Quote from Dr. Garrett Smith on November 14, 2018, 9:30 pm

Grant Genereux discusses this topic in his first e-book, so please read that.

You will see the protein and/or zinc and/or iodine deficiency connection (among othernutrients)  show up everywhere that vision issues and "Vitamin A deficiency" are discussed.  DHA deficiency is also implicated, as this is the natural ligand for the incorrectly named RXR (Retinoic Acid Receptor, see other thread on this).  First, we will cover protein malnutrition/deficiency as a cause of so-called "Vitamin A deficiency conditions".

Chapter 7. Vitamin A

http://www.fao.org/docrep/004/Y2809E/y2809e0d.htm
"Night blindness is usually an indicator of inadequate available retinol, but it can also be due to a deficit of other nutrients, which are critical to the regeneration of rhodopsin, such as protein and zinc, and to some inherited diseases, such as retinitis pigmentosa"

Remember the protein deficiency, it will be important.

Vitamin A

https://www.dsm.com/markets/anh/en_US/Compendium/ruminants/vitamin_A.html
"Deficiencies of dietary protein, phosphorus, zinc and iodine during gestation can also impair vitamin A metabolism in the cow"

Vitamin A Deficiency in Beef Calves

https://vetmed.iastate.edu/sites/default/files/vdpam/Extension/Vitamin-A-deficiency-in-Beef-Calves.pdf (also attached)
[my comments in brackets]
"Calves that are born with signs of vitamin A deficiency due to abnormal development will probably not benefit from supplemental vitamin A.
[This makes NO sense unless the root cause is NOT "Vitamin A deficiency"...correcting a TRUE deficiency while still in development phases should correct at least some of the problems.]

Abnormal bone development that constricts the optic nerve leading to blindness or muscle incoordination from spine abnormalities will probably not respond to vitamin A.
[Because it is not a "Vitamin A deficiency" maybe? Remember the protein deficiency connection I mentioned above, it will be important below in connecting one possible nutritional cause of the optic nerve, blindness, and muscle incoordination issues]

Normal calves will be born with adequate levels of vitamin A but require additional vitamin A from consumption of milk that has satisfactory levels vitamin A.
[How can a calf have an "adequate level" of Vitamin A yet still require additional consumption? What does the blood test really mean then, exactly?]

It is also important to remember that cows and calves that are deficient in vitamin A are probably deficient in other vitamin and minerals such as vitamin E, copper, manganese, selenium and zinc."

Let's make a list from the above papers on possibly/probably connected nutrient deficiencies that seem to often & "coincidentally" happen together with so-called "Vitamin A deficiency":

• Protein
• Zinc
• Iodine
• Phosphorus
• Vitamin E
• Copper
• Manganese
• Selenium
• DocosaHexanoic Acid (DHA), I will make this case on my own, it is not mentioned above.

Back to the optic nerve, blindness, and muscle coordination issues mentioned above.  Did you know that all of those issues could be potentially caused by just ONE thing, a PROTEIN malnutrition/deficiency?  Let's do this.  First, the optic nerve.

Functional development of the visual system in normal and protein deprived rats. II. Morphometric and biochemical studies on adult optic nerve.

https://www.ncbi.nlm.nih.gov/pubmed/4072710
"The optic nerve of normal (C) and protein deprived (PD) adult rats was examined by morphometry and biochemistry. The mean cross-sectional area of the optic nerve was reduced by 15% and the number of axons per unit area increased by 17% in the PD rats. Calibre spectrum analysis of axons revealed a reduction in median diameter from 0.49 micron in controls to 0.45 micron in PD rats. The number of axons with a diameter larger than 1 micron was reduced by 35% in PD rats. These reductions were probably due to a general reduction in size, since the calculated total number of axons in the optic nerve was almost identical in C and PD rats (126 X 10(3) and 124 X 10(3), respectively). The increased packing density of axons in the nerve was not only due to thinner axons. The biochemical measurements showed a marked reduction in myelin basic protein in the optic nerves of PD rats, without an alteration in the composition of the total protein. This confirms the persistent hypomyelination which has been reported previously in other malnutrition models. The possible relations between the structural and biochemical changes affecting optic nerve fibres and physiological findings on cortical visual evoked response and on optic nerve in vitro in PD rats are discussed."

Here's how I look at the above:

• Protein deficiency resulted in overall "thinner nerves" (lower cross-sectional area).  Could thinner nerves have been misinterpreted in the "Vitamin A Deficiency in Beef Calves" paper above as "abnormal bone development that constricts the optic nerve"?  Is it that the bones were too big, or that the nerves were too small?  It's all in how one looks at it.
• Protein deficiency made the axons (the long fibers of neurons/nerve cells that act somewhat like fiber-optic cables carrying outgoing/efferent messages) SMALLER.  Think of the nerve like a cable, and the axons like the individual wires within the cable.  Just like with computer data and electric power, the bigger/thicker the cable (and individual wires inside the cable), the faster & easier the flow along it.  The opposite is true as well, smaller/thinner makes for slower and more difficult flow.
• There was less myelin in the optic nerves of protein-deficient rats, and this has been shown in studies before. That's not good.

Next, night blindness and protein malnutrition/deficiency.

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

https://www.ncbi.nlm.nih.gov/pubmed/8985529
"The occurrence of night blindness and serum vitamin A concentrations among children in rural Bangladesh were studied in relation to protein energy malnutrition, dietary habits and intake of vitamin A capsules. In 1992, 124 night-blind children were registered in a cross-sectional survey in the northern part of Bangladesh, and age-, sex- and neighbourhood-matched controls were selected. Of these, the first reported night-blind child from a household (n = 105) and their controls were included in the analyses. 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)."

And on to muscle incoordination (in humans, we might call this motor development delays, muscle weakness, etc.), two large papers.  First, in infants and children:

Neurological consequences of protein and protein-calorie undernutrition.

https://www.ncbi.nlm.nih.gov/pubmed/1934090
"Malnutrition is a worldwide problem of enormous magnitude. The growth of the central nervous system in human beings is retarded in case of malnutrition in the very early part of life. Likewise, the peripheral nerves in infants and children and young growing animals appear susceptible to nutritional deprivation including protein as well as protein-calorie deficiency. Motor weakness, hypotonia, and hyporeflexia in infants and children are the essential clinical neurological signs in protein-calorie malnutrition (PCM). Motor and sensory nerve conduction are significantly impaired in children with PCM as well as in animals subjected to protein or protein-calorie deficiency. Histological studies have revealed reduced diameter of myelinated nerve fibers, retardation of myelination, segmental demyelination and remyelination, axonal degeneration, and shortened longitudinal growth of internodes. Diffusion barrier by perineurium may be broken. There is reduction in myelin lipids and impaired synthesis of myelin as shown by the biochemical and radioisotope incorporation studies. Presence of cholesterol esters in the biochemical synthesis of nerves suggests degeneration changes. Experimental studies have revealed that most effects of PCM on peripheral nerves can be reversed by nutritional rehabilitation, although complete recovery in the sensory nerve action potential, fiber size of dorsal nerve roots, and myelin-specific lipids does not occur. Skeletal muscle also shows many changes including muscle fiber atrophy, reduction in duration and amplitude of motor unit potentials, and/or fibrillation on electromyography (EMG) and biochemical estimation of muscle enzymes. These changes may be the reflection of a direct effect of PCM on muscles or secondary to the abnormal structural or biochemical changes in the peripheral nerves. PCM affects the central nervous system, especially the neuropsychological functions, in a lasting manner. Learning deficits and impairment of manual dexterity are the most obtrusive features. Neurotransmitter abnormalities and maturation lag in electroencephalogram have been demonstrated in experimental animals. Spinal cord dysfunction sometimes manifests overtly as clinical myelopathy. Degenerative changes in the cerebellum have been noted."

Next, in "adults" (rats):

Protein-Energy Malnutrition Causes Deficits in Motor Function in Adult Male Rats

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5469620/
"Conclusions
PEM [Protein-Energy Malnutrition] in adult male rats causes a variety of sensorimotor abnormalities that develop at different stages of malnutrition. This model can be used in combination with disease models of sensorimotor deficits to examine the interactions between nutritional status, other treatments, and disease progression."

To be incorporated later:

Zinc deficiency

Iodine deficiency:
https://www.ncbi.nlm.nih.gov/pubmed/1659516 (Vitamin A inhibited iodine uptake and thus inhibited cAMP production)
http://diabetes.diabetesjournals.org/content/18/12/797
https://www.sciencedirect.com/science/article/pii/B9780080450469009219 "Cyclic adenosine monophosphate is a key intracellular regulator of retinomotor movements, triggering dark-adaptive movements in all three cell types."

So, we have multiple known, connected nutritional deficiencies that supposedly "impact Vitamin A metabolism" negatively.  What if Poison/"Vitamin A" isn't a vitamin at all, is actually a poison, and many of the problems we think are caused by its so-called "deficiency" are related to other known nutritional deficiency patterns?