Quote from Dr. Garrett Smith on January 25, 2019, 10:24 pm

I will add more research as it comes in.

As I went through my own personal detoxification of Poison/"Vitamin A", I realized (through paying attention to dream recall frequency, lack of dream recall can imply B6 deficiency, while excess B6 supplements can cause significant issues) that I didn't need to take any Vitamin B6 any longer.  I started to wonder if there was any connection between Poison/"Vitamin A" and B6 deficiency.  It has proven difficult to find any direct connections, however, we can establish some possible indirect ones.

In some of the paid-access-only Sara's Diet information (a lutein aka carotenoid-free diet said to help autism), it was stated that "Carotenoids are B6 binding and these are being greatly reduced in this diet recommendation."  If carotenoids bind B6 in a bad way, this could effectively induce a deficiency...therefore restricting them could correct a deficiency, which is what I personally observed.  There is no reference I can find to back this up, at least to this point.

There is this one study, which correlates very high carotenoid intakes in Zambian children with low Vitamin B6 (aka PLP) levels:

High provitamin A carotenoid serum concentrations, elevated retinyl esters, and saturated retinol-binding protein in Zambian preschool children are consistent with the presence of high liver vitamin A stores1

First, what is the study giving these children to cause the high levels of all things Poison/"Vitamin A" in the study title?

Design: A randomized, placebo-controlled, biofortified maize efficacy trial was conducted in 140 rural Zambian children from 4 villages.

Before we go further, I need to include something.  Nowhere in the entire study did they specifically mention how long the trial was going to be!  Being the Nutrition Detective I am, I had to go to ClinicalTrials.gov and look up the study by its number in order to find out how long it was:

This study will determine the change in total body stores of vitamin A in response to feeding orange maize for 90 days.

90 days of "biofortified" orange maize.  We're going to take a quick detour here.  What is this stuff, exactly?

Carotenoid retention in biofortified maize using different post-harvest storage and packaging methods

Orange maize is being promoted as a source of provitamin A carotenoids (pVAC) in Zambia.
[...]
The first group of biofortified orange maize varieties, which has been conventionally bred as an alternative to improve vitamin A status of populations

Well, at least it isn't GMO, I guess?  Maize bred to produce so many carotenoids it turned orange.  NOT fortified through the addition of exogenous Vitamin A. Before we go further into the original study I linked above. you need to catch this.  The below toxicity and deficiency was caused within 90 DAYS of eating a totally natural source of carotenoids (NOT synthetic)!!!  Let me repeat that.  All the hypervitaminosis A and Vitamin B6 (PLP) deficiency you are about to read below was caused by carotenoids from foods IN 90 DAYS. Back to that paper:

Because of surprising findings that indicated adequate through hypervitaminotic VA status of Zambian preschoolers (7), these assumptions have been challenged (8).

Let's be clear here from the start.  They already know they are poisoning these Zambian kids with Poison/"Vitamin A" with this plant food, in a twisted attempt to "prevent deficiency" that isn't really causing the problem.  The lack of animal foods is the problem.  That's a whole different story though.

Calculated mean liver reserves for all subjects were 1.13 +/- 0.41 micromol retinol/g liver, with 59% >1 micromol/g (7), which is the current cutoff for defining hypervitaminosis A (2). No reserves were <0.1 micromol/g, which is the deficiency cutoff (2).

Nearly 60% of these kids were TOXIC by medical definition!!!  In 90 days.

A common reference range for serum carotene is 0.9–3.7 micromol/L (28), which would encompass the overall mean. Sixteen samples (13%) had total carotenoid concentrations >3.7 micromol/L, which were considered hypercarotenemic.

13% of the kids had too many carotenoids! In 90 days.

In all participants, 16% of subjects had retinyl esters >5% of serum total VA, whereas 2% of subjects had retinyl esters >10% of serum total VA.

Measuring retinyl esters is a way of showing how much Poison/"Vitamin A" is stored in the liver.  Above 5% indicates toxicity.  By this test, 16% of these kids were toxic.  In 90 days.

With so many kids being toxic with this so-called pro-vitamin, the researchers expected to see elevated ALT levels (a liver enzyme that goes up in hypervitaminosis A).  They didn't see this happen, so they suspected B6 aka PLP deficiency:

The liver enzyme ALT was evaluated in serum to determine whether liver damage was present because of the hypervitaminotic state of some children. ALT activity was below normal (range: 0.83–11.4 U/L), and only one child tested had normal activity (10-40 U/L). ALT activity was not related to any other factors evaluated. Because ALT activity was low, PLP concentrations were determined and were also below normal; 79% of children had serum concentrations <20 nmol/L, which is the suggested deficiency cutoff (29), and 29% of values were in the extremely low range of <10 nmol/L.

Seems like a mini-epidemic of B6 (PLP) deficiency is going on in these four villages. In 90 days.  The way the authors talk, and the fact they were surprised by this finding (rather than expecting it) makes it sound like this is NOT common in other villages.  This was a trial study, after all!

The findings of hypercarotenemia, saturated RBP, and elevated retinyl esters in some of the children support excessive stores of VA in this community.

This disaster was done in 90 days.  

Hypervitaminosis A is linked to a major increase in INFLAMMATION.  What does inflammation do to B6 requirements? It increases them!

Vitamin B-6 Intake Is Inversely Related to, and the Requirement Is Affected by, Inflammation Status

In conclusion, our large, general-population study confirmed the association between inflammation and low plasma PLP concentration...

To recap what I have on this topic so far:

• My personal experience that the Poison/"Vitamin A" Detox restored my dream recall and eliminated my need for extra B6
• Sara's Diet author states that carotenoids bind B6
• Trial study on Zambian children shows very low B6 levels with excessive carotenoid intake and hypervitaminosis A
• Low B6 levels correlate with increased inflammation, and increased inflammation is implicit in hypervitaminosis A

Not the most direct connection.  I hope more comes out on this.  In the meantime, I will go by the combination of my clinical observations with the above research trail.

Calculated mean liver reserves for all subjects were 1.13 +/- 0.41 micromol retinol/g liver, with 59% >1 micromol/g (7), which is the current cutoff for defining hypervitaminosis A (2). No reserves were <0.1 micromol/g, which is the deficiency cutoff (2).