Quote:
Originally Posted by dmplaura
I was reading reviews of it here:
http://www.revolutionhealth.com/drug...remitting-rrms
And this:
http://www.centurywellness.com/newsl...20Fight_MS.htm
ALA is a powerful antioxidant. Thirty-seven multiple sclerosis subjects were given alpha lipoic acid 1200 mg a day for 14 days. The results were positive. ALA was able to lower levels of two markers for multiple sclerosis called MMP-9 and CAMP-1. The researchers say, "ALA may prove useful in treating multiple sclerosis by inhibiting MMP-9 activity and interfering with T-cell migration into the CNS." MMP-9 is a matrix metalloproteinase substance which is high in multiple sclerosis patients. MMP-9 has been implicated in the pathogenesis of cancer, autoimmune disease, and various pathologic conditions characterized by excessive fibrosis. The fact that ALA was able to reduce it is a positive indication.
Although this study in no way says ALA will be a cure or long term benefit for those with multiple sclerosis, it does open the door for further exploration. I think the dose of 1200 mg is extremely high, and I would not recommend more than 50 mg a day of R-Alpha Lipoic Acid for long term use.
Another study which was completed in 2005 on ALA in MS, had also shown to beneficial for MS patients. ALA is an antioxidant that suppresses and treats an animal model of MS, experimental autoimmune encephalomyelitis. The purpose of this study was to determine the pharmacokinetics (PK), tolerability and effects on matrix metalloproteinase-9 (MMP-9) and soluble intercellular adhesion molecule-1 (sICAMP-1) of oral Alpha Lipoic acid in patients with multiple sclerosis. Thirty-seven multiple sclerosis subjects were randomly assigned to one of four groups: placebo, Alpha Lipoic acid 600 mg twice a day, Alpha Lipoic acid 1200 mg once a day and Alpha Lipoic acid 1200 mg twice a day. Subjects took study capsules for 14 days. The study found that subjects taking 1200 mg Alpha Lipoic acid had substantially higher peak serum Alpha Lipoic acid levels than those taking 600 mg and that peak levels varied considerably among subjects. The study also found a significant negative correlation between peak serum Alpha Lipoic acid levels and mean changes in serum MMP-9 levels. There was a significant dose response relationship between Alpha Lipoic acid and mean change in serum sICAM-1 levels. The case study conclude that oral Alpha Lipoic acid is generally well tolerated and appears capable of reducing serum MMP-9 and sICAM-1 levels. Alpha Lipoic acid may prove useful in treating multiple sclerosis by inhibiting MMP-9 activity and interfering with T-cell migration into the CNS. |
Other THINGS that reduce MMP-9s
Things that reduce MMP-9s (AKA gelatinase B)
This list of GOOD "things" for MS should seem familiar - This is WHY???
QUERCETIN..........................REDUCES MMP-9s
VIT D3 .................................REDUCES MMP-9s
RESVERATROL (Grape Skin Extract) ...REDUCES MMP-9s
(NOT GRAPE SEED EXTRACT)
GREEN TEA EXTRACT(EGCGs)... REDUCES MMP-9s
ALPHA LIPOIC ACID (R-lipoic/ R-Dihdro-LipoicAcid) ... REDUCES MMP-9s
NAC N-Acetyl-L-Cysteine .......REDUCES MMP-9s
STATIN DRUGS (i.e Zocor) .....REDUCES MMP-9s
Omega-3s (ie Fish oil) ...........REDUCES MMP-9s
Minocycline/Doxycycline.........REDUCES MMP-9s
Curcumin.............................REDUCES MMP-9s
Pycnogenol (Pine bark extract)..REDUCES MMP-9s
Chondroitin sulfate (CS) and CS plus glucosamine sulfate (GS) ..REDUCES MMP-9s
Interferon Betas 1a/1b...........REDUCES MMP-9
(of course Steroids ....REDUCES MMP-9s)
***NOTE*** ( gelatinase B = MMP-9) ***NOTE***
I have lots more information on this MMP - MS - INTERFERON-beta connection and will elaborate it if there is some interest in this subject here.
Jack n dalton - jackD
Lancet Neurol. 2003 Dec;2(12):747-56.
Functional roles and therapeutic targeting of gelatinase B(MMP-9) and chemokines in
multiple sclerosis.
Opdenakker G, Nelissen I, Van Damme J.
GO, IN, and JVD are at the Rega Institute for Medical Research, University
of
Leuven, Belgium
Multiple sclerosis (MS) is a demyelinating disease of the CNS of unknown
cause. Pathogenetic mechanisms, such as chemotaxis, subsequent activation of
autoreactive lymphocytes, and skewing of the extracellular proteinase
balance, are targets for new therapies.
Matrix metalloproteinase gelatinase B (MMP-9) is upregulated in MS and was
recently shown to degrade interferon beta, one of the drugs used to treat
MS.
Consequently, the effect of endogenously produced interferon beta or
parenterally given interferon beta may be increased by gelatinase B(MMP-9)
inhibitors. Blockage of chemotaxis or cell adhesion molecule engagement, and
inhibition of hydoxymethyl-glutaryl-coenzyme-A reductase to lower expression
of gelatinase B(MMP-9), may become effective treatments of MS, alone or in
combination with interferon beta. This may allow interferon beta to be used
at lower doses and prevent side-effects.
PMID: 14636780 [PubMed - in process]
1: Brain. 2003 Jun;126(Pt 6):1371-81.
Gelatinase B/matrix metalloproteinase-9(MMP-9) cleaves interferon-beta and is a
target for immunotherapy.
Nelissen I, Martens E, Van den Steen PE, Proost P, Ronsse I, Opdenakker G.
Rega Institute for Medical Research, Laboratory of Molecular Immunology,
University of Leuven, Leuven, Belgium.
Parenteral administration of interferon (IFN)-beta is one of the currently
approved therapies for multiple sclerosis. One characteristic of this
disease is the increased production of gelatinase B(MMP-9), also called matrix
metalloproteinase (MMP-9) Gelatinase B is capable of destroying the
blood-brain barrier, and of cleaving myelin basic protein into
immunodominant and encephalitogenic fragments, thus playing a functional
role and being a therapeutic target in multiple sclerosis. Here we
demonstrate that gelatinase B(MMP-9) proteolytically cleaves IFN-beta, kills its
activity, and hence counteracts this cytokine as an antiviral and
immunotherapeutic agent. This proteolysis is more pronounced with
IFN-beta-1b than with IFN-beta-1a. Furthermore, the tetracycline
minocycline, which has a known blocking effect in experimental autoimmune
encephalomyelitis, an in vivo model of acute inflammation in multiple
sclerosis, and other MMP inhibitors prevent the in vitro degradation of
IFN-beta by gelatinase B(MMP-9). These data provide a novel mechanism and rationale
for the inhibition of gelatinase B(MMP-9) in diseases in which IFN-beta has a
beneficial effect. The combination of gelatinase B(MMP-9) inhibitors with better
and lower pharmacological formulations of IFN-beta may reduce the
side-effects of treatment with IFN-beta, and is therefore proposed for
multiple sclerosis therapy and the immunotherapy of viral infections.
PMID: 12764058 [PubMed - indexed for MEDLINE]