Quote from Dr. Garrett Smith on November 25, 2018, 12:50 pm

The "normal range" for laboratory values is typically determined to fit 95% of the population that takes the test:
http://www.clinlabnavigator.com/reference-ranges.html

The population who is going to visit the doctor and getting lab testing--for the most part--is biased towards SICK people.  This skews the "normal" range towards the major trends that would show up in sickness, not health.

https://www.labcorp.com/test-menu/36636/vitamin-a# (screenshot attached)

https://www.questdiagnostics.com/testcenter/BUOrderInfo.action?tc=921&labCode=SJC (screenshot attached)

Why are the ranges different for children and adults?  What justifies this? Why do the ranges steadily go up by age?

My answers:  Children have the lowest levels because they are simply less saturated with Poison/"Vitamin A", so their "normal ranges" as determined by the lab's calculation methods are simply lower.  It progresses up by age because it is indicative of a accumulative (gathering or growing by gradual increases) disease process.

Quest's reference ranges below:

Reference Range(s)

1-6 Years	20-43 mcg/dL
7-12 Years	26-49 mcg/dL
13-19 Years	26-72 mcg/dL
Adult	38-98 mcg/dL

Unit conversion link for Vitamin A here: http://unitslab.com/node/212

Doctors like to tell people that their worsening health is just "part of getting older, you have to deal with it".  What if much of that is not true, and it is simply that Poison/"Vitamin A" is behind most of the suffering that we've been brought to believe is just a part of aging?

- Discuss excessive % of retinyl esters causing hypervitaminosis A in spite of low serum Vitamin A

From the LabCorp link:

Vitamin A exists in humans in several forms and is tightly controlled.

Why is it tightly controlled?  The reason is it is extremely toxic to the system in "excessive" amounts.

Naturally occuring forms of vitamin A include retinol, retinol esters, retinal and retinoic acid. The alcohol form, retinol, predominates in the circulation, but it is too toxic for storage.

The admission that retinol is toxic is right there.  This is the form of Poison/"Vitamin A" that people ingest via animal sources, such as eating liver and taking cod liver oil.

Instead, the liver stores as retinyl esters - principally palmitate. The active form of vitamin A in the visual cycle is the aldehyde form, retinal. Retinoic acid is the form in tissues responsible for the biological actions of vitamin A in cellular division and differentiation.¹¹

Retinoic acid is used in dermatology as a "chemical peel".  "Chemical Peels may be defined as “controlled wounds” of the skin made by the dermatologist to multiple purposes."  This should be assumed to be toxic and damaging when inside the system as well.

The most important measurand [sic] for the estimation of vitamin A status is circulating vitamin A as retinol. Serum retinol levels do not accurately reflect liver retinyl ester levels.

The amount of Poison/"Vitamin A" in the blood is NOT reflective of the amount (storage) of Poison/"Vitamin A" in the liver.  Ergo, a low blood test cannot rule out Poison/"Vitamin A" toxicity in the liver.

Despite this limitation, serum retinol is still useful because the levels will diminish once the supply from the liver is diminished.

Read both of these quotes again.  The first one says that the serum retinol doesn't reflect liver stores, the second one is trying to make a case that all low serum retinol levels must indicated depleted liver stores.  The second one is incorrect.

The serum retinol level at which vitamin A deficiency occurs will coincide with the manifestation of night blindness, due to the interruption of the visual cycle by lack of retinal. Other more serious symptoms will occur later when retinoic acid is depleted by even less available hepatic retinyl esters.¹²

Why are there normal lab ranges when a symptom occurs (night blindness), which can have MULTIPLE other causes (protein deficiency, Caloric deficiency, zinc deficiency, and DHA deficiency are all potential and LIKELY causes *add blog-forum hyperlinks*), then magickally becomes the "deficient serum retinol level"?  Shouldn't science be more straightforward than this?  Did that second sentence try to imply that one type of Poison/"Vitamin A" depletes another type?

Vitamin A deficiency only manifests when liver stores are depleted by prolonged reduction of dietary intake.^1,10 In healthy individuals, serum retinol concentrations are homeostatically controlled and do not begin to decline until liver reserves of vitamin A are dangerously low.^2,4,10

But previously they said that serum Vitamin A was NOT indicative of liver stores? If Poison/"Vitamin A" is so crucial to health, how can "healthy individuals" ever have been found with "dangerously low liver reserves of Vitamin A"?  Do you see the disconnect?

From the WHO:

Biomarkers of vitamin A status: what do they mean?

http://www.who.int/nutrition/publications/micronutrients/background_paper2_report_assessment_vitAandIron_status.pdf

"For example, in rats given three different levels of daily vitamin A supplements, serum retinol concentrations did not differ despite a sixfold difference in liver reserves of vitamin A (17).

Serum retinol is not a reflection of the vitamin A liver stores because it is homeostatically controlled and it does not drop until liver reserves are very low. The cut-off value for definition of deficiency has been discussed. In children certainly values <0.35 μmol/L and in women 0.70 μmol/L may indicate deficiency. However, if no infection is present in the population under study, 0.70 and 1.05 μmol/L for children and women, respectively, may be more descriptive of the actual status. If the population has access to a source of preformed vitamin A, serum retinol concentrations will be higher but not necessarily reflective of status,

[...]

Although isotope dilution testing is usually too expensive to consider as a means to evaluate a programme, a sugar-fortification programme was evaluated in a small group of Nicaraguan children (52). The baseline mean liver retinol concentration was 0.57 μmol/g liver, well above what is currently considered deficient (0.07 μmol/g liver). All the children had serum retinol concentrations between 0.74 and 1.31 μmol/L. One year after sugar fortification was implemented, liver reserve concentrations increased to an average of 1.2 μmol/g liver. In 9 of 21 children, liver vitamin A concentrations were calculated to be >1.05 μmol/g liver after fortification, which was defined as toxic in 1990 (53). Because many foods are now being considered for fortification, this sensitive methodology may have to be used, as no other method except liver biopsy is able to diagnose hypervitaminosis A."

From a hypervitaminosis A case study paper:

Vitamin A Toxicity: When One a Day Doesn’t Keep the Doctor Away

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/lt.21007

"Despite massive quantities of total plasma vitamin A levels, the measured levels of the vitamin in the serum do not reflect plasma and tissue levels. Patients with hypervitaminosis A may have low, normal, or high serum levels of vitamin A."

Magnesium deficiency lowers the serum retinol without affecting liver reserves, one mechanism how liver toxicity can occur while blood tests show "low".  Add evidence of magnesium deficiency epidemic.

Inflammation interferes with the assessment of vitamin A status in magnesium deficiency.
https://www.ncbi.nlm.nih.gov/pubmed/19271422

"Hyporetinemia is observed in several pathological conditions including a primary deficiency of vitamin A and has also been reported to accompany inflammatory diseases. Experimental magnesium (Mg) deficiency in rodents is accompanied by an inflammatory syndrome. The present study was designed to determine whether the acute phase response in Mg-deficient rats can modify vitamin A status. Clinical symptoms of acute phase response were observed in Mg-deficient rats and were accompanied by a reduction in plasma retinol and of plasma retinol binding protein (RBP). Mg deficiency in rats resulted in hyporetinemia without a significant decrease in liver retinol reserves. Consequently, the data strongly suggest that the decrease in plasma retinol concentration, resulting from the level of its binding protein, is related to the inflammatory effect of Mg deficiency. These results point to the possible interference of Mg deficiency on the use of plasma retinol as an indicator of vitamin A status."

Have you seen Grant Genereux's blog post about how his serum retinol is almost down to ZERO without any negative health effects? This is a proof in what I said above, that healthy individuals can have almost NO Vitamin A in their system and be TOTALLY HEALTHY, because the problems that are ASSumed to be from "Vitamin A deficiency" are problems of significant/severe malnutrition in other areas.

Do you realize that they are making up stories about this compound and trying to call it science?

Metabolism of retinol-binding protein and vitamin A during hypervitaminosis A in the rat

Vitamin A transport in human vitamin A toxicity.

The plasma retinol transport system was studied in three patients with chronic hypervitaminosis A. The toxic state in each was associated with increased plasma concentrations of total vitamin A, and particularly of retinyl esters. The concentrations of plasma retinol-binding protein and prealbumin were, in contrast, normal, and there was a molar excess of total vitamin A in relation to retinol-binding protein. These limited clinical data support conclusions from detailed studies with hypervitaminotic rats, which suggest that vitamin A toxicity occurs when excessive amounts of vitamin A are presented to cell membranes in association with plasma lipoproteins, rather than specifically bound to retinol-binding protein. Retinol-binding protein may not only regulate the supply of retinol to tissues but also protect tissues from the surface-active properties of the vitamin.

"For example, in rats given three different levels of daily vitamin A supplements, serum retinol concentrations did not differ despite a sixfold difference in liver reserves of vitamin A (17).

Serum retinol is not a reflection of the vitamin A liver stores because it is homeostatically controlled and it does not drop until liver reserves are very low. The cut-off value for definition of deficiency has been discussed. In children certainly values <0.35 μmol/L and in women 0.70 μmol/L may indicate deficiency. However, if no infection is present in the population under study, 0.70 and 1.05 μmol/L for children and women, respectively, may be more descriptive of the actual status. If the population has access to a source of preformed vitamin A, serum retinol concentrations will be higher but not necessarily reflective of status,

[...]

Although isotope dilution testing is usually too expensive to consider as a means to evaluate a programme, a sugar-fortification programme was evaluated in a small group of Nicaraguan children (52). The baseline mean liver retinol concentration was 0.57 μmol/g liver, well above what is currently considered deficient (0.07 μmol/g liver). All the children had serum retinol concentrations between 0.74 and 1.31 μmol/L. One year after sugar fortification was implemented, liver reserve concentrations increased to an average of 1.2 μmol/g liver. In 9 of 21 children, liver vitamin A concentrations were calculated to be >1.05 μmol/g liver after fortification, which was defined as toxic in 1990 (53). Because many foods are now being considered for fortification, this sensitive methodology may have to be used, as no other method except liver biopsy is able to diagnose hypervitaminosis A."