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General Mitochondrial & Wellness Protocol
(Technical Edition)
by
Joshua Leisk | (@joshual_tm on X/Twitter)
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Summary
This is an experimental protocol based on the disease model by Leisk et al., (preview here - https://bornfree.life/2024/the-disease-model/) which may be helpful for supporting the unique nutritional and wellness / lifestyle requirements of teenagers and adults with chronic illnesses that share various common features, including mitochrondrial dysfunction, hormone dysregulation, ferritin and other mineral deficiencies, microbiome dysbiosis, biofilms, neurotransmitter regulation and immune dysregulation, etc., such as:
| Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME/CFS) | Long COVID, Post-Vaccine Syndrome | Viral / Post-Viral Chronic Fatigue |
| Post-Exertional Malaise (PEM) | “Floxed” | Guillain-Barre syndrome (GBS) |
| Chronic Inflammatory Response Syndrome (CIRS) | Breathlessness | Hypoxia |
| Acidosis / Alkalosis / pH Dysregulation | Dysregulated Cortisol | Dyslipidemia |
| Post Finasteride Syndrome (PFS) | Post SSRI Sexual Dysfunction (PSSD) | Post Accutane Syndrome |
| Small Fibre Peripheral Neuropathy (SFPN) | Mast Cell Activation Syndrome (MCAS) | Diamine Oxidase (DAO) Deficiency |
| Stiff Person Syndrome | Gut Fermentation Syndrome | Glycogen Storage Disease (functional) |
| Histamine intolerance | Brain Fog | Sleep disorders |
| Anxiety | Postural Orthostatic Tachycardia Syndrome (POTS) | Autism Spectrum Disorders (ASD) |
| Fibromyalgia | Dysautonomia | Frequent Urination |
| GI Disorders | “Small Intestinal Bowel Overgrowth” (SIBO) | Vitamin B6 Toxicity |
| Vitamin A Toxicity | Candidiasis | Aspergillosis |
| Ehlers Danlos Syndrome (EDS) | Joint Pain | Connective Tissue Disorders |
| Tinnitus | Polycystic Ovary Syndrome (PCOS) | Erectile Dysfunction |
| Elevated Cholesterols / Fasting Glucose / D-Dimer | Hashimotos | Alopecia |
| Major and other types of Depression | Cataracts | Migraines |
Contents
Warning: This documentation contains a significant amount of information and it is expected that you will need multiple read-throughs and a number of hours to absorb and / or action the information.
How to Navigate This Information
There are multiple ways to approach this material:
First Reading: We suggest that you read everything from start to finish in a linear fashion. This will help you become acquainted with all of the concepts.
Guided Navigation: If you decide to act on the information, return here and use the visual navigation tool below to step through the protocol in a logical and structured manner.
- AI-supported (experimental): If you would like AI assistance in understanding the model and/or protocol, Google's NotebookLM is able to perform this function for free. A setup guide is available here - https://bornfree.life/2024/notebooklm-ai/
Disclaimer
Please read this entire document before taking any action based on its contents.
Important Notice:
While we strive to minimize adverse effects, you may experience some temporary symptoms when starting this protocol:
- Paradoxical Effects: As deficiencies are corrected and neurotransmitter balance is restored, you might notice short-term increases in adrenaline and heart rate.
- Copper Deficiency Correction: Addressing a severe copper deficiency may cause temporary kidney pain and nausea.
- Immune Activity Increase: An initial boost in energy availability can heighten immune activity and symptom severity. This might be psychologically challenging and may cause hesitation in continuing the process.
- Herxheimer Reactions: You may experience effects from microbial die-off, such as increased "burning" sensations and headaches.
- Hormonal Changes: Temporary changes in libido or menstrual cycles can occur.
- Inflammation and Flu-like Symptoms: Improvements in adaptive immune function might lead to brief periods of inflammation, fever, flu-like symptoms, nausea, and fatigue.
Support:
We host an online discussion and support group on Discord. Feel free to join us:
Monitoring Recommendations:
In addition to the tests used in the protocol, we suggest regular blood tests to monitor:
- D-dimer Levels
- Vitamin B6 Levels
- Cholesterol Levels
- Fasting Glucose Levels
This protocol is for research and educational purposes only. Always consult your doctor to determine if this information is appropriate for you, especially if you are taking medications like SNRIs/SSRIs, beta-blockers, MAO inhibitors, or drugs metabolized by CYP2D6 enzymes.
Overview of the Protocol
This protocol is based on a disease model that identifies a blind spot in the immune system as the root cause of certain syndromes. This gap allows harmful microorganisms to hide within biofilms located in mucosal and other tissues such as the nose, mouth, lungs, gut, sex organs, and even the bloodstream. These biofilms can begin forming in small quantities early in childhood. Under normal circumstances, they grow slowly over many years and are now being associated with aging processes. Various immunological events can rapidly accelerate biofilm growth.
Formation and Growth of Biofilms
The immune system typically halts biofilm growth by detecting and attacking microorganisms during their free-moving (planktonic) stage outside the biofilms. However, this defense can be compromised by factors such as infections, injections, drugs, trauma, malnutrition, and stress.
Toxins and Immune Response
A primary toxin produced by these bacteria is acetaldehyde, which is also a byproduct of alcohol metabolism, as seen in Gut Fermentation Syndrome. This toxin interferes with energy production and affects the immune system and gut lining. The disruption allows more microorganisms to breach bodily barriers, triggering an innate immune response involving interferon-gamma (IFN-γ) and reactive oxygen species to eliminate them. Other endotoxins and mycotoxins have relevance, also.
Challenges in Diagnosis and Treatment
Chronic inflammation can turn functional mineral deficiencies into long-term systemic issues. Measuring intracellular minerals during chronic inflammation is problematic due to altered transporter behavior in cell membranes, in different tissues. The cyclic nature of the disease and impaired absorption in the duodenum make it challenging to correct deficiencies through diet or oral supplements. Absorption and homeostasis of up to ten metals may be inhibited at different times, depending on inflammatory states and signaling.
Ongoing Research Insights
Our ongoing research has found that IFN-γ immune dysregulation and a persistent cyclic inflammatory process involving a peptide hormone called hepcidin disrupt homeostasis for at least 11 biologically active metals. These metals rely on common transporters: divalent metal transporter 1 (DMT-1) and ferroportin.
Additional mineral deficiencies have been observed. eg. Silicon may be excreted or depleted as a microorganism-produced Si-acetaldehyde compound. Dietary restrictions and toxins produced by bacteria or fungi can also alter zinc and other mineral homeostasis. Mineral deficiencies can create cascades of other issues; for example, lithium and rubidium deficiencies can worsen catecholamine metabolism and kidney function. Kidney problems may lead to electrolyte deficiencies, disrupting energy metabolism, neurotransmitter function, immune activity, and muscle contractions—including those of the heart and skeletal muscles.
Mineral Deficiencies and Dysregulation
Specific mineral deficiencies can disrupt your immune response, leading to further energy dysregulation and damage to nearby cells and tissues. This results in severe imbalances in the gut and other microbiomes, weakening the immune system.
Additional Dysregulations
This complex cascade
affects neurotransmitters, cortisol levels, vitamin B6, cholesterol,
histamine, hormones, kidney function, and body temperature regulation,
among others.
Reversing the Trajectory
To reverse this progression, several key issues need to be addressed:
Fixing mineral and other deficiencies is crucial, as it helps restore energy production, manage oxidative stress, and resolve issues with chronic human herpesviruses, among others.
Correcting imbalances in the microbiome, biofilms, and infections by treating all mucosal surfaces and the bloodstream. This removes reservoirs of pathogens and endotoxins. Employing lifestyle changes which cultivate healthy microbiomes helps create ongoing resilience against future dysbiosis / infections.
Addressing structural problems involving the lymphatic system and related structures can improve neural blood flow and reduce hypoxia.
Dealing with trauma and PTSD is also essential for complete recovery, as it addresses limbic system influences affecting neurotransmitters, energy metabolism, and immune activity.
Current Findings and Research
Early testing shows that some individuals achieve long-term remission, while others significantly improve on their way to remission. Clinical trials are currently being organised.
Broader Implications
This metabolic cascade appears in many infections and chronic conditions. Associated dysfunctions include severe mitochondrial dysfunction, low intracellular oxygen levels, nervous system dysfunction, histamine dysregulation, collagen synthesis issues, and immune deficiency. This is not an exhaustive list.
Future Directions
Elemental deficiency patterns can predict various disease features and severity when linked to related enzyme impairments. Ongoing improvements are continuously reflected in protocol updates.
This protocol involves several steps that require multiple tests and a wide range of important supplements. While the expected results are unlikely to be realized without completing all these steps, efforts have been made to simplify them as much as possible. The steps are as follows:
- Collect Your Data
- Lifestyle Changes
- Stage 1: Remineralization, increasing collagen synthesis rates, and performing a controlled initial “die-off” (at least two weeks)
- Stage 2: Enhanced gastrointestinal and mucosal interventions (at least two weeks)
- Stage 3: Stimulate and support a strong immune response while breaking (circulating) biofilms (at least four weeks)
- Optional Follow-Up
- Ongoing Preventative Maintenance
We fully anticipate that individuals exploring this protocol may be highly sensitive to supplements. The reasons for this sensitivity are detailed in the disease model and have been accounted for within the protocol. The sensitivity to supplements and foods is expected to resolve as part of the protocol.
This protocol is designed to stimulate immune activity and may produce a “J-curve” trajectory, meaning you might feel progressively "quite sick" at the beginning of each stage. Increasing energy availability allows for heightened immune activity, which prioritizes energy metabolism toward these goals and can temporarily intensify symptoms. Carefully maintaining levels of electrolytes, copper, zinc, iron, manganese, selenium, glycogen, and B vitamins may help prevent severe symptoms and post-exertional malaise (PEM) or "crashing."
Your individual experience may vary based on factors such as the pace of protocol implementation, the pathogens involved, your initial baseline condition, and the consistency and accuracy of your daily participation. Avoiding or delaying parts of the protocol can hinder progress and potentially lead to unnecessary discomfort. Support is available through our Discord discussion group.
Before beginning, assess your lymphatic system as described in the “2.2.2 Lymphatic Maintenance” section. Note any tissues that have been or continue to be sore, stiff, or inflamed—these areas are expected to flare during increased immune activity and may be adjacent to other infected tissues.
To help reduce expected symptoms when correcting deficiencies and experiencing Herxheimer reactions (fungal die-off effects) due to improved immune activity, a recommended starting sequence has been provided.
The "die-off effect" can cause a range of temporary but highly debilitating symptoms, including headaches, nausea, additional fatigue, dizziness, swollen glands, bloating, gas, constipation or diarrhea, joint or muscle pain, tachycardia, chills, cold hands or feet, itchiness, rashes, sweating, and fever resembling the "disulfiram effect."
A schedule of specific products is available, with vendor website links provided for different regions (see “5. Ordering Products”). These are not affiliate marketing links. With the exception of the Oxalobacter.com
website (which was created out of necessity to address worldwide supply issues for
"Oxalobacter formigenes" probiotics and is not intended as a for-profit
endeavor), there are no financial incentives or benefits from providing links to products or tests. If you encounter supply shortages, please try to find the same product from another vendor or ask for help in the online Discord discussion group.
Deviating from the recommended starting order or substituting products may lead to avoidable and unpleasant symptoms or may simply be ineffective. You can space out the stages further if needed. Despite the extensive list of supplements—aside from one or two items included to make your experience more tolerable—all are necessary. Attempts to create a "lite" version of this protocol by swapping or omitting items have consistently resulted in failure.
Stage 1 focuses on delivering missing minerals and other nutrients to the body, sometimes via non-oral routes, to resolve measurable deficiencies caused by inhibited oral absorption of these micronutrients at levels typically found in foods. While this helps restore normal metabolism, these nutrients are also accessible to the microorganisms inhabiting your body. Therefore, an additional goal of selectivity is required, targeted by a combination of probiotics and antimicrobial interventions. Some of these interventions are included in Stage 1, while others are introduced in Stages 2 and 3.
It is not advisable to take the Stage 1 metabolic support supplements for an extended period without progressing to the parts of the protocol that address microbiome dysbiosis, such as dietary optimisation. Otherwise, you may feel increasingly better at first, but over time this may lead to amplification of existing microbiome issues. Nutrients that benefit your cells also benefit microorganisms that depend on you, and vice versa.
Fulvic Acid Usage
Fulvic acid is used in Stage 3 of the protocol. Due to its potent ability to "liberate" and recirculate metals sequestered during chronic inflammation; it is recommended to test your response to a single drop of Good State Ionic Man (fulvic acid multi-mineral) diluted in a glass of water during Stage 2. Increase the dosage slowly. Fulvic acid is also a potent biofilm breaker. If you experience any unpleasant effects, take a few days to gradually increase from a smaller dose—for example, place a drop in a bottle of water, mix it, and then transfer a drop from this first dilution into another glass of water—until you can consume a standard serving without adverse effects.
Nasal Inflammation Considerations
If you have nasal inflammation or notice any airway resistance or restriction when breathing, it may be appropriate to perform a nasal microbiome test. Unwanted microorganisms such as Candida, Aspergillus, Streptococcus, Staphylococcus, and Klebsiella species are sometimes found in the nasopharynx. These tests may also indicate the susceptibility of detected strains to interventions like fluconazole, itraconazole, voriconazole, or amoxicillin.
Aldehyde Metabolism Insufficiency
If your levels of magnesium, zinc, molybdenum, selenium, iron, iodine, or calcium are low, you may experience additional symptoms related to aldehyde metabolism insufficiency. These symptoms can be exacerbated by consuming excess alcohol, histamine, polyethylene glycol (PEG), vitamin A, or vitamin B6.
Issues with neurotransmitter metabolism, histamine regulation, and gut function are common and to be expected.
Correcting Deficiencies and Potential Effects
Correcting severe electrolyte deficiencies can temporarily create paradoxical effects, including increased metabolism rates and heart rate. Consuming certain minerals like copper or zinc on an empty stomach can easily induce nausea.
If taurine or magnesium affects your sleep or causes palpitations, tremors, or if you feel worse upon starting them, this may indicate a calcium deficiency. Adding 1–2 grams of elemental calcium per day, along with vitamin D3 and vitamin K2 MK-7, may help correct this. Be aware that addressing a calcium deficiency can initiate the process of oxalate dumping, which is necessary but may cause muscle pain. Low calcium levels may coincide with strontium and phosphorus deficiencies. The tests included in this protocol will help identify these issues. Low strontium levels in hair testing may serve as a proxy indication for calcium deficiency.
Correcting an iodine deficiency is likely to temporarily increase anti-thyroid peroxidase antibodies (anti-TPO) and Thyroid Stimulating Hormone (TSH), enhancing the activity of the sodium-iodide symporter (NIS) while improving levels of triiodothyronine (T3) and thyroxine (T4).
Simplifying Supplement Intake
We recognize that the extensive list of individual supplements required for this protocol presents a new challenge. We are collaborating with compounding pharmacies to simplify this process—transforming most of Stage 1 into two sublingual lozenges (troches) and a tub or bag of premixed powder. A DIY powder recipe is also included for those who prefer to mix their own.
Inositol and Glycogen Replenishment
Consuming mixed inositols will signal your cells to increase glucose uptake and glycogen synthesis, promoting glycolysis over other energy pathways. Inositol inhibits catalase, which may decrease your capacity to handle oxidative stress during immune activity, necessitating additional antioxidant support. If your liver and muscle glycogen stores are low—which is expected—you may initially feel extremely hungry or experience hypoglycemic symptoms such as dizziness, depression, and extreme fatigue. Consuming up to 500 grams of additional net carbohydrates and water over two to three days to replenish glycogen stores should help you feel significantly better. Glycogen binds with water at a 1:3 ratio, so your total body mass may increase by around 2 kilograms. Note that inositol can be problematic if you are following a ketogenic diet. D-chiro-inositol should be started at approximately 2.5 mg and very slowly increased as tolerated.
(Optional) Pre-protocol support
While getting started (ideally after sending off your baseline tests), you may help stabilise critical parts of the metabolism and help avoid unwanted MCAS + other symptoms by;
a) Consuming the suggested food items in 2.2.1 Diet.
b) Making a DIY "Sipper" of specific electrolytes and amino acids to put in a 500ml drink bottle and slowly sip between meals (see 4.1 Electrolytes and 4.3 DIY "shake" and "sipper"). You can start at 1/8 daily doses and increase. This can be combined with eg. green or other tea, lemon juice, lime juice, etc for flavour. (NB. Consuming too much at once may cause diarrhoea, headaches, nausea, water retention and/or rapid urination. Shake before each use, as dicalcium phosphate is largely insoluble.)
c) Taking [high dose Vitamin B1 as thiamine HCL, (sublingual) Vitamin B2 - FMN and (sublingual) Vitamin B3 - NMN] (or the compounded troches - see 4.2 Custom troches) at different times throughout the day.
d) Liberally applying the magnesium gel after showering, can be highly effective for magnesium absorption.
e) Working on your lymph flow - see 2.2.2 Lymphatic maintenance - this is especially important if addressing the electrolyte deficiencies allows immune activity to initially increase, which is more likely when these deficiencies are severe.
Product ordering links can be found in 5 Ordering products.
2.1 Collect your data
This protocol begins with a data collection process that helps you to identify specific deficiencies and microbial influences relevant to your metabolism.
There are multiple tests required to collect this data and the protocol is unlikely to succeed without them.
2.1.1 Blood tests
Testing blood is a helpful way to understand specific aspects of immune activity and metabolism. Minimally, it’s useful to have markers for blood group (needed for Oligoscan), red blood cell (RBC) and white blood cell (WBC) counts, comprehensive metabolic panel (CMP) and lipids, LDH isoenzymes, iron studies (iron, transferrin, transferrin saturation %, ferritin), vitamin B6 and vitamin D (inactive form). Your doctor is usually the best person to assist you with these, however private lab services are also available in many countries, should these be helpful.
USA
Australia
Lactate dehydrogenase (LDH) isoenzymes
Lactate dehydrogenase (LDH) is an enzyme primarily involved in converting pyruvate to lactate (and vice versa). It has five isoenzymes (LDH-1 to LDH-5), each consisting of different combinations of two subunits: H (heart) and M (muscle). Further, there are individual LDH isoforms - LDH-A/B/C which make up these isoenzymes. These isoforms have specific roles / functions. LDH is also a metalloenzyme, affected by zinc status and NAD+:NADH ratio. LDH isoenzymes are distributed across various tissues based on their metabolic needs.
The terms "H" (heart) and "M" (muscle) subunits were historically named based on the tissues where these subunits were first observed in high concentrations. The H (heart) subunit was first identified in cardiac tissue, which relies on aerobic metabolism. The M (muscle) subunit was discovered in skeletal muscle, which often utilizes anaerobic glycolysis, especially during high activity.
This test allows you to see if an elevation of a specific isoenzyme or pattern of elevations is present, further suggesting if a particular tissue is experiencing energy metabolism dysregulation, and/or upstream influences affecting energy metabolism.
eg. If LDH-4 and LDH-5 (which contain more M subunits, characteristic of anaerobic glycolysis) are elevated, it can be indicative of reduced oxygen availability or prolyl hydroxylase inhibition for other reasons (oxidative stress, low Fe/Si, low Zn, low alpha-ketoglutarate, elevated succinate). These isoenzymes are more prevalent in tissues that rely on anaerobic metabolism, such as skeletal muscle and liver, and their elevation suggests a shift towards lactate production due to reduced oxygen, a common feature of hypoxic conditions and / or various issues which inhibit prolyl hydroxylase activity (see Figure 1).
2.1.2 Intracellular minerals / nutrients
Use at least one of the following two testing methods (hair mineral testing no longer supported for measuring most deficiencies due to unavoidable limitations in the methodology).
There are limitations to any testing methodology and potential ways for errors in sampling to occur. Some of these problems can be identified and avoided. Others can relate to eg. unpredictable sample transport delays.
To identify potential data errors, best practice is to triangulate and validate markers, deficiencies and issues from multiple data sources, eg. direct measurements of minerals and patterns in metabolites of enzymatic reactions which rely on these minerals.
White blood cells (WBC)
Currently, there are 3 competing laboratories which specialise in measuring the intracellular nutrient status inside WBCs - Cell Science Systems CMA (part of their CNA offering), SpectraCell Micronutrients and Vibrant America Micronutrients.
WBCs are used as a proxy to infer the nutrient status of other cell types, eg. brain, muscle, liver, etc. This data is very different to what is reported in serum (data sourced from outside the cells and any/all related mineral transporter function) or red blood cells, which lack mitochondria and therefore have very different metabolism. Vibrant America Micronutrients test does an excellent job of highlighting this issue in their report. It's frankly astonishing that serum testing is still considered the "gold standard" by public health systems, in light of these issues. However, this also highlights why chronic diseases have been difficult to research and solve.
Although all of these laboratories measure WBC nutrients, each of these tests has a different methodology and included array of markers. Therefore, the advantages and disadvantages for each have been carefully considered. Primarily due to the expansive array of markers more closely matching our requirements, Cell Science Systems CMA is used by this protocol. However, there are limitations to accommodate.
NB. Due to the preparation methodology used by the CMA assay, it's possible under certain circumstances for the report results to appear almost "normal" in the more severe patients with SEVERE deficiencies that affect how the cells behave, even when other deficient nutrients are added. This can be identified by cross-referencing OAT metabolites and other data. Usually these are eg. phosphate and/or sulphur, however a severe enough deficiency of eg. B1 or magnesium can also limit cellular activity sufficiently to mask the effect of correcting other nutrient deficiencies.
By checking OAT results before ordering the CMA test, you can help identify if you're likely to have issues:
1. If you see elevated lactic acid (22), relative to pyruvic acid (23), elevated oxalic acid (21), and/or low phosphorus (76), this pattern is suggestive of excessive anaerobic glycolysis / lactic acid metabolism, metabolic acidemia and renal phosphate dumping.
2. A relative drop from citric acid (29) to aconitic acid (28), with similarly low 2-oxoglutaric acid (27) may indicate severe deficiency of magnesium.
The Pre-Protocol Support mentioned at the end of "2 The Protocol" may be helpful in bringing up the baseline metabolism enough to perform the test without issues. Alternatively, you could use the Oligoscan without this limitation.
However, if you receive a CMA report which is verifiably affected by this issue, you may be able to partially salvage the results by reinterpreting the markers as follows:
1. Any marker not all the way to the left, yet still green is re-interpreted as yellow.
2. Any marker that is yellow is re-interpreted as red.
3. Any marker that is red is re-interpreted as severely deficient.
Advantages:
1. Highly accurate and directly actionable data from an accredited laboratory.
2. Significant array of markers included.
3. Data is considered a snapshot of "current status", without any lag.
4. Blood sample can be collected at home, using a mobile phlebotomist.
Limitations:
1. 8–12 hours fasting is required.
2. Does not include fluorine, sulphur, silicon, various toxic metals, and some of the electrolytes – phosphorus, sodium and potassium
3. Does not indicate excess nutrient data, although this hasn't been a concern.
4. Transport of the sample needs to be rapid, to accommodate eg. cytokine half-life and nutrient transporter behaviour in the cellular membrane, otherwise report sensitivity can be lost. For non-US citizens, an express FedEx courier service is supplied by the laboratory (with an additional cost), along with any import/export clearance paperwork needed for getting blood samples through border security.
5. Sensitivity in the reporting appears to be significantly impacted by phosphate, sulphur and other deficiencies. I would suggest consuming eg. approximately 1.5g of dicalcium phosphate or monosodium phosphate, and 1g of taurine 3x/day for a week or more prior to testing. (Product links available in 5 Ordering products.)
6. Intracellular iron status does not capture systemic iron status data, as 75% of iron is circulating in RBC and serum. A separate test is required.
This comprehensive test is available internationally from a US laboratory. The test normally costs USD$239 - 264, plus express FedEx shipping (usually quoted / invoiced separately, shortly after purchase) and any phlebotomist costs.
Low iodine may be used to infer high fluorine.
Phosphorus data from the Organic Acids Test (OAT) can infer phosphorus status, although there are some differences, being urine / excretory data.
The protocol uses daily targets for electrolytes, however you won’t have an understanding of the baselines for these markers.
Skin
Research suggests that an Oligoscan, So/Check or Zell Check report can provide an approximation of your ACTUAL mineral status, using the skin of your hand as a data source. Note that “OligoLab” / “OligoHealth” / “Scantest” branded reports are currently not supported. This is normally an in-clinic test and a local practitioner will be required.Your blood type, age, height and weight affect the sample calibration used to generate this report, so this information will be requested when you visit a clinic. Any inaccuracies can dramatically alter your results.
While not happy with the level of published evidence currently supporting this emerging methodology, our testing showed a clear pattern of deficiencies in ME/CFS, Long Covid and Covid19 vaccine injured people, with minor variability, which was not observed in controls.
Follow up Oligoscan reports have also matched supplements taken and previous results. The array of elemental markers collected is almost the same as the Doctors Data HTMA reports, however it also includes silicon and usually fluorine. Unfortunately, it does not show rubidium or strontium markers.
1. As over 75% of systemic iron is circulating, Oligoscan / skin data for iron will be an unreliable proxy for systemic levels – blood tests for serum iron studies (iron, transferrin, tsat% and ferritin) would be needed via your doctor or private lab testing.
Low manganese may also provide a hint for low iron, unless IV iron has recently been administered.
2. Calcium markers in skin data will be similarly unreliable – 99% of calcium is stored in skeletal tissue. This also makes serum calcium insensitive. As strontium and calcium can potentially substitute for each other in biological processes, using the “strontium” marker from the hair test as a proxy to indicate systemic calcium may be possible, but needs further study. Tremors and/or heart palpitations, especially in response to taurine or magnesium could indicate low calcium, also. Low phosphorus may indicate low calcium.
3. Copper and zinc appear to be over-estimated in some cases.
4. Due to an unusual quirk in methodology / reporting, highly elevated minerals need to be re-interpreted as highly deficient.
5. Highly elevated zinc in skin tissue may also indicate low protein / histidine intake and mask an actual zinc deficiency.
Oligoscan and CMA results are not known to be directly affected by the inflammatory cascade, meaning that these reports provide an actionable set of objective markers to use when choosing most mineral supplements to address deficiencies. (HTMA data can be referenced to help supplementation planning for rubidium and strontium, also inferring calcium).
For more information about the effects of specific mineral deficiencies, see the “Rationale for protocol inclusions and general notes” section. The Oligoscan and SO/Check reports include a number of vitamin markers, which appear to track relatively well with other data. A good general target for these is to exceed 55%.
Hair minerals (deprecated / limited use)
Research suggests that a Hair Toxin Mineral Analysis (HTMA) may provide an approximation of your functional mineral status, averaged over the period of follicle growth, sampled adjacent to the transporter alterations from inflammation – where circulating minerals can be sequestered inside various brain, liver and kidney cells and consequently low in other cells. It cannot accurately report on the intracellular levels or systemic levels, as sequestered minerals are not shown in this data.
The results obtained from the HTMA data may be used to infer averaged intracellular mineral availability, downstream of any chronic inflammation, for the period of time in which the hair follicles grew, in a similar way to read HbA1C for glucose metabolism. This mechanism is largely relevant to the ten elements transported by DMT-1 and ferroportin.
A list of vendors offering a compatible list of markers and reference ranges is provided below. Doctors Data and other compatible laboratories
| US | https://www.walkinlab.com/products/view/dd-hair-elements-profile-doctors-data (not available in NY/ NYC and other areas.) |
| AU | https://www.toxno.com.au/articles/heavy-metals/hair-tissue-mineral-analysis-hma-or-htma-in-australia/ (can manually add rubidium) |
| EU / UK | https://regeneruslabs.com/products/hair-toxic-essential-elements-1 |
| EU | https://www.biocoherence.eu/en/shop/htma/ (doesn't include rubidium) |
| EU | https://www.lifelinediag.eu/en/product/eha-standard-en/#products (doesn't include rubidium) |
| NZ | https://www.houseofhealth.co.nz/product/hair-toxic-mineral-analysis/ |
| PL | https://analizawlosa.com.pl/produkt/analiza-wlosa/ |
| UK / some EU | https://www.lauristonlabs.co.uk/product/hair-elements-doctors-data/ |
- Ignore any conflicting vendor-specific instructions.
- The hair needs to be clean, well-rinsed, dry, untreated and uncoloured. Unwashed hair may provide false (elevated) data for sodium and potassium, from dried sweat. Use gloves.
- Select suitable areas of sideburn, scalp and/or neck hair. If the hair is longer than 2.5cm / 1", first trim the sample area to this maximum length with clean stainless steel scissors. By using shorter hair, the report data relates to a more recent period of time.
- Cut the (remaining) hair to be sampled as close to the skin as possible. Do not use clippers or an electric razor – metal contamination from tungsten blades may occur. Collect at least two heaped tablespoons worth of hair, or approximately 250mg, or the sample may be rejected.
- Place the hair sample in the sample kit envelope provided, or in a clean, clearly labelled envelope or sachet. Whilst Trace Elements Inc says not to use resealable plastic bags as apparently hair “sweats” and the sample may be rejected, whereas Doctors Data supplies plastic bags in their kit.
2.1.3 Mosaic DX Organic Acids Test (OAT)
A Mosaic Diagnostics (Mosaic DX, formerly Great Plains) Organic Acids Test (OAT) is a comprehensive report on urine metabolites.
While there are various OAT vendors, eg. Genova Diagnostics, Vibrant, Nutripath, etc., the preferred vendor for this protocol is Mosaic DX, for reasons of reliability, results consistency and marker inclusion.
This test is available through local vendors, or these websites:
International - https://mosaicdxinternational.com/products/mx-organic-acids-test-oat
US - https://www.integrativepsychiatry.net/shop/the-great-plains-laboratory/urine-organic-acids-test/
UK / EU - https://smartnutrition.co.uk/shop/great-plains-oat-organic-acids-test/
AU - via a RN Labs registered practitioner
Note: if there is a pattern of “left shift” or “suspiciously
low” microbial markers on page 1 of the OAT results, it’s possible the
sample has thawed in transit and the integrity compromised, AND/OR the concentration of the sample was out of range (hydration levels). You may need
to repeat the test.
For best results a very short shipping time is
needed and creatinine levels (marker 77) should ideally be between 80-180 mg/dL.
Mosiac DX automatically scale the report markers against the creatinine levels, which can induce a false LEFT-shift with very high concentrations and RIGHT-shift with very low-concentrations. Overall, it's something I think the lab could improve on.
In addition to allowing interpretation of metabolic impairment from the patterns observed in these markers, page 1 of the report shows various markers for microbial interference. The remaining pages show your metabolic impairments from infection and malnutrition. Elevation of yeast, bacterial and fungal metabolites in OAT results have been seen consistently in our collected data, with matching symptoms. A further MycoTOX test may provide further clarity on species and expected metabolic impairments, if required.
A clinician’s guide to interpreting OAT results is being drafted. Example interpretations of these reports can be found on our Discord online discussion group.
A basic OAT interpretation guide for the purposes of supplement selection can be found in 4 Calculating supplement doses.
2.1.4 Cronometer
Cronometer (https://cronometer.com) is a freemium online app which can visualise the performance of your current eating strategy / habits / restrictions and allow you to make positive changes. It has a mobile app for data collection and basic reporting. Using a desktop / laptop allows access to richer reporting options and diary view.
Logging at least two days of eating in Cronometer would be very helpful for identifying problems and also help you rebuild / restore your relationship with food, especially as any sensitivities are reduced / resolved over the duration of the protocol. (see “2.2.1 Diet”)
People usually find this process eye-opening.
When selecting food items to enter into the virtual diary, choosing NCCDB or USDA listed food items will provide more micronutrient data. CRDB (user-entered, moderated entries) only contain information displayed on the product labels rather than laboratory identified data.
An example day of eating, with nutritional report:
2.1.5 Microbiome testing
Dysbiosis and biofilms in the various microbiomes sits at the root of this disease model. Given the implications and progression described in the disease model,
reviewing your medical history, from early childhood forward would be
suggested. A common progression would be an early childhood infection /
biofilm formation in the ears/nose/throat/sinuses that progresses to the
gut (and sometimes lungs), before translocating to sex organs and
urinary tract. Skin microbiome dysbiosis - eczema, acne, dandruff,
fungal nails, etc is also common.
Gut microbiome
Certain gut microbiome tests are useful in getting a rough understanding of the species present in your GI tract, the metabolites they consume and produce and if any of these are toxic / relevant to your metabolic alterations. Currently there is no single "perfect" microbiome test available. There are a range of tests with strengths and weaknesses.
As the stool specimens are not homogenised, very different counts of species can be obtained from different parts of the same specimen. False negatives are common. This can create confusion for anyone who is used to interpreting various reports at face value. Any species counts need to be interpreted with low confidence.
However, the “overall trends” of species diversity and overgrowth can be useful in making decisions around changes to eating habits, supplements and other interventions, for example, consuming bismuth compounds and / or codonopsis / Dang Shen tea for inhibiting sulphur reducing bacteria and promoting bifidobacteria, or taking Akkermansia probiotics and/or pomegranate, if low or missing, along with a supportive diet.
Biomesight
For diversity / abundance testing and recommendations around dietary changes, Biomesight provide some useful reports and importantly, allows record-level data export to CSV for further detailed analysis, which can be used with the information here to make decisions around interventions. NB. fungal species are not reported.
A Biomesight data analysis tool is now available (beta), which will quickly interpret exported Biomesight CSV files against the disease model:
https://bornfree.life/2024/biomesight-tool/
Biomesight are offering a discounted test for people with Long COVID and you can also use the code "RemissionBiome" for any other Biomesight products, thanks to our ongoing collaboration with Remission Biome:
https://shop.biomesight.com/products/long-covid19-study-gut-microbiome-test
GI-MAP
For enhanced pathogen testing, also including parasites, along with reporting on GI related markers, a GI-MAP report provides more information, however the report lacks the detailed species diversity information provided by eg. Biomesight.
USA vendors:
https://www.dhalab.com/shop/gi-map-gi-microbial-assay-plus/
https://labtestshop.com/tests/gi-map-stool-test/
AU vendors:
https://healthandharmony.net.au/shop/gi-map-test-kit-gut-microbiome-stool-sample
https://elementalhealthandnutrition.com.au/product/gi-map-diagnostic-solutions/
UK, EU vendors:
https://smartnutrition.co.uk/shop/comprehensive-stool-test-gi-map-pathogen-plus-uk-and-europe-igimap/
https://www.ibsclinics.co.uk/product/gi-map/
https://ifu-wolfhagen.de/shop/stuhl-test/stuhl-und-verdauungsanalyse-pilze-gr-parasitologie-bakterien-bauchspeicheldruese-entzuendungsparameter/
IN vendors:
https://www.ithrive.shop/products/gi-map-stool-analysis-offered-by-diagnostic-solution-laboratory-us?variant=44135044612310
Other – sinuses, oral, lung, urinary tract and sex organ microbiome
If you have a known or suspected infection in any mucosal tissue, then combining qPCR and Next Generation Sequencing (NGS) 16S methodology can help identify the species present and help with decision-making processes around remediation. Reviewing your entire medical history since birth and highlighting / testing tissues with recurring issues would be highly appropriate.
They normally supply a "Level 1" report (targeted qPCR), followed by a "Level 2" report (NGS), a few days later. It's common that the Level 1 report results will be less than helpful.
MicrogenDX offer a range of different testing and reports, for different tissues. These are available to US and international customers.
https://microgendx.com/patients/microgendx-patient-test-service-dm-intl
Limitations:
1. Does not show Lyme species.
Circulating microorganisms - tick-borne, systemic infections
As anyone who has spent time around Lyme disease and tick-borne infections will tell you, getting good data on circulating and intracellular microorganisms is traditionally very, very difficult. Even if you have access to quality testing, the lifecycle of these species can make many of them difficult and expensive to quantify. However, Legionella and Rickettsia species frequently show up in Biomesight and other microbiome reports.
If you have a reason to suspect intracellular species are going to be included in your collection of pathogens:
MicrogenDX can provide "shotgun" metagenomic sequencing of samples to
US customers for "research only" purposes and an extra fee, if your
doctor contacts them.
ArminLabs EliSpot and TickPlex tests are able to detect a wide range of pathogenic species - https://arminlabs.com/en/tests/elispot
MDL can provide comprehensive data via their OneSwab test - https://www.mdlab.com/testing/vector-borne/
Vibrant Wellness Tick-borne test has a wide range of inclusions and uses multiple methodologies - https://shop.drjabanmoore.com/products/copy-of-vibrant-wellness-tickeborne-complete-1-0
Similarly, elimination of intracellular species has additional challenges to other microorganisms. Getting the immune system restored to normal functionality and ongoing use of circulating biofilm breakers is a key part of resolving these infections. Specific anti-microbials can be used to manage and accelerate this process.
Fermenting species identification
Once you have collected accurate microbiome data, you can use it to identify overgrowth of any species which produce alcohol and/or acetaldehyde using this table.
Notes and considerations:
1. Some species produce alcohol from carbohydrates or lactic acid.
2. Other species produce acetaldehyde when provided with alcohol and may otherwise be harmless.
3. Some produce both.
4. Some probiotic species are also included for accuracy, however these are not considered problematic under normal circumstances.
5. Some species found outside the gut that only produce acetaldehyde may benefit from alcohol produced in the gut or from dietary intake. Therefore, you may have difficulties remediating overgrowth of these species in other tissues until moderate - severe fermentation by the gut microbiome is remediated.
6. This list is comprehensive, but not exhaustive. It will be added to as a comprehensive literature review is completed and GenBank entries processed.
7. It's a very interesting observation that all of the species known to be causal for common issues like acne and dandruff to various cancers are found in this list.
2.2.1 Diet
Planning and consuming an appropriate / strategic diet are complex topics for most people, even without a chronic disease.
For those with a chronic disease, it's significantly more complex. One common challenge is selectivity - trying to ensure that your cells
are receiving these dietary nutrients, while avoiding feeding them to certain
microorganisms residing in your GI tract - which then produce endotoxins
/ mycotoxins that poison your energy metabolism and neurotransmitter
pathways. Acetaldehyde is one of the toxins discussed heavily in the disease model, as part of Gut Fermentation Syndrome (GFS).
Failure to adapt your diet around your personalised microbiome dysbiosis and chronic disease metabolism will invariably lead to "getting stuck" or even back-sliding. Unlike minerals deficiencies, which are normally slow to develop and slow to resolve, microbiome dysbiosis can rapidly shift during immune activity or by feeding the wrong microorganisms over a number of weeks. What you eat determines which microorganisms get promoted or inhibited.
Diet plays a pivotal role in chronic disease by influencing substrate availability for fermenting microbes and shaping the gut microbiota composition. High-carbohydrate diets provide ample fuel for microbial fermentation, exacerbating acetaldehyde production and metabolic disruptions. Conversely, low-carbohydrate diets can reduce substrate availability, potentially decreasing microbial fermentation and acetaldehyde levels, however these can also exacerbate glycogen storage issues and contribute to various symptoms like POTS, fatigue, depression and other neurological symptoms. This has been labelled by some as “low carb limbo”.
Depending on the functionality of different energy pathways, while first starting this protocol, you may also find you respond better to certain type of macronutrients, ie. carbohydrates, fats and proteins than others.
The performance of your diet can be predicted in the Organic Acids Test (OAT) results, by looking at the relevant pathways for metabolites of each macronutrient, eg. glycolysis, fatty acids, amino acids. Some of the adjacent pathway markers, such as ketogenesis, lactic acid and oxalate metabolism are also helpful in identifying impaired pathways, indirectly.
Therefore, before we go into detailing specific foods and their attributes, it helps to understand a little more about the different energy pathways and how dietary macronutrients can be turned into energy:
Instant / burst energy (muscle tissue)
ATP-PC (Phosphocreatine) System
Where: Not used in liver and adipose tissue.
Substrates: Phosphocreatine (PC) stored in muscles.
Requirements: Dietary creatine. Creatine produced from the urea cycle, using dietary protein. Dietary phosphorus intake. Promoted by sex and thyroid hormones.
Uses: High-intensity, short-duration activities (e.g., sprinting, weightlifting).
Availability / Duration: 10-15 second bursts.
Trigger/Signaling: Immediate energy demand; catecholamines increase utilization.
High intensity energy demands
Glycolysis
Where: Not used in red blood cells (RBCs), as they rely entirely on anaerobic glycolysis, and white adipose tissue prefers fatty acid metabolism.
Substrates: Glucose or glycogen.
Requirements: Dietary carbohydrate intake or gluconeogenesis. Phosphorus. Biotin. Vitamin B3 (as NAD+). Zinc. Magnesium / Manganese. Potassium. Chromium. Vanadium. Thyroxine (calcium, iodine, selenium, heme, tyrosine). Vitamin B1 (as TPP). Lipoamide. Promoted by sex and thyroid hormones.
Uses: Brain activity. Moderate to high-intensity activities (eg., walking / running upstairs, thinking).
Availability / Duration: Muscles - up to 2-3 minute bursts, subject to glycogen reserves.
Trigger/Signaling: Increased ADP levels; catecholamines enhance glucose availability via cAMP-PKA signaling, inhibiting glycogen synthase and activating glycogen phosphorylase.
Glutaminolysis (anaplerosis)
Where: Not used in red blood cells due to lack of mitochondria and adipose tissue due to limited metabolic flexibility.
Substrates: Glutamine.
Requirements: Dietary glutamine, or glutamine created from citric acid cycle activity. Vitamin B3 (as NAD+). Zinc. Magnesium / Manganese. Promoted by sex hormones.
Uses: Rapid cellular proliferation (eg., immune response) and intense brain activity.
Duration: Continuous during demand.
Trigger/Signaling: Stress-induced catecholamine elevation may indirectly upregulate this pathway.
Sustained energy demands
Fatty Acid Oxidation
Where: Not used in brain cells due to fatty acids not crossing the blood-brain barrier, nor red blood cells due to lack of mitochondria.
Substrates: Fatty acids
Requirements: Dietary fats or lipolysis. Carnitine for the carnitine shuttle. Vitamin B2 (as FAD). Vitamin B5 + cysteine (as Coenzyme-A). Lymphatic system is used to transport dietary fats.
Uses: Basal daily metabolism. Low to moderate-intensity activities (eg., walking, endurance sports).
Duration: Indefinite.
Trigger/Signaling: Prolonged energy demand; catecholamines promote lipolysis, increasing free fatty acids for oxidation.
Branched Chain Amino Acid (BCAA) Catabolism
Where: Low activity in the smooth muscle, brain and liver. Primarily used in skeletal muscle, heart, and kidney tissues.
Substrates: Leucine, isoleucine, valine.
Requirements: Dietary protein intake. Vitamin B2 (as FAD). Biotin. Vitamin B12 (as adenosylcobalamin). P5P.
Uses: Prolonged exertion, especially with low glycogen.
Duration: Sustained.
Trigger/Signaling: Catecholamines promote protein breakdown, increasing BCAA availability.
Backup energy pathways for excessive load and various mitochondrial dysfunction
Anaerobic Glycolysis / Lactic Acid Metabolism
Where: Not used in liver (under normal conditions) and heart (prefers aerobic metabolism). Promotes neurogenesis and myogenesis.
Substrates: Glucose.
Requirements: Dietary carbohydrate intake or gluconeogenesis. TBC.
Uses: High-intensity activities with limited oxygen.
Duration: Short bursts, up to 2-3 minutes.
Trigger/Signaling: High ADP/ATP ratio, catecholamines enhance lactate production through glycogenolysis.
Astrocyte-Neuron Lactate Shuttle (ANLS)
Where: Found in the brain. Lactate can also circulate and participate in the Cori Cycle.
Substrates: Glucose (astrocytes), lactate (neurons).
Requirements: Dietary carbohydrate intake or gluconeogenesis.TBC.
Uses: Neural activity, intense cognitive tasks where glycolysis is insufficient.
Duration: Continuous during brain function.
Trigger/Signaling: IFN-gamma, others. Norepinephrine enhances glucose uptake in astrocytes, promoting lactate production for neurons, similar to an intra-brain Cori cycle.
Cori Cycle / Lactic Acid Cycle
Where: Systemic
Substrates: Lactate (from muscles, brain).
Requirements: Dietary carbohydrate intake or gluconeogenesis. TBC.
Uses: High-intensity exertion / mitochondrial dysfunction.
Duration: Normally short-term, during recovery.
Trigger/Signaling: Epinephrine increases lactate production, fueling the Cori cycle.
Ketogenesis + Ketosis
Where: Ketones are generated in the liver, but not used by it. Red blood cells cannot use ketones due to lack of mitochondria.
Substrates: Fatty acids.
Requirements: Dietary fats and/or lipolysis. TBC.
Uses: Prolonged fasting, low carbohydrate intake / impaired glycolysis, or low liver glycogen.
Duration: Sustained during glycogen depletion.
Trigger/Signaling: Catecholamines promote lipolysis, increasing fatty acids for ketone body production.
Examples of some less utilised pathways, which may be promoted / abused when primary pathways fail
Tyrosine Catabolism
Where: Not used in red blood cells and adipose tissue due to limited enzymatic activity for this pathway.
Substrates: Tyrosine.
Requirements: Dietary intake of tyrosine and/or microbiome synthesis. P5P. Ferritin. Calcium. Magnesium.
Uses: Various, including stress, mitochondrial dysfunction.
Duration: Continuous, where tyrosine exists.
Trigger/Signaling: Catecholamines do not directly regulate but are derived from tyrosine.
GABA Shunt
Where: Not used in liver and skeletal muscle as they are not involved in neurotransmitter metabolism.
Substrates: GABA via glutamate or polyamine metabolism.
Requirements: P5P, magnesium.
Uses: Neural activity, especially during TCA cycle impairment and oxidative stress.
Duration: Continuous.
Trigger/Signaling: Catecholamines influence neurotransmitter release but do not directly regulate GABA metabolism.
Urea Cycle (Argininosuccinate)
Where: Not used in brain and muscle tissue since the urea cycle is primarily hepatic.
Substrates: Amino acids (arginine).
Requirements: Dietary protein intake. Aspartate.
Uses: Ammonia elevation, protein metabolism / high protein intake.
Duration: Continuous.
Trigger/Signaling: Catecholamines indirectly increase ammonia load, requiring urea cycle activity.
Food Intolerances
You also may have already developed a number of food intolerances.
Some of these intolerances are "simply" endotoxins being produced by overgrowth of unwanted microbial species living in biofilms inside your GI tract, consequently being sustained by your intake of various dietary carbohydrates and/or other nutrients, such as sulfur-rich compounds These endotoxins can inhibit energy metabolism, neurotransmitter homeostasis, histamine degradation and various other pathways.
"Sometimes the easiest way to solve a problem is to stop participating in the problem." - Unknown
(In this context, "You cannot efficiently eliminate or reduce overgrown species while you're also feeding them.")
Standard Mixed Diets vs. Ketogenic Diets
Standard Mixed Diet
A standard mixed diet typically includes a balanced intake
of carbohydrates, proteins, and fats. In the context of the disease model, this diet may
inadvertently contribute to increased fermentation and unwanted biofilm development. The high carbohydrate
content fuels microbial ethanol and acetaldehyde production, leading to
continued impairment of energy pathways due to elevated acetaldehyde. Symptoms
such as fatigue, cognitive impairment, and metabolic abnormalities may persist
or worsen under this dietary regimen.
Depending on the species and locations of the biofilms
containing these microbial species, you may have more success avoiding
symptoms by consuming different types of carbohydrates.
eg.
a.
Simple carbohydrates / sugars may feed any existing microbial
overgrowth in the mouth / throat / oesophagus / stomach / small
intestine. In the absence of dysbiosis in those tissues, simple
carbohydrates can also be readily absorbed in the small intestine,
before reaching any dysbiosis in the large intestine, should it exist.
b.
Complex carbohydrates may not be broken down until further along the GI
tract and may skip feeding some of the populations residing in biofilms
in the small intestine.
c. Different types of dietary fibres and starches may selectively feed some species and not others. (see "2.2.3 -- Prebiotics"")
d.
Gliadin in gluten may generate an immune response due to molecular
mimicry of the protein in the "hook" of Candida's hyphae form. Gliadin
is also used by a particular pathogenic strain of Streptococcus
salivarus to produce an antigen that punches holes in enterocytes,
leading to gut barrier degradation, immune response and inflammation. Giardia infections are also known to create gluten intolerance.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4368562/
https://pubmed.ncbi.nlm.nih.gov/22617359/
In some types of more severe dysbiosis (and where your B vitamin and mineral status also supports this), you may find swapping more carbohydrates for
protein can be helpful in avoiding endotoxemia symptoms such as
nausea, bloating, diarrhoea, histamine reactions, tachycardia,
headaches, etc. These will resemble die-off symptoms, as the same toxins
are involved (see: 2.3.1-Herxheimer / die-off / acetaldehyde-support).
Here is an example 2000kcal mixed-diet, visualised in Cronometer:
Ketogenic Diet
The ketogenic diet, characterized by high fat, moderate
protein, and very low carbohydrate intake, offers a contrasting approach to
a standard mixed diet or a low carbohydrate diet.It also avoids "low carb limbo" by promoting generation of ketone bodies in the liver.
In extreme gut microbiome dysbiosis cases, changing to a
ketogenic diet for a period of time can also be very helpful in reducing
fermenting species, however will require commitment to endure an often
unpleasant induction (1 week) and then adaptation phase (2 weeks). If
your OAT results already show elevated ketone markers, this is much
easier. Studies suggest the acute effects of a ketogenic diet on your
gut microbiome will last around 12 weeks, before the microbiome adapts.
Combining this window of opportunity with other interventions in this protocol can allow
you to break the existing cycle with lasting results.
By significantly reducing carbohydrate consumption, this diet limits the
substrates available for microbial fermentation. As a result, endogenous
ethanol and acetaldehyde production may decrease significantly in response to food
intake, alleviating some of the metabolic disruptions caused by GFS.
However, circulating acetaldehyde and other endotoxins will still be
experienced, making the first 1-2 weeks of a ketogenic (the induction phase)
more unpleasant than it would be for someone without GFS.
A key point of difference is that the ketogenic diet promotes fatty acid oxidation and ketone body production as alternative energy sources. Ketone bodies can cross the blood-brain barrier and provide energy to the brain (much more efficiently after weeks of being on a ketogenic diet), potentially improving cognitive function and reducing fatigue. Additionally, this diet may alter the gut microbiota significantly, reducing fermenting microbial populations and promoting a healthier balance.
Mechanisms of Ketogenic Diet's Impact on GFS
Carbohydrate Restriction
Limiting carbohydrate intake directly reduces the amount of glucose and other fermentable sugars in the gut. This reduction in substrates can lead to decreased microbial fermentation activity, resulting in lower ethanol and acetaldehyde production. With less acetaldehyde burden, the inhibitory effects on metabolic enzymes are alleviated, helping to restore the cellular redox balance and improve the function of gluconeogenesis and fatty acid oxidation pathways.
Fatty Acid Oxidation and Ketogenesis
The ketogenic diet's high-fat composition encourages the body to utilize fats as the primary energy source. This shift promotes the production of ketone bodies in the liver through a process called ketogenesis. Ketone bodies serve as an efficient alternative energy source for various tissues, including the brain and muscles. By providing a consistent energy supply, the diet addresses the energy deficits caused by acetaldehyde-induced metabolic disruptions. Additionally, relying less on impaired glucose production pathways reduces the risk of hypoglycaemia.
Benefits of a Ketogenic Diet in GFS
Implementing a ketogenic diet in GFS management offers
several potential benefits. By reducing acetaldehyde levels, the diet can help
restore normal metabolic functions, improving energy production and overall
well-being. The provision of ketone bodies as an alternative energy source may
alleviate symptoms such as fatigue and cognitive impairments. Furthermore, the
reduction in carbohydrate intake may lead to favourable shifts in gut
microbiota composition, decreasing the population of fermenting microbes
responsible for excessive acetaldehyde production.
Potential Challenges
Despite its potential advantages, the ketogenic diet
presents challenges that must be carefully considered. The restrictive nature
of the diet can make long-term adherence difficult for some people. There is
also a risk of nutrient deficiencies, particularly in electrolytes, fibre,
vitamins, and minerals, if the diet is not properly managed. Monitoring thyroid
function is also helpful, as very low carbohydrate intake can sometimes reduce
T3 levels, potentially affecting metabolic rate. Additionally, high-fat diets
can impact beneficial gut bacteria, necessitating careful planning to maintain
gut health.
A manganese deficiency will significantly impact hepatic gluconeogenesis, as will zinc and magnesium deficiencies.
These should be somewhat addressed before attempting keto induction.
NB. The reduction in glucose availability may affect cognitive function where neural hypoxia exists - due to eg. structural issues, coagulation and/or transport issues, severe iron deficiency, and also blocked lymph nodes in the neck and/or nasopharynx (usually relating to localised infection). The reduced glucose affects lactic acid metabolism involved in the Astrocyte-Neuron Lactate Shuttle and ultimately energy availability in neurons.
Strategic Implementation
Successful implementation of a ketogenic diet for GFS
requires proper planning to ensure safety and efficacy. A personalised
nutritional plan tailored to individual needs and tolerances can enhance
adherence and effectiveness. Cronometer
is very helpful in planning and visualising a successful day. Setting expectations ahead of time will help allow you to "keep calm and keto on" during unpleasantness.
Supplementation with essential electrolytes, vitamins, minerals, and probiotics
like the ones in this protocol may be necessary to address deficiencies and
support gut health.
A gradual transition into the diet, by slowly reducing carbohydrate intake, prolongs
keto adaptation and exacerbates energy crisis symptoms. It is not recommended.
A rapid transition normally creates temporary symptoms of "keto flu",
which can be managed by using GoBHB exogenous ketone supplements and essential
amino acids (EAAs) during the dietary transition.
Strictly restricting carbohydrate intake is paramount to the
diet, which involves eliminating sugars and refined carbohydrates like
sweets, sugary drinks, white bread, and pastries. Removing starchy foods
such as potatoes, rice, pasta, and grains is also necessary. Instead, consuming
non-starchy vegetables like broccoli, cauliflower, kale, and bell peppers (capsicum)
provides essential nutrients with minimal carbohydrates. The target daily net
carbohydrate (total carbohydrates, minus fibre) upper limit is 25g.
Increasing the intake of healthy fats supports the
ketogenic approach. This includes consuming monounsaturated fats found in olive
oil, avocados, and nuts, as well as omega-3 fatty acids from fatty fish such as
salmon and mackerel. Saturated fats from sources like coconut oil and butter
can be included. Butter is also a good source of butyrate, which may trigger rapid,
beneficial changes to the microbiome, however, this will also trigger die-off
symptoms and potentially induce rapid alcohol withdrawal symptoms.
Protein intake is important for essential amino acids and to
allow the liver to perform hepatic gluconeogenesis for brain and other tissues.
Balancing protein intake is important because excessive protein can be
converted into glucose, potentially triggering an insulin response that
inhibits keto induction / adaptation, while also fuelling microbial fermentation,
depending on the location of the biofilms. The longer the protein take to
digest, the further along the GI tract it will be before potentially feeding
the microbiome.
Keto induction is easier with more fats than protein, initially.
For example,
During keto induction, you could consume:
170g fat @ 1530 kcal +
100g protein @ 400 kcal
= 1930kcal
After keto induction, you can transition to consuming roughly 1:1 of fat:protein, on a per-gram
basis:
150g fat x9 = 1350kcal
150g protein x4 = 600kcal.
= 1950kcal.
(Scale this by your calorific needs.)
High-quality protein sources such as lean meats, poultry, eggs (a great source of
lecithin for phosphatidylcholine), and plant-based proteins like nuts (good
mineral sources) and tofu (some people may have tolerance issues) are
recommended.
Maintaining proper hydration and electrolyte balance is
essential. Adequate water intake supports detoxification and metabolic
processes, while sufficient electrolytes help prevent imbalances that will
reliably occur during the initial stages of a ketogenic diet, as glycogen
stores are intentionally depleted.
Here is an example 2000kcal ketogenic diet, visualised in Cronometer:
Inflammation and/or gut membrane permeability issues due to microbiome dysbiosis and related immune activity often leads to further histamine elevation and temporary IgG antibodies being produced. This is normal behaviour in response to complete foreign proteins getting through the barrier and triggering an immune response. In this state, foods which trigger mast cell activation and histamine release should be avoided for 6-8 weeks before reintroducing them, preferably after the barrier dysfunction has been sufficiently improved / resolved.
Due to metabolic impairments being described in this disease model, other food intolerance issues are entirely expected. The disease model and collected data shows that aldehyde toxicity / impaired aldehyde metabolism leads to elevations of serum Vitamin B6, creates issues metabolising "inactive" forms of Vitamin A into the active forms, creates issues degrading histamine and separately, other issues promoting lactic acid metabolism also elevate endogenous biosynthesis of oxalate.
In this state, additional intakes of these nutrients / compounds may exacerbate existing symptoms. These issues are targeted in Stage 1 of the protocol and allows dietary intakes to become more flexible. Overall, foods need to be carefully managed and reintroduced as the related
metabolic impairments and barrier function issues are resolved.
Meal composition and timing is also important when energy metabolism is impaired. Part of the metabolic cascade includes type-2 diabetes and metabolic syndrome, so the dietary strategies will look very similar.
In the context of the disease model including glucose uptake and glycogen storage issues, the BCAA content of dietary protein intake may be very helpful in refilling glycogen stores via an alternate route, depending on your manganese, zinc, magnesium, biotin, B1, B2, B3, P5P and B12 status. In addition to general energy availability improvements, the model shows this is helpful for preventing PEM and crashes, providing oxidative stress and coagulation is being managed.
A table of microbiome transforming foods is provided in 2.2.3 -- Prebiotics and should be considered a required part of the protocol and any strategic diet.
The concept of "roughage" and its role in helping to disrupt and remove mucous + biofilms, especially when combined with additional biofilm breaking food items / compounds is often underappreciated in meal planning.
Foods to generally consume as part of the protocol (as tolerance allows / increases):
Foods to generally avoid or otherwise consume cautiously as your aldehyde metabolism, etc normalises (monitor serum cholesterols, B6, beta-carotene):
In the tables below, you'll find food items and their relevant attributes, which you can use to help you get started building meals.
These tables are best viewed on a computer or tablet. On mobile devices, some columns will be hidden to fit the screen.
The columns can be sorted and cautions or elevations of potentially inappropriate nutrients in foods items when getting started have been highlighted in red.
These tables are not intended to replace https://cronometer.com, which is incredibly helpful in visualising and planning your dietary strategy.
Protein sources:
Carbohydrate sources:
Micronutrient sources:
2.2.2 Lymphatic maintenance
The lymphatic system is a network which spans the majority of the human body. Until quite recently, it was not known that this also included the brain.
The lymphatic system has a number of important roles in immunity and circulation. Lymphoid organs are the source of B and T lymphocytes. The system transports dietary fats and collects extracellular fluid and metabolites from tissues, returning them via lymphatic vessels to the bloodstream, preventing lymphoedema or catastrophic fluid build-up, pressure / pain and metabolic backlog.
A friendly primer on the lymphatic system can be found here: https://www.britannica.com/science/lymphatic-system
The lymphatic system relies on breathing and muscle contractions to maintain healthy circulation and waste excretion. Calendula creams can also help move lymph.
In any disease where movement is being restricted, this creates additional difficulties for maintaining immune function, fat transport and metabolite circulation. The lymphatic system can become blocked. This may be observed as being stiff, or having sore swollen tissues that
can feature enlarged lymph nodes, such as in the neck, groin and/or
armpits, relative to adjacent infections. Failure to maintain the lymphatic system may create a serious roadblock to recovery.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5954877/
A session with a massage therapist who specialises in lymphatic drainage may help you assess and remediate any recurring lymphatic blockages. There are also some helpful videos online with comprehensive instructions.
A daily regimen to maintain any problematic areas by hand or
vibrating massage gun (used on a glancing angle), may also assist
unlocking functional gains and preventing pain in chronic illnesses /
infections.
https://youtu.be/ccV24hCOe5A
https://youtu.be/dDrJajg2ZII
Localised pressure / oedema, numbness, hypoxia, impaired
blood flow, "burning" sensations, pain and lactic acidemia can be expected when lymph nodes
become blocked from nearby immune activity.
eg.
Intracranial pressure is regulated by nasopharyngeal, occipital and cervical lymph nodes in the face and neck. If these lymph nodes become blocked, crippling head pressure can be experienced. This is especially noticeable if immune activity increases from eg. improved energy metabolism / resolving deficiencies. Intracranial pressure can be a blocking issue to making any forward progress, if left unresolved. Chronic intracranial pressure issues and nasal / sinus inflammation are commonly found where environmental mould issues are unresolved, see 2.2.3 Living without chronic dysbiosis.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10808075/
https://www.nih.gov/news-events/nih-research-matters/lymphatic-vessels-discovered-central-nervous-system
NB.
The nasopharyngeal lymph nodes are largely inaccessible via manual manipulation, although a soft attachment and glancing angle with a vibrating massage tool on either side of the nose may help. Resolving infections in the nasopharynx reduce load on those lymphatic vessels. The occipital and cervical lymph nodes are much easier to access and clear.
https://bornfree.life/images/neck-lymphatic.mov
Face and sinuses can become acutely painful if related lymph nodes are blocked. These nodes are usually very easy to access with your fingers or a vibrating massage tool.
Here is a diagram you can follow to help improve lymphatic flow, by dragging your fingers in the same locations and directions of the arrows. Areas with multiple arrows side by side may benefit from using multiple fingers:
Hands and arms can be significantly affected by blocked lymph nodes in the neck and armpits. These nodes are usually very easy to access with your fingers or a vibrating massage tool.
Feet and legs
can be significantly affected by blocked lymph nodes either side of the groin and backs of
the knees. These nodes are also easy to access with your fingers or
vibrating massage tools.
NB.Most lymphatic drainage / massage specialists will skip the groin nodes due to being intimate areas, however these are commonly blocked, presumably from immune activity in the gut and/or sex organs.
A strong paradoxical effect may be felt the first time a blockage is cleared.
2.2.3 Living without chronic dysbiosis
Yeasts, moulds and fungi are found everywhere in nature and have an important role. They decompose animals, plants and other organisms, recycling their elements and other nutrients, thereby continuing the circle of life.
Usually, these decomposing animals are not alive, however when an organism’s immune response is incapable of maintaining a defence against the normal daily background level of fungal challenge, the living organism will become food for yeast, mould and/or fungi. Various lifestyle influences contribute positively and negatively to maintaining this daily defence.
Lack of exposure to sunlight, lack of sufficient activity to maintain a specific immune function and/or lack of a balanced, protective microbiome can also contribute to an organism being more susceptible to mould. It has been previously said “we don’t grow old, we mould!”
Antibiotics are powerful tools in controlling bacterial infections, however they are also broadly indiscriminate in their effects and are overused in food production + minor infections, leading to a loss of microbiome diversity and also the development of drug-resistant strains. Acute use of them decreases systemic levels of both "good" and "bad" bacteria, creating opportunities for opportunistic fungal overgrowth. Without paying careful attention to diet, probiotics, prebiotics and host metabolism, using broadly destructive interventions against your microbiome can have deleterious effects on your health and happiness.
eg. If you pour weedkiller all over your garden, killing almost all of the flora and then don't replant and cultivate the garden again afterwards, you'll find that over a short time, the plant life now growing back is made up of the most hardy, versatile, adaptable species either left behind or reintroduced by natural processes. These are often the species of weeds you were trying to remove in the first place.
Growing a beautiful garden means making space for what you want to flourish, planting the seeds and then feeding the species you want to keep, so they can out-compete the others. Selective weeding is also helpful. Some fertilisers are selective for species, also. These will be discussed in the Probiotics and Prebiotics sections below.
Maintaining a protective gut microbiome in modern times has a number of challenges due to the germicidal effects of stomach acid, metabolic acidemia and chronic disconnection from our natural source of probiotics via our industrialised food chain / use of preservatives and general preference for cooked food.
The barrier function of the skin and mucosal layers play an important part in resilience against pathogens. Unfortunately, the human body has a number of tissues that are opportunistic for yeast / mould / fungal and bacterial infections to thrive with minimal interference from direct immune activity, thanks to their ability to form biofilms.
https://www.sciencedirect.com/science/article/pii/S0016508524050546
Subgrouping for ME/CFS, PFS, PSSD and other patients may have a
relationship with the locations of infected tissues. Localised
pathogenic biofilm accumulation and chronic innate immune activation.
Nasopharnyx
One example for possible subgrouping relates to the nasopharynx (and surrounding areas), which have a direct route to the central nervous system. Swollen / enlarged lymph nodes can often be found nearby infected tissues. If these blocked lymph nodes include the nasopharyngeal, occipital and cervical vessels in the neck and face, then crippling intracranial pressure can also be expected, as these nodes regulate intracranial pressure. This can cause debilitating pain, also creating a blocking issue / preventing remineralisation unless resolved beforehand. You can read more about this topic in 2.2.2 Lymphatic maintenance.
Do you have a history of cracked lips / ears / toes / feet / rectum,
flaking skin, severe acne, dandruff, hair loss, red / inflamed skin patches / rashes,
eczema, psoriasis, nasal inflammation, tonsillitis, sleep breathing
disorder, gut pain / issues, cystitis, prostatitis, mastitis,
epididymitis, white or green/black film on tongue or discharge?
These are strong indicators for potentially invasive microbiome dysbiosis. The extent / severity of the invasiveness of these microbes has a direct correlation with the intensity and duration for activation of chronic innate immune response pathways. These alter energy metabolism towards specific immune functions and generate predictable symptoms, such as neurotransmitter and endocrine dysregulation, POTS, dysautonomia, elevated cholesterols, insomnia, frequent urination, etc., especially where coenzyme or mineral deficiencies are also present.
Orifices and tissues such as the nasopharynx, sinuses, throat, Eustachian tubes, ears, GI tract, rectum, vagina, feet, toes are areas which are not regularly exposed to direct sunlight. This list might well include all tissues, where someone is bed-bound or house-bound. These tissues provide “safe spaces” for any pathogenic microorganisms to colonise, create biofilms and thrive, without appropriate immune surveillance.
[source: https://commons.wikimedia.org/wiki/File:Paranasal_Sinuses_ant.jpg]
[source: https://commons.wikimedia.org/wiki/File:Paranasal_Sinuses_lat.jpg]
Gastrointestinal biofilms and pathogens
In the case of a GI tract infection, this may also
affect dietary absorption efficiency and cause endotoxemia, sometimes
leading to gastroparesis, nausea / vomiting in response to food
consumption, along with other potential systemic impairments.
The timing of symptoms onset, in relation to meals may be helpful in identifying the location of unhelpful biofilms / colonies and also which interventions may be the most appropriate. Generally, the shorter the duration between meals and symptom onset, the closer the biofilm / overgrowth is to the stomach.
Upper GI / small intestine dysbiosis / overgrowth may benefit from oral dosing of specific biofilm breakers and related interventions, whereas lower GI / large intestine dysbiosis / overgrowth can be more easily targeted by administration of eg. robusta coffee enemas.
Similarly, upper GI microorganism colonies bloom in response to dietary intakes of simple sugars, BCAAs, etc., whereas colonies in the large intestine benefit more from more complex carbohydrates and proteins, which break down into simple sugars and BCAAs further along the digestion journey.
Different strategies are needed for different parts of the GI tract.
[adapted from source: https://in.pinterest.com/pin/640355640799063911/]
This protocol currently includes a number of staged interventions to address biofilms and pathogens in different locations inside the GI tract, such as Candex, Biofilm Phase 2 Advanced, NAC, spirulina, curcumin, fulvic acid, prebiotics, targeted probiotics, biofilm flushes, dietary interventions and water-fasting, with an aim of not unduly circulating endotoxins / acetaldehyde in the process of eliminating them, if at all possible. These strategies have been testing well and we are always exploring ways to improve on this process (please join the Discord online community to join the discussion).
Professional endoscopic biofilm removal is possible, however there appears to be a significant problem with general awareness of biofilm issues amongst gastoenterologists, so finding a willing clinician is currently challenging. A paper and video of removal here - https://x.com/joshual_tm/status/1825355958568304834
One of the key challenges is that invasive microorganisms which breach the (mucosal) barrier function can trigger an IFN-γ response, which causes collateral damage and inflammation to infected tissues in the process of oxidising pathogens, using reactive oxygen species.
If the rate of collateral oxidative damage + pathogenic damage exceeds the regenerative capacity of the tissue, this could further compromise the barrier function and dysregulate IFN-γ activity, leading to a “deadlocked” cycle / state. External indicators for insufficient collagen synthesis rates may include hEDS symptoms, poor skin texture, chronic cranial instability, slipped rib syndrome, thoracic outlet syndrome, etc.
A healthy microbiome appears to play a very important role in providing protection against invasive bacterial, yeast, mould and fungal infections.
Apart from generating gaseous toxins, ethanol and acetaldehyde – depleting silicon and other metals in compensation, many yeasts / mould / fungi and bacteria can cause dramatic metabolic alterations. They have an ability to break through our skin / epithelial tissue / mucosal barrier function from immune-evasive biofilms and cause recurring / chronic immune activation during the invasion. This immune activation inhibits specific mitochondrial metabolism and reconfigures a number of other metabolic pathways toward combating these pathogens. However, while ultimately beneficial, these alterations can be quite debilitating, under certain conditions.
Mammary glands and lactiferous ducts are present in both male and female anatomy. A less well-known fact is that males
are also capable of lactating under unusual circumstances that involve
low dopamine and elevated prolactin. These tissues are also another common area for microbial
biofilm formation.When diagnosed with an infection, this is known as
non-lactational mastitis.
Collecting any data on this microbiome is rather difficult when not lactating. It's possible that repurposing eg. MicroGenDX's WoundKEY panel could be useful, if a sample can be obtained.
For women, where biofilms in these microbiomes contain pathogenic species, it is expected that immune activity and inflammation in these (and any other infected) tissues will ramp up during oestradiol elevation, by allowing more IFN-gamma activity.
This immune activity elevation occurs as a short spike during pre-ovulation and for a range of days during the second half of the luteal phase, pre-menses. (see "2.2.7 Reproductive-health")
Sore and bumpy breasts during these times are common and inflammation may be observed in both the mammary glands and lactiferous ducts, with or without accompanying swollen inframammary, anterior axillary and parasternal lymph nodes.
While traditionally, many women have received advice about reducing oestradiol levels to prevent these symptoms, this logically leads to persistence of the infection.
Working with the body's natural signalling, while helping to manage the localised biofilm, oxidative stress and pathogens may help you break out of this unpleasant monthly cycle.
Topical use of 70% DMSO / 30% water (or 30% aloe vera gel), as a transport enhancer, combined with various biofilm breakers and anti-microbial interventions listed in this protocol may be an effective way to shorten this journey. This intervention can also be used with other tissues.
NB. DMSO is expected to create a localised histamine response when applied to skin, which will feel itchy for a short period. It's best applied with clean hands or gloves.
[source: Human Anatomy Atlas, by Visible Body.]
Parasites
Co-infections of flesh-eating parasites such as worms, flukes, amoebas, etc.,
can temporarily induce severe ME/CFS symptoms by directly attacking the
epithelial layer and allowing opportunistic invasion by any/all
microbial species.
Any of these can become systemic and create a chronic, recurring immune response in different tissues.
If you suspect you have a parasitic infection, over-the-counter
and/or prescription pharmaceutical interventions such as ivermectin,
fenbendazole, mebendazole, albendazole, methylene blue and pyrantel may be appropriate.
Some of these anti-parasitics also have anti-fungal and other
properties. These are commonly taken as either a single or multi-dose
intervention by all inhabitants of a household, per your pharmacist’s or
doctor’s advice.
For other species, such as amoebas, paromomycin and similar prescription drugs can be highly appropriate. Additionally, various herbal products based on black walnut, cloves and wormwood have also shown as highly effective, eg.
https://www.australianhealthfoods.com/product/ppc-herbs-herbal-tri-plex
The GI-Synergy product in Stage 2 already includes many of these ingredients.
Interventions
Whenever our efforts or immune system is successful in killing these microorganisms, their death can cause “dumping” and circulation of these toxins which contribute to a well-known “die-off effect” occurring. This die-off effect is responsible for a number of highly debilitating symptoms, such as headaches, nausea, additional fatigue, dizziness, swollen glands, bloating / gas, constipation or diarrhoea, joint or muscle pain, tachycardia, chills, cold hands / feet, itchiness, rashes, sweating and/or fever which resembles the “disulfiram effect”. Read more here: https://www.thecandidadiet.com/candida-die-off-symptoms/
This cascade can cause an ongoing / recurring cycle of extreme unpleasantness, if these infections and their original “safe spaces” (biofilms) are not fully resolved and a protective microbiome restored.
We have been actively researching a combination of some innovative and existing strategies to help kill these microorganisms and minimise the die-off symptoms (see 2.3.1 Herxheimer / die-off / acetaldehyde support). Some additional challenges relating to biofilms, which provide further protection against our immune activities are also targeted.
In addition to the metabolic supplement schedule included in this protocol, a more rapid clearance of any (somewhat) accessible microorganisms may be achieved by direct or topical interventions for these infected tissues. Commercial preparations are available with various levels of efficacy.
However, the quality of your data will determine the quality of your results. Having known targets allows for precision interventions to be used, whereas having unknown targets leaves you no choice other than "throwing darts in a dark room, hoping one of more of them lands". With a competent immune system, targeting the biofilms allows the immune system to see the pathogens and throw precision "darts".
Binders
Area of effect: localised and systemic interventions exist.
Limitations: somewhat selective interventions - matching products with toxins is important.
Risk profile: "Final binders" are usually non-toxic, some binders can also bind to nutrients, such as minerals, causing deficiencies over a short time.
Silicol Gel, Enterosgel: Both of these readily-available products are non-absorbing silica-based gels that act as “sponges” for endotoxins / LPS / acetaldehyde and salts of heavy metals, backed by clinical trials. These are consumed around mealtimes or interventions that induce die-off, to mitigate the Herxheimer effect symptoms.
Zeolite: Zeolite is a natural volcanic mineral with a high affinity for binding heavy metals, environmental toxins, and radioactive isotopes. It acts as a molecular sieve, trapping toxins within its cage-like structure. Zeolite is non-toxic and passes through the body without being absorbed, making it a popular detox aid. It is often used in detox protocols to support the elimination of lead, mercury, and other harmful substances.
Bentonite Clay: Bentonite is a type of absorbent clay known for its ability to bind toxins, chemicals, and heavy metals. When hydrated, it swells and creates an electrical charge that attracts toxins like a magnet. It is often consumed mixed with water and is widely used for digestive issues, detoxification, and skin health. It can be especially useful after exposure to environmental toxins or as part of a regular detox regimen.
Diosmectite (Smecta): Diosmectite is a natural clay-based binder with potent adsorption capabilities, specifically targeting bacterial toxins, viruses, and harmful substances in the gut. It forms a protective layer over the gut lining, reducing inflammation and aiding in the healing of gut mucosa. Diosmectite is commonly used for gastrointestinal issues like diarrhea and leaky gut and can be helpful in reducing symptoms of food poisoning and infections.
Activated Charcoal: Activated charcoal is one of the most popular and widely available binders. It has a porous surface that traps toxins, chemicals, and gases, preventing their absorption into the bloodstream. Often used for acute poisoning or in situations involving gastrointestinal distress, it can also be part of regular detox protocols. It is taken in capsules or powder form and is effective in reducing bloating, gas, and Herxheimer reactions during detoxification.
Fulvic Acid: Fulvic acid is a natural organic compound found in soil and water sources. It has strong binding properties and can help chelate heavy metals and toxins, making them more water-soluble and easier to eliminate through the kidneys. Fulvic acid is also known for its ability to enhance nutrient absorption and support cellular detoxification. It is often consumed in liquid form as a supplement for detox and overall health.
Humic Acid: Humic acid is a large molecule that works alongside fulvic acid to bind heavy metals, glyphosate, mycotoxins, and other environmental toxins. Its complex structure allows it to act as a natural chelator, pulling toxins from the body and supporting liver and kidney detoxification. Humic acid is commonly used to help restore gut health and improve immune function.
Spirulina: Spirulina is a blue-green algae rich in nutrients and known for its detoxifying properties. It is particularly effective at binding to heavy metals such as mercury, lead, and arsenic, promoting their elimination from the body. Spirulina is often used as part of heavy metal detox protocols and can be consumed in powder or tablet form.
Chlorella: Chlorella, another algae, is renowned for its detoxifying capabilities, especially in binding heavy metals, pesticides, and other toxins. It contains a unique outer cell wall that traps and removes these substances from the body. Like spirulina, chlorella is used in detox protocols and is available in various forms, including tablets and powders.
Pectin: Citrus pectin, especially in modified form, is a powerful binder that helps remove heavy metals and environmental toxins. It works by binding to these toxins in the bloodstream and digestive tract, preventing their reabsorption and facilitating their excretion through urine. Modified citrus pectin is often included in protocols for reducing toxic burden, particularly for lead and mercury.
Chitosan: Derived from the shells of crustaceans, chitosan is a natural polymer that acts as a binder for fat-soluble toxins, heavy metals, and excess lipids. It has therapeutic effects against LPS. It is often used to support weight loss and detoxification by reducing the absorption of fats and toxins from the digestive system. Chitosan supplements are available in capsule form and can be helpful in detox protocols.
Cilantro (Coriander): Cilantro is a natural herb known for its ability to mobilize heavy metals, particularly mercury, from tissues. While it may not be as potent as synthetic chelators, cilantro is often used in combination with other binders like chlorella to promote the safe excretion of heavy metals. It is a common addition to natural detox protocols and is consumed as fresh leaves, tinctures, or supplements.
A number of these binders are already included in the protocol at different stages.
Bacteriophages
Area of effect: localised, replicating and systemic (nebuliser, IV).
Limitations: highly selective intervention - matching products with species and strain are important.
Risk profile: Non-toxic, can create die-off symptoms.
A bacteriophage is a virus which doesn't infect human cells, however it does infect and kill bacteria with high specificity,
unlike antibiotics. They've been studied for over a hundred years and
Russia is well-established as the world-leader in this area.. which makes things a little
tricky in 2024.
Bacteriophages have been studied against gut microbiome dysbiosis in long COVID, with positive results.
https://www.mdpi.com/1999-4915/14/12/2614
A little-known fact about bacteriophages is that they can be found in seawater in concentrations of up to 107 mL−1,
however this does not automatically mean that random doses of seawater
will contain the relevant bacteriophages that eg. match your collections
of pathogenic species.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7150976/
If you have data from a microbiome report that indicates particular species of pathogenic bacteria,
you may be able to use a bacteriophage product in that tissue to help
eliminate them - very, very selectively.
However, on the basis of various species
regularly appearing in different tissues, bacteriophage products are
also available which target a range of common pathogenic species. It's
possible you may need more than one product to target all of the species
reported in your data.
A product selection table and various product instructions translated from Russian to English are provided in 5 Ordering products.
For
GI related targets, oral + rectal administration is recommended by
product manufacturers, presumably to avoid being degraded by stomach
acid.
The same W302 nebuliser mentioned in the DIY antiseptic recipe section is also appropriate for bacteriophage delivery to lungs and circulating targets.
Luer slip syringes can be used for other tissues / orifices.
NB.
Just like when using any other any other well-targeted anti-microbial,
die-off is expected. The more potent the anti-microbial, the larger the
wave of toxins you need to metabolise and/or excrete. Some support for
this can be found in 2.3.1 Herxheimer / die-off / acetaldehyde support.
DIY antiseptic recipe: mucosal clean and flush, rinse, topical spray
Area of effect: localised, with some systemic absorption / effects in some cases, eg. black seed oil.
Limitations: broad spectrum, can harm good and bad species. Requires follow-up probiotics.
Risk profile: Negligible toxicity, can create significant initial inflammation and die-off symptoms.
Popular antifungal soaps, shampoos and creams containing zinc pyrithione can be effective at inhibiting fungal overgrowth. However, these products are now banned in Europe due to concerns around causing DNA damage.
Part of a successful "untargeted" intervention for these tissues may also include first administering a solution to break up any protective biofilms, leaving this solution to incubate for 20–30 minutes before (where possible / appropriate) wiping the area clean and then administering a second solution to selectively inhibit these foreign cells. These two solutions can also be applied simultaneously. The process may be repeated daily for 1–2 weeks, or as necessary.
Getting started:
Ongoing testing and literature review has suggested that a simple solution of NAC and hypertonic sodium bicarbonate water solution can reliably break up many biofilms and lyase cells. Breaking biofilms exposes any remaining microbes to immune surveillance and any other interventions you may explore. Using this recipe in a Neilmed Sinugator, douche or other appropriate tool can be a gentler way to start clearing biofilms and remodelling microbiomes, such as the nasopharynx and sex organs.
Further research has also suggested that a solution containing diluted tea tree oil, clove oil and other oils, when applied with or immediately following NAC yields a tolerable, yet significant inhibitory effect on bacteria, yeasts, moulds and fungi which may rival or exceed existing pharmacological interventions and is appropriate for a range of applications.
Commercial preparations made from tea tree oil and clove oil, are also readily available as shampoos, vaginal douches, topical sprays, mouthwashes, creams and suppositories.
Available from your local chemist, Neilmed make sinus washing products – such as “Sinugator” and “Sinus Rinse”, which can be highly effective at pre-rinsing these difficult-to-reach mucosal tissues, 20 minutes prior to application of any antiseptic products.
2g boric acid and 5–10mg of liquid iodine can also be added to the Neilmed solution, for additional potency, however this may not be appropriate for daily use. A temporary smell of iodine and some burning / stinging would also be expected where infected tissues exist.
Note: Due to the die-off effect when killing fungi, using this antiseptic recipe while not using the other supplements from Stage 1 may be unnecessarily unpleasant and exacerbate symptoms.
| Part 1: Mix 500mg of NAC powder (preferably not from a capsule, as these usually have fillers, although these could also be filtered / strained after stirring), 500mg of sodium bicarbonate (baking soda), 1g of xylitol and >5 ml of water. |
| Part 2: Separately, mix essential oils – 20 drops of tea tree oil, 80 drops of black seed oil, 6 drops of oregano oil, 6 drops of clove oil, 1 capsule of Biofilm Phase 2 Advanced (BP2A). (You can add more black seed oil if you find this too strong.) |
| Mix both parts together to form your final solution – allow a 2 week shelf life. Store in an empty glass bottle with a dropper for convenient dosing. Shake well before use. |
To test this as a nasal antiseptic: while laying on your back, with your head tilted back and breathing through your mouth, drip about 6 drops of the solution into each nostril.
Let the solution run into the nasopharynx and incubate for a minute or so, while you suffer through some shockingly unpleasant burning for a few minutes (the first time), assuming you have infected tissue. (See the experiences reported in the Discord server for more information.)
Healthy tissues won’t be irritated at this concentration, so if it "burns" – repeat this process every 1-3 days until irritation / inflammation is not observed. It will get progressively much easier.
Rotating your head slowly to each side and gently “equalising” (like pinching your nose, gently exhaling through the nose against the close nostrils and "popping your ears", like on an aeroplane) with fluid in the nasopharynx may allow the solution to access the Eustachian tubes. (Performing the same in reverse and inhaling against closed nostril can evacuate the tubes, also.) After some time, blow / purge your nose, leaving some residue behind. A follow-up nasal probiotic may be very helpful after eg. 5-7 days of this, assuming there is no significant inflammation in response to the antiseptic.
To test this as a topical antiseptic: simply clean the area and then spray / apply the solution. A cotton tip could assist application to the ear canal or rectum (don’t use this in enemas).
To test this as a dental pre-rinse: apply a few drops to your tongue, teeth and gums, or more to gargle and spit. Wait a few minutes, then brush / floss as usual. Note: unpleasant flavour. Note: as an antiseptic, small amounts reaching your throat isn’t likely to cause toxicity, whereas drinking it intentionally could be harmful.
Sensitive tissues
Recipe 2:
Combine a “squirt” of Johnson & Johnson Baby Shampoo (it contains a gentle detergent and EDTA as a biofilm breaker. NB. We are currently exploring organic alternatives) ,
plus;
1 x "Neilmed hypertonic sodium sachet" (or a teaspoon of sodium bicarbonate / baking soda), for osmolality,
in 240mL of clean water.
This recipe makes a gentle, yet potent, biofilm breaking intervention that can be used in a Neilmed Sinugator/Sinus Rinse tool, vaginal douche, Waterpik, etc.
Alternatively, you can also make another DIY rinse recipe
Recipe 3:
Per 500mL of boiled / cooled water -
Mix 5g of sodium bicarbonate (baking soda) with 5g NAC. This allows an acid:base reaction (and gas release) to occur, which helps create a pH balanced solution.
This can then be combined with ¼ teaspoon of boric acid (making a 1½–2% solution) and 10 drops of the 5% Lugol’s iodine or 25 drops of 2% Lugol’s iodine.
To administer recipe 2 or 3:
- Eyebath: Use 30mL of the solution to bathe each eyeball, also cleaning the eyelids, lashes.
- Urethra: Administer 5–30mL of the solution via a large (needleless, Luer slip) syringe to the opening.
- Vagina: Administer 50-120mL, using a suitable douche tool or syringe and keep your hips and legs elevated for 30 mins.
- Lungs: (Use "Recipe 3" only) Administer 1-3mL via a drop-feed ultrasonic nebuliser, such as a "W302", found in most online marketplaces
- Sinuses, Eustachian tubes: This recipe can also be added to the Neilmed Sinugator reservoir.
The colostrum from Stage 2 can also be successfully used in mucosal tissues to neutralise unwanted species, antigens, etc.
Rotating between the “potent” recipe and the “gentle” recipes for 1–2 days is recommended if intense inflammation for more than 30 minutes is experienced. Continue with the nasal probiotics from the next section once an inflammatory response can’t be provoked by the normal antiseptic recipe.
Regardless of the recipe used, strong die-off effects can be expected the first time and should only be implemented after metabolic and detox support supplements are added in Stage 1 of the protocol.
Links to ingredients and tools mentioned can be found in the "5 Ordering products" section.
Biofilm breakers
Area of effect: some are localised, others are systemic.
Limitations: does not directly kill microorganisms - requires immune activity, probiotic species and/or other interventions to eliminate the species inside. Different biofilm compositions respond to different biofilm breakers - more than one may be required in chronic diseases with more than one pathogen indicated.
Risk profile: usually broad effects on biofilms for both good and bad species. Can trigger elevated immune activity and redistribution of microorganisms. If misused or overused, can damage microbiome diversity and abundance profiles.
Biofilm Phase 2 Advanced (BP2A): a localised bismuth-thiol biofilm breaker. Doesn't absorb. Included in Stage 2 and DIY antiseptic recipe.
NAC: a systemic biofilm breaker, particularly at higher doses.
Glutathione: a systemic biofilm breaker, particularly at higher doses.
Fulvic acid / humic acid: a systemic biofilm breaker, even at lower doses.
R-Alpha lipoic acid: a systemic biofilm breaker and metal chelator, particularly at higher doses.
Soap / detergent: a localised biofilm breaker, when used externally.
Ethylene Diamine Tetraacetic Acid (EDTA): a localised biofilm breaker and metal chelator, usually supplied bound to an electrolyte or mineral. Doesn't absorb well, orally - 5%. Can be used IV for circulating biofilms.
Dimercaptosuccinic acid (DMSA): a systemic biofilm breaker and metal chelator. Doesn't absorb well, orally - 25-30%. Can be used IV for circulating biofilms.
Dimercaptopropane-1-sulfonic acid (DMPS): a systemic biofilm breaker and metal chelator. Can be used orally or IV.
Microdacyn / hypochlorous acid: a localised biofilm breaker. Some absorption.
Ethyl acetate: a systemic biofilm breaker, even at very low doses. Found in robusta coffee and various acetone-free nail polish remover products.
Silver: a systemic biofilm breaker, even at very low doses.
Compounds found in foods: Allicin (Garlic), Curcumin (Turmeric), Epigallocatechin gallate (Green tea), Quercetin (Onions, Apples), Resveratrol (Grapes, Red wine), Eugenol (Cloves), Cinnamonaldehyde (Cinnamon), Sulforaphane (Broccoli, Brussels sprouts), Apigenin (Parsley, Celery, Chamomile), Berberine (Goldenseal, Barberry), Thymol (Thyme, Oregano), Carvacrol (Oregano, Marjoram), Fisetin (Strawberries, Apples), Linalool (Coriander, Lavender), Gallic acid (Blueberries, Pomegranates), Cinnamic acid (Honey, Cinnamon), Citric acid (Citrus fruits), Naringenin (Citrus fruits), Rosmarinic acid (Rosemary, Basil), Catechin (Cocoa, Dark chocolate), Ellagic acid (Pomegranates, Raspberries), Diallyl disulfide (Garlic), Capsaicin (Chili peppers), Piperine (Black pepper), Hydroxytyrosol (Olive oil), Xylitol (Berries, Plums), Isothiocyanates (Kale, Mustard greens), Ferulic acid (Rice bran, Oats), Kaempferol (Spinach, Kale), Pterostilbene (Blueberries), Saponins (Beans, Legumes), Chlorogenic acid (Coffee, Potatoes), Luteolin (Peppers, Carrots)
Probiotics: many of the probiotic species included in the protocol have potent functions as biofilm degraders and inhibitors. (see "Protective probiotics").
A number of these biofilm breakers are already included in the protocol. Overall, biofilm breakers should be considered an integral part of any microbiome dysbiosis or infection intervention and food sources should be included in any dietary strategy.
There are some additional strategies being tested which may feature in future updates, for example:
Upper GI biofilm flush, bind and purge recipe (advanced):
This a 3 step process, with similarities to a colonoscopy prep or gallbladder flush procedure. This
is not intended to ever be used a daily routine, as this intervention is
significantly broad spectrum and is highly destructive to the entire microbiome in the
upper GI. It would be used in limited circumstances only.
Step 1
contains a potent mix of biofilm breakers and anti-microbials, plus
some starch and warm water. Some of these items are not normally
consumed, however they are successfully used for pre-faecal microbiome
transplant (FMT) procedures. The mixture of anti-biofilm and
anti-microbial interventions is
adapted from Dr Thomas Borody’s excellent pre-FMT biofilm flush protocol and uses 2g biocompatible detergent (baby shampoo), 4mL of 1% iodine and 50mL Microdacyn).
The biofilm
flush recipe adaptation includes some additional items - an extra
biofilm degrader (ethyl acetate, from 2 shots of ground robusta coffee), 1 spoonful of diatomaceous
earth as a bulking agent and binder, along with an optional (opened) capsule of cascara to irritate / stimulate the bowels and increase GI motility. All of
these items are added to an empty glass and half a glass of hot water is
stirred in.
3 large spoonfuls of sifted potato starch (to prevent clumping) slowly stirred in to make a
rubbery mass that helps dislodge and drag / sweep along the broken biofilms. Fill the remaining part of the glass with cool water.
(This delightful concoction needs to be consumed quickly, or it'll polymerise in the glass.)
Step 2,
20 mins later - binders to help absorb toxins instead of allowing them
to circulate, which was a concern with the original pre-FMT protocol.
This next step includes a generous mix of binders, being 1/2 tablespoon of charcoal, 1/2 tablespoon of zeolite, 1/2 tablespoon of pectin and
1/2 tablespoon ofslippery elm powder, mixed into a glass of water.
Step 3,
20 mins later - this functions just like a colonoscopy prep or
gallbladder flush recipe. A large amount of electrolytes (Epsom salts / magnesium
sulphate) and lots of water are consumed. The large volume of magnesium
sulphate draws water into the bowel and purges the contents in a predictably dramatic fashion.
Add 1 teaspoon of Epsom salts (magnesium sulphate) to a glass of water. Stir until dissolved and consume.
Repeat this step 2 more times - 60 and 120 minutes later.
Overall, this allows the original biofilm breaking concoction from Step 1 around 40 minutes of travel throughout the GI tract, before being chased and diluted by the flush, reducing the impact of the biofilm breakers on the remaining length of bowel. It can potentially be adapted around the timing of peak gas output during a SIBO breath test, or reactivity timing to food.
Expect some unpleasant die-off symptoms / herxheimer-style reactions,
diarrhoea, nausea shortly afterwards. Exclusive bathroom access would be advisable for the next 12-18 hours.
Step 4, 12-24 hours later - consume S.boulardii, Bifidobacteria and Lactobacillus probiotics + prebiotics, related foods.
This flush could be performed
1-3 times, if
severe upper GI overgrowth exists, as evidenced by reactions to food in
under 1 hour. Excessive use of this recipe would NOT be recommended.
Protective probiotics
Area of effect: localised, however can translocate to other tissues.
Limitations: probiotics may not provide a comprehensive solution in isolation.
Risk profile: Non-toxic, can create significant die-off symptoms. The literature suggests some species can be opportunistic pathogens in highly immunocompromised people.
Following on from any efforts in clearing unwanted biofilms and microbial species overgrowth in the eyes, sinuses, nasopharynx, mouth, throat, oesophagus, lungs, GI tract, vagina, urethra and other mucosal tissues, further restorative efforts are usually needed in repopulating these tissues with helpful species to promote and maintain a healthy microbiome. (Links to these products can be found in the “5 Ordering products” section.)
These helpful species assist in inhibiting unwanted species, degrading biofilms and preventing opportunistic growth. They can also provide helpful functions, such as metabolism of oxalates, acetaldehyde, histamine, plus production of short chain fatty acids and other compounds beneficial to humans. Please note inclusion of these probiotics are based on an observed pattern of
diversity loss and are included for specific functions, to generally
promote a healthier balance in the microbiome, when combined with remineralisation and dietary changes.
They are not intended to replace MARCoNS, vaginal swabs, “GI-MAP” or Biomesight gut microbiome tests.
Many of these species were traditionally found in the Bacillus, Lactobacillus and Bifidobacterium genus, although recent taxonomy changes have relabeled / reclassified some of them, providing some minor confusion when researching species.
Bacillus subtilis:
Key Mechanism: Produces enzymes and antimicrobial compounds that degrade biofilms.
Notable Features: Spore-forming bacterium, resilient and able to survive harsh conditions, which allows it to act more potently against biofilms.
Effective Against: Both Gram-positive and Gram-negative bacteria.
Additional Benefits: Supports overall gut health and resilience against environmental stressors.
Lactobacillus fermentum ME-3:
Key Mechanism: Produces glutathione (antioxidant), disrupts pathogenic biofilms, reduces oxidative stress.
Notable Features: Dual-action as a biofilm breaker and antioxidant producer. Glutathione production sets it apart from many other probiotics, as it supports cellular detoxification.
Effective Against: Harmful gut pathogens and biofilm-forming bacteria, also including H. pylori..
Additional Benefits: Supports immune function, reduces inflammation, and has cardioprotective effects.
Lactobacillus reuteri:
Key Mechanism: Produces reuterin, a powerful antimicrobial compound that breaks down biofilms.
Notable Features: Strong antimicrobial activity, especially effective in the oral cavity and gut.
Effective Against: Pathogens like E. coli, H. pylori, and oral biofilm formers.
Additional Benefits: Promotes oral and gut health, reduces inflammation.
Lactobacillus rhamnosus:
Key Mechanism: Produces bacteriocins and SCFAs, which inhibit biofilm formation.
Notable Features: Excellent at inhibiting gut biofilms and maintaining gut balance.
Effective Against: E. coli, Pseudomonas aeruginosa, and other biofilm-producing pathogens.
Additional Benefits: Supports immune system, often used in combating gastrointestinal infections.
Lactobacillus plantarum:
Key Mechanism: Produces hydrogen peroxide and antimicrobial peptides that break down biofilms.
Notable Features: Broad-spectrum biofilm inhibition, active in the gut and oral cavity.
Effective Against: Gut and oral pathogens, including Candida and Staphylococcus aureus.
Additional Benefits: Improves digestive health, supports immune system function.
Lactobacillus casei:
Key Mechanism: Disrupts biofilms through production of bacteriocins and lactic acid.
Notable Features: Particularly effective against Helicobacter pylori biofilms in the gut.
Effective Against: H. pylori and other gut pathogens.
Additional Benefits: Supports digestive health, beneficial in addressing stomach ulcers.
Bifidobacterium bifidum:
Key Mechanism: Produces SCFAs like acetate, which create an acidic environment that disrupts biofilms.
Notable Features: Prevents biofilm formation by pathogenic bacteria in the gut.
Effective Against: Pathogens like Clostridium difficile and other harmful gut bacteria.
Additional Benefits: Supports overall gut health, improves digestion and immune system.
Bifidobacterium longum:
Key Mechanism: Like B. bifidum, B. longum produces SCFAs that lower the pH in the gut, which can inhibit biofilm formation. It also promotes the production of antimicrobial peptides and enzymes that disrupt pathogenic biofilms.
Notable Features: One of the most common Bifidobacterium species in the human gut, B. longum is well-adapted to the gut environment and plays a crucial role in maintaining microbial balance. It is especially good at outcompeting pathogenic bacteria.
Effective Against: Effective against a range of harmful bacteria, reducing biofilm formation in the gut.
Additional Benefits: Enhances immune function and promotes gut health, further protecting against biofilm-related infections.
Bifidobacterium lactis:
Key Mechanism: B. lactis can modulate immune responses, leading to the production of compounds that degrade biofilms or prevent their formation. It also produces lactic acid and acetic acid, which inhibit the growth of biofilm-forming pathogens.
Notable Features: Known for its resilience in the gastrointestinal
tract, B. lactis is widely used in probiotic supplements due to its
strong ability to survive stomach acid and bile. It's particularly
effective at adhering to the gut lining, enhancing its biofilm
prevention capabilities.
Effective Against: Has shown effectiveness in reducing biofilm formation by Escherichia coli and other gut pathogens.
Additional Benefits: Improves gut barrier function and promotes overall digestive health.
Bifidobacterium breve:
Key Mechanism: B. breve produces metabolites that interfere with pathogen adhesion and biofilm formation. It can inhibit the colonization of harmful bacteria by promoting a balanced gut microbiome and maintaining a lower gut pH through lactic acid and acetate production.
Notable Features: B. breve is one of the earliest colonizers of the human gut in infancy, making it especially important in the development of a healthy microbiome. It plays a significant role in maintaining gut integrity and has strong antimicrobial activity against pathogens.
Effective Against: Effective against Clostridium difficile and other gut pathogens that form biofilms.
Additional Benefits: Helps alleviate symptoms of gut dysbiosis, supports digestion, and reduces inflammation in the gut.
Bifidobacterium adolescentis:
Key Mechanism: Produces SCFAs and antimicrobial peptides that help prevent pathogenic biofilm formation. B. adolescentis can also enhance gut mucosal immunity, providing an additional layer of protection against biofilm-forming bacteria.
Notable Features: B. adolescentis is prevalent in the adult gut and plays a crucial role in breaking down complex carbohydrates, contributing to overall digestive health. Its ability to stimulate immune cells makes it particularly effective in preventing gut infections.
Effective Against: Reduces biofilm formation by pathogens in the gut, such as Salmonella and Escherichia coli.
Additional Benefits: Supports the immune system, promotes gut health, and reduces inflammation.
Saccharomyces boulardii:
Key Mechanism: Inhibits biofilms and outcompetes pathogens in the gut.
Notable Features: Effective against Candida and Clostridium difficile biofilms. Not susceptible to antibiotic influence.
Effective Against: Fungal pathogens and gut pathogens, particularly in cases of infection or dysbiosis.
Additional Benefits: Supports gut health, reduces diarrhea and inflammation, commonly used in traveler's diarrhea prevention.
Also potentially helpful is Oxalobacter formigenes, as an oxalate degrading species. When present in the small intestine, it also signals the host to secrete oxalates into the gut, instead excreting them via the kidneys. However, acidemia will override this.
Bifidobacterium are largely pH sensitive. You will have difficulties in restoring diversity and abundance while lactic acid metabolism is overused and zinc is low (hypoxia, impaired glycolysis, low minerals, anxiety disorders). Your OAT results should help indicate if lactic acid (+ oxalates) markers are elevated or the lactic acid : pyruvic acid ratio is elevated.
Studies and dosing information for these microorganisms in different mucosal tissues can be found on the Discord online discussion group and/or the literature. This protocol currently includes a number of key probiotics relating to these studies and their described functions / benefits:
- Life Extension Florassist: (Oral microbiome)
Probiotics - BLIS M18 S. salivarius M18, L. plantarum L-137 - DrFormulas Nexabiotic for Women: (Acid resistant capsule)
PaCran®SP (Cranberry fruit 50:1 extract), D-Mannose,
Probiotics - Saccharomyces boulardii, Lactobacillus helveticus, Lactobacillus delbrueckii LE, Enterococcus faecium, Bifidobacterium bifidum, Bifidobacterium longum, Bacillus coagulans, Lactobacillus rhamnosus LB3, Lactobacillus plantarum LM, Lactobacillus acidophilus, Lactobacillus rhamnosus, Bifidobacterium animalis lactis (formerly named Bifidobacterium infantis), Lactobacillus fermentum, Lactobacillus gasseri, DE111® (Bacillus subtilis), Lactococcus lactis, Lactobacillus casei, Lactobacillus salivarius, Lactobacillus brevis, Lactobacillus reuteri, Streptococcus thermophilus, Bifidobacterium lactis, Low moisture rice dextrin, delayed release capsule (hydroxypropyl methylcellulose, pectin, and water), silica. Allergen warning: Contains milk. - DrOhhira RegActiv Essential ME-3: (Survives stomach acid.)
Probiotics - Lactobacillus fermentum ME-3®, maltodextrin, magnesium salts of fatty acids (anti-caking agent). Vegetable capsule (hydroxypropylmethylcellulose). - CFUful 300 Billion CFU: (Acid resistant capsule)
Probiotics - Bifidobacterium longum BB536, Bifidobacterium longum HRVD90b, Bifidobacterium breve BR3, Bifidobacterium breve HRVD521, Lactiplantibacillus plantarum LP1, Lacticaseibacillus rhamnosus LR6, Lacticaseibacillus rhamnosus HRVD113, Lacticaseibacillus rhamnosus GG, Bifidobacterium infantis M63, Bifidobacterium lactis BS5, Bifidobacterium lactis HRVD524, Bifidobacterium lactis SD150, Lactobacillus crispatus LCR01, Lacticaseibacillus casei HRVD300, Limosilactobacillus fermentum LF8, Lactobacillus reuteri RD830, Lactobacillus acidophilus, Ligilactobacillus salivarius LS1, Bifidobacterium longum CECT7347, Lactobacillus casei CECT9104, Bifidobacterium bifidum, Lactiplantibacillus plantarum LPLDL, Bifidobacterium lactis MB2409.
Prebiotics - Fructooligosaccharides (FOS), Organic Barley Grass Powder, Organic Wheat Grass Powder, Organic Alfalfa Grass Powder, Organic Oat Grass Powder, Organic Beet Juice Powder, Organic Spinach Powder, Organic Suma Root Powder, Organic Licorice Root Powder, Organic Dandelion Root Powder, Organic Astragalus Root Powder, Organic Milk Thistle Seed Extract, Organic Ginkgo Leaf Extract, Organic Bilberry Extract, Organic Ginger Root Powder
- General Biotics Equilibrium Boost MegaDose Probiotic: (2 x acid resistant capsules per container.)
Probiotics - 115 strains, which have their own page, here - https://www.generalbiotics.com/equilibrium/strains/ - Ochek: (Only needed if indicated as missing in gut microbiome data. Promoted by dietary oxalates.)
Probiotics - O. formigenes, L. acidophilus, L. rhamnosus, B. lactis
Prebiotics - FOS - Pendulum Akkermansia: (Only needed if indicated as missing in gut microbiome data. Promoted by pomegranate.)
Probiotics - Akkermansia muciniphila - (Various sources, Kimchi) - L. sakei: (Anti-microbial. Also used in food production to prevent spoilage, etc.)
Probiotics: Lactobacillus Sakei
For example:
Nostrils: cotton tip / fingertip and apply inside the nostrils. Eustachian tubes: place drops of liquid into the nose and use the “equalisation” technique.
Mouth / throat / oesophagus / upper GI: gargle and swallow.
Lungs: nebuliser, 1-2 mL.
Vagina: add to a 5ml vaginal douche and elevate hips/legs for 15 minutes, while laying down, or place recently moistened, unopened capsule deep into fornix and allow it to dissolve.
Lower GI tract: use a probiotic rectal syringe (no tip) with <50mL of water, then “down dog” yoga pose for 15 mins to bypass stomach acid. Achieves a similar colonisation rate to FMT.
Eyes: place drops of liquid into the corners of the eyes and / or under the eyelids.
Prebiotics
Area of effect: localised, with systemic benefits.
Limitations: can be highly selective for promoting helpful species, if well-selected.
Risk profile: Non-toxic, can create die-off symptoms. Can promote unwanted species, if poorly selected.
You cannot solve dysbiosis by probiotics alone. Strategically feeding your microbiome and correcting symbiotic host metabolism, via remineralisation, etc. is the best way to make any lasting transformations. If you've ever made yoghurt, you'll have a good understanding of just how rapidly 2L of milk can turn into a (probiotic) fermentation product. 8 - 12 hours can turn eg. 2L of milk into 2L of yoghurt with just a spoonful of starter culture / microorganisms.
Your GI tract is no different, in this respect. Your choice of foods (substrates) allows you to achieve some selectivity in the species being fed and promoted. What you eat matters.
Inulin + fructooligosaccharides (FOS) are types of soluble fiber found in a variety of plants. Some common food sources include:
Chicory root (one of the richest sources), Jerusalem artichokes, Garlic, Onions, Leeks, Asparagus, Bananas, Dandelion greens, Wheat
Galacto-oligosaccharides (GOS)
is often added to foods as a prebiotic fiber, but it is also found in
trace amounts naturally in certain foods. Some food sources include:
Human breast milk (high content of GOS), Cow's milk, Lentils, Chickpeas, Green peas, Soybeans
Resistant starch is a type of starch that resists digestion and feeds beneficial gut bacteria. Common sources include:
Green
(unripe) bananas, Cooked and cooled potatoes (cooking and cooling
increases resistant starch), Cooked and cooled rice, Oats, Legumes
(lentils, chickpeas, beans), Barley, Corn
Polyphenols are compounds found in many fruits, vegetables, and beverages. Some common polyphenol-rich foods include:
Berries
(blueberries, strawberries, raspberries), Pomegranates, Cranberries,
Dark chocolate (high in cocoa content), Green tea (especially rich in
EGCG), Red wine, Olive oil, Nuts (walnuts, almonds), Herbs and spices
(turmeric, cloves, oregano)
These should be considered as high priority food items to introduce when planning your diet. However, they'd be expected to create some die-off reactions, gas and digestive discomfort at first. (see "2.2.1 Diet" for information on food items which also includes prebiotics)
Herbal Anti-microbials
Area of effect: localised and systemic
Limitations: may have broader effects on metabolism.
Risk profile: over-the-counter, generally regarded as safe. Can create significant initial die-off symptoms. Can alter drug metabolism.
There are a number of very effective and highly selective, plant-based anti-microbial products / foods.
Some of these interventions can simultaneously promote good species at the same time as inhibiting unwanted species. These would ideally be introduced in Stage 2 and will relate to your microbiome report data.
Notes:
Vanillin is often used at 2g, 2x per day and has been shown to kill sulphur-reducing and other unwanted species, however these species can be producing metabolites which have an antidepressant-like effect. Removing these species can create antidepressant-like 'rapid withdrawal' symptoms for up to 2 weeks.
Resveratrol has broadly beneficial effects at 300-600mg, 3x per day, but can inhibit aldehyde dehydrogenase activity, especially in larger doses.
Short-chain fatty acids (SCFAs) such as butyrate can have highly positive effects on the microbiome and epithelium, however can create significant alterations which induce multi-day long die-off. Starting slowly is advisable.
Quercetin has many beneficial effects, but can inhibit aldehyde dehydrogenase activity, especially in larger doses.
Berberine has potent effects against Clostridia, but has similarly potent effects on enhancing fatty acid transport at CD36 and inhibiting mitochondrial complex 1. May not be well tolerated by some people, especially before Stage 2.
Here is a table of direct and indirect promoters and inhibitors, by genus / species (sorry, this table is too large for mobile and tablet screens):
A highly potent, combination herbal anti-microbial product is available called GI-Synergy. It features many of the interventions listed in the table above. It would be advisable to start slowly and work up to a full dose, in Stage 2.
(Prescription-based interventions and other options)
Area of effect: some are somewhat localised, however usually systemic.
Limitations: highly non-selective and broadly harmful to many species - good and bad. Antibiotic resistance can be created.
Risk profile: may harm mucosal tissues. May inhibit host metabolism. Can create potent die-off symptoms. Requires probiotics, prebiotics and dietary optimisation to prevent deleterious effects on microbiomes. Creates risk for fungal overgrowth, if not combined with anti-fungal interventions.
It’s expected that for “PSSD” symptoms that a UTI or sex organ infection may be present. With good data and a discussion with your doctor, specific antibiotics may be appropriate to treat an indicated infection, as these tissues are difficult targets, especially in males. Bacteriophages may also be an option for many cases.
Once you have collected quality data, you should be empowered to make better decisions around how to move forward. To assist this process, a database of pathogens and overgrowth vs interventions is being developed to help you decide what the best course of action is and will grow, over time. Most of these inhibitors are prescription antibiotics that require a discussion with your doctor, who can also advise you on the risks and benefits of pairing any antibiotic use with anti-fungal medications like itraconazole and fluconazole, to prevent the opportunistic overgrowth of fungal species during any significant microbiome remodelling. Careful attention will also be needed towards probiotics, prebiotics and diet.
Ideally, any antibiotics and anti-fungal interventions would not be started until Stage 2, or very late in Stage 1, if some urgency is required.
The table below will hide columns on smaller screens. You can use complete or partial words eg. "kleb" or "Klebsiella" for searching genus, species or inhibitors.
When a person is chronically ill and confined to their bed / house, the transfer of pathogenic microbes from their body to their surroundings becomes a significant concern. Pathogenic microbes can transfer easily from the body to the environment and back again, causing an ongoing challenge to an already compromised immune system.
One of the primary concerns is the transfer of pathogenic microbes to the bed, pillows, sheets, and mattress. These surfaces can harbour pathogens and continue a cycle of infection.
Bed linen – sheets, pillowcases, and blankets – should be changed frequently and washed in hot water, with a hygienic detergent to kill any pathogens present and arrest the cycle of reinfection.
Mattresses and pillows should also be rotated and disinfected regularly. A waterproof mattress protector can also help prevent the accumulation of moisture and bacteria. These will also need regular cleaning.
Another concern is the transfer of airborne pathogens through air conditioning systems. Air conditioning systems can spread pathogens throughout a room, increasing the risk of infection. It is important to clean / change the air filter frequently and consider using an air purifier to help remove pathogens from the air.
Wet areas are a common issue - bathrooms and kitchens, etc. Mould and fungi can be found in extractor fans, drains, towels, rugs and soft furnishings, tile grout, spaces / voids around baths, showers and sinks, before being transferred to other locations. These microbial species produce mycotoxins in the form of gases, which can be silently poisoning household occupants - inhibiting energy metabolism and neurotransmitter homeostasis.
Nasopharyngeal inflammation and even intracranial pressure can sometimes be a "helpful" clue to investigate if there is a potential mould issue.
Carpets, window frames, walls, skirting boards, ceilings, books and bookcases, etc should also be inspected and maintained appropriately. Commercial air quality testing and mould remediation services are also available.
If not completely bed-bound and where the room doesn't have plants and/or pets (which can be excluded from the room for an hour), a relatively cheap ozone generator can be used to disinfect entire rooms, very effectively. Sunlight is also helpful in inhibiting certain microorganisms.
Overall, it is essential to maintain good hygiene practices – regularly disinfecting surfaces and fabrics, to prevent ongoing reinfection and unnecessary delays in progress.
We also share our microbiomes with close contacts. This happens in both directions, which can create interesting challenges and yet another reinfection cycle, in some cases. A host with a competent microbiome and immune system should be resilient against new challenges, helping to prevent this.
Where possible, getting outside of the home environment regularly can boost microbiome diversity and improve the efficiency of microbiome remodelling. There are many anecdotes of short-term remission events occurring, simply by taking a holiday away from home. Unfortunately, these normally revert within 1-2 months of returning to the original environment, or eg. staying in the same hotel room for more than 1-2 months.
2.2.4 The importance of “pacing” or “just enough activity”
Anyone who has experience with ME/CFS is likely to have gained a significant appreciation for the symptoms associated with “crashing” and Post Exertional Malaise (PEM).
A daily fear that too much activity will “crash” you and leave you with fatigue / malaise, flu-like symptoms and often tinnitus. A further fear that this may persist for days / weeks / months.
A hypothesis surrounding the mechanisms involved in PEM is being described in the upcoming paper, however the work-in-progress diagrams are available on the Born Free website.
Unfortunately, due to the trauma surrounding PEM, some people choose to severely limit their activity. This unfortunately has an impact on the capabilities of their immune system to deal with chronic infection.
One of the primary tools the innate immune system can use against microbial challenges is creating reactive oxygen species (ROS) to oxidise these pathogens. IFN-γ inhibits Complex I, which means that NADH generated by the TCA cycle can be diverted towards elevating NADPH, also powering NADPH oxidase (NOX) and nitric oxide synthase, which then (like xanthine oxidase, which uses NAD+ instead) create reactive oxygen species to oxidise pathogens, damaging your cells in the process. This can also lead to fungal die-off symptoms.
Excess NADPH / low NADP with elevated NADH / low NAD+ can be observed / inferred by elevated cholesterols, impaired glucose metabolism, elevated cortisol / inverted diurnal release profile, low aldosterone, low testosterone, low BH4, impaired methylation and various other compensations.
For optimal immune response and hormones, “pacing” should always be attempted – testing the appropriate upper threshold for activity, each day, unless that threshold has been exceeded already. Over sufficient time, inactivity leads to “rotting”, which is wholly undesirable, as the immune response is expected to be insufficient for maintaining resilience against pathogens.
The combination of supplements here should help improve the exertion threshold and buffer against “crashing”. However, you may have already noticed that fungal “die-off” symptoms share some common features with PEM and crashing, as does any immune activity. This will add some challenges for identifying your upper limits for exertion / glycogen synthesis rate.
Note the upper limit for exertion will be artificially reduced when IFN-γ is elevated and Complex I is inhibited, during any intense immune response. Increasing temperature elevates IFN-γ levels potentially ten-fold. Spirulina, schisandra and curcumin modify this pathway, favourably, by inhibiting NOX.
Proceed carefully, however the age-old phrase “no pain, no gain” absolutely applies here.
2.2.5 Structural issues
Thoracic Outlet Syndrome (TOS)
The lower traps and rhomboids are essential muscles responsible for scapular control and stability. Weakness in these muscles can lead to poor scapular control, which can result in chronically pronated shoulders and TOS.
Pronated shoulders occur when the shoulder blades “wing” and rotate forward, leading to a hunched posture. This can occur when the lower traps and rhomboids are weak and unable to maintain proper scapular alignment and is common in people with hypermobile Ehlers Danlos Syndrome (hEDS) metabolism. hEDS metabolism is described in the disease model as a "normal feature"
whenever innate immune response pathways are activated and/or specific
mineral deficiencies are present. The resulting forward shoulder position can cause tension and compression in the neck and shoulder region, leading to TOS.
TOS is a condition where the nerves, lymphatic thoracic duct and blood vessels that pass through the thoracic outlet become compressed, leading to pain, numbness, and weakness in the arm and hand. This can be bilateral or unilateral. Forward head position will further contribute to the progression of this syndrome. This can cause impaired immune response and water retention / lymphoedema.
To prevent TOS and other related conditions, it is essential to maintain proper scapular control and stability. This can be achieved through exercises that strengthen the lower traps and rhomboids, such as scapular retraction and shoulder blade squeezes. Additionally, maintaining good posture and avoiding activities that require prolonged shoulder and arm elevation can help prevent TOS, however when this position occurs during sleep, it can be hard to avoid.
Slipped Rib Syndrome, costochondritis and chest pain
Slipped rib syndrome, costochondritis, and worrying chest pain can all be downstream effects of a poorly seated rib – usually between T6–T8. When a rib is not properly aligned, it can cause thoracic instability, leading to overworked intercostal muscles and inflammation in the surrounding tissues. This is a common issue where hEDS metabolism is present.
Slipped rib syndrome occurs when a rib slips out of place and moves too easily, causing pain and discomfort. Costochondritis is inflammation of the cartilage that connects the ribs to the breastbone, which can also cause significant chest pain, which can mimic having a cardiac event.
When a rib is poorly seated, it can create an unstable environment for the intercostal muscles that are responsible for breathing. With mitochondrial dysfunction, these overworked muscles can become fatigued and inflamed, leading to scary chest pain and difficulty breathing.
It is wise to seek medical attention if you experience chest pain, as it can be a symptom of more severe conditions such as a heart attack or pulmonary embolism. However, if you have chronic chest pain that is related to slipped rib syndrome or costochondritis, treatment may include correcting the alignment of the rib and regular physical therapy, once any hEDS metabolism is corrected. Like any other resistance training, this tissue rehabilitation process will normally take weeks or months to complete.
A (free for the Born Free community) online posture rehabilitation course can be found here, using code: Free4Me - please carefully observe the modification to the advanced stretching technique for working around hEDS metabolism.
Atlas and / or upper cervical misalignment
Another potential structural issue can come from neck alignment
issues, relating to trauma and / or chronic cranial instability.
This
can severely affect blood-flow to and from parts of the brain via impingement of eg.
vena and arteria vertebralis, leading to neural hypoxia and a range of other symptoms. This is more likely to occur with someone
who has hEDS metabolism / collagen synthesis issues - which is described
as a feature in this disease model.
Various tests and interventions are available, with different
levels of risk / return. One particularly interesting approach is Atlas
Orthogonal (AO). Unlike the "high risk" neck manipulation techniques
used by everyday chiropractors, the AO method is gentle and uses a
special machine to perform the atlas adjustment.
https://youtu.be/O-cjIq7s6mM
As a precursor or replacement for AO, there are also some specialised stretches you can perform at home for free. These are included as part of the posture rehabilitation course above, however there are also some standalone videos on upper cervical stretching by various specialists.
https://youtu.be/NATds3r1zxw
If
you've had a previous history of neck trauma from vehicle accidents,
sports, chiropractic or other interventions, etc., visiting an AO
practitioner could be a worthwhile investment.
Practitioners can be found in many parts of the US, Australia and only sparsely in EU, by eg. searching Google for "atlas orthogonal near me"
2.2.6 Cortisol, limbic system, glycogen and IFN-γ
Cortisol is the “master” negative regulator for IFN-γ related immune activity and promotes catabolic energy availability via epinephrine (adrenaline).
What this means is that any/all influences which promote cortisol also decrease IFN-γ activity and provide some “relief” for many of the symptoms observed in ME/CFS.. while potentially creating others. This allows periods of increased functionality, while simultaneously inhibiting the necessary suppression of the pathogens that are triggering the innate immune response pathways.
In the disease model, we have described how cortisol acts as a “sensor” and signalling relay for insufficiencies of NAD+, P5P and glucose / glycogen, via phosphatidylserine and 11HSDβ1/2 flux (see figure 4). The metabolism for NAD+ and P5P is altered by IFN-γ and they act as upstream sensors for specific IFN-γ activities which can upset the metabolism or cause excessive tissue damage via oxidative stress. An inverted diurnal cortisol release pattern is expected.
When any of the sensed metabolites are insufficient, cortisol increases, signalling for an increase of epinephrine. This promotes energy "scavenging" or "catabolism", while inhibiting IFN-γ immune activity. This allows some of the cofactors and metabolites to replenish and by doing so, it helps restore normal metabolism. However, the same cortisol -> epinephrine elevation also signals for your cells to stop storing glycogen and instead use the existing glycogen pools for energy (see figure 1, upper right). Glycogen storage can therefore become problematic when cortisol -> epinephrine is dysregulated and chronically elevated.
As the metabolites reach sufficiency, cortisol levels normalise. If any triggers for IFN-γ are still present, then IFN-γ activity will resume and the cycle will repeat, as necessary.
Exercise, sex hormones and heat can increase IFN-γ. Dietary supplements can support IFN-γ activity. Cortisone medications are potent immunosuppressants and will inhibit IFN-γ.
Appropriate carbohydrate and protein intake (with uninhibited metabolism) supports optimal glycogen homeostasis. Sublingual and liposomal NMN can efficiently support NAD+ biosynthesis. Creatine can reduce the methylation “costs” associated with use of this pathway and also increase glucose transport. Magnesium and zinc can support B6 -> P5P metabolism. Manganese sufficiency is required for conversion of other substrates (protein -> amino acids, fats -> fatty acids) into glycogen, usually via the TCA cycle to the glycolysis pathway, however flowing in reverse.
Hypothyroidism affects both glucose metabolism and “B6 toxicity” / P5P insufficiency. The thyroid hormone, T3 (tyrosine, heme iron, iodide, selenium, calcium) is required to maintain FMN levels, needed for P5P recycling and to induce pyruvate flux into the TCA cycle.
The primary sex hormones (testosterone / DHT in males, estradiol in females) sense the elevation of NADPH (created during physical / metabolic activity), with sufficiency of NAD+, magnesium and zinc. These primary sex hormones then promote creatine synthesis and glucose uptake. They inhibit cortisol levels, promote nitrogen metabolite recycling and glycogen synthesis. This also allows IFN-γ activity to increase, which is also needed for tissue adaptations to exercise. Non-optimal sex hormones can cause chronic cortisol increase.
Importantly, lifestyle factors and learned responses to stimulus – namely stress / fear / anxiety – cause the limbic system to promote cortisol levels and inhibit the IFN-γ pathway / immune response, while decreasing glycogen stores. As this also decreases “ME/CFS” symptoms, a persistent cycle of fear / anxiety and immune suppression can also be learned / imprinted.
Has your life been entirely devastating for many months or years? Have you lost nearly everything? Are you lonely? Have you been medically gaslit (or abandoned) during this time and have therefore spent many of your days isolated from your friends, loved ones and former life, while laying in your own filth and usually a mouldy bedroom?
These events can reliably create trauma.. and guess what? No one - literally, no one - can deal with their trauma, alone.
If you are constantly in "fight or flight" mode, which is not resolving by correcting relevant nutritional deficiencies, or you think you are someone who is prone to habitually seeking out new things to trigger anxiety, you are going to face significant difficulties in maintaining glycogen stores. This may cause you to be in a somewhat "permanently crashed" state.
If you find yourself in this situation and believe it relates to trauma or any other unresolved psychological issues (either of which are entirely expected after living with ME/CFS or any other named entry-point to the disease model), then getting help is highly advisable.
Trauma counselling / therapy and brain retraining programs like DNRS can be game-changing for people who are suffering from chronic "fight or flight" programming. However, this protocol also describes an anxiety -> phobic response trap that can cage people and ways to navigate this successfully. From my observations, this affects at least 10% of people.
If you are affected by this subconscious programming, you will struggle to make forward progress while still in a chronic "fight or flight" state, due to the downstream metabolic consequences:
The "fight or flight" and/or "crashed" state may also lead to significant amounts of lactic acid and oxalates being generated. If the lactic acid can't be metabolised efficiently to usable energy, this can cause swollen / inflamed / numb / tingling body parts, especially in areas with smaller blood vessels, such as hands, feet, face and lungs.
Lactic acidemia can also make it very difficult to restore missing bacteria which are pH sensitive, eg. bifidobacterium, as excess lactic acid is secreted into the GI tract and also excreted via your kidneys, leading to frequent urination, "sandy urine", kidney stones, etc.
If you are feeling lost or in a crisis, THRIVE Lifeline offers 24/7 international text-based crisis support to anyone aged 18+, with a specific focus on multiple marginalized communities. They do not engage in non-consensual "active rescue" and they prioritise the texter's consent + autonomy.
For urgent help
SMS: +1.313.662.8209
General enquiries
Website: https://thrivelifeline.org/
Email: info@thrivelifeline.org
Anxiety, isolation, and phobia
Before continuing, for clarity, I'll restate my previously published, long-standing position against using CBT and GET as a primary therapy for ME/CFS and similar diseases:
I anticipate that there is a special place in hell reserved for clinicians who negligently misdiagnose ME/CFS patients with a purely psychological disease or "anxiety", or force patients with measurable mitochondrial dysfunction from chronic infections / dysbiosis / induced malnutrition to perform "graded exercise".
You wouldn't initially prescribe a diagnosed septicaemia patient CBT and GET as their primary therapy, so it's appalling that this continues to be the "gold standard approach" taken by numerous clinicians for ME/CFS patients. There are decades of evidence against this.
Yes, once the infections and malnutrition are sufficiently resolved and mitochondrial metabolism allows for it, physical rehabilitation is absolutely encouraged as part of the recovery process.
Yes, there are neurological and psychological issues created in this disease model - biochemically and from trauma, isolation, coping mechanisms and learned fear responses. These each require different interventions.
[/RANT]
This section explores the connections between anxiety, isolation, and phobic responses to symptoms in individuals with ME/CFS or similar chronic diseases. Drawing on parallels between chronic pain, fibromyalgia and ME/CFS, it aims to provide a clearer understanding of these challenges and how to exit another closed-loop / cycle which can be present in some patients.
Understanding the fear-avoidance cycle
A fear-avoidance model, initially developed in the context of chronic back pain by Dr Sarno as "Tension Myositis Syndrome (TMS)" and later extended by Dan Buglio as "Perceived Danger Pain (PDP)", also provides a working description for an observed pattern of daily experiences, physiological responses and behaviour that may create a further trap for some people already suffering from ME/CFS.
A popular example of perceived danger pain is the "Rubber Hand
Illusion" - a psychological experiment that demonstrates how the brain
can be tricked into perceiving a fake hand as part of one's own body. In
this setup, a participant's real hand is hidden from view, and a rubber
hand is placed in front of them. Both the hidden real hand and the
visible rubber hand are simultaneously stroked with brushes. Over time,
many participants begin to feel as though the rubber hand is their own.
This illusion highlights the brain's ability to integrate visual and
tactile information to create a sense of body ownership. https://youtu.be/sxwn1w7MJvk
In chronic pain, the fear of pain or "perceived danger pain" can lead to avoidance behaviors, which ultimately reinforce fear and reduce / prevent pain-free movement. The brain creates a genuine sensation of pain and measurable metabolic alterations to a perceived danger, to try and keep you safe. This is described as a learned phobic response that happens even when the original danger has been removed.
https://journals.lww.com/pain/fulltext/2022/08000/impaired_pain_related_threat_and_safety_learning.18.aspx
Similarly, some people with ME/CFS may fear pain from triggering or exacerbating existing metabolic symptoms such as mast cell activation syndrome (MCAS), post-exertional malaise (PEM), inflammation, sleep deprivation, etc, leading them to increasingly avoid foods, supplements and people, along with physical and mental activities. This avoidance can result in severe deconditioning, increased isolation, and a greater severity of symptoms, perpetuating a closed-loop / cycle of fear and avoidance.
Notably, even the possibility of avoiding discomfort can paradoxically increase fear over time. Studies show that individuals who are given the option to avoid pain experience increased fear when that option is removed, highlighting how avoidance can amplify anxiety rather than reduce it.
https://academic.oup.com/abm/article-abstract/55/3/216/5876277
Anxiety, isolation, and heightened threat response
Anxiety is a significant factor for individuals living with ME/CFS, similar to its role in chronic pain. People with ME/CFS often experience heightened anxiety - created by the mitochondrial dysfunction and downstream energy crisis. Neural hypoxia is one of the more common influences, downstream of immune activity, impaired iron homeostasis, oxidative stress, blood-flow and structural issues.
Additional anxiety can also sometimes be driven by feelings of inadequacy and/or fear from not being able to participate in life and fulfil roles as parents, lovers, workers, or friends. This anxiety is often compounded by fear of the unknown, thanks to inadequate medical care and also anticipatory fear - worrying about potential symptoms exacerbation by taking even small actions. This leads to heightened stress and worsened symptoms.
Isolation and unrefreshing sleep further intensifies this anxiety. For those with ME/CFS, reduced social contact can enhance the brain’s threat-detection systems, making individuals more likely to interpret normal bodily sensations as signs of danger. Studies indicate that even brief periods of social isolation can increase vigilance to perceived threats, which contributes to the cycle of fear and avoidance.
https://royalsocietypublishing.org/doi/10.1098/rsos.240101
Moreover, as a "perceived danger syndrome", symptoms related to immune activity and die-off, such as inflammation, pain, elevated histamine, rashes, nausea, diarrhoea or flu-like sensations, can be misinterpreted by the brain as a danger signal.
This heightened threat perception can create a feedback loop where normal immune responses are seen as threatening, further amplifying anxiety, acting as a "fight-or-flight" trigger, chronically depleting glycogen stores, altering blood-flow and leading to more avoidance behaviors.
This misinterpretation by your subconscious brain reinforces the fear-avoidance cycle, making it more difficult for people to break free from the loop of symptom exacerbation and fear. The brain can even create real, measurable symptoms of physical pain and emotional fatigue in the process of keeping you safe.
The phobic response to symptoms
Repeated experiences of PEM, MCAS, etc., can result in a conditioned, phobic response to certain triggers. This means that the brain starts to associate specific activities—such as physical exertion or even mental tasks—with symptom exacerbation, leading to an increased fear response. The brain, in a state of chronic stress or "under siege", may misinterpret normal sensations as threats, reinforcing feelings of vulnerability and the development of phobic responses to a wide range of stimuli.
People with ADHD and/or OCD-like traits are expected to have a
more difficult time with this, as the subconscious hyper-focus and
pattern-recognition traits can easily be fixated on the symptoms,
instead of the recovery progress. As an analogy, I'm reminded of a lesson once given by my motorcycle riding instructor:
When
riding a motorcycle, you seamlessly "merge" with the bike, to the point
that wherever you're looking is where the bike will travel towards.
Imagine a scenario where you're riding a motorbike around a large
paddock that has a single tree in the middle of it. The paddock is so
large that there is absolutely no reason that the tree should present a
significant risk of collision - you have a lot of wide open space to
enjoy. However, if you're consciously or subconsciously afraid of
hitting the tree, you'll keep glancing or looking over at it to make
sure you're safe. Consequently, by these actions, you'll increase the
risk of actually hitting the tree, or perhaps succeed in doing so. By
simply focusing on the wide open space where you want to actually be
riding, you will be significantly safer and enjoy your ride more.
This lesson applies to ME/CFS in the same way: don't focus on the symptoms - focus on the destination. Trust your body. The symptoms that we worry about the most may persist the longest. We give energy and life to things by paying attention to them.
Steps towards recovery
Several strategies can help people with ME/CFS navigate the complex interplay of physical and psychological symptoms:
Recognizing the Role of the Mind: Understanding the powerful connection between the mind and body is crucial. Anxiety and fear can perpetuate symptoms, so addressing these emotions is an essential part of recovery.
Daily Mantras / Replacing Unhelpful Thoughts: This can help re-frame negative thoughts and beliefs about symptoms, thereby removing unnecessary obstacles, fears and anxiety,
eg.
1. "This is a chapter in my life, not the whole story."
This
mantra puts the illness experience into perspective, reminding people
that their lives are not defined by their symptoms. It encourages them
to look beyond the present moment and envision a future filled with
possibility. It helps to counteract the sense of hopelessness that can
accompany chronic illness. It reminds people that their lives are still
unfolding and that their illness, while a significant challenge, does
not have to define their identity or their future.
2. "I choose to focus on what I can do, not what I can't."
This
mantra promotes a positive outlook and encourages individuals to find
joy and fulfillment in the present moment, even within the constraints
of their illness. This affirmation helps to shift attention away from
limitations and towards possibilities. It encourages people to explore
activities that bring them joy and a sense of accomplishment, however
small, to counteract the sense of loss and frustration that can
accompany chronic illness.
3. "Every step I take, no matter how small, is a victory."
This
mantra celebrates small wins and acknowledges the courage it takes to
move forward even when faced with fear and uncertainty. It encourages
people to appreciate their efforts, no matter how seemingly
insignificant. It emphasizes that progress is not always linear and
that even small steps forward contribute to overall healing.
4. "I am not alone in this journey."
This
mantra reminds people that they are part of a larger community of people
who understand their struggles. It helps to combat feelings of
isolation and foster a sense of belonging. It underscores the importance
of connecting with others who have experienced the challenges of living
with ME/CFS. Sharing experiences, offering support, and learning from
one another can be a powerful source of healing and hope.
5. "I am learning to listen to my body with kindness and curiosity."
This
mantra encourages a compassionate and non-judgmental approach to
symptom management. It fosters a sense of collaboration with the body
rather than seeing it as an adversary. This affirmation helps to shift
the internal dialogue from one of self-criticism and blame to one of
understanding and acceptance. It encourages people to pay attention to
their body's signals and respond with care and compassion.
6. "My body is healing, even when I can't see it."
This
mantra fosters patience and hope, reminding people that recovery is a
process that may not always be visible. It encourages trust in the
body's innate capacity to heal. It helps to counteract the
discouragement that can arise when progress feels slow or setbacks
occur. It reminds people that healing is happening on multiple levels,
even when it's not immediately apparent.
7. "My symptoms are a signal, not a sentence."
This mantra helps to re-frame symptoms as messengers rather than threats. It acknowledges that symptoms are trying to communicate something, but they don't dictate the future or define one's limitations. It draws on the idea that pain, fatigue, and other symptoms in ME/CFS are often amplified by fear and anxiety. It encourages a shift in perspective from viewing symptoms as inherently dangerous to seeing them as signals that need to be understood and addressed.
8. "I am safe, even when I experience symptoms."
This mantra directly addresses the fear response, offering a powerful message of reassurance. It emphasizes the distinction between experiencing a sensation and being in actual danger. It is particularly helpful in breaking the cycle of fear and avoidance. By repeating this affirmation, people can begin to retrain their nervous systems to associate symptoms with safety rather than threat.
9. "I am stronger than my fear."
This mantra
empowers people to face their fears and challenge the limitations they
have imposed on themselves. It emphasizes that fear does not have to
control their lives. This affirmation promotes self-efficacy and
encourages individuals to take an active role in their recovery. It
reminds them that they have the inner strength to overcome their fears
and gradually expand their boundaries.
These mantras, when repeated regularly and with intention, can help to rewire the brain's threat response, reduce anxiety, and foster a sense of safety and empowerment in the face of challenging symptoms. With practice and persistence, belief in these mantras strengthen. It only takes a few wins or reductions of something to see this approach is helping.
Gradual Exposure and Pacing: Gradually increasing exposure to normal activities and day-to-day life, along with appropriate pacing, can help desensitize the nervous system and break the fear-avoidance cycle.
Emotional Processing: Techniques such as journalling, therapy, or other methods for exploring and expressing emotions can be key in addressing underlying emotional issues that may contribute to symptom persistence. Recovery is not linear. Record your wins as a list. On bad days go back to the listed wins list and focus on the positive.
Somatic Practices: Practices like mindfulness, gentle movement, and breath-work can help people with ME/CFS develop a greater sense of safety and connection with their bodies, shifting the nervous system from sympathetic to parasympathetic mode.
Self-Compassion: Cultivating patience and kindness towards oneself during the recovery journey is crucial, as ME/CFS recovery can be a slow, non-linear and challenging process.
Building Social Support: Connecting with others who understand the experience of ME/CFS and critically, are supportive of the process you are undertaking can reduce feelings of isolation, provide validation, and offer emotional peace.
Recovery from ME/CFS is a deeply personal journey of "putting Humpty Dumpty back together again". Everyone has slightly different shaped pieces to reassemble.
2.2.7 Reproductive health, menstrual cycles, UTIs and PSSD
As part of normal female reproductive health, oestradiol normally elevates on days 10–12 and 22–26 of the menstrual cycle. This decreases cortisol levels and promotes IFN-γ activity. Without chronic infection, these alterations would allow for increased energy availability and libido. With chronic infection, these alterations allow for increased immune activity, pain / inflammation, neurological and emotional challenges, etc. Conversely, oestradiol is low on days 1–8, allowing cortisol to increase – decreasing immune activity and increasing anxiety.
[source: Feingold KR et al., editors. South Dartmouth (MA): MDText.com, Inc.; 2000-.]
Both of these situations are ultimately helpful, long-term. However, no one enjoys the symptoms of immune activity. Supplements like DIM, found in broccoli and calcium d-glucarate can help reduce the effect of these hormonal alterations.
Metabolism described in this disease model can significantly influence urinary tract infections by weakening the immune system, promoting bacterial growth in the urinary tract due to elevated glucose levels, renal excretion of oxalates, impaired nerve function and bladder emptying.
Similarly, pathogenic species found in the nasopharynx, oral, gut and other microbiomes may translocate or be transferred to urinary and sexual organs, potentially leading to further sexual dysfunction, pain and inflammation.
This may be more prevalent in PSSD, PCOS, endometriosis, cystitis, prostatitis and epididymitis sufferers, however dysbiosis and biofilm formation in urinary and sexual organs is generally found across the entire scope of chronic diseases.
For renal and urinary tract infections, methylene blue protocols and the ‘purple foods’ containing anthocyanins may be particularly relevant. Elderberries and chokeberries appear to be the richest sources of anthocyanins and will provide the same benefits in other tissues. Bacteriophages and protective probiotics can be extremely helpful.
2.2.8 Sleep
Sleep is often viewed as a simple daily routine, but it is far more than just rest for the body and mind. It is a complex and essential physiological process that plays a pivotal role in maintaining overall health, particularly when it comes to the brain.
Sleep is a naturally recurring state of altered consciousness and decreased physical activity. It is divided into several stages, including non-rapid eye movement (NREM) and rapid eye movement (REM) sleep, each serving different purposes in the sleep cycle.
Dopamine is a neurotransmitter that plays a vital role in mood regulation, motivation, and reward systems in the brain. However, the metabolism of dopamine produces toxic by-products. If these metabolites accumulate excessively, they can lead to oxidative stress and damage to brain cells.
The glymphatic system is a relatively recent discovery that has revolutionised our understanding of brain health during sleep. This system acts as the brain’s waste clearance system, similar to the lymphatic system in the rest of the body. It operates primarily during sleep and is responsible for removing metabolic waste products from the brain.
Melatonin is a hormone produced by the pineal gland in response to darkness. It plays a crucial role in regulating the sleep-wake cycle. Melatonin levels rise at night, promoting the onset of sleep and maintaining sleep duration. What’s fascinating is that melatonin has been shown to enhance the efficiency of the glymphatic system during sleep. It does this by causing a temporary contraction of brain cells, which allows cerebrospinal fluid to flow more freely, aiding in the removal of waste products. Oxytocin -> Prostaglandin F2α signalling also controls glymphatic activity.
https://www.nature.com/articles/s43587-024-00691-3
When we don’t get enough sleep, the glymphatic system’s efficiency is compromised. This can lead to the accumulation of toxic metabolites in the brain. Over time, this build-up can contribute to cognitive decline and increased risk of neurodegenerative diseases like Alzheimer’s, Parkinson’s and severe mood disturbances.
To benefit from this natural brain-cleansing process, it’s essential to establish a healthy sleep routine. Aim for 7–9 hours of quality sleep per night, starting ideally before 10pm. Maintain a consistent sleep schedule, create a comfortable sleep environment, and limit exposure to blue light from screens before bedtime.
The protocol targets issues which cause low serotonin, GABA and high cortisol levels at night, preventing quality sleep. If you fall asleep and wake up quickly with myoclonic jerks, you may have a calcium or other electrolyte deficiencies, hypometabolism as energy insufficiency from catabolic pathways and/or liver glycogen, and/or respiratory depression / airway restrictions. Another influence is low vitamin C from oxidative stress, further inhibiting dopamine beta hydroxylase, the enzyme which makes norepinephrine from dopamine. This is more likely to occur with increased immune activity and/or exertion. Low glycogen can reliably cause cortisol increase and is one of the major influences in post exertional malaise.
Hypometabolism can also occur during rapid microbiome changes and withdrawal from microbial / endogenous alcohol -> acetaldehyde -> morphine and/or GHB, see ("2.3.4 Rapid withdrawal symptoms, hypo/hyper-metabolism").
Following the dietary guidelines, plus correcting chromium, vanadium and other deficiencies will help prevent this.
2.2.9 PEM prevention and recovery
One of the hallmark symptoms of ME/CFS, Long COVID / Long Haulers and various other named syndromes is post-exertional malaise (PEM).
The disease model shows that exertion promotes IFN-γ and oxidative stress, which further inhibits glycolysis, fatty acid oxidation, methylation and other key energy metabolism.
Part of the glycolysis impairment relates to inhibited glycogenesis (glycogen synthesis). This is acutely influenced by elevated cortisol -> epinephrine in response to the energy crisis, however there are additional "background" influences from elevated microbiome-related acetaldehyde and various cofactor + nutrient deficiencies. This part of the disease cascade is described as a reversible glycogen storage disease.
Glycolysis insufficiency is frequently accompanied by tinnitus, vision reduction, dizziness, reduced mobility / muscle activation, muscle spasms / tremors, tachycardia and nausea.
The protocol addresses these upstream influences and the glucose uptake and glycolysis rate has been shown to improve / revert, however some daily variability around glycogen usage will exist relative to your exertion and immune activity levels.
During increased exertion, your immune activity creates oxidative stress, hence your carbohydrate and protein intake may need to be increased to match your glycogen expenditure. This would normally be additional carbohydrates, protein and a large additional intake of vitamin C and/or other antioxidants.
However, in a crash / PEM, the priority is restoring glycogen (and sodium) levels. Spoonfuls of NZ Manuka honey are one of the least risky sources for simple carbohydrates, as it has an antimicrobial profile thought to be related to the methylglyoxal content and various phenols.
You can also target restoration of energy availability and glycogen synthesis via alternative pathways, if they are functioning. These pathways may include (non-exhaustive):
- Branched-chain amino acids (BCAAs) catabolism. BCAAs are found in dietary protein sources. BCAA catabolism requires sufficiency of manganese, Vitamin B1 (as thiamine pyrophosphate), P5P, biotin and Vitamin B12 (as adenosylcobalamin, for 2 of the BCAAs - L-leucine has a different pathway). Assuming you are supporting these co-factors with the protocol, you can simply take 5-10g of BCAAs or L-leucine alone to rapidly help initial recovery and then increase carbohydrates and/or protein to prevent reoccurence.
https://www.bulksupplements.com/search?q=bcaa - Ketogenesis - supplying beta-hydroxybutyrate (BHB). This pathway requires phosphatidylcholine (PC) and NAD+ sufficiency. Assuming you are supporting phosphatidylcholine and NAD+ biosynthesis and redox with the protocol, you can also take 10–20g of a BHB supplement, as needed to help recovery and then increase carbohydrates and / or protein to prevent reoccurrence.
https://www.bulksupplements.com/search?q=hydroxybutyrate
If you have an asthma inhaler (salbutamol), it can be very helpful to increase catabolic activity and provide emergency energy availability for a period of time, but may also inhibit glycogen storage if used too frequently.
For best results, this schedule should be printed, laminated and ticked off with a whiteboard marker, each day.
Note that this schedule has been prepared using the custom troches and DIY "shake" and "sipper" recipes. Details for these can be found in the "4.2 Custom troches", "4.3 DIY shake and DIY sipper" and “5 Ordering products”
sections.
These preparations significantly reduce the daily complexity and
cost of the protocol, however it is also still possible to utilise individual
supplements. Links to those products are also provided in “5 Ordering products”.
However, if you aren't planning on using the custom troches, and / or DIY shake, you will instead need to optimally schedule a large array of individual products. (An alternative for the DIY sipper is not provided, or suggested.)
Details for these alternative schedule options are provided here:
2.3A Alternative daily supplement schedule - [no troches] - (if you intend on using the DIY shake recipe and not the custom troches)
2.3B Alternative daily supplement schedule - [no DIY shake] - (if you intend on using the custom troches and not the DIY shake recipe)
2.3C Alternative daily supplement schedule - [no DIY shake or troches] - (if you intend on not using the custom troches or the DIY shake)
.. please be aware, these schedules are considerably less convenient.
Stage 1: Remineralisation, increasing collagen synthesis rates and performing a controlled initial “die-off”
This stage will typically last at least two weeks and can be initially unpleasant due to the microbial “die-off” effect – even though it is being minimised by various supplements.
If necessary, slow things down, as needed / use reduced doses and build up. If tolerated, 100mg/day aspirin can be helpful at this stage to help inflammation / hypoxia.
However, many items are complementary to each other, therefore moving too slowly during Stage 1 implementation may lead to an unsupported / unsustainable increase of immune activity, ultimately reducing energy availability and leading to lower glycogen and increased oxidative stress induced damage.
Stage 2: Increased GI / mucosal interventions
Whilst continuing all items from Stage 1, add the following elements. Note that the Stage 1 DIY sipper and shake recipes are replaced with a Stage 2 DIY sipper and shake recipes that contains additional ingredients.
Stage 2 is expected to trigger additional gastrointestinal immune activity, which is likely to be observed as diarrhoea lasting a few days and sometimes nausea. Extra water and diosmectite / Diarelieve may be a useful binder during this time.
https://wikipedia.org/wiki/Diosmectite
Methylene blue is being tested as Stage 2 intervention.
https://bornfree.life/download/methylene_blue_protocol.xlsx
If your doctor has prescribed any anti-fungals and/or antibiotics, Stage 2 is the most appropriate place to introduce them.
However, these may have an impact on your existing efforts to restore microbiome diversity – some additional focus on probiotics, prebiotics and diet may be required. Ideally, any antibiotic use should be followed by Biomesight and/or other microbiome reports.
When you have completed Stage 2, repeat an Oligoscan / CMA test and don't proceed to Stage 3 until you have confirmed successful remineralisation. Similarly, iron status via standard pathology should be confirmed, if needed - iron, ferritin, transferrin saturation%, transferrin.
Stage 3: Stimulate and support a strong immune response
Important: confirm successful remineralisation of copper, zinc, selenium and manganese via CMA / Oligoscan and iron status via blood tests before proceeding to this stage.
This stage will typically require 4+ weeks.
If your cortisol / heart rate becomes elevated for long periods (>6 hours), or immune-related tissue pain/inflammation extends beyond 3 days per localised tissue, take a few days off the mushrooms, double the vitamin C and simultaneously decrease spirulina to 500mg during this “recovery break”. 100mg aspirin may again be helpful.
Expect temporary die-off symptoms, heavy immune response, pain / inflammation, POTS, fatigue, nausea, diarrhoea, headache, etc.
You will likely feel temporarily worse than your pre-protocol baseline, as the intensity of the innate immune response induces most of the ME/CFS symptoms. This may add some additional psychological challenges to this stage.
Continue items in all previous stages, apart from any minerals now measuring as “Normal+” on the Oligoscan report. Whilst continuing all Stage 1 and Stage 2 items, add the following elements. Note that the Stage 2 DIY sipper and shake recipes are replaced with a Stage 3 DIY sipper and shake recipes that contains additional ingredients.
2.3.1 Herxheimer / die-off / acetaldehyde support
Acetaldehyde is one of the primary toxins released during microbial die-off events and also in smaller amounts, multiple times per day, in response to normal dietary intake of nutrients. Our food intake also feeds our resident microorganisms – including the pathogenic species – which allows them to produce (toxic) metabolites and poison us following each meal.
Acetaldehyde potentially places a difficult burden on our metabolism in key places – histamine degradation, neurotransmitter degradation, collagen synthesis, carnitine synthesis (needed to transport longer chain fatty acids), fatty acid degradation, glucose transport and glycolysis, GABA metabolism, choline metabolism, methylation, vitamin B6 degradation, vitamin A degradation, lysine degradation, pyruvate metabolism and other pathways. Aldehyde dehydrogenase enzymes (ALDH2, 1A1, 1A2, etc.) detoxify acetaldehyde into acetate as a priority over their normal substrates. Having low NAD+ as a result of chronic IFN-γ activity exacerbates this problem significantly, as ALDH normally requires NAD+, magnesium and zinc.
Taurine, NAD+, magnesium, zinc and molybdenum help promote ALDH activity and restore normal metabolism. Cultivating acetaldehyde metabolising probiotic species like bifidobacterium and reducing acetaldehyde producing species is the long-term goal, however using one of these short-term interventions can be very helpful pre-meal and during die-off:
Kislip - https://ase-onlinestore.com/products-list/asetablet-1box/, worldwide shipping from Japan
-
Acetium - https://www.biohitshop.com/product/3/acetium-capsules-3-x-60-pcs, EU shipping only
ZBiotics - https://zbiotics.com/products/zbiotics, too expensive for daily use
NAC - small amounts after meals are now included in the DIY Sipper recipe.
DHM - now included in Stage 1, though additional amounts can be taken
2.3.2 Remineralisation
One of the biggest challenges for remineralisation with chronic disease and inflammation is absorption. The
disease model shows this is mostly related to elevated TNF-α, IL-1β, IL-6, IL-10, IL-22 -> hepcidin, which then inhibits 2 metal transporters - Divalent Metal Transporter (DMT-1) &
ferroportin. This further inhibits uptake and/or export of at least 11
metals in some cell types - Iron (Fe), Manganese (Mn), Copper
(Cu), Zinc (Zn), Cobalt (Co), Molybdenum (Mo), Nickel (Ni), Cadmium
(Cd), Lead (Pb), Vanadium (V) and Selenium (Se), in their 2+ state.
According to the literature, a 70kg human body normally maintains an
optimal level of many elements needed for enzymatic and other processes:
| element | mass | element | mass | element | mass | element | mass |
| Oxygen | 45kg | Gallium | 700mg | Nickel | 15mg | Lanthanum | 800μg |
| Carbon | 13kg | Rubidium | 680mg | Chromium | 14mg | Tellurium | 700μg |
| Hydrogen | 8kg | Strontium | 320mg | Manganese | 12mg | Yttrium | 600μg |
| Nitrogen | 1.8kg | Bromine | 260mg | Arsenic | 7mg | Bismuth | 500μg |
| Calcium | 1kg | Lead | 120mg | Lithium | 7mg | Thallium | 500μg |
| Phosphorus | 780g | Copper | 72mg | Ruthenium | 7mg | Indium | 400μg |
| Potassium | 140g | Aluminium | 60mg | Mercury | 6mg | Gold | 200μg |
| Sulphur | 140g | Cadmium | 50mg | Caesium | 6mg | Scandium | 200μg |
| Sodium | 100g | Cerium | 40mg | Molybdenum | 5mg | Tantalum | 200μg |
| Chlorine | 95g | Barium | 22mg | Germanium | 5mg | Vanadium | 110μg |
| Magnesium | 19g | Tin | 20mg | Cobalt | 4mg | Thorium | 100μg |
| Iron | 4.2g | Iodine | 20mg | Antimony | 2mg | Uranium | 100μg |
| Fluorine | 2.6g | Titanium | 20mg | Silver | 2mg | Samarium | 50μg |
| Zinc | 2.3g | Boron | 18mg | Niobium | 1.5mg | Tungsten | 20μg |
| Silicon | 1g | Selenium | 15mg | Zirconium | 1mg | Beryllium | 36μg |
Oral absorption of certain minerals will be inhibited throughout the day, relative to the inflammatory state.
Oral absorption is directly inhibited by the inflammatory cascade. The more severe someone's state, the more difficult it is to absorb minerals from food and oral supplements. For this reason, the protocol specifies sublingual mineral supplements as a "MUST", along with various coenzymes.
Combined with difficulties in absorption, various metabolic alterations will be causing enhanced excretion of electrolytes, and endotoxins (acetaldehyde, gliotxin, etc) can cause deficiency of silicon and zinc. Relative to the disease model, these can have significantly deleterious effects on energy metabolism, immune function and barrier function.
https://www.atsjournals.org/doi/10.1164/rccm.201301-0061OC
https://journals.physiology.org/doi/full/10.1152/ajpgi.00350.2009
Intravenous, intramuscular, subcutaneous, sublingual, rectal and transdermal routes bypass this mineral transporter blockade in the duodenum.
Compounded sublingual vitamins and minerals are now available internationally from an Australian pharmacy.
Please see the “4.2 Custom troches” section on how to order this product.
Magnesium spray is one example of a transdermal supplement. Dead Sea
mud is another very rich transdermal source for a number of minerals and
electrolytes, eg. calcium, magnesium, bromine and silicon. However,
while reportedly highly successful at helping resolve these
deficiencies, it's also a little cumbersome and time inefficient to use.
An alternate source of bromine (and iodine) is kelp, now found in the
protocol's DIY powder schedule.
Depending on the skin microbiome,
a rash or biofilm may develop. This can be prevented by pre-rinsing and cleaning the
skin with a NAC-based solution (e.g. 5g NAC in 250mL of water) when
showering and washing the area with a cloth. Be sure to thoroughly clean
and dry your skin, especially the areas where transdermal supplements
are being used.
Notes and cautions:
1) Intravenous and intramuscular administration of minerals and other nutrients may be offered by local IV nutrients clinics or your doctor. Unfortunately, without these are normally not customised around your data and doses used may be closer to those commonly found in total parenteral nutrition. These are not appropriate for resolving moderate-to-severe deficiencies.
2) IV iron / ferritin administration is well-known for causing a high rate of hypophosphatemia. The disease model suggests this is largely due to an effect which is very, very similar to "refeeding syndrome". As such, IV iron and other minerals would likely have a significantly reduced risk of triggering this state, if the dietary electrolytes, vitamins and other micronutrients are being well-managed. Stage 1 of the protocol targets these variables and would be recommended as a precursor to any IV iron infusions. This can be discussed further with your doctor.
https://pmc.ncbi.nlm.nih.gov/articles/PMC8279965/
3) The safety profile of any "nano" mineral compounds is not well-established and the data on a number of them is already concerning. I would avoid being exposed to these materials at this time.
4) In the interests of harm minimisation, I am also aware of reports that
some people have been self-administering non-prescription injectable
mineral products used in agriculture and veterinary applications out of desperation and/or frustration with the medical system, as a
way to rapidly alter their mineral status. Some of these products have seriously inappropriate ratios
and concentrations of minerals for use in humans and could cause harm.
eg. Yes, it's true that veterinary products, such as "Multimin Evolution Injection for Cattle" sold in Australia provides (elemental) zinc
@ 30mg, copper @ 7.5mg, manganese @ 5mg and selenium @ 2.5mg, per 0.5mL
subcutaneous dose. While you may consider that hypothetically, 3-4 x 0.5mL doses over 1-2 weeks
may help provide a rapid resolution for a deficiency of those minerals (apart from zinc - which has a much larger 2g+ total store in human tissues), I would strongly encourage people not to take shortcuts like these. These products are not made for humans. They're unlikely to be produced with any consideration around pH, osmolality and/or compound concentration. They may have undisclosed ingredients in the product formulations. There is a high probability of these products creating tissue damage and serious post-injection pain.
Please seek competent medical supervision / management and use registered / approved products only.
2.3.3 Blood-flow, hypoxia and fibrin-amyloid
Understanding Reduced Blood Flow in Chronic Disease: Impact on Quality of Life and Symptoms
Reduced blood flow, or impaired circulation, is a common issue in many chronic diseases. It can significantly affect a person's quality of life by exacerbating symptoms, slowing healing processes, and increasing the risk of complications. Understanding the factors that influence blood flow is essential for both medical professionals and patients managing chronic conditions. Addressing these influences not only alleviates symptoms
but also enhances overall well-being and disease outcomes.
Infections in the Bloodstream
Bacteremia, fungemia, and septicemia refer to the presence of bacteria, fungi, and toxins in the bloodstream, respectively. These infections can lead to systemic inflammation, causing blood vessels to constrict and reducing blood flow. In chronic disease patients, compromised immune systems make them more susceptible to these infections, which can worsen their condition and delay recovery.
Oxidative Stress and Vascular Health
Oxidative stress occurs when there's an imbalance between free radicals and antioxidants in the body, which is a significant factor in this disease model and relates to dysregulation of IFN-γ. Excessive free radicals can damage the lining of blood vessels, leading to stiffness and reduced elasticity. This damage impedes proper blood flow and can contribute to the progression of chronic diseases like diabetes and hypertension. Additional dietary antioxidant can assist during elevated immune activity.
The Role of Zeta Potential and pH
Zeta potential is a measure of the electrical charge on particles, such as red blood cells, in a fluid. A healthy zeta potential keeps cells evenly dispersed, promoting smooth blood flow. Changes in blood pH can alter zeta potential, causing cells to clump together and slow circulation. Maintaining a balanced pH is crucial for optimal blood viscosity and flow.
Nitric Oxide Synthase and Vasodilation
Nitric oxide synthase is an enzyme responsible for producing nitric oxide, a molecule that relaxes blood vessels and improves circulation. In chronic diseases, the production of nitric oxide can be impaired by oxidative stress and mineral deficiencies, etc., leading to vessel constriction and reduced blood flow. Enhancing nitric oxide levels can help alleviate symptoms by promoting vasodilation.
Fibrin, Fibrinogen, and Amyloid Aggregates
Fibrin and fibrinogen are proteins involved in blood clotting. In chronic conditions, elevated levels can lead to excessive clot formation, obstructing blood vessels. Additionally, fibrin-amyloid aggregates can accumulate, further hindering circulation. Monitoring and managing these protein levels are vital to prevent blockages and maintain healthy blood flow. NAC, nattokinase and DMSO may assist in degrading aggregates, along with biofilms. Aspirin and various prescription anticoagulants are also known to be helpful in managing symptoms in chronic disease.
Neutrophil Extracellular Traps (NETs)
Neutrophils are white blood cells that release extracellular traps to capture pathogens. However, excessive formation of these traps can increase blood viscosity and contribute to clot formation. In chronic diseases with persistent inflammation, NETs can play a role in reducing blood flow and exacerbating symptoms.
Sodium Levels and Blood Volume
Sodium insufficiency can lead to decreased blood volume, known as hypovolemia. Sodium helps retain water in the bloodstream, maintaining adequate blood pressure and flow. Low sodium levels can cause dehydration, reducing blood volume and impairing circulation. Ensuring sufficient sodium intake is important for patients unless contraindicated by their condition. (see "4.1 Electrolytes")
Dehydration and Hypovolemia
Dehydration reduces the total volume of blood in the body, leading to hypovolemia. This condition decreases the amount of blood available to transport oxygen and nutrients, negatively affecting organ function and energy levels. Staying hydrated is essential to support adequate blood flow and overall health.
Structural Influences on Circulation
Structural issues like chronic cranial instability can compress blood vessels, impeding blood flow to critical areas like the brain. Similarly, blocked lymphatic vessels hinder the removal of waste products and excess fluids, leading to swelling and increased pressure on blood vessels. Addressing these structural problems can significantly improve circulation and symptom management. (see "2.2.5 Structural issues")
2.3.4 Rapid withdrawal symptoms, hypo/hyper-metabolism
The metabolic consequences of Small Intestinal Bacterial Overgrowth (SIBO) and Gut Fermentation Syndrome are often not immediately clear. These conditions can create complex biochemical disruptions in the body, similar to the effects seen in chronic alcohol users.
https://www.ncbi.nlm.nih.gov/books/NBK513346/
Much like in alcohol dependence, individuals with SIBO may experience metabolic impairments due to the fermentation of sugars into alcohol and acetaldehyde within the gut. This process can disrupt homeostasis, precisely mimicking the metabolic challenges faced by chronic alcohol users.
When treating alcoholism, the typical approach involves gradually reducing alcohol intake, supported by high doses of thiamine (Vitamin B1) and adequate amounts of Vitamin C. In addition, psychological counseling is often recommended as part of the recovery process
https://pmc.ncbi.nlm.nih.gov/articles/PMC8302359/
In some cases, doctors may prescribe Naltrexone, a medication that can help regulate dopamine and GABA metabolism, offering relief from alcohol cravings. Naltrexone has additional benefits beyond this primary use, such as improving mood and reducing anxiety - however there is are some additional benefits.
https://pmc.ncbi.nlm.nih.gov/articles/PMC2565602/
What has not been fully understood or appreciated is that alcohol -> acetaldehyde elevation further elevates endogenous synthesis of morphine, codeine and gamma-hydroxybutyrate (GHB).
For endogenous morphine and codeine synthesis, the mechanism related to dopamine metabolism. When ALDH1A1 and/or ALDH2 are inhibited, elevated dopamine and DOPAL cause an elevation of Tetrahydropapaveroline (THP) (also known as (S)-norlaudanosoline), which is the first step in the morphine biosynthesis pathway. This altered metabolism leads to behavioural changes that overlap ADHD, coupled with homeostasis alterations and dependence .
https://onlinelibrary.wiley.com/doi/10.1111/j.1755-5949.2009.00114.x
https://www.pnas.org/doi/10.1073/pnas.050324410
https://www.science.org/doi/10.1126/science.557839
THP has also been observed in Alzheimer's and Parkinson's disease patients, however the model suggests it will be found in numerous others. Morphine and DHMA has been observed in collected data by younger members of the Born Free community, without any exogenous use.
https://www.mdpi.com/1420-3049/28/5/2166
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3560700/
https://pubmed.ncbi.nlm.nih.gov/1545408/
Naltrexone, particularly in its low-dose form (LDN), is a well-known therapeutic intervention for managing opioid use disorder. It is also increasingly used to treat conditions such as Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), Long COVID, and Post-Vaccine Syndrome. The disease model suggests additional mechanisms for its observed therapeutic benefits.
https://pubmed.ncbi.nlm.nih.gov/38267326/
The body’s production of gamma-hydroxybutyrate (GHB) is linked to changes in GABA metabolism through a process connected to the GABA shunt. In this pathway, GABA is normally converted into succinic acid via an intermediate called succinic semialdehyde (SSAL). However, when the enzyme ALDH5A1 is inhibited, often due to low NAD+ levels, while NADPH levels are elevated, SSAL is instead metabolized into GHB.
https://www.ncbi.nlm.nih.gov/books/NBK1195/
GHB is marker #75 on the OAT results and is often quite elevated in more severe patients:
As we gain a better understanding of how the gut microbiome interacts with these metabolic processes, it becomes crucial to anticipate potential withdrawal symptoms during microbiome remodelling. A rapid improvement in gut health, especially after a significant dietary shift or use of antimicrobials and/or biofilm breakers, can lead to sudden withdrawal from multiple endogenous narcotics.
The more rapidly any successful gut fermentation syndrome remediation is performed, the more likely that someone will go into rapid withdrawal symptoms for multiple simultaneous narcotics.
For instance, transitioning to a ketogenic diet or using antimicrobials can trigger an initial wave of endotoxemia (toxins released from dying bacteria), which may temporarily suppress withdrawal symptoms. However, as microbial production of alcohol and its byproduct acetaldehyde decreases, there is a corresponding reduction in the synthesis of morphine and GHB. This may result in metabolism and symptoms expected during chronic alcohol, opioid, and GHB withdrawal, which can peak about a week after significant microbiome changes.
Depending on the significance of the alcohol / endogenous narcotic reduction, symptoms may include:
Insomnia, Nausea and Vomiting, Sweating, (Severe) Fatigue, Hypothermia (Low Body Temperature), Diarrhea, Abdominal Cramping, Hypometabolism, Tremors, Tachycardia (Rapid heartbeat), Muscle Aches/Cramps, Seizures, Hypertension (High blood pressure), Anxiety, Agitation, Reduced Motivation, Difficulty Concentrating, Hallucinations, Delirium/Confusion, Depressed Mood, Psychosis, Yawning, Goosebumps (Piloerection), Runny Nose (Rhinorrhea), Lacrimation (Tearing), Dilated Pupils, Internal Vibrations, "Band Around Head" Pressure (warning, this is an indication for severe withdrawal, ahead of seizures).
These can be potentially life-threatening / self-harm inducing. Ironically, the logical solution is fairly simple, although it may understandably raise some initial concerns.
It has often been said that "alcohol is the cause of and solution to all of life's problems" and never more literally than in this instance.
This observation has been shared by various well-known people with ME/CFS and related online groups such as https://www.reddit.com/r/hangovereffect/.
Although this author's opinion is bound to attract some criticism, I'd also advocate that using exogenous alcohol, as an over-the-counter tapering schedule against withdrawal from the microbial-sourced alcohol (and the 2 downstream endogenous psychoactive substances) is a far simpler and less problematic therapeutic intervention than administering exogenous opioids and/or benzodiazepines, in an attempt to create an effective tapering schedule.
These 2 classes of drugs are both well-known to be "drugs of dependence" and will likely require high doses to be effective symptomatically. High doses of these interventions can create a long tapering schedule of their own that may last 6 months to a year and is known to be highly unpleasant.
Following a strict alcohol tapering schedule and avoiding dosing at levels which induce alcoholic intoxication is required. The goal is to remain in a tolerable level of withdrawal symptoms during the taper, rather than attempting to make the process "feel pleasurable". This will be highly personalised and likely involve multiple doses over the day / night, which decrease over time. Having appropriate monitoring and management would be highly advisable.
Caveats and Risks
1) It would be optimal to avoid alcohol reaching the gut microbiome.
Neat alcohol such as gin, vodka or whiskey, when taken in small sips
and absorbed largely via the mucous membranes found in the mouth, throat
and oesophagus would be a preferred route of administration.
2) While alcohol add-back therapy is known to be problematic in chronic alcohol use withdrawal due to the risk of behavioral disorders, such issues are less likely to arise in conditions like ME/CFS or Long COVID where alcohol consumption was not voluntary or habitual. However, professional oversight and adequate peer support is still recommended to manage the process effectively and provide a safety-net.
In addition to alcohol tapering, certain supplements may also help manage withdrawal symptoms relating to hypometabolism.
These include:
Coffee or caffeine.
Forskolin (will need tapering).
Hesperidin.
2.4 Optional follow-up
When the elements reported by your Oligoscan are optimal, a 3+ day “water fast” may provide additional benefits. This is not advisable with severe mineral deficiencies.
If this is your first water fast, it is generally advisable to have someone monitoring you during this time. Avoid driving vehicles, stress and excessive exertion.
Fasting protocol requirements (per day):
- No food or other supplements
- 3L water
- 5g (teaspoon) of sodium chloride (5g table salt contains 2.5g elemental sodium)
- 3g NAC (mucolytic, oxidative stress)
- 1000mg magnesium oxide (will induce diarrhoea)
Optional add-ons:
- EGCG 500mg, 3× per day
- Resveratrol 120mg, 3× per day
- Hesperidin 500mg, 2× per day
- “Upper GI biofilm flush, bind and purge recipe” (see: "2.2.3 -- Biofilm breakers"), the night before starting day 1 only.
Important safety consideration:
To break a water fast “early”, use two or more apple cider vinegar doses – without capsules – as a succinate source. This is only a requirement if EGCG has been dosed in the previous 6 hours. Failure to observe this safety consideration may result in rapid cyclical blackouts and convulsions until the EGCG is fully metabolised or until someone else administers apple cider vinegar. This could easily be fatal, for example if operating a motor vehicle. You have been warned.
2.5 Ongoing preventative maintenance
After successfully remineralising and remediating dysbiosis sufficiently enough to enjoy a normal quality of life, you may be inclined to adopt lifestyle changes and dietary strategies to prevent sliding back down the slippery slope to poor health:
Real food, lots of coloured vegetables and diversity. Eat the right ballpark targets for carbohydrates, fats and proteins. You can use an app such as https://cronometer.com to help structure your diet and learn what micro and macronutrients are in each food until it becomes second nature.
Now that your dietary absorption is working, your micronutrients should be coming from food, rather than supplements. The protocol’s diet is still a good foundation, however you won’t need to be mindful of avoiding excessive oxalates, vitamin B6, histamine or vitamin A.
Vitamin D3 is a good supplement to maintain.
Maintenance supplement
Here are 3 product examples for very similar daily shakes with "lite" versions of the protocol ingredients, albeit in forms which aren't suitable for someone in a moderate / severe state . These could be highly appropriate as a maintenance / preventative strategy, alongside busy lifestyles and imperfect diets.
The first two products contain 75+ ingredients. Huel Daily Greens has 91 ingredients and may be a superior product (does not ship to Canada).
Athletic Greens 1 (AG1) - https://drinkag1.com/ [There have been some recent AG-1 concerns circulating on social media and this is being investigated.]
Nuzest "Good Green Vitality" - https://www.nuzest.com.au/products/good-green-vitality
Huel "Daily Greens" - https://huel.com/products/huel-daily-greens
One of the main macronutrient differences between Good Green Vitality, Daily Greens and AG1 has additional pea protein "for digestive comfort" and costs a little more.
Your hormone synthesis, methylation and immune activity are promoted by physical exertion. This benefits your energy metabolism, sleep, neurotransmitters and helps prevent disease. Posture rehabilitation and maintenance is also important.
Eat foods which degrade biofilms, such as;
Herbs and spices like turmeric and black cumin, which contain tannins, phenolics, flavonoids, aromatics, etc. Sugar replacements such as xylitol and stevia. Mushrooms, especially reishi.You can perform a periodic biofilm disruption / challenge interval – e.g. a large oral dose of eg. tetrasodium EDTA or robusta coffee (ethyl acetate) once every 2–4 weeks and a similar interval for nasal / sinus and other microbiomes, using a relevant tool where necessary. Ocean swimming can be helpful. Yearly water fasting intervals would be advantageous. Occasional "robusta coffee enemas" are also rather useful for biofilm maintenance in the large intestine.
Checking your mineral status every 3–6 months is a good way to see how your diet is performing and make corrections. It can also be used to infer your levels of inflammation and potentially dysbiosis, which could justify further testing, e.g. OAT / microbiome.
4 Calculating supplement doses
It is generally expected that many intracellular deficiencies for eg. silicon, magnesium, iodine, selenium, molybdenum, copper, zinc and others may show in your CMA and / or Oligoscan data (and that functional deficiencies for iron, manganese, copper and six others may exist in any HTMA data, indicating inflammation severity over time.)
Assuming inflammation and pH imbalances are correctly managed, resolving these deficiencies may take, eg.
2 or more months, via non-oral routes, eg. sublingual / transdermal / rectal.
1 - 2 weeks via appropriately dosed parenteral administration. This can then be easily maintained via non-oral routes.
NB. These deficiencies are likely not going to resolve at all using standard oral dosing, due to mineral transport inhibition in the duodenum.
If your Oligoscan and/or OAT data shows low phosphorus, the upstream causes for this need to be addressed as a priority, or else remineralisation will be highly problematic. Common upstream influences include the various issues affecting mitochondrial metabolism, to the point of triggering lactic acid metabolism (anaerobic glycolysis). Some of these include insufficient pacing, zinc status, oxidative stress support and oxygen transport / coagulation.
If you are using the custom troches, a number of these minerals
and various vitamins are combined in a sublingual dose, which greatly simplifies this part of the protocol. The
default formulation should suffice for most
people, unless your transferrin saturation is at or above 40%, in which
case you would reduce the ferritin content to zero. (see “4.2 Custom troches” section)
Please recheck your CMA / Oligoscan for progress on remineralisation regularly (and HTMA, as desired, for progress on inflammation, strontium and rubidium). Adjust mineral supplements as needed if remineralisation is slow. There appears to be a bell curve response for absorption of many metals, where around 5-10% of the total system stores is the upper limit, per day and further efforts result in active blockade. Similarly, absorbing a reasonable amount of excess minerals is not normally problematic unless you have, for example, Wilson’s disease, hemochromatosis or beta thalassemia. These diseases are rare, however need careful management.
Where an element is indicated as non-optimal, you can use these suggested (elemental) minimum daily doses below, relative to the interpreted lower threshold.
Based on our collected data, we interpret Oligoscan / SO/Check reports using different upper and lower thresholds than the provider’s report layout indicates.
For Oligoscan reports, VISUALLY, the "Low" threshold is relocated to halfway between the original Low and OK vertical lines, (ie. where the “a” in “Normal” is located, to the left of “OK”) and the "High" for all markers except fluorine is relocated to halfway between OK and original High vertical lines (ie. where the “o” in “Normal+” is located, to the right of “OK”).
Numerically, if you wanted to do this computationally, Oligoscan "Low" and "High" threshold values for each marker would be recalculated as:
Low=(((Low+High)/2)+Low)/2
High=(((Low+High)/2)+High)/2
NB. According to the 2024 Oligoscan practitioner's guide*, due to an unusual quirk in methodology / reporting, highly elevated minerals (to the right of our vertical blue line / upper threshold in the image below and usually indicated as yellow or red bar) need to be re-interpreted as highly deficient. This also applied to SO-Check reports. If you see this anomaly in your data, it would be advisable to confirm this by taking a CMA test, if possible. Otherwise, default to reinterpreting the marker as proportionally "low".
*The practitioner's guide discusses zinc transport blockade as the reason for the marker elevation. From our comparisons with CMA data, the issue also applies to other markers and appears to be something do to with the "trade secret" Oligoscan algorithm. Ultimately, I think this could be improved.
For So/Check branded reports, these have a different format / layout and markers are shown as a percentage deviation from “normal” instead of values. You can ignore this report’s two outer columns to use the dosing guide image above.
1. The same methodology "quirk" relating to elevated values in Oligoscan applies to So/Check, as do the higher sensitivity thresholds for interpretation.
2. So/Check Calcium and Iron are discarded / ignored for the same reason as Oligoscan.
3. So/Check Copper and Zinc markers may also be over-stated.
4. Numerically, the So/Check mineral and electrolyte markers have a reinterpreted lower in-range threshold of -14% and an upper in-range threshold of +14%, instead of +/-25%.
Marker values which are INSIDE the +/- 14% threshold are interpreted normally as progressively lower or higher than the ideal target, which is 0%, ie. "in-range, low" and "in-range, high".
Marker values which are OUTSIDE of these +/- 14% thresholds in either direction are both interpreted as "LOW" and are considered progressively worse on a scale, the further the value deviates from 0%, OUTSIDE of the new thresholds. For example, +/- 30% would be "VERY LOW", +/- 50% would be "CRITICALLY LOW".
5. In-range low markers should still be supported by diet and/or supplementation.
Although no longer used in this protocol, elevations of electrolyte excretion in hair tests can indicate low cellular uptake with dietary sufficiency, causing enhanced excretion. Where a hair mineral profile shows low potassium and similarly low rubidium, the rubidium deficiency will need correcting or else potassium levels may be difficult to restore. Similarly, calcium with strontium and magnesium with lithium. High zinc can indicate low histidine / insufficient protein.
Low phosphorus in Oligoscan or OAT data can indicate parathyroid issues, acetaldehyde and/or (metabolic/respiratory or renal) acidemia. ¼ teaspoon of sodium bicarb in water away from meals 1–3 times per day can be helpful in “patching” downstream issues of acidemia, until resolved.
Low sulphur in Oligoscan or So/Check data can indicate elevated transsulfuration, sulphur metabolising microorganisms or microbial oxalate issues.
Low iodine is often observed with fluorine excess. Fluorine is found in medicines, toothpaste and town water. Consuming 10g of tamarind paste per day can dramatically increase excretion of fluorine.
If you have taken a blood test for iron, transferrin, transferrin saturation% and ferritin and the transferrin saturation% is below 18%, you have a critical need for iron supplementation before Stage 3. However most oral supplements will not absorb and can feed pathogens.
For other supplement selection criteria:
“Do I need P5P?”
38, 39, 40, 75 – where no SSRI, melatonin or 5-HTP supplement is being used, if these markers are all in the lower range, this can infer low P5P levels, via (38) aromatic L-amino decarboxylase (AADC) [+ P5P] ⇒ monoamine oxidase (MAO) [+ riboflavin as FAD], via (39) kynureninase (KYNU) [+ P5P, less oxidative stress] and via (40) kynurenine aminotransferase (KAT) [+ P5P / zinc / magnesium], via (75) as 4-aminobutyrate transaminase (4ABT) [+ P5P] ⇒ SSAL [+ NADPH] -> GHB}. Part of this pattern assumes dietary tryptophan is sufficient.
51 – Pyridoxic acid / pyridoxate is a degradation metabolite of B6 / pyridoxal, which can be used to infer pyridoxal LESS any aldehyde dehydrogenase (ALDH) activity [NAD+ / magnesium / zinc deficiency, acetaldehyde], pyridoxine 5'-phosphate oxidase (PNPO) activity [riboflavin as FMN, tissue damage / TGF-b1 inhibition, hypoxia] and aldehyde oxidase (AO) activity [riboflavin as FAD, molybdenum, heme, iron+sulphur, hypoxia].
“Do I need biotin?”
57 – Methylcitric is used to indicate biotin availability. If this marker is out-of-range in either direction, sublingual biotin will need to be carefully used in Stage 2.
“Do I need trimethylglycine (TMG) / betaine?”
37 (36:33) – The lower the integer in 37, the more likely you are to benefit from some methylation support. 3,4-dihydroxyphenylacetic acid (DOPAC) ⇒ homovanillic acid (HVA) involves 1 enzymatic reaction – catechol O-methyltransferase (COMT), which requires S-adenosylmethionine (SAMe) as a cofactor. SAMe is produced by the methylation cycle. These markers can be confounded by overgrowth of certain bacteria and by renal synthesis of dopamine.
41:42 – This ratio can also help interpret methylation status. An unbalanced ratio of uracil:thymine can indicate low activity at thymidylate synthase. If uracil is also low, this could further indicate dietary protein insufficiency.
“Do I need Vitamin B5”
52 – This marker can help indicate a vitamin B5 deficiency, which will affect lipolysis and pathways reliant on coenzyme-A (many). Elevated 16 / HPHPA may also benefit from more B5 to produce CoA. If in doubt, include B5 - it's not known to have tolerance issues.
“Does my OAT and Oligoscan / CMA data correlate?”
50 - Vitamin B12
52 - Vitamin B5 / pantothenic acid
53 - Vitamin B2 / riboflavin
54 - Vitamin C / Ascorbic acid
55 - CoQ10
76 – Phosphoric acid should correlate well with the Oligoscan phosphorus marker. If they do not, please share your data and report this in our Discord discussion group for further analysis.
4.1 Electrolytes
Maintaining electrolytes can be challenging, due to expected renal dysfunction in this disease model. If you are suffering from any pre-existing kidney disease consult your doctor prior to supplementing any of these elements.
Maintaining your electrolytes is arguably one of the most critical goals for your daily micronutrient intake, relative to your quality of life. According to the intracellular data collected and disease modelling, these are highly problematic in many chronic diseases, yet poorly captured by standard serum testing.
Electrolytes include potassium, sodium, calcium, magnesium, phosphate, chloride and bicarbonate. Electrolytes are required for ion channels / transporters, signalling pathways, blood pressure regulation any many important metabolic pathways.
When electrolytes are deficient, neurological symptoms, fatigue, muscle spasms and pain/inflammation may occur (skeletal, smooth and cardiac tissues). Digestion and nutrient absorption may be impaired. Serum levels of electrolytes are tightly regulated and often fail to help indicate intracellular or systemic levels until an emergency hospital visit is required.
Electrolytes can “exchange” at the cellular membrane as pairs by pumps called "ATPases", which consume approximately 2/3 of ATP produced inside the cell, to maintain functional levels of each electrolyte inside and outside the cells.
For example:
The Na+K+-ATPase exchanges sodium : potassium.
The Ca2+-Mg2+-ATPase exchanges calcium : magnesium.
Under extreme metabolic conditions, alternate exchangers, such as the Na+/Ca2+ exchanger (NCX) can exchange sodium : calcium, too.
This is not an exhaustive list.
For this reason, a deficiency of one electrolyte in the pair can create
issues absorbing and retaining the other, creating a secondary
deficiency. Ideally, deficiencies for electrolytes should be addressed as pairs, or all at once, to prevent exacerbating an existing imbalance.
Intracellular deficiencies for each electrolyte can come from various influences other than simple dietary deficiency of it and / or its "exchanging partner", eg.
Calcium deficiency can also be created by parathyroid hormone (PTH) issues downstream of eg. low iron and phosphate. Other influences include elevated oxalate synthesis, low Vitamin D, low Vitamin K2 mk7 and excessive NCX activity.
Common symptoms include low energy, low neurotransmitter synthesis, sleep disturbances, muscle tremors and osteopenia.
Magnesium deficiency can also be created by silicon deficiency and chronic diarrhoea.
Common symptoms include low energy, low neurotransmitter synthesis, sleep disturbances, muscle tremors and constipation.
Sodium deficiency can also be created by chronically elevated IFN-gamma and CYP2D6 enzyme activity in the kidneys, which produces renal dopamine and promotes renal sodium excretion. Other influences include frequent diarrhoea, vomiting or sweating. Above daily values of sodium intake are required during periods of immune activity.
Common symptoms include low energy, dizziness, nausea, muscle tremors and low blood pressure.
Potassium deficiency can be created by chronic alcohol / acetaldehyde, chronic kidney disease / infection, diabetic ketoacidosis, frequent diarrhoea, vomiting or sweating, folate deficiency, chronic elevation of aldosterone.
Common symptoms include low energy, low neurotransmitter synthesis, muscle tremors and high blood pressure.
Phosphate deficiency can also be created by chronic alcohol / acetaldehyde elevation and also acidemia, triggering renal excretion of phosphorus. This can come from metabolic or respiratory acidemia. Elevated lactic acid + low intracellular zinc is one mechanism which can allow elevated lactic acid from an energy crisis, mineral deficiencies or hypoxia to progress to acidemia.
Common symptoms include low energy, muscle tremors / poor strength, seizures, rhabdomyolysis, respiratory suppression, softening of bones and teeth.
Bicarbonate deficiency can also be created by metabolic acidosis, chronic diarrhoea, elevated oxalate levels and chronic kidney disease / infection.
Common symptoms can include tachycardia, confusion and fatigue.
Chloride deficiency has not been commonly observed.
Most electrolytes should be consumed slowly over the day. They may cause diarrhoea and other symptoms in large doses.
Transdermal administration has been demonstrated as a superior route for magnesium absorption due to the "slow-release" aspect. Rapid absorption and downstream elevation of serum electrolytes triggers rapid excretion to restore homeostasis, resulting in poor electrolyte retention and wasted effort. This can be exacerbated by low activity levels and intracellular deficiency of the corresponding partner in the electrolyte pair.
Electrolytes are commonly available as salts, and the second table below outlines the relative amounts of each electrolyte in these salts.
The weekly DIY "sipper" recipe contains suggested amounts based on poor dietary intakes from food sources and can be adjusted where necessary.
TOTAL daily elemental targets from all food / supplement sources
| Element | Target Daily Amount | Notes and Sources |
| Sodium Na | >4g | (Daily value is 2300mg. More is required than normal, due to elevated excretion rate.) 5g (1 teaspoon) of table salt contains 2.5g Na |
| Potassium K | >5g | (Daily value is 4700mg.) 10g of Nu-Salt (potassium chloride) contains 5g of K. 3 large potatoes (900g) contains roughly 5g of K. |
| Magnesium Mg | >500mg | Supplemental regimen should include transdermal route, where deficient. |
| Calcium Ca | >750mg | Increase supplementation to 1.5–2g if deficient. Cronometer can help visualise your calcium intake. CMA results show intracellular deficiencies. Low phosphorus and also low strontium in hair testing may also infer calcium status. Oxalate dumping can be expected initially. |
| Phosphate Pi | 1g | Meat, dairy, pumpkin seeds / pumpkin seed oil, red lentils, sunflower seeds, potatoes. Supplement if deficient. Supplements which combine phosphorus with various electrolytes, e.g. calcium phosphate, may be available in some regions. |
| Bicarbonate HCO3 | As needed | Commonly found in sodium bicarbonate / baking soda (NOT baking powder) and/or potassium bicarbonate. Typical dose is 1/4 teaspoon AWAY FROM MEALS, multiple times per day, if lactic acid is elevated and/or phosphorus is either high OR low in OAT results, or phosphorus is low in Oligoscan. |
Reference material: Elemental weights, by compound, for calculating servings of various electrolytes
| Electrolyte Compound | % Proportions | Weight Proportions |
| Sodium Chloride NaCl | Na 39%, Cl 61% | 6.4g contains 2.5g sodium & 3.9g chloride |
| Sodium Bicarbonate NaHCO3 | Na 27% | 5g contains 1.4g sodium & 3.6g bicarbonate |
| Potassium Chloride KCl | K 52%, Cl 48% | 9.6g contains 5g potassium & 4.6g chloride |
| Potassium Citrate C6H5K3O7 | K 38% | 13g contains 4.9g potassium & 8.1g citrate |
| Dicalcium Phosphate CaHPO4 | Ca 29%, P 23% | 3.8g contains 1.1g calcium & 870mg phosphorus |
| Disodium Phosphate Na2HPO4 | Na 32%, P 22% | 7.73g contains 2.5g sodium & 1.7g phosphorus |
| Monosodium Phosphate NaH2PO4 | Na 19%, P 26% | 6.6g contains 1.25g sodium & 1.7g phosphorus |
| Dipotassium Phosphate K2HPO4 | K 45%, P 18% | 10g contains 4.5g potassium & 1.8g phosphorus |
| Magnesium Aspartate C8H12MgN2O8 | Mg 8% | 6g contains 500mg magnesium 5.5g aspartate |
4.2 Custom troches
The custom troches / lozenges are available from an Australian compounding pharmacy. To order, use the order form at:
https://bornfree.life/download/troche_order_form.xlsx
Leave all “targets” at default values, unless your data shows a transferrin saturation above 40%, in which case set ferrous fumarate to "0" and review your cobalt status.
NB. LITHIUM CANNOT BE INCLUDED IN THE TROCHES DUE TO AN AUSTRALIAN LEGISLATIVE MISMATCH VERSUS DIETARY GUIDELINES. (Prescription only, unless <0.01%). Lithium will therefore need to be purchased and consumed separately. Oral absorption works.
Note and limitations
1. If you experience mouth ulcers / lesions / sores with use, pause for a few days and address your oral microbiome using eg. bacteriophages, antiseptic recipe and follow with oral probiotics in 2.2.3 Living without chronic dysbiosis.
2. These troches aren't overly palatable and are available to use as a suppository, if desired. It is suggested to avoid peppermint flavouring if this is your intended administration route, as it can trigger bowel movements. Troche 1 now has "vanilla butternut" flavouring, which is much more tolerable for either application.
3. The ferrous fumarate may cause a black / brown hairy tongue at times, if you have inflammation.
4. The ferrous fumarate may cause a false positive for occult blood on a GI test.
5. The ferrous fumarate and riboflavin will stain biofilms / plaques orange and/or brown. These can be dissolved by using a NAC + sodium bicarbonate rinse before brushing. See the 'gentle' antiseptic recipe in 2.2.3 Living without chronic dysbiosis.
4.3 DIY "shake" and DIY "sipper"
For convenience, weekly batches of powder can now be prepared ahead of time to simplify dosing and improve time management. You can still adjust / modify your weekly batches around any individual dosing requirements.
The weekly DIY preparation task is best created as 2 separate weekly recipes -
a. DIY "shake" - a supplements shake, consumed 3 times per day.
b. DIY "sipper" - an electrolyte + amino acid "sipper", consumed slowly across the day, in between meals. (Shake bottle before each use, as dicalcium phosphate is insoluble).
The tables below indicate the amount of powder to be added (or capsules to be opened) and thoroughly mixed together in a suitable kitchen mixer / grinder, such as the ones used for making sauces and Indian meal preparation. Ideally this device should have a stainless steel jar, support dry materials and have at least 1.5L capacity, eg. Philips HL7759/00, Philips HL7756/00, Thermomix, etc.(see "5 Ordering products" or search Google / Amazon / eBay for "indian mixer grinder" and double-check that any imported overseas models match your power plug / input voltage, eg. AU/EU 220-240V, US 110V)
In the absence of a suitable mixer, the destination tub itself can be
filled and shaken vigorously / used as a manual dry mixer (if your
energy allows or someone can assist).
Empty 1.5L or larger tubs / buckets are needed to store the finished powders. (see "5 Ordering products")
For the DIY shake: To calculate your serving size, divide the total net weight of your finished weekly powder by 21 to reach a single serving, taken 3x/day.
For example, 615g net / 21 servings = 29.3g per serving. Large kitchen scales will be required. (see "5 Ordering products")
The DIY shake is taken 3 times per day, 15–30 minutes before meals, replacing the existing schedule for those supplements, even those which may have been previous dosed only once per day.1
In Stage 2 and 3, there are items such as NAC and Spirulina which are present in Stage 1, yet have increased doses. These differences are shown in the table.
If you are just starting out, you can still prepare a full week of powder, start with smaller servings, e.g. ¼ the normal dose and increase the serving size over time to reach a full dose.
a. DIY "shake" recipe (weekly preparation)
| Product Name | Stage 1 | Stage 2 | Stage 3 | Notes | |
|---|---|---|---|---|---|
| 2 | B8 Myo & D-Chiro Inositol | 3 caps | 3 caps | 3 caps | For AU source, 1.5g = 3 caps. DE source has 20% more per cap. |
| 3 | B5 Pantothenic Acid | 0.7-3.5g | 0.7-3.5g | 0.7-3.5g | |
| 4 | Candex | 21 caps | 21 caps | 21 caps | |
| 5 | PQQ+CoQ10 | 7 - 21 caps | 7 - 21 caps | 7 - 21 caps | |
| 6 | Apigenin | 7 - 56 caps | 7 - 56 caps | 7 - 56 caps | |
| 8 | Psyllium husk | 35g | 35g | 35g | |
| 9 | Kelp | 7g | 7g | 7g | |
| 11 | Hesperidin | 7 caps | 7 caps | 7 caps | |
| 13 | Lecithin | 77g | 77g | 77g | |
| 19 | Trimethylglycine | 3.5g | 3.5g | 3.5g | Only needed if indicated by OAT |
| 20 | L-Lysine | 14g | 14g | 14g | |
| 21 | L-Proline | 14g | 14g | 14g | |
| 22 | L-Glycine | 35g | 35g | 35g | |
| 23 | L-Serine | 14g | 14g | 14g | |
| 25 | L-Glutamine | 35g | 35g | 35g | |
| 26 | Bamboo (Silica) | 14g | 14g | 14g | |
| 27 | Green Tea (EGCG) | 1.75-3.5g | 1.75-3.5g | 1.75-3.5g | |
| 28 | R-ALA | 4.2g | 4.2g | 4.2g | |
| 30 | Spirulina | 3.5g | 3.5-35g | 3.5-35g | Slowly increase in Stage 2 |
| 31 | a-GPC | none | 3.5g | 3.5g | Pause if it creates a headache. |
| 32 | Schisandra | none | 8.3g | 8.3g | |
| 33 | Elderberry | none | 3.5g | 3.5g | |
| 34 | Apple Cider Vinegar (ACV) | none | none | 16.8g | |
| 35 | Beta-glucans | none | none | 1.75g | |
| 38 | Dihydromyricetin (DHM) | 10.5g | 10.5g | 10.5g | |
| 48 | C Ascorbate | 14g | 14g | 14g | |
| 50 | Curcumin | 7 caps | 7 caps | 7 caps | |
| 71 | Colostrum | none | 28g | 28g | |
| 112 | GI-Synergy (K-64) | none | 7 sachets | 7 sachets | 1 sachet / day. Start slowly / separately, can cause potent die-off. |
b. DIY "sipper" recipe (weekly preparation)
This can be combined with eg. green or other tea, lemon juice, etc to modify the flavour of your "seawater-tasting" concoction and
then put into a 500mL drink bottle to be slowly consumed over the day, eg.50mL / hour,
ideally in-between meals - preferably 1 hour either side. (Shake bottle before each use, as dicalcium phosphate is insoluble)[If you find any particularly enjoyable combinations, please feel free to share them with the group!]
Individual electrolytes in the DIY sipper recipe can be reduced by amounts already obtained from food items, using your food logging results (see 2.1.4 Cronometer). This is relative to meeting or even somewhat exceeding the daily targets set in "4.1 Electrolytes".
For the DIY sipper:
NB.The amounts listed below for dicalcium phosphate 28g, potassium citrate 91g, etc are the amounts needed for a week. (4g and 13g, etc. per day, respectively)
To calculate your daily serving size, divide the total net weight of your finished batch of weekly powder, eg. 396.5g, by 7 to reach a single daily serving, eg. 56.6g.
For each day, approximately 56.6g of the batch is dissolved in 500mL of water, with any flavour enhancements and sipped over the day at eg. 50ml per hour, between meals and ideally 1 hour away from them.
NB. Consuming too much at once may cause diarrhoea, headaches, nausea, water retention and/or rapid urination.
5 Ordering products
While the Oligoscan provides instant data, it will typically take 1–3 weeks to get other results (CMA, OAT, microbiomes, etc.) and a potentially similar timeframe to order / receive supplements from vendors. For time efficiency, consider ordering any/all supplements which do not require personalisation while you are still collecting your data.
Some products are not available domestically in all regions and will need to be imported from USA. As such, the order list is based around two primary USA suppliers, however some alternative local vendors / supplements for some regions have been provided where possible.
Apologies, this table is too large for mobile devices and is best viewed on a computer, where it can also be exported as a spreadsheet to aid product ordering accuracy.
The default table selection shown is for US (and international) orders. You can select a different region (eg. EU, AU) to see a merged list of US + region-specific products, where available. You can sort the table by columns. Sorting by 'Product Vendor Link', will group products by vendor.
Notes:
1. Quantities in grams or bottle counts are indicated are for a 90 day supply. The products will be sold in amounts or multiples matching or somewhat exceeding 90 days.
2. Products highlighted in purple are already included in the "custom troches" and therefore do not need ordering if you are intending to use the troches.
3. The European Commission has unfortunately determined that use of the word "probiotic" and/or "prebiotic" on a label is making a health claim - which needs to be authorised, effectively banning import of any products with matching labels within EU countries, at least via any of the compliant online marketplaces such as Amazon and eBay. A workaround is to use https://www.shipito.com which provides a "free" US mailing address, for these or any other products with similar problems.
At this time, there are 3 products in the schedule affected where no other direct solution has been found.
These can be quickly identified by setting the Region to "EU" and entering "amazon.com" in the Search field in the area above the table below.
4. Magnesium L-Aspartate appears to have erroneous restrictions for some EU countries. The product link in the table for the EU region has the country "Austria" embedded in the link, to add it to the cart more smoothly. The correct EU destination country can be set at the checkout, or you can use https://www.shipito.com, as per Note 3.
5. A UK-based bulk powder vendor https://www.lifelabsupplements.com/ is likely to be added in the next update. They ship worldwide.. apart from EU.
Custom troches
| order using this form https://bornfree.life/download/troche_order_form.xlsx and request how many days’ worth you require (in multiples of 30) |
Bacteriophage product selector
Clicking on any product link symbol in the bacteriophage "Pathogen vs Product" table below will take you directly to a vendor's webpage in Belarus called Cosmoll.org. (In the event their website is unavailable, they're also contactable via WhatsApp messaging, during their business hours on +7 904 751-48-55). They have been friendly and reliable to deal with. Shipping to eg. Australia may take 2-3 weeks.
NB. Due to difficulties with cross-border payments to this region, Cosmoll uses payment processors such as Wise.com and Paysend.com to facilitate orders. The overall process is a little clunky, but much smoother if you set up a Wise or Paysend account and mobile app before placing your order. The company will try to contact you on WhatsApp or email and manually send a payment request, once the order is received and ready to be processed.
If you run into show-stopping difficulties with the order process, some of the bacteriophage products, eg. Intestifag, Sextaphag and the other bacteriophage products that come in sterile vials are also available at RU-Pills, however they use a Bitcoin intermediary for payments. Overall, access to these products needs to get simpler.
If you have a suitable budget, you can also contact the Phage Therapy Center in Georgia, who have thousands of phages in their biobank and make custom phage cocktails, based on your sample specimens.
The bacteriophage "Pathogen vs Product" table below can help you choose the correct products for your application. For online users, you can also type in (part of) the species or genus name into the search field and the table contents will shrink to just those records, eg. typing "kleb" will return all products targeting Klebsiella species.
Apologies, this table is too large for mobile devices and is best viewed on a computer.
Product notes:
1. Whilst the Viera products have very broad coverage for pathogenic species eg. combining "Spray for women" and "Hand spray", these products are sold as 'prophylactic' doses - you may need to use more of the product to achieve the same results. They also contain PEG, for anyone with sensitivity. Interestingly enough, although these are marketed as external use products, a number of the Viera sprays broadly target the Bacteroides genus. This has implications for selectively correcting elevated Bacteroides : Firmicute ratios and may be (potently) helpful at eg. 8-10 sprays per day, orally for 1-2 weeks. Anecdotal reports are favourable, accompanied by initial die-off symptoms.
2. The Micormir gel bacteriophage products, eg. Phagodent, Fagogin, Phagoderm, Otofag are 'therapeutic doses' and potent.
3. All of the bacteriophage products which come in sterile vials are extremely potent. These will require eg. 20-30ml syringes and detachable eg. 23-27G 1/2 -1" needles to draw up liquid from the vials, before removing the needle to administer them to various mucosal tissues.
4. Nebuliser usage - the Micromir Gel products contain a carbomer base which readily dissolves in water, meaning it is able to be used in a nebuliser at roughly 1mL of gel to 3mL of water. Target dose is typically 1-2mL per session. The sterile vials can be used without dilution in a nebuliser. Nebulising phages has been used in at least one study to achieve systemic distribution, also noting that circulating bacteriophages via this route would normally trigger a systemic immune response, just like IV phage administration.
https://www.mdpi.com/1999-4915/14/12/2614
https://pubmed.ncbi.nlm.nih.gov/26691737/
5. Translated product manuals from Russian to English for Sextaphag, Pyofag and Intesti-fag are provided, courtesy of ChatGPT. Original manuals, etc., can be found on the manufacturer's websites: https://www.bacteriofag.ru/, https://micromir.bio/eng, https://www.veira.net/
6. Peer-reviewed literature exists for various products, eg. https://journals.uran.ua/index.php/2307-0404/article/view/221232
6 Frequently asked questions (FAQ)
This section contains an ongoing effort to curate frequently asked questions which can't be easily preempted / prevented by clarity updates to the existing protocol documentation.
You can use the search field for keywords, and / or browse through the question / answer pairs.
Changelog
You can browse the changelog as-is, or use the filter tools to show only the changes between version numbers and / or date ranges by entering a value in one of the relevant "From" fields.
You can also filter by Type to eg. show only "Product" changes, which can be helpful for people already doing the protocol.