Byron White Herbal Formulas

The Byron White Formula A-FNG And Chronic Fungal Infections

Biology
There are thousands of members of the fungi community including mold, mildew and yeast. They are nature’s decomposers recycling organic material through a complex enzymatic process that breaks down complex biopolymers such as starch and cellulose. Molds reproduce through spores that can survive hard conditions waiting for moisture to activate their growth process. Spores can be airborne traveling great distances and attach to our mucous membrane.

The immense Fungal Kingdom has members that have important beneficial applications both for medication and food. They can be simple irritants as in airborne allergies, or can cause a variety of delayed chronic immune mediated reactions resulting in chronic fatigue-like symptoms.

Mold organisms colonize on our skin and the surface of our mucous membrane including the sinuses, throat, lungs, gut, vagina, and the lining of the bladder. The immune system will not allow mold to survive in the body. Only in severely compromised patients with cancer or AIDS will mold be active in the blood.

Pathogenicity of Mold and Yeast
There is still much to learn about the pathogenicity of mold and yeast organisms. Very generally mycosis (fungal infection or disease) can be problematic in three ways.

1. Acute (immediate, IgM) reaction: Local irritants from airborne exposure to the mucous membrane causing an immediate allergic reaction.
2. Chronic (delayed, IgG) reaction: The colonized mold or yeast on our mucous membrane secretes a waste produce that is absorbed into the blood.
3. Hypersensitivity (immediate or delayed) IgG reaction: An excessive or hypersensitivity immune response after exposure.

The Main Theory of Biotoxin Illness
Dr Shoemaker in Mold Warriors said, “The pathway includes the dynamic interaction of genetics, cytokines, autoantibodies, vascular growth factors, central hypothalamic hormones, pituitary hormones, peripheral honorees and opportunistic growing microbes.”

Mold as a member of the Neurotoxin Family
Many of the pathogenic (toxin excreting) mold and yeast species secrete neurotoxins as a byproduct of their metabolism. These toxins can be located on the mucosal membrane or be excreted into the blood to be absorbed into the cell.

The Neurotoxin Family includes:

• The mold and yeast organism that have this excreted toxin.
• Lyme disease.
• The co-infections (Babesia, Bartonella, Mycoplasma, Erhlichia, Rocky Mountain Spotted Fever just to name a few).
• Chemical toxins including pesticides, insectides and solvents.
• Heavy metal.

Many of our patient with difficult to treat, multi-system, multi-symptom illness have chronic mold infection along with other members of the Neurotoxin Family.

Chronic Fungal Infections (Mycosis) along with Neurotoxin Family shared a Common Mechanism of Action.
When colonized on the mucous membrane these irritants can result in local inflammation. When these toxins find their way inside the cells these same inflammatory effects of can cause systemic symptoms that can be very similar to the Chronic Lyme disease patient. The family of neurotoxins shares these characteristics:

• Symptoms are related to inflammation.
• They are lipophilic (they stick to our fat).
• They absorb through the bi-lipid membrane to deposit inside the cell.
• They disrupt cell function.
• They have an additive inflammatory effect.
• They compromise homeostasis.
• They disrupt the brain and nervous system, endocrine system, immune system and gut.

The patient with a chronic mold overgrowth and the patient with Lyme disease can have many of the same symptoms. Both target the brain and nervous system as these fat-loving globs have an affinity for the fat of the brain. They have a synergistic effect, disrupting energy, memory, behavior, and sleep, among others.

The immune suppressing effect of having a Borrelia infection can predispose a patient to have a more active fungal infection. Patients with Lyme disease often have fungal related problems, as do patients with chronic fungal overgrowth are more likely to have a more aggressive Lyme infection.

Differential Diagnosis of Chronic Fungal Infections.
Differential Diagnosis: Signs and symptoms of mycosis can be local and/or systemic. They often simultaneously affect multiple organ systems and defy conventional diagnosis and lab test. Treatment protocols are often ineffective.

Superficial symptoms: Chronic sinusitis, stuffy nose, otitis media and externus, sore throat, cough, asthma, SOB, esophogitis, nausea, belching, abdominal bloating, gas, IBS, anal itching, vaginosis, vaginitis, cystitis, frequent and urgent urination, skin lesions, irritations and itching, opacity of the nails.

Systemic symptoms: Chronic fatigue is common. Significant depression with sleep disturbance, anxiety states and mood swings. Mycotoxin related neuropathy with bilateral numbness and tingling, which does not follow dermatome nerve distribution. Behavioral disorders, difficulty learning, autism, memory and concentration dysfunction, headaches, must be considered related to these pathogens.

Summary of Mycosis Symptomatic Presentation.
Think mold when a patient has inflammation of the mucous membrane and neurological symptoms.

• The patient’s mucous membrane symptoms often involve the sinuses, sore throat, asthma, allergies, IBS with gas and bloating, vaginitis, urgency to urinate.
• These areas are itchy and irritated.
• These inflamed areas are worse in the winter or during the wet season.
• Symptoms are worse with mold exposure.
• When the mood is dark and depressed.
• Can have disruptive effects on behavior, attention, and learning.
• Pain is usually mild and bilateral.

Mold must be considered in the differential diagnosis of any neurological symptom from simple neuropathy to seizures.

Considering the Diagnosis.

First: We need to have to a high index of suspicion for chronic mold infection in our “wired-tired” patients. Patients that already have a diagnosis of Chronic Fatigue Syndrome, Fibromyalgia, Lyme disease, allergic or chemical sensitivity, autoimmune diseases will likely have concomitant fungal infections.

Second: (General principle) “There is wisdom in our patient’s symptom presentation.” Our immune system is prioritizing as best to protect us. As practitioners it is our responsibility to interpret it’s signs and symptoms.

Third: (General Principle) “Mold as well as other neurotoxin illness can have a disruptive effect on the endocrine and immune system.” Variability’s and inconsistencies in the following labs can be indicators of Neurotoxin illness.

Useful Labs:
Mold Antibodies: Esoterics (LabCorp) Mold IgG Antibodies.
Genetic: HLA-DRB, Methylation Panel, KPU, HPL.

Immune System: Complements C4a, C3a, TNF alpha, MMP9, IL-1B, IL-6, CRP, Total IgE Total IgG and subsets.

Hypothalamic Hormones: MSH, Leptin.
Pituitary Hormones: ADH, ACTH, TSH, and urine Osmo.
Peripheral Hormones: Cortisol, DHEA-S, Testosterone, fT3, fT4, Total T3/Reverse T3.

Opportunistic Organisms: Gastrointestinal evaluation for parasites, mold opportunistic and bacteria by saliva and stool.

MARCoNS (Multiply antibiotic resistant coagulase negative staphylococci- biofilm producing bacteria) evaluated by nasal swab and culture.

Autoimmune antibodies: ANA, Anticardiolipin, Myelin Basic Protein, Antigliadin, Tissue Trans-Glutaminase IgA, TPO, Antithyroglobulin antibodies.

Others: Erythropoietin, VEGF (Vascular Endothelial Growth Factor), VIP (Vasoactive Intestinal Peptide).
Visual Contrast Screening (VCS)

Is this patient’s fungal overgrowth their primary or secondary problem?
General Principle: “Patients with the same exposure will be affected by their individual strengths and weaknesses.”
As a way to prioritize treatment protocols I find HLA-DRB, is a marker for the patients predisposition to fungal infections. With defects in these allele strands they can be genetically susceptible to biotoxin illness. This can identify patients who lack the antibody producing capacity to adequately defend themselves from mold overgrowth and toxins. (Needs to be done at LabCorp #012542, ICD-9: 297.10)

T helper 17 role in Cell Mediated Response.
A new model of cell-mediated immunity could give us a better understanding into the systems response to mold. Th 17 stimulates tissue inflammation by proinflammatory cytokines IL-6, TNFa and chemokines that recruit macrophages and neutrophils to the site of inflammation. This pathologic inflammatory IgG response is mediated by IL-17, IL-23 and IL-22.

Confirming the Diagnosis with A-FNG.
General Principle: The patient’s predicted response to a isolated variable challenge is the only way to confirm the diagnosis. After doing a complete assessment of the patient, taking a comprehensive history, physical exam and laboratory assessment you have arrived at a possible diagnosis. Now is time to challenge with a therapeutic variable that is specific to fungal pathogens. In my experience the BWF product A-FNG can be used for this purpose.

Challenge Protocol using A-FNG
Step 1: Start with 1 to 5 drops, 2 times daily, of this herbal energized extract depending on the sensitivity of your patient.
Step 2: Increase quickly, again depending on the patient’s sensitivity, but quick enough that you will elicit a response. If it is a provoking variable there should be an aggravation (Jarisch-Herxheimer) response. An average increase during this challenge phase could be 2 to 5 drops (2 x daily), every 3 to 5 days, to a maximum dose to 20 droops 2 times daily.
Step 3: Instruct the patient to report their specific aggravated symptoms along with their intensity and duration.
Step 4: If the aggravated response is too disruptive, the patient can stop the challenge, or lower the number of drops and there should be a 1 to 3 day washout of symptoms, bringing the patients symptoms back to their pre challenge baseline.
Step 5: If the patient is unsure if the worsening of their symptoms was related to the provoking agent then go back to the same dose that caused the aggravation. If the response if the same this is as good as it gets at confirming the diagnosis.

Symptoms to look for as a Herx response to A-FNG.
These should be the very symptoms that resulted in the consideration of mold and its toxins. The most consistent symptom is depression, as the brain is very sensitive to fungal die-off. And any neurologic symptom and/or mucous membrane irritation should be considered. The individual patients Herx response will represent their Target Symptoms and will be predictable to follow during the course of treatment.

Treatment Protocol.
After confirming fungal as the pathogens that the immune systems is currently prioritizing, it is time to treat it.
Step 1: Instruct the patient to go back to a low dose of A-FNG. This should be well below the number of drops that resulted in their Target Symptoms. This could be one drop 2 x daily, or 10 drops 2-x daily, depending on the patient’s response to the Challenge Protocol.
Step 2: From this non-provoking dose increase the number of drops slowly by one drop two times daily. At this gradually increase dose the patient will become aware of the early signs of their symptoms being stirred up. Upon the first awareness of this the patient should hold at that dose and observe these symptoms ease.
Step 3: After the patient experiences a plateau of their Target Symptoms, they can go up by one-drop 2-x daily. This should result in a minor response to the same symptoms.
Step 4: Continue this gradual increase to a maximum of 20 drops 2-x daily.

Post Treatment Provocation with A-FNG.
After stabilizing on 20 drops 2-x daily the patient could experience a significant improvement in mold toxin related symptoms. At this point another challenge could give further information about the patients need for further treatment, Step 1: Increase the number of A-FNG drops from 20 drops 2-x daily to 25 drops 2-x daily. An aggravated response could mean further work is needed on this patients biotoxin load. Step 2: If the patient has an uncomfortable aggravation in their target symptoms then go down to 20 or 21 drop 2-xdaily and continue to move up slowly. Step 3: If the patients experiences mild but tolerable aggravation of their target symptoms they can go to 30 drops 2-x daily for additional therapeutic response.

The Role of the Jarisch-Herxheimer Response.
When we have found the provoking agent that is appropriate for this individual patient they will have a characteristic Herx response. We now understand this to be the activation of immune cytokines as the immune system is stimulated into improved awareness of these intracellular pathogens. This flood of cytokines can result in an excessive reaction of inflammatory symptoms. It is unnecessary to over provoke this response. Not only is the patient uncomfortable but also it can be disruptive to the immune system. If we can unload these toxins in a systematic way the immune system can continue to maintain homeostasis. Having an agent that can be effective with a sliding dosage has obvious value both therapeutically and for patient compliance