{"id":363,"date":"2024-07-08T07:04:17","date_gmt":"2024-07-07T20:04:17","guid":{"rendered":"https:\/\/bornfree.life\/2024\/?p=363"},"modified":"2026-05-06T08:34:17","modified_gmt":"2026-05-05T21:34:17","slug":"4-calculating-supplement-doses","status":"publish","type":"post","link":"https:\/\/bornfree.life\/learn\/4-calculating-supplement-doses\/","title":{"rendered":"4 Calculating supplement doses"},"content":{"rendered":"\n\n\n

\n 4 Calculating supplement doses <\/h1><\/a>\n\n <\/div>\n\n

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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 (deprecated) HTMA data, indicating inflammation severity over time.)

Assuming inflammation and pH imbalances are correctly managed, resolving these deficiencies may take, eg. <\/strong>
2 or more months, via non-oral routes, eg. sublingual \/ transdermal \/ rectal,
or
1 – 2 weeks via appropriately dosed parenteral administration, providing cytosolic + mitochondrial ATP synthesis, (metabolic) acidaemia, and any enhanced renal excretion has been resolved. This can then be easily maintained via non-oral routes.

NB. Many of these deficiencies are likely not going to resolve at all using standard oral dosing, due to inflammatory cascade related mineral transport inhibition in the duodenum.<\/strong>

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 and ATP synthesis, to the point of triggering lactic acid metabolism (anaerobic glycolysis). Some of these include inappropriate metabolic load (insufficient pacing), zinc status, heavy metals status \/ oxidative stress support and oxygen transport \/ coagulation.

If you are using the compounded nutrients, a number of these minerals \nand various vitamins are combined using a sublingual or DMSO-enhanced route, which greatly simplifies this part of the protocol. The \ndefault formulation should suffice for most \npeople, unless your transferrin saturation is at or above 35-40%, in which \ncase you would reduce the ferritin content to zero. Where the transferrin saturation exceeds 45%, ie. “iron overload”, checking for and remediating cobalt deficiency is suggested, along with excluding any causes of severe oxidative stress \/ impaired Cytochrome c \/ methemoglobinemia.<\/strong> (see \u201c4.2 Compounded nutrients<\/a>\u201d section)

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Please recheck your intracellular mineral data 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, according to ongoing data collection and literature review, absorbing a “reasonable amount” of excess \/ unnecessary dietary minerals is not normally problematic unless you have, for example, Wilson\u2019s disease<\/a>, hemochromatosis<\/a> or beta thalassemia<\/a>. 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.
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<\/strong>An Oligoscan and SO\/Check report analysis tool can be found here.

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Based on our collected data, we interpret Oligoscan \/ SO\/Check reports using different upper and lower thresholds than the provider\u2019s 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 \u201ca\u201d in \u201cNormal\u201d is located, to the left of \u201cOK\u201d) and the “High” for all markers except fluorine is relocated to halfway between OK and original High vertical lines (ie. where the \u201co\u201d in \u201cNormal+\u201d is located, to the right of \u201cOK\u201d).

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*<\/sup>,<\/strong> 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 deficien<\/u><\/strong>t<\/u>.<\/strong> This also applied to SO\/Check reports. <\/strong>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”. <\/strong>

*<\/sup>The practitioner’s guide discusses zinc transport blockade as the reason for the marker elevation. From our comparisons with intracellular (white blood cell) data, the issue also applies to all other mineral markers and appears to be something off-target with the <\/strong><\/em>“black box” <\/em><\/strong>Oligoscan algorithm.<\/strong> Ultimately, I think this could be improved and ongoing discussions with the lab are have been optimistic. <\/em>
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For So\/Check branded reports, these have a different format \/ layout and markers are shown as a percentage deviation from \u201cnormal\u201d instead of values. You can ignore this report\u2019s 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”.<\/strong> 
    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. <\/strong>In-range low markers should still be supported by diet and\/or supplementation.<\/strong><\/p>\n\n


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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 potassium and rubidium both appear low on a hair\/mineral profile, rubidium can be treated as a hypothesis to review rather than a confirmed barrier to potassium restoration. Similarly, calcium with strontium and magnesium with lithium. High zinc can indicate low histidine \/ insufficient protein.

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An important note on “hypoxia” and acidosis:<\/h4>

Low phosphorus in Oligoscan or OAT data can indicate parathyroid issues, poor glycolysis \/ ATP synthase activity, elevated acetaldehyde and\/or (metabolic\/respiratory or renal) acidaemia.

(Lactic) acidaemia is commonly seen with (chronic infection -> immune activity -> coagulation ->) hypoxia<\/a>.

Elevated oxalate and\/or relative elevation of lactic acid vs pyruvic acid in the OAT results are further indication for “hypoxia”-related anaerobic glycolytic shift, ie prolyl hydroxylase inhibition -> HIF-<\/a>1alpha stabilisation and cytosolic NAD+ redox via lactate dehydrogenase and GPD1\/2. ie. The glycolysis pathway output diverts to lactate instead of entering the TCA cycle via acetyl-CoA. 

If chronic “hypoxia” metabolism is present, additional support may well be required. (see: “2.3.3 Blood-flow, hypoxia and fibrin-amyloid<\/a>“)

NB. Correcting “hypoxia” is expected to help remove innate immune bias towards IFN-alpha response and assist IFN-gamma activity. Initial elevated immune response, fatigue and die-off symptoms could be expected when starting these interventions. <\/strong>Pre-protocol support items may be useful in supporting this period.

Failure to address hypoxia \/ acidemia will stall remineralisation and microbiome remediation. (see: “2.3.2 Remineralisation<\/a>“)<\/strong>
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Low sulfur in Oligoscan or So\/Check data can indicate elevated transsulfuration, sulfur metabolising microorganisms or hyperoxaluria issues and up-regulated transport.

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Low iodine is often observed with fluoride excess and impaired retinoic acid metabolism (retinol -> retinal -> retinoic acid requires functioning NAD+ redox). Fluoride is found in some medicines, toothpaste and town water. Human studies suggest tamarind ingestion can increase urinary fluoride excretion in specific fluorosis-exposure contexts, but this should not be treated as a universal detoxification claim. [107]<\/a> [108]<\/a>

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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.<\/strong>

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For other supplement selection criteria:

An automated OAT interpretation tool is available here, which provides detailed information on inferred intracellular nutrient \/ cofactor deficiencies and lots of other information.
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