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Born Free
2 The protocol

2 The Protocol


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:

  1. Collect Your Data
  2. Lifestyle Changes
  3. Stage 1: Remineralisation, increasing collagen synthesis rates, and performing a controlled initial “die-off” (at least two weeks)
  4. Stage 2: Enhanced gastrointestinal and mucosal interventions (at least two weeks)
  5. Stage 3: Stimulate and support a strong immune response while breaking (circulating) biofilms (at least four weeks)
  6. Optional Follow-Up
  7. Ongoing Preventative Maintenance


"Be thankful for your triggers, for they show where you are not free."


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.

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 - 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.


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."


trajectory

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 (microbial 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 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. 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.


If you have nasal inflammation or notice any airway resistance or restriction when breathing, it may be appropriate to perform a nasal microbiome test 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.

Issues with neurotransmitter metabolism, histamine regulation, and gut function are common and to be expected.


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).


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.

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


Remineralisation Will Alter (Restore) Neurotransmitter Homeostasis or "Managing Transitional Neuropsychiatric Symptoms"

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.

p5p_v3


However, this problem isn’t 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.

fad-fmn


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 H₃-mediated inhibition of tyrosine hydroxylase. It acts as both a primary disruptor and a multiplier of vulnerability in neurotransmitter and cofactor systems.

catecholamines_v2


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 “weird” or “off” feeling.


Onboarding

The fix isn’t to push harder, it’s to intervene smarter - a staged approach works better.

For severe cases / people with elevated susceptibility to (neuropsychiatric) symptoms from supplements, etc.,  a very gentle ramp up with tiny doses of non-methylated B vitamins can be very helpful, before moving to the compounded multi-mineral products. Metabolics (UK) produce a range of liquid B vitamins which are ideal for these purposes, although they don't carry all products and some other vendors are required.

You can find these in 5 Ordering supplements in the "Onboarding (Severe)" category.


One example of a suggested optimal sequence:

1. Stabilise the redox and mineral terrain. This includes VERY SLOWLY introducing :
        a) electrolytes, taken slowly over the day. Calcium and potassium may temporarily increase adreneric / glutaminergic sensitivity and need to be increased more slowly than others.
        b) antioxidants and mitochondrial cofactors (Vitamin C, Vitamin E, R-ALA, CoQ10, GSH donors like NAC), taken 2-3x/day. These may need TINY doses, initially, eg. 50mg of Vitamin C.
        c) (usually less slowly) L-carnitine / acetyl L-carnitine, creatine (for fatty acid transport and ATP-PC pathway), uridine monophosphate (sublingual - ramp up, starting from 10, to 50-100mg, 2x/day) and slowly ramp up d-ribose, starting from 500mg, to 10g, in the daily DIY "sipper/shot". Expect insulin sensitivity and glycogen synthesis to increase - be prepared to increase intakes of carbohydrates to facilitate glycogen synthesis and potentially sodium + other electrolytes, towards their daily targets.
        d) mineral cofactors like zinc, copper, iron, manganese, selenium, iodine, lithium, rubidium, cobalt, boron, and molybdenum, etc. This helps balance the neurotransmitter synthesis pathway (and precursors), lowers the burden on ALDH and MAO pathways and reduces oxidative stress, allowing safer processing of neurotransmitter metabolites. 

2. Introduce B1 and B2 in active or near-active forms, such as FMN and TPP / cocarboxylase. These support mitochondrial redox balance, glycolysis, and the Pentose Phosphate Pathway. Depending on the severity of dysbiosis / acetaldehyde burden, the total daily B1 dosing can range from 50-600mg of the active form, cocarboxylase, starting from a low dose. Additional B1, in any form, can be added for further acetaldehyde adduct-forming and detoxification support, over time. Adding B1 can increase B9 transporter activity and SAMe availability, allowing some adrenergic signalling increase unless B2 and NAD+ are restored in balance.

3. Slowly layer in B5, B6 (as P5P), biotin, D-chiro inositol, B9 and B12 (as methylcobalamin or hydroxocobalamin) only after upstream redox stress is under better control. B9 and B12 can increase methylation -> SAMe availability, unblocking epinephrine synthesis at PNMT and also COMT activity, leading to hyper-adrenergic signalling if TOO MUCH is introduced quickly, ie. without sufficient B2 for MAO and NAD+ (+ redox) for ALDH. In the context of unresolved aldehyde or monoamine overload, these can also be disruptive (unless P5P is eg. dissolved in DMSO, bypassing impaired alkaline phosphatase (ALP) and pyridoxal kinase (PK) steps) and BH4 synthesis (dietary queuine - see "Vitamin Q deficiency").

NB. Reducing acetaldehyde and/or restoring NAD+ status corrects a lot of impaired metabolism, including the pathway that promotes endogenous morphine synthesis.
Stay keenly observant for rapid withdrawal symptoms and manage them proactively.


Then;
3a. Introduce NAD+ pool support (apigenin - P38 inhibitor), NAD+:NADH redox support (0.05-0.1mg of methylene blue, once per day), and

3b. Add sublingual NAD⁺ / NADH (NOT precursors, for severe) at 5-10mg doses, 2x/day and increase to 20-40mg 2x/day. Expect and watch for alcohol / opioid withdrawal symptoms.

A schedule of standard products and dosing can be found below, in "Getting started (standard schedule)".

Use non-oral routes to bypass known bottlenecks. Transdermal, sublingual, or parenteral delivery helps sidestep transporter saturation, liver metabolism, or dysregulated GI environments. Dissolving nutrients in DMSO is another useful strategy.

P5P in DMSO is one example of an advanced strategy - dissolving P5P in a DMSO solution bypasses multiple upstream steps: it does not rely on ALP, avoids compromised membrane transporters, and skips over PK activation. This makes it ideal in states where P5P is known to be low despite B6 repletion. It may also enter intracellular compartments more efficiently, including mitochondria.

In this context, neurotransmitter restoration is more about kinetics, cofactor availability, and redox context. A patient may be taking all the right nutrients, but if those nutrients are stuck upstream, degraded by peroxynitrite, or unable to bind to their target enzymes due to low zinc, the net effect is failure. Worse, poorly timed repletion can destabilise the system further.

The half-life of each vitamin is frequently overlooked. Dosing vitamins 2-4 times per day is often necessary to achieve sufficient benefit.
eg. Vitamins B1, B2, B3, B5, B6, B7/H, B8, B9, B12 and C are taken 2-3x/day, often sublingually.

In the context of restoring severe deficiencies, strategic sequencing matters. B vitamins are powerful, especially in active forms, however they also act as signals in a complex control system. If introduced out of order or in isolation, they may trigger compensatory reactions that mimic toxicity, when in fact they are just unmasking hidden dysfunction.

Many of these mechanisms may also help explain why certain neuropsychiatric conditions appear during chronic illness and how they can act as precursor states to systemic collapse.

ADHD, for instance, is often characterised by signs of noradrenaline and dopamine dysregulation, impaired impulse control, and chronic restlessness, traits which may reflect an early-stage compensation for failing neurotransmitter recycling or low-grade redox and metabolic dysfunction, downstream of chronic endogenous acetaldehyde and opioid synthesis. If these compensations begin to fail, especially under stress, infection, or prolonged nutritional depletion downstream of chronic lactic acid metabolism and mineral transporter alterations, the system may tip into a more energy-conserving, downregulated state, as observed in ME/CFS, long COVID, post vaccination syndrome, etc.

Bipolar disorder may reflect a different kind of instability, one in which neurotransmitter tone swings between overcompensation and collapse, and this too may be compounded by aldehyde load, especially acetaldehyde, which inhibits ALDH enzymes responsible for clearing dopamine breakdown products like DOPAL.

Dietary contributions to acetaldehyde burden, such as excessive intake of alcohol, sugar, or fermentable carbohydrates, can further amplify this inhibition by fuelling microbial overgrowth and endogenous ethanol production in the gut. When ALDH function is compromised, neurotoxic intermediates accumulate, further impairing redox balance and downstream dopamine synthesis. Over time, this may shift the system toward an oscillatory or collapsing state, where any attempt to stabilise mood or energy is undermined by bottlenecks in detoxification and neurotransmitter recycling These cycles could, in part, emerge from fluctuating availability of critical cofactors like P5P, B2, or SAMe, or episodic redox crashes that disrupt normal mood-regulating feedback.

Getting started (standard schedule)


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, while also integrating the phases described in 2.2.3 - Gastrointestinal.
b) Making a DIY "sipper/shots" 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, acai, berry, etc for flavour. (NB. Consuming too much at once may cause diarrhoea, headaches, nausea, water retention and/or rapid urination. Shake before each use.)
c) Taking [high dose Vitamin B1 as thiamine HCL, (sublingual) Vitamin B2 - FMN and (sublingual) Vitamin B6 - P5P] (or the compounded troches - see 4.2 Custom troches) and (sublingual) uridne monophosphate at different times throughout the day. Add methylene blue microdosing, when ready to restore NAD+ redox and push into endogenous morphine withdrawal, then add Vitamin B3 - NADH. (The compounded nutrients are potent and starting at eg. 1/8th doses, may be helpful to soften / slow the metabolic shift when restoring severe deficiencies.)
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.)
f) Testing for and and addressing blood-flow / hypoxia issues. (see 2.3.3 Blood-flow, hypoxia and fibrin-amyloid).

The product ordering links for the full protocol can be found in 5 Ordering products. However, you can also download a time-saving spreadsheet of the starter items ONLY, using the section below:

This protocol is a comprehensive framework which addresses how to quantify and remediate different aspects of chronic diseases that share mitochondrial dysfunction as a common feature. 

However, the protocol also spans over 240 printable pages - so it's also completely understandable if you find yourself feeling a bit overwhelmed by the volume of new information needing to be absorbed.. likely while still battling brain fog and energy envelope issues, chronic feelings of fight/flight and other challenges.. 

Removing some or all of these debilitating issues should help improve the absorption and retention of new information. The focus of this section is to order JUST the essential items needed to get started on stabilising the key metabolic pathways.

You can simply choose your shipping region from the drop-down box and click on the Excel or CSV icon to download a spreadsheet of some starter items, with product ordering links and relevant information for preparation of time/effort-saving weekly recipes.