Taurine could be added to an multiple sclerosis therapy regime in order to boost mature oligodendrocyte production, and therefore remyelination. In doing so, the hope is it would ultimately reduce relapses for multiple sclerosis patients. Taurine boosts oligodendrocyte production in multiple sclerosis. Taurine promotes and resparks remyelination with high dose biotin which is crucial for repairing damage from multiple sclerosis restoring function which serves as a co-factor for essential carboxylase enzymes required for fatty acid synthesis that has recently been demonstrated to provide benefit in patients with non-active progressive multiple sclerosis. Also, triiodothyronine (T3) is a thyroid hormone that is a “well-known” and most potent agent that induces rapid re-myelination of nerves along with the crucial role of cholesterol. Patients on statins never experience remission and often have the worst form of the disease- primary progressive multiple sclerosis which biotin is found to be very beneficial for. https://www.mdmag.com/medical-news/metabolite-taurine-boosts-oligodendrocyte-production-in-ms

I was diagnosed with multiple sclerosis two years ago by the Department of Veteran affairs. I experience several symptoms that come and go after a couple of days. Early this year i lost my eyesight (left eye) and developed weakness in the left side of my body. Eyesight came back but not the left side mobility. Muscles of my left foot are weak, making it hard to walk in a normal heel-toe pattern. As a result, my foot drags on the ground when I walk. Two months ago I ordered two bottles of MS herbal remedy from Best Health Herbal Centre, which I only used for six weeks and the result was extremely marvellous, all symptoms was terminated and my MS was totally reversed. Thanks to Best Health Herbal Centre, I will never stop sharing my testimony till the whole world know about this wonderful MS herbal remedy and Am so happy to see myself living normal life again.

I started using multiple sclerosis (MS) herbal remedy i purchased from Best Health Herbal Centre January this year. I only used it for a month and two weeks, my condition changed automatically, all my symptoms are gone. Remaining positive have helped me during this treatment. Now am living MS FREE.
Hope this will help somebody, remember, do your own research and make your own decisions based on information you have received and digested. Thanks to Best Health Herbal Centre for their amazing work. Forever Grateful!

Progesterone is produced in high amounts in the ovaries (by the corpus luteum) from the onset of puberty to menopause, and in the testes in males, and is also produced in smaller amounts by the adrenal glands after the onset of adrenarche (preteen age years) in both males and females. No progesterone is made in women after menopause. Progesterone levels in men are as high as women’s levels during the follicular phase of the menstrual cycle. Progesterone is also produced by cells in the body’s nervous system, where it helps form the protective layer around nerve endings known as the myelin sheath. The nervous system depends on the myelin sheath for insulation and for neurotransmission speed. Normal brain function is not the only thing progesterone is required for in the nervous system. An important role of progesterone is to protect the brain from damage and promote repair after injury. It actually does this by promoting the growth and repair of the myelin sheath that protects the nerve fibers. In fact, both estradiol and progesterone promoted the differentiation of oligodendrocyte progenitors in culture, but whereas progesterone increased cellular branching, estradiol stimulated myelin sheath formation. There is also evidence that the addition of progesterone can also help remyelinate damaged axons due to trauma, restoring some lost neural signal conduction. Another way progesterone aids in regeneration includes increasing the circulation of endothelial progenitor cells in the brain. https://en.wikipedia.org/wiki/Progesterone#cite_note-pmid14667980-86

This study below shows progesterone therapy switches off demyelination of the central nervous system associated with reactive microglia in neurodegenerative disorders such as multiple sclerosis.
https://www.ncbi.nlm.nih.gov/pubmed/28830026 Progesterone therapy induces an M1 to M2 switch in microglia phenotype and suppresses NLRP3 inflammasome in a cuprizone-induced demyelination mouse model. Demyelination of the central nervous system (CNS) has been associated to reactive microglia in neurodegenerative disorders, such as multiple sclerosis (MS). The M1 microglia phenotype plays a pro-inflammatory role while M2 is involved in anti-inflammatory processes in the brain. In this study, CPZ-induced demyelination mouse model was used to investigate the effect of progesterone (PRO) therapy on microglia activation and neuro-inflammation. Results showed that progesterone therapy (CPZ+PRO) decreased neurological behavioral deficits, as demonstrated by significantly decreased escape latencies, in comparison to CPZ mice. In addition, CPZ+PRO caused a significant reduction in the mRNA expression levels of M1-markers (iNOS, CD86, MHC-II and TNF-α) in the corpus callosum region, whereas the expression of M2-markers (Trem-2, CD206, Arg-1 and TGF-β) was significantly increased, in comparison to CPZ mice. Moreover, CPZ+PRO resulted in a significant decrease in the number of iNOS+ and Iba-1+/iNOS+ cells (M1), whereas TREM-2+ and Iba-1+/TREM-2+ cells (M2) significantly increased, in comparison to CPZ group. Furthermore, CPZ+PRO caused a significant decrease in mRNA and protein expression levels of NLRP3 and IL-18 (~2-fold), in comparison to the CPZ group. Finally, CPZ+PRO therapy was accompanied with reduced levels of demyelination, compared to CPZ, as confirmed by immunofluorescence to myelin basic protein (MBP) and Luxol Fast Blue (LFB) staining, as well as transmission electron microscopy (TEM) analysis. In summary, we reported for the first time that PRO therapy causes polarization of M2 microglia, attenuation of M1 phenotype, and suppression of NLRP3 inflammasome in a CPZ-induced demyelination model of MS.

This study below shows that luteolin is the strongest phytoestrogen that inhibits the breakdown of progesterone in the liver. A phytoestrogen is a plant-derived hormonally-active compound known to cause varied reproductive, immunosuppressive and behavioral effects in vertebrates. Other research shows that luteolin is the most powerful aromatase inhibitor by inhibiting the synthesis of aromatase, plus luteolin was the best estradiol inhibitor. It inhibiits estradiol synthesis. Luteolin may increase progesterone levels as kaempferol increases progesterone levels in the body.
https://www.ncbi.nlm.nih.gov/pubmed/15748835 Inhibitory effects of flavonoids on the reduction of progesterone to 20alpha-hydroxyprogesterone in rat liver. The first aim of this study is to characterize the reduction of progesterone in rat liver. Progesterone was mainly reduced to 20alpha-hydroxyprogesterone in the cytosolic fraction of rat liver. The amount of 20alpha-hydroxyprogesterone formed from progesterone in the cytosolic fraction was significantly larger in the males than in the females and this enzyme reaction proceeded not only in the presence of NADPH, but also in the presence of NADH. Furthermore, we attempted to evaluate the inhibitory effects of 15 flavonoids on the NADPH-dependent reduction of progesterone to 20alpha-hydroxyprogesterone in liver cytosol of male rats. The order of the inhibitory potencies was luteolin>apigenin>quercetin>myricetin=fisetin=kaempferol. Other flavonoids exhibited lower inhibitory potencies. Energy-minimized molecular models demonstrated that a planar benzopyrone ring (A and C rings) with a coplanar phenyl ring (B ring) is a structural characteristic determining the inhibitory effects of flavonoids other than isoflavones.

This study below shows that catalpol jumpstarts and promotes adrenal/corticol hormone production and rebalances estrogen and progesterone levels.
https://www.ncbi.nlm.nih.gov/pubmed/25177027Ovarian failure-resistant effects of catalpol in aged female rats. Catalpol, an iridoid glycoside obtained from various natural sources, has many biological functions. However, its ovarian failure-resistant effect has scarcely been studied. The present study used senile 14-month-old Sprague-Dawley female rats to examine the in vivo ovarian failure-resistant activity of catalpol. Daily oral graded doses of catalpol (1, 3, or 5 mg/kg/d) for 4 weeks significantly increased the levels of serum 17β-estradiol (E2) and progesterone (P4) but reduced follicle-stimulating hormone and luteinizing hormone levels. Electron microscopic analysis and flow cytometry showed that catalpol significantly retarded apoptosis of the ovarian granulocytes of the rats. These findings suggest that catalpol works on the sex organs by nourishing ovarian tissues and improving both the quality and quantity of follicles, thus leading to rebalanced E2 and P4 levels in aged rats so that catalpol has a direct in vivo antiaging effect on the rat ovarian system.

Fecal Matter Transplants (FMT) seems to be very important in the curing or halting of MS.

Multiple sclerosis

An infectious cause of multiple sclerosis (MS) has been speculated, though the potential for gastrointestinal pathogens to exert neurological effects remotely (as seen with many Clostridium species) has not been considered likely. In 2011, Borody et al.[38] reported three wheelchair-bound patients with MS treated with FMT for constipation. Bowel symptoms resolved following FMT; however, in all cases, there was also a progressive and dramatic improvement in neurological symptoms, with all three patients regaining the ability to walk unassisted. Two of the patients with prior indwelling urinary catheters experienced restoration of urinary function. In one patient of the three, follow-up MRI 15 years after FMT showed a halting of disease progression and ‘no evidence of active disease’.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3868025/

A couple of additional considerations:

The Membrane Stabilizing Diet as described in the PK Protocol developed by Patricia Kane PhD has been used successfully in many patients with multiple sclerosis:

This regimen encourages the use of phosphatidylcholine, bioactive oils, short chain fatty acid butyrate, and other nutrients and micro nutrients to restore the cell membrane integrity and function. Therapies directed to demyelinating pathology is included.

The regimen is individualized by the use of the RBC membrane fatty acid analysis done at Johns Hopkins Kennedy-Krieger Institute Laboratory which can identify the presence of abnormal fatty acids as well as deficiencies and excesses in normally occurring membrane fatty acids.

Another therapy for multiple sclerosis is that of Vincenzo Simonetti in Italy who has pioneered a protocol using IV ozone with a very good success rate. This has multi-factorial benefits to enhance the immune system, speed healing, and to eliminate pathogens.

One can imagine that by combining such modalities a synergistic treatment effect could be achieved.
This theoretical needs to be demonstrated in clinical trials, and remains anecdotal at present.