{"id":308,"date":"2024-07-06T05:55:18","date_gmt":"2024-07-05T18:55:18","guid":{"rendered":"https:\/\/bornfree.life\/2024\/?p=308"},"modified":"2026-10-10T16:56:47","modified_gmt":"2026-10-10T05:56:47","slug":"2-the-protocol","status":"publish","type":"post","link":"https:\/\/bornfree.life\/learn\/2-the-protocol\/","title":{"rendered":"2 The protocol"},"content":{"rendered":"\n\n\n

2 The protocol<\/h1><\/a><\/p>


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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:

<\/p>

  1. 1) Collect your data<\/strong><\/li>
  2. 2) Protocol onboarding: Mineral and electrolyte repletion, toxic metals chelation, mitochondrial remediation and support, diet and lifestyle changes, glycogen and collagen synthesis improvements, nasal dysbiosis remediation, structural assessment, cardiovascular assessment, initial immune activity phase, plus ongoing transition from sympathetic overdrive -> parasympathetic balance<\/strong><\/li>
  3. 3) Stage 1<\/strong>: Microbiome re-seeding and performing a controlled initial \u201cdie-off\u201d (at least two weeks)<\/li>
  4. 4) Stage 2<\/strong>: Enhanced gastrointestinal and mucosal interventions (at least two weeks)<\/li>
  5. 5) Stage 3<\/strong>: Stimulate and support a strong immune response while breaking (circulating) biofilms (at least four weeks)<\/li>
  6. 6) Optional follow-up<\/strong><\/li>
  7. 7) Ongoing preventative maintenance
    <\/strong><\/li><\/strong><\/strong><\/ol>


    <\/span><\/strong><\/strong><\/strong><\/p>\n

    “Be thankful for your triggers, for they show where you are not free.”<\/span>
    <\/strong><\/p>\n


    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.<\/strong> The sensitivity to supplements and foods is expected to resolve as part of the protocol.

    One of the most important lessons learned through this process is that ultimately, whenever a basic, essential nutrient triggers an initial reaction – either good or bad<\/em> – you need it, although you may also unmask other deficiencies \/ compensations in the process of correcting one.

    That stated, blindly charging your way through barriers is not a sensible way to achieve success, and there is a structured process to follow which makes nutrient repletion much more tolerable.<\/strong><\/p>\n


    This protocol is designed to stimulate immune activity and may produce a \u201cJ-curve\u201d 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. Maintaining electrolytes, selected minerals, glycogen and active B-vitamin status may help reduce risk of severe symptoms or PEM in this protocol model, but should not be presented as guaranteed prevention.<\/p>


    <\/p>\n\n

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    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.

    <\/p>

    Before beginning, assess your lymphatic system as described in the \u201c2.2.2 Lymphatic Maintenance<\/a>\u201d section. Note any tissues that have been or continue to be sore, stiff, or inflamed\u2014these areas are expected to flare during increased immune activity and may be adjacent to other infected tissues.

    <\/p>

    To help reduce expected symptoms when correcting deficiencies and experiencing Herxheimer reactions (microbial die-off effects) due to improved immune activity, a recommended starting sequence has been provided.

    <\/strong><\/p>

    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 diarrhoea, joint or muscle pain, tachycardia, chills, cold hands or feet, itchiness, rashes, sweating, and fever resembling the “disulfiram effect.”<\/strong>

    <\/p>

    A schedule of specific products is available, with vendor website links provided for different regions (see \u201c5. Ordering Products<\/a>\u201d). These are not affiliate marketing links. With the exception of the Oxalobacter.com<\/a> \nwebsite (which was created out of necessity to address worldwide supply issues for \n“Oxalobacter formigenes” probiotics and is not intended as a for-profit \nendeavor), 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.

    <\/p>

    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\u2014aside from one or two items included to make your experience more tolerable\u2014all are necessary. Attempts to create a “lite” version of this protocol by swapping or omitting items have consistently resulted in failure.<\/span>

    <\/p>

    Onboarding and Stage 1<\/strong> 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. A further protocol goal is selectivity: reducing unwanted organisms while preserving or rebuilding beneficial species through diet, probiotics and carefully chosen antimicrobial strategies. Some of these interventions are included in Stage 1, while others are introduced in Stages 2 and 3.<\/p>


    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.
    <\/strong>
    Fulvic acid is used extensively 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. <\/strong>If you experience any unpleasant effects, take a few days to gradually increase from a smaller dose\u2014for 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\u2014until you can consume a standard serving without adverse effects.<\/p>


    <\/strong><\/p>

    If you have nasal inflammation or notice any airway resistance or restriction when breathing, it may be appropriate to perform a nasal microbiome test<\/a> and investigate for environmental mould issues. 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.

    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.<\/p>

    Issues with neurotransmitter metabolism, histamine regulation, and gut function are common and to be expected.<\/p>

    <\/strong>
    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.<\/p>


    If taurine or magnesium worsens sleep, palpitations or tremor, treat this as a protocol signal to evaluate thyroid status and temporarily adjust electrolyte dosing. If calcium deficiency is suspected, calcium, vitamin D3 and vitamin K2 may be reviewed, and 1-2g\/day elemental calcium (a high supplemental range) could be individualised against diet, labs, kidney-stone risk and medications. Addressing calcium status may change oxalate handling in the protocol model and can coincide with muscle or tissue symptoms. this is a possible transitional issue, not a necessary process. 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.<\/p>


    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).<\/p>


    <\/strong><\/p>

    We recognise 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 sublingual lozenges (troches) or DMSO-based multivitamin, and a tub or bag of premixed powder. A DIY powder recipe is also included for those who prefer to mix their own.

    <\/p>

    Mixed inositols may influence insulin\/glucose signalling and glycogen handling. 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. 

    During the protocol onboard phase, there is expected to be a transition from sympathetic dominance and lipolysis to parasympathetic balance and glycogen \/ glycolysis preference. It is expected that consuming potentially >400 grams of net carbohydrates and water, per day, for typically two to three days, to replenish glycogen stores should help you feel significantly better, and continuing at >250g net carbohydrates per day should keep you that way. 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.

    <\/strong><\/p>\n

    Pre-protocol support<\/a><\/h4>\n


    Remineralisation Will Alter (Restore) Neurotransmitter Homeostasis or “Managing Transitional Neuropsychiatric Symptoms”<\/strong><\/p>In complex chronic illness, neurotransmitter imbalances are almost never occurring in isolation. They emerge from a landscape riddled with microbiome dysbiosis, nutrient insufficiencies, redox imbalance, enzyme inhibition, and compensatory feedback loops. Restoration of neurotransmitter function therefore requires much more than supplementing amino acids or throwing SSRIs at the wall. It requires understanding why key cofactors, especially active B vitamins and minerals, are almost always functionally low.

    It’s critical to note that most of the enzymes responsible for synthesising, degrading, or recycling neurotransmitters are B-vitamin dependent, and their active forms, such as FMN, FAD, TPP, P5P, and methylcobalamin, are functionally deficient in the data of people with chronic illness. This is not always due to dietary inadequacy, even relative to general population requirements. The applied data shows this is due to cofactor bottlenecks, impaired enzymatic activation, oxidative degradation, and zinc- \/ magnesium-dependent enzyme instability.

    This is evident, for example, in the metabolism of vitamin B6. As shown in this detailed diagram of B6 metabolism, converting dietary B6 into its active form P5P involves a cascade of steps: alkaline phosphatase (ALP) activity outside the cell, membrane transport, and intracellular phosphorylation via pyridoxal kinase (PK). Each of these steps is dependent on magnesium and zinc, and many are redox-sensitive. Acetaldehyde, chronic inflammation, and low ATP all interfere. It’s no surprise, then, that functional P5P levels are low, even when blood levels of pyridoxine or pyridoxal appear normal or highly elevated.

    \n\n


    However, this problem isn\u2019t limited to Vitamin B6.

    eg. Riboflavin must be converted to FMN and FAD, a process impaired by low ATP, oxidative stress, zinc or magnesium loss. Thyroid synthesis and related minerals, substrates also influence this. 

    <\/p>\n\n


    Thiamine must become TPP via thiamine pyrophosphokinase. B12 must be converted to methylcobalamin, a zinc- and glutathione-sensitive step. These are often affected by chronic acetaldehyde, either directly or indirectly.

    Acetaldehyde burden affects not only ALDH directly, but also indirectly interferes with zinc-dependent enzymes, magnesium availability, and redox-sensitive pathways throughout this entire cascade. It also stimulates mast cell activation, promoting histamine release, while simultaneously impairing histamine degradation through inhibition of ALDH and depletion of cofactors like P5P and copper. This can disrupt the balance of neurotransmitters by overactivating histamine receptors, and indirectly suppressing dopamine synthesis via H\u2083-mediated inhibition of tyrosine hydroxylase. It acts as both a primary disruptor and a multiplier of vulnerability in neurotransmitter and cofactor systems.

    <\/p>\n\n


    The result is that small efforts to stimulate or correct neurotransmitter production can trigger paradoxical responses, including overshooting, agitation, anxiety, “brain on fire”, insomnia, sedation, getting “stoned” \/ “high”, or what many patients call a \u201cweird\u201d or \u201coff\u201d feeling.<\/p>\n\n

    \n \n \n\n \n \n \n \n\n\n wdt_ID<\/th> wdt_created_by<\/th> wdt_created_at<\/th> wdt_last_edited_by<\/th> wdt_last_edited_at<\/th> Compound<\/th> General Effect<\/th> Sensations When Low<\/th> Sensations When Excessive<\/th> Relationship<\/th> Notes<\/th> <\/tr>\n<\/thead>\n \n\n \n \n\n\n
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    \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n
    1<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n Dopamine<\/td>\n Motivation, reward, goal-directed behaviour<\/td>\n Apathy, low motivation, anhedonia, fatigue<\/td>\n Anxiety (if ALDH inhibited \/ \"Disulfiram effect\"), hyperfocus, paranoia, addictive behaviour<\/td>\n Upstream: Tyrosine, Tyrosine Hydroxylase (TH); Downstream: DOPAC, HVA, THP<\/td>\n Synthesis inhibited by low [(Zinc, Magnesium->) P5P, (Queuine->) BH4, Tyrosine | Iron | Copper | Calcium | Potassium | Lithium | Oxygen], elevated [Histamine, oxidative stress]<\/td>\n <\/tr>\n
    2<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n Serotonin<\/td>\n Mood regulation, satiety, sensory filtering<\/td>\n Irritability, insomnia, gut discomfort, sensory sensitivity<\/td>\n Emotional numbness, lethargy, flattened affect<\/td>\n Upstream: Tryptophan, Tryptophan Hydroxylase (TPH); Downstream: 5-HIAA, Melatonin<\/td>\n Tied to Oestrogen, gut microbiota, Tryptophan metabolism. Influenced by IDO1\/TDO activation during innate immune responses.<\/td>\n <\/tr>\n
    3<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n Norepinephrine<\/td>\n Alertness, arousal, vigilance<\/td>\n Brain fog, low energy, insomnia, poor concentration<\/td>\n Panic, insomnia, sympathetic overdrive<\/td>\n Upstream: Dopamine, Dopamine Beta-Hydroxylase (DBH); Downstream: Normetanephrine, VMA<\/td>\n DBH is sensitive to oxidative stress and low Copper.<\/td>\n <\/tr>\n
    4<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n Epinephrine<\/td>\n Acute stress response, mobilisation<\/td>\n Low physical energy, poor response to stress<\/td>\n Hyperarousal, restlessness, palpitations<\/td>\n Upstream: Norepinephrine, Phenylethanolamine N-Methyltransferase (PNMT); Downstream: Metanephrine, VMA<\/td>\n PNMT sensitive to elevated Cortisol, low Vitamin D, stress immobilisation (rats).<\/td>\n <\/tr>\n
    5<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n GABA<\/td>\n Inhibition, calm, anti-seizure, muscle relaxation<\/td>\n Anxiety, restlessness, insomnia<\/td>\n Sedation, reduced alertness, depression<\/td>\n Upstream: Glutamate, Glutamate Decarboxylase (GAD); Downstream: SSA, Succinate<\/td>\n Synthesised from Glutamate; linked to P5P and ALDH5A1<\/td>\n <\/tr>\n
    6<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n Glutamate<\/td>\n Excitation, memory, learning<\/td>\n Poor focus, cognitive fatigue, low learning retention<\/td>\n Neurotoxicity, anxiety, agitation, excitotoxicity<\/td>\n Upstream: Glutamine; Downstream: GABA, \u03b1-KG (via Glutamate Dehydrogenase (GDH))<\/td>\n Requires P5P, Magnesium, Zinc and GSH balance<\/td>\n <\/tr>\n
    7<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n Acetylcholine<\/td>\n Learning, attention, parasympathetic tone<\/td>\n Memory loss, low attention, dry mouth, poor digestion<\/td>\n Overstimulation, cramps, sweating, nausea<\/td>\n Upstream: Choline, Acetyl-CoA; Downstream: Acetate, Choline<\/td>\n Synthesised from Choline and Acetyl-CoA. Degradation inhibited by Aflatoxin B1, Territrem B, p-Cresol.<\/td>\n <\/tr>\n
    8<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:42 AM<\/td>\n Histamine<\/td>\n Arousal, immune modulation, gastric secretion<\/td>\n Sedation, poor gastric acid, low immune alertness<\/td>\n Itching, hives, insomnia, irritability<\/td>\n Upstream: Histidine, Histidine Decarboxylase (HDC); Downstream: Imidazole acetaldehyde, Methylhistamine<\/td>\n Released by Acetaldehyde. Degraded by Diamine Oxidase (DAO) - requiring Copper, then ALDH2 (inhibited by Acetaldehyde) and Histamine-N-Methyltransferase (HNMT) - requiring SAMe, MAO - requiring FAD, then ALDH3A1 (inhibited by Acetaldehyde); Inhibits TH.<\/td>\n <\/tr>\n
    9<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n Endorphins \/ Enkephalins<\/td>\n Pleasure, pain suppression, emotional buffer<\/td>\n Pain sensitivity, low mood, emotional lability<\/td>\n Emotional blunting, addiction potential, hormonal suppression<\/td>\n Upstream: Proopiomelanocortin (Proopiomelanocortin (POMC)); Downstream: \u03bc-opioid receptor binding<\/td>\n Linked to Dopamine, Oxytocin, and \u03bc-opioid tone<\/td>\n <\/tr>\n
    10<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n Anandamide \/ 2-AG<\/td>\n Stress modulation, appetite, mood, memory<\/td>\n Anxiety, heightened stress response<\/td>\n Amotivation, reduced memory, low arousal<\/td>\n Upstream: Arachidonic acid, N-Acylphosphatidylethanolamine (NAPE); Downstream: CB1\/CB2 receptor activity<\/td>\n Part of endocannabinoid system; modulates Dopamine and GABA<\/td>\n <\/tr>\n
    11<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n Melatonin<\/td>\n Circadian rhythm regulation, antioxidant<\/td>\n Insomnia, poor sleep quality, circadian disruption<\/td>\n Drowsiness, fatigue, vivid dreams<\/td>\n Upstream: Serotonin, Serotonin N-Acetyltransferase (SNAT)\/Acetylserotonin O-Methyltransferase (ASMT); Downstream: Sulfated\/oxidised metabolites<\/td>\n Synthesised from Serotonin; impacted by light and inflammation<\/td>\n <\/tr>\n
    12<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n DOPAL<\/td>\n Dopamine catabolite, redox-sensitive aldehyde<\/td>\n N\/A<\/td>\n Neurotoxicity, mitochondrial stress, Monoamine Oxidase (MAO) overload<\/td>\n Upstream: Dopamine via Monoamine Oxidase (MAO); Downstream: THP, DOPAC<\/td>\n Implicated in Parkinson\u2019s, ALDH1A1\/1A2\/2 sensitivity, Tyrosine Hydroxylase (TH) inhibition.<\/td>\n <\/tr>\n
    13<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n THP<\/td>\n Tetrahydropapaveroline, opioid-like dopamine derivative<\/td>\n N\/A<\/td>\n \u03bc-opioid effects, suppression of Tyrosine Hydroxylase (TH), altered mood perception<\/td>\n Upstream: DOPAL + dopamine; Downstream: opioid receptor influence<\/td>\n Formed under ALDH1A1\/1A2\/2 inhibition, increases under Acetaldehyde burden<\/td>\n <\/tr>\n
    14<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n GHB<\/td>\n CNS depressant, GABAergic mimic<\/td>\n Anxiety, agitation, hypersensitivity<\/td>\n Sedation, dissociation, altered consciousness<\/td>\n Upstream: SSAL via 4-HBDH; Downstream: GHB receptor, GABA-B<\/td>\n Built up during ALDH5A1 inhibition \/ low NAD+; depresses respiration and cAMP<\/td>\n <\/tr>\n
    15<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n Tyramine<\/td>\n Indirect sympathomimetic, displaces norepinephrine<\/td>\n N\/A<\/td>\n Headache, hypertension, panic episodes<\/td>\n Upstream: Tyrosine decarboxylation; Downstream: Monoamine Oxidase A (MAO-A) degradation<\/td>\n High in fermented foods; sensitive to Monoamine Oxidase (MAO) inhibitor levels<\/td>\n <\/tr>\n
    16<\/td>\n 3dghs<\/td>\n 20\/04\/2025 04:24 AM<\/td>\n 3dghs<\/td>\n 21\/04\/2025 03:08 AM<\/td>\n Autoantibodies (Receptor-Modulating)<\/td>\n Variable; modulates neurotransmitter receptor function<\/td>\n N\/A<\/td>\n Receptor overstimulation, desensitisation, or rebound suppression<\/td>\n Targets: dopamine, serotonin, histamine, GABA, others; Modulate signalling dynamics<\/td>\n Typically IgG-based; estimated half-life ~21 days; may enhance or inhibit receptor signalling based on binding site and context. Likely represent an adaptive attempt to restore homeostasis in failing or suppressed pathways.<\/td>\n <\/tr>\n <\/tbody> \n\n \n \n \n <\/table>\n\n<\/div>