Quote from Dr. Garrett Smith on November 8, 2018, 12:43 pm

I'm going to try to put together some inconsistencies in the way that medicine diagnoses a deficiency of Poison/"Vitamin A".  I will make sure to use VERY conventional sources.

First, can a person have very low serum Vitamin A levels and NOT have problems?  YES.  See Grant Genereux's blog here on his quest for a blood level of ZERO retinol, having been on a near-zero Poison/"Vitamin A" diet for 5+ years now, without any negative symptoms to report. Sort of bucks the idea that we need any of it at all, right?  His level of 0.1 umol/L is well below the common low end of the "normal" range, which is 0.7 umol/L in most places I've seen.

So, being that I don't believe Grant is some sort of genetic freak in any way, how is he able to get his serum retinol SO LOW without ANY symptoms?  Could it be because Poison/"Vitamin A" isn't really a vitamin at all?  That should be the obvious conclusion.

Next, it is VERY straightforward in the literature that carotenoids (carotenes and xanthophylls, the most famous one being beta-carotene) are NOT essential nutrients ("essential nutrients" meaning that we must get enough of them from our diet or else we will DIE of deficiency).  The precursors to retinol (the liver converts a minor amount of carotenoids to retinol) are not actual ESSENTIAL nutrients.  Isn't this sort of strange?  If people are adopting vegan diets without any pre-formed retinol to eat in them, wouldn't that make carotenoids essential nutrients for their survival then? How does nutritional science ignore this fact, unless it is true that we don't need ANY carotenoids for health?

How is "Vitamin A deficiency" diagnosed then?  Well...from the MERCK MANUAL:
https://www.merckmanuals.com/professional/nutritional-disorders/vitamin-deficiency,-dependency,-and-toxicity/vitamin-a
"Diagnosis is based on typical ocular findings and low vitamin A levels."

Here's the grand question based on the above, one that is being demonstrated in Grant's LOW serum retinol level without any negative symptoms:
IF someone has a confirmed extremely low blood level of Vitamin A (serum retinol and/or serum Retinol Binding Protein aka RBP), and DOESN'T have any eye problems or any other problems, doesn't that imply the possibility that the things modern medicine suggests are related to a "Vitamin A deficiency" are NOT ACTUALLY CORRECT?

What if the symptoms that modern medicine has decided to correlate with "Vitamin A deficiency" are well-known to:

• Correlate with other nutrient deficiencies, including protein malnutrition and zinc deficiency (both would happen extremely commonly in places where the population doesn't eat animal protein on a regular basis, for whatever reason it happens).
• Those same deficiencies also interfere with the production of RBP, which means the liver does not have the nutrients it needs to release toxic Poison/"Vitamin A" out of the liver into the circulation to GET RID OF IT without damaging the body (including the eyes) further.  See the Rules thread in this forum for more info on this.

What nutrient deficiency might also go along with a supposed "Vitamin A deficiency" disease like xerophthalmia ("abnormal dryness of the conjunctiva and cornea of the eye, with inflammation and ridge formation"), that ALSO would negatively impact the liver's production of RBP?

Protein malnutrition:

• Less protein equals more xerophthalmia problems:
  https://www.ncbi.nlm.nih.gov/pubmed/113519
  "Xerophthalmic inpatients were older and had more severe hypoproteinemia than inpatients without eye signs, and were more undernourished by anthropometric criteria than a comparison group matched for age, sex, and type of PCM."
• Protein (amino acids) are necessary for the production of RBP:
  https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcp.1041300103
  "Studies were conducted to explore hormonal and nutritional factors that might be involved in the regulation of retinol‐binding protein (RBP) synthesis and secretion by the liver. The studies employed primary cultures of hepatocytes from normal rats. When cells were cultured in Dulbecco's modified Eagle's medium alone, a high rate of RBP secretion was observed initially, which declined and became quite low by 24 hr. Supplementing the medium with amino acids maintained RBP and albumin secretion at moderate (but less than initial) rates for at least 3 days."
• Not enough protein = more xerophthalmia = tests then show *correlated, not causative* low serum retinol and/or serum RBP

What about night blindness, a supposed dead giveaway symptom of "Vitamin A deficiency"?  That should be a slam dunk diagnosis, right?  My comments interspersed within the non-italicized brackets:

https://www.merckmanuals.com/professional/nutritional-disorders/vitamin-deficiency,-dependency,-and-toxicity/vitamin-a#v884910
"Diagnosis

Ocular findings suggest vitamin A deficiency. Dark adaptation can be impaired in other disorders (eg, zinc deficiency, retinitis pigmentosa, severe refractive errors, cataracts, diabetic retinopathy). If dark adaptation is impaired, rod scotometry and electroretinography are done to determine whether vitamin A deficiency is the cause.

[Hey, there's that ZINC DEFICIENCY again!  Also, other things besides "Vitamin A deficiency" cause night blindness too! ]

Serum levels of retinol are measured. Normal range is 28 to 86 mcg/dL (1 to 3 mcmol/L). However, levels decrease only after the deficiency is advanced because the liver contains large stores of vitamin A. Also, decreased levels may result from acute infection, which causes retinol-binding protein and transthyretin (also called prealbumin) levels to decrease transiently.

[The bolded part is a distinct attempt to imply that one could have night blindness from a supposed "Vitamin A deficiency" YET somehow it isn't showing up "correctly", as in the way they want it to, on the blood test because the liver isn't in an "advanced enough deficiency", did you catch that?  If the liver still has enough Vitamin A to maintain blood levels, how is the eye running short???]

A therapeutic trial of vitamin A may help confirm the diagnosis.

[Wishy-washy words throughout..."suggest"..."may"...these are not words that should be used when a mechanism is correct.  IF it is a "Vitamin A deficiency", and they give Vitamin A, the ONLY thing that should happen is it SOLVES the problem.]"

If the light receiving cells (photoreceptor cells) of the eyes are reliant upon a PROTEIN called opsin, does it make sense that a PROTEIN DEFICIENCY in the diet would strongly impact night blindness too?

What's that you say?  Protein malnutrition has been STRONGLY connected with night blindness?

Protein energy malnutrition, vitamin A deficiency and night blindness in Bangladeshi children.

https://www.ncbi.nlm.nih.gov/pubmed/8985529
"Our results showed that night blindness was associated with protein energy malnutrition when using the mid-upper arm circumference (MUAC) as a measure of nutritional status. The odds ratio for a confirmed diagnosis of night blindness among children with a MUAC < 80% of the reference versus normal children was 5.4 (CI 1.9-15.5)."

In conclusion:

• Grant's self-experimentation (and his pet experiments, see his first book) have shown that there are NO, NONE, ZERO negative effects of getting and keeping Poison/"Vitamin A" completely out of the diet.  I will eventually be posting more laboratory and eye exam results to bolster this fact as I accumulate them from myself and willing clients.  In fact, people are reporting to Grant and I that the low-to-no Poison/"Vitamin A" dietary approach is actually IMPROVING their eyesight.  Crazy, huh?  It won't be once you truly understand this stuff.
• Many of the problems associated with supposed "Vitamin A deficiency" are likely CAUSED BY either protein malnutrition and/or zinc deficiency, both of which will result in the observed/correlated lab results of "low serum Vitamin A".
• I can look to simple blood tests to assess for zinc status, protein intake status, and the level of Poison/"Vitamin A" toxicity in a person, so we can fix all three issues at once.