of the cell itself. Apoptosis or “programmed cell death” is a normal process of growth and development, as well as a defense against pathogens. In a healthy state, cells are replaced, differentiated, and reconnected with neighboring cells.

Disease develops when the cellular healing process gets stuck; this can occur when mold and mycotoxin exposure is ongoing. Dr. Neuenschwander points out that if the host is sick, the host microbiome will also be out of balance and show signs of dysbiosis.

The full presentation includes the role of mitochondria, thought of primarily as energy producers, but which are very involved in the cellular response to stress. The presence of ATP outside the cell is part of cellular danger signaling, along with the appearance of various caspase enzymes at several points in the apoptosis process. The cell resorts to aerobic glycolysis, oxidative stress and glutamate level increase, and glutathione is diverted, vitamin D production drops, and methylation reactions are impaired.  Eventually, thyroid function is thrown off, and histamine increases. Patients with a chronic toxic load may develop MCAS and other indications of immune upregulation.

Dr. Neuenschwander mentions the myriad patient symptoms that can result from toxic processes instigated by mycotoxin exposure: psychiatric and cognitive symptoms, any chronic syndrome, respiratory symptoms, as well as POTS and other vagal symptoms. He uses Organic Acid Test (OAT) results as well as MycoTOX Profile results to illustrate possible responses to mycotoxins such as trichothecenes, aflatoxins, zearalenone, and ochratoxins. He also discusses the utility of specific immune and neurological testing.

An individual patient workup is included in this presentation and emphasis is placed on removal of mycotoxin exposure as determined by environmental testing. Food can also be a source of mycotoxins, particularly ochratoxin for which digestive binders are useful. Dr. Neuenschwander points out that unsprayed, organic food can often have higher mold content. He notes that the sickest patients have both mold colonization and an upregulated immune response to mycotoxin exposure and notes when antifungal treatment is called for.

Order a Test or
Open an Account

GPL improves health treatment outcomes for chronic illnesses by providing the most accurate, reliable, and comprehensive biomedical analyses available.

Workshop Q+A Part 2 - Mitochondria and Toxins

On August 5-7, 2022, GPL Academy hosted the Mitochondria and Toxins: Advanced Strategies & Protocols in Chicago and live-streamed online. The following Q+A is a grouping of responses from the workshop presentations.

The material contained within this article is not intended to replace the services and/or medical advice of a licensed healthcare practitioner, nor is it meant to encourage diagnosis and treatment of disease. It is for educational purposes only. Any application of suggestions set forth in the following portions of this article is at the reader's discretion and sole risk. Implementation or experimentation with any supplements, herbs, dietary changes, medications, and/or lifestyle changes, etc., is done so at your sole risk and responsibility.


Joseph Pizzorno, N.D.

Joseph Pizzorno, ND is a world-leading authority on science-based natural medicine, a term he coined in 1978 as founding president of Bastyr University. A naturopathic physician, educator, researcher and expert spokesman, he is Editor-in-Chief of PubMed-indexed IMCJ, Chair of Board of IFM, board member of American Herbal Pharmacopeia, and a member of the science boards of the Hecht Foundation, Gateway for Cancer Research and Bioclinic Naturals. Author or co-author of six textbooks and 7 consumer books (Encyclopedia of Natural Medicine, The Toxin Solution), he has been an intellectual, political and academic leader in medicine for four decades.

Q: What was the supplement you recommended when using NAC for a patient?   

A: N-acetylcysteine is readily available from many good companies. I use Natural Factors/Bioclinic Natural since I am a scientific consultant for them. I like adding fiber to help bind the toxins that NAC helps excrete. 

Q: How do you detox arsenic? What nutrients or binders do you use to detox arsenic?  

A: The best detox for arsenic is avoidance. Its half-life is typically 2-4 days, so avoidance is effective. The rate of detox can be increased by consuming dietary folates, not folic acid, and flavonoids such as phloretin.  

Q: What are your thoughts on NAD and Glutathione IV therapy?  

A: IV therapy can be helpful but should only be done by those who are very skilled and when the safer oral interventions are not adequate. Before giving anyone IV glutathione, be sure the blood is cleared of mercury. 

Q: For someone with deletions in glutathione-S-transferase, what is the best way/form to increase GSH?  

A: This is really two different issues. Glutathione-S-transferase uses glutathione, does not produce it. Oral NAC and liposomal glutathione increase GSH. 

Q: With a sulfa allergy which is directly correlated with that deletion, is glutathione supplementation not recommended or cautioned?  

A: I am not aware of sulfa allergy being a contraindication for glutathione. 

Q: Is there any connection between the malate you are speaking about in your lecture and supplements with malate, such as calcium and magnesium malate?  

A: Same molecule. Several minerals have been bound to Krebs cycle intermediates, supposedly to improve absorption and utilization. 

Q: Do you have data on the effects of Metformin on Cplx 1 - causing acidosis?  

A: Yes, Metformin does indeed cause pericellular acidosis. Anything which increases lactic acidosis causes acidosis, such as biguanides (metformin), antiretrovirals, statins, many more. 


Elena Villanueva, D.C.

Dr. Elena Villanueva, producer and co-host of the 5 Part Series Mental Health Masterclass, the 5 Part Series Inflammation Masterclass, and The Leaky Brain Summit, is an internationally recognized crusader for ending the global chronic illness & mental health crisis by educating both the public and health professionals that mental health & other chronic illnesses are actually a body or brain health issue and not a disease. Elena has been featured on multiple occasions on FOX news, MSN, Healthline, Houston Chronicle, Anxiety and Depression Secrets Docu-Series, and several other documentaries. Dr Villanueva teaches on stages around the globe on evidence-based approaches for finding the underlying causes of chronic illness and brain-related conditions and how to use holistic and 'whole person' approaches to restore brain-related disorders and other chronic diseases.

 

Q: Do you have any experience with devices such as the NanoVi, to assist with mitochondrial function and proper folding of proteins? 

A: I do not. I do however have experience with bioenergetics and how that shows improvement of mitochondrial function. In fact, a recent study was just completed by a university out of California showing the biological improvements in mitochondrial function and replication with the use of bioenergetics. 

Q: What is your glyphosate protocol? 

A: Glyphosate has a short half-life and is one of the toxins that can leave the body without help of added supplementation. However, the client must discover and stop his/her exposure to the glyphosate for levels to come down. When we detox, our protocols are designed to detox ALL toxins, chemical, myco, and HM’s… this simplifies the protocols (and reduces the costs) for patients/clients and makes them much more compliant and with that compliance you and your patients/clients will see more consistent positive outcomes. 

Q: Are you concerned when toxins don't increase on testing between months 4-6 indicating they are not coming out as much? 

A: Not as much of a concern as it is an indicator that the client/patient is not compliant with the protocols. By month 4-6, if they are compliant with reducing their exposure and taking their recommended supplements and food protocols, you will see one of the following two scenarios: 

  1. Their toxins will show higher indicating they are releasing toxins from their body 

  2. Their toxins will show lower because they have already released a good portion of their toxic load quickly. 

If they are still showing the same levels after 3 months on deep detox, they are either still exposing themselves, not taking their protocols as recommended, or both. Keep in mind this is reflective for the protocols in our practice and may vary based on the protocols you establish. 

Q: For a colonized fungal infection in the gut do you cycle, rotate, or use one over-the-counter anti-fungal at a time? 

A: It depends. If the client/patient is not showing symptoms directly related to the fungal infection I focus instead on the broader picture with my deep detox protocols which also address fungal infections. If they are having considerable symptoms from the fungal infection, then yes, I put them on a fungal protocol first to mitigate their symptoms. Then I resume with my 12-month protocol system. 

Q: I have a 34-year-old female with extreme CFS, ADHD and depression for 12 years. Organic Acids Test results are within normal limits except for borderline high arabinose and low Vitamin C. MycoTOX Profile results are positive for ochratoxin A, citrinin, and chaet (from previous home). Dealing with severe debilitating brain fog, memory issues, poor executive function. She wants to go back on Adderall but worried that it will affect mitochondria/adrenals. Any insight on the negative effects of psychostimulants on CFS? 

A: We prefer to avoid those at all costs because of the negative side effects and potential damage they can have. If you are using effective protocols your client should be able to detox her mold toxins in an average of 9 months and you can include added brain and energy support during this time to help her… that could look like added high dose DHA, phospholipids, AA therapy, adrenal support, or even addressing vitamin and /or mineral deficiencies (according to labs) because those are common and can exacerbate brain fog, memory, etc. 

Q: Can you comment on use of Vitamin D with Vitamin K? Why do you use Vitamin K? 

A: High level overview on this: there are a percentage of people who have the VDR taq genetic variant and need Vitamin K to process their Vitamin D. Also, it simply ensures that the Vitamin D has the best chance at being utilized by the body. So, we are covering the bases without having to add more costly testing like genetic testing to their overall costs.  

Q: Just wondering the rationale for doing just the methyl B12/folate vs. a good B complex with activated forms? How do they replete the other B vitamins if given just the folate and B12? 

A: We do like using a good B complex with the methylated B12 and folate. However, at this time we have not found, nor have we been able to formulate a B complex that has the high therapeutic grade doses of methyl B12 methyl folate we prefer to use… therefore we use just the Methyl B12 and Methyl folate that we created in our brand at BioOne Sciences. There are some clients that we will put on additional B Complex. And all our clients that go into a year 2 program with us (which is most of them), get switched over to a B Complex (with the methylated B12 and Folate). We haven’t had an issue with repletion of the other B’s. 

Q: Could we get your pdf form for patients to record their lab results and significance? 

A: Please reach out to us at info@modernholistichealth.com We will be emailing our practitioners who are interested in learning our systems with information on our first live, in person training that we want to do and from that training we will share all our forms and protocols with you. 

Q: What is in your tox bundle? OAT, MycoTOX Profile, Heavy Metals and what else?  

A: Yes, those plus the environmental toxins and Glyphosate

Q: What was the biofilm agent you said you used?  

A: It’s our TCG Activation product that is humic/fulvic based.  

Q: Is it normal for a patient to get full body edema during a detox? 

A: No, it is not normal. It sounds like their detox pathways are not open and you should have your patient stop immediately. Be sure you check their blood labs for kidney and liver function, make sure they are having full evacuation bowel movements, and check for methylation challenges with some genetic testing. You might also get a history on any issues with their lymphatic system as well and determine if they have any allergies or sensitivities to any of the ingredients in the supplements you have them on. 


LEARN NEW WAYS TO HELP PATIENTS WITH DIFFICULT-TO-DIAGNOSE AND CHRONIC HEALTH ISSUES.

The tests discussed throughout each workshop are all used to help identify exposure sources and biochemical imbalances in individuals with chronic health conditions. The Organic Acids Test (OAT) contains multiple markers which may be influenced by environmental and mold toxins. Often, the combination of the OAT, MycoTOX Profile, and GPL-TOX Profile can be used to help identify how a patient might be getting exposed, as well as assist with correlating their symptoms back to these sources. Determining the underlying causes of chronic illnesses for patients is the key to integrative medicine, not just treating the symptoms. The Great Plains Laboratory continues to find new ways to detect these causes of many illnesses and study the correlations between the results and conditions.

Registration includes:

  1. Ability to purchase GPL tests discussed throughout the program at special workshop-only discounted rates.

  2. 60-day access to the full conference recordings.

  3. Permanent PDF access to each speaker’s slides.

  4. The option to purchase continuing education credits (5 credits per day), whether you attend in-person, watch Live Online, or watch the conference recordings at a later date! See detailed information about credits.

  5. An interactive Workshop Hub website where you can live chat and network with attendees and ask questions to the speakers.

  6. And last, but most certainly not least, qualified practitioners will receive a free OAT.

Workshop Q+A Part 1 - Mitochondria and Toxins

On August 5-7, 2022, GPL Academy hosted the Mitochondria and Toxins: Advanced Strategies & Protocols in Chicago and live-streamed online. The following Q+A is a grouping of responses from the workshop presentations.

The material contained within this article is not intended to replace the services and/or medical advice of a licensed healthcare practitioner, nor is it meant to encourage diagnosis and treatment of disease. It is for educational purposes only. Any application of suggestions set forth in the following portions of this article is at the reader's discretion and sole risk. Implementation or experimentation with any supplements, herbs, dietary changes, medications, and/or lifestyle changes, etc., is done so at your sole risk and responsibility.


Kurt Woeller, D.O.

Kurt N. Woeller, D.O. has been an integrative medicine physician and biomedical Autism specialist for over 20+ years. He is an author of several health books including Autism – The Road To Recovery, Methyl-B12 Therapy For Autism, Methyl-B12 for Alzheimer’s Disease and Dementia, and 5 Things You MUST Do Right Now To Help With Your Rheumatoid Arthritis. He is an international speaker, educator, and practicing clinician offering specialized interventions for individuals with complex medical conditions. His health consulting practice for Autism alone is multinational with families from various countries. Dr. Woeller serves as a clinical and lab consult for Functional Medicine Clinical Rounds, as well as provides educational seminars for Great Plains Laboratory. He is co-founder of Integrative Medicine Academy (www.IntegrativeMedicineAcademy.com), which is an online training academy for health practitioners learning integrative medicine.

Q: How much more is covered in your Advanced OAT Mastery Course?

A: We go over every marker on the Organic Acids Test from Great Plains, as well as certain other markers commonly seen on other OATs.

Q: Do you ever delay addressing the bacterial/fungal dysbiosis to gently detox the patient first so that the removal of the biofilm is more effective and is only done once?

A: Yes, this can be done for some people.

Q: I have a patient who gets recurrent vaginal yeast infections monthly. She is told by her gynecologist that it’s hormonal. Could it be from a yeast/mold issue within the gut and environment? Should I run an Organic Acids Test on her?

A: Absolutely run an OAT.

Q: Do you typically avoid fungus plants in mold/mycotoxin patients? Do you use saccharomyces boulardii?

A: I use this from time to time. It can be helpful overall, but some people are sensitive to it.

Q: If the test shows candida or mold does that mean it is currently active?

A: On the OAT its active.  

Q: Or could it be showing that you did at one time have candida and there are antibodies or organic acids still present?

A: The IgG Food MAP can indicate past problems, but the OAT is current and active.

Q: Once you see the clostridia markers high on the OAT, do you run a stool test to confirm Clostridia presence before treating?

A: No, only unless they have significant bowel problems and want to rule out C. difficile with toxins and A and B.

Q: Polyethylene glycol is used widely in nursing homes for older people with constipation. It is also a component in some drugs and foods, how much of a health risk is this?

A: It’s a risk and certainly not ideal to use. There are many other options for constipation in the natural medicine world worth looking into.

Q: I understand, from other information I've viewed, that the OAT test can be hit-or-miss for oxalates because of cyclical excretion. Are you familiar with this phenomenon or its implications?

A: Yes. It’s called dumping. However, most of the time it is picked up on the OAT.

Q: For patients taking high doses of quercetin ascorbate (i.e. 2-8g/day) for mast cell hyperactivity, do you think there is a high probability of oxalate issues from such high doses of Vitamin C? Would a downward taper be a good idea, to avoid possible dumping when coming off it again?

A: Yes. Oxalates can manifest through this. For people who are very sensitive this would be a good idea. Not necessary for many people though.

Q: I've heard of good results with AURO topical glutathione. Your thoughts? Have you used it? vs Tri Fortify?

A: I have not used it.

Q: Would ADD medication affect the HVA value on the OAT?

A: Anything that drives up dopamine can affect the HVA value.

Q: What D-lactic free probiotics do you use/how do you know if the probiotic is D-lactic free?

A: It has to do with the type of bacteria in the probiotic. You will need to do some research on which bacteria produce D-lactic.

Q: Which marker on the OAT could indicate a coinfection of virus interfering with mitochondria function or getting damaged inducing the cell danger response?

A: There is no specific marker for viruses and no markers per se specific to the CDR.

Q: Do you have any thoughts or preferences on the form of CoQ10 to use, ie. Ubiquinol or Ubiquinone?

A: Ubiquinol.

Q: Do you have any thoughts on supplementing with Calcium Citrate for Oxalates and K2 amounts to address uptake? Does it matter if the Calcium is getting bound with the oxalates?

A: Vitamin K helps with bone mineralization so less availability for oxalate binding. It is a good idea to use too.

Q: Do molds that are known to be toxic that show up on the OAT not always produce toxins that would show up on the MycoTOX Profile?

A: Correct. There may not always be mycotoxins present, but they often are.

Q: Is Gliotoxin just produced by fungus or also candida?

A: There seems to be controversy around it, but it appears more likely that Candida can produce it too.

Q: Do you avoid using saccharomyces boulardii as an antifungal in those with fungal or mold related illness due to it being in that family of organisms, or do you find it still beneficial?

A: I do not use SB a lot. It can be helpful for some people, but watch out for reactions in people with inflammatory bowel disease.

Q: Can colonized molds create mycotoxins?

A: Yes

Q: Does the nephrotoxicity associated with ochratoxin, etc, tend to reverse once the detoxification has been done? 

A: It should if the problem has been more of a recent onset.

Q: Any experience using modified citrus pectin?

A: Some. It is another type of binder.

Q: At what level of a positive MycoTOX Profile do you treat mycotoxins? 

A: Any level outside the green. If its in the green than I mostly leave it alone unless the patient has known exposure and there is a high suspicion of mold/mycotoxin exposure.


James Greenblatt, M.D.

A pioneer in the field of integrative medicine, James M. Greenblatt, M.D., has treated patients since 1988. After receiving his medical degree and completing his psychiatry residency at George Washington University, Dr. Greenblatt completed a fellowship in child and adolescent psychiatry at Johns Hopkins Medical School. He currently serves as the Chief Medical Officer at Walden Behavioral Care in Waltham, MA and serves as an Assistant Clinical Professor of Psychiatry at Tufts University School of Medicine and Dartmouth College Geisel School of Medicine. Dr. Greenblatt has lectured internationally on the scientific evidence for nutritional interventions in psychiatry and mental illness.  He is the author of seven books, including Finally Focused: The Breakthrough Natural Treatment Plan for ADHD. He is the founder of Psychiatry Redefined, an educational platform dedicated to the transformation of psychiatry, which offers online CME-approved courses, webinars, and fellowships for professionals about functional and integrative medicine for mental illness. jgresources@gmail.com www.PsychiatryRedefined.org www.JamesGreenblattMD.com

Q: Do you think that the safety profile differs much between lithium carbonate, lithium citrate, and lithium orotate or are they all primarily dose-dependent?

A: I believe that the side effect profile is most often due to the amount of elemental lithium not the carrier model (i.e., Carbonate, citrate, or orotate). It is important to remember 150 mg of lithium carbonate only has 28 mg of elemental lithium.

Q: For patients with brain fog associated with long COVID, have you found Lithium helpful? Any protocols specific for long COVID?

A: Other than “the basics,” the most effective supportive supplements for long-haul COVID involve the use of lithium and OPC’s. Lithium (Lithium (Orotate) 1mg | Pure | Doctors and Patients Access (pureencapsulationspro.com) and Lithium (Orotate) 5mg | Pure | Doctors and Patients Access (pureencapsulationspro.com)) is recommended for patients with starting dose at 1-2 mg and titrate up if tolerated or needed to 5-10 mg. The OPC product is usually 2-3 times per day and we use the Curcumasorbmind (Cognitive Support Supplement* | Pure | Doctors and Patients Access (pureencapsulationspro.com)

Q: What kind of doses of lithium (or lithium levels) show the greatest effect on inflammation?

A: Using nutritional lithium for irritability, prevention of dementia, and neuroinflammation, we often use dosages that do not result in blood levels. There is very little research correlating blood levels with efficacy on any disorder except for bipolar disorder.

Q: It looks like some studies were done in the 90s showing “no effect” in OCD, but theoretically lowering neuro-inflammation would improve OCD. Have you seen any benefit of low dose lithium on PANS/PANDAS/OCD? How long would you trial it for in a pediatric patient before concluding it has no effect on them?

A: I have seen tremendous benefit in patients with PANS/PANDAS/OCD. I think the problem in our field is that we oversimplify our treatment response and simply assume every PANS/PANDAS/OCD patient with respond. As you know, there are multiple genetic and environmental factors that contribute to these illnesses and the exacerbation of symptoms. Lithium often plays a critical stabilizing role but without adequate testing and targeted treatments for the infection and other drivers of inflammation, lithium by itself is usually not enough.

Q: Is low lithium excretion on the urinary essential elements test equivalent to low lithium on hair mineral analysis?

A: I am not familiar with urine tests and am not convinced of utility of urine tests for assessment of lithium status. I know a few labs have developed these very quickly. I have not yet found them useful in clinical practice.

Q: Who offers lower than 5 mg dose in supplement form for Lithium?

A: Pure Encapsulations offers a 1 mg lithium orotate.

Q: What is the appropriate dosage for a suicidal person in an emergency and how soon will it calm the patient?

A: Any patient that is suicidal should be in an emergency room and low dose lithium is not an agent that is used for acute suicidal behavior.

Q: With the 1-2mg dosing in irritable children, is that 1-2mg of Lithium Orotate, or elemental?

A: Both. They should be the same. It should be elemental lithium, most commonly found as lithium orotate. For younger children under 6 years of age, I would recommend to start with 500 micrograms.

Q: How does lithium impact the Orotic marker on the OAT?

A: Lithium orotate simply will raise Orotic acid.

Q: Would there be any value in administering Lithium via IV?

A: I have not investigated IV lithium and, since lithium is so easily absorbed, it likely won’t be significantly advantageous.

Q: Can stress from living in a low social economic environment deplete lithium and require higher need?

A: Stress is unlikely to deplete lithium directly but all the related inflammatory markers and disruption in neurotransmitter utilization will likely require higher lithium.

Q: What are the parameters for dosing carbonate, as well as orotate in adults and then for children?

A: I can only share 150 mg lithium carbonate and 28 mg of lithium orotate. These should be dosed according to a physician’s clinical experience based on symptoms and underling diagnoses.

Q: What is the dosage range of lithium for generalized anxiety disorder?

A: I would recommend sticking to lower doses 1-5 mg.

Q: Which SNPs are related to higher lithium needs?

A: There are SNPs associated with lithium but not well understood. The only SNP that I consistently look at is BDNF.

Q: Would low dose lithium be acceptable for patient with Hashimoto’s and elevated levels of TSH when patient has Lithium deficiency?

A: I have utilized low doses of 2-5 mg with patients with thyroid disorder with good success, but this should be done carefully by monitoring thyroid function.

Q: Do you suggest Lithium carbonate or Lithium orotate with patient who is deficient?

A: Based on the dose, I usually use 1-20 mg lithium orotate. If I am looking for 30 mg or higher, I use lithium carbonate.

Q: What is dosage for adult female 115 lbs.?

A: Lithium is not dosed per body weight. We always start with 1-2 mg and titrate as we monitor symptoms and possible side effects.

Q: Would a thyme supplement be an alternative for lithium micro dosing?

A: I have not found that for any patients with clinical symptoms that herbal supplementation is sufficient.


LEARN NEW WAYS TO HELP PATIENTS WITH DIFFICULT-TO-DIAGNOSE AND CHRONIC HEALTH ISSUES.

The tests discussed throughout each workshop are all used to help identify exposure sources and biochemical imbalances in individuals with chronic health conditions. The Organic Acids Test (OAT) contains multiple markers which may be influenced by environmental and mold toxins. Often, the combination of the OAT, MycoTOX Profile, and GPL-TOX Profile can be used to help identify how a patient might be getting exposed, as well as assist with correlating their symptoms back to these sources. Determining the underlying causes of chronic illnesses for patients is the key to integrative medicine, not just treating the symptoms. The Great Plains Laboratory continues to find new ways to detect these causes of many illnesses and study the correlations between the results and conditions.

Registration includes:

  1. Ability to purchase GPL tests discussed throughout the program at special workshop-only discounted rates.

  2. 60-day access to the full conference recordings.

  3. Permanent PDF access to each speaker’s slides.

  4. The option to purchase continuing education credits (5 credits per day), whether you attend in-person, watch Live Online, or watch the conference recordings at a later date! See detailed information about credits.

  5. An interactive Workshop Hub website where you can live chat and network with attendees and ask questions to the speakers.

  6. And last, but most certainly not least, qualified practitioners will receive a free OAT.

Diagnosing Molds, Mycotoxins, and Things that Go Bump in the Night

SUMMARY

Mold is found in the environment and grows in water-damaged buildings. When exposed to mold and mycotoxins, patients will have no reaction, an allergic reaction, or a toxic reaction. Common toxic effects from mycotoxins include their ability to be neurotoxic, hepatotoxic, nephrotoxic, GI irritants, immune suppressant and modulating, skin irritants, hematologic toxins, carcinogenic, cardiovascular toxins, endocrine toxins, etc. This post discusses mold and mycotoxin exposure and recommends how a combination of diagnostic tools like the the Organic Acids Test, MycoTOX Profile, and the Mold IgE Allergy Test can guide your treatment.

By: Jasmyne Brown, N.D.

Functional medicine practitioners are not only healers but investigators of the root cause of runny eyes and noses. It’s our job to determine if a person’s allergic symptoms stem from seasonal triggers like grass and pollen or environmental triggers such as pet dander, mold, or mycotoxins. 

Mold and its mycotoxins seem to be ever present in the lives and sometimes the bodies of our clients. For some practitioners, mold and mycotoxins exposure and treatment may not have been taught during their training. So, what is mold exactly? Is it a yeast, a fungus or something completely different?  


Fungis, Molds, Yeasts, and Microorganisms that Cause Dysfunction 

In the animal kingdom, mold falls under the classification of fungi. These are eukaryotic microorganisms(3). Mold exists here along with yeasts and mushrooms (3). So indeed, it is a fungus making it closely related to yeasts like Candida. Unlike yeast, mold does not reproduce by budding. It reproduces by formation of multicellular hyphae via apical extension(4,6).  

Mold is found ubiquitously in the environment and found to grow in water-damaged buildings. Mold can contaminate foods that must be dried and stored, and mold is used in foods like in the production of cheese.  

Source: World Health Organization and Mycotoxins. Clinical microbiology reviews. Bennett, J. W., & Klich, M 

We’re constantly exposed to mold when we’re outdoors even though we can’t see it. Our forecasters tell us it’s there and how much of it is in the air during the evening weather forecasts. 

On days when the count is moderate to severe, we can see a rise in allergy-type symptoms in individuals with allergies.  

Another common source of mold exposure is from our diet. Certain foods are more prone to mold growth due to the way they are stored and/or grown. There are checks and balances that limit the number of mold/mycotoxins that are allowable before it is sent to market. This limits our exposure from food unless we overindulge in these foods. Common foods include coffee, grains, corn, dairy, wine, etc. Learn more about mold and mycotoxins in food here.  

Mold decomposes dead organic matter so it can grow on wood, the paper facing on gypsum board (drywall) and other materials made from wood. To grow, mold requires oxygen, heat and moisture. Due to this, mold commonly contaminates water damaged buildings. Materials often found to be contaminated include wallpaper, gypsum board, adhesives, pastes, and paints(1,5).  

Although it doesn't grow on non-organic matter like concrete and glass and metal, the dirt on these materials when in the right environment will allow for the growth of mold (1). This is where people get overly exposed to mold and its mycotoxins. The most common are Penicillium chrysogenum, Aspergillus versicolor, and Chaetomium globosum (1).  

When we get exposed to mold, we’ll either have no reaction, an allergic reaction, or a toxic reaction. In certain cases, we’ll experience both allergies and toxicity. So, what's the difference between an allergy and toxicity?   

How the Body Fights Back From Mold Exposure 

When an allergy is present, exposure to the offending substance or antigen triggers a response. This response is made by the immune system. In a true allergic situation, immunoglobulin E (IgE) antibodies are produced by the body. These IgE antibodies attack the antigen, in this case mold, and bind to cells like mast cells and basophils(7). This then triggers the release of chemical mediators like histamine. These chemicals are what induce the symptoms associated with allergies.   

Allergic reactions can also happen to common household molds rather than just molds that produce mycotoxins in water damaged spaces. Commonly people experience itchy watery eyes, sneezing, coughing, urticaria, sinusitis, asthma and wheezing, etc.(7) In sensitive individuals, whenever exposed to the antigen these symptoms will arise.  

During peak mold months in the summer and fall, you may be one of the millions of consumers combing your local drugstore for over-the-counter allergy medications and nasal sprays to find any relief from common allergens like pollen, and mold. You might also watch the weather forecast to prepare for the air quality and level of mold spore spikes in the air.  If you’re unfortunate enough to live in a water-damaged building, you can expect to see a chronic persistence of these allergic type symptoms.  

When Mold Exposure Elevates to a Chronic Illness 

Mold toxicity is different from mold allergy. In a toxicity, there is an over exposure to toxic metabolites that are produced by mold organisms. Toxicity states do not require immune mediated responses to be harmful or to cause what is experienced by the affected party.  

Mold toxins are considered mycotoxins. These compounds have activities that are harmful to humans, animals, and even other microorganisms. Their toxic nature includes neurotoxicity, nephrotoxicity, hepatotoxicity, immune dysregulation and suppressive properties, GI toxicity, cardio toxicity, carcinogenic, hematologic toxins, endocrine toxins, and more (2, 8).  

Myotoxicity has been referred to as the great masquerader in some scientific circles as it can present in many ways for different individuals. Exposure and symptomatology associated with mycotoxins is known as mycotoxicosis(2). It can be acute with a rapid onset that is clearly a large toxicity, or chronic which is a longer-term low-level exposure that usually results in cancers and more irreversible symptoms(2). 

Myotoxicity differs from mold allergy due to the lack of an immune mediated response. The symptoms you may experience from toxins are due to the toxic nature that they already have. An allergy, on the other hand, is the body’s immunologic response mounted to protect us from a foreign substance. Symptoms arise due to the degranulation of mast cells and basophils and the release of chemicals like histamines(7).  

This release is what causes allergic-like symptoms. In a pure toxicity state, you would not experience allergy symptoms. Also, someone without allergies could still feel the effect of mycotoxin overload, but wouldn’t suffer from congestion, itchy watery eyes etc. during allergy season. At least not from mold.  

When people are going through a toxicity state they are often dealing with an active exposure. This exposure is less likely due to the outside air alone, but maybe experienced in high outdoor air exposure rates. During high mold spore count months (summer and fall) those who compost, garden, forage, or do other activities in the soil, toxicity can be seen from these activities and situations(5).  

Though this is not what I commonly see. Water-damaged buildings and cars are the most common culprits for mold overexposure, in my experience. As said earlier, mold decomposes organic materials. Woods, wallpaper, and gypsum board are their fuel, due to the cellulose content, and happen to be extremely common building materials (1,5). When the mold is in ideal conditions it will grow in prominent levels and emit its toxic byproducts.  

Mold Affects Each Person Differently 

During large exposure levels toxicoses can occur. Various toxins can lead to different experiences, and individuality of people can lead to different manifestations. What does this mean? For example, you may have a stay-at-home mother and young child complaining of fatigue, anxiety, skin rash, ASD, GI issues etc., along with a partner and older child with no symptoms or mild fatigue or headache symptoms. Why is this?  

Usually, in these cases the mother and child spend an exponentially greater time in the moldy home than the older child and partner. As they may be going out of the home for work/school. There are also four different, yet similar, genetic make ups that allow for or do not allow for adequate detoxification and may make them more susceptible to the toxin’s effects.  

Situations also arise where the mold is concentrated in one person’s main living space that other family members do not frequent. Thus, increasing their exposure comparatively. All these factors are considered in mycotoxicosis. By understanding these differences and environmental spaces you can better pinpoint where the exposure is coming from.  

Common toxic effects from mycotoxins include their ability to be neurotoxic, hepatotoxic, nephrotoxic, GI irritants, immune suppressant and modulating, skin irritants, hematologic toxins, carcinogenic, cardiovascular toxins, endocrine toxins, etc. due to the wide range of effects and the endless toxic profile someone could present with, the manifestations that can occur are also endless and look different in each person (2). Because of this, looking into mold toxicity would be a good place to start or to rule out for someone with a chronic disease or a new onset of symptoms. 

Mold Exposure Diagnosis and Treatment 

Now that we understand the diverse ways mold can affect our bodies, are they interconnected in disease states? Of course, they are. It is common to see an allergic patient who also presents with a chronic disease or a new onset of symptoms. You may be dealing with a mold exposed client.  

On the other hand, these two manifestations of mold exposure can happen independent of each other. An allergic person not living or working in water damage can just have allergy symptoms. They wouldn't also present with toxic symptoms. This would also be limited to certain seasons when outdoor mold is higher. These individuals would also have significant relief in their home since mold is not growing there.  

In someone without an immune reaction, they would present with strictly toxic symptoms like fatigue, anxiety, pain, dizziness, headaches, etc. These would not be relieved while in the home/workplace/car and they may see relief when away from the exposure for a time.  

When you have someone come to you and you are thinking that they may be dealing with a mold issue, a combination of diagnostic tests can guide your treatment. When I suspect mold exposure, I like running the Organic Acids Test, MycoTOX Profile, and the Mold IgE Allergy Test. These three test will clarify what type of exposure you are dealing with. Is it toxicosis, allergies, or both. A full comprehensive mold workup includes all three of these reports.  

With this information, you will have better insight on what tools are needed to help heal your client from their mold exposure. Overall, an overexposure to mold can lead to two different experiences: allergic response and/or toxicity. When we understand how our clients respond to mold, we can better support them in their healing. 

Order a Test or
Open an Account

GPL improves health treatment outcomes for chronic illnesses by providing the most accurate, reliable, and comprehensive biomedical analyses available.


JASMYNE BROWN, N.D.

Jasmyne Brown is a board certified and licensed naturopathic doctor. She earned her Bachelor of Science in chemistry with a minor in biology from Alabama Agricultural and Mechanical University in 2013. Then she earned her Doctor of Naturopathic Medicine and Master of Human Nutrition degrees from the University of Bridgeport College of Naturopathic Medicine in 2017. Her professional training allows her to be able to interpret the GPL lab tests in a clinical manner, plus she enjoys identifying the biochemical pathways within our bodies and how nutrition and lifestyle impact them. Her educational background and her experience as a WIC nutritionist with the Florida Pasco County Department of Health allows her to convey complex concepts in a manner that can be grasped by anyone on multiple levels.


References  

  1. Andersen, B., Frisvad, J. C., Søndergaard, I., Rasmussen, I. S., & Larsen, L. S. (2011, June). Associations between fungal species and water-damaged building materials. Applied and environmental microbiology. Retrieved August 3, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131638/ 
  2. Bennett, J. W., & Klich, M. (2003, July). Mycotoxins. Clinical microbiology reviews. Retrieved August 3, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC164220/ 
  3. Classification of animals: The complete guide. AZ Animals. (2022, February 19). Retrieved August 3, 2022, from https://a-z-animals.com/reference/animal-classification/ 
  4. Lakna. (2017, November 16). Difference between yeast and mold: Definition, structure, function, similarities. Pediaa.Com. Retrieved August 3, 2022, from https://pediaa.com/difference-between-yeast-and-mold/#:~:text=The%20main%20difference%20between%20yeast,of%20sexual%20or%20asexual%20spores. 
  5. Lstiburek, J., Brenna, T., & Yost, N. (2002, January 15). RR-0208: What you need to know about mold. Building Science Corporation. Retrieved August 3, 2022, from https://www.buildingscience.com/documents/reports/rr-0208-what-you-need-to-know-about-mold/view 
  6. McGinnis, M. R., & Tyring, S. K. (1996). Introduction to mycology - medical microbiology - NCBI bookshelf. National Library of Medicine. Retrieved August 3, 2022, from https://www.ncbi.nlm.nih.gov/books/NBK8125/ 
  7. Sánchez, P., Vélez-del-Burgo, A., Suñén, E., Martínez, J., & Postigo, I. (2022, March 9). Fungal allergen and mold allergy diagnosis: Role and relevance of Alternaria alternata alt a 1 protein family. MDPI. Retrieved August 3, 2022, from https://www.mdpi.com/2309-608X/8/3/277/html 
  8. World Health Organization. (n.d.). Mycotoxins. World Health Organization. Retrieved August 3, 2022, from https://www.who.int/news-room/fact-sheets/detail/mycotoxins#:~:text=Mycotoxins%20are%20naturally%20occurring%20toxins,under%20warm%20and%20humid%20conditions.  

Kidney: The Often-Forgotten Part of Detoxification

Quick glance

  • Toxicants can be absorbed via three main pathways: respiratory tract via inhalation, integumentary system via direct skin contact, or gastrointestinal tract (GI) via consumption (2).

  • Chemical toxicants passing through the kidneys can be measured in urine.

  • Included are recommendations that can be put in place to ensure your patients’ kidneys function well and are prepared to do the work of detoxification of any type of toxic intruder.

By: Lindsay Goddard, M.S., R.D.N., L.D.

Too often the liver and the GI tract are the first two organs that spring to mind when the word detoxification is mentioned.  Granted, these two systems do a lot of important work in removing toxins from the body, but another vital organ that detoxifies the body are the kidneys.

The kidneys are instrumental in detoxifying a wide range of end products of metabolism. Toxins which have gone through phase II liver detoxification or direct excretion, and excess water-soluble nutrients such as B vitamins and Vitamin C are also filtered out by the kidneys (1). The kidneys allow these compounds to be removed from the body via urine, which along with stool, is the major pathway of elimination. Sweat, tears, saliva, hair, nails, and milk, all are a part of elimination as well, but to a lesser degree (2). In this blog we will discuss the kidneys and the roles they play in elimination of toxins, especially ones found on the MycoTOX Profile and the GPL-TOX Profile.


How the Kidney Works

Let’s first review the kidney and its function. It is a complex, and sophisticated organ that is so important, nature felt two were necessary. These bean shaped organs have many functions, but one of the major roles is filtering out excess water and cleaning the blood from toxins. They are so efficient, they can clean all the blood in the body in just under an hour on average (3).

The three layers of the kidney are the cortex (outer layer), medulla (inner part), and the central pelvis. Unfiltered blood travels through the cortex via the renal artery into the nephron. The nephrons are basically the blood filtering units composed of bundles of blood vessels called glomerulus, within the Bowman capsules.

When the blood passes through the glomeruli, within the medulla, waste and excess water diffuse into the capsule. The excess is then carried away by tubules to form urine, while useful substances that can be recycled are absorbed by the capillaries. The filtered blood is sent back to the heart via the renal vein. The urine is then carried through the tubules to the central pelvis, which is then emptied into two tubes called ureters, ultimately going to the bladder (2).

To be fair, the kidneys have other notable functions as well, such as release of certain hormones, stimulation of red blood cell production, and supporting fluid homeostasis within the body, but those details are outside the scope of this blog.

Figure 1: Basic Structure of the Kidney. Adapted from the University of Michigan. http://websites.umich.edu/~elements/web_mod/viper/kidney_function.htm (4).


Eliminating Toxicants

How do toxicants enter our systems? Toxicants can be absorbed via three main pathways: respiratory tract via inhalation, integumentary system via direct skin contact, or gastrointestinal tract (GI) via consumption (2).

The pulmonary route of absorption can be quite significant as the lung tissue is highly vascularized and has a larger surface area. The GI tract also has a larger surface area, but pH has a greater influence on this systems ability to absorb.

The skin isn’t as permeable (unless there is an opening), and it’s mainly the lipid-soluble compounds that are the most worrisome, as they can be absorbed more efficiently via passive diffusion. In a very, very simplistic view, once the toxicant is absorbed via the skin or respiratory tract, it ultimately ends up in the blood where it can travel throughout the system.

The GI tract absorption is different in that if it passes through the membranes, it will likely pass through the liver before it enters general circulation. Ultimately, the body’s goal is to eliminate toxicants. As noted previously, urinary excretion via the kidney is an extremely important mechanism for this to occur.

When toxicants enter the kidney, a large amount are filtered across the glomerulus with relative ease if they are not protein bound in the plasma and/or are relatively small. Ionized toxicants tend to remain in the urine, while toxicants that are more lipophilic can re-enter renal circulation through reabsorption (2). This is the case with Ochratoxin A (OTA) from Great Plains Laboratory’s MycoTOX Profile.

OTA is quite nephrotoxic, and this is likely because as it is going through organic anion transport in the tubules of the kidney, it is actively being reabsorbed. It is also transported with smaller carrier proteins, allowing the compound to pass through the glomerular membrane at an increased rate (5-7). Other than OTA, there are other mycotoxins that can impact the kidneys while they pass through it.

Other Ochratoxins, particularly C, can be damaging to the kidney, though the direct mechanism of action is still being investigated (8). Mycotoxins from Fusarium and Aspergillus, particularly some of the aflatoxins (B2, G1, M1 and M2), and the T2 toxin have all been documented in literature to influence the kidneys during excretion (9-12).

Evidence also indicates that Gliotoxin has cytotoxicity to renal epithelial cells, even at lower concentrations (13). Verrucarin A and Roridin E have both been found to be highly absorbed into the kidneys, even more so than the liver or lungs (14, 15).

Mycophenolic Acid (MPA) goes through glucuronidation in the kidneys, and is mainly eliminated via urine by active tubular secretion and glomerular filtration (16-18). These mycotoxins are all measured on the GPL’s MycoTOX Profile, and can be a helpful clue into what assaults are occurring on the kidneys, along with the other added benefits of running a MycoTOX Profile.



Eliminating Chemical Toxicants

Chemical toxicants passing through the kidneys can be measured in urine. The structure of the chemical compound has a large influence on its excretion through the kidneys. The more lipophilic the compound, the more likely it will be reabsorbed, or in other words, have a difficult time eliminating. The more hydrophilic compounds are, the easier they are to eliminate (1,2).

Please do not think of chemicals that are easy to eliminate as not as toxic as others. Though they may not bioaccumulate as well, the damaging effects they can have while in the system prior to elimination are still of concern, especially with chronic exposure.

Saturation plays a factor in the kidney’s ability to eliminate, meaning it only has a certain capacity it can filter. Mitochondrial function can also be a factor since the ATP generated from the citric acid cycle can help actively move the toxicants out (1).

When you look at toxicants on the GPL-TOX Profile, one can get an idea of the more water-soluble compounds by the metabolite name. If the metabolite is the same name as the parent compound, then it did not have to go through much metabolism to be eliminated. Toxicants such as Diphenyl Phosphate, Perchlorate, and 2,4-Dichlorophenoxyacetic Acid (2,4-D) all fit that description. The others are more complex, and it gets even more complex with heavy metals, but we can save that for another blog.

How to Support the Kidneys

So, we now know what the kidneys do, and what assaults can negatively impact them, the next question  is how can I support it? How do we take care of the kidneys so they can do their job(s) well?

If you have been looking into the world of environmental toxins, it is abundantly clear that the most important thing to do is remove/reduce the toxicant loads. That is a whole other topic, and some really great blogs/webinars have been produced that already delve into mold testing for your body and your home as well as identifying toxins in your environment. If you don’t remove the source, no matter what you do, the problem will persist.



Additional Recommendations

Below are some additional recommendations that can be put in place to ensure our kidneys function well and are prepared to do the work of detoxification of any type of toxic intruder.

  1. Drinking enough clean water. Keeping fluid moving through the body and the kidneys will help them run efficiently and get the toxicants out quicker. There is no specific amount, as everyone is different, but a good general guideline is half the body weight in ounces (e.g. a 120lb person should consume around 60oz of water, minimum). Also, check the urine color to help. Too yellow means more water, clear urine means too much water, as it should have a tinge of yellow to it.

  2. Decrease Sodium and Phosphorus Intake. Sodium and Phosphorus in excessive amounts (not the kind in natural foods, rather the kind in processed foods) can cause imbalances in the kidneys and put additional strain on them, causing them to work harder.

  3. Movement. Improving blood and lymph flow through movement can help the kidneys function optimally. Walking, Yoga (added bonus with the breathing - that’s a part of detoxing too believe it or not!), bicycling, etc. Whatever movement brings joy, it will help.

  4. N-acetyl Cysteine (NAC). NAC has been known to protect kidneys from various assaults. A meta-analysis found that supplementation with NAC improved glomerular filtration rate and serum creatinine, indicating supportive effects (19).

  5. Functional Foods. Various foods can have direct effects on kidney improvement. Beets can support better blood flow throughout the system, in particular the kidneys (20). Blueberries and cabbage have been shown to help with reducing inflammation in the kidneys (21, 22). Curcumin has evidence suggesting it can be helpful in protecting the renal mitochondria (23). Cinnamon, although the effects are not directly towards the kidneys, can help control blood sugar which in turn helps support the kidneys (24).

  6. Be aware that some herbals can be toxic for the kidneys, while other herbs may have influences on kidney function, if the kidney is already in distress. Be mindful with herbal tinctures depending on the current state of the kidney (25).

There are other supports for the kidneys out there, but these should at least be a good start.

The kidneys are incredibly important in helping with the elimination of toxicants, and it is important to support them with lifestyle and diet. We need to support our bodies for the environment in which we live and take care of our systems to ensure they can work properly to withstand the challenges.

Order a Test or
Open an Account

GPL improves health treatment outcomes for chronic illnesses by providing the most accurate, reliable, and comprehensive biomedical analyses available.


Lindsay Goddard, M.S., R.D.N., L.D.

Lindsay Goddard is a Registered Dietitian, with a Master’s Degree in nutrition. She has been involved in integrative and functional nutrition for over 10 years. She has worked in a variety of specialty areas such as genetic and metabolic disorders along with NICU and pediatrics. She also had a private practice where she specialized in gastrointestinal disorders. Lindsay now works as a GPL consultant and is currently earning her graduate certificate in Toxicology through The University of South Florida.


References: 
  1. Pizzorno J. The Kidney Dysfunction Epidemic, Part 1: Causes. Integr Med (Encinitas). 2015 Dec;14(6):8-13. PMID: 26807064; PMCID: PMC4718206.
  2. Richards I and Bourgeois M. Principles and Practice of Toxicology in Public Health. 2014. ISBN: 9781449645267
  3. A, Fardon J, Friend J, Temple N, Routh, K. et al. The Amazing Body. Smithsonian. 2017. First American Edition. Pg. 154-155. ISBN: 978-1-4654-6239-8
  4. University of Michigan. Kidney Function. http://websites.umich.edu/~elements/web_mod/viper/kidney_function.htm
  5. Khoury A and Atoui A. Ochratoxin A: General Overview and Actual Molecular Status. Toxins. 2010. 2(4): 461-493. PMID: 22069596
  6. Gupta, Ramesh C. Veterinary Toxicology. Basic and Clinical Principles 3rd edition. 2018. 
  7. Plumlee KH. Mycotoxins Toxicokinetics. Clinical Veterinary Toxicology. 1st Edition. 2004
  8. Abramson D. MYCOTOXINS Toxicology. Encyclopedia of Food Microbiology. 1999. Pages 1539-1547. ISBN 9780122270703. https://doi.org/10.1006/rwfm.1999.1150.
  9. Mohan J, Sheik Abdul N, Nagiah S, Ghazi T, Chuturgoon AA. Fumonisin B2 Induces Mitochondrial Stress and Mitophagy in Human Embryonic Kidney (Hek293) Cells-A Preliminary Study. Toxins (Basel). 2022 Feb 25;14(3):171. doi: 10.3390/toxins14030171. PMID: 35324667; PMCID: PMC8954924.
  10. Coppock RW, Dziwenka MM. Mycotoxins. Biomarkers in Toxicology. 2014. Pages 549-562.ISBN 9780124046306. https://doi.org/10.1016/B978-0-12-404630-6.00032-4. https://www.sciencedirect.com/science/article/pii/B9780124046306000324. 
  11. Nassar AY, Megalla SE, El-Fattah HM, Hafez AH, El-Deap TS. Binding of aflatoxin B1, G1 and M to plasma albumin. Mycopathologia. 1982 Jul 23;79(1):35-8. doi: 10.1007/BF00636179. PMID: 6811900.
  12. Adhikari M, Negi B, Kaushik N, Adhikari A, Al-Khedhairy AA, Kaushik NK, Choi EH. T-2 mycotoxin: toxicological effects and decontamination strategies. Oncotarget. 2017 May 16;8(20):33933-33952. doi: 10.18632/oncotarget.15422. PMID: 28430618; PMCID: PMC5464924.
  13. Gayathri, L., Akbarsha, M. & Ruckmani, K. In vitro study on aspects of molecular mechanisms underlying invasive aspergillosis caused by gliotoxin and fumagillin, alone and in combination. Sci Rep 10, 14473 (2020). https://doi.org/10.1038/s41598-020-71367-2
  14. Amuzie CJ, Islam Z, Kim JK, Seo JH, Pestka JJ. Kinetics of satratoxin g tissue distribution and excretion following intranasal exposure in the mouse. Toxicol Sci. 2010;116(2):433-440. doi:10.1093/toxsci/kfq142
  15. Amuzie CJ, Islam Z, Kim JK, Seo JH, Pestka JJ. Kinetics of satratoxin g tissue distribution and excretion following intranasal exposure in the mouse. Toxicol Sci. 2010;116(2):433-440. doi:10.1093/toxsci/kfq142
  16. Food and Drug Association. Mycophenolic acid (Myfortic). https://www.accessdata.fda.gov/drugsatfda_docs/label/2008/050791s002lbl.pdf
  17. Lamba V, Sangkuhl K, Sanghavi K, Fish A, Altman RB, and KE.PharmGKB. Mycophenolic Acid Pathway. Pharmacogenetics and genomics.2014. PMID:24220207. https://www.pharmgkb.org/pathway/PA165964832
  18. Hooijmaaijer E, Brandl M, Nelson J, Lustig D. Degradation products of mycophenolate mofetil in aqueous solution. Drug Dev Ind Pharm. 1999 Mar;25(3):361-5. doi: 10.1081/ddc-100102183. PMID: 10071831.
  19. Ye M, Lin W, Zheng J, Lin S. N-acetylcysteine for chronic kidney disease: a systematic review and meta-analysis. Am J Transl Res. 2021 Apr 15;13(4):2472-2485. PMID: 34017406; PMCID: PMC8129408.
  20. Kolluru GK, Kevil CG. Beets, bacteria, and blood flow: a lesson of three Bs. Circulation. 2012 Oct 16;126(16):1939-40. doi: 10.1161/CIRCULATIONAHA.112.136515. Epub 2012 Sep 19. PMID: 22992323; PMCID: PMC4078643.
  21. Nair AR, Masson GS, Ebenezer PJ, Del Piero F, Francis J. Role of TLR4 in lipopolysaccharide-induced acute kidney injury: protection by blueberry. Free Radic Biol Med. 2014 Jun;71:16-25. doi: 10.1016/j.freeradbiomed.2014.03.012. Epub 2014 Mar 19. PMID: 24657730.
  22. Asiwe JN, Kolawole TA, Anachuna KK, Ebuwa EI, Nwogueze BC, Eruotor H, Igbokwe V. Cabbage juice protect against lead-induced liver and kidney damage in male Wistar rat. Biomarkers. 2022 Mar;27(2):151-158. doi: 10.1080/1354750X.2021.2022210. Epub 2022 Jan 3. PMID: 34974788.
  23. Trujillo J, Chirino YI, Molina-Jijón E, Andérica-Romero AC, Tapia E, Pedraza-Chaverrí J. Renoprotective effect of the antioxidant curcumin: Recent findings. Redox Biol. 2013 Sep 17;1(1):448-56. doi: 10.1016/j.redox.2013.09.003. PMID: 24191240; PMCID: PMC3814973.
  24. Khan A, Safdar M, Ali Khan MM, Khattak KN, Anderson RA. Cinnamon improves glucose and lipids of people with type 2 diabetes. Diabetes Care. 2003 Dec;26(12):3215-8. doi: 10.2337/diacare.26.12.3215. PMID: 14633804.
  25. National Kidney Foundation. Use of Herbal Supplements in Chronic Kidney Disease. 2009. https://kidneyhi.org/use-of-herbal-supplements-in-chronic-kidney-disease/

Mycotoxin, Glyphosate & IgG: Q&A With Elena Villanueva, DC, Shanhong Lu, MD, William Shaw, PhD & Lindsay Goddard, RD

On June 10-12, 2022, GPL Academy hosted Beyond the Basics: Advanced Organic Acids Testing Strategies live-streamed online. This three-day event focused on advanced Organic Acids topics. Those who attended the summit learned how to use effective diagnostic and treatment protocols for their patients to help get them on the road to recovery.

The following Q+A is a grouping of responses from the Day 3 workshop presentations. Click each presentation title to expand the answers from each speaker.

The material contained within this article is not intended to replace the services and/or medical advice of a licensed healthcare practitioner, nor is it meant to encourage diagnosis and treatment of disease. It is for educational purposes only. Any application of suggestions set forth in the following portions of this article is at the reader's discretion and sole risk. Implementation or experimentation with any supplements, herbs, dietary changes, medications, and/or lifestyle changes, etc., is done so at your sole risk and responsibility.


Day 3 Q+A: Toxin Exposure and More


William Shaw, PhD

Organic Acids and Mycotoxins: Correlations With Mold in Various Chronic Illnesses | Speaker Panel

Q: Why not add Volatile Organic Compounds to your MycoTOX Profile?

A: Volatile organics would have to be extracted by a different method than mycotoxins. 

 

 

Q: Farmed chickens are fed corn. Do you think chicken meat may contain mycotoxins?

A: Very likely, unless corn feed is tested for mycotoxins.

  

 

Q: Do you use 240 mg/kg/day to calculate the dosage of cholestyramine for children or how do you calculate pediatric dosage? Would you use cholestyramine in infants as well?

A: The usual dosage in children (0-17 years) is 240 mg/kg of body weight per day of anhydrous cholestyramine resin taken in 2 to 3 divided doses. Most children won’t need more than 8 grams per day.

 

 

Q: Which medication or herbal combinations are best for both Candida and Aspergillus simultaneously?

A: The big problem is that there is a lack of published studies for herbals used as antifungals. Amphotericin and itraconazole have been used for both Candida and many molds, but there are resistant strains that require other drugs.

 

 

Q: For children with liver toxicity due to Sporanox, how do you approach that? Maybe half dose for twice as long?  Do you have ideas for alternatives for Itraconazole/ Sporanox?

A: I would recommend oral nystatin, if there is evidence of liver toxicity with Sporanox. This is because nystatin is not absorbed from the GI tract.

 

 

Q: Why do some people get so sick when exposed to mold? Could it be the genetic component HLA gene possibly? 

A: All of the mycotoxins are extremely toxic and may be fatal. The dose of mycotoxin is likely the main factor determining the degree of illness. Neil Nathan, MD states that he found HLA testing of little use in mold treatment.

 

 

Q: What may be the other likely causes of mold exposure for adults apart from damp houses?

A: Food or water damaged buildings are the most common causes of mold exposure. Food is unlikely source in USA and EU where food testing is required for foods commonly mold contaminated.

 

 

Q: I was told that you should not use bleach because it causes the mold spores to open up and release the mycotoxins and that hydrogen peroxide is a better option. Can you comment on this? 

A: Chlorine bleach can help eliminate mold on hard non-porous surfaces like sinks, bathtubs, tiles, or glass. This is because the roots of the mold do not penetrate through this surface and so it is easily wiped off.

However, when mold grows on a porous material like wood or drywall, it spreads its roots deep into the material to reach more nutrients. So when you apply bleach to such a surface, you are merely changing the mold’s color on the surface. Bleach quickly dries off on the surface and will not reach into the deeper part of the material to the mold’s root. So, in a few days or weeks, the mold regains its color and grows back to become even worse than it was before you applied the bleach.

I would suspect that hydrogen peroxide would also be ineffective on these porous materials which is why replacement of these materials is the most effective treatment.

 

 

Q: Recently, it was suggested that we could use effective microorganisms (EM) to kill mold on the walls. Using good bugs to kill bad bugs. What are your thoughts on this?

A: I don’t know. Never saw articles on such treatment.

 

 

Q: If there is only an elevation of tartaric acid in the Organic Acids Test, can we be confident that the patient is definitely affected by Aspergillus?

A: Several pharmaceuticals contain tartaric acid salts in their drugs so you need a complete drug history before you can conclude that Aspergillus is the cause of high tartaric acid.

 

 

Q: If you are only treating the GI tract, why not use amphotericin, which isn't absorbed?   I use itraconazole nasal spray as I find colonization is usually cured by treating sinuses. 

A: Amphotericin B is comparable to itraconazole for several molds and may be preferable since it is not absorbed from the GI tract so will not cause liver toxicity. However, amphotericin B may be liver toxic when administered intravenously rather than given orally. I know one physician who lost his medical license because of his use of amphotericin given orally. His medical board did not appreciate the difference in toxicity between oral and IV administration.

 

 

Q: Shoemake and Heyman have indicated that the mold smell had a higher correlation to the bacteria actinomycetes than mold. Could that explain inconsistencies at times?  Have you seen WDB with actinomycetes and have you treated it any differently than you would mold, i.e. antibiotics, and which one?

A: I would not use smell to determine mold contamination. The best way is to use a professional mold inspector who uses laboratory testing.



Lindsay Goddard, RD

Food to Treat: Using the IgG to Help Your Patients | Speaker Panel

Q: Is a dried blood spot (fingerstick) sample as accurate as a blood draw?

A: Yes. The accuracy is the same. The option is given to accommodate patients who blood draws are more complicated.

 

Q: In your clinical experience, do people who have candida or aspergillus overgrowth react badly to saccharomyces boulardii?

A: That has not been my overall clinical experience. There have been patients that have reacted poorly to it, but not the majority. Since it is not consistent, it is one of the benefits to running the test, to understand how an individual might respond based on their own individual immune response.


Q: Is there any way to get the OAT and /or MycoTOX Profile covered by insurance?

A: The OAT can sometimes be covered by Medicare or TRICARE (military), but the MycoTOX Profile is rarely covered.

 

Q: Is it of benefit to also check peptide level reactions to food in addition to whole blood protein?

A: Testing the peptide levels makes a case by eluding that they are measuring individual parts of the protein versus the whole protein. However, they are still measuring IgG4 and IgA, which do not induce complement, and therefore not inflammation.. I was not able to find any studies showing the efficacy of this method in the literature. If you find any independent studies on this methodology, I would be very interested to see them.  

 

Q: Can you see certain trends in OAT markers for Long Covid patients?

A: Not specifically. Quinolinic acid is often elevated in the beginning, and/or recently post infection or vaccines. There are times the mitochondria are also stressed.  



Shanhong Lu, Md

Glyphosate and GBH as an EDC, a Slow, Multisystem Corruptor to Hormone Optimization and How to Become Glyphosate Resilient

Q: Thank you for your mineral connection (i.e. mercury and iodine). You mentioned Hyper Zinc. What should I be thinking with high zinc if there is no obvious source? Or high ferritin, if there is no obvious HFE or fatty liver?

A: A complete mineral profile will be extremely important and also GPL-TOX Profile and Glyphosate Test will also help to determine where the excessive zinc comes from as many pesticides use zinc as a carrier. 

Q: Can glyphosate pass to cow's milk which is sold to humans?

A: Yes

 

Q: If we see neuroinflammatory symptoms when we give patients glutamine, should that excessive glyphosate exposure be on the differential diagnosis?

A: Absolutely – I have tested so many people with autoimmune, cancers, ALS MS PD and endocrine disruption and elevated SHBG. Glyphosate is always present.

 

Q: When should we suspect a glyphosate problem and do a glyphosate test?

A: I recommend getting that test done right away along with a mineral heavy metal profile and genomic test. Do an environmental workup, if supplements do not work.

 

Q: In your experience, when you removed glyphosate load from the Parkinson's/ dementia patients, do their symptoms reduce substantially?

A: With immune – depolarization, removing glyphosate as soon as possible absolutely improve symptoms. One patient with PD over 10 years on triple drugs improved walking down stairs and started riding horses and hiking. Neuroinflammation in the brain is definitely a result of M1 M2 polarization.

 

Q: How do you determine Individual Tolerant Level?

A: I look at genetic (such as methylation, PON1, COMT, SOD, Dopamine receptors, Vitamin D receptor IL6 TNFa) plus their hormonal age (adrenal sex thyroid and pituitary) people with traumatic brain injuries are more sensitive also.

Q: Do you recommend intermittent fasting as a way to trigger autophagy and a means to help the body become more resilient?

A: I no longer recommend fasting because it causes more stress. Many women are genetically in-between-meal eaters, compliance is low, and the pituitary is not working well when fasting.

 

Q: What do you do for patients that are deficient in glutathione synthetase?

A: I use systemic detox binders (cleardrrops www.zoiglobal.com/drlumd and practitioners with a license can apply professional detox pro), Ca-D-glucarte 2000 mg a day and skip the conjugation relying glutathione pathway, which is not strong for BPA metals and so on.

 

Q: Could you explain once more how to increase/support phase 1 detoxification of the liver?

A: Metals and glyphosate both block phase 1 cytochrome P450 and drugs too. Decreasing exposure and systemic detox support is the key. Genetic studies on cytochrome P450 and PON1 are important.

Q: Is there a way that you can perform the OligoScan on somebody that is not in your presence? (e.g. via some sample of skin or something?)

A: Unfortunately no. A pathologist is needed for biopsies and I recommend going to www.theoligoscan.com to find providers. Feel free to text me at 530-925-0565.

Q: It seemed that you were saying in your presentation that PON1 acts on phase 1 intermediates. Did I hear that correctly, and if so, is PON1 considered a phase 2 enzyme? 

A: For water soluble pesticides (organophosphates ) PON1 is much needed to render the intermediate substrate nontoxic – still phase 1 process. 

Q: Which nutrigenomic software do you use?

A: I use puregenomic from pure encapsulation the most and I also use gxsciences.com.

Q: Since you listed X39 and AEON in association with stress control and other products that balance the branches of the ANS, does that mean you find that they help to balance the ANS? I use them but had not known of a mechanism that would affect the ANS aside from reducing oxidative stress.

A: X39 has been studied to balance blood flows in various regions and enhancing GABA Dopamine and Otropin has been tested by MAX pulse machine using HRV.   We have found over 90% people with significant improvement of SNS vs PSNS balance-parasympathetic improvement with 3 minutes after 4 sprays of Otropin.

Q: What do you use as an immune modulator?

A: I use ultimate immune (containing a patented formula muramyl peptide beta glucan and Glucarate). Please email me drlu@drlumd.com and we can open an account for you.



Elena Villanueva, DC

Managing the Complex Patient: Using the GPL-TOX and OAT in Clinical Practice | Mycotoxins: Considerations, Case Studies and Protocols

Q: What are the top three mind therapies that you have found to be most effective for healing? 

A:  It really depends on what is going on with the individual as to which tools and modalities will be the most effective. If we are looking at how to down regulate the SNS using mind-based therapies, tools like QTT (quantum time therapy), perceptual positions exercises, resonance repatterning, hypnosis, hypnobreath therapy, and meditation exercises can be super beneficial.  

If a client has dis-ease that is rooted in unresolved trauma or unprocessed emotions, incorporating a sequence of a combination of both mind and body therapies is how I see the best outcomes. For example, first teaching the client awareness of how their thoughts, emotions, trauma can effect their physiology and mental health. Then teaching them to master their own down regulation of their SNS and how to activate their PNS using tools like breath therapy, yoga breath therapy, EFT tapping, bilateral touch, and watching their stress metrics improve as they master their own 'circuit board'. Then moving into teaching them awareness around their conscious and unconscious mind, their thoughts, and what tools are available to address and resolve their unprocessed emotions and unresolved trauma using tools like somatic experiencing, QTT, parts integration, P positions, language, light, color, sound therapy, etc.

Q: What are the top three spiritual therapies that you have found to be most effective for healing? 

A: Teaching awareness of who we are as humans has been very powerful with my clients. 'Who we are' being a mind, body, and a spirit with both a conscious and an unconscious mind. And teaching our clients how to integrate their 'parts' so they can speak and live their authentic truth without shame, fear, anger, etc.

Helping them become aware also that they are living a human experience and that all they experience is happening for them, not 'to' them; that THEY are the ones creating their realities through their thoughts, stories, beliefs, and actions. The power for them to heal comes from within them more so than anything outside of them.  

I wouldn't say that we teach spiritual therapies, but rather we teach awareness of the power they have within ourselves to master our own minds, and ultimately our own realities. We focus on empowerment and awareness of their sovereignty. 

Q: How long do your patients/clients typically stay on maintenance? How often do they return for visits? 

A: Once our clients are back to 'baseline' with their health, we start teaching them about longevity and anti-aging and how to biohack for higher performance without compromising their long-term health. We encourage them to do their full functional blood labs, and hormones annually and we encourage them to do their toxins labs every other year to ensure they are not unknowingly building up and re-exposing themselves to toxins. They typically see us 2 to 3 times per year for their wellness programs with us. 



Learn new ways to help patients with difficult-to-diagnose and chronic health issues.

The tests discussed throughout each workshop are all used to help identify exposure sources and biochemical imbalances in individuals with chronic health conditions. The Organic Acids Test (OAT) contains multiple markers which may be influenced by environmental and mold toxins. Often, the combination of the OAT, MycoTOX Profile, and GPL-TOX Profile can be used to help identify how a patient might be getting exposed, as well as assist with correlating their symptoms back to these sources. Determining the underlying causes of chronic illnesses for patients is the key to integrative medicine, not just treating the symptoms. The Great Plains Laboratory continues to find new ways to detect these causes of many illnesses and study the correlations between the results and conditions.

Registration includes:

  1. 60-day access to the full conference recordings.

  2. Permanent PDF access to each speaker’s slides.

  3. The option to purchase continuing education credits (5 credits per day), whether you attend in-person, watch Live Online, or watch the conference recordings at a later date! See detailed information about credits.

  4. An interactive Workshop Hub website where you can live chat and network with attendees and ask questions to the speakers.

  5. And last, but most certainly not least, qualified practitioners will receive a free OAT.

Mycotoxin Properties and Metabolism: Part 2

This blog is a continuation of Mycotoxin Properties Part 1. Here, we discuss the less common, but arguably some of the more toxic mycotoxins that may come up on the MycoTOX Profile (Mold Exposure).


As a mycotoxin classified under the Aspergillus category, Gliotoxin has an average elevation range for people who are suspicious of mycotoxins between 200-2000 ng/g of creatinine. More extreme cases have been shown to be in the 20,000-25,000 ng/g of creatinine range. Although Aspergillus (particularly the fumigatus species) and Penicillium have been shown to produce Gliotoxin, some yeast can as well, particularly Candida (1). A study that looked at A. fumigatus strains from silos contaminated with mold found only 11% of the cultures to be gliotoxin producers (2). On the other hand, a study performed at MD Anderson Cancer Center, found 93% of A. fumigatus strains from respiratory and tissue samples produced gliotoxin (3). Other studies that compared environmental versus clinical A. fumigatus producing gliotoxin, have not only found geographical variations, but overall as the evidence suggests, it is found more commonly as the result of internal colonization rather than contaminated environmental sources (4). Gliotoxin is also commonly found in the soil, but in that case, it is most commonly produced by Trichoderma virens to support competition among the other fungus and bacteria (4). 

Toxicology

Gliotoxin has been shown to inhibit phagocytosis by neutrophils and transcription factor NF-kB, causing immunosuppression, which can potentially further influence cytokine production and mast cell degranulation (5,6). Apoptosis in monocytes and dendritic cells has also been observed. Research has also demonstrated that gliotoxin can inhibit NADPH oxidase and Glutaredoxin enzymes, influencing the system’s ability to tolerate oxidative stress (7). Other studies on laboratory mammals have found that gliotoxin exposure causes a decrease in blood pressure, gastrointestinal hypermobility, and altered sleep patterns (8,9). It has also been identified as a potent antiviral, antibacterial, and anti-fungal agent (e.g. Rhizoctonia solani, Botrytis cinerea, Colletotrichum spp., Pythium ultimum, Fusarium spp (10). 

Properties

Gliotoxin is a compound from the epipolythiodioxypipeazines family, which includes an internal disulfide bridge. It is this disulfide bridge that allows the cross-linkage with cysteine residues, which produces reactive oxygen species (11). It can be produced by A. fumigatus near the temperature of the human body at around 37 degrees Celsius (98.6 degrees Fahrenheit), which is unique for mycotoxin production (12). Gliotoxin has a melting point between 200 °C and 202 °C (392-396 °F) and has a solubility of 0.5-5 mg/L depending on the solvent, where organic solvents increase the solubility (13). Stability increases in acidic, dry environments, but Gliotoxin is extremely unstable and degrades quickly in alkaline and neutral environments with high moisture. There is little literature regarding the half-life of gliotoxin, however, a soil study found the half-life is highly variable and dependent on pH and moisture. In acidic conditions (pH 4), gliotoxin was stable for >30 days, but in alkaline water (pH 7.5), only 35% was stable on the 10th day of measurement. However, when in dry soil versus moisture-rich soil, regardless of pH, gliotoxin was completely degraded on the 10th day (10). 

Metabolism

There is limited data on the pathways utilized by gliotoxin in the human system. However, we do know that it can enter the cytoplasm of the cell, which can arrest the cell cycle possibly by interfering with DNA (9). Its oxidized disulfide structural form allows for glutathione conjugation which reduces it to the dithiol form. This is how it is taken up into the cell and increases its accumulation (9, 14). This reduced form is how it is generally found in the cells, and there is a maximum concentration allowance dictated by cell density. When glutathione levels decrease, the oxidative intracellular toxin creates an increased outflow from the cells, allowing for minimal amounts to have more of an impact (14). As it moves through the system, through the kidneys for elimination, it has been documented to be highly cytotoxic to renal epithelial cells at lower concentrations (9). 

Similar in structure to aflatoxins, particularly B1 (15), Sterigmatocystin (ST) is most commonly produced by Penicillium and Aspergillus (mainly A. Versicolor and A. nidulans), but can also be produced by FusariumBipolarisand even Stachybotrys and Chaetomium (16, 17). It is not currently monitored in food due to the lack of occurrence. Stored cheese and grains are the only documented contaminated circumstances and there have been no outbreaks associated with ST reported to date (16). It is mostly associated with being a potent liver carcinogen (18). The data was limited on ST, and information was difficult to obtain. 

Toxicology

ST has been found to be highly carcinogenic because it can easily react with DNA and be highly mutagenic. However, this only applies to the exo-epoxide formed post conjugation through phase II detoxification. The endo-epoxide has been shown to be less reactive (18). This is one reason it is said to be less toxic than Aflatoxin B1. It has been documented in mice to be hepatotoxic, with chronic and consistent exposures, and with mutagenic actions (16). Also known to increase production of reactive oxygen species, with enhanced lipid peroxidation (16). 

Properties

ST contains a dihydrofurofuran core, with a xanthone nucleus, and an attached bisfurn structure (16,18). It is insoluble in water, with a half-life in plasma of 46.5 to 55.8 hours and a melting point of 246 °C (474 °F) (19).

Metabolism

ST goes through cytochrome P450 oxygenase systems, which produces endo and exo-isomers. They are incredibly unstable, and so they are difficult to isolate from biological systems, hence measuring the toxin itself is likely more efficient than measuring the metabolites generated from metabolism (18). Human studies are limited. However, rodent studies have found the greatest tissue distribution resided within the gastrointestinal tract tissue with 100% elimination in 96 hours, 80% excreted in the first 24 hours in urine (19). Although, when tissue accumulation was compared to blood levels, they remained significantly higher in the tissue, though still with decreasing levels by a factor of 8 over 96 hours. This makes sense because ST also goes through enterohepatic recirculation via the bile, which is likely why tissue amount is extended over serum and urine (19). 

Both Roridin E and Verrucarin A mycotoxins categorized under the Stachybotrys mold, are relatively similar, though differences will be discussed as they arise. Roridin E is produced by Fusarium, Myrothecium, Trichothecium, Stachybotrys, and less commonly, the Betula cordifolia (the mountain paper birch tree) and the Podostroma cornu-damae mushroom (20, 21). Verrucarin A is also produced by Fusarium, Myrothecium, Trichoderma, and Stachybotrys, but differs in that Trichothecium, Cephalosporium, and Verticimonosporium can also produce it. Though not as common to come up positive on the testing, these are some of the more toxic mycotoxins measured. When exposed to trichothecenes the effects can be quite toxic. For Roridin E; irritation of the skin, mucosal layers of the intestines, and the nasal passage have been observed, sometimes leading to blisters and bleeding.  Ocular symptoms have been described as burning, blurred vision, conjunctivitis, and pain. Hypotension, nausea, vomiting, and potentially shock have also been documented (22).  Symptoms can be variable for Verrucarin A, but can be extreme and have cascading effects. The symptoms include bone marrow damage, nervous disorders, cardiovascular alterations, hemostatic derangements, immunodepression, gastric inflammation and lesions, anorexia, and dermatological lesions potentially leading to necrosis (23,24).

Toxicology

Trichothecenes are different than other mycotoxins in that they do not require metabolic activation, rather they react with biological systems, directly. Exposure can be through oral, dermal, inhalation, and parenteral routes, and once absorbed, they are able to move across the plasma membrane freely (22,23). Roridin has been shown to inhibit receptor tyrosine kinase, impact glucose-6-ph,osphatase in liver tissue, and also deplete glutathione (20, 25). One of the major components of Verrucarin A’s toxicity is their ability to bind to ribosomes, particularly at the 3’ end of large 28S ribosomal RNA. This inhibits initiation, elongation, or termination steps, therefore influencing protein synthesis and polyribosomal disaggregation (23). These mycotoxins can alter membrane structure, influencing the mitochondria, and have also been noted to inhibit RNA and DNA synthesis along with mitosis. Verrucarin A is known as a potent antibacterial and antifungal (23). 

Properties

Trichothecenes, including these two mycotoxins, contain a distinct 9,10 double bond, and a 12,13 epoxide ring, with an additional hydroxyl or acetyl groups at certain positions (20, 22,23, 26). They are lipophilic in nature but have a relatively short half-life. It is estimated that trichothecenes, in general, have a half-life of minutes to hours (27, 28). Both have low water solubility, with Roridin E at 0.01 g/L and Verrucarin A at 0.043 g/L (22, 23). There is no data on melting points for either one of these toxins.       
                                                                                                                                                                                                                                                                

Metabolism

Once absorbed into the system, they are metabolized in the liver by cytochrome P-450 enzymes and trichothecene-specific carboxylesterases. Through phase II detoxification, the major pathway utilized is glucuronidation and deepoxidation (22,23, 27). They are mainly excreted through urine and feces, but additional data beyond these pathways was difficult to find. One study that was done on a similar trichothecene produced by S. Chartarum, Satratoxin G, found that it was detectable in the blood of the mice being exposed intranasally from 5-60 min after exposure (26). Noting that the clearance from plasma was rapid and single compartment kinetics was observed. The highest concentrations were found in the nasal passage (480 ng/g), then the kidneys (280 ng/g), lungs (250 ng/g), and spleen (200 ng/g) had the next elevated amounts. Interestingly, the liver did not have as high of a concentration (140ng/g). The half-lives were variable in the tissues as well, with 7.6-10.1 h in the nasal passage and the thymus, and 2.3-4.4 hours in the other organs. When the urine and feces were evaluated, the cumulative excretion over 5 days was 0.3% of the total dose administered. The two mycotoxins were difficult to compare but do give some insight into the biochemical pathways of these toxins (26). 

Ennaitin B comes from the fusarium species, and though it is common in foods due to its resistance to food processing techniques, and being unregulated, it has also been found in water damaged buildings (29). It has been shown to be more toxic than Ennaitin A, and just as common in our environment (29). Research has shown it acts as an antibacterial (particularly to certain species of Escherichia, Enterococcus, Salmonella, Shigella, Listeria, Yersinia, Clostridium, Psuedomona, and Staphylococcus), and antifungal (Beauveria and Trichoderma) (29, 30).  

Toxicology

ENN B is most commonly known to inhibit acyl-CoA and cholesterol acyl transferase activity, which will inherently influence lipidemic levels, particularly with decreased free fatty acid availability and triglyceride biosynthesis (29). EEN B has also been shown to affect the mitochondria directly by influencing potassium uptake and decreasing calcium retention capacity of the matrix. This can cause the mitochondrial membrane potential to collapse. Cell cycle disruption, and apoptotic death, have also been observed with the presence of ENN B (31). Adrenal endocrine influences via reducing progesterone, testosterone, and cortisol have been noted even in smaller amounts (29, 32). Higher concentrations (10 µM) were noted to reduce testosterone and estradiol (33). It has been shown to be a potent cytotoxin in several human and animal cell lines, even at very low levels. This is amplified when other mycotoxins are present (29). 

Properties

ENN B is a cyclohexadepsipeptides that is composed of mostly valine, isoleucine, and leucine residues, and three hydroxy acids, usually hydroxyisovaleric (29, 31, 34). It is lipophilic in nature, giving it the ability to incorporate into the phospholipid bilayers of the cell membrane. They are ionophores, which allows them to have a lot of other variabilities in their activity (29). This leads to its ability to influence the selectivity of the pores and disrupt cation levels. Also, it has the ability to form complexes with alkali metal ions, with selectivity in the following order: K+ > Ca2+ ≥ Na+ > Mg2+ > Li+. Solubility is 0.018 g/L in water (31). With regards to half-lives, a study that evaluated the degradation rate within a human gastrointestinal tract model found a degradation rate of 79 ± 5% within the GI tract, with even more degradation of enniatin B in the colon after 24 hours (35). The melting point is 229°C (444 °F), which is the main contributing factor as to why it is not affected by food processing (31).  

Metabolism

ENN B enters the system via oral, dermal, or inhalation route. From the aforementioned study on the GI model and ENNs behavior, they found metabolites from ENN were adsorbed within the GI tract (more than the parent compound) and observed moderate blood-brain-barrier crossing (35). It has been noted to bioaccumulate in the lipid tissue in rats and disseminate throughout the tissue in chickens (29). It utilizes the P450 enzyme CYP3A4, which to note, is one of the main enzymes that metabolizes numerous drugs, and other contaminants (31,36). 

Chaetoglobosin A is one of the most toxic mycotoxins on the test with even small amounts being deadly. It is very common in water damaged buildings, and in fact, one study that looked at the prevalence found that out of 794 water- damaged building material, 49% had isolated Chaetomium species (37). Chaetoglobosin A is one of the major mycotoxins produced by the Chaetomium species (mainly Chaetomium globosum) and some Penicillium species (38, 39). There are 18 natural chaetoglobosin mycotoxins that have been identified and have been known to be an antimicrobial agent with some neocicidal and antifungal influences (40, 41). Unfortunately, the literature is sparse on this mycotoxin, and details regarding properties and metabolism were limited. 

Toxicology

Chaetoglobosin A has been shown to influence cell division by inhibiting cell movement, cytoplasmic division, and multinucleation (40). It has also been found to be a P450 inhibitor and influence apoptosis (40, 42). Research has shown it to be quite toxic to mammals. In rats, exposure by injection caused necrosis of the thymus and spleen, and degeneration of the spermatocytes (40). Evidence also suggests it to be cytotoxic, particularly in cancer cells, and influences the cytoskeleton, accompanied with apoptosis (40 and 41). There is evidence of it being teratogenic in mice fetuses, with documented skeletal malformations, micromelia of the forelimbs, fused ribs, and death (43).

Properties

Chaetoglobosin A is a member of the cytochalasan-type (48).  All 8 types have a similar 13-member macrocycle and perhydroisoindole skeleton, with an indolymethyl substituent on C-3, but vary in oxidation level, C-11 and C-12 methyl substituents additions (40). They have a melting point of 165°C-170°C (329°F - 338°F), but no data was available on solubility or half-life at this time (40).

Metabolism

The data is very limited on the metabolic pathways of Chaetoglobosin A in the animal system, with in vitro studies very much lacking in the literature. A dated study in 1978 found higher toxicity load through parental exposure versus oral dosing in rats and mice, alluding to low oral absorption (44). In this study, when the rats were injected with this mycotoxin, death was observed 10 minutes to 2 hours post-administration, with visceral congestion noted on autopsy (44). At lower injection doses, 36% mortality rate was observed in 6-48 hours accompanied by necrosis throughout the spleen, decreased thymocytes, spermatocyte degeneration, and pulmonary congestion. The other 64% that recovered, after 3 days, the only effects were on the thymus and testes, with no histological abnormalities after 7 days (44). In another study where the rats and mice were fed an oral diet contaminated with a 50% concentration of Chaetoglobosin A for 10-15 days, decreased weight was observed (38). 

This concludes the evaluation of each mycotoxin on the MycoTOX Profile. Hopefully, it helps in the understanding of these mycotoxins in nature, and potentially in our bodies. 

 

  1. Shah DT, Larsen B. Clinical isolates of yeast produce a gliotoxin-like substance. Mycopathologia. 1991 Dec;116(3):203-8. doi: 10.1007/BF00436836. PMID: 1724551.
  2. Dos Santos VM, Dorner JW, Carreira F. Isolation and toxigenicity of Aspergillus fumigatus from moldy silage. Mycopathologia. 2003;156:133–138. 
  3. Lewis RE, Wiederhold NP, Lionakis MS, Prince RA, Kontoyiannis DP. Frequency and species distribution of gliotoxin-producing Aspergillus isolates recovered from patients at a tertiary-care cancer center. J Clin Microbiol. 2005;43:6120–6122.
  4. Kwon-Chung KJ, Sugui JA. What do we know about the role of gliotoxin in the pathobiology of Aspergillus fumigatus?. Med Mycol. 2009;47 Suppl 1(Suppl 1):S97-S103. doi:10.1080/13693780802056012
  5. Pahl HL, Krauss B, Schulze-Osthoff K, et al. The immunosuppressive fungal metabolite gliotoxin specifically inhibits transcription factor NF-kappaB. J Exp Med. 1996;183:1829–1840.
  6. Niide O, Suzuki Y, Yoshimaru T, Inoue T, Takayama T, Ra C. Fungal metabolite gliotoxin blocks mast cell activation by a calcium- and superoxide-dependent mechanism: implications for immunosuppressive activities. Clin Immunol. 2006;118:108–116.
  7. Dolan SK, O'Keeffe G, Jones GW, Doyle S. Resistance is not futile: gliotoxin biosynthesis, functionality and utility. Trends Microbiol. 2015 Jul;23(7):419-28. doi: 10.1016/j.tim.2015.02.005. Epub 2015 Mar 10. PMID: 25766143.
  8. National Center for Biotechnology Information (2022). PubChem Compound Summary for CID 6223, Gliotoxin. Retrieved March 31, 2022 from https://pubchem.ncbi.nlm.nih.gov/compound/Gliotoxin.
  9. Gayathri, L., Akbarsha, M. & Ruckmani, K. In vitro study on aspects of molecular mechanisms underlying invasive aspergillosis caused by gliotoxin and fumagillin, alone and in combination. Sci Rep 10, 14473 (2020). https://doi.org/10.1038/s41598-020-71367-2
  10. Jayalakshmi, R., Oviya, R., Premalatha, K. et al. Production, stability and degradation of Trichoderma gliotoxin in growth medium, irrigation water and agricultural soil. Sci Rep 11, 16536 (2021). https://doi.org/10.1038/s41598-021-95907-6
  11. Waring P, Beaver J. Gliotoxin and related epipolythiodioxopiperazines. Gen Pharmacol. 1996;27:1311–1316.
  12. Kamei K, Watanabe A. Aspergillus mycotoxins and their effect on the host. Med Mycol. 2005 May;43 Suppl 1:S95-9. doi: 10.1080/13693780500051547. PMID: 16110799.
  13. Cayman Chemicals. Gliotoxin Product Information. https://cdn.caymanchem.com/cdn/insert/11433.pdf
  14. Bernardo PH, Brasch N, Chai CL, Waring P. A novel redox mechanism for the glutathione-dependent reversible uptake of a fungal toxin in cells. J Biol Chem. 2003 Nov 21;278(47):46549-55. doi: 10.1074/jbc.M304825200. Epub 2003 Aug 28. PMID: 12947114.
  15. Díaz Nieto CH, Marcelo Granero A, Zon MA, Fernández H. Sterigmatocystin: A mycotoxin to be seriously considered. Food and Chemical Toxicology. 2018. 118 (Pages 460-470). ISSN 0278-6915. https://doi.org/10.1016/j.fct.2018.05.057.
  16. Tabata S. Yeasts and Molds | Mycotoxins: Aflatoxins and Related Compounds. Encyclopedia of Dairy Sciences (Second Edition). 2011. Pages 801-811. https://doi.org/10.1016/B978-0-12-374407-4.00369-1. (https://www.sciencedirect.com/science/article/pii/B9780123744074003691)
  17. Wishart D, Arndt D, Pon A, Sajed T, Guo AC, Djoumbou Y, Knox C, Wilson M, Liang Y, Grant J, Liu Y, Goldansaz SA, Rappaport SM. T3DB: the toxic exposome database. Sterigmatocystin (T3D3663) Nucleic Acids Res. 2015 Jan;43(Database issue):D928-34. 2537831 http://www.t3db.ca/toxins/T3D3663
  18. Gates KS. Covalent Modification of DNA by Natural Products. Comprehensive Natural Products Chemistry. 1999. Pages 491-552.https://doi.org/10.1016/B978-0-08-091283-7.00074-6. (https://www.sciencedirect.com/science/article/pii/B9780080912837000746). 
  19. Walkow J, Sullivan G, Maness D, Yakatan GJ. Sex and Age Differences in the Distribution of 14C-Sterigmatocystin in Immature and Mature Rats. 1985. Journal of the American College of Toxicology.4(1). https://journals.sagepub.com/doi/pdf/10.3109/10915818509014504
  20. Cayman Chemical. Product Information: Roridin E. 2019. https://cdn.caymanchem.com/cdn/insert/26955.pdf
  21. Zhu M, Cen Y, Ye W, Li S, Zhang W. Recent Advances on Macrocyclic Trichothecenes, Their Bioactivities and Biosynthetic Pathway. Toxins (Basel). 2020;12(6):417. Published 2020 Jun 23. doi:10.3390/toxins12060417
  22. Wishart D, Arndt D, Pon A, Sajed T, Guo AC, Djoumbou Y, Knox C, Wilson M, Liang Y, Grant J, Liu Y, Goldansaz SA, Rappaport SM. T3DB: the toxic exposome database. Roridin E (T3D3711) Nucleic Acids Res. 2015 Jan;43(Database issue):D928-34. 2537831 http://www.t3db.ca/toxins/T3D3711#references
  23. Wishart D, Arndt D, Pon A, Sajed T, Guo AC, Djoumbou Y, Knox C, Wilson M, Liang Y, Grant J, Liu Y, Goldansaz SA, Rappaport SM. T3DB: the toxic exposome database. Verrucarin A (T3D3720) Nucleic Acids Res. 2015 Jan;43(Database issue):D928-34. 25378312 http://www.t3db.ca/toxins/T3D3720https://pubmed.ncbi.nlm.nih.gov/25378312/
  24. Chu FS, Mycotoxins Toxicology. Encyclopedia of Food Sciences and Nutrition (Second Edition). 2003. Pages 4096-4108. ISBN 9780122270550. https://doi.org/10.1016/B0-12-227055-X/00823-3. (https://www.sciencedirect.com/science/article/pii/B012227055X008233). 
  25. Hossam El-Din M. Omar, Nagwa M. El Sawi & Abdel-Raheim M.A. Meki (1997) Acute Toxicity of the Mycotoxin Roridin E on Liver and Kidney of Rats, Journal of Applied Animal Research, 12:2, 145-152, DOI: 10.1080/09712119.1997.9706200
  26. Amuzie CJ, Islam Z, Kim JK, Seo JH, Pestka JJ. Kinetics of satratoxin g tissue distribution and excretion following intranasal exposure in the mouse. Toxicol Sci. 2010;116(2):433-440. doi:10.1093/toxsci/kfq142
  27. Fung F. Chapter 157 - T-2 Toxin (Trichothecene Mycotoxins) Attack. Ciottone's Disaster Medicine (Second Edition). 2016. Pages 801-803. ISBN 9780323286657. https://doi.org/10.1016/B978-0-323-28665-7.00159-X.(https://www.sciencedirect.com/science/article/pii/B978032328665700159X)
  28. Fæste CK, Ivanova L, Uhlig S. In vitro metabolism of the mycotoxin enniatin B in different species and cytochrome p450 enzyme phenotyping by chemical inhibitors. Drug Metab Dispos. 2011 Sep;39(9):1768-76. doi: 10.1124/dmd.111.039529. Epub 2011 May 26. PMID: 21622627.
  29. Prosperini A, Berrada H, Ruiz MJ, et al. A Review of the Mycotoxin Enniatin B. Front Public Health. 2017;5:304. Published 2017 Nov 16. doi:10.3389/fpubh.2017.00304
  30. Meca G, Sospedra I, Valero MA, Mañes J, Font G, Ruiz MJ. Antibacterial activity of the enniatin B, produced by Fusarium tricinctum in liquid culture, and cytotoxic effects on Caco-2 cells. Toxicol Mech Methods. 2011 Sep;21(7):503-12. doi: 10.3109/15376516.2011.556202. Epub 2011 Mar 21. PMID: 21417626.
  31. Wishart D, Arndt D, Pon A, Sajed T, Guo AC, Djoumbou Y, Knox C, Wilson M, Liang Y, Grant J, Liu Y, Goldansaz SA, Rappaport SM. T3DB: the toxic exposome database. Enniatin B (T3D3758) Nucleic Acids Res. 2015 Jan;43(Database issue):D928-34. 2537831 http://www.t3db.ca/toxins/T3D3758
  32. Prosperini A, Juan-García A, Font G, Ruiz MJ. Reactive oxygen species involvement in apoptosis and mitochondrial damage in Caco-2 cells induced by enniatins A, A1, B and B1. Toxicol Lett (2013) 222(1):36–44.10.1016/j.toxlet.2013.07.009
  33. Kalayou S, Ndossi D, Frizzell C, Groseth PK, Connolly L, Sørlie M, et al. An investigation of the endocrine disrupting potential of enniatin B using in vitro bioassays. Toxicol Lett (2015) 233(2):84–94.10.1016/j.toxlet.2015.01.014
  34. Stroka, J.  Gonçalves, C. Mycotoxins in Food and Feed: An Overview. Encyclopedia of Food Chemistry. 2019. Pages 401-419. ISBN 9780128140451. https://doi.org/10.1016/B978-0-08-100596-5.21801-5https://www.sciencedirect.com/science/article/pii/B9780081005965218015
  35. Pallarés N, Righetti L, Generotti S, Cavanna D, Ferrer E, Dall'Asta C, Suman M. Investigating the in vitro catabolic fate of Enniatin B in a human gastrointestinal and colonic model. Food Chem Toxicol. 2020 Mar;137:111166. doi: 10.1016/j.fct.2020.111166. Epub 2020 Jan 27. PMID: 32001315.
  36. Ivanova L, Denisov IG, Grinkova YV, Sligar SG, Fæste CK. Biotransformation of the Mycotoxin Enniatin B1 by CYP P450 3A4 and Potential for Drug-Drug Interactions. Metabolites. 2019;9(8):158. Published 2019 Jul 27. doi:10.3390/metabo9080158
  37. Fogle, Matthew & Douglas, David & Jumper, Cynthia & Straus, David. (2007). Growth and mycotoxin production by Chaetomium globosum. Mycopathologia. 164. 49-56. 10.1007/s11046-007-9023-x
  38. CPSC Staff Statement on Toxicology Excellence for Risk Assessment (TERA) Report “Review of the Health Risks of Mold, Health Effects of Molds and Mycotoxins”. 2015. https://www.cpsc.gov/s3fs-public/CPSCStatementmoldmycotoxinhealtheffectsJuly2015.pdf
  39. Knudsen, P., Hanna, B., Ohl, S. et al. Chaetoglobosin A preferentially induces apoptosis in chronic lymphocytic leukemia cells by targeting the cytoskeleton. Leukemia 28, 1289–1298 (2014). https://doi.org/10.1038/leu.2013.360
  40. Ichihara A, Oikawa H. Polyketides and Other Secondary Metabolites Including Fatty Acids and Their Derivatives: Chaetoglobosins. Comprehensive Natural Products Chemistry. 1999
  41. Zhang G, Zhang Y, Qin J, et al. Antifungal metabolites produced by Chaeyomium globosum No. 04, an endophytic fungus isolated from Ginko biloba. Indian J Microbiol. 2013 Jun; 53(2): 175-180. PMID: 24426105.
  42. Tsunematsu Y, Watanabe K, et al. Structural Diversity and Biosynthesis of Natural Products: Polyketides, Terpenes. Chaetoglobosin.  Comprehensive Natural Products III. 2020. 1.15.2.4. 
  43. Smith JE and Henderson RS. Mycotoxins and Animal Foods. 2000. Pages 478-479. ISBN 0-9493-4904-4.
  44. Ohtsubo K, Saito M, Sekita S, Yoshihira K, Natori S. Acute toxic effects of chaetoglobosin A, a new cytochalasan compound produced by Chaetomium globosum, on mice and rats. Jpn J Exp Med. 1978 Apr;48(2):105-10. PMID: 713122.
  45. Ichihara A., Oikawa H. The Diels–Alder Reaction in Biosynthesis of Polyketide Phytotoxins. Comprehensive Natural Products Chemistry. 1999. Pages 367-408. https://doi.org/10.1016/B978-0-08-091283-7.00015-1. (https://www.sciencedirect.com/science/article/pii/B9780080912837000151). 
  46. Walkow J, Sullivan G, Maness D, Yakatan GJ. Sex and Age Differences in the Distribution of 14C-Sterigmatocystin in Immature and Mature Rats. 1985. Journal of the American College of Toxicology.4(1). https://journals.sagepub.com/doi/pdf/10.3109/10915818509014504


LINDSAY GODDARD, RDN, LD/N

Lindsay Goddard is a Registered and Licensed Dietitian (RDN, LD/N), with a Masters in Nutrition, and a Bachelor's in Biology with a concentration in Human Physiology and Ecology. Her background allows for a comprehensive understanding of the connections and interactions between the body, the environment, and nutrition. Her experience consulting in functional medicine practices and hospital settings (Tampa General Hospital, University of Arkansas for Medical Sciences), has enabled her to take the biochemical information and apply it clinically, while bridging the gap between conventional and functional perspectives. She is excited to be a part of the GPL team, and hopes to support your mission in greater knowledge.

Webinar Q+A: The Toxicity of Trichothecenes - Insights Into This Unique Group of Mycotoxins

On February 16, 2022, The Great Plains Laboratory hosted The Toxicity of Trichothecenes - Insights Into This Unique Group of Mycotoxins webinar with Kurt Woeller, DO. Mycotoxins are toxic compounds produced by many different types of molds. A certain group of mycotoxins called trichothecenes are a large group of chemically related compounds produced by such molds as Fusarium and Stachybotrys. Trichothecenes have some unique toxicity effects, including on cellular production of proteins, DNA synthesis, and more. This lecture explored various mycotoxins within the trichothecene family and some of their related cytotoxicities.

The following Q+A is a grouping of responses from Dr. Woeller’s presentation.


Webinar Attendee Q+A

Q: Is it true that ammonia is an electron donor that degrades the integrity of the epoxide ring?

A: Amines are derived from ammonia and amines can act as nucleophile which attack the epoxide ring - 

 

Q: Dr. Ritchie Shoemaker has deemphasized mycotoxins as a cause of CIRS, saying they are less than 7% of gene activations. He has substituted endotoxins and actinomycetes. Many of his practitioners are saying this doesn't matter, because the structure of these toxins is "all the same.” This has caused them to discount Stachybotrys. Can you address Dr. Shoemakers altered position on toxic mold?

A: I have not dived deeply in Dr. Shoemaker’s claims. From my research, various mycotoxins can be significantly problematic for various reasons through their biological functions. A chemical may have a similar chemical structure on paper, but even subtle differences based on changing functional groups, positions of these groups on the molecule which can alter the chemicals orbital configurations, etc. are sometimes enough to change its cellular reactivity. 

 

Q: Do the same things occur in the body when these are inhaled vs being absorbed in the GI or skin? 

A: Yes, from my research and understanding. Now, there certainly could be some differences in specific cellular responses within the gut versus the skin, but when these toxins find their way into the lymphatic system, and eventually the bloodstream their distribution throughout the body to other organ systems should be the same.

 

Q: Which probiotics are low in histamine? 

A: Here is the link from presentation. This article is a good place to start your research.

 

Q: I am curious of your thoughts on the carnivore diet for patients?

A: I have not looked into this.

 

Q: What does PQQ mean?

A: Pyrroloquinoline Quinone – stimulates mitogenesis


The material contained within this article and webinar is not intended to replace the services and/or medical advice of a licensed healthcare practitioner, nor is it meant to encourage diagnosis and treatment of disease. It is for educational purposes only. Any application of suggestions set forth in the portions of this article is at the reader's discretion and sole risk. Implementation or experimentation with any supplements, herbs, dietary changes, medications, and/or lifestyle changes, etc., is done so at your sole risk and responsibility.



Kurt Woeller, DO

FOUNDER OF INTEGRATIVE MEDICINE ACADEMY
Kurt N. Woeller, DO, has been an integrative medicine physician and biomedical Autism specialist for over 20+ years. He is an author of several health books including Autism – The Road To Recovery, Methyl-B12 Therapy For Autism, Methyl-B12 for Alzheimer’s Disease and Dementia, and 5 Things You MUST Do Right Now To Help With Your Rheumatoid Arthritis. He is an international speaker, educator, and practicing clinician offering specialized interventions for individuals with complex medical conditions. His health consulting practice for Autism alone is multinational with families from various countries. Dr. Woeller serves as a clinical and lab consult for Functional Medicine Clinical Rounds, as well as provides educational seminars for Great Plains Laboratory. He is co-founder of Integrative Medicine Academy (www.IntegrativeMedicineAcademy.com), which is an online training academy for health practitioners learning integrative medicine.

Webinar Q+A: Mycotoxin Induced Mitochondrial Dysfunction And Cytotoxicity

On December 15, 2021, The Great Plains Laboratory hosted the Mycotoxin Induced Mitochondrial Dysfunction and Cytotoxicity webinar with Kurt Woeller, DO. Various mycotoxins can have significant adverse effects with regard to cellular function. Through DNA and RNA disruption and/or induction of oxidative stress mycotoxins can lead to various diseases, including cancer. A major target of intracellular mycotoxins are the mitochondria. This lecture by Dr. Kurt Woeller discussed some of the cytotoxic effects of mycotoxins on mitochondrial function.

The following Q+A is a grouping of responses from Dr. Woeller’s presentation.


Mycotoxin Induced Mitochondrial Dysfunction And Cytotoxicity Q+A

Q: Is it recommended for all patients who have mycotoxins to have some form of multivitamin therapy since vitamins have a huge impact on the ECT cycle?

A: I think so. I have most everyone on foundational supplements such as a multivitamin.

Q: If you have mold and candida, do you deal with them both simultaneously, or which do you treat first generally?

A: Depends on the severity of the condition, but in general mold because it can make candida worse.

Q: Maple Syrup Urine Disease is a genetic disorder in which a person is unable to break down the branched-chain amino acids. Would riboflavin make a difference in this disorder?

A: Great question and I do not know. It probably might help some.

Q: Is any other way to measure ochratoxin than the Organic Acids Test?

A: Ochratoxin is measured on the MycoTOX Profile from GPL. The OAT does not measure Ochratoxin or any other mycotoxins.

Q: Please indicate treatment strategies for aspergillus mold exposure and mycotoxins for patients with respiratory rx MAST CIRS.

A: This is a very in-depth topic and there are some webinars on the GPL site that address this, as well as seminars that are put on via the GPL Academy.

Q: I had a patient who was higher in gliotoxin than that, and we were able to completely eliminate it in less than 9 days using Ascorbic Acid and Ascorbates. We repeated this several times and got the same results using testing immediately before and immediately after the use of IV-Vitamin C. The whole process took about 9 or 10 days.

A: Awesome. I do see the value in ascorbic acid intervention too.

The material contained within this article and webinar is not intended to replace the services and/or medical advice of a licensed healthcare practitioner, nor is it meant to encourage diagnosis and treatment of disease. It is for educational purposes only. Any application of suggestions set forth in the following portions of this article is at the reader's discretion and sole risk. Implementation or experimentation with any supplements, herbs, dietary changes, medications, and/or lifestyle changes, etc., is done so at your sole risk and responsibility.



Kurt Woeller, DO

FOUNDER OF INTEGRATIVE MEDICINE ACADEMY
Kurt N. Woeller, DO, has been an integrative medicine physician and biomedical Autism specialist for over 20+ years. He is an author of several health books including Autism – The Road To Recovery, Methyl-B12 Therapy For Autism, Methyl-B12 for Alzheimer’s Disease and Dementia, and 5 Things You MUST Do Right Now To Help With Your Rheumatoid Arthritis. He is an international speaker, educator, and practicing clinician offering specialized interventions for individuals with complex medical conditions. His health consulting practice for Autism alone is multinational with families from various countries. Dr. Woeller serves as a clinical and lab consult for Functional Medicine Clinical Rounds, as well as provides educational seminars for Great Plains Laboratory. He is co-founder of Integrative Medicine Academy (www.IntegrativeMedicineAcademy.com), which is an online training academy for health practitioners learning integrative medicine.

Review of Mold and Mycotoxin Health Effects

GPL_Blog_MoldExposure_Woeller_0921_Graphics-12.png


By Kurt Woeller, D.O.

A mold by definition is “a fungus that grows in the form of multicellular filaments called hyphae” (1). One of the most common mold fungal species is aspergillus. In contrast, “fungi that can adopt a single-celled growth habit are called yeasts” (2), which includes the many species of candida. Both candida and aspergillus are types of fungus, but candida is not a mold, and aspergillus is not a yeast.   Molds (and other fungus) can produce different chemical compounds known as mycotoxins which are secondary metabolites (3) that can cause disease and death in humans and animals (4). An example of a group of dangerous mycotoxins of aspergillus mold is aflatoxins. These substances are some of the most carcinogenic compounds known in the field of biological toxins (5). Other mycotoxins from various molds such as penicillium, fusarium, and Stachybotrys chartarum are categorized as immunotoxic, hepatotoxic, nephrotoxic, neurotoxic (6). Molds are ubiquitous in the environment and mold spores can inhabit soil, certain food products such as grains, as well as dust particles. Several species of aspergillus, including A. fumigatus and A. niger can grow in damp, humid, and warm environments (7) and may even be found in bedding and pillows (8).

A person’s reaction to mold can range from typical allergic symptoms such as nasal congestion, itching, sneezing, and a mild cough to more severe manifestations linked to mycotoxin poisoning and associated adverse health effects such as immune suppression or organ damage. Listed here is a brief overview of different, but common physical reactions to various components of mold exposure:

GPL_Blog_MoldExposure_Woeller_0921_Graphics_Header Block.png

A mold allergy is an abnormal immune reaction mediated through immunoglobulin E (IgE) production in response to exposure to mold spores or cellular components of the mold. This immune reaction causes various inflammatory chemicals to be produced which can appear as simple nasal congestion, watery eyes, and mild cough, to more severe reactive airway disease and asthma (9).

When mold spores are inhaled intact, they can embed in lung tissue and cause an infection. This is particularly serious for any individual with immune disorders or other diseases such as asthma, cancer, chronic obstructive pulmonary disease, emphysema, diabetes, etc.

The infection linked to invasive fungus is called fungemia which is defined as a fungus found in the bloodstream. The most common form of fungemia is candidemia linked to invasive candida but can occur from aspergillus invasion. An aspergillus infection is termed aspergillosis and can ultimately lead to invasive aspergillosis (10). A common form of aspergillus is A. fumigatus which is significantly opportunistic in immunocompromised individuals (11).

The most common form of mold hypersensitivity is linked to the direct exposure to inhaled mold spores. It does not matter if the mold spore is alive or dead because reactivity can also occur to hyphal fragments that trigger inflammation in the upper airways, lungs, and systemically. Mold hypersensitivity has been linked to sick building syndrome (12) where people experience heightened symptoms and health problems when they encounter environments known to have mold contamination.

Many research papers have been written about sick building syndrome, including a 2018 review. This comprehensive analysis reviewing 16 previous studies concluded that individuals exposed to molds and associated mycotoxins had “symptoms affecting multiple organs, including the lungs, musculoskeletal system, as well as the central and peripheral nervous systems” (13). The symptoms associated with sick building syndrome could occur in almost anyone with mold illness and is likely associated with mycotoxin exposure and toxicity

GPL_Blog_MoldExposure_Woeller_0921_Graphics_Header Block copy 3.png

As discussed previously, these toxins of mold as secondary metabolites, have a wide array of negative health effects. There are many different types of medically significant mycotoxins, including ochratoxin A, gliotoxin, mycophenolic, and trichothecenes:

GPL_Blog_MoldExposure_Woeller_0921_Graphics_Main_3.png
GPL_Blog_MoldExposure_Woeller_0921_Graphics_Main_2.png
GPL_Blog_MoldExposure_Woeller_0921_Graphics_Main_1.png
 

There are two popular methods for analyzing the existence of mycotoxins in the body. One is called enzyme-linked immunosorbent assay (ELISA) and the other is liquid chromatography-mass-spectrometry (LC-MS).

ELISA – this method works on a “lock and key” method where a specific antigen (a substance that can stimulate the production of an antibody) is attached to a binding surface such as a polystyrene plate. A matching antibody is applied over the surface of the binding plate which allows the antibody a chance to bind to the antigen. The binding antibody, which is linked to a specific enzyme, then reacts with an added enzyme substrate. The substrate-enzyme reaction produces a chemical change signal indicating a positive match for the identified mycotoxin.

LC-MS – this method utilized by Great Plains Laboratory (GPL) is popular in chemical analysis because each technique is synergistically enhanced. The liquid chromatography separates multiple chemical components, while the mass spectrometry provides structural identity of the individual components with high molecular specificity and chemical detection sensitivity. In essence, LC-MS provides high accuracy of chemical detection of seemingly similar appearing compounds.

Both methods help to identify the existence of various mycotoxins, but with the ability for LC-MS to analyze specific chemical configurations it greatly reduces the false positive detection of similar compounds.

The discussion focused on treatment of mold exposure and mycotoxicosis is about as extensive and complicated as they come in integrative medicine. From a simplistic standpoint, if an individual is having allergic reactions to a mold the easiest thing to do is remove oneself from the environment. Anti-allergy medications may provide some temporary relief, but these do nothing to treat an underlying infection or manage the accumulation of mycotoxins. In most cases when it comes to mold illness, the situation is often more complex than a common mold allergy.

The difficulty with long-standing mold exposure is it often leads to systemic toxicities that greatly affect health. Each person needs to be analyzed individually to determine if they are suffering from common mold hypersensitivity, fungemia and/or mycotoxin toxicity.

Because mold organisms can colonize various areas within the human body, e.g., sinuses, lungs, gastrointestinal tract, comprehensive diagnostic approaches often need to be taken to determine at what level someone is affected. This can include performing a Mold IgE Allergy Test from GPL which identifies a multitude of environmental molds known to activate IgE antibody production.

The mycotoxin profile, (MycoTOX Profile) from GPL evaluates for various medically significant mycotoxins as discussed previously. However, these mycotoxins can exist for long periods of time in the human body even though an individual is no longer acutely exposed to mold. For example, it is possible to have a normal Mold IgE Allergy Test but have elevated levels of mycotoxins.

The Organic Acids Test (OAT) from Great Plains Laboratory has specific markers found in the Yeast and Fungal section on page one. The aspergillus and fusarium organic acids identify digestive colonization of these mold exposures. When the OAT is done along with a MycoTOX Profile and/or Mold IgE Allergy assessment, these tests may or may not show elevated findings. Therefore, when considering laboratory tests for mold exposure, it is often necessary to do multiple tests, as well as obtaining a thorough clinical history of exposure and symptoms.

It is critical for any practitioner working with a mold exposed individual to have a broad understanding of the various reactivity mechanisms and adverse health effects of mold and mold toxins.


GPLA_EmailGraphics_ETS_Nov_Header_2.png

To learn more about environmental toxins and mold toxicity, the Great Plains Laboratory's next event is heavily focused on these topics.

The Environmental Toxin Summit in San Diego, CA and streaming live online on November 12-14, 2021.

This three-day event will focus on the epidemics of toxin exposure, including both toxic chemicals in our environment and mycotoxins from mold. These toxins can cause symptoms of many acute and chronic health disorders. Attend this summit and learn how to use effective diagnostic and treatment protocols for your patients with toxin exposure and get them on the road to recovery. CLICK HERE for more details.


In October 2021, Integrative Medicine Academy will be hosting a comprehensive online course called Toxicity Mastery Course designed for health professionals on the topic of mold and mycotoxin exposure, along with environmental chemical and heavy metal toxicity. This course will cover details on laboratory testing, mechanisms of toxicity, and various treatment strategies. For more information, please visit Toxicity Mastery Coursehttps://toxicitymasterycourse.com.

Kurt N. Woeller, D.O.
Integrative Medicine Academy
Functional Medicine Clinical Rounds


References

1. Candidiasis. Fungal Diseases. (2019). United States: Centers for Disease Control and Prevention. 
2 Moore D, Robson GD, Trinci AP, eds. (2011). 21st Century Guidebook to Fungi (1st ed.). Cambridge University Press. 
3. Richard JL (2007). "Some major mycotoxins and their mycotoxicoses – an overview". Int. J. Food Microbiol. 119 (1–2): 3–10.
4. Bennett, J. W.; Klich, M (2003). "Mycotoxins". Clinical Microbiology Reviews. 16 (3): 497–516.
5. Hudler GW (1998). “Magical Mushrooms, Mischievous Molds: The Remarkable Story of the Fungus Kingdom and Its Impact on Human Affairs.” Princeton University Press.
6. Bennet, J.W., Klich, M (2003). “Mycotoxins”. Clinical Microbiology Reviews. 16 (3): 497–516.
7. Latgé JP (April 1999). "Aspergillus fumigatus and aspergillosis". Clinical Microbiology Reviews. 12 (2): 310–50.
8. "Pillows: A Hot Bed Of Fungal Spores". (2017). Science Daily.
9. Fisk WJ, Eliseeva EA, Mendell MJ (2010). "Association of residential dampness and mold with respiratory tract infections and bronchitis: a meta-analysis". Environmental Health. 9: 72.
10. Simicic S, Matos T, “Microbiological diagnosis of invasive aspergillosis.” Zdravnisji vestnik-slovanian medical journal. (2010). Vol. 79, Issue 10, pp. 716–25.
11. McCormick A, Loeffler J, Ebel F (2010). "Aspergillus fumigatus: contours of an opportunistic human pathogen". Cellular Microbiology. 12 (11): 1535–43.
12. Hardin BD, Kelman BJ, Saxon A (2003). "Adverse human health effects associated with molds in the indoor environment". Journal of Occupational and Environmental Medicine. 45 (5): 470–78.
13. Ratnaseelan AM, Tsilioni I, Theoharides TC (2018). "Effects of Mycotoxins on Neuropsychiatric Symptoms and Immune Processes". Clinical Therapeutics. 40 (6): 903–917.
14. Ringot D, Chango A, Schneider YJ, Larondelle Y. Toxicokinetics and toxicodynamics of ochratoxin A, an update. Chemico-biological Interactions, 15 Nov 2005, 159(1):18-46.
15. Annie Pfohl-Leszkowicz, Richard A Manderville. Mol Nutr Food Res. 2007 Jan;51(1):61-99.
16. Belmadani A, et al. (1999). "Selective toxicity of ochratoxin A in primary cultures from different brain regions". Arch Toxicol. 73 (2): 108–114.
17. Sava V, et al. (2006). "Acute neurotoxic effects of the fungal metabolite ochratoxin A". Neurotoxicology. 27 (1): 82–92.
18. Brankica Aleksic, Marjorie Draghi, Sebastien Ritoux, Sylviane Bailly, Marlène Lacroix, Isabelle P Oswald, Jean-Denis Bailly, Enric Robine. “Aerosolization of Mycotoxins after Growth of Toxinogenic Fungi on Wallpaper.” Appl Environ Microbiol. 2017 Aug 1;83(16). 
19. Mycophenolate Monograph for Professionals". Drugs.com. Retrieved 28 October 2019.
20. Prossnitz, Eric R.; Barton, Matthias (2014). "Estrogen biology: New insights into GPER function and clinical opportunities". Molecular and Cellular Endocrinology. 389 (1–2): 71–83.
21. Etzel RA (2002). "Mycotoxins". JAMA. 287 (4): 425–7.
22. Kiessling K (1986). "Biochemical mechanism of action of mycotoxins" (PDF). Pure and Applied Chemistry. 58 (2): 327–338.
23. Zorov DB, Juhaszova M, Sollott SJ (July 2014). "Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release". Physiological Reviews. 94 (3): 909–50.

Mycotoxin Properties and Metabolism: Part 1


By LINDSAY GODDARD, MS, RDN, LD

It appears mycotoxins are gaining a significant amount of interest as the literature increases on their toxic effects on humans and other animals. Just with any topic, as more data surfaces, more questions arise. Mycotoxin sources, testing, impacts, and treatments have been discussed in other blogs that you can review.

What has received less attention is how these compounds behave, particularly within our bodies, and what levels are commonly observed. The latter being particularly ambiguous.  In this article, properties and the metabolism of the top four most common mycotoxins will be explained to help further understand their behaviors, along with common ranges that are typically observed in Great Plains Laboratory. It is important to keep in mind that most of this research is done within the agriculture communities and laboratories, since human evaluations can be difficult to assess, for obvious reasons. It is the intent to use as much data from human studies as possible, but it may not always be feasible. It is also important to understand that although the typical ranges are provided, this does not assess the severity of those mycotoxins to an individual. Humans and other animals deal with these mycotoxins very differently, and it appears to be highly individualized within the species and current state of health of the individual.

Ochratoxin A (OTA) is the most common mycotoxin to show up on the test. Average positive ranges are generally from 15-30 nanograms/g of creatinine for people who are suspicious of mycotoxins. Results have been shown to be much higher in more extreme cases, with levels reaching up into the hundreds and even thousands range.

Toxicology

OTA is most notably a nephrotoxin, especially as it relates to the proximal tubule, which has been observed in several phylums. It also can impact the immune system; however, the exact mechanism is variable among different species. Studies have been observed the presence of OTA and the depletion of lymphoid cells, and stimulation of cytokine production especially with IL-2 and IL-5. Other influences are linked to inhibition of various enzymes such as phenylalanine hydroxylase, phenylalanine-tRNA synthetase, renal phosphoenolpyruvate carboxykinase, and carboxypeptidase A. OTA also can enhance lipid peroxidation, which is another aspect of the cellular damage caused by this mycotoxin. It also has the potential to cause proliferation of the cell via the interference with hormonal Ca2+ signaling, and therefore impairing Ca2+ cAMP homeostasis. 

Properties

Structurally, OTA consists of a para-chlorophenolic group, which contains a dihydroisocoumarin moiety, which is linked to L-phenylalanine via an amide link. At a neutral pH, OTA is slightly soluble in water, and soluble in polar organic solvents. Once alkaline conditions occur, it becomes soluble in all the aqueous solutions. Its melting point is between 90 °C (194 °F) to 169 °C (336.2 °F) depending on the solvent, proving it’s high stability especially in food processing.

Metabolism

It is absorbed into the system, via oral, skin or inhalation routes. From the ingestion standpoint, OTA is absorbed in the GI tract through various points. Taking note that the hydroxyl group of OTA is more in the nonionized form at low pH, which improves its absorption, therefore a significant amount of OTA is absorbed in the stomach. It is also readily absorbed in the intestines via passive diffusion, which is aided by the OTA binding to serum albumin. This complex also increases the half-life with a single dose of OTA lasting about 35 days. It is thought that this binding capacity is what allows OTA to transfer from blood to milk.

The human body attempts to eliminate some OTA via the bile, however enterohepatic recycling makes that less efficient. Once in the liver, the cytochrome P-450 microsomes along with NADPH, metabolize OTA further into hydroxyochratoxin A for elimination.  OTA itself is mainly excreted through the urine, yet the organic anion transport system in the proximal and distal tubules of the kidney actively reabsorb OTA. At this point, OTA is being transported with smaller carrier proteins, which allow the compound to pass through the glomerular membrane at an increased rate. This further increases the bioaccumulation and contributes to the extended half-life, leading to the cause of the nephrotoxicity that ensues with consistent, larger exposures.

GPL_Blog_MycotoxinPropedrties_Graphics_Header Block copy 7.png

Mycophenolic Acid (MPA) is one of the better understood mycotoxins within the medical community since it is used by the pharmaceutical industry. The average positive range tends to be between fifty and the mid hundreds. In more extreme cases, it can be in the thousands. If someone is taking the drug that contains MPA, the amount excreted tends to be between 40,000-100,000 nanograms/g of creatinine.  

Toxicology

The main mechanism of action for MPA is as an inhibitor of inosine monophosphate dehydrogenase, leading to an inhibition of the de novo pathway of guanosine nucleotide synthesis. This significantly reduces T- and B- lymphocytes since they are dependent on de novo synthesis of purines for their proliferation.

Properties

MPA is a polyketide compound, which is not soluble in water, and has a melting point around 141 °C (285 °F). Similar to OTA, it has a high affinity for albumin. When albumin is in lower amounts because of a disease or inflammatory state, the free MPA concentration may increase.  MPA is metabolized by glucuronidation via glucuronyl transferase, primarily in the liver, but also in the intestines and kidney. This ultimately forms MPA glucuronide (MPAG). This metabolite has little activity on the immune system, however the other metabolite that is formed, acyl glucuronide, will also impact the immune system, similarly to MPA. When analyzing the metabolism of MPA in stable transplant patients, 28% of the MPA taken orally was converted to MPAG, and the ratio of MPA:MPAG:acyl glucuronide was about 1:24:0.28.  

Metabolism

MPA, as observed through oral administration, is absorbed in the small intestines, and primarily eliminated in the urine by active tubular secretion and glomerular filtration, with approximately 60% or more as MPAG, and about 3% as MPA. Keep in mind here that the MPAG has less impact on the immune system versus the MPA, so measuring that would have less clinical significance as it relates to assessing toxicity. MPAG also utilizes bile in its elimination, however it can be deconjugated by certain flora in the gut back to MPA, leading it to be reabsorbed. Some of the enzymes involved in MPA glucoronidation (particularly UGT1A8 and UGT1A9), are expressed outside of the liver, thus contributing to the metabolism within the GI tract. The half-life of MPA is between 8-16 hours, therefore when extreme elevations are occurring, it is likely from a very recent exposure.

GPL_Blog_MycotoxinPropedrties_Graphics_Header Block copy 8.png

Previously known as F-2, Zearalenone (ZEA) is another mycotoxin that has a large amount of recognition. It is a very common contaminate of grains to the point it is regulated closely by numerous countries. What sets it apart from other mycotoxins is that it has a unique application in regulating hormones in livestock due to its estrogenic effects. This pharmaceutical drug is called zeranol and is approved to be used in livestock within the US, though the FDA has banned it for human use. It should be noted here that the World Anti-Doping Agency has been tracking zeranol since 2003 in athletes (who typically consume a significant number of livestock products) and has only found 6 positive tests globally. Typical ranges found on the GPL MyCoTOX Panel tend to be below 20, and in more extreme cases, can get up in the hundreds or above.

Toxicology

ZEA’s main mechanism of action is activating estrogenic receptors, creating estrogenic responses. It is therefore classified as an endocrine disrupter. The impact of ZEA on estrogenic effects varies significantly throughout animal species. Swine tend to be the most sensitive to it, while humans require a more chronic exposure to be significantly harmful. Cascading effects have been identified in the uterine organ and mammary tissue, like estradiol elevations.  ZEA also has the capacity to act on the hypothalamus and pituitary, mimicking estrogenic effects. There is some discussion of its association with hepatotoxicity and immunotoxicity, but these are not as well understood.

Properties

The structure of ZEA is a phenolic resorcylic acid lactone and is extremely similar to the estradiol structure. There are various forms, with at least seven derivatives identified just with corn, alone. They have all been shown to impact estrogen receptors. It has a melting point of 164 °C (328 °F), and solubility in water is very limited (0.002g/100mL). However, it is soluble in various solutions, particularly in aqueous alkali. ZEA is fairly heat stable but can be partially destroyed with extrusion cooking. The heat degradation is dependent on the solution it is in, but overall, it is completely degraded at 225 °C (437 °F). It is half-life from oral dosage is approximately 86 hours in swine, and 72 hours in hens. Not much information exists on humans except for one study by Mukherjee et al. where it was estimated to be around 11.98 hours in young girls. It has been shown to bioaccumulate within adipose tissue and reproductive tissue of females, and interstitial cells within the testes. 

Metabolism

Ingestion or inhalation seems to be the most common routes of exposure, though ZEA does have the ability to permeate through human skin. Absorption of ZEA occurs within the intestinal lumen for most animals. In swine observations, somewhere between 80-85% was absorbed through a single dose. ZEA is mainly conjugated through glucaronidation in the liver and the intestinal mucosa. It then goes through enterohepatic circulation and biliary excretion, with stool being the major route of elimination. Rumen and microbiota metabolism is also a potential; however, this is dependent on absorption, enzymes, and receptor availability and/or presence in particular species.

GPL_Blog_MycotoxinPropedrties_Graphics_Header Block copy 9.png

Citrinin (CTN) is likely the second most common mycotoxin to be reported, but unfortunately it has the least amount of recognition in the literature. It is very common to find alongside OTA, especially since they typically come from the same species (Aspergillus niger). General ranges found for positive results are below a hundred. 

Toxicology

The mechanism of action for CTN toxicity is not as well understood as the other mycotoxins. It has been found to cause oxidative stress and increased permeability of mitochondrial membranes, however, not cellular membranes themselves. In these mitochondrial preparations, CTN inhibited succinate oxidase and NADH oxidase, while also completely inhibiting cellular respiration.  The target organ appears to be the kidney in a variety of phylums. Embryocidal, fetotoxic, and genotoxic have been suspected, and proven in some organisms. Immunotoxicity and hepatotoxicity is also a potential, but data is lacking. When CTN and OTA are together within the system, they work cooperatively in reducing the activity of RNA synthesis in the renal tissue.

Properties

CTN is a polyketide mycotoxin that is insoluble in cold water, barely soluble in hot water, and soluble in polar organic solvents. It can breakdown in acidic and alkaline solutions. CIT’s melting point is around 100 °C (212 °F).  Relative to other mycotoxins, CTN is fairly heat sensitive, and unstable in temperature elevations. When heated (>175 °C, in dry conditions, >100 °C in water), it has the potential to degrade to CIT H1, which is more toxic, and CIT H2, which is less toxic, than CTN. It also has a short half-life in the human blood (~9 hours), and in urine (6-8 hours), and for this reason, it is thought it does not bioaccumulate in organisms unless there is repeated, large exposures.

Metabolism

Oral, inhalation, and skin tend to be the major routes of exposure. Unfortunately, there is very limited data as to the exact route and elimination of CIT in humans, however excretion moves through the kidney’s, which is where it has the potential to bioaccumulate.


Stay tuned for part II, where the next review will be of the less common, but potentially more toxic, group of mycotoxins measured on the MycoTox. 


References

1. Gupta, Ramesh C. Veterinary Toxicology. Basic and Clinical Principles 3rd edition. 2018. 
2. Khoury A and Atoui A. Ochratoxin A: General Overview and Actual Molecular Status. Toxins. 2010. 2(4): 461-493. PMID: 22069596
3. Plumlee KH. Mycotocins Toxicokinetics. Clinical Veterinary Toxicology. 1st Edition. 2004
4. Gruber-Dorninger C., Novak B, Nagl V, and Berthiller F. Emerging Mycotoxins: Beyond Traditionally Determined Food Contaminants. Journal of Agricultural and Food Chemistry2017 65 (33), 7052-7070. SOURCE
5. Food and Drug Association. Mycophenolic acid (Myfortic). SOURCE
6. Lamba V, Sangkuhl K, Sanghavi K, Fish A, Altman RB, and KE.PharmGKB. Mycophenolic Acid Pathway. Pharmacogenetics and genomics.2014. PMID:24220207. SOURCE
7. Hooijmaaijer E, Brandl M, Nelson J, Lustig D. Degradation products of mycophenolate mofetil in aqueous solution. Drug Dev Ind Pharm. 1999 Mar;25(3):361-5. doi: 10.1081/ddc-100102183. PMID: 10071831.
8. Haschek WM, Voss KA,  Beasley VR.  Selected Mycotoxins Affecting Animal and Human Health. Handbook of Toxicologic Pathology (Second Edition).2002. Pages 645-699. SOURCE
9. United States Anti-Doping Agency. Zeranol FAQ. 2021. SOURCE
10. National Center for Biotechnology Information (2021). PubChem Compound Summary for CID 5281576, Zearalenone. SOURCE
11. Ryu D, Hanna MA, Eskridge KM, and Bullerman LB. Heat Stability of Zearalenone in an Aqueous Buffered Model System. Journal of Agricultural and Food Chemistry 2003 51 (6), 1746-1748. DOI: 10.1021/jf0210021. 
12. Gil-Serna J, Vázquez C, Patiño B. Mycotoxins | Toxicology. Reference Module in Food Science. Elsevier. 2019. ISBN 9780081005965. SOURCE
13. Doughari, J. The Occurrence, Properties, and Significance of Citrinin Myctoxin.  Plant Pathol Microbiol 2015, 6:11 DOI: 10.4172/2157-7471.1000321
14. Arce-López B, Lizarraga E, Vettorazzi A, González-Peñas E. Human Biomonitoring of Mycotoxins in Blood, Plasma and Serum in Recent Years: A Review. Toxins (Basel). 2020;12(3):147. Published 2020 Feb 27. doi:10.3390/toxins12030147

8 Binders for Mycotoxins

GPL_SpeakerGraphiC_JasmyneBrown.png


BY JASMYNE BROWN, ND, MS

After a positive Organic Acids Test and MycoTOX Profile, the presence of mold and mycotoxins are usually significant answers for many symptomatic clients. When working with mycotoxicosis, choosing the correct binder can present a challenge.  Oftentimes I get the question: which binder is correct for which toxin? Since the research for the binding capacity of each binder isn't as heavily researched as other agents, it can be daunting to sift through the information. Below is a collection of research connecting mycotoxins to a good binder choice.

In our bodies, toxins are detoxed and excreted through a few pathways. Routes of elimination include urine, stool, bile and through our skin. Other routes include tears and saliva but are negligible in the realm of detoxification. Another route is breast milk. Since breast milk is a route of excretion this means toxins can be transferred to another life this way. This fact makes binders even that much more crucial in childbearing age women.

When it comes to binders, bile and stool are the target routes of elimination. Fat soluble substances such as dietary lipids, certain vitamins and fat-soluble toxins like mycotoxins get packaged into bile for absorption and detoxification. During bile’s life cycle it gets excreted into the GI tract and is what gives stool its brown color. In the colon most of the bile is reabsorbed so the liver and gallbladder do not have to work as hard to make more bile. It is recycled and reused. Dysfunction of this phenomenon, bile acid malabsorption, chronic diarrhea is the main symptom.  Since bile is reabsorbed, in the ileum and jejunum, if toxins are packaged in the bile then the toxins can be reabsorbed as well. They would then re-enter circulation via the hepatic portal system. This is where binders come in handy. Binders will adhere to the bile that packages the toxins and then it cannot be reabsorbed. Due to the nature of this adherence, it cannot be trusted that the bond is irreversible. This bond is more like static cling, as described by Dr. Neil Nathan. The lack of a tight bond allows for the bile to be released if not excreted regularly. Meaning, irregular bowel movements from constipation, lack of fiber, or motility issues could cause resorption of toxins even with binder usage. Binders by nature are constipating and this should be mitigated and assessed regularly during binder usage. Properly moving bowels through diet and supplements should be achieved prior to adding in any binding agent. View products for gut motility on the New Beginnings Nutritionals Website

GPL_Blog_BindersforMycotoxins_Graphics_Header_1.png
GPL_Blog_BindersforMycotoxins_Graphics_Box_1.png

In the world of prescriptions, cholestyramine and colesevelam hydrochloride, more commonly known as Welchol, are often binders of choice. They are known for their intended use and design, which is their lipid lower activity and use in glycemic control in patients with type 2 diabetes mellitus. They work by directly binding bile in the GI tract. This causes a reduced bile resorption and an increased conversion of cholesterol to bile, via 7a-hydroxylation, thus lowering cholesterol levels. In this process toxin laden bile is bound and thus excreted via stool.

These two binders are often used in mycotoxin detoxification protocols. As seen above, this is for good reason. The mycotoxin that responds best to these prescriptions is ochratoxin a (OTA), according to the research. This is a notorious mycotoxin. OTA is produced by many species of Apergillus and Penicillium molds. These are two of the most ubiquitous molds in the environment. This fact makes OTA the most common mycotoxin. It is so common that even regular ingestion of commonly moldy foods will most likely expose you to small, negligible amounts of OTA - We outline this in our article: Mycotoxins in Food. In cases of water damage building exposure these drugs are valuable assets to binding this mycotoxin. 

GPL_Blog_BindersforMycotoxins_Graphics_Header_2.png
GPL_Blog_BindersforMycotoxins_Graphics_Box_2.png

A few years ago, activated charcoal was the new buzz trend. It was popping up in drinks, snacks, even ice cream. Due to this most people are familiar with this binder. It is commonly used for firming loose stools, binding toxin from food poisoning, and now for mycotoxin binding. According to the research most binders will bind to just about anything, including nutrients necessary for life. They are non-discriminating. This fact made the charcoal trend rather troubling for those engaging in high intake of this substance with no regard to its potential danger if not taken responsibly. But, due to this, activated charcoal is an effective toxin binder to just about any toxin that is excreted in the gut. It works similarly to cholestyramine by adsorbing to toxins packaged in bile.

Research shows that in food stuff and in the body activated charcoal is beneficial in mycotoxin binding. OTA is bound effectively by charcoal products. This a good alternative for non-prescribing practitioners. Charcoal has also shown efficacy in adsorbing to macrocyclic trichothecenes. Two of the most common are verrucarin a and roridin e, and these are assessed on the MycoTOX Profile. Other subvarieties of verrucarin, including ‘J’ have shown binding efficacy with charcoal administration. Also T-2 toxins from fusarium are bound by charcoal.

GPL_Blog_BindersforMycotoxins_Graphics_Header_3.png
GPL_Blog_BindersforMycotoxins_Graphics_Box_3.png

Another common binding agent is bentonite clay and zeolite clay. These two clays have been touted as working wonders in the cosmetic arena by pulling toxins from the skin. These clays have been shown to bind greatly to toxins in animal feed, reducing the toxic load before consumption. Another clay is montmorillonite clay, also known as Novasil. This clay has ample research as a mycotoxin adsorbent in animal feed, a highly mycotoxin contaminated source. Great news, these clays do the same adsorbing action in the GI tract. Both agents show great affinity for binding aflatoxins best. These clays do not have much other research connecting them as strong adsorbents to other toxins as they do with aflatoxins. Although they can be useful in clients with these toxins and zearalenone, OTA, and gliotoxin as there is some adsorbing activity with these toxins.

GPL_Blog_BindersforMycotoxins_Graphics_Header_4.png
GPL_Blog_BindersforMycotoxins_Graphics_Box_4.png

This water-soluble polysaccharide is a well touted weight loss solution. It comes from the elephant yam, konjac. It is a hemicellulose fiber with beta-D-glucose and beta-D-mannose with acetyl groups with beta 1–4 linkages. Due to the lack of enzymes in human saliva to break these linkages, glucomannan goes through the GI tract unchanged. This allows for it to bind without absorption. Due to its content, this fiber can adsorb up to 50 times its weight. Glucomannan has shown efficacy in binding various mycotoxins.  Aflatoxin and OTA are major toxins affected by this binder. Others include zearalenone and Toxin T-2. not much efficacy was seen in binding DON-1 (Deoxynivalenol). Since glucomannan is a fiber this may be an option to consider in more constipated clients with ample water intake.

GPL_Blog_BindersforMycotoxins_Graphics_Header_5.png
GPL_Blog_BindersforMycotoxins_Graphics_Box_5.png

Speaking of fiber, in general fibrous supplements and foods can act as simple overall binders. Fiber from oats, wheat bran, alfalfa, lignans in flax and chia, guar gum, etc have been used as early interventions in lowering cholesterol. It has the same effect that cholestyramine has on cholesterol. It is due to the bile sequestering activity of these fibers that work to lower cholesterol. In turn this will also lower toxic load. Even though fiber doesn't have much direct research in the binding of specific mycotoxins, it is always a good dietary change to implement. Barley and oats showed highest absorptive capacity amongst other fibers when tested. Another great fiber binder to consider is modified citrus pectin (MCP). This binder has shown great efficacy in binding heavy metals such as lead. Though this isn't a mycotoxin, this shows us that MCP has a great potential utility in any detox protocol.

GPL_Blog_BindersforMycotoxins_Graphics_Header_6.png
GPL_Blog_BindersforMycotoxins_Graphics_Box_6.png

This next binding agent is a common plant-based agent. Chlorella is a type of freshwater algae that is packaged into a tablet, liquid extracts, and powders. It is often touted as a superfood due to its highly nutritious profile. It is high in protein, vitamins A, C, and E and is a great source of fiber. Because of its nutrition, chlorella is known for its wound healing, anti-cancer, anti-aging, and immune boosting potential. In breastfeeding mother’s chlorella intake increased circulating immunoglobulins in breast milk. This plant is great as a heavy metal binder and as a binder of aflatoxins. It has even been shown to inhibit aflatoxin B1 induced liver cancer.

Due to the safety profile of chlorella, it is a great binder for all populations. It is difficult to detox a constipated child or a woman expecting a child and is planning to breastfeed. Since so many other binders bind not only toxins, but also nutrients it can be difficult to support detox. Adding in small doses of chlorella is a safe and effective way to add in supportive detox without stimulating too much toxin release to the unborn fetus or breastfeeding child. 

GPL_Blog_BindersforMycotoxins_Graphics_Header_7.png
GPL_Blog_BindersforMycotoxins_Graphics_Box_7.png

Humic acid and its related counterpart, fulvic acid, are the final products of decomposition of organic matter. They are formed through humification of plant and animal matter via biologic processes of microorganisms. This byproduct acts as an adsorbent in soil to bind to toxic substances. Agriculturalists use these substances as soil additives to boost the growth and health of their crop due to its concentrated amount of nutrients. Due to its rapid lifecycle humic acid doesn't compete for nutrients with the plant or any other organism that uses it. This makes this biotoxin binder simpler to utilize when taking a variety of nutritional supplements.

Not only is humic acid a great biotoxin binder, but it also has shown efficacy as an anti-inflammatory. It also has shown promise in stimulating apoptosis in promyelocytic leukemia cells. This substance, along with fulvic acid, is a wonderful well-rounded addition to any detoxification protocol. 

GPL_Blog_BindersforMycotoxins_Graphics_Header_8.png
GPL_Blog_BindersforMycotoxins_Graphics_Box_8.png

This section of biotoxin binders may come as a surprise. Probiotics are best known for their activity in repopulating the GI microbiome after antibiotic use, killing of pathogenic organisms like C. difficile, and as a support in a whole host of chronic diseases. What many do not realize is that these organisms can also directly bind to mycotoxins. Strain of lactobacillus work to directly bind aflatoxins especially the B1 variety. The specific strains are L. pentosus and L. beveris. Another promising strain is L. plantarum C88. This strain works not only to bind to aflatoxins, but it also works by upregulating the antioxidant activity of glutathione s- transferase. It also shows great binding capacity to the common mycotoxin, sterigmatocystin.

Strains of saccharomyces also work well to bind mycotoxins. S. cerevisiae has been shown to bind tightly to aflatoxins. It has also shown great efficacy to bind to OTA and zearalenone. Saccharomyces boulardii, clinically, has shown great efficacy against gliotoxin. It has also shown efficacy in reducing Aspergillus and Fusarium molds in the GI tract. This will indirectly reduce mycotoxins, as it is reducing the producers of mycotoxins including zearalenone, enniatin b, OTA, gliotoxin, and aflatoxins. Mannan oligosaccharides (MOS) are prebiotics derived from the outer cell wall of S. cerevisiae. This prebiotic has been shown to bind to citrinin, which a wide variety of molds produce.  Using a variety of these strains will round out not only your gut treatment but also the detoxification process.


All in all, binding agents are an integral part of mycotoxin illness detoxification. Whether someone has 1 or 10 mycotoxins populate on the MycoTOX Profile, having the correct binders can be a challenge. Hopefully, this can be used as a resource to guide you in planning toxin binder regimens to best help your clients. Using a combination of binding agents will allow for well-rounded binding capacity in any mycotoxin toxicity case. View a wide variety of binding agents at New Beginnings Nutritionals to support you in choosing the best biotoxin binders.

This is a table matching mycotoxin with binders that have research to their binding affinity

GPL_Blog_BindersforMycotoxins_Graphics_Table.png

References

1. Agawane, S. B., and P. Lonkar. “Effect of Probiotic Containing Saccharomyces Boulardii on Agawane, S. B., and P. Lonkar. “Effect of Probiotic Containing Saccharomyces Boulardii on Experimental Ochratoxicosis in Broilers: Hematobiochemical Studies.: Semantic Scholar.” Undefined, 1 Jan. 1970, SOURCE. 
2. Ardeshir Mohaghegh,Mohammad Chamani,Mahmoud Shivazad,Ali Asghar Sadeghi &Nazar Afzali. “Effect of Esterified Glucomannan on Broilers Exposed to Natural Mycotoxin-Contaminated Diets.” Taylor & Francis, SOURCE. 
3. Armando, M.R., et al. “Adsorption of Ochratoxin A and Zearalenone by Potential Probiotic Saccharomyces Cerevisiae Strains and Its Relation with Cell Wall Thickness.” Journal of Applied Microbiology, vol. 113, no. 2, 2012, pp. 256–264., doi:10.1111/j.1365-2672.2012.05331.x. 
4. “Chlorophyll and Chlorophyllin.” Linus Pauling Institute, 1 Jan. 2021, SOURCE. 
5. D. Lloyd-Jones, R. Adams, et al. “Impact of Daily Chlorella Consumption on Serum Lipid and Carotenoid Profiles in Mildly Hypercholesterolemic Adults: a Double-Blinded, Randomized, Placebo-Controlled Study.” Nutrition Journal, BioMed Central, 1 Jan. 1970, SOURCE. 
6. De Mil, Thomas, et al. “Characterization of 27 Mycotoxin Binders and the Relation with in Vitro Zearalenone Adsorption at a Single Concentration.” Toxins, MDPI, 5 Jan. 2015, SOURCE. 
7. Devreese M;Girgis GN;Tran ST;De Baere S;De Backer P;Croubels S;Smith TK; “The Effects of Feed-Borne Fusarium Mycotoxins and Glucomannan in Turkey Poults Based on Specific and Non-Specific Parameters.” Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association, U.S. National Library of Medicine, SOURCE. 
8. El Khoury, Rhoda, et al. “OTA Prevention and Detoxification by Actinobacterial Strains and Activated Carbon Fibers: Preliminary Results.” MDPI, Multidisciplinary Digital Publishing Institute, 24 Mar. 2018, SOURCE. 
9. Garcia Diaz, Tatiana, et al. “Use of Live Yeast and Mannan-Oligosaccharides in Grain-Based Diets for Cattle: Ruminal Parameters, Nutrient Digestibility, and Inflammatory Response.” PloS One, Public Library of Science, 14 Nov. 2018, SOURCE. 
10. Guo M;Hou Q;Waterhouse GIN;Hou J;Ai S;Li X; “A Simple Aptamer-Based Fluorescent Aflatoxin B1 Sensor Using Humic Acid as Quencher.” Talanta, U.S. National Library of Medicine, SOURCE. 
11. Hamidi, Adel, et al. “The Aflatoxin B1 Isolating Potential of Two Lactic Acid Bacteria.” Asian Pacific Journal of Tropical Biomedicine, vol. 3, no. 9, 2013, pp. 732–736., doi:10.1016/s2221-1691(13)60147-1. 
12. Hope, Janette. “A Review of the Mechanism of Injury and Treatment Approaches for Illness Resulting from Exposure to Water-Damaged Buildings, Mold, and Mycotoxins.” The Scientific World Journal, Hindawi, 18 Apr. 2013, SOURCE. 
13. J;, Santos RR;Vermeulen S;Haritova A;Fink-Gremmels. “Isotherm Modeling of Organic Activated Bentonite and Humic Acid Polymer Used as Mycotoxin Adsorbents.” Food Additives & Contaminants. Part A, Chemistry, Analysis, Control, Exposure & Risk Assessment, U.S. National Library of Medicine, SOURCE. 
14. Jay Y. Jacela, DVM; Joel M. DeRouchey, PhD; Mike D. Tokach, PhD; Robert D. Goodband, PhD; Jim L. Nelssen, PhD; David G. Renter, DVM, PhD; Steve S. Dritz, DVM, PhD. Fact Sheet: Mold Inhibitors, Mycotoxin Binders, and Antioxidants, SOURCE. 
15. Jubert, Carole, et al. “Effects of Chlorophyll and Chlorophyllin on Low-Dose Aflatoxin B(1) Pharmacokinetics in Human Volunteers.” Cancer Prevention Research (Philadelphia, Pa.), U.S. National Library of Medicine, Dec. 2009, SOURCE. 
16. Kerkadi A;Barriault C;Tuchweber B;Frohlich AA;Marquardt RR;Bouchard G;Yousef IM; “Dietary Cholestyramine Reduces Ochratoxin A-Induced Nephrotoxicity in the Rat by Decreasing Plasma Levels and Enhancing Fecal Excretion of the Toxin.” Journal of Toxicology and Environmental Health. Part A, U.S. National Library of Medicine, SOURCE. 
17. Kraljević Pavelić, Sandra, et al. “Critical Review on Zeolite Clinoptilolite Safety and Medical Applications in Vivo.” Frontiers in Pharmacology, Frontiers Media S.A., 27 Nov. 2018, SOURCE. 
18. Kumar, C. B. ; Reddy, B. S. V. ; Gloridoss, R. G. ; Prabhu, T. M. ; Suresh, B. N. “ Effect of MOS Based Toxin Binder on Low Level Citrinin Toxicity in Commercial Broilers.” Mysore Journal of Agricultural Sciences, vol. 48, no. 1, 2014, pp. 75–82. 
19. L,Haus M;Žatko D;Vašková J;Vaško. “The Effect of Humic Acid in Chronic Deoxynivalenol Intoxication.” Environmental Science and Pollution Research International, U.S. National Library of Medicine, SOURCE. 
20. Lauterburg BH, Dickson ER, Pineda AA, Carlson GL, Taswell HF. “Removal of Bile Acids and Bilirubin by Plasmaperfusion of U.S.P. Charcoal-Coated Glass Beads.” Europe PMC, 30 Sept. 1979, SOURCE. 
21. Li, Yan, et al. “Research Progress on the Raw and Modified Montmorillonites as Adsorbents for Mycotoxins: A Review.” Applied Clay Science, Elsevier, 30 July 2018, SOURCE. 
22. Naumann, Susanne, et al. “In Vitro Interactions of Dietary Fibre Enriched Food Ingredients with Primary and Secondary Bile Acids.” Nutrients, vol. 11, no. 6, 2019, p. 1424., doi:10.3390/nu11061424. 
23. Riaz, Sana. “Cholestyramine Resin.” StatPearls [Internet]., U.S. National Library of Medicine, 25 May 2020, SOURCE. 
24. Rotter, R G, et al. “Influence of Dietary Charcoal on Ochratoxin A Toxicity in Leghorn Chicks.” Canadian Journal of Veterinary Research = Revue Canadienne De Recherche Veterinaire, U.S. National Library of Medicine, Oct. 1989, SOURCE. 
25. Vahouny, George V., et al. “Dietary Fibers: V. Binding of Bile Salts, Phospholipids and Cholesterol from Mixed Micelles by Bile Acid Sequestrants and Dietary Fibers.” Lipids, vol. 15, no. 12, 1980, pp. 1012–1018., doi:10.1007/bf02534316. 
26. “Verrucarin A (T3D3720).” T3DB, SOURCE. 
27. S,Baker; W,Shaw. “Case Study: Rapid Complete Recovery From An Autism Spectrum Disorder After Treatment of Aspergillus With The Antifungal Drugs Itraconazole And Sporanox.” Integrative Medicine (Encinitas, Calif.), U.S. National Library of Medicine, SOURCE. 
28. Wang JS;Luo H;Billam M;Wang Z;Guan H;Tang L;Goldston T;Afriyie-Gyawu E;Lovett C;Griswold J;Brattin B;Taylor RJ;Huebner HJ;Phillips TD; “Short-Term Safety Evaluation of Processed Calcium Montmorillonite Clay (NovaSil) in Humans.” Food Additives and Contaminants, U.S. National Library of Medicine, SOURCE. 
29. Yang, Hsin-Ling, et al. “Humic Acid Induces Apoptosis in Human Premyelocytic Leukemia HL-60 Cells.” Life Sciences, Pergamon, 25 June 2004, SOURCE. 
30. Zhao ZY;Liang L;Fan X;Yu Z;Hotchkiss AT;Wilk BJ;Eliaz I; “The Role of Modified Citrus Pectin as an Effective Chelator of Lead in Children Hospitalized with Toxic Lead Levels.” Alternative Therapies in Health and Medicine, U.S. National Library of Medicine, SOURCE.

Oxalates, Mold & Bacteria - Q&A with Andrew Rostenberg, DC, James Neuenschwander, MD & Emily Givler, DSC

GPL-Blog_Graphics_2021_MasterPractitioner_Mar2021_Q+A-04.png

The Great Plains Laboratory has been educating practitioners for over 15 years on how to help patients heal through cutting-edge testing, research and protocols. In our recent 3-Day Master Practitioner Workshop, speakers shared detailed information on how the MycoTOX Profile, IgG Food MAP and Glyphosate Test can work for you. As well as gave additional information about markers in the OAT and GPL-TOX.

The following Q+A is a response to remaining questions speakers were unable to answer during their presentations.

The material contained within this article is not intended to replace the services and/or medical advice of a licensed healthcare practitioner, nor is it meant to encourage diagnosis and treatment of disease. It is for educational purposes only. Any application of suggestions set forth in the following portions of this article is at the reader's discretion and sole risk. Implementation or experimentation with any supplements, herbs, dietary changes, medications, and/or lifestyle changes, etc., is done so at your sole risk and responsibility.


GPL-Blog_Graphics_2021_MasterPractitioner_Mar2021_Q+A_Rostenberg.png

Andrew Rostenberg,
DC, DIBAK

Bacterial Phenol Overload - A Hidden Cause of Gut-Brain Dysfunction

Andrew Rostenberg, D.C., DIBAK, is a chiropractor, kinesiologist, functional medicine expert, methylation researcher, author, and director of Red Mountain Natural Medicine in Boise, ID.

Q: So if patient with likely phenol overload from SIBO, but also has mycotoxin and oxalic acid issue, what to treat first - the gut?

A: The gut is Phase 0 detoxification – literally detoxification starts in the gut before it even begins in the body. If we are trying to cleanse the metabolic tissues of a toxic patient, but the gut is completely out of order and dysfunctional, then we will not see the best results. Always treat SIBO and other chronic, hidden gut infections first as that opens up the pathways for improved detoxification as the treatment process goes on. You might treat SIBO for 3- or 4-months max, then shift to helping with mycotoxins, mold, heavy metals, xenoestrogens, etc…just depends on what your patient needs.

Q: What if a patient with this high dopamine presentation does WORSE on taurine and TUDCA bile salts?

A: Some people just do not tolerate taurine well. It is a very small minority of people, but they do exist. Studies have shown a relationship to people with psoriasis and an intolerance to taurine. So even though certain supplements are very neutral and well tolerated, you will always find one or two people who are just sensitive in ways that are different from everyone else.

Q: What if someone is missing their Ileocecal valve, (cancer cut out), PLUS no gall bladder? Plus, daily PCN due to no spleen and immune deficiency? What is this person at risk for and how do they fix SIBO?

A: In our experience herbs and natural anti-microbials are well tolerated even by complex patients such as this. Someone without their ICV could perform bowel massages to help regulate peristalsis in the correct direction. They will likely need long-term herbal support to kill excess bacteria and yeast that inevitably get into the small intestine. They will need support for their upper GI tract like betaine HCl, pancreatic enzymes, and bile support (choline, methionine, taurine, ox bile, etc.). They can only fix SIBO by helping to correct the environment in the small intestine, and that will require consistent attention.

Q: So then what can that patient do? Also they have PPI due to GESR and ever increasing brain fog (used to think just due to chemo but suddenly has worsened significantly in the last year, since the pandemic).

A: PPI therapy is a guarantee of nutritional deficiency. That is what we see in practice as the number one problem in our patients – poor nutrient status be it Vit. C, or Vit. D, or any other of the 50 nutrients we need. The goal is to get patients off these PPI medications using any and all available natural medicine tools. Anything that improves the stomach function of our patients will improve their health, and any drug that interferes with normal stomach physiology is a big problem for the long-term health of our patients.

Q: Is this why certain service dogs can smell BS, blood sugar drops? Cancer etc.? phenols vocs, mind blowing…

A: Most likely yes.

Q: What causes flushing when taking high quality B complexes-- SIBO?

A: Any strange or paradoxical reaction to supplements should be investigated as a hidden gut problem until proven otherwise.

Q: So mycotoxins increase aldehydes and also clog up pathway towards COMT and glyphosate can inhibit aromatic aminos, so could things "balance" out, but still be toxic?

A: It’s possible that there are many mechanisms at play and that people can be “balanced out” but still heavily toxic. Best idea is to test and treat these hidden problems and get the balanced without the toxic side effects.

Q: How does mold affect dopamine?

A: Mold inhibits the ability of the body to breakdown catecholamines, so the higher the mold the more slowly dopamine and other catecholamines will be processed which can lead to dangerously high levels of half-way-broken-down dopamine. Mold produces toxic VOC chemicals (essentially indoor pollution) that must be metabolized through Phase 2 pathways in the liver and kidney. If mold levels are high, there is less bandwidth available for dopamine to get processed correctly. We tend to see people with mold exposure as individuals who cannot adequately metabolize their catecholamines due to the interference from the mold poisons the liver is trying to break down.

Q: Could you provide references for the nutrients to decrease/increase Dopamine?

A: References can be found by searching the PubMed library…sorry nothing convenient to share or hand out on this one.

Q: Patient with intermittent PVCs for several years after mold exposure intermittent anxiety completely resolved with B6 50mg daily. What’s the mechanism?

A: Could be multiple things, but B6 with lower SIBO and it is a cofactor for ALT enzyme in the Liver so it will upregulate detox reliably as well.

Q: Same protocols for SIFO as SIBO…. ? What do you think SIFO is?

A: SIBO protocol is more strict than a protocol required to treat SIFO, so if you treat SIBO you will also help reduce the fungal burden in parallel with the bacterial overgrowth.

Register now for our upcoming events and workshops.


GPL-Blog_Graphics_2021_MasterPractitioner_Mar2021_Q+A_Neu.png

James Neuenschwander, MD

Identifying and Treating Complex Patients with Mold Toxin Induced Illness

A graduate of the University of Michigan with both a Bachelor of Science degree in Molecular and Cellular Biology as well as a MD degree. He is dually board certified in both Emergency and Integrative Medicine and has been the owner of the Bio Energy Medical Center since its opening in 1988.

Q: Prefer IV Voriconazole or oral, and what doses?

A: Oral: 200mg twice daily.

Q: Are there special considerations for treating a patient with diverticulitis (on a third round of antibiotics) with Hx of chronic fatigue, ebv, and mold. I’m not her physician, she’s my sister.

A: I can’t give treatment recommendations for someone that is not my patient.

Q: What do you think about testing as a preventative - even if you don’t have symptoms - it may be brewing and present as a problem later on?

A: Testing for mold toxins is not that helpful if you are not symptomatic—most people don’t have problems.

Q: Have you found any treatment particularly useful to eradicate MARCONS, possible explanations for non-resolution of MARCONS and how do you treat low MSH?

A: Usually from persistent exposure. Need to regular Neti pot or saline rinses in addition to the antiseptic nasal sprays. Can use PT141 to try to increase MSH, but MARCONS will continue to break it down.

Q: On one panel, all mycotoxins were 0 except for OCHRATOXIN, which was high. Could this be from her excess coffee drinking alone?

A: It depends on the degree of elevation. Food sources will typically elevate levels slightly.

Q: I've heard other practitioners say that S.boulardi produces oxalates, so not good for those who already have mold/fungal issues and too much oxalates. Do you have any thoughts on this?

A: Not in my experience. The balance of the microbiome by S. boulardii usually reduces oxalates. There are some people that don’t tolerate any yeast.

Q: Do you check for adrenal fatigue and how do you treat it if present?

A: That is a two hour lecture.

Q: Do you consider EMFs in your patients?

A: Yes, but extremely difficult to treat.

Q: How do you give Itraconazole dose and interval ? With binders?

A: I use voriconazole.

Q: How do you fix VAGAL dysfunction in your practice? fix underlying mold, but how do you stimulate MMC after the eradication of toxicity?

A: I typically use DNRS. LINK

Q: What is the electron transport chain test called?

A: MitoSwab

Q: Any specific lab for AVH alpha MSH?

A: Not really—you need to know your ranges.

Q: Any recs for alternative to tenting for termites?

A: Not an exterminator.

Q: Vocabulary check POP (persistent organic pollutants)?

A: Yes.

Q: Can you say more about the origins and mechanisms involved in generating high osmolality / low sodium?

A: Don’t know the specific mechanism, but has to do with both renal and brain signaling dysfunction.

Q: What is the conference you were referring to in August in Arizona and are you presenting?

A: August 2021 is Integrative Medicine for Mental Health in Atlanta - use promo code: 50MPW21 for $50 off! The Arizona Conference is MAPS and will be 9/30-10/2 in Scottsdale.

Q: High ANA but no other elevated typical Autoimmune panel-would mycotoxins and/or environmental toxins be a potential cause?

A: Yes.

Q: Since binders are absorbing toxins why would too much of a binder cause a Herxheimer Reaction

A: Too quick of a detox will create symptoms.

Q: Can mycotoxins be responsible for persistent fever?

A: Any immune activation can cause a persistent fever.

Q: In the chronically ill patient with known history of Lyme, co-infections, mold toxicity, long term antibiotics, does the OAT help you differentiate what issues are still active and priorities? Any pearls?

A: It won’t differentiate between Lyme and co-infections, but will tell you about mold and toxicity.

Register now for our upcoming events and workshops.


GPL-Blog_Graphics_2021_MasterPractitioner_Mar2021_Q+A_Givler.png

Emily Givler, DSC

Oxalates & Mold: A Hidden Source of Inflammation

Emily Givler, DSC is a Functional/Genetic Nutrition Consultant and Dietary Supplements Counselor with the NutriGenetic Research Institute and Tree of Life. She specializes in food sensitivities, utilizing genetically influenced dietary protocols designed to maximize health outcomes while maintaining a healthy relationship with food.

Q: Anything to consider during treatment for clients with NO gallbladder?

A: These individuals are vulnerable to hyperoxaluria without adequate digestion support with something like TUDCA or ox bile. They may benefit from including calcium alongside higher oxalate foods to aid in the excretion of oxalic acid in stool.

Q: Could you recommend a lab for urine sulfate testing?

A: I use over the counter Quantofix sulfite and sulfate test strips. These are a urine dipstick and are good for home testing.

Q: I've heard Dr. Grace Liu say that O.forminges gets too much attention and that other bifido bacteria and lacto bacteria are actually powerful oxalate degraders.  What are you thoughts on this?

A: There are other organisms that can degrade oxalate under various conditions, but the research currently shows that O formigenes plays a primary role in degrading oxalic acid under any physiological conditions. Ideally, we should have a robust microbiome that has a large diversity of symbiotic organisms. I agree that we should not overstate the importance of any one organism. I do find the association between disruption of O formigenes by certain classes of antibiotics helpful to know when taking a history.

Q: How can you increase O. formigenes if not in a probiotic?

A: I try spore-based probiotics like MegaSpore. The goal would be to create diversity even if we cannot target that specific species.

Q: Please be specific with the prebiotics that you use that help the body regrow O.Formigenes

A: I have had good success with MegaSporebiotic, but there aren’t any studies that I can point to on it, only anecdotal evidence.

Q: Lichen Sclerosis not on list, do you suspect any link here?

A: I see associations in my own clients, but it isn’t there in the literature yet. LINK

Q: Where do you get the sulfate test strips?

A: Amazon.

Q: So, what comes first treating the mold or the oxalates? Or do you treat both at same time?

A: This must be an individual decision, but you can start reducing oxalate at any point (as long as a slow reduction approach is taken). You may not see full resolution of the oxalate issue until the mold is addressed if that is the primary driver, but it does not need to be gone before you start the oxalate reduction process.

Q: Do you ever use a Ca Mg citrate combo or the like?

A: Yes, that can be a great choice with meals.

Q: Which product or manufacturer for urinary sulfate testing and what was the range?

A: Quantofix Sulfite optimal 0-10; Sulfate range 400 - 800 optimal; <200 is insufficient, >1200 consider sulfate dumping.

Q: If you see high glycolic or glyceric but oxalic in normal range.  We think Genetic, but how do you get them to start excreting the oxalate?  Sulfate supplementation?

A: Yes, sulfate is likely going to be effective to start mobilizing trapped oxalate, but I would always start slowly in these cases. Epsom salts are generally my starting point. If sulfite is elevated, molybdenum can increase sulfate. Adding B6 can also help reduce oxalic acid production in cases where there is a genetic cause.

Q: Can you use P5P instead of B6 therapy when glyceric or glycolic markers elevated?

A: Yes, that would be my own preference.

Q: Could a patient's worsening of Symptoms if supplemented with B6 or zinc or B1 be because the oxalates where dumped more?

A: Potentially.


The MycoTOX Profile in Action - Elaboration from William Shaw, PhD

GPL-Blog_Graphics_2021_MasterPractitioner_Mar2021_Q+A-04.png

The Great Plains Laboratory has been educating practitioners for over 15 years on how to help patients heal through cutting-edge testing, research and protocols. In our recent 3-Day Master Practitioner Workshop, speakers shared detailed information on how the MycoTOX Profile, IgG Food MAP and Glyphosate Test can work for you. As well as gave additional information about markers in the OAT and GPL-TOX.

The following Q+A is a response to remaining questions Dr. Shaw was unable to answer during his presentations.

The material contained within this article is not intended to replace the services and/or medical advice of a licensed healthcare practitioner, nor is it meant to encourage diagnosis and treatment of disease. It is for educational purposes only. Any application of suggestions set forth in the following portions of this article is at the reader's discretion and sole risk. Implementation or experimentation with any supplements, herbs, dietary changes, medications, and/or lifestyle changes, etc., is done so at your sole risk and responsibility.


GPL-Blog_Graphics_2021_MasterPractitioner_Mar2021_Q+A_Shaw.png

William Shaw, PhD

IgG Food Allergy Testing: Scientific Evidence of its Validity in Chronic Illness

William Shaw, PhD, is board certified in the fields of clinical chemistry and toxicology by the American Board of Clinical Chemistry. Before he founded The Great Plains Laboratory, Inc., Dr. Shaw worked for the Centers for Disease Control and Prevention (CDC), Children's Mercy Hospital, University of Missouri at Kansas City School of Medicine, and Smith Kline Laboratories.

Q: Could you explain a little bit about the process of testing the environment and mold removal techniques from home/car for patient tested positive?

A: Clients can choose from about 3 different choices of home testing. The ERMI, mold air sampling plates, and a home inspector are the most common options. Here is a resource for more info on all of these options.

Q: If the OAT is not to be used in place of the MycoTOX Profile, and a client cannot follow up with a MycoTOX Profile after findings of mold in the OAT test, should one address it in some way? I am guessing it is wise to do so.

A: If mold is showing up on the Organic Acids Test and the client cannot test the MycoTOX Profile further investigation of the home/workplace/car/school should take place. This will help you as a practitioner know if they are currently exposed to mold. This will guide your treatment in whether or not to address the fungus with antifungals right away or post remediation/removal of exposure source. Retesting should include at lest a MOAT/OAT and MycoTOX.

Q: Does eating mushrooms or using medicinal mushrooms contribute to mycotoxins in your body?

A: If the mushrooms are contaminated with mold, then they can contribute to mycotoxin exposure. Also, they would most likely need to be ingested at extremely high levels to cause substantial mycotoxin increases. It would be best to investigate a WDB exposure prior to saying it is just the medicinal mushrooms.

Q: If someone is doing a mold protocol and is getting inflammation in the joints how can you support these toxins from excreting properly do you support more of lymph?

A: Lymphatic support is beneficial. Also consider increasing the binder dose if the client’s bowels can handle it. Consider reducing detox support during flares. This may be an aggravation reaction of detoxing too quickly. Supporting oxalate reduction and increasing anti-inflammatory support will also reduce joint pain.

Q: If a patient has a furan-2,5 dicarboxylic value above the average (15), would you treat him with antifungals?

A: This is not a positive result and should be confirmed with a positive MycoTOX Profile. If after consistent detox there is a plateau of progress, antifungals can support healing. I am finding most often people must do antifungal therapy for full resolution in most cases.

Q: How do you gauge whether the oxalate level on the organic acids can be from food? Is there a range that dietary oxalates can fall into?

A: There is not a specific range for any one person. It would be dependent on oxalate food intake you may see from a diet diary or diet history during your intake. Also if fungal markers are elevated on the OAT then its more than likely from that unless they eat a high amount of oxalate rich foods.

Q: Any hypothesized connection between autism, vaccines and mold?

A: Mold and mycotoxins have been implicated in autistic children. There may be a possibility of potential immune alteration of mycotoxins potentially causing adverse effects after vaccination administration.

Register now for our upcoming events and workshops.

Q: How do you manage a patient with autism who has a severe herxheimer reaction during treatment with itraconazole? do you keep the same dose?

A: This is up to the you and client. If they aggravate where they cannot function you can give them permission to reduce or skip a dose until symptoms subside. You may find that some clients that herx give up due to being uncomfortable and not feeling they have any control over their treatment if it gets to be too much. Giving an option to reduce can increase compliance. Also consider increasing the binder dose if their bowels can handle it.

Q: A patient has low Pyroglutamic and Oxalic, but high Glycolic, Glyceric and N Acetylaspartic - what significance of that?

A: These values don’t directly have anything to do with each other at the levels described but, low pyroglutamic acid means glutathione is being made sufficiently. Low oxalic and elevate glycolic and glyceric may be from fungal overgrowth, collagen, or bone broth intake, genetic hyperoxaluria (rare), B6 deficiency. Elevated N-acetylaspartic is associated with Carnavan’s disease (rare) if severely elevated. If mildly elevated this is more than likely due to increased nutrient need and/or gut dysbiosis.

Q: How would one test well water for mold?  and wouldn’t you be able to smell or taste it?

A: Mold testing plates could be used. Just add you water to the plate and see if mold grows. Could have it analyzed by Immunolytics potentially.

Q: What botanicals work against aspergillus?

A: Many antifungal botanicals work against molds like oregano and garlic. Please see 5 Herbal Agents for Antifungal Therapy for more information.

Also check out www.nbnus.net for herbal supplements that will kill mold and fungus.

Q: To clarify, Dr. Shaw believes that no glutathione should be used before mycotoxins testing because the toxins will bind to the glutathione and not be assessed correctly by the mass spec?

A: Correct. We are looking at the toxin unbound NOT bound to glutathione. It will be missed if its bound.

Q: Dr. Shaw disagrees with Shoemaker’s refusal to use anti-fungal drugs. Presumably, this not for all cases? Which molds typically require drugs to kill the organism? Only cases where repeat testing shows returning toxins despite removal of contaminants?

A: If the person is not colonized, then anti-fungal therapy is not needed. However, if continued detox of toxins and removal from exposure source still populates toxin on the MycoTOX Profile, then more than likely this person is going to need anti-fungal therapy. Also, any mold, if colonized, typically needs antifungals to kill them. Pharmaceuticals are beneficial in killing almost all species of mold. There is no one mold that absolutely NEEDs drugs to be killed. Mold is susceptible to natural agents.

Q: Is the mold on cheese toxic? How about if you trim it off and eat the rest? Are some cheeses more prone to toxic molds?

A: Mold on cheese is typically penicillium. In the case of blue cheese mycophenolic acid, a mycotoxin from penicillium, is the main ingredient that gives the cheese its blue color. So yes, mold on cheese can be toxic. If you are to remove the visibly molded spots you are more than likely reducing your exposure but there is no way to rule out microscopic mold growth and mycotoxins that are not visible. If you are not mold toxic then it should not harm you to eat this, but you may want to avoid molded foods to not add to the toxic load.

Register now for our upcoming events and workshops.

Q: Why do males have worse mycotoxin reactions than females?

A: I not sure this is a proven observation. There are many cases where men and women have the same exposure, and the woman has the worst reaction. All vice versa happens. It is more dependent on the individual and their susceptibility to the toxic effects of the mycotoxins.

Q: What is the glutathione challenge? and what were you trying to imply re it? To just not do before testing or you might not pick up the mycotoxins?

A: Glutathione challenge is giving the compound to provoke toxins prior to testing. GPL does not recommend doing this as the mas spec if not looking at the toxin bound to glutathione but unbound toxin. Bound toxin will be missed during sample testing.

Q: What over the counter antifungals were you referring to instead of the prescription ones?

A: Herbal and nutraceutical supplements. Check out www.nbnus.net for OTC anti-fungal options.

Q: Is there a marker in the OAT for actinomycetes?

A: No

Q: Just confirming the need to test liver enzymes twice a week? While on Sporonox.

A: Once a week is sufficient unless they increase and you want to assess sooner that that, then 2x that week would be warranted.

Q: And if mycotoxins are positive, how do you know which species of mold you have?  or does it even matter to know?  in other words, sporonox will treat them all?

A: You can evaluate which species of each genus excretes which mycotoxins to know which mold species you are directly dealing with or at least narrow it down. You could also do a sputum/nasal culture to determine which species is present. In the grand scheme of things, the specific species isn’t necessary to treat as Sporonox works on the ergosterol in the fungal cell wall to kill fungus in general.

Q: How likely are organic blue corn chips to be free of mycotoxins?

A: Not very likely. Corn is a commonly contaminated grain. Also, organic foods do not use pesticides so there is nothing there to kill the potential mold. In other words, organic food has an increased risk of being moldy due to the lack of fungicide use.

Q: What’s the research on seizure disorders and the testing?

A: Here is some info.

Register now for our upcoming events and workshops.


Organic Acids, Mycotoxins & Heavy Metals - Common Questions

GPL-Blog_Graphics_2021_MasterPractitioner_Mar2021_Q+A-04.png

The Great Plains Laboratory has been educating practitioners for over 15 years on how to help patients heal through cutting-edge testing, research and protocols. In our recent 3-Day Master Practitioner Workshop, speakers shared detailed information on how the MycoTOX Profile, IgG Food MAP and Glyphosate Test can work for you. As well as gave additional information about markers in the OAT and GPL-TOX.

The following Q+A is a response to remaining questions Dr. Woeller was unable to answer during his presentations.

The material contained within this article is not intended to replace the services and/or medical advice of a licensed healthcare practitioner, nor is it meant to encourage diagnosis and treatment of disease. It is for educational purposes only. Any application of suggestions set forth in the following portions of this article is at the reader's discretion and sole risk. Implementation or experimentation with any supplements, herbs, dietary changes, medications, and/or lifestyle changes, etc., is done so at your sole risk and responsibility.


GPL-Blog_Graphics_2021_MasterPractitioner_Mar2021_Q+A_Woeller.png

Kurt Woeller, DO

Functional Medicine
and the Organic Acids Test

Kurt N. Woeller, D.O. has been an integrative and functional medicine physician and a biomedical autism specialist for over two decades. He is an author, lecturer and clinical practitioner offering specialized diagnostic testing and health interventions for individuals with complex medical conditions such as autism, autoimmune conditions, gastrointestinal and neurological disorders.

Q: How does viral genome interfere with this intracellular mechanisms - EBV for example?

A: Viral infections would likely trigger oxidative stress in the cell leading to mitochondrial damage. One of the reasons for high quinolinic acid is interferon production secondary to viral infection.

Q: What’s the difference between blood spot and blood serum vitamin d test?

A: Best to ask Great Plains directly From my understanding there is no difference when looking at 25(OH)D.

Q: Which stool test do you recommend?

A: The CDSA that Great Plains Laboratory has is very good. I also do the Doctors Data GI 360 Profile too.

Q: What markers could correlate with ALS and what other tests would be recommended?

A: No specific pattern for ALS. In anyone with a chronic degenerative condition like ALS I would personally be running the OAT, GPL-TOX, Glyphosate, MycoTOX and Hair Metals Test.

Q: If a patient comes to you with medications, antibiotics, etc. And you recommend doing the OATs. Do you suspend the medications to take the sample?

A: No. I do not have them stop their medications.

Q: Do you use botanicals for yeast overgrow instead of nystatin for some individuals who cannot tolerate Nystatin?

A: Yes, all the time.

Q: This is off the yeast/mold topic but now that Dr. Shoemaker believes that most of CIRS is due to Actinomycetes, is there a test you use that is specific to this bacteria?

A: Not that I know of.

Q: Do you compound this, or do you feel that pharmaceutically available is fine?

A: Usually, the regular pharmacy is okay, but I will compound for sensitive patients.

Q: What is wrong with higher doses, e.g. 100,000 BID?

A: Only the potential for die-off.

Q: Will these also bind helpful nutrients?

A: Yes. They can and should be taken away from supplements and medications by at least a few hours.

Q: To clarify will the zeolite etc.. also bind nutrients, how to avoid this?

A: Likely, it will. Separate by at least a few hours from other medications and supplements.

Q: Is isocitrate lyase a Candida enzyme that disrupts the Krebs Cycle?

A: It’s a enzyme within its own kreb cycle that produces oxalate. So, if you have candida in the gut it has the ability to produce oxalate in the digestive system.

Q: Can you give core biotics to young children? Age 2

A: I have, but conservatively like one capsule.

Q: I'm sure you have heard speculation that there may be correlation between glyphosate use in agriculture in our country starting in the 1950's (I believe) and increasing since that time. I understand that glyphosate is very inflammatory and is a microbiome disruptor.

A: It is a major toxin to the gut microbiome from my research.

Q: Can saccharomyces boulardi impact the arabinose marker?

A: It won’t cause the Arabinose or produce it. But, instead go after Candida that produces it.

Q: Do you test the glyphosate level in your patients with a lot of abnormalities on the OAT?

A: I combine that with the GPL-TOX Profile. I am always concerned about Glyphosate with recurrent clostridia.

Register now for our upcoming events and workshops.

Q: What’s the significance of 5 hydroxybenzoic?

A: Could come from Paraben exposure.

Q: What was the name of the site for practitioners ?

A: Functional Medicine Clinical Rounds – https://functionalmedicineclinicalrounds.com.

Q: Can you speak about SIFO in relation to OATS test?

A: Could cause a lot of markers seen on page #1. But, in my experience the OAT only suggests SIBO/SIFO and is not absolutely diagnostic for it.

Q: I have used Geova neutraval for several years. Can you please comment on why OAT is "better" test?

A: The GPL OAT has the HPHPA and 4-cresol which are really important to obtain because of their significant toxicity. Also, it has the oxalate information which is also important to obtain.

Q: Can supporting these deficiencies (B-6 etc) cause dumping of oxalates into tissues, how to avoid?

A: It is not going to drive dumping, but instead help to divert substrate away from being converted into oxalic acid.

Q: Are there specific metals that may have a higher affinity to oxalates than others? Nickel for example?

A: I do not know of all metal specificities, but Lead and Mercury are certainly high.

Q: Can collagen 20 gram increase oxalates? What about High dose vitamin c at 25 GMs? All of this is possible.

A: The prevalence with regards to this happening I do not know specifically.

Q: So is this SNPs testing to know? Or is this on the OATS Test?

A: The OAT does not have the SNPS. The genetics for oxalates would have to tested through genetic testing.

Q: Any headaches associated with oxalate?

A: Yes. They could be.

Q: Does someone need to stay on a lifelong low oxalate diet or temporarily?

A: It depends on what is causing the oxalates to be high. If it is primarily genetic based then a low oxalate diet is going to be necessary. If the oxalates are from poor nutrients, e.g. B1, B6 and/or mold or yeast produced, then the diet is likely just temporary.

Q: Can you explain your take on fat malabsorption and oxalates? I believe it is important to aid fat digestion when dealing with high oxalates.

A: Fat maldigestion will cause increase oxalate absorption.

Q: What if a patient has high arabinose and oxalic acid, but is unable to tolerate B6 and B1 supplementation?

A: Then you have to work on reducing high oxalate foods in their diet and treat the yeast as best as possible. Hopefully, in time they become more tolerant of these B-vitamins.

Q: When you do the Epsom salts baths how long do you sit in it to be effective?

A: Could be done nightly or at least 3 to 4 times per week. 15 to 20 minutes is a bath is often sufficient.

Q: What kind of diet is suggested before taking OATS test? How many days previous?

A: There are no specific diets needed prior to testing.

Q: Also, I believe there is a Epsom salt cream. Is that effective?

A: It can be, but I think the baths work better.

Q: Do you recommend avoiding high oxalate foods in the days before collecting the oat?

A: No.

Register now for our upcoming events and workshops.

Q: Do you know how phosphatidylcholine compares to CDP-choline? Is there a reason you prefer one over the other for PLA2 inhibition? Any thoughts on Choline Bitartrate?

A: The CDP-Choline combination is what lowers PLA2. Just choline with bitrate will not do it.

Q: If you have nigh arabinose, would you avoid taking extra Vitamin C?

A: No.

Q: What does HVA/VMA ratio means?

A: it is related to the ratio between HVA (dopamine) and VMA (norepinephrine). If the ratio is high than not enough dopamine is getting converted to norepinephrine.

Q: And HVA/DOPAC indicate?

A: Ratio between HVA and DOPAC.

Q: What do it mean when all markers of Beta-Oxidation are high?

A: Problem in fatty acid metabolism with the cell.

Q: Where is lithium listed on OATS, under which heading?

A: It is not in the OAT. It is measured in a Hair Analysis.

Q: What if you’ve been taking NAC (600 mg 2 times a day) and it is not showing up on the OAT test. Why would that be? Will taking glutathione be the next step?

A: That it likely is getting converted over to Cysteine. If the glutathione is still deficient than giving glutathione directly is the next best option.

Q: Oxo-4-methiolbutyric what would cause this to be high?

A: That is a rare genetic disorder linked to Maple Syrup Kidney Disease. Low levels could occur from consuming beets, blueberries and cashews.

Q: Any thoughts come to mind with consistent eye pupil dilation in a 23-year old with AU?

A: I would first start looking at heavy metal toxicity.

Q: Is serotonin syndrome clinically significant in patient on SSRI who wants and try L-tryptophan or 5-http?

A: I personally have never seen serotonin syndrome. It is always possible if too much tryptophan or 5-HTP were taken, but not common in my experience. There may be other doctors who have more experience with this.

Q: Can you say how long you need to treat candida with botanicals, Treatment duration?

A: At least two months. It may require longer.

Q: Do you find twice daily dosing work with Biocidin?

A: Not as great compared to three times daily, but for a low level infection that is not overly bothersome for someone twice a day can work. I have some people where twice daily did the trick.

Q: Do you have to get rid of mold in the environment before you do the antimicrobial treatment for clostridia?

A: No. It is always best to work on the mold, but I have people where I am treating them while they are doing remediation.

Q: What are you favorite soil-based probiotics brands?

A: I use a lot of CoreBiotic from Researched Nutritionals and Proflora 4R from BioBotanical Research.

Q: NADB since the west coast fires have been burning so much? Or is it elevated from rubber mostly? What happened to the RA when clostridia treated?

A: Improved.

Register now for our upcoming events and workshops.

Q: What was the dose of Biocidin you used in the RA patient for 3 months?

A: From what I recall it was two capsules three times daily.

Q: Why test when additional testing with expected positive results will not change your treatment? Or how would you change the treatment if mycotoxins, chemicals were elevated.

A: Because if the person has high Mycotoxins they are going to need to figure out where the mold is coming from. Also, I have seen patients where all the mold markers are normal on the OAT, but they have very high levels of mycotoxins.

Q: What else to look at when #56 NAC is elevated, and Indicators of Detoxification are in the normal range?

A: It could be a deficiency of the enzyme that deacetylates the NAC. I do not know of a specific test for this though.

Q: How do you dose GI Detox, when and how many?

A: For adults I have them start at one capsule twice daily between meals with a range of 1 to 3 capsules as tolerated. If a person can handle three times daily that may be preferred in real bad mycotoxin scenarios. It is all based on tolerance and person must watch out for constipation. I would suggest contacting BioBotanical Research directly for more insight and their recommendations on dosing of their products.

Q: Regarding Small Intestinal Fungal Overgrowth, is there any OAT Info that would equate to diagnosing SIFO? Perhaps Arabinose marker, plus other marker?

A: In my experience, most people with SIBO and SIFO have underlying yeast and fungal problems. Sometimes, they have clostridia too. I always run the OAT on anyone with SIFO or SIBO or who is suspected of having these issues.

Q: If a patient cannot tolerate even one drop of Biocidin do to die off, who has problems with clostridium, candida, and mold, what do you do?

A: This would require a much larger discussion about the various things going on with the patient, their environment, history, etc. In some of these cases there are not easy answers. We developed a website called Functional Medicine Clinical Rounds – https://functionalmedicineclinicalrounds.com to help practitioners work through some of these details. Research the Cell Danger Response. This is likely what is happening with your patient.

Register now for our upcoming events and workshops.


Elaboration on the Organic Acids Test

GPL-Blog_Graphics_2021_OATTOXWorkshopQ+A-04.png

The Great Plains Laboratory has been educating practitioners for over 15 years on how to help patients heal through cutting-edge testing, research and protocols. In our recent 2-Day OAT + TOX Workshop, speakers extolled the virtues of comprehensive metabolic tests like the Organic Acids Test (OAT) and the MycoTOX Profile to help with difficult-to-diagnose patients.

The participants heard ways of how to implement these tests along with other diagnostic assessments, as well as effective treatment methods.

The following Q+A is a response to remaining questions Dr. Woeller was unable to answer during his presentations.

The material contained within this article is not intended to replace the services and/or medical advice of a licensed healthcare practitioner, nor is it meant to encourage diagnosis and treatment of disease. It is for educational purposes only. Any application of suggestions set forth in the following portions of this article is at the reader's discretion and sole risk. Implementation or experimentation with any supplements, herbs, dietary changes, medications, and/or lifestyle changes, etc., is done so at your sole risk and responsibility.


GPL-Blog_Graphics_2021_OATTOXWorkshopQ+A_Profile 5.png

Kurt Woeller, DO

Functional Medicine
and the Organic Acids Test

Kurt N. Woeller, D.O. has been an integrative and functional medicine physician and a biomedical autism specialist for over two decades. He is an author, lecturer and clinical practitioner offering specialized diagnostic testing and health interventions for individuals with complex medical conditions such as autism, autoimmune conditions, gastrointestinal and neurological disorders.

Q: Is high fatty acids due to coconut oil in the diet clinically significant? Is that showing a problem or just a false positive?

A: It is not necessarily a problem that I know of that would cause toxicity at the cellular level. But, it does point out that our cells can only take up so much lipid at any given time to function effectively.

Q: If there is a problem with medium-chain fatty acid beta-oxidation, how does that manifest in omega-oxidized organic acids? Do all of 47, 48, 49 become elevated, or is there some other pattern to 47, 48 and 49?

A: The first two fatty acids are strongly linked to ketosis, but there is a relationship with poor cellular metabolism of certain amino acids like isoleucine, leucine, and valine metabolism. Other individual fatty acids are linked to other specific biochemical pathways that can from various enzyme defects or mitochondrial problems. The biochemistry is complicated, and we go into this extensively in Module #10 of our Advanced OAT Mastery course.

Q: What of add ADHD and yeast metabolism? Is it worthwhile to be doing the testing?

A: It is important to always do the OAT for ADD/ADHD. I also make sure to do the Hair Metals Test and Food IgG MAP from Great Plains Laboratory as initial testing too.

Q: I don't see, Avoid Vitamin C, Tryptophan, Coffee in manual. Should this food and supplements be avoided before test and how many hour?

A: No. I do not personally have people stop their supplements prior to testing.

Q: If you have only hydroxybutyric elevated and the patient is not on a keto diet what is the cause?

A: Need for additional antioxidants. The body is most commonly pulling things into the pathway for glutathione production.

Q: What chemical pathway did you say indicates aggravation of POTS?

A: Dopamine-Beta-Hydroxylase, which converts Dopamine to Norepinephrine.

Q: Is the inflation of the fatty acids a bad thing?

A: It depends on what is causing it. There are disease states that can inflate these numbers. The biochemistry is complicated, and we go into this extensively in Module #10 of our Advanced OAT Mastery course.

Q: Would the high markers that could be associated with high usage of coconut oil be a sign of food sensitivity?

A: Not that I know of.

Q: Please explain what is meant when all detox markers are elevated. What is happening metabolically with patient?

A: Let’s focus on Pyroglutamic and 2-hydroxybutyric. If those two are elevated the patient is glutathione deficient from some toxin or toxins. The 2-hydrobutyric is linked to glutathione production or the demand for more glutathione.

Q: Any other reasons for elevated glutaric in someone taking B complex supplements and other b vitamins normal?

A: There are many, but the most common is increased need for mitochondrial support and high levels of candida toxin acetaldehyde.

Register now for our upcoming events and workshops.

Q: For patients not toilet-trained, try to capture a concentrated urine after how many hours?

A: First morning urine. The parents can have their child stand up in the bathtub and run warm water over their feet. This will usually trigger them to urination.

Q: Why is arabinose range of value on the lecture slides normal range <50? On my recent test it is <20. Did entire range get changed?

A: Range changes based on age and sex. Greater than 13 years old male and female, and less than 13 years old male and female, will have different reference ranges.

Q: How often should someone do an OAT?

A: At least once yearly as a screening assessment.

Q: Please explain again, how to interpret the nutritional markers that do not have an * (indicating possible deficiency if high).

A: The asterisk markers are only significant when elevated. If elevated, that means a deficiency of the respective nutrient. The non-asterisk markers are direct assessments. It gets tricky with NAC because levels are typically on the lower end of the scale which can be normal as NAC is converted to glutathione. Low levels of ascorbic are not valid for ascorbic acid determination since it is unstable in urine samples.

Q: How long do you have to avoid B12 supplements to get true/accurate picture of patients B12 status from MMA marker.

A: Good question. I am not sure exactly. It likely would only be a few days since B-vitamins like B12 are water soluble and the effects biochemically on the pathway linked to MM is constantly ongoing.

Q: 3 oxoglutaric acid. What is it? What is it correlated with?

A: It is an organic acid produced by various species of yeast organisms

Q: If a patient is highly positive for Aspergillus and is treated (Nystatin, N-acetyl L Cysteine, Acetyl Lcarnitine, activated charcoal, home remediation to eliminate mold) , do you expect markers to go down and what is timeframe? What is succerate?

A: Yes, the markers on the OAT should go down and could do so quickly within a few weeks. The same would be true of Succinic or other markers being influenced by yeast/mold toxins.

Q: Do you recommend following up a nutrition marker out of range with a blood test? How long refrain from supplements to get accurate test of nutrition markers on OAT?

A: I do not personally have people stop their supplements prior to testing. I typically do not have patient do follow-up blood testing for nutrients unless there was really strong clinical evidence to do so.

Q: How variable is microbial part of OAT day to day?

A: There may be slight fluctuations, but not dramatic unless there has been some massive surge in toxin production in the gut.

Register now for our upcoming events and webinars.


From Mycotoxins to Mold, William Shaw, PhD Has Answers

GPL-Blog_Graphics_2021_OATTOXWorkshopQ+A-04.png

The Great Plains Laboratory has been educating practitioners for over 15 years on how to help patients heal through cutting-edge testing, research and protocols. In our recent 2-Day OAT + TOX Workshop, speakers extolled the virtues of comprehensive metabolic tests like the Organic Acids Test (OAT) and the MycoTOX Profile to help with difficult-to-diagnose patients.

The participants heard ways of how to implement these tests along with other diagnostic assessments, as well as effective treatment methods.

The following Q+A is a response to remaining questions Dr. Shaw was unable to answer during his presentation.

The material contained within this article is not intended to replace the services and/or medical advice of a licensed healthcare practitioner, nor is it meant to encourage diagnosis and treatment of disease. It is for educational purposes only. Any application of suggestions set forth in the following portions of this article is at the reader's discretion and sole risk. Implementation or experimentation with any supplements, herbs, dietary changes, medications, and/or lifestyle changes, etc., is done so at your sole risk and responsibility.


GPL-Blog_Graphics_2021_OATTOXWorkshopQ+A_Profile 4.png

William Shaw, PhD

William Shaw, PhD, is board certified in the fields of clinical chemistry and toxicology by the American Board of Clinical Chemistry. Before he founded The Great Plains Laboratory, Inc., Dr. Shaw worked for the Centers for Disease Control and Prevention (CDC), Children's Mercy Hospital, University of Missouri at Kansas City School of Medicine, and Smith Kline Laboratories.

Q: Are organic meats allowed to have mycotoxins?

A: Agriculture in the US have high standards for toxins. But realize organic food stuffs will have a higher risk of mycotoxins as there is no pesticides used in the growth/feeding of the food and thus more chance for mold growth and mycotoxin contamination.

Q: How does renal function influence accuracy of results of  MyCoTOX & OAT? Will a patient with impaired renal function benefit from testing? Do you know the minimum kidney glomerular filtration rate needed in order to get accurate results? If they can’t use urine tests, do you recommend different test(s)?

A: If renal function impairs your client to concentrate their urine, then the sample will be rejected and you will get a notice of this. There isn’t a set GFR. If the urine sample is not able to be used, consider the IgE Mold Test.

Q: Can Ochratoxin cause seizures?

A: The potential is there as this is a neurotoxin. Click here for more info.

Q: When treating mycotoxins, do you see further immune suppression on labs - neutropenia, thrombocytopenia, increase in autoimmune markers etc.? Is this d/t “reactivation” of these mycotoxins throughout the body?

A: You can see changes on lab work depending on the patient and their reaction to the toxins. This is because toxins are not harmless when they are coming out of the cells until they are bound by binders and glutathione. The reactivation is more of a release into the blood stream from storage in the tissue and fat cells for ultimate detoxification and elimination.

Q: If there are markers indicating candida and C. difficile and extremely high Ochratoxin A and Mycophenolic Acid, what do you treat first or do you treat simultaneously?

A: You would want to treat simultaneously. If the immunosuppressive and immune toxins are not detoxed it will be difficult to fully clear the candida and C. difficile. Just be sure the clients are aware of the importance of timing of the their binders, antifungals, and other supplements.

Q: Would it be more beneficial to take the binders before bed so as to bind mycotoxins dumped into the GI tract from the liver during detoxification through the night?

A: This is a good strategy and usually easier for clients to remember and to take away from other foods/supplements/meds.

Q: Can you address how bleach is not recommended as it can cause spores from penicillium to explode?

A: Bleach can only kill mold on impermeable surfaces some of the times. It can clear the color of mold growth, but this typically grows back. It is not guaranteed to kill mold in all cases and cannot penetrated permeable and porous materials like wood. This could cause a false sense of security in a home that isn’t truly mold free.

Q: How significant is citrinin elevation if all other markers have been cleared?

A: This depends on the level of citrinin. Citrinin can come from a variety of molds and a significant elevation of this marker could be indicative of an ongoing mold exposure.

Q: Do you provoke prior to testing, be it GSH, infrared sauna, etc? Recommendations for provocation protocol? Patients to consider provoking/not provoking?

A: We do not recommend provoking for the mycotoxin test. The LC/MS measures the mass of the toxin alone, not bound to GSH. The GSH molecule attached to the toxin during provocation will hide the toxin from the LC/MS as the mass is now changed from what we are assessing. For this reason patients, should be off of GSH/NAC/ binders for 1 week prior to sample collection.

Q: Gliotoxin adds to the same reduced-sulfur enzyme systems known to be inhibited in Alzheimer’s disease. Which drugs have mycophenolic acid?

A: Myfortic and Cellcept

Q: Does Mycophenolic Acid help with high histamine intolerance?

A: Mycophenolic acid is an immunosuppressant and would more than likely be a contributor to the cause of a histamine intolerance.

Q: What lab will test immune suppressant drug for Mycophenolic acid? Is it a contaminant in the drug, or included as an ingredient?

A: There are certain drugs, myfortic and cellcept, that are made with mycophenolic acid as its active ingredient. It is used due to its immunosuppression activity. These drugs are used to reduce rejection of a new organ like a kidney due to immune rejection.  I do not know of any labs that test drugs for mycophenolic acid.

Q: Could you please speak to treatment for children under 5? What are they able to take to treat mycotoxins

A: They can take binders, antioxidants, and antifungals just like adults. The dosing would need to be lower. The forms of the supplements/drugs would need to be child friendly so they can easily take them. Think of more powders and liquids over capsules.

Q: What percentage of mycotoxin in the urine is conjugated (phase-II) with glutathione, sulfate or glucuronic acid, and can you identify these by testing?

A: That percentage is difficult to determine as is varies from person to person, day to day based on detox capability. And, no, we do not identify these conjugates on the MycoTOX Profile.

Q: Has atrial fib been associated with mycotoxin exposure?

A: I do not have any direct research for a fib. But mycotoxins have been shown to be cardiotoxic. See more information here.

Q: You mentioned lactobacillus sp for fungal overgrowth/ mold - is there a favorite probiotic you have? Thoughts on spore forming probiotics like Megaspore for mold? also thoughts on serum derived immunoglobulins/SBI?

A: Spore probiotics can be helpful in inhibiting the growth of mold.

Saccharomyces boulardii has also shown efficacy in reducing mold.

Here are other studies of lactobacillus in the overgrowth of mold: HERE & HERE

Q: Is there literature to support the specific strain recommendation for probiotics: L. pentosus and L. beveris

A: This study is looking at the benefit of these two strains in adsorbing alflatoxin B1.

Q: Would Amoxicillin carry penicillium mold as it’s made from penicillin?

A: Penicillin and other derived antibiotics are made from a protein from penicillium mold. They do not contain the whole organism itself and no mycotoxins.

Q: A patient on OAT has a value of marker 2 (5-hydroxymethyl-2-furoic) 3037, and marker 4 the value is 759. Have you ever seen higher values?

A: Values of this level have been recorded. This isn’t a common occurrence, but it does happen.

Q: How does testing differentiate if the mold is colonized in the intestines or just passing through?

A: If it were passing through, we would see very minimal amounts of the furan compounds. When elevated this is evidence that the mold has colonized. To be 100% sure it has not passed on you can always retest and assess if it is still there prior to treatment.

Q: You mention 20-30 yrs, so if that much time has passed since the exposure is it unlikely for the person to be still colonized?

A: It is unlikely but the possibility is there. It is assumed that the body would have cleared the mold by then if the exposure was removed.  But if someone hasn’t had a mold exposure in 20 years, yet has elevated mold markers, it could be inferred that this was from 20 years ago.

Register now for our upcoming events and workshops.

Q: Are antifungals the only way to kill off colonization? And can they be used at the same time as binders?

A: Antifungals are the most direct way to kill a colonization. Probiotics are a great adjunct. These can be used along with a binder but it should be taken 2 hours away from the antifungal and other supplements, meds, and foods.

Q: How do you treat sinuses directly if a patient is intolerant to nasal sprays and nebulized medications (severe discomfort, nose bleeding, severe pressure for days after)?

A: Oral antifungals and removal of moldy environment will help reduce irritation. This should be the beginning of the treatment. Detox with binders and antioxidants will reduce the toxic load. Slowly add in nasal sprays of saline to flush the area and then work up to antifungal nasal sprays. Go at the pace of the patient and their irritation.

Q: Are the treatment options in the order they need to be implemented on the patient infected by mold?

A: The treatment options listed are in order, yet after finding the source all these things should be implemented for full healing. They can be started simultaneously. But gauge your client and their ability to handle each part of the protocol. If they cannot get out of the exposure right away consider detoxing but holding off on the antifungals as the treatment will most likely need to start again after removal of the source.

Q: What about using NAC instead of glutathione?

A: If the person is making glutathione (assess pyroglutamic acid marker on the OAT) then NAC can be used. If they are glutathione deficient, consider investing in glutathione as the supplement of choice.

Q: Would you use the Antifungal if the patient does not have colonized mold?

A: Due to the lack of colonization testing for every mold it is difficult to determine if the person is or isn’t colonized even with the OAT. Because mycotoxins come from mold it is safe to assume mold is in the persons body if mycotoxins are being excreted, especially if they are no longer being exposed. If this is the case, or if the person plateaus in detox, antifungals are the next step.

Q: Are you saying you must use antifungal drugs with binders to rid the body of the mycotoxins that have colonized?

A: You must address the mold with antifungal therapy. It does not have to be drugs. You can use herbs and nutraceuticals.

Q: I have a case of an adolescent with autism. I have recently received the results of OATs with the results of markers of clostridium 15 and 18 elevated, elevated methylsuccinic, elevated ochratoxin and dihydrocitrine 1714, currently and after the oats presents constant fever, in sputum they found e coli. Other doctors have treated her with ciprofloxacin without being able to lower her fever. In this case, what do you treat first, clostridium, mycotoxins, e.coli?

A: If she still has a fever you may consider doing a blood culture for mold to be sure this isn’t a systemic infection. If not systemic, detox the mold toxins and address the bacterial overgrowths (clostridia/e. coli) with antimicrobials and probiotics (Core Biotic/ S. boulardii).  Get her out of her moldy exposure as soon as possible and then begin antifungal therapy. For more support with treatment options contact customer service for a complimentary consult with one of our qualified GPL consultants to review her results and case.

Q: You skipped over Chlorophyllin. How does this work with treating myco?

A: The chlorophyllin directly binds to the mycotoxins especially aflatoxin. See more information here.

Q: Can we get references showing effectiveness of your list of treatments of Mycotoxins?

A: Here are a few references. Please see the Great Plains Laboratory website for additional resources. Also on your MycoTOX reports the PMID after the interpretations are articles from PubMed you can reference for treatment.

See the following links for research based options for treatment of mold: HERE & HERE

Q: What is the best timing for when you prescribe the antifungals and then the binders during the day.  Biocidin dose is often TID, and the binder I have used BID.  My understanding is Biocidin is best away from meals - this leaves little time to get the binder in.  What times of day have you found is the best treatment?

A: You can consider taking the binder before bed, 2 hours after dinner, and/or first thing in the morning an hour prior to any other supplements/meals/ meds.

Q: What is a starting dose of Mg and Vit C (citrate?) to avoid constipation when using clays and charcoals for detox?

A: This depends on the clients and bowel history. But consider starting with 500mg of one and slowly adding the other agent at 500mg. then they can add more by 250-500mg until they have a proper bowel movement. Also check out these bowel supportive supplements: TruFiber and Oxy-Powder by New Beginnings Nutritionals.

Q: Could you clarify what foods (from where or in which states or countries) we can trust as having been tested for mycotoxins?

A: The FDA monitors food for mycotoxins. More research would need to be done on all other countries regulatory practices when it comes to monitoring mold.

Q: What is the recommended length of time to treat for mycotoxins once remediation has occurred?

A: At least 3-6 months, but treatment can take longer

Q: Where can we find dosing for children for MOLD/CIRS treatment? Supplements, rx, binders, etc.

A: New Beginnings Nutritional has many supplements for mold/CIRS and there is child dosing for many products.

Q: Do the charcoal, zeolite or bentonite clay or other binders not disrupt enterohepatic circulation similar to cholestyramine if taken in similar fashion?  It was my understanding that all the binders had that capacity.

A: They work by binding bile in the GI tract as does cholestyramine.  This stops the recirculation of bile through enterohepatic circulation. Bile production should be supported in long term use.

Q: How long is protocol for mold treatment before retesting?

A: 3-6 months

Q: Can a chronic mold infection be exacerbated with pregnancy? Can it be transmitted to the baby in utero? Or after through the breastmilk?

A: A chronic mold colonization and myotoxicity can be complicated by pregnancy. The mycotoxins can be transmitted to baby via placenta and breastmilk.

Q: What are the usual symptoms of mycotoxins?  I know typical allergy symptoms, but I would guess digestive symptoms as well

A: Top symptoms are chronic sinusitis, constipation, diarrhea, bloating, gas, nausea, vomiting, inability to lose/gain weight, etc.

Q: You mentioned that only 1% of labs you see are negative for ochratoxin A...are you referring to first tests only and not follow up testing, or do you mean ALL testing including follow up labs?

A: All tests that are run by GPL

Q: Are lipomas in people also a sign of mold issues?

A: They have been documented in mold toxic patients: HERE

There is also evidence of lipomas filled with mycotoxins in mold exposed dog: HERE

Q: can the lymphomas go away using mycotoxin binders after stopping grains?

A: If mycotoxins and mold are the sole cause for the lymphoma it is possible that it could resolve after mycotoxin detox and mold colonization treatment. This cannot be guaranteed if there are other causes stimulating the lymphoma.

Register now for our upcoming events and webinars.

Q: If positive mycotox results for all family members living together aren’t shared, can you assume the source of mycotoxins is not the home but instead food or outside the home?

A: This could be implied but please be aware people all detox differently and release mycotoxins at their own rate and in their own pattern. The way to know for sure is by checking the home and culturing the molds growing there. If someone has mold toxins from an unidentified mold then you can assume it is from another source of exposure.

Q: If no fungal markers are elevated on OAT, would high Ochratoxin A (55) mean it came from penicillium most likely? Thank you

A: It could be assumed that is coming from penicillium but it could also be from aspergillus colonized in the lungs or nasal passages. Or it could be a combination of the 2 molds. Mold doesn’t have to colonize the GI tract to be an issue. Remember the OAT can only give GI colonization info. Cross reference with mold inspection of the moldy environment.

Q: Do you need to use a provoking agent before a mycotoxin test? Can a patient have difficulting detoxifying mycotoxins from their body that they may get a false negative test even if they are in symtomatic and living in a water damaged home

A: GPL doesn’t recommend provoking due to the nature of the LC/MS technology. It is specific to unbound toxins not GSH bound toxins. If there is concern about the patient not detoxing well, they can intermittently fast or exercise then night prior to collection to induce the release of toxins. Please remember this is not how the reference ranges were developed though. If someone is living in a water damaged building with visible mold a mycotoxin test is more confirmatory evidence of exposure and gives you a base line of toxic load. Similarly, with all lab testing, results should be taken in consideration with all the other information you have about the client.

Q: If you have a Fibro, Autsitic, ADHD or CFS patient would you start with OAT and Mycotox right away or wait to see what shows up on OAT first?

A: If you have evidence of a past or current mold exposure do both panels. If not start with the OAT and let it guide you to what tests to do next. Or start with the EnviroTOX Complete Panel: HERE

Q: Can you clarify--in pt w/ aspergillus colonization improved on nystatin--is the point that nystatin treats gut, doesn't get into blood stream, therefore is treating aspergillus in gut and eliminating the colonization, which is in the gut, is the explanation for improvement

A: Correct-aspergillus markers reducing when nystatin is given, provides us the conclusion it was in the gut, since nystatin is not absorbed through the mucous membranes or the GI tract. 

Q: I have many patients with multiple lipomas, do you suppose this could be a similar process to what happens in dogs?

A: It’s one possibility. You might find this article helpful; HERE

Q: Can the mold the dog is exposed to, expose the family to that mold?

A: There is the thought that mycotoxins can be in the dog’s fur, and then therefore one may be exposed in that manner. If that is true, there are dog washes that claim to neutralize them.

Q: Is chronic hepatitis and cachexia without symptom (negative autoimmune Hep A, B, C, no neurological issue, no fatigue) is it worth to check Mycotoxin?

A: If their clinical history alludes to mold in their environment, absolutely.  Mycotoxins are known hepatotoxins, and Chaetomium can cause unintended weight loss.

Q: I like the fact we are addressing when people are living in food insecurity there’s a tendency to still eat food contaminated by mold. How would you respond to someone who says- “Oh I just removed the moldy part of the food and use the rest in my cooking?”

A: It would be advised against since a lot of mycotoxins are heat resistant.

Q: Just an FYI, I did a consult with GPL for one of my pts mycotoxin test and was told that a low level did not matter.  Not true according to Dr. Shaw.

A: It is HIGHLY dependent on the entire clinical picture and situation.

Q: Would you please provide the citation for the recent study published in Nature you discussed about autistic children & their mothers found to have high antibodies to a mold?

A: HERE

Q: dosing guidelines for itraconazole and sporonox? adult and peds please

A: Sporonox: HERE

Intraconozole: HERE

Q: what are some antifungals that are non-prescription that a nutritionist can provide as a protocol?

A: The literature supports utilizing caprylic acid to target yeast and mold. Combination antimicrobials are best to prevent resistance. A recent article written by Dr. Brown illuminates other botanicals that function as antifungals. HERE

Q: any recommendations for collecting urine from non-toilet trained patients?

A: There are bags that fit over the penis that can be requested from the lab to help with urine collection. The Chinese method for potty training can also be a helpful tool.

Q: What is recommended to prevent further mycotoxin infection after successful treatment?

A: With regards to the environment post remediation, ensuring low humidity, areas kept clean and dust free, air purifiers suitable for filtering mycotoxins, sufficient lighting, increased air flow, and to be very cautious of water leaks. For the body, keeping the immune system and points of entry into the body (skin, nasal, mouth, and GI tract) strong and supported, as well as, supporting the body’s removal of toxins.

Q: Is there a test we can run to determine if the gastrointestinal tract is colonized?

A: The Organic Acid Test (Markers 2.,4.,5., and sometimes 6.)

Q: how do you know if the gastroinstenial tract is colonized? would this be something to do a stool test for? or are their spceific symtoms that a patient would be experiencing

A: The OAT can help determine if the GI tract is colonized (looking at Markers 2.,4.,5., and sometimes 6) . To date, no stool test to my knowledge can test for mold. Symptoms typically present similar to yeast overgrowth.

Q: Does the OATS show colonization of mold in the body vs. mycotoxin exposure?

A: The OAT can determine if mold is colonized, but does not always indicate mycotoxin exposure. If a colonization is present, one can assume there are mycotoxins, but it is not always evident mycotoxins are present based on the OAT alone when no mold markers are elevated. There are other markers on the OAT that can perhaps elude to mycotoxins, but it is best to run the mycotox if there is suspicion of mycotoxin exposure to get confirmation.

Q: Would an OAT on a dog be accurate or relevant the same way as the MycoTox test?

A: If you can apply the differences from human metabolism to canine metabolism, then potentially you could. I know of one veterinarian that utilize the OAT in their practice.

Q: What are good antifungals for Ochratoxin A and Mycolphenolic Acid?

A: Mycotoxins are not always indicative of colonization. The OAT should be done concurrently to confirm colonization. If high values are found for the specific aspergillus markers on the OAT, use of antifungals is warranted. If colonization is confirmed, nystatin, intraconozole, and/or caprylic acid or GSE have been shown to decrease aspergillus in the gut.

Register now for our upcoming events and webinars.

Q: A patient tested for Myctoxins and it showed the Ochratoxin A is 17.87 and Mychophenolic Acid is 4397 - what would be the appropriate protocol for this patient?

A: It would probably be best to set up a consultation with the lab to further discuss this.

Q: since there are no food restrictions prior to mycotox collection, but food restrictions prior to OAT, can you please explain why those foods affect the OAT, but not the mycotox profile.

A: The OAT is measuring metabolic metabolites produced by humans and other organisms in the body. Arabinose is the main metabolite that is noted to be directly influenced by consuming specific foods. To ensure elevations are contributed to yeast overgrowth rather than food components, foods that contain arabinogalactans (which are partly composed of arabinose) should be avoided 48 hrs prior to testing. On the other hand, the mycotox test is measuring the specific toxin in the urine, and is not influenced by food components.

Q: Do you recommend a GSH challenge for 5 days prior to collecting the urine like Dr Nathan suggests?

A: No. The ranges are based on people who were NOT provoking, and therefore if a provocation was administered, the ranges are no longer comparable. Furthermore, when GSH is conjugated with the mycotoxin, it changes the structure of the compound, and due to the specificity of LC/MS, it reduces the ability for the mass spec to measure it.  

Q: Have you used medical ozone to remove the fungal infection?

A: No, but some practitioners have.

Q: if oxalates can form from intake of higher phenol foods, and estradiol is a phenol, could prescription HRT/estradiol therapy contribute to oxalates, histamine intolerance?

A: There is data that indicates that higher levels of estradiol in the system correlates with less calcium oxalate stone formation (HERE), and that estrogen intervention may actually decrease the risk of stone formation by lowering urinary calcium and calcium oxalate saturation (HERE)

I am not sure about histamine intolerance.

Q: did Dr. Shaw say a level about 50% is notable for toxic panel?

A: Above the 95% in a toxic panel is considered clinically significant.

Q: Does this include an interpretation or is there an option to hire someone to interpret?

A: The laboratory provides a free consultation with each test, to help with interpretation of the results.

Q: Is there an affordable lab that you would recommend for testing water from our taps for some of these chemicals?

A: www.watercheck.com- National Testing Laboratories Ltd.

Q: Do you know if there is any company producing phthalate-free tubing for IV treatments, reverse-osmosis water filtration systems,?

A: Not to my knowledge. Sounds like a good investigation.

Q: Have you heard of Relax Sauna brand, in which you sit inside but your head is outside? Wondering if still effective.

A: Inducing sweating is what is of most benefit, so anything that will accomplish this will be helpful.

Q: breast implant patients and saunas ok?

A: Dependent on status of implants, and tolerance.

Q: Are hot baths and/or exercise an option to saunas?

A: Yes. Hot baths tend to be used for heat sensitive patients, and some people can generate a significant amount of heat during exercise.

Q: Would the IR Sauna wraps be a good option?

A: As long as the patient is able to increase body temperature and sweat, it should work.

Q: Dr. Shaw. I have heard that IgG food allergy testing is not valid because if the person has leaky gut, then they will react to many things.  Is this the case?  Or you may show high levels in the foods you often eat.  This happened to me. I found it ironic that all the foods that showed up were foods I ate often in my diet.  How reliable is a mod/high IgG response in terms of correlation with patient improvement when said foods are eliminated?

A: Validity is not what is in question, but rather the potential reasoning for the inflammation. Often when you improve the gut (and the immune system), food intolerances improve.  As it relates to your question with increased levels with foods that are often eaten; perhaps there were more food antigens to bind to. In other words, inflammation was being caused by that food, but with more food antigens present, the peaks were higher on the results. There is a significant amount of data that shows relief of symptoms with elimination of high reactive foods, both clinically, and in the research literature.

Q: also I need information on the email for functional medicine rounds again please

A: HERE

Q: What could be the source of the high exposers to:

3-hydroxypropylmercapturic acid (3-HPMA), Diphenyl phosphate, Diethyl phosphate (DEP), 2-Hydroxyisobutyric Acid (2HIB) MTBE/ETBE, N-acetyl(3,4-dihydroxybutyl) cysteine (NADB).

Patients are older children, grew up on a mountain and drink bottled Fiji water and Arrowhead water, family is consumer conscientious about chemicals in products, and uses EWG shampoo/cleaners and cleaning products. Father drives diesel truck. Consumed very littler sugar or processed food. They also burn wood for six months a year for many years.

A: It is probably best to discuss this with a consultant.

Q: I am going to run your new IgG tests but I ran IGG testing through a different company and my kids showed high IGG to almost all of the 150 foods. Many of the foods they have never eaten. Thoughts?

A: It would be important to look at the immune function if a reaction is that high with GPL’s IgG testing as well. Something to also consider is the DPPIV enzyme levels.

Q: What is the relationship between blood testing for milk allergy and results from IgG testing? Could the traditional lab corp serum test show no problem, but the IgG food allergy be positive?

A: If you are referring to the IgE milk test they have, the two are not necessarily comparable. One can have an IgG reaction and not an IgE, or vice versa since they are two different type of immunoglobins, creating two different reactions in the body. If you are referring to their IgG test, it seems limited with only looking at milk, especially since the epitopes vary for dairy sources because of food processing manipulating the proteins, potentially yielding varying results for dairy- based foods.

Q: If someone shows as having a food sensitivity on the test, is it typically something that will be present for life? Meaning if they eat the food say ten years later the body will react?

A: Not necessarily. Depends on why the immune response is occurring.

Q: doesn't food change molecularly when cooked?  I have people that react to a food raw but not cooked.

A: Yes;  proteins can change, depending on the method of cooking. If it is higher heat and/or more acidic than the digestive environment, then it could manipulate the proteins enough to not cause a similar reaction. Also, consider the changes in fiber and nutrient release/degradation with cooking too.

Q: I know that Dunwoody Labs looks at IgE, IgG, IgG4 and complement. They claim that he complements reaction is very important to reduce the elimination. Why does your test give more data or can you clarify the differences?

A: GPL measures IgG1-4 for a more specific response.

This article can provide more details. HERE

Register now for our upcoming events and webinars.


Glyphosate, Parkinson’s Disease & Mycotoxins Questions Answered

GPL-Blog_Graphics_2021_OATTOXWorkshopQ+A-04.png

The Great Plains Laboratory has been educating practitioners for over 15 years on how to help patients heal through cutting-edge testing, research and protocols. In our recent 2-Day OAT + TOX Workshop, speakers extolled the virtues of comprehensive metabolic tests like the Organic Acids Test (OAT) and the MycoTOX Profile to help with difficult-to-diagnose patients.

The participants heard ways of how to implement these tests along with other diagnostic assessments, as well as effective treatment methods.

The following Q+A is a response to remaining questionsour participating speakers were unable to answer during their presentations.

The material contained within this article is not intended to replace the services and/or medical advice of a licensed healthcare practitioner, nor is it meant to encourage diagnosis and treatment of disease. It is for educational purposes only. Any application of suggestions set forth in the following portions of this article is at the reader's discretion and sole risk. Implementation or experimentation with any supplements, herbs, dietary changes, medications, and/or lifestyle changes, etc., is done so at your sole risk and responsibility.


GPL-Blog_Graphics_2021_OATTOXWorkshopQ+A_Profile 1.png

Evan Brand

Mold, Mycotoxins, Case Studies & Protocols

Evan Brand, CFMP, FNTP is a Podcast Host, Certified Functional Medicine Practitioner and Nutritional Therapist. He is passionate about healing the chronic fatigue, obesity, and depression epidemics after solving his own IBS and depression issues. His Evan Brand Podcast has over 7 million downloads and counting.

Q: please repeat info on companies that have lymphatic support supplements.

A: Beyond balance and wish garden have lymph supports

Q: With the legalization of marijuana, I have not heard anyone discuss the mold in marijuana.

A: I have heard of moldy cannabis; you could grind it up and put it on a mold petri dish to test it

Q: How can you detect mold in coffee which is drank daily for thousands?

A: It’s a very common issue.

Q: Can you talk about how to detox children under five from mycotoxins?

A: Would prefer to discuss this on a consult, but in general, gentle binders like liquid chlorella, small doses of charcoal mixed with applesauce. Email me at office@evanbrand.com if you need more help.

Q: Do the mycotoxins cross into the eggs produced by exposed poultry?

A: Sounds reasonable to me.

Q: Which markers on the OAT are indicative of mold toxicity? And what levels are considered high?

A: Page one shows mold colonization but the MycoTOX Profile is what looks at actual toxin levels.

Q: Where would we find a source for nebulizable glutathione and a protocol?

A: Thernaturals carries the one for the nebulizer, we mix it with 2-3ml of saline and 1 cap glutathione and put into nebulizer to breathe it in

Q: Are you not concerned with using medicinal mushrooms with mold and fungal overgrowth?

A: No, I’ve never found it to be an issue, even with those that have histamine issues.

Q: What do you think about treating heavy metals with mold? Do you have an order of operations with that? And what about with EBV as well?

A: The binders are broad spectrum and we likely fix both at the same time.

Q: Is it harder to treat mold when eating high histamine foods?

A: Histamine issues due to mast cell activation and mold issues are common, lower histamine diets can be helpful to lower the work.

Q: Are you familiar with Beth O’Hara’s work with Mast Cell Activation Syndrome?

A: Yes, Beth is a very nice woman and has done a great job of educating the public about mast cell and histamine issues

Q: What sauna do you recommend? If you can’t afford a big one, what about the portable one.  Is it effective?

A: I have the ClearLight, tell them Evan sent you for a discount. I don’t know much about portable ones but heard Therasage 360 is decent.

Register now for our upcoming events and workshops.

Q: For high dose choline, have you seen blood sugar problems increase?

A: Never

Q: Do you use either phosphatidylserine or phosphatidylcholine or use both at same time?

A: I use both at the same time for different purposes.

Q: What herbs did you use to treat H. Pylori?

A: My microbiome support 1 formula on auraroots.com

Q: Have you had much success in treating mycoplasma infection and what did you use?

A: I have success with mycoplasma using astragalus and cats claw.

Q: How did you do the test for babies from a distance? What company are you using for lyme and co-infection testing?

A: DNA connexions urine test

Q: I have a patient on binders and he can’t live without them. Given binders inhibit absorption of everything, how long can I keep him on them?

A: Forever. Ask Dr. Neil Nathan

Q: Can you state again the company you use for the petri-dishes?

A: Immunolytics

Q: Thoughts on ERMI home testing?

A: It is ok. I like petri dishes better.

Q: Herbs can be very powerful, are you concerned about doing damage to the microbiome?

A: No

Q: What have you researched to be the best HVAC filtering?  Do you recommend UV light in the HVAC system?

A: I recommend point of contact filters like Austin Air. UV is ok.

Register now for our upcoming events and webinars.


GPL-Blog_Graphics_2021_OATTOXWorkshopQ+A_Profile 3.png

Shanhong Lu

Glyphosate, Neuroinflammation Nation, & Parkinson’s Disease

Dr. Shanhong Lu, MD, PhD is a Internal Medicine Specialist in Mount Shasta, CA and has over 34 years of experience in the medical field. She graduated from Beijing Med University medical school in 1987.

Q: What are your best tools for detox of glyphosate?

A: Decrease exposure, Ultimate immune 8 a day, ultimate eaze 1-3 a day and OPC, with OR WITHOUT GLYCINE 4-5 GRAM TWICE A DAY- most of my 90 day data are based on 8 ultimate immune a day, please email drlu@drlumd.com for complimentary case discussions

Q: Does her approach / treatment help with epilepsy/seizure disorders patients?

A: Yes, please email drlu@drlumd.com for complimentary case discussions

Q: Cytokine storm Ebola virus works by this as probably SIDS from vaccine administration. No one has looked at routine vaccination but since vaccines with adjuvants produce a nonspecific immune provocation, wouldn’t that also be factor in Parkinson’s disease?

A: Vaccine injuries are not the cause of adult PDs because most of them have not received vaccines

Q: Even though organic foods are contaminated, do you recommend them as a better choice?

A: Absolutely

Q: Do you think an organic, plant based diet is safer overall than let’s say carnivore, with regard to levels of glyphosate?

A: I wish I could say that because I am a vegan and have been finding vegans are tested high in glyphosate (more often than meat eaters) but we have had less consequences … please email me drlu@drlumd.com since the keto people are more toxic with fat soluble toxins EDCs.

Q: Because glyphosate is a glycine mimic, would glycine supplementation help to detoxify by binding to its receptor and preventing glyphosate from binding? Do you prescribe supplemental Glycine to mitigate the effects of glyphosate exposure-injury?

A: In theory, but glycine alone will not be adequate

Q: What are your favorite tests to assess Toxic Burden?

A: The GPL-TOX Profile (Toxic Non-Metal Chemicals) and the Great Plains Laboratory Glyphosate Test.

Q: Would you name a few immune modulators please?

A: Muramyl peptide, beta glucans

Q: What lab/ tests do you use for total body burden & antioxidant SnPs? I use GPL and detox project and HRIlabs.org

A: GXsciences.com for SNPs and GPL-tox and GPL-glyphosate and oligoscan for tissue levels of minerals heavy metals and vitamins

Register now for our upcoming events and webinars.

Q: Is L-glutamine a concern for Parkinson. I heard it may pass the blood brain barrier.

A: Do you mean glyphosate? Yes glyphosate accesses the brain via BBB also the vagal nerve from the gut enteric plexus.

Q: You said heavy metals take forever to detox. What about kiddos with mouths full of mercury amalgam fillings? Thoughts about considering that fact?

A: ClearDetox pro for life and remove amalgam fillings

Q: More specifically, how do you activate PON1 for detox of glyphosate?

A: Email me drlu@drlumd.com

Q: What are your favorite detox methods?

A: WFPB organic diet+ A systemic core detox system please email or text me at 530-925-0565 drlu@drlumd.com and we can email you a recorded webinar

Q: How do we join the group?

A: Email me drlu@drlumd.com

Q: Since glyphosate is pretty much everywhere, even if we eat organic and minimize environmental toxins… how else can we counteract the effects of it?

A: Email me drlu@drlumd.com

Q: I don’t see glycine for detoxing from glyphosate. Where is it?

A: Glycine can replace glyphosate in theory but most of our data comes from glucarate 3000 mg a day and leaky gut and stress prevention

Q: I was wondering if glyphosate is also found in organic pea protein isolate? You mentioned it is present in the organic pea protein.

A: YES and that is why I take a regimen daily to prevent accumulation- I call a cellular shower) please email me drlu@drlumd.com

Q: Is it best Ca-d-glucarate on an empty stomach. Any suggestion dose wise. Once daily BID etc mg. please and thank you

A: 3000 mg a day with or without food in my experience and make sure Glutathione deficiency is corrected and Th1 and Th2 immune system is balanced (often time during detox Th1 switches to Th2 – cytokine storm)

 

Dr. Shanhong Lu is looking for participants to join a national and international detox project by first making toxins visible and gather data in relationship to clinical illnesses. If interested, please contact her at drlu@drlumd.com


GPL-Blog_Graphics_2021_OATTOXWorkshopQ+A_Profile 2.png

Suzanne Gazda

The Neurological Effects of Mold and a Look into Integrative Neurology

Dr. Suzanne Gazda, MD has uniquely combined a dedication to outstanding care with an authentic commitment to patients as people first. From this desire to find more ways to achieve wellness as a means of treating illness came Integrative Neurology, providing you with individualized solutions specific to your health.

Q: Do you incorporate Botanical anti-fungals in your protocols?

A: Yes, I love to use botanicals . But , like Dr Shaw, I believe in most patients, antifungal RX like Itraconazole is needed to fully remove fungal colonization but I can imagine that if we use antifungal botanicals (which can also boost immune health) .. long enough, patients can improve as well.

Q: What would be your sequence of evaluations for a child with ADHD and dysgraphia, tremors after testing w/ OAT, and MOAT?

A: The same as an AE patient : MRI, NQ , Lab, Cunningham panel and in some w/u for mold and lyme and heavy metals etc.

Q: Any good practical resources how to fight the mold? EMF exposure?

A: I will defer to Dr. Shaw on this one.

Q: I am a mother with five sons 2 of which have been diagnosed with Pans/pandas. One of those two have Lyme. According to labs, we have high levels of strep in the gut, how would you suggest to break the cycle?

A: This is such a complicated question. You are welcomed to email me so we can set up a time to speak about your sons.

Q: Small amount of Chitinase is endogenous to humans no ? Chitinase in CSF would mean the body is trying to break down fungi no?

A:I believe so in a certain subset of patients , especially those that we worry have mold exposure.

Q: Which lake in Shasta is high in aluminum?

A: HERE

Q: I see a lot of recommendation for chlorophyll and spirulina but I think there would be a potential risk of BMAA exposure by ingesting these?

A: Yes, I agree depending on the source.

Q: I am a physician in OK. How do i order the Cunningham and neuroquant tests?

A: You can ask Moleculera labs to send you some kits and for the NQ…go to the Core Techs website and send info and ask for a center near you that does NQ HERE.

Q: Do you get concerned with use of D-ribose and increased acetylated glycolic endpoints?

A: This is a question I will defer to Dr Shaw . Take good care!!

Q: More on the NeuroQuant please?

A: I am soon going to have a blog on my website about the NQ …. Check back within a couple of weeks. But, I already have quite a bit of info HERE.

Q: Is the neuroquant and MRI that needs to be ordered by a physician?

A: Since in most cases they are private pay (about 300 dollars ) I suspect anyone could order / not sure.

Q: are you working with MS patients doing plasmalogen replacement?

A: I am excited to explore more and am doing that now. In my experience, so much of what we would like to do in FM…well, the patients just can’t afford to do it all. I hope that changes one day.

Q: which is Dr. Dan Goodenowe's plasmalogen replacement work?

A: The data is strong. Check back with me in a few months after I have had a few patients try this.

Register now for our upcoming events and webinars.

5 Herbal Agents for Antifungal Therapy

Dr-Brown-Headshot.png


By JASMYNE BROWN, ND, MS

Throughout life, almost everyone will experience some type of microbial overgrowth or infection. Whether it be as common as a cold or as debilitating as a systemic mold infection, pretty much everyone will go through this. Being aware of as many antimicrobial agents is beneficial in treatment. We are finding fungal overgrowths to be quite common. Our offered profiles including: OAT, MycoTOX, and the Comprehensive Stool Analysis, all can help to diagnose and understand the effect of a fungal overgrowth. Herbal agents are effective in treating fungal overgrowths and are great options in most clinical cases. This post will aim to shed light on a few herbs that have shown antifungal properties.

GPL_Blog_Webinar_AntifungalHerbs_Graphics_Header Block.png
GPL_Blog_Webinar_AntifungalHerbs_Graphics-03.png

The first herb to discuss is a popular one. Hydrastis canadensis, more commonly known as goldenseal, has been used for many decades for its antimicrobial effects. The active ingredient of goldenseal is berberine. Berberine is an isoquinoline alkaloid. This is the component that gives the plant its antifungal properties. This alkaloid is cytotoxic. It works by affecting the cell membrane of fungus. Ergosterol is the most prevalent and abundant sterol in the cell membrane, giving fungal cells their permeability and fluidity. Berberine acts to inhibit ergosterol synthesis. By inhibiting the synthesis, the cell membrane of the fungus becomes unstable and increases its permeability. This causes a loss of internal contents, DNA and protein, of the fungus and subsequently death. Berberine also plays a role in direct lipid peroxidation of the membrane, acting directly to destroy the membrane. Other herbs with berberine as a constituent include Oregon grape root, barberry and goldthread. Any of these, including goldenseal, are valuable components of any antifungal therapy.

GPL_Blog_Webinar_AntifungalHerbs_Graphics_Header Block copy.png
GPL_Blog_Webinar_AntifungalHerbs_Graphics-05.png

This herb, also known as Juglans nigra, is widely known and used as an antiparasitic agent. It is also a potent antifungal herb. The active component is called juglone. Juglone is a type of organic compound called naphthoquinone. It has shown antifungal properties against topical, intestinal and vaginal candida overgrowth. This compound, in its nanoparticle form, has shown promising efficacy against aspergillus and fusarium mold species. When acting, the juglone also increases cellular catalase and superoxide dismutase. These are common defense enzymes that act at the cellular membrane of the fungal cell to cause damage and death.

Juglone has also shown direct inhibition in cellular respiration of Fusarium mold, a common mold exposure as depicted by the OAT and MycoTOX Profile. It stimulates the increase of glutathione reductase enzyme in addition to its antifungal properties. This enzyme helps to reduce the increase in ROS. Other compounds, phenols, have also been extracted from black walnut. Some include: 3- and 5-caffeoylquinic acids, 3- and 4-p-coumaroylquinic acids, p-coumaric acid, quercetin 3-galactoside, quercetin 3-pentoside derivative, quercetin 3-arabinoside, quercetin 3-xyloside and quercetin 3-rhamnoside. These phenolic compounds have also shown antifungal properties, in particular to candida. With juglone and these phenolic compounds working synergistically, black walnut is a potent option to consider in fungal overgrowth treatment. 

GPL_Blog_Webinar_AntifungalHerbs_Graphics_Header Block copy 4.png
GPL_Blog_Webinar_AntifungalHerbs_Graphics-11.png

This next herb is a common immune boosting supplement known and used by many. Echinacea purpurea has been long touted for its immunomodulatory effects and antiviral nature. It has also shown efficacy against fungal infections and overgrowths. Vaginal candidiasis and Saccharomyces cerevisiae have been successfully treated with this herb. It acts using its polysaccharide rich composition. They work by enhancing the natural killer cells and macrophages of the host. This causes an increase in the phagocytosis of the fungal cells. Other active compounds in Echinacea that give it its immune modulating properties include the alkamide and caffeic acid derivatives. Echinacea’s direct antifungal, along with UV light therapy, is from the acetylenic isobutyl amides it contains. The UV light therapy isn't necessary, but its addition does enhance Echinacea’s antifungal property.   

Echinacea also works in a different way to exert antifungal properties. Fungi, including Aspergillus and Candida, have been studied tirelessly and it has been found that they possess lipoxygenase (LOX) enzymes. Their LOX is like the ones found in humans. Echinacea exerts its anti-inflammatory nature by inhibiting these types of enzymes. So, in the presence of LOX enzyme in fungus, Echinacea exhibits the same inhibitory effect, thus affecting the fungal cell negatively. This makes it more susceptible to the polysaccharide function of enhancing immunity. Echinacea is a great addition to any formula for immune support and for antifungal properties. 

GPL_Blog_Webinar_AntifungalHerbs_Graphics_Header Block copy 2.png
GPL_Blog_Webinar_AntifungalHerbs_Graphics-07.png

Another herbal option for antifungal therapy is grapefruit seed extract (GSE). This potent extract is used often over the counter for many antimicrobial needs. Its antifungal nature is due to a few mechanisms. One includes its flavone content. The flavones are found in high concentrations in all citrus including grapefruit. The flavones in question are naringin and hesperidin and their derivatives like prunin decanoate. They have been shown to inhibit mycelial growth of not only Candida yeast, but also Aspergillus, Fusarium, and Penicillium. 

GSE works by inhibiting fungal cell growth and energy production. It works at the mitochondrial level of the fungal cell. The GSE induces apoptosis by destroying the 60S and L14-A ribosomal proteins found in the mitochondria. Through this inhibition, the conversion of pantothenic acid to coenzyme A. This inhibition disrupts the fungal cellular respiration needed for its own energy production and cellular function. The blockage caused eventually will kill the fungus and disrupt replication. GSE also works by eliminating biofilms that are already present. It also inhibits the formation of new biofilms. GSE can be used not only as a star antifungal player in treatment, but also as a novel biofilm disruptor set in place to enhance the activity of other potent antifungals being used.

GPL_Blog_Webinar_AntifungalHerbs_Graphics_Header Block copy 3.png
GPL_Blog_Webinar_AntifungalHerbs_Graphics-09.png

For centuries, Allium sativum, more commonly known as garlic, has been used for its medicinal properties. Now, most people use garlic only as a nice addition to many savory meals for enhanced flavor. Luckily, its medicinal properties have not been forgotten. Garlic has been touted as antilipidemic, antiproliferative, anti-inflammatory, amongst other great properties. For our purpose we will focus on the more antimicrobial properties and effects of the amazing plant. Allium has shown great efficacy as an antimicrobial agent and as an antifungal. 

This plant has various active compounds that give it its medicinal properties. Two are ajoene and allicin. Allicin is the commonly known active compound in garlic. In its pure form, allicin is a potent antifungal with great efficacy against Candida albicans. It has been shown to inhibit candida growth with topical and internal application. The allicin is released from the plant by the alliin that is acted upon by the phospho-pyridoxal enzyme alliinase. Therefore, it's best to crush garlic cloves and let them sit before adding to your dish when cooking. This time allows for the allicin to be fully released. Once the active allicin is released it can exert its antifungal properties. It works due to its sulfur content. The sulfur, when in contact with the fungus, enters the fungal cell and binds to the sulfur in the DNA and proteins of the fungus and disrupts synthesis thus killing the organism. One would be suspicious that this compound would do the same to human cells when ingested. This is prevented as the sulfur in the glutathione our cells possess binds synergistically with the allicin and thus inactives this action of the garlic. It’s pretty interesting how plants can be helpful to one organism, yet harmful to another. Allicin has also been shown to cause 100% mycelial growth inhibition of Aspergillus niger.

This other compound ajoene is also an organosulfur compound from garlic. It happens to be from allicin. The further degradation of the allicin, allows for the release of this other potent compound. Ajoene has also shown great efficacy in the killing of fungus. Studies have shown its success in treating Candida and Aspergillus. Some other molds that have been found to be common in water damage building exposure that ajoene can combat include Fusarium and Penicillium. Another plant, highly related to garlic, Allium cepa or onion, has also shown great efficacy in killing mold and yeast. With the same compounds found in both these plants, both would be beneficial to any antifungal protocol.


In the discovery of fungal overgrowths, whether yeast or mold, treatment options are vast. These 5 herbs discussed: goldenseal, echinacea, grapefruit seed extract, garlic, and black walnut are options that should be considered. When deciding which herbs to use to treat your clients consider formulations that include these options. For a convenient place to procure supplementation consider visiting New Beginnings Nutritionals at www.nbnus.com.


References

1. Aboody, M., & Mickymaray, S. (2020, January 26). Anti-Fungal Efficacy and Mechanisms of Flavonoids. Retrieved December 24, 2020, SOURCE
2. Ankri, S., & Mirelman, D. (2001, June 19). Antimicrobial properties of allicin from garlic. Retrieved December 24, 2020, SOURCE
3. Arasoglu, T., Mansuroglu, B., Derman, S., Gumus, B., Kocyigit, B., Acar, T., & Kocacaliskan, I. (2016, September 16). Enhancement of Antifungal Activity of Juglone (5-Hydroxy-1,4-naphthoquinone) Using a Poly (d,l-lactic-co-glycolic acid) (PLGA) Nanoparticle System. Retrieved December 24, 2020, SOURCE 
4. Bagheri, M., Mahmoudi Rad, M., Mansouri, A., Younespour, S., & Taheripanah, R. (1970, January 01). A comparison between antifungal effect of Fumaria officinalis, Echinacea angustifolia, vinegar, and fluconazole against Candida albicans and Candida glabrata isolated from vagina candidiasis. Retrieved December 24, 2020, SOURCE 
5. Binns SE; Purgina B;Bergeron C;Smith ML;Ball L;Baum BR;Arnason JT;. (n.d.). Light-mediated antifungal activity of Echinacea extracts. Retrieved December 24, 2020, SOURCE 
6. Bona, E., Cantamessa, S., Pavan, M., Novello, G., Massa, N., Rocchetti, A., . . . Gamalero, E. (2016, October 24). Sensitivity of Candida albicans to essential oils: Are they an alternative to antifungal agents? Retrieved December 24, 2020, SOURCE 
7. Cao S; Xu W;Zhang N;Wang Y;Luo Y;He X;Huang K;. (2012). A mitochondria-dependent pathway mediates the apoptosis of GSE-induced yeast. Retrieved December 24, 2020, SOURCE 
8. Clark, A., Jurgens, T., & Hufford, C. (2006, January 11). Antimicrobial activity of juglone. Retrieved December 24, 2020, SOURCE 
9. Dantas, A., Day, A., Ikeh, M., Kos, I., Achan, B., & Quinn, J. (2015, February 25). Oxidative stress responses in the human fungal pathogen, Candida albicans. Retrieved December 24, 2020, SOURCE 
10. Ho, K., Lei, Z., Sumner, L., Coggeshall, M., Hsieh, H., Stewart, G., & Lin, C. (2018, September 29). Identifying Antibacterial Compounds in Black Walnuts (Juglans nigra) Using a Metabolomics Approach. Retrieved December 24, 2020, SOURCE 
11. Irkin, R., & Korukluoglu, M. (2007). Control of Aspergillus niger with garlic, onion and leek extracts. Retrieved December 24, 2020, SOURCE 
12. Kumar, K. M., & Ramaiah, S. (2011). PHARMACOLOGICAL IMPORTANCE OF ECHINACEA PURPUREA. International Journal of Pharma and Bio Sciences, 2(4), 0975-6299, 304-314. Retrieved December 24, 2020, SOURCE 
13. Merali, S., Binns, S., Paulin-Levasseur, M., Flicker, C., Smith, M., Baum, B., . . . Brovelli, J. T. (2008, September 29). Antifungal and Anti-inflammatory Activity of the Genus Echinacea. Retrieved December 24, 2020, SOURCE 
14. Mikaili, P., Maadirad, S., Moloudizargari, M., Aghajanshakeri, S., & Sarahroodi, S. (2013, October). Therapeutic uses and pharmacological properties of garlic, shallot, and their biologically active compounds. Retrieved December 24, 2020, SOURCE
15. Naganawa, R., Iwata, N., Ishikawa, K., Fukuda, H., Fujino, T., & Suzuki, A. (1996, November 01). Inhibition of microbial growth by ajoene, a sulfur-containing compound derived from garlic. Retrieved December 24, 2020, SOURCE 
16. Pereira, J. A., Oliveira, I., Sousa, A., Valentao, P., Andrade, P. B., Ferreira, I. C., . . . Estevinho, L. (2002, November). Walnut (Juglans regia L.) leaves: Phenolic compounds, antibacterial activity and antioxidant potential of different cultivars. Retrieved December 24, 2020, SOURCE 
17. R; L. (2006, June). [Ajoene the main active compound of garlic (Allium sativum): A new antifungal agent]. Retrieved December 24, 2020, SOURCE 
18. Rodrigues, M. (2018, November 07). The Multifunctional Fungal Ergosterol. Retrieved December 24, 2020, SOURCE 
19. S; C. (2004, September). Antimicrobial activity of grapefruit seed and pulp ethanolic extract. Retrieved December 24, 2020, SOURCE 
20. Sahibzada MUK; Sadiq A;Faidah HS;Khurram M;Amin MU;Haseeb A;Kakar M;. (n.d.). Berberine nanoparticles with enhanced in vitro bioavailability: Characterization and antimicrobial activity. Retrieved December 24, 2020, SOURCE 
21. Salas, M., Céliz, G., Geronazzo, H., Daz, M., & Resnik, S. (2010, August 02). Antifungal activity of natural and enzymatically modified flavonoids isolated from citrus species. Retrieved December 24, 2020, SOURCE 
22. SR; D. (2005, March). An overview of the antifungal properties of allicin and its breakdown products--the possibility of a safe and effective antifungal prophylactic. Retrieved December 24, 2020, SOURCE 
23. Suleiman, E., & Abdallah, W. (2014, July 15). In vitro Activity of Garlic (Allium sativum) on Some Pathogenic Fungi. Retrieved December 24, 2020, SOURCE 
24. VK; M. (2001, February). [Adaptation of the phytopathogenic fungus Fusarium decemcellulare to oxidative stress]. Retrieved December 24, 2020, SOURCE 
25. VK; M. (2002, April). [Respiratory activity and naphthoquinone synthesis in the fungus Fusarium decemcellulare exposed to oxidative stress]. Retrieved December 24, 2020, SOURCE 
26. Vu, D. C., Lin, C., Coggeshall, M. V., & Vo, P. H. (2018). Identification and Characterization of Phenolic Compounds in Black Walnut Kernels. Retrieved December 24, 2020, SOURCE
27. W; K. (2001). [Effects of 33% grapefruit extract on the growth of the yeast--like fungi, dermatopytes and moulds]. Retrieved December 24, 2020, SOURCE
28. Yin, M., & Cheng, W. (1998, January 01). Inhibition of Aspergillus niger and Aspergillus flavus by Some Herbs and Spices. Retrieved December 24, 2020, SOURCE 
29. Yoshida, S., Kasuga, S., Hayashi, N., Ushiroguchi, T., Matsuura, H., & Nakagawa, S. (1987). Antifungal activity of ajoene derived from garlic. Applied and Environmental Microbiology, 53(3), 615-617. doi:10.1128/aem.53.3.615-617.1987
30. Zorić, N., Kosalec, I., Tomić, S., Bobnjarić, I., Jug, M., Vlainić, T., & Vlainić, J. (2017, May 17). Membrane of Candida albicans as a target of berberine. Retrieved December 24, 2020, SOURCE