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Carotenoids and retinoids--Poison/"Vitamin A" absolutely do accumulate in many tissues, especially the EYES--and cause long-term problems

I would like to start this post by "popping a belief balloon".  What does the research say about carotenoids and health?  Is the evidence strong or WEAK?

Rooibos (Aspalathus linearis) and its Major Flavonoids — Potential Against Oxidative Stress-Induced Conditions

Empirical evidence for carotenoids being important antioxidants in vivo is weak [105,139]. Recent reports on birds showed that carotenoids have a very low contribution to protection against oxidative damage under stressful conditions [140144]. Many human trials where carotenoids and other dietary antioxidants (vitamin C and E) were administered singly or together did not show any positive effect and even contributed to mortality among study subjects [145148].

People DIED EARLY (that what "contributed to mortality" means!) from beta-carotene supplements (see the reference links at the end of the above quote).  THREE STUDIES have shown that!

Metabolism of Carotenoids and Retinoids Related to Vision

The third family member, RPE65 (retinal pigment epithelium 65-kDa protein), was the first animal CCE molecularly identified (15), but RPE65 was regarded for a long time as a retinoid-binding protein (1617). Mutations in RPE65 can cause Leber congenital amaurosis in humans (18). Analysis of mouse models revealed that this enzyme's dysfunction disrupts chromophore synthesis and leads to the accumulation of retinyl esters (REs) in the retinal pigment epithelium (RPE) (19). It was later shown that RPE65 is the retinoid isomerase in the vertebrate visual cycle that catalyzes the conversion of all-trans-REs to 11-cis-retinol (2022).
Genetic disruption of Bcmo1 results in β,β-carotene accumulation in the fat pads of mice.

Mutations in the ninaB gene lead to carotenoid accumulation in the eye.

Genetic disruption of the Bcdo2 gene results in a yellow color of isolated liver mitochondria due to carotenoid accumulation.
Mutant analyses of the silk worm Bombyx mori identified molecular players in a pathway for tissue-specific accumulation of carotenoids in the silk gland. In this pathway, carotenoid absorption is mediated by a NinaD-related protein encoded by the Yellow Cocoon gene (37). For cellular accumulation, Bombyx expresses a specific carotenoid-binding protein encoded by the Yellow Blood gene that is a member of the family of StAR (steroidogenic acute regulatory) proteins (37).
BCDO2 is critical for the catabolism of carotenoids in cells. In Bcdo2−/− mice, carotenoids accumulate in several tissues and cause mitochondrial oxidative stress (13).
The natural occurrence of such an aberrant side reaction is documented by the presence of the bisretinoid A2E, formed by a condensation reaction of two molecules of RAL
[RetinALdehyde] with the membrane lipid phosphatidylethanolamine. Ocular accumulation of A2E and A2E-mediated redox reactions have been implicated in the pathology of eye diseases such as age-related macular degeneration (68). The importance for rapid clearance of the photoproduct is also demonstrated by the consequences of mutations in RDH12 and ABCA4 in humans (6970). Mouse models with impaired retinal clearance have been established to characterize the underlying pathology (71).

Accumulation of Poison/"Vitamin A" (bisRETINOID A2E) has been implicated in age-related macular degeneration.

Mouse models that cannot get rid of Poison/"Vitamin A" (impaired retinal clearance) characterizes the underlying pathology (aka the cause of the disease) of eye diseases.

One of their reference papers showing that if Poison/"Vitamin A" is not cleared (aka DETOXED) from the eye properly, then retinopathy (disease of the retina which results in impairment or loss of vision) is the result: Retinopathy in Mice Induced by Disrupted All-trans-retinal Clearance

Back to the original review paper:

In contrast, genetic disruption of RPE65 abolishes both cone and rod vision in mice. In Rpe65−/− mice, some residual light sensitivity has been attributed to rods (90) and is mediated by 9-cis-retinal and isorhodopsin (91). Furthermore, RPE65 is critical for chromophore production and vision in Nrl−/− mice, which possess a cone-only retina due to developmental defects (92). However, this dependence of chromophore production on RPE65 does not contradict an additional cone-specific pathway if we consider that ROL uptake in the eyes occurs via the RPE and is driven by esterification by LRAT (76). This all-trans-RE must be metabolized by RPE65 to the cis-chromophore as noted by the tremendous accumulation of REs in Rpe65−/− mice (19).

My interpretation...accumulation of REs (Retinyl Esters, the storage form of Poison/"Vitamin A") completely destroys rod and cone vision.

Two more studies on monkeys and canthaxanthin (a carotenoid) accumulation, turning into Poison/"Vitamin A" crystals in their eyes:

Occurrence of birefringent retinal inclusions in cynomolgus monkeys after high doses of canthaxanthin.

PURPOSE: To reproduce and investigate in a primate animal model the phenomenon of the red carotenoid canthaxanthin (beta, beta-carotene-4'4'-dione) to induce crystal-like retinal deposits as they have been observed in the ocular fundus of humans after high canthaxanthin intake (i.e., more than 30 mg/day).
Twelve of the 24 canthaxanthin-treated animals showed yellow, golden birefringent inclusions in the macula. Retinas of placebo-treated monkeys were free of birefringent, crystal-like inclusions. The HPLC confirmed the presence of all-trans canthaxanthin, and 4-OH-echinenone and isozeaxanthin as well, in the retinas of all canthaxanthin-treated animals. 
CONCLUSIONS: A high intake of canthaxanthin for 2.5 years led to the deposition of crystal-like birefringent inclusions in the inner layers of the peripheral retina and, to some extent, the central retina of cynomolgus monkeys.

Dose dependency of canthaxanthin crystals in monkey retina and spatial distribution of its metabolites.

CONCLUSIONS: The grade of crystals in monkey retinas was dose dependent with a threshold level at 0.6 mg canthaxanthin/kg body wt/d. It correlated in the retinal periphery with the concentrations of all-trans-canthaxanthin and in the macula with its metabolites.

If you like your eyes, you shouldn't like Poison/"Vitamin A".

Dr. Garrett Smith, the "Nutrition Detective"
Licensed Naturopathic Physician (NMD) in Arizona
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