Vitamin A

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Vitamin A

Postby gibbledygook » Tue Oct 29, 2013 4:24 am

I think I have noticed an improvement since starting 10,000 iu of vitamin A (palmitate) although it has only been about 4 days! Check out the Pubmed stuff on it though. It's quite encouraging. Par exemple:

PLoS One. 2011;6(9):e24590. doi: 10.1371/journal.pone.0024590. Epub 2011 Sep 13.
All-trans retinoic acid promotes TGF-β-induced Tregs via histone modification but not DNA demethylation on Foxp3 gene locus.
Lu L, Ma J, Li Z, Lan Q, Chen M, Liu Y, Xia Z, Wang J, Han Y, Shi W, Quesniaux V, Ryffel B, Brand D, Li B, Liu Z, Zheng SG.
Source
Division of Rheumatology, Department of Medicine, Saban Research Institute, Children's Hospital Los Angeles, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Abstract
BACKGROUND:
It has been documented all-trans retinoic acid (atRA) promotes the development of TGF-β-induced CD4(+)Foxp3(+) regulatory T cells (iTreg) that play a vital role in the prevention of autoimmune responses, however, molecular mechanisms involved remain elusive. Our objective, therefore, was to determine how atRA promotes the differentiation of iTregs.
METHODOLOGY/PRINCIPAL FINDINGS:
Addition of atRA to naïve CD4(+)CD25(-) cells stimulated with anti-CD3/CD28 antibodies in the presence of TGF-β not only increased Foxp3(+) iTreg differentiation, but maintained Foxp3 expression through apoptosis inhibition. atRA/TGF-β-treated CD4(+) cells developed complete anergy and displayed increased suppressive activity. Infusion of atRA/TGF-β-treated CD4(+) cells resulted in the greater effects on suppressing symptoms and protecting the survival of chronic GVHD mice with typical lupus-like syndromes than did CD4(+) cells treated with TGF-β alone. atRA did not significantly affect the phosphorylation levels of Smad2/3 and still promoted iTreg differentiation in CD4(+) cells isolated from Smad3 KO and Smad2 conditional KO mice. Conversely, atRA markedly increased ERK1/2 activation, and blockade of ERK1/2 signaling completely abolished the enhanced effects of atRA on Foxp3 expression. Moreover, atRA significantly increased histone methylation and acetylation within the promoter and conserved non-coding DNA sequence (CNS) elements at the Foxp3 gene locus and the recruitment of phosphor-RNA polymerase II, while DNA methylation in the CNS3 was not significantly altered.
CONCLUSIONS/SIGNIFICANCE:
We have identified the cellular and molecular mechanism(s) by which atRA promotes the development and maintenance of iTregs. These results will help to enhance the quantity and quality of development of iTregs and may provide novel insights into clinical cell therapy for patients with autoimmune diseases and those needing organ transplantation.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Re: Vitamin A

Postby CureOrBust » Wed Oct 30, 2013 1:06 am

All-trans-retinoic acid (atRA), a Vitamin A derivative
I hadn't heard of of "atRA", so searched for what it was, and found that the above article was my best bet. The article in full can be found at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3172235/

In the immune system, atRA plays important roles in regulating the functions of many different cell types [3]. Vitamin A and its derivatives are capable of ameliorating several models of autoimmunity, including inflammatory bowel disease, rheumatoid arthritis, type I diabetes, and experimental encephalomyelitis [4]–[5].


Reference [5] looks interesting...
Retinoid treatment of experimental allergic encephalomyelitis. IL-4 production correlates with improved disease course.
http://www.ncbi.nlm.nih.gov/pubmed/7527821
All-trans-retinoic acid (tRA) inhibited the proliferation of MBP-specific LNC in vitro. However, the capacity of these cells to transfer EAE was markedly reduced by concentrations of tRA that only mildly inhibited T cell proliferation


I have always remembered seeing warnings of too much Vitamin A. Maybe you should look for something to take to ameliorate that issue
Toxicity has been shown to be mitigated through vitamin E (tocopherol), cholesterol, zinc, taurine, and calcium.
Cholesterol has been shown to prevent retinol induced golgi fragmentation.[9]
In rats, the toxic effects of vitamin A were significantly reduced when diets were supplemented with taurine or Cholestin

https://en.wikipedia.org/wiki/Hypervitaminosis_A
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Re: Vitamin A

Postby gibbledygook » Wed Oct 30, 2013 2:05 am

Hey Cureo! Well after all these years of necking vitamin D without any noticeable effect I would definitely say I have observed a change since starting the vitamin A in that my night spasms are better or milder and the walking somewhat stiffer about 5 hours after taking the vitamin a but not substantially more difficult. Perhaps the combination of saffron and vitamin a is making the change...
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Re: Vitamin A

Postby Scott1 » Wed Oct 30, 2013 2:46 am

It's not just the all trans retinoic acid. The Vitamin A helps you get 9 cis retinoic acid into your system. This form upregulates the retinoid X receptor (RXR). This receptor is the master switch that controls the thyroid like group of receptors which include Vitamin D. The point is Vitamin D needs to form a complex with RXR to function so if RXR is down then Vitamin D receptors won't function properly.
I'm not that keen on taking Vitamin A as a supplement as it can accumulate in the system and become toxic (you turn yellow). This is why I prefer freshly juiced carrot juice as it is synthesised into retinoids as your body requires.
If you dig deep enough you will find literature about Vitamin A and the adrenal glands in neonates. There is some sort of malfunction at this phase that I think is quite important in the development of MS as a metabolic disorder but we are not newborn babies so don't get stuck on it.
Please try a big glass of Carrot juice each day in preference to a Vitamin A tablet.

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Re: Vitamin A

Postby CureOrBust » Wed Oct 30, 2013 11:49 pm

Scott1 wrote:... taking Vitamin A as a supplement as it can accumulate in the system and become toxic (you turn yellow). ...
I thought that downing a lot of carrot juice caused your skin to go orange if the Betacarotene is not converted.
https://en.wikipedia.org/wiki/Hypervitaminosis_A
Betacarotene, a precursor form of vitamin A typical of vegetable sources such as carrots, is selectively converted into retinoids, so it does not cause toxicity; however, overconsumption can cause carotenosis, a benign condition in which the skin turns orange.
It also lists the effects of overdose of Vit A as
Signs of acute toxicity include nausea and vomiting, headache, dizziness, blurred vision, and loss of muscular coordination.
With "loss of muscular co-ordination" being my biggest red flag.


I actually went through a phase of having carrot juice regularly and it wasn't just me that noticed my skin had a slight tinge of orange to it.
Scott1 wrote:Please try a big glass of Carrot juice each day in preference to a Vitamin A tablet.


gibbledygook wrote:I have observed a change since starting the vitamin A in that my night spasms are better or milder and the walking somewhat stiffer about 5 hours after taking the vitamin a but not substantially more difficult
So your spasm were improved (ie less) but your walking deteriorated (ie you were stiffer)? Maybe the "stiffer" was actually a "loss of muscular co-ordination" :confused:
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Re: Vitamin A

Postby Scott1 » Thu Oct 31, 2013 3:02 am

I'd rather turn yellow (or orange) on carrot juice than take Vit A and have it build up. At least I could see what was happening. The point is too much Vit A is not a good thing. You body needs to take what it needs not store the surplus.
RXR still needs to be active for a range of functions , including Vit D receptors, to work properly.

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Re: Vitamin A

Postby LR1234 » Thu Oct 31, 2013 4:52 am

I have to say I agree with Scott....When I studied nutrition many moons ago they warned us of how Vitamin A and Vitamin D (and I think possibly E) gets stored in the Liver and can become very toxic.
Beta Carotene is the safe version of Vitamin A as you guys have mentioned as it can be excreted but Im not sure how that differs in function to retinoic Acid.

(btw Im doing the carrot juicing thing everyday and Im not orange yet.......my vision is getting better after the 8th bout of ON and strangely enough so is my thyroid function......I have had to lower my thyroxine from 50mcg now down to 25mcg on advice of my Dr 6 weeks ago and my TSH is still low and in normal range (1.5) and my FT4 is still up near the top 18 ish!) In another six weeks we will test again to decide whether to I can stay on 25mcg or I need to come up or down.
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Re: Vitamin A

Postby gibbledygook » Tue Nov 05, 2013 9:02 am

Honestly, this vitamin a and saffron supplement regime has gone hand in hand with a reduction in spasms. About 3 to 5 hours after taking the vitamin A my walking gets a bit harder, a bit more spastic so I have started taking it at tea time and the spasms just aren't there when I lie in bed. Weird. Okay it's early days and I shouldn't get excited but I reckon we should all be taking vitamin A as well as D and maybe saffron which is a POWERFUL ANTIOXIDANT. This has not for me been associated with the negative sequelae of nigella sativa or ocimum sanctum (tenuiflorum) or anatabine... I've been trying these all this year and the latter 3 made me worse. So I tried the saffron and it didn't have a noticeable negative effect but it definitely felt like it was doing something to the damaged nerve areas...then I added the vitamin A and wow something is definitely happening and it is GOOD. WOW.

Mult Scler. 2013 Apr;19(4):451-7. doi: 10.1177/1352458512457843. Epub 2012 Aug 20.
Retinol levels are associated with magnetic resonance imaging outcomes in multiple sclerosis.
Løken-Amsrud KI, Myhr KM, Bakke SJ, Beiske AG, Bjerve KS, Bjørnarå BT, Hovdal H, Lilleås F, Midgard R, Pedersen T, Benth JS, Torkildsen Ø, Wergeland S, Holmøy T.
Source
Department of Neurology, Innlandet Hospital Trust, Lillehammer, Norway.
Abstract
BACKGROUND:
Vitamin A has immunomodulatory properties and may regulate the transcription of genes involved in remyelination.
OBJECTIVE:
To investigate the association between retinol and disease activity in multiple sclerosis (MS).
METHODS:
Cohort study of 88 relapsing-remitting MS patients, originally included in a randomised placebo-controlled trial of omega-3 fatty acids in MS (the OFAMS study), followed prospectively for 24 months with repeated assessments of serum-retinol and magnetic resonance imaging (MRI). All patients were initiated on interferon β-1a after month 6.
RESULTS:
Each 1 µmol/L increase in serum-retinol reduced the odds (95% confidence interval) for new T1 gadolinium enhanced (Gd(+)) lesions by 49 (8-70)%, new T2 lesions by 42 (2-66)%, and combined unique activity (CUA) by 46 (3-68)% in simultaneous MRI scans, and 63 (25-82)% for new T1Gd(+) lesions, 49 (3-73)% for new T2 lesions and 43 (12-71)% for CUA the subsequent month. Serum-retinol also predicted new T1Gd(+) and T2 lesions six months ahead. The associations were not affected by HLA-DRB1*15, or serum levels of 25-hydroxyvitamin D, eicosapentaenoic acid or docosahexaenoic acid.
CONCLUSION:
Serum retinol is inversely associated with simultaneous and subsequent MRI outcomes in RRMS.
Comment in
Vitamin A: yet another player in multiple sclerosis pathogenesis? [Expert Rev Clin Immunol. 2013]
PMID: 22907941 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/22907941

Arch Neurol. 1998 Mar;55(3):315-21.
All-trans retinoic acid potentiates the ability of interferon beta-1b to augment suppressor cell function in multiple sclerosis.
Qu ZX, Dayal A, Jensen MA, Arnason BG.
Source
Department of Neurology and the Brain Research Institute, University of Chicago, Ill 60637, USA.
Abstract
OBJECTIVE:
To determine the effects of combination all-trans retinoic acid (RA) and interferon beta-1b therapy on immune system functions potentially relevant to multiple sclerosis (MS).
DESIGN:
Interferon gamma-secreting cells, T suppressor cell function, and lymphocyte proliferative responses were assayed using peripheral blood mononuclear cells from patients with MS and control subjects under control conditions and in the presence of interferon beta-1b, RA, and the 2 combined.
SETTING:
A university hospital MS clinic.
PARTICIPANTS:
Seventeen patients with secondarily progressive MS and 25 control subjects.
RESULTS:
Interferon beta-1b use increased interferon gamma-secreting cell counts, augmented T suppressor cell function, and inhibited T-cell proliferation. Therapy with RA decreased interferon gamma-secreting cell counts, had a minimal positive effect on T suppressor cell function, and had no effect on T-cell proliferation. When RA and interferon beta-1b were combined, the inhibitory effect of RA on interferon gamma-secreting cells predominated, T suppressor cell function increased synergistically over the increment observed with interferon beta-1b use alone, and the inhibitory effect of interferon beta-1b alone on T-cell proliferation remained unchanged.
CONCLUSIONS:
Treatment with interferon beta-1b partially restores defective T suppressor cell function in patients with MS. This potentially beneficial action is synergistically potentiated by RA. Interferon beta-1b increases the number of interferon gamma-secreting cells in the circulation when treatment is initiated. A similar increment in interferon gamma-secreting cells is observed when interferon beta-1b is added to cultural peripheral blood mononuclear cells in vitro. This potentially deleterious action of interferon beta-1b is reversed by RA. Interferon beta-1b inhibits lymphocyte proliferation modestly but reproducibly. This action of interferon beta-1b is unaltered by RA. These data provide a rationale for a trial of combination treatment with interferon beta-1b and RA in patients with MS.
PMID: 9520005 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/9520005
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Re: Vitamin A

Postby LR1234 » Tue Nov 05, 2013 12:26 pm

Good to hear Gibbs :) I hope u continue to see positive changes.
Did u mean to write your walking gets harder or easier after taking the supps?
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Re: Vitamin A

Postby gibbledygook » Tue Nov 05, 2013 1:08 pm

Well, it changes, it doesn't get much harder like on the anatabine or the ocimum sancturm. But it seems a bit stiffer and less prone to spasming in bed at night!
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Re: Vitamin A

Postby NHE » Wed Nov 06, 2013 2:00 am

gibbledygook wrote:Interferon beta-1b use increased interferon gamma-secreting cell counts


What... :?: :?: :?: The very drug that's prescribed to us to help "modify" the disease is increasing the cell type responsible for the secretion of a cytokine which makes MS WORSE? No wonder Cochrane Reviews and the like have found no long term benefit of DMDs. This is ludicrous :!: I can smell a class action lawsuit brewing on the horizon.


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Re: Vitamin A

Postby jimmylegs » Thu Nov 07, 2013 5:34 am

Serum Levels of Antioxidant Vitamins and Lipid Peroxidation in Multiple Sclerosis (2002)
http://www.ownmultiplesclerosis.com/wp- ... ler-02.pdf

"The present study indicates that antioxidant vitamins (alpha tocopherol, beta-carotene, retinol and ascorbic acid) are decreased in sera of MS patients during an attack..."

TABLE I Characteristics and some analytical data of patients with MS and control groups
Parameters.........................MS patients …n=24..................Control …n=24†
Analytical data
Retinol (mmol/l) .................2.07+/-0.21* (1.39–2.48).......2.53+/-0.26 (1.67–3.29)
Beta carotene (mmol/l)........0.41+/-0.13* (0.12–0.72).......0.63+/-0.08 (0.34–0.87)

I am sure there are some interesting interactions going on there amongst the various cofactors involved.... we know that uric acid levels are down in an attack too.
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