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.
Department of Neurology, Innlandet Hospital Trust, Lillehammer, Norway.
Vitamin A has immunomodulatory properties and may regulate the transcription of genes involved in remyelination.
To investigate the association between retinol and disease activity in multiple sclerosis (MS).
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.
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.
Serum retinol is inversely associated with simultaneous and subsequent MRI outcomes in RRMS.
Vitamin A: yet another player in multiple sclerosis pathogenesis? [Expert Rev Clin Immunol. 2013]
PMID: 22907941 [PubMed - indexed for MEDLINE]
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.
Department of Neurology and the Brain Research Institute, University of Chicago, Ill 60637, USA.
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).
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.
A university hospital MS clinic.
Seventeen patients with secondarily progressive MS and 25 control subjects.
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.
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]
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,