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Vision
These first two papers could well go under the Topics of PubMed Research Papers and PhotoBioModulation, respectively, but I think Vision deserves a category all its own. Someone very close to me has AMD and that reality has driven a lot of my study over the years. I'm still trying to grok the idea that all the "research" on vision and the retinoids could be so completely screwed-up, but papers like the first one here readily show how they're stumbling all over themselves trying to match reality to theory. Check it out.
https://www.ncbi.nlm.nih.gov/pubmed/27830507
Subcell Biochem. 2016;81:231-259.
Vitamin A and Vision.
Saari JC1,2.
Author information
Abstract
Visual systems detect light by monitoring the effect of photoisomerization of a chromophore on the release of a neurotransmitter from sensory neurons, known as rod and cone photoreceptor cells in vertebrate retina. In all known visual systems, the chromophore is 11-cis-retinal complexed with a protein, called opsin, and photoisomerization produces all-trans-retinal.
In mammals, regeneration of 11-cis-retinal following photoisomerization occurs by a thermally driven isomerization reaction.
Additional reactions are required during regeneration to protect cells from the toxicity of aldehyde forms of vitamin A that are essential to the visual process.
Photochemical and phototransduction reactions in rods and cones are identical; however, reactions of the rod and cone visual pigment regeneration cycles differ, and perplexingly, rod and cone regeneration cycles appear to use different mechanisms to overcome the energy barrier involved in converting all-trans- to 11-cis-retinoid.
Abnormal processing of all-trans-retinal in the rod regeneration cycle leads to retinal degeneration, suggesting that excessive amounts of the retinoid itself or its derivatives are toxic.
This line of reasoning led to the development of various approaches to modifying the activity of the rod visual cycle as a possible therapeutic approach to delay or prevent retinal degeneration in inherited retinal diseases and perhaps in the dry form of macular degeneration (geographic atrophy). In spite of great progress [ha, that’s funny] in understanding the functioning of rod and cone regeneration cycles at a molecular level, resolution of a number of remaining puzzling issues will offer insight into the amelioration of several blinding retinal diseases.
JF comment: that abstract is quite the confirmation of Grant's critique that Nature wouldn't be so stupid to have our vision rely on such a family of molecules. I don't understand the molecular evidence that the house-of-cards relies upon, but as long as researchers are pointing out the above problems, I'm going with the simple thesis - i.e. we don't need it at all - and as a Pascal's Wager, if we do, after many years of eating very little of it, then there's plenty of it around in a pinch.
Now here comes the really cool paper describing PhotoBioModulation at 670nm Red Light wavelength therapy.
https://www.ncbi.nlm.nih.gov/pubmed/?term=29167189
Diabetes. 2018 Feb;
67(2):291-298. doi: 10.2337/db17-0803. Epub 2017 Nov 22.
Photobiomodulation Inhibits Long-term Structural and Functional Lesions of Diabetic Retinopathy.
Cheng Y1,2, Du Y1, Liu H1, Tang J1, Veenstra A1, Kern TS3,4.
Abstract
Previous studies demonstrated that brief (3 to 4 min) daily application of light at 670 nm to diabetic rodents inhibited molecular and pathophysiologic processes implicated in the pathogenesis of diabetic retinopathy (DR) and reversed diabetic macular edema in small numbers of patients studied.
Whether or not this therapy would inhibit the neural and vascular lesions that characterize the early stages of the retinopathy was unknown. We administered photobiomodulation (PBM) therapy daily for 8 months to streptozotocin-diabetic mice and assessed effects of PBM on visual function, retinal capillary permeability, and capillary degeneration using published methods.
Vitamin D receptor and Cyp24a1 transcripts were quantified by quantitative real-time PCR, and the abundance of c-Kit+ stem cells in blood and retina were assessed.
Long-term daily administration of PBM significantly inhibited the diabetes-induced leakage and degeneration of retinal capillaries and also significantly inhibited the diabetes-induced reduction in visual function.
PBM also inhibited diabetes-induced reductions in retinal Cyp24a1 mRNA levels and numbers of circulating stem cells (CD45-/c-Kit+),
but these effects may not account for the beneficial effects of PBM on the retinopathy.
PBM significantly inhibits the functional and histopathologic features of early DR, and these effects likely are mediated via multiple mechanisms.
© 2017 by the American Diabetes Association.
[JF: the Free Article is available]
Hello Guest,
There's a very good report to read on this regarding retinoic acid and eye damage it causes.
UC Berkeley Previously Published Works
Title
Effects of isotretinoin on meibomian glands
Permalink
https://escholarship.org/uc/
It documents that accutane is released from the meibomian glands and spreads across the eye in the tear film within days of consumption.
But, it is also known that just consuming moderately high vit A meal can also produce a rise in RA levels.
Retinoic acid is present in both the fasting and postprandial circulations where it is bound to albumin. 505 Immediately following consumption of a retinol-rich meal (~1 mg/kg body weight), mean plasma 506 concentration of retinoic acid was observed to reach 254 nmol/L but was quickly restored to fasting 507 concentrations of 14 nmol/L in 10 male volunteers (Arnhold et al., 1996).
Source:
DRAFT SCIENTIFIC OPINION 1
Scientific Opinion on Dietary Reference Values for vitamin A1 2
EFSA Panel on Dietetic Products, Nutrition, and Allergies (NDA)2, 3 3
European Food Safety Authority (EFSA), Parma, Italy
Yesterday I read Dr. Garrett Smith's new post on his forum entitled,
"Carotenoids and retinoids--Poison/Vitamin A absolutely do accumulate in many tissues, especially the EYES--and cause long-term problems".
I'm presently on my iPhone and though I can email and text links, I can't seem to send a link for this article to this forum. The article shows research validating that Vitamin A and carotenoids accumulate in the eyes of macular degeneration patients. Though the type of macular degeneration tested in the research was an early inset type, age related macular degeneration is similar.
DWL
Quote from DWL on February 18, 2019, 3:09 amYesterday I read Dr. Garrett Smith's new post on his forum entitled,
"Carotenoids and retinoids--Poison/Vitamin A absolutely do accumulate in many tissues, especially the EYES--and cause long-term problems".
I'm presently on my iPhone and though I can email and text links, I can't seem to send a link for this article to this forum. The article shows research validating that Vitamin A and carotenoids accumulate in the eyes of macular degeneration patients. Though the type of macular degeneration tested in the research was an early inset type, age related macular degeneration is similar.
DWL
I read that too. That’s pretty exciting for me because I have a couple genes that put me at higher risk for macular degeneration. Bella
Quote from DWL on February 18, 2019, 3:09 amYesterday I read Dr. Garrett Smith's new post on his forum entitled,
"Carotenoids and retinoids--Poison/Vitamin A absolutely do accumulate in many tissues, especially the EYES--and cause long-term problems".
I'm presently on my iPhone and though I can email and text links, I can't seem to send a link for this article to this forum. The article shows research validating that Vitamin A and carotenoids accumulate in the eyes of macular degeneration patients. Though the type of macular degeneration tested in the research was an early inset type, age related macular degeneration is similar.
DWL
Here is the link for those interested:
Orion, thank you for posting the link!!!
DWL
Retinoid receptors trigger neuritogenesis in retinal degenerations https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3250249/
The full consequences of retinal degeneration for retinoid metabolism are unclear. But it is certain that prolonged bleaching events can release very high levels of all-trans-retinal, which is potentially retinotoxic (67). Rod photoreceptor outer segments are estimated to contain 3–5 mM rod opsin (68) based on protein mass, but the effective membrane concentration is likely much higher (69), representing a massive depot for 11-cis-retinal provisioned by the RPE. Under normal homeostasis, most all-trans-retinal formed by bleaching is converted to 11-cis-retinol by photoreceptor RDH, and little or none appears to reach the neural retina, consistent with the absence of detectable neuritogenesis in the normal retina. However, coincident with the rapid degeneration of photoreceptors in either light damage or retinal degeneration, it is evident that sufficient all-trans-retinal reaches cells containing ADH to result in RA production, consistent with prior reports (26) and our finding of elevated RA-like species in retinal degeneration
This study is an eye-opener!!
Relationship between dietary retinol and lipofuscin in the retinal pigment epithelium.
Katz ML, et al. Mech Ageing Dev. 1986.
Show full citation
Abstract
A variety of evidence suggests that autoxidation of cellular components probably plays a significant role in the age-related accumulation of lipofuscin, or age-pigment, in the mammalian retinal pigment epithelium (RPE). Among the likely candidates for conversion into RPE lipofuscin fluorophores via autoxidative mechanisms are vitamin A compounds, which are present in the retina and RPE in high concentrations. Vitamin E, an important lipid antioxidant, is likely to inhibit vitamin A autoxidation. Experiments were conducted to evaluate the significance of vitamin A autoxidation in the deposition of lipofuscin in the RPE. Albino rats were fed diets either supplemented with or lacking vitamin E. Each of these two groups of animals was further subdivided into three groups which were fed different levels of vitamin A palmitate: none, 14.0 mumol/kg diet, and 80.5 mumol/kg diet. After 26 weeks, the animals were killed and the RPE lipofuscin contents were determined by both fluorescence measurements and quantitative ultrastructural morphometry. Vitamin A palmitate deficiency led to significant reductions in RPE lipofuscin deposition, relative to the amounts of this pigment present in the groups receiving vitamin A palmitate in their diets. The relative magnitude of the vitamin A effect was greater in the vitamin E-supplemented groups than in the groups fed the diets deficient in vitamin E. This finding suggests that vitamin E interacts with vitamin A ester metabolites in vivo in a more complex manner than simply acting as an antioxidant protectant. Rats fed the diets containing the higher level of vitamin A palmitate failed to display elevated RPE lipofuscin contents relative to those in the rats fed 14.0 mumol of vitamin A palmitate/kg diet. Failure of high vitamin A intake to enhance RPE lipofuscin deposition may have been due to the fact that intake of vitamin A above normal levels did not lead to an elevation in vitamin A content of the retinal tissue. Establishing an effect of vitamin A deficiency on RPE lipofuscin deposition and characterization of the interactions between vitamins E and A are important steps toward defining precisely the molecular and cellular mechanisms underlying age-pigment accumulation in the RPE.
PMID 3773574 [Indexed for MEDLINE]
Full text
Full text at journal site
The first thing that occurs to me (besides the fact that I wish google had a translator for scientific-ese to layman-ese) is that they chose albino rats.
What is an albino rat going to do with orange color pigments? haha. But really. I'm one step above albino LOL and wonder if that is one of the reasons I can't deal with pigments.