Candidiasis

Concerns for Children: Can Hidden Hunger Affect Mental Health?

Jill Craig, MS, CN, CNS

SUMMARY

Mental health issues for children is now one of the top 10 reasons for children to be admitted to the hospital in the United States, according to an article in US News and World Reports.

This past September in an article in the Dayton Ohio News cited mental health concerns were the most common reasons for the admission of children to the Dayton Children’s Hospital.  

This articles explains why what we eat impacts our mental health.
 

A Happy Child by Kate Greenaway1

A September newspaper ran this story:  

Mental health now most common cause for admissions at Children’s 

The article cited that over 900 children since the start of 2022 had been admitted to a local hospital for depression or suicidal thoughts. One in seven returned within 30 days. Why? Adverse childhood experience, stress and conflict were a few reasons given.2
A 2020 National Survey of Children’s Health upholds this sad reality – many children are not happy.3 

As a consultant with Great Plains Laboratory, I routinely ask practitioners, “What can you tell me about the patient?” At times, I hear, “Well, she (or he) had a traumatic childhood.” In one case, a patient named “Nancy” was in great distress because she had just been diagnosed with bipolar disorder. Her “crazy-wild” mother received the same diagnosis when Nancy was young. While all cases are unique, two parts of Nancy’s story are common with others I hear – malnutrition coupled with mental instability. A Happy Child was written long ago when life seemed simpler, and cake was an occasional treat. As we will see, what we eat or do not eat can have influence. 

Obstacles to Good Nutrition 

A recent systematic review showed a significant, cross-sectional relationship between unhealthy dietary patterns and poorer mental health in children and adolescents. Childhood-learned dietary habits most often segue into adulthood. Clearly, depression, anxiety, suicidal and bipolar tendencies are common in all stages of life.4 However, depression in young adults in a randomized controlled trial improved when given a
3-weeks’ intervention of a diet rich in fruit, vegetables, fish, and lean meat.5
Yet, for some families, wholesome foods may not be readily available or preferred.  

Food deserts” or “low-access communities” are areas where fresh food is hard to find and are a reality for millions of Americans. Grocery stores are not conveniently located and convenient stores at nearby gas stations mostly carry only processed food options. From my experience with community nutrition, children in food deserts often do not know names of most vegetables and fruit. Many have not even seen them.
However, it seems food swampsare of more concern to health for those of lower socioeconomic status where the prevalent presence of fast food and junk food overshadow available healthy alternatives.6, 7  

As a growing problem in European regions, as well, a recent study corroborates this.
The primary dilemma for children and adolescents when it comes to food environment is the profusion and marketing of cheap, unhealthy food, not the inaccessibility to healthy options.8, 9 And even many “healthy” foods are of concern, as well. 

He’s gluten-free and dairy-free.” I hear this often from practitioners since an elimination diet for a time may help correct GI complaints. Yet some food options are not so healthy. According to Dr. Dariush Mozaffarian of the Tufts Friedman School of Nutrition Science and Policy in Boston, “…you could create any kind of Frankenstein food that met the nutrient criteria and label it as healthy.”10   

Overall, the two primary reasons behind the food people choose to buy and eat is founded in their knowledge about nutrition and their food preferences.11  Yet, societal factors play huge roles, as well.12 This is known as “foodways”, where food and culture converge: campfires and S’mores; birthdays with cake and ice cream; Halloween and candy, candy, candy. 

Foodways, American style 

We would not want to live without traditions and the memories they bring, but 3 cups or 144 teaspoons is the average amount of sugar ONE child eats on Halloween. That is a lot of sugar. Yet, a newspaper article quotes an expert in nutrition who says three cups of sugar for a kid on a single day is “not that bad.” If they eat it and get a stomachache, well then, they will learn their lesson.13  

On top of that, Halloween is just the kick-start to the holiday season. Then come the Thanksgiving pies and sweet potato-marshmallow casseroles; Hanukkah "sufganiyot" (jelly donuts) and latkes; and Christmas cookies and candy canes. So, foodways seem to give license to increased sugar intake. Besides, the Food and Drug Administration (FDA) gives sugar a generally recognized as safe (GRAS) status with no limitations for its content in foods, other than current good manufacturing practice.14 Yet, does the stomach solely suffer? 

An ecological analysis of international differences in food supply relative to epidemiological data on the outcome of schizophrenia and the prevalence of depression showed that consumption of refined sugar worsens both.15 Yes, sugary seasonal indulgences during the holidays can be detrimental to mental health, yet, the overall increase of sugar intake in the Western diet is of greater concern, especially for children.16 Basically, sugar supplants the sense of taste for nutritious foods which can result in hidden hunger.17  

Hidden hunger, a lack of essential nutrients, is a global reality. At least half of all children under five suffer from stunted growth because of it. For several reasons, which could include displacement due to the influences of sugar, these children don’t eat enough variety of foods to support healthy growth and development.18
A pattern-analysis of the Organic Acid Test (OAT) can reflect the effects of such malnutrition upon metabolism as seen in the following case. 

Metabolic evidence of hidden hunger  

Five boys in one family with behavioral issues all appeared to be on the autistic spectrum. Toxic mold exposure was a likely part on their story, as well, yet the greatest concern was for the middle son, “Ben”, whose dietary intake was dangerously limited.
If there was something Ben liked, he’d eat. If not, he’d be content not to. In addition to showing signs of stunted growth, his symptoms included headaches, dyslexia, vision problems, symptoms associated with Pediatric Acute-onset Neuropsychiatric Syndrome (PANS), and episodes of rage.  

Ben’s OAT revealed decreased levels of many metabolites, a pattern I’ve seen commonly in children. The first analyte I noticed was lower hippuric acid (#10). This likely reflected Ben’s low intake of colorful vegetables and fruits on which bacteria feed to generate butyrate, a needed cofactor to produce hippuric acid. The beneficial bacterial analyte, DHPPA (#15), is concurrently low which implied insufficiency dysbiosis likely due to his lack of dietary fiber.19 

Secondly, the Krebs Cycle metabolites were below the mean. Because of Ben’s low caloric intake, the intermediates leave the cycle to convert to glucose, fatty acids, and non-essential amino acids. This puts a demand upon his body’s amino acid supply as the intermediates need to be refilled by amino acids at various points along the cycle to support its continued function. For example, succinate is replenished by isoleucine, valine, and methionine; fumarate with phenylalanine and tyrosine.20  So, lower Krebs Cycle metabolites suggest both suboptimal diet, an overall low amino acids status and the metabolic evidence of hidden hunger.  

Also, I observed that the end-byproducts of essential amino acids involved in neurotransmission were below the mean (#33) #34) (#38). Lower HVA and VMA are related to the decrease of fumarate and its association with phenylalanine and tyrosine. The lower HIAA may reflect low tryptophan in Ben’s diet and body stores, as well. 

Though the HVA/DOPAC ratio is only slightly lower, it may indicate slower catachol-o-methyltransferase (COMT) activity.21 Magnesium, vitamin C and S-adenosyl-methionine (SAMe) support COMT function and many other enzymatic reactions. Furthermore, SAMe is a byproduct of methionine, an essential amino acid primarily found in animal protein.22

All these were likely limited in Ben’s diet, as well, which could negatively affect COMT function. Also, several of Ben’s symptoms are common with COMT genetic defects. 

Additionally, the HIAA may be lower due to a genetically slow monoamine oxidase (MAO) enzyme and/or insufficiencies of its cofactors, vitamin B2 and iron. Iron is commonly low in infants and children.23 Genetic mutations in the MAO enzyme are also associated with mental disorders that include autism, anxiety, impulse-control disorders, and ADHD.24   

Hidden hunger in Ben’s OAT is also evident in the pattern of the following metabolites that fall below the mean.  

Lower ketones (43 - 44) and fatty acid (45 – 49) analytes common with lower dietary intake 

Lower vitamins B6, B5, and C / 50, 53 lower due to low amino acid precursors.

58 – 59 lower due to low amino acid precursorsxxv / 60 may indicate low protein intake / 76 possible low vitamin D and/or low animal protein in the diet.

A simple answer to address a complex
concern – in part
 

Current newspaper headlines relay daily the grave reality that many children suffer from mental health distress. A Happy Child. A simpler life of long ago. A piece of cake, a treat. Why are so many children not happy in our day? Surely there are many varied reasons for this as each child’s story comes with its unique, complex set of circumstances. However, malnutrition, or hidden hunger, is a common thread in Nancy’s and Ben’s stories. I would not be surprised if it also appears someplace in the narratives of the
900 admitted to Children’s. It is worth considering as what we eat or don’t eat does
have influence. 

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References
  • Nutrition for Kids: Tips on Getting Children to Eat Healthier - webinar by Dr. Tracy Tranchitella, N.D. https://vimeo.com/386074107embedded=true&source=vimeo_logo&owner=2820515 
  • Refined to Real Food: Moving Your Family Toward Healthier, Wholesome Eating ISBN: 9781880158487 
  • Feeding Baby Green: The Earth Friendly Program for Healthy, 
    Safe Nutrition During Pregnancy, Childhood, and Beyond ISBN: 9780470425244 
  • Brain Health from Birth: Nurturing Brain Development During Pregnancy and the First Year ISBN: 099967613X 
  1. Benoit, C. F. (1922) Children's Poems That Never Grow Old, for Little Folks from Six to Twelve Years Old. [Chicago, The Reilly & Lee co] [Image] Retrieved from the Library of Congress, https://www.loc.gov/item/22013224/. 
  2. Perry, Parker.(2022) Mental health now most common cause for admissions at Children’s 
    https://www.daytondailynews.com/local/
    mental-health-issues-most-common-admission-reason-now-at-daytonchildrens/DMBEHEQL7BH4BFII7UKPBUZY5U/#:~:text=More%20than%20900%20children%20have,doctor%2 0at%20the%20hospital%20said. 
  3. Mental and Behavioral Health NSCH Data Brief (2020) https://mchb.hrsa.gov/sites/default/files/mchb/data-research/
    nsch-data-brief-2019-mental-bh.pdf  
  4. O'Neil A, et. al. (2014) Relationship between diet and mental health in children and adolescents: a systematic review. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4167107/#bib1/  
  5. Francis, HM., et. al (2019) A brief diet intervention can reduce symptoms of depression in young adults – A randomised controlled. https://journals.plos.org/plosone/article/file id=10.1371/journal.
    pone.0222768&type=printable  
  6. Cooksey-Stowers, K. (2017) Food Swamps Predict Obesity Rates Better Than Food Deserts in the United States. https://media.ruddcenter.uconn.edu/PDFs/ijerph-14-01366.pdf 
  7. Chen, T. (2017) Food Deserts and Food Swamps: A Primer.  https://www.ncceh.ca/sites/default/files/Food_Deserts_Food_Swamps_Primer_Oct_2017.pdf  
  8. Smets, V. (2022) The Changing Landscape of Food Deserts and Swamps over More than a Decade in Flanders, Belgium. https://www.mdpi.com/1660-4601/19/21/13854/htm  
  9. Harris, J. et. al., (2021) Fast Food Facts https://media.ruddcenter.uconn.edu/PDFs/FACTS2021.pdf  
  10. New York Times. (September 29, 2022) https://www.nytimes.com/2022/09/29/well/fda-healthy-food.html  
  11. Ver Ploeg, M. (2016) Recent Evidence on the Effects of Food Store Access on Food Choice and Diet Quality. https://www.ers.usda.gov/amber-waves/2016/may/recent-evidence-on-the-effects-of-food-store-access-on-food-choice-and-diet-quality/ 
  12. The Factors that Influence Our Food Choices. (2006) https://www.eufic.org/en/healthy-living/article/the-determinants-of-food-choice  
  13. Avril, T. (2022) Should kids eat all their Halloween candy all at once, or spread it out? Dentists and nutritionists help you with the sticky questions. https://www.spokesman.com/stories/2022/oct/27/should-kids-eat-all-their-halloween-candy-at-once-/  
  14. Code of Federal Regulations Title 21 (2022)https://
    www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?fr=184.1854  
  15. Peet, M. (2018) International variations in the outcome of schizophrenia and the prevalence of depression in relation to national dietary practices: and ecological analysis.  https://www.cambridge.org/core/journals/the-british-journal-of-psychiatry/article/international-variations-in-the-outcome-of-schizophrenia-and-the-prevalence-of-depression-in-relation-to-national-dietary-practices-an-ecological-analysis/D226B13D07E36AB09016A2EED81049B6  
  16. Mills, C. (2022) The haunting facts of eating too much sugar.
    https://www.statefoodsafety.com/Resources/Resources/
    the-haunting-facts-of-eating-too-much-sugar
  17. Drewnowski, A., et. al. (2012). Sweetness and food preference. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3738223/  
  18. UNICEF (2019) The state of the world’s children 2019. https://features.unicef.org/state-of-the-worlds-children-2019-nutrition/  
  19. Cronin, P., et. al (2021). Dietary Fibre Modulates the Gut Microbiota. https://doi.org/10.3390/nu13051655  
  20. Owen, O. (2002) The Key Role of Anaplerosis and Cataplerosis for Citric Acid Cycle Function. 
    https://www.jbc.org/action/showPdf?pii=S0021-9258%2820%2970110-9  
  21. Bilder, R., Volavka, J., Lachman, H. et al. (2004) The Catechol-O-Methyltransferase Polymorphism: Relations to the Tonic–Phasic Dopamine Hypothesis and Neuropsychiatric Phenotypes. https://doi.org/10.1038/sj.npp.1300542
  22. Elango, R. (2020) Methionine Nutrition and Metabolism: Insights from Animal Studies to Inform Human Nutrition. https://doi.org/10.1093/jn/nxaa155 
  23. Wang, M. (2016) Iron Deficiency and Other Types of Anemia in Infants and Children 
    https://www.aafp.org/dam/brand/aafp/pubs/afp/issues/2016/0215/
    p270.pdf  
  24. Bortolato, M. Shih JC. (2014) Behavioral outcomes of monoamine oxidase deficiency: preclinical and clinical evidence. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3371272/  
  25. Human Metabolomic Database (2021) https://hmdb.ca/metabolites/HMDB0000008  

How Candida Can Cause an Autoimmune Response and Ways to Neutralize the Fungus

Kurt Woeller, DO

SUMMARY

Candida albicans is the most commonly encountered human fungal pathogen and is frequently found on the digestive tract. Host defense against Candida is dependent upon a finely tuned implementation of innate and adaptive immune responses, enabling the host to neutralize the invading fungus. Dr. Kurt Woeller explains how the Th1 and Th17 cells play an important role in defending the body against candida.


Overview of the Immune System, Mucosal Pathogen Detection, and Inflammation Activation

The complexity of the immune system comes from its multiple cell types and overlapping functions that coordinate in their activity to recognize, combat, and initiate acute and prolonged defenses against different pathogens. The main categories of the immune system are referred to as innate and adaptive, aka acquired. The physical barriers which include the skin and mucus membranes are often described as part of innate immunity:

  • The physical barriers provide a protective defense against opportunistic and invading pathogens. If one of these barriers are breached, either from injury or inflammation, immune chemicals are produced to stop the infection. If this is not successful, then more specific innate immune cells such as monocytes are activated.

  • The innate immune system includes granulocytes like basophils, neutrophils, and eosinophils, as well as other specialized cells such as monocytes and macrophages. These innate immune cells are not intrinsically affected by prior antigen exposure and typically respond similarly with each new encounter.

  • The adaptive immune system, aka acquired immune system, is highly specialized to react to various pathogens. This includes the B-cell and T-cell lymphocytes. Adaptive immunity has an important immune memory capacity for pathogens of previous exposure.

Neutrophils and monocytes play an important role in innate immunity in the early stages of infection and injury. Macrophages, known as “big eaters,” are derived from circulating monocytes, and are critical for engulfing antigen which has first been recognized and processed by tissue infiltrating neutrophils. For simplicity, the focus here will be on the relationship between neutrophils and macrophages in a process of apoptotic neutrophil activation for macrophage engulfment.

When a bacteria or fungus invades a tissue such as the mucosal lining of the digestive system there is a flood of immune chemicals, i.e., cytokines and chemokines, released that signal circulating neutrophils to the site of activity. The end goal of this reaction is to destroy the invading pathogen. After the neutrophil has neutralized the pathogen, it transforms into an apoptotic neutrophil. This neutrophil form needs to be quickly cleared from the tissue before its breaks down and causes more tissue damage through release of its enzyme granules. The macrophage that is residing in the same tissue area is called into action to engulf (“eat”) the apoptotic neutrophil and then clear it through the locally draining lymph system. If this process does not occur in a timely fashion, the apoptotic neutrophil will degrade, release its toxic granules, and cause more tissue inflammation.


PRR and PAMP

Another important aspect of innate immunity is its ability to communicate with the adaptive arm of the immune system for a systemic and more comprehensive response. This occurs, in part, through pattern recognition receptors (PRR) and pathogen associated molecular patterns (PAMP).

The immune system is linked to various tissue receptors such as those in the gastrointestinal tract containing pattern recognition receptors. Each PRR is unique to a specific pathogen associated molecular pattern. Candida contains various PAMPs unique to its cellular structure, particularly within its complex membrane layers. For example, β-glucan, part of the candida cell membrane, is a type of PAMP that our PRRs can recognize. Candida will attempt to shield the β-glucan PAMP from the host immune surveillance system. When a fungal organism such as candida contacts the epithelial surface there are various PAMPs recognizable by host cell PRRs. Uniquely, candida interacting with the epithelial cell also triggers a series of behavioral changes within the candida organism to become invasive. The PRR-PAMP interaction is crucial with regards to immune recognition and action against a pathogen.

Dendritic Cells and Antigen Presentation

The innate immune system has additional cells called antigen presenting cells (APC). These cells relay information about a specific PAMP to the adaptive immune system. Specific APCs known as dendritic cells (DC) communicate with naïve T-cells to bring into action adaptive immune activity. This interaction between the DC and naïve T-cells induces various other T-cell types, including T-helper cells (CD4) such as Th1 and Th2, and cytotoxic T-cells (CD8). Two additional T-cell types called Th17, and T-regulatory (Treg) cells are important with regards to this discussion about candida and immune activation.  


Candida, Autoimmunity, and Autoinflammation

Autoinflammation is inflammation that occurs as a result of an autoimmune reaction. Autoimmunity is a condition that happens when the immune system attacks self-tissue. Rheumatoid arthritis and Chron’s disease are two types of autoimmune diseases where components of the immune system attack the joints and digestive system tissues, respectively, causing autoinflammation. Candida, in some cases, can be a trigger for autoimmune and subsequently autoinflammation.


T-Cell Immunity Plays Pivotal Role Fighting Candida

T-cells are part of the adaptive immune system. They play an important role in immune surveillance of both intracellular and extracellular pathogens, as well as immune tolerance. Here is a brief description of the actions of Th1, Th2, Th17, and Treg cells:

  • Th1 cells are directed towards intracellular pathogens such as viruses. For many years imbalances in Th1 cells levels or its regulation were felt to play a major role in autoimmune reactions. This was the case until Th17 cells were discovered.

  • Th2 cells are directed towards extracellular parasites and can be involved in allergy, asthma, and similar conditions.

  • Th17 cells are directed towards extracellular bacteria and fungus. They are now recognized to play a significant role in autoimmunity. Th17 cells are important for mucosal reactivity against fungus, e.g., Candida albicans.

  • Treg (T-regulatory) cells are regulators of overall immune responses, immune tolerance (to aid against immune attack against self-tissue), and homeostasis.

 

The Dance of T-Cells

The relationship between these T-cells is a complicated dance coordinated by various cytokines such as TGF-β, INF-α, and IL-6, as well as cell membrane receptors, second messenger reactions, and induction of genetic influencing transcription factors which influence protein production. As a general overview as it relates to candida and autoimmunity, the following is key information:

  • Increased Th17 cells producing IL-17 against candida can have a suppressive effect on Treg.

  • Decreased Treg can lead to reduced immune tolerance

  • Reduced immune tolerance increases the potential for autoimmune reactions

  • Reduced Treg decreases its influence on Th1 and Th2 which may also lead to increased activity of these T-cells in response to other existing pathogens.

  • Non-regulated immune activity of Th1, Th2, and Th17 in various tissues can lead to increased inflammation causing tissue destruction and cellular degradation.

  • Increased cellular degradation can lead to cellular structure exposure which can increase self-antigen immune recognition and drive autoimmunity.

Although there is always more to learn about the immune system and means of intervention. The next short section are some basic strategies which can be implemented for improved health, digestive function, and reduced potential for candidiasis triggering of autoimmunity.


Basic Strategies for Reducing Gastrointestinal Candida and Potential Mucosal Immune Activation

The following is a short list and descriptions of things that can be helpful in improving digestive system health, microbiome diversity, and eliminating/reducing opportunistic candida:

  • Microbiome diversity can be greatly enhanced through a high plant-based diet, fiber, and the use multi-strain probiotics. The improved microbiome diversity aids in pathogen reduction, mucosal barrier integrity, and reduced capacity for fungal overgrowth.  

  • The mucosal immune function helps to maintain optimal signaling between the mucosal immune mechanisms and innate and adaptive immune reactivity. Multi-strain probiotics, i.e., lactobacillus and bifidobacteria species, secretory IgA (SIgA) stimulators such as colostrum, Saccharomyces boulardii (which helps combat opportunistic candida and promotes SIgA production), can all be helpful.

  • Elimination or reduction of opportunistic pathogens through antimicrobial support, including individual or combination botanicals.

  • Elimination of gut mold colonization and mycotoxins

  • Elimination or reduction of environmental chemicals known to alter immune and gut function.

  • Incorporating omega-3 fatty acids (DHA & EPA), resveratrol, and curcumin to aide in inflammation control and oxidative stress.  

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References
  1. Candidiasis. Fungal Diseases. United States: Centers for Disease Control and Prevention. 13 November 2019. 
  2. Candidiasis. cdc.gov. February 13, 2014. Archived from the original on 29 December 2014. 
  3. Cottier F, Hall R. Face/Off: The Interchangeable Side of Candida albicans. 2000. Frontiers in Cellular and Infection Microbiology. 
  4. Roe K. How major fungal infections can initiate severe autoimmune diseases. 2021. Microbial Pathogenesis. Science Direct. 
  5. Nydiaris, H.S., et.al. Th17 Cells in Immunity to Candida albicans. 2012. Cell Host & Microbe Review. 
  6. Peter J. Delves, Seamus J. Martin, Dennis R. Burton, Ivan M. Roitt. Roitt’s Essential Immunology 13th. 2017. Wiley-Blackwell Publishing. 

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.

Functional Medicine Answers with Kurt Woeller, DO

On November 12-14, 2021, GPL Academy hosted the Environmental Toxin Summit in San Diego, CA as well as streamed online simultaneously. This three-day event focused 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. Those who attended the summit learned how to use effective diagnostic and treatment protocols for their patients with toxin exposure and get them on the road to recovery.

The following Q+A is a grouping of responses from Dr. Woeller’s 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, 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, LLC. He is co-founder of Integrative Medicine Academy, which is an online training academy for health practitioners learning integrative medicine.

Q: If you have been supplementing with Lithium orotate 10mg and the hair test comes back HIGH do you back down, stop, or just continue at the same dose? The child has high Glutamate marker on Neurotransmitter test.

A: I would personally back down to the 4.8 mg dose and retest again in 90 days, particularly if there have been some positive changes. If there is no significant change, then I would likely just discontinue the supplement.

Q: Based on various research studies, it has been shown Biocidin can treat primary hyperhidrosis. Would you recommend long-term daily Biocidin dosing or implementation of a cyclic protocol over a shortened period?

A: For this, I would recommend a long-term daily dosing versus cyclical dosing.

Q: Why did you choose Biocidin capsules vs drops?

A: I do not remember the specifics for that particular case. Usually, it comes down to taste sensitivity of a child versus their ability to swallow capsules.

Q: Did you increase the dose slowly?

A: No.

Q: Was there a die-off at full dose?

A: It did not happen in that case, but that is a possibility. Therefore, starting at a lower dose is okay to do if you get the sense die-off could happen.

Q: How did you choose Flagyl dose of 250 mg tid for the 2-year-old?

A: The medications were being handled by another physician since the child lived in another state. It was a higher dose for sure with the child having already been through multiple other treatments up to that point that were unsuccessful.

Q: I am a bit unclear but is it ok to continue Vit C with high oxalates?

A: This is a controversial situation, and it is not clear cut in every situation. There are quite a few studies and reference websites for kidney stone sufferers that describe up to 2000mg daily oral of Vitamin C to be okay. Therefore, in my experience modest dosing of ascorbic acid, e.g., 250mg to 500mg daily has been fine. I have even gone to 2000mg daily and not seen any problems. However, in most situations, I keep the dosing to less than 500mg daily but do not stop it entirely.

Q: What cholesterol triggers your concern as I find iCNS issues with 120 -135? Is it a variable number depending on the severity of the CNS presentation?

A: Yes. I have seen people who have a total cholesterol of 120 (or lower) and seem fine. In others that value is problematic for them.

Q: Can you augment a 165?

A: At this level I would not be supplementing with Sonic Cholesterol.

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Considerations And Protocols For The Complex Patient With James Neuenschwander, MD & Elena Villanueva, DC (Copy)

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 focused on the epidemic of environmental toxin exposure, from the many chemicals we encounter every day to mycotoxins released from mold. Attendees learned about many common environmental pollutants from the 173 chemicals tested by the GPL-TOX Profile.

The following Q+A is a grouping of responses from a distinguished pool of speakers who participated in the OAT+TOX Workshop with his own unique topics and lectures as labeled.

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.


James Neuenschwander, MD

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. Dr. Neu (as he is also known) 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: What cutoff is ‘Lots” on an ERMI? 

A: I typically start paying attention if the number is over 2; but in my state (Michigan), many houses are over 2. The ERMI score also does not take into account how moldy the house is in general, only the difference between toxin producing mold and non-toxin producing mold. I will use the mold numbers to calculate a HERSMI Score.  If it is over 16, the house is a problem. 12-16 might be a problem if the person is sensitive.

Q: Can mycotoxins cause a progressive pulmonary fibrosis?

A: I think that anything that causes consistent immune activation (like mold toxins) can cause pulmonary fibrosis.

Q: How about triphala? Ayurvedic herb that helps with constipation and detoxifier, antioxidant and more.. 

A: I frequently use Triphala to help with constipation. I don’t use is it as a detoxifier/antioxidant/etc—I think there are better options for that.

Q: Are you familiar with phenomenal AIRE? It produces ions? Is this ozone?

A: It is not ozone, but it incidentally generates ozone from room air. The idea behind an ionizer is to charge particles so they stick to each other and surfaces. The energy needed to create the ions can also create ozone from the oxygen in the air. I am not a fan.

It is said to join particles to bond together known as agglomeration.

Q: What are your thoughts regarding treating mold with thermal fogging with a solution like BioBalance vs. treating with ozone generator? 

A: I think ozonation is probably the most effective way of treating mold after you have removed the obvious contamination (this won’t get mold off of wood joists or rafters because it won’t penetrate the wood deeply enough) with other techniques. This requires that people are out of the building and requires an industrial strength, whole house ozonator.

Q: In a patient with Gilbert’s, what precautions are needed?

A: The issue with Gilbert’s is that they will be more susceptible to certain environmental toxins. Supporting glutathione (NAC, ALA, liposomal glutathione supplements, Setria) can help with glucuronidation (the problem with Gilbert’s).

Q: I also live in Michigan. What water filter do you find works well with our water?

A: Every water system will have different issues. I am on a well. I have completely different issues than someone that is on Detroit City water. I use the Zero Water filter—this is a pour through, multi-stage system that removes almost everything. My biggest problem is iron and bacteria—not any issues with other water supplies. This system will also remove chlorine and fluoride and heavy metals. Most of the time, a combination charcoal/reverse osmosis water filtration system works for most things, but does not remove all the thyroid.

Q: Can you just take ox bile with binders so patients have more time flexibility?  Some must take meds before eating.

A: Yes. You can take them together.

Q: Patients with severe MCS that have such a hard time taking ANY med/supplement...where do you start with mold or mycotoxin treatment? Slow small amounts of binder until tolerating?

A: First, I will start with supportive supplements (like vitamin C) before I start with detox supplements. Then, I will start with a single binder (not a combination) at low dose and work my way up. Many of the symptoms MCS patients have are related to histamine, so I also tend to start with things like luteolin (and quercetin if they are not sensitive to salicylate).

Q: Is Cholestyramine constipating?

A: It is almost always constipating. I always start something (like magnesium citrate or sodium ascorbate) to help with the constipation.

Q: Do you have any protocols for people to detox from the CV injections and their injuries?

A: I assume you are referring to the COVID vaccines—check out the FLCCC.org website. They have a protocol for long-haul COVID. It works for most vaccine injuries. Above and beyond that, it requires someone familiar with detox from vaccine injuries—that is an entire workshop, not a simple answer.

Q: It’s been shown that DMSA, etc. provoking sends toxins all of the body, into joints, etc. Do you see this?

A: Not really. DMSA will bind metals in tissues. Because it is a sulfur bond, it is not easily reversible. The metal can be displaced by another metal with a higher affinity, so you can have some distribution. I also give DMSA according to the Cutler protocol—every three hours for three days every two weeks. I also make sure that patients have adequate glutathione and that they don’t have intestinal yeast. There is no way to remove metals without some distribution, but that is better (when managed properly) than leaving the metals in the body.

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Elena Villanueva, DC

Elena Villanueva is an internationally recognized health coach and crusader for ending the global mental health crisis and educating the public and other health professionals that mental health conditions are actually ‘brain health’ issues and when the underlying causes are found, the brain health conditions can be reversed.

Q: Do you have a toxic exposure history form that you like?

A: The questions we ask in this area of our intake include the following. We also ask if they have any history of these exposures from their past.

Q: Would you be willing to share your symptom sheet and what you are utilizing for these patients to track symptoms?

A: Thank you for asking! Great question! We offer this and much more for our practitioners who go through our MHH certification program.

Q: What home mold testing do you recommend?

A: Home testing kits are not effective. We recommend our clients find a local mold testing company in their area to come out and test the house for mold. The price, depending on the state can range between $600-$800 for the testing and report.

Q: What do you use to break up the biofilm?

A: There are many different substances that can break up biofilm. The humic/fulvic compounds (like the ones found in the Cellcore product lines are effective at breaking up biofilm.  

Biofilm X and Interphase are also great biofilm busters, as are coffee enemas, and Biocidin also breaks up biofilm. Keep in mind that biofilm, depending on how dense and how much build-up there is, can take as little as 8 weeks to as long as 8 months to fully break up and come out. I am basing this comment on our experience with our clients.

Q: Are you giving biofilm disrupters alongside the binders in your patients that had new molds show up in later tests, or do you think just using binders alone was lowering the load enough to allow the body to break up the biofilm on its own?

A: The protocols we put them on do break up biofilm, so it’s not common that we need to add something extra like Interphase or some added additional biofilm buster.

Q: Is the “chemical toxin” test the GPL-TOX?

A: Yes.

Q: I do see a lot of sick patients that have high B12 lab readings.  What are your thoughts on that?

A: Such a great question! They could be showing high levels of blood serum B12 or urinary metabolite patterns of high B12 for the following reasons:

  1. They are taking B12 currently.

  2. They have specific genetic methylation SNPS (MTRR A66G) that may be ‘mal expressing’ where they are not able to uptake the B12 into the cell … so they may show ‘high’ levels in blood serum or in urine, but are actually cellularly ‘deficient’ - in these cases either a sublingual or transdermal delivery method for methylated B12 is going to be the ideal delivery method for cellular uptake.

Q: Can you comment on when you choose Liposomal Glutathione vs N acetylcysteine for detox?

A: There are definitely varying opinions on this one. We actually use BOTH, glutathione, and NAC. Previously, a few years ago, we were using glutathione and saw marked improvements in homocysteine, CRP, and MCV numbers, which can indicate methylation issues, which can cause inefficiency of phase 1 AND 2  detox pathways, leading to excessive inflammation (of course we also had clients on methyl folate/methyl B12 as well, per their genetics -- to make sure phase 1 and 2 Detox pathways were optimized). In the last year or so we have added NAC as well.

Q: I am interested in what exactly she is using for kidney/liver detox

A: We vary what we use from LVGB by DFH, to SP products, to Cellcore liver gallbladder support. There are many different brands that all work well.

Q: do you add in digestives like bile or HCL etc for support?

A: When we see it’s needed, yes we do.  We definitely do when we are doing specific gut repair (after removing the toxins and confirming with labs) It’s a fine line when we are not wanting to overload the client with supplements. We want them to be able to take the least amount of supplements with the greatest effect. Too many supplements make the clients/patients feel overwhelmed and often they lose compliance.

Q: Please expand on biofilm treatment protocol… list options and when to use in the overall treatment protocol.

A: Discussed biofilm in the above questions.

Q: What is TUDCA and what is inside Para 1;2;3

A: Tudca provides liver/gallbladder support. You can go to HERE to see the labels on the Para’s.

Q: Do you see 3-4 week cough as a herx symptom?

A: I would ask more questions and get a deeper history on this. The client/patient may be having an IgG type of inflammatory reaction to an ingredient in one of the supplements that is causing the cough. Or it could be a recent food they recently started eating. More times than not, a herx is more ‘severe’ symptom wise, than a cough. So definitely ask more questions. You could also do an ‘elimination’ test by having them stop all supplements to see if the cough goes away, and then one at a time every 5 days or so, start adding in one more of the supplements on their list…. and record if sx comes back with one of the supplements.

Q: …But you are putting them on new supplements.  So how do you tell the difference between a reaction and a herx?

A: It’s not as common to have a true ‘reaction’ to food/herb/nutraceutical based protocols. More than likely the sx are because the client is detoxing which can lead to mild sx or more severe ones (herx). If you are suspecting a true reaction, talk to the patient/client to get a history … they usually are already aware of their allergies to certain things. Use your discernment and if needed, take them off all supplements and slowly have them add one in at a time, sometimes micro dosing them with each supplement even. You’ll learn with experience!

Lyme, Mold, Mycotoxins & Testing Answers with Jasmyne Brown, ND, Darin Ingels, ND & More!

On November 12-14, 2021, GPL Academy hosted the Environmental Toxin Summit in San Diego, CA as well as streamed online simultaneously. This three-day event focused 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. Those who attended the summit learned how to use effective diagnostic and treatment protocols for their patients with toxin exposure and get them on the road to recovery.

The following Q+A is a grouping of responses from a distinguished pool of speakers who participated in the Environmental Toxin Summit with their own unique topics and lectures as labeled.

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.


Jasmyne Brown, ND

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.

The Clinical Approach of a GPL Consultant
on GPL Testing

Q: Please comment about Chaetoglobosin A and appropriate treatment protocols?

A: Treatment for this toxin is like others. You would need to remove the source and detox the toxins. Binders like charcoal bind all mycotoxins at some level and can be effective for this toxin too. Consider a combo binder product.

Q: If zearalenone is very elevated (90) but the patient has low estrogen, would you believe the results?

A: Yes. Zearalenone does not necessarily increase your own estrogen but has its own estrogenic effects. Also, the LC/MS is specific to the toxins so if it’s populating there is an exposure. Also realize all toxins do not cause the same symptoms in every person.

What would be a good next step if you have a sensitive patient with mold who reacts poorly to binders such as GI Detox? Is there a binder that works better for sensitive individuals or something that needs to be done first?

A: You can use another product that doesn’t contain strong binders like charcoal and clay. Consider ToxinPul™ Multi-Function Detox by New Beginnings Nutritional’s.

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Darin Ingels, ND

Dr. Ingels is a licensed naturopathic doctor with more than 30 years of experience in the healthcare field. He is a Fellow of the American Academy of Environmental Medicine and has been published extensively. Dr. Ingels is the author of “The Lyme Solution: A 5-Part Plan to Fight the Inflammatory Autoimmune Response and Beat Lyme Disease”, a comprehensive natural approach to treating Lyme disease. Dr. Ingels specializes in Lyme disease, MS, mold/mycotoxins, and chronic immune dysfunction. He uses diet, nutrients, herbs, homeopathy, and immunotherapy to help his patients achieve better health.

Lyme, Mold and Mycotoxins: Strategies For Navigating Complex Illness

Q: What's the dosing of TRISALTS for Herx?

A: Take 1 tsp every 2-3 hours until feeling better. May cause loose stools at higher doses, so warn patients.

Q: If you are exposed to mycotoxins at the office, do you carry a risk of bringing the toxin home through your clothes and belongings?

A: It is possible that porous material can contaminate other objects, so if the exposure at work were high enough and gets in your clothes when you sit on a chair, or bed it is possible to contaminate those surfaces. However, this is not likely the way most people get exposure, and it seems this contributes to a minimal form of exposure.

Q: For treatment of molds/mycotoxins, do you treat with antifungal medication (Diflucan, Nystatin) concurrent with binders?

A: If you are treating actual mold colonization, you need itraconazole as other azoles are not effective at killing mold. They are good for yeast, but not for mold. Yes, I use concurrent with binders as they are doing different things in the body.

Q: If you use binder products from CellCore Biosciences, does that mean you do not need to use Cholestyramin or Welchol?

A: Generally speaking, yes. You do not necessarily need to have multiple binders on board. Just monitor your patient’s progress and make sure their mycotoxin levels are dropping.

Q: One of my patients decided to try this ionic foot bath instead of the IonCleanse: Regain Health & Vitality ionic foot cleanse. Are you familiar with this version and do you think it will work? She purchased it since it costs less than $200.

A: I can’t speak to other ion foot baths but know that IonCleanse has a patent on their device, so it is unlike other ion generators out there. My personal experience with IonCleanse from AMD is that most people have a good response to it. I have had other patients get different devices and they do not seem to work as well, so I’m betting you get what you pay for.

Q: Could celiac symptoms be from contamination of the wheat with mold/toxins? Instead of allergy?

A: Not likely as Celiac disease is a genetic disorder in breaking gliadin down. No doubt, mycotoxin and mold contamination can aggravate both Celiac and non-celiac gluten enteropathy.


Mark Su, MD

Mark Su is a board-certified family physician of 18 years, practicing in Newburyport, MA. He founded Personal Care Physicians as a functional medicine practice in 2014, where he and 4 other clinicians provide both primary care as well as consultation services for chronic complex illness patients. As such, he's been evaluating and treating patients for mold and other related conditions across a variety of symptom and severity stages, creating a rather diverse experience beyond treating only severely dysfunctionally ill patients. He is currently the vice president of ISEAI, and also a member of the IFM and ILADS, among other organizations.

EnvironmnetAl Illnesses
and treatment Protocols

Q: B/W salicylate, oxalate and histamine/MCAS issues, what to test for/address first?

A: I view all 3 of these matters as "back 9", or secondary, root cause problems. Commonly, there are deeper, primary root cause problems causing each of these, so I'd look for those root causes. Reflective of the very essence of my presentation, one is not likely to find a singular cause - I believe it would be very, very rare for a practitioner to cast a wide enough net and yield only one cause for any or all of these problems. But at this point in time, if I was forced to name one most likely cause, or name the one cause that is likely to be having the greatest contribution to these issues (among the many found), I'd suspect it to be mycotoxins. That's likely to be the case with histamine/MCAS, certainly, with high oxalates a close second (commonly because where there are mycotoxins, yeast is likely to be a problem as well, and oxalates are common with the latter). With high salicylate levels, if we're talking about the marker under the "toxin" biomarkers within the GPL OAT results, my suspicion would more likely lie within a gut dysbiosis root cause, but even that is commonly going to be associated with mycotoxin illness. Whereas, any other exposome/"non-self" condition (incl. tickborne illnesses, heavy metals, viruses, etc) or other "self" condition (incl. immune deficiencies, hormone imbalances, methylation dysfunctions, etc) is not nearly as likely to (singularly) cause these problems.... A decent second suspicion would be to look at gut health, which is arguably unfair in comparison since it is a more categorical answer than mycotoxins being a more focal/singular response - gut health could include bacterial dysbiosis that is driving salicylate marker abnormalities; genetic-based deficiencies in histamine metabolism (leading to excess histamine in the gut); and/or fungal dysbiosis leading to high oxalates.

Q: What are the best way to lower oxalate levels?

A: Look for root causes. Dr. Woeller/GPL staff often teach that 3 of the most common causes are yeast, oxalate rich foods, and B6 deficiency. In my experience, yeast, as reflected by high arabinose levels (marker 7 on the OAT), is a common problem, even in a more generalized health population (vs. the chronic, complex illness patients). Given such, and my clinical impression that not many patients, as a generalized population, are likely to be eating a large enough amount of oxalate foods, yeast is likely to be the most common culprit among these three. (B6 deficiency, on some level, may be pretty common, but my suspicion is that this isn't likely to be a strong enough deficiency in most people to cause high oxalates - again, across the generalized population).

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Emily Givler, DSC

Emily Givler is a Functional/Genetic Nutrition Consultant, researcher, and lecturer with a thriving clinical practice at Tree of Life Health in Lancaster County, Pennsylvania. She holds advanced degrees and certifications in Nutrition, Herbalism, and Nutrigenomics from the Holt Institute of Medicine, PanAmerican University of Natural Health, and Functional Genomic Analysis where she now serves as an adviser and supplement formulator. In her practice, Ms. Givler utilizes personalized dietary and nutritional protocols based on genetic predispositions, environmental and epigenetic influences, and functional lab testing to help her clients regain their health.

Oxalates and Mold: A Hidden Source
of Inflammation

Q: What about stone dissolving herbal therapy?

A: There are several herbal preparations that may be beneficial for high oxalate individuals. This paper, Dietary Plants for the Prevention and Management of Kidney Stones: Preclinical and Clinical Evidence and Molecular Mechanisms, summarizes their potential benefits and specific mechanisms.

Q: Do you see a pattern of lactose intolerance in genetic testing with patients with high oxalates?

A: Not necessarily, though lactose intolerance can be an exacerbating factor. Far more people will be lactose intolerant than will have a problem with oxalates.

Q: Do you have a protocol for oxalate that you can share with us?

A: The first step would be to assess which mechanisms for over absorbed oxalates are coming into play. Next, we would add Epsom salt soaks, working progressively up to 20 min 3-5x/week as tolerated. Evaluate the diet for volume of oxalates and start reducing/binding oxalates at roughly 10% per week. The next steps depend on the individual presentation and may be bile support, probiotics, antimicrobials, B1, and/or B6. The individual presentation will typically dictate the order and necessity of those pieces.

Q: Can you repeat the brand name of the sulfate/sulfite test strips you're using?

A: Quantofix

Q: Where do you get the sulfate test strips?

A: Amazon

Q: What would be considered "high" for a child when using the sulfate strips?

A: 10

Q: Can you expand on the use of sulfate test strips if/when oxalate markers aren't elevated on an Organic Acids Test? Would we expect to see low to no reported sulfate on the strip because of wasting?

A: Typically, in this scenario you will see high sulfate as the oxalate is being retained and the sulfate is being excreted.

Q: If oxalate crystals are insoluble in tissue, how can they dissolve to show up in the urine?

A: They are present in urine, not dissolved in it.

Q: Can urine be a false low?

A: Absolutely! Therefore we need to look for other clinical indications such as sulfate wasting.

Q: Can you repeat the gene that you mentioned that helps with sulfation?

A: SUOX

Q: And you suggested giving molybdenum?

A: Yes, it is the cofactor and can help when there are polymorphisms or when the transulfuration pathway is upregulated and sulfites are high.

Q: If you have high oxalates and positive for mycotoxins (i.e ochratoxin and gliotoxin) - which anti-fungal medication would you recommend starting + dosage and duration?

A: I would use an antifungal if there was evidence of colonization but am not a doctor and cannot prescribe. This also needs to be personalized for the individual. I do like Biocidin for these cases.

Q: How much baking soda are you recommending in water in between meals as prevention for oxalate dumping?

A: Very little; typically, ⅛ tsp

Q: How much Epsom salt do you typically recommend adding to a bath to help mobilize oxalates?

A: ¼c in a foot basin or 2 cups in a bath. There are sensitive individuals who do need to start more slowly.

Q: What is your favorite recommendation for dealing with fat malabsorption/digestion?

A: TUDCA and/or the combination of Quicksilver BittersX and Pure PC. Adding castor oil packs over the liver and gallbladder and using coffee enemas can be helpful if there is “sludgy” bile.

Q: Can oxalates pull calcium from bone and cause osteoporosis?

A: There are several studies exploring the associations between kidney stones and osteoporosis, but a causal link, to my knowledge, has not been clearly established. Please refer to Kidney Stones and Risk of Osteoporotic Fracture in Chronic Kidney Disease as well as Unravelling the links between calcium excretion, salt intake, hypertension, kidney stones and bone metabolism.

Organic Acids, Invasive Candida, Clostridia & More With Kurt Woeller, DO

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 focused on the epidemic of environmental toxin exposure, from the many chemicals we encounter every day to mycotoxins released from mold. Attendees learned about many common environmental pollutants from the 173 chemicals tested by the GPL-TOX Profile.

The following Q+A is a grouping of responses from Kurt Woeller, DO, who participated in the OAT+TOX Workshop with his own unique topics and lectures as labeled.

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, DO

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.

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Q: Can you see parasite infection on here and can that impact dopamine? Dopamine markers are elevated / too low but no clostridia in ASD child.

A: There is no specific marker absolutely diagnostic for parasites on the OAT. You would need to do stool testing.

Q: Hippuric acid - is this indicative of bacterial infection i.e. parasites?

A: It is indicative of increased normal digestive bacterial activity in the presence of chlorogenic acid found in many foods, e.g. fruits, potatoes, and other vegetables. There is a full list of foods in the interpretation section of the OAT.

Q: If 61 is high but no sweeteners in diet what could be the cause?

A: Often seen with bacterial markers found on page 1 of the OAT. Could also be phenols found naturally in foods.

Q: Is there an issue if ALL amino acid metabolites are low?

A: No. This section of the test is only significant when the values are elevated. This section of the OAT is to evaluate for certain metabolic diseases. Therefore, when the values are low it indicates that there is no evidence of a genetic disease linked to the specific marker.

Q: Ascorbic acid is extremely low in a child on a very high veg whole food diet - what would be the reason?

A: Ascorbic acid is commonly low on the OAT because it is an unstable acid in urine. The main reason the marker is on the OAT is to pick up on high values that might be associated with high oxalic acid.

Q: Do you recommend treating candida, when values are high, even if patient is asymptomatic?

A: Yes. I feel it is still worthwhile to treat.

Q: Does the high vitamin C ascorbic increase oxalate?

A: In some circumstances it might.

Q: Will uracil be elevated in those recently vaccinated?

A: I do not know. This would be a good thing for you to watch for in your practice.

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Q: If a person had pseudomonas aeriginosa and never took antibiotics for it, curing it naturally is there still the possibility of having a biofilm present?

A: Yes. It appears many of these bacteria produce biofilm as a natural part of their existence.

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Q: What is your opinion on the effectiveness of Botanical treatment versus Abx/Antifungal prescription medication?

A: It depends on what you are treating and how severe the condition is. I mostly try and use botanicals and reserve antibiotics for more severe conditions.

Q: I have a patient with 3 oxoglutaric acid which is listed in the intestinal overgrowth panel. He has elevated HPHPA and arabinose also. Is the 3 oxoglutaric different?

A: It gets produced from different types of intestinal yeast. Remember, candida is a type of yeast too, but there are different yeast species.

Q: What is the significance of 3-Oxoglutaric acid?

A: It gets produced from different types of intestinal yeast. Remember, candida is a type of yeast too, but there are different yeast species.

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Q: For fungal markers, do you do a course of binders and if no response prescribe?  What would make you add itraconazole/other antifungal?

A: I will typically add binders for any infections, e.g., candida, mold, bacteria. The use of Itraconazole would be based on the severity of the condition and known exposure to environmental mold. It is not a medication I will typically start with. I have seen good success with digestive mold, e.g., aspergillus, with oral Amphotericin B (from a compounding pharmacy).

Q: Has Dr. Woeller ever worked with people (children especially) with Bardot Biedl Syndrome (BBD)?  Parts of the Schizophrenia case seem similar to traits of this especially with inability to absorb or break down fats and low cholesterol.

A: I have not. In fact, I have never heard of this syndrome before. I will look into it.

Q: The question is about what trips the trigger to make him add the antifungals.

A: I am always going to treat yeast regardless of how high the OAT markers are. As a basic level this would be a botanical like Biocidin and probiotic. However, if I feel the severity of the condition warrants medications, I will use these too such as Nystatin. If I have a autistic child that is extremely yeast reactive such as inappropriate laughter, high self-stimulatory behavior, bloating, excessive flatulence than Nystatin may be needed. However, I have seen botanicals work too. As a general rule, I attempt botanicals first, then go with meds if these do not work.

Q: How do you treat a 2.5 year old with high arabinose, oxalic acid and quinolinic acid, mold exposure (+ penicillium)?

A: First, you need to find out if the mold exposure is causing high mycotoxins. The high oxalic should be addressed with a low oxalate diet and calcium/magnesium with meals, minimally. But, oxalic can often occur from mold exposure, so this needs to be addressed too. High arabinose is linked to invasive candida. Both the mold and candida might be able to be addressed with botanicals and probiotics. Medications are not my first option in most cases. The quinolinic acid can often be helped with niacinamide. This type of scenario is really based on the severity of the condition and what type of child we are supporting. Are they autistic? Do they have self-injurious behavior? How well do they take supplements? All of these questions and more need to be asked and determined before proceeding with any type of treatment program.

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Chronic Candidiasis: Mechanisms of Pathogenicity and Laboratory Testing Options

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By Kurt Woeller, DO

Chronic candida has been a well-recognized problem in functional and integrative medicine for many years. It too is a problem acknowledged in conventional medicine, although at times for different reasons, i.e., oral thrush or skin infections.

Candidiasis is defined as a fungal infection linked to any form of candida species. These infections can occur in various places on or inside the body from the mouth, esophagus, intestines, as well as on the skin and scalp. Oral candida overgrowth (a.k.a. thrush), evidenced by white patches on the tongue or other areas in the mouth, is common in immune compromised individuals, the elderly, but also infants. Oral candida can cause mouth sores and make it difficult to chew food and swallow which can be extremely detrimental to the elderly through reduced nutrient intake. Esophageal candidiasis can occur with advancing infection making swallowing even more painful. Systemic candidiasis can occur too leading to candidemia which is defined as a candida infection within the bloodstream. Candida albicans is the species of candida most common in chronic candidiasis, but there are other types in existence known to cause problems as well.

Gastrointestinal candidiasis (GC) is a well-known problem recognized by functional and integrative medicine providers but is an underappreciated condition by many conventional medicine practitioners despite decades of clinical research. In autism, for example, GC commonly causes or contributes to digestive symptoms, e.g., bloating, constipation, flatulence. GC also can contribute to the accumulation of various toxic compounds such as chemical aldehydes known to affect cellular function through various biochemical alterations.

There are multiple mechanisms of pathogenicity associated with chronic candidiasis. Two common occurrences through the production of a toxic organic acid called arabinose and candida’s ability to cause leaky gut will be discussed.

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Arabinose, closely related to a sugar alcohol known as arabinitol, is a toxic aldehyde, which has been used for years as an indicator of invasive candidiasis. Aldehydes (-CHO) characterized by a carbon atom double bonded to an oxygen and single bonded to a hydrogen can be a reactive functional group involved in radical formation and oxidative stress. An article in 1995 by W. Shaw, Ph.D. detailing high levels of arabinose in twins with autism eventually led to further research into this compound and its prevalence to various other health disorders, e.g., Alzheimer’s disease. These conditions are often linked in part to chemical imbalances that are oxidative in nature.

Arabinose through its aldehyde group can bind with the amino acid lysine. This essential amino acid found in various proteins when complexed with arabinose can cross-link with the amino acid arginine. Arginine is involved in many physiological functions such as ammonia regulation, release of hormones, immune function, and wound healing. This interaction of arginine and the arabinose-lysine complex can alter normal biological function through the development of a toxic compound called pentosidine. Pentosidine, a glycation end-product, damages neuronal structures and has been linked to myelin damage, neurofibrillary tangle development, and Alzheimer’s disease.

Lysine is a functional component of many enzyme systems that depend on binding cofactors such as vitamin B6, lipoic acid and biotin. Therefore, high amounts of pentosidine formation being driven by excessive arabinose production from the invasive nature of candida may lead to functional vitamin deficiencies even when nutritional intake of these nutrients seems sufficient.

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Invasive candida within the digestive system can lead to leaky gut (LG), a.k.a. increased intestinal permeability. This problem is brought about by invasive candida piercing through the apical membrane of an epithelial cell or damaging the tight junctions between these cells.

The lining of the digestive system is a complex network of epithelial structures that are involved in nutrient absorption, toxin neutralization, and mucosal immune function, a.k.a. mucosal barrier. When the mucosal lining is disturbed a leaky gut scenario can develop which allows gut toxins to breach the epithelial barrier and gain access to the lymphatic system and bloodstream. LG is known as a causative or contributing factor in various health conditions such as chronic fatigue, allergies, arthritis, autoimmune diseases/disorders, and other inflammatory diseases.

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The detection of candida can occur from various laboratory methods such as serum antibody testing and stool analysis identification. Often a stool analysis may not show the existence of candida, but when organic acid testing is done the presence of invasive candida is recognized through the measurement of arabinose. Unfortunately, some conventional medicine practitioners overlook the existence of candida that may show up in stool testing and even push aside the existence of elevated immunoglobulin G analysis based on the notion that “everyone has candida in their body” (author’s emphasis).

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Organic acids are metabolic compounds containing carbon, oxygen, and other atoms such as hydrogen, sulfur, and nitrogen. They are naturally occurring compounds linked to cellular metabolism and may be elevated because of problems in biochemical processing.

Many organic acids are produced by bacteria, candida, and other fungal organisms in the digestive system. These gut-produced organic acids get absorbed systemically then highly concentrate in the urine. They are measured through a laboratory profile called an Organic Acids Test (OAT). Certain organic acids from fungal metabolism represent overgrowth within the digestive tract, while the previously discussed arabinose is linked to the invasive nature of candida at the mucosal level. Arabinose is a prevalent marker seen on the OAT.

In the stool collection method, fecal samples are analyzed by microscopic visual appearance of yeast, as well as growth of the organisms in a culture medium. Being that candida and other forms of yeast are common to the digestive system, it is not unusual to see a positive finding on microscopy. This is commonly listed as “moderate” or “many” yeasts detected, but the actual type of species is determined by stool culture analysis.

The culture component is specific in isolating which type of organisms are present. For example, Candida albicans is the most common type of candida found in the digestive system, but the culture method may detect others such as Candida glabrata or Candida tropicalis.

One of the benefits of differentiating candida types through culture is the ability of the lab to provide sensitivity testing that can help determine which botanical or medication is most effective in eradicating the organism. As mentioned previously, stool analysis for candidiasis through culture is not 100% effective and miss detection even though an individual may be symptomatic of candida overgrowth. It is common to see elevated arabinose on the OAT, while the stool culture for candida is not detected.

Some labs provide polymerase chain reaction (PCR) analysis for candida detection. PCR technology helps make billions of copies of DNA accessible for study (13).  Unfortunately, PCR testing does not differentiate between non-viable (non-living, not capable of reproducing) from viable (capable of reproduction) candida. Other considerations regarding PCR testing are that it can detect multiple pathogens but may not differentiate the causative organism and it may show false positives if the stool sample is collected too soon after previous antifungal treatment.


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Chronic candidiasis can be a challenging condition for many individuals. Effective intervention requires reliable diagnostic testing, as well as understanding the various pathogenic mechanisms inherent to these sophisticated organisms. 

There are many testing options available for the detection of intestinal candida that can determine overgrowth and the degree of invasiveness. Candidiasis, defined as a fungal infection linked to any form of candida species that is detected via serum, stool or organic acid analysis does not necessarily indicate that a patient is suffering from candidemia which is linked to actual intact fungal organisms cultured from the bloodstream. Unfortunately, blood cultures for candida are often unreliable (14) but understanding the clinical application of the methods discussed in this article can provide specific data to help identify individuals clinically affected by candida overgrowth.

In short, the organic acids test is a preferred option because it shows mucosal reactivity to invasive candida even when a stool analysis reports no evidence of candida overgrowth. Often, a serum IgG test will report high levels of candida which may correlate with an elevated arabinose on the OAT.  However, this is not always the case. Therefore, my preference is to use the OAT as a primary test for candida assessment and incorporate stool analysis and/or serum testing as complementary methods.


In May 2021, Integrative Medicine Academy will be hosting a comprehensive online course designed for health professionals on the topic of chronic candidiasis and related fungal infections as they relate to various chronic health conditions. This course will cover details on laboratory detection of candida, mechanisms of pathogenicity, and various treatment strategies. For more information, please visit Candida Mastery Coursehttps://candidamasterycourse.com.


References

1. Candidiasis. Fungal Diseases. United States: Centers for Disease Control and Prevention. 13 November 2019. 
2. Candida infections of the mouth, throat, and esophagus. Fungal Diseases. United States: Centers for Disease Control and Prevention. 13 November 2019. 
3. Symptoms of Oral Candidiasis. cdc.gov. February 13, 2014. Archived from the original on 29 December 2014. 
4. Candidiasis. cdc.gov. February 13, 2014. Archived from the original on 29 December 2014. 
5. Martins N, Ferreira IC, Barros L, Silva S, Henriques M. Candidiasis: predisposing factors, prevention, diagnosis and alternative treatment. Mycopathologia. 2014. 177 (5–6): 223–40.
6. Sell D, Monnier V. Structure elucidation of a senescence cross-link from human extracellular matrix. Implication of pentoses in the aging process. J Biol Chem. 1989;264(36): 21597-21602.
7. Kiehn T, Bernard E, Gold J, Armstrong D. Candidiasis: detection by gas-liquid chromatography of D-arabinitol, a fungal metabolite, in human serum. Science. 1979; 206(4418): 577-580.
8. Shaw W, Kassen E, Chaves E. Increased excretion of analogs of Krebs cycle metabolites and arabinose in two brothers with autistic features. Clin Chem. 1995;41(8):1094-1104.
9. Sell D, Monnier V. Structure elucidation of a senescence cross-link from human extracellular matrix. Implication of pentoses in the aging process. J Biol Chem. 1989;264(36): 21597-21602.
10. Smith MA, Taneda S, Richey PL, et al. Advanced Maillard reaction end products are associated with Alzheimer disease pathology. Proc Natl. Acad. Sci U S A. 1994; 91(12): 5710-5714.  
11. Mahler H, Cordes E. Biological Chemistry. 1966; Harper and Row, NY. Pgs 322-375.
12. Ludovic Giloteaux, Julia K. Goodrich, William A. Walters, Susan M. Levine, Ruth E. Ley, Maureen R. Hanson. Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome. Microbiome, 2016.
13. Saiki, R.; Gelfand, D.; Stoffel, S.; Scharf, S.; Higuchi, R.; Horn, G.; Mullis, K.; Erlich, H. Primer-directed enzymatic amplification of DNA with a thermostable DNA polymerase. 1988; Science. 239 (4839): 487–491. 
14. Cornelius J. Clancy and M. Hong Nguyen. Finding the Missing 50%” of Invasive Candidiasis: How Nonculture Diagnostics Will Improve Understanding of Disease Spectrum and Transform Patient Care, 2013-04-04 Oxford Journals, Medicine & Health, Clinical Infectious Diseases, Volume 56, Issue 9 Pp. 1284-1292.
87–92

IgG FOOD MAP FAQs

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LINDSAY GODDARD, MS, RDN, LD

Great Plains Laboratory recently launched a new IgG panel, utilizing an upgraded methodology with additional food antigens. I want to take this opportunity to answer some frequently asked questions, in the hopes it will save some time in literature reviews and data interpretation of results. I’ve provided an overview of IgG testing here, but to reduce repetition and for more information on methodology, please visit the main page for the IgG testing.

Why IgG?

When trying to heal the system, or relieve idiopathic symptoms, identifying food sensitivities can be a piece to the puzzle, or sometimes the direct cause. When IgG immune complexes are over produced due to a specific antigen, and unable to clear, they can cause significant inflammation throughout the body. IgG Food Sensitivity testing can be a simple and effective way to identify foods that are causing an inflammatory response without having to implement an elimination/reintroduction diet, which can take a significant amount of time and effort. This is especially true since reactions to foods can take up to several days to create noticeable symptoms. Furthermore, testing for IgG reactivity has numerous published case reports showing positive results with implementation.

What’s new about this test?

Prior to this, our laboratory used the long-accepted ELISA methodology, but when a substantially improved method becomes available, it is important to evolve. Our new XMAP technology increases the precision of identification by using intense signaling from fluorescents; the testing procedure is fully automated for greater precision and reliability, produces less waste by using multiplexed magnetic beads and requires less blood to run the sample for easier collection. We have also added specific allergens to problematic food categories, providing a more inclusive panel.

Why are Candida albicans and Saccharomyces cerevisiae on separate reports?

Yeasts’ primary antigens are not appropriate for protein-specific assays because their antigens are richer in glycans. Therefore, ELISA is the better methodology for assessing the immune response as it relates to yeasts, so sub-samples are run on separate equipment, generating a separate report. We are still able to use the same sample for both methods.

How does it compare to other food sensitivity testing?

There are several tests available, employing different methodologies, all claiming to be the best for food sensitivities. Below is a table that describes the differences, and how they compare with IgG.

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It should be noted that GPL includes all 4 subtypes of IgGs, to ensure more accuracy and we are only measuring IgG levels responses, not IgAs, since IgA is unable to bind complement and trigger generalized inflammation. To read more about why this is important, CLICK HERE

What is meat glue?

Meat glue is one of the new antigens on the test, interestingly enough, it is common for it to be elevated. Its source seems to be a bit obscure to some, but there may be more to the story than just an addition to processed foods. Meat glue is the transglutaminase enzyme, which can be derived from multiple sources: animals (vertebrates and invertebrates), plants, and bacteria (mainly the Streptoverticillium sp), the latter being the most common sourcing in commercial food products. Culinarily speaking, it is helpful in forming isopeptides between proteins, increasing viscosity, elasticity, firmness, and water-binding capacity in foods. The most common source of meat glue is in processed or imitation meat, cheese and other dairy products, and baked goods. Since it is considered vegan when derived from plants or bacteria, it may be in some plant-based products, as well. If you are trying to avoid meat glue, look for TG enzyme or TGP enzyme in the ingredients. Also be aware of manufactured meats, and meats described as reformed or formed. The USDA requires all companies disclose this ingredient on the food label, and there are no exemptions.  

Transglutaminase is also involved in our biological chemistry. Transglutaminases are a family of enzymes categorized as transferases and mainly catalyze isopeptide bond formation, which can be difficult to degrade.  You know, kind of like glue. They are found in several organs, and their specific functionality is dependent on their location: intracellular versus extracellular, as well as the type of tissue. For example, intracellular tissue transglutaminase plays an important role in apoptosis, while extracellular tissue transglutaminase can influence extracellular matrix stabilization, likely from its ability to bind fibronectin.

Although transglutaminase enzymes are diverse, they do have significance in several diseases. The disease most associated with this enzyme is celiac disease. Tissue transglutaminase cross links to gluten, stimulating a specific B-cell response that can result in production of anti-transglutaminase antibodies, which are measured as a part of the diagnosis of Celiac. The dysregulation that follows may impact the intestinal lining, causing the structural changes seen in Celiac disease.  A high reactivity to meat glue on the IgG test is not diagnostic of Celiac Disease, but can provide justification of further testing of anti-transglutaminase antibodies if other factors are pointing to Celiac as well.

Why are there different derivatives of the same food?

First, it will be helpful to review how food proteins, which can serve as food antigens, bind to antibodies.

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Adapted from Fundamentals and Methods for T- and B- Cell Epitope Prediction. Sanchez-Trincado JL,  Gomez-Perosanz M, Reche PA. Journal of Immunology Research, vol. 2017

In this figure, we can see that on the antigen, the epitopes (i.e., where the antibody molecules dock) are very specific and end up with somewhat different structures, even though they may originally be from the same source. This is in part because protein structure can change significantly during food processing, potentially creating structures and epitopes so different they are not recognized by antibodies nor do they bind.

Measuring various components of a food allows for more detailed analysis as to which compound may be causing the inflammatory response, as well as increasing specificity and decreasing the chance of missing a potential source of inflammation. This not only pertains to the dairy section (cows’ and goats’ milk, casein, whey, beta-lactoglobulin, sheep’s yogurt, yogurt, mozzarella and cheddar cheese), but also gluten components (Wheat gluten, whole wheat, gliadin, barley, rye), and  pineapple components (bromelain).

Does the casein differentiate between A1 vs A2 Casein?

No. The ability to differentiate between A1 and A2 caseins is not possible at this time.

If I stopped eating a particular food, and it is not showing up on the results as a problem, do I still need to remove it?

It can take up to 6 months after removing a food from the diet to not see an elevated IgG response to that particular food antigen. If a person is not consuming the food (or hasn’t done so in over 6 months), it likely will not trigger a large immune response, and will not show up as elevated on the test. A low reactivity to a certain food does not indicate that the person is now able to tolerate it or that the food can be safely reintroduced. It only means they have been vigilant in keeping it out of their diet. On the other hand, if the person has abstained from consuming a specific food and it does show positive on the test, then cross contamination with structurally similar proteins in the diet is likely the culprit.

Will the lipid derivative of foods on the IgG test be a problem?

The IgG response is to proteins, not lipids. However, people often question if they are sensitive to casein, can they consume butter? Or if they are sensitive to soy, can they consume soy lecithin? During the processing of extraction for these components, trace levels have been found of the corresponding protein, however, the protein is in such small amounts it is unlikely to be a problem. Most people seem to be able to tolerate it, though there are a select few who do not. An elimination/reintroduction phase may be helpful for further investigation in those rare cases.

Hopefully, this blog helps answer some of the common questions. If you still need help before ordering, you may contact customer service, or if you have a result that you need help interpreting, please schedule a consultation with the consultant staff.


Resources: 
1. Sanchez-Trincado JL, Gomez-Perosanz M, Reche PA, "Fundamentals and Methods for T- and B-Cell Epitope Prediction", Journal of Immunology Research, vol. 2017, Article ID 2680160, 14 pages, 2017. SOURCE
2. Kemeny DM, et al Sub-class of IgG in allergic disease. I. IgG sub-class antibodies in immediate and non-immediate food allergy. Clin Allergy. 1986; 16:571-81.
3. Williams F. Use of the LEAP mediator release test to identify non-IgE mediated immunologic food reactions that trigger diarrhea predominant IBS symptoms results in marked improvement of symptoms through use of an elimination diet. American Journal of Gastroenterology: October 2004 – Volume 99 – Issue – P S277-S278. SOURCE.
4. Lomangino, Kevin Food Sensitivity Testing: Evidence-Based Practice or Pricey Placebo?, Clinical Nutrition Insight: March 2013 - Volume 39 - Issue 3 - p 1-5 doi: 10.1097/01.NMD.0000428066.22177.2
5. Mullin, GE, Swift, KM, Lipski L, Turnbull LK, Rampertab SD. Testing for Food Reactions: The Good, the Bad, and the Ugly. Nutrition in Clinical Practice: April 2010-Volume 25-Issue 2-pg192-198 SOURCE
6. Kieliszek M, Misiewicz A. Microbial transglutaminase and its application in the food industry. A review. Folia Microbiol (Praha). 2014;59(3):241-250. doi:10.1007/s12223-013-0287-x
7. United States Department of Agriculture, Food Safety and Inspection Service. Safety of Transglutaminase Enzyme (TG enzyme). 2017. SOURCE
8. Sakly W, Thomas V, Quash G, El Alaoui S. A role for tissue transglutaminase in alpha-gliadin peptide cytotoxicity. Clin Exp Immunol. 2006 Dec;146(3):550-8. doi: 10.1111/j.1365-2249.2006.03236.x. PMID: 17100777
9. Patel S, Patel H. Technical Report: Understanding the Role of Dairy Proteins in Ingredient and Product Performance. U.S. Dairy Export Council. 2015. DMICMAIM5063_Dairy_Protein_Report_r6.pdf
10. Griffin M, Casadio R, Bergamini CM. Transglutaminases: nature's biological glues. Biochem J. 2002 Dec 1;368(Pt 2):377-96. doi: 10.1042/BJ20021234. PMID: 12366374

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5 Herbal Agents for Antifungal Therapy

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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.

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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.

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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. 

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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. 

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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.

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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

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Webinar Recap: Clinical Considerations of Chronic Candidiasis

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By Kurt Woeller, DO

Various candida organisms can be a normal inhabitant of the digestive system and part of our microbiome in low levels. However, candida has the potential to overpopulate the bowel leading to various symptoms of bloating, gas, constipation, etc. Candida can also become invasive within the digestive system leading to leaky gut increase immune activity and systemic reactivity. This lecture will highlight unique aspects of candidiasis, including certain pathogenicity mechanisms, laboratory tests, and treatment interventions.

The full webinar can be viewed here:


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During the course of the Webinar, individuals were able to ask questions of the speaker. Because of time constraints, not all the questions were able to be answered in real time. We are happily able to answer those questions below:

Q: One of the slides about vulvodynia mentions adding oral calcium citrate. I have two questions:
1. How does adding calcium reduce oxalates? I thought the oxalate combines with calcium to cause the calcium oxalate crystals, which can cause vulvodynia.
2. Are other forms of calcium also effective such as calcium magnesium or maleate?

A: The calcium citrate helps with oxalate binding in the digestive system preventing it from being absorbed. Once the salt is formed in the gut it doesn’t get absorbed. Instead, it is released out of the body in the stool. The citrate component helps with moving more oxalate out of the digestive cells into the lumen of the gut where is can combine with the calcium. This, along with a low oxalate diet, lessons the total body load of oxalate. Therefore, there will be less to react at the tissue level. Other forms of calcium and magnesium do not appear to be as effective as calcium citrate and magnesium citrate.

Q: Will a plant based diet make candida worse? Is coconut oil bad for candida? Heard it increases leaky gut.

A: In general, a plant-based diet would be better as it helps to improve the diversity of the microbiome. I am not sure about coconut oil, but not likely to make it worse.