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Correcting impaired cerebral venous drainage (CCSVI) apparently restores proper oxygenation, influx of glucose/nutrients, and proper waste removal. CCSVI could potentially impact the effect of androgens. If androgen signaling and production are disrupted due to hypoerfusion and iron accumulation in the deep gray matter it could possibly present another feedback mechanism that negatively impacts CNS function.

These recent studies are very interesting.

Estrogen and testosterone therapies in multiple sclerosis
http://www.ncbi.nlm.nih.gov/pubmed/19660660

Testosterone acts as an efficacious vasodilator in isolated human pulmonary arteries and veins: evidence for a biphasic effect at physiological and supra-physiological concentrations.
http://www.ncbi.nlm.nih.gov/pubmed/19535892

Do androgens play a beneficial role in the regulation of vascular tone? Nongenomic vascular effects of testosterone metabolites.
http://www.ncbi.nlm.nih.gov/pubmed/20228257

Endothelial regulation of eNOS, PAI-1 and t-PA by testosterone and dihydrotestosterone in vitro and in vivo
http://www.ncbi.nlm.nih.gov/pubmed/20547636
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Is CCSVI thickening the IJV veins & valves due to shear stress & hypoxia (stimulating the release of "endothelin 1" factors)? What part do androgens play...how are they related?

MegansMom wrote:These veins are made of mesenchymal tissue, mesenchymal tissue responds to hormones, especially female hormones, the tissue is much more " stretchy" during pregnancy/ lactation. This may explain why there are less MS events during these times

2. Sheer stress and hypoxia both make the endothelium produce "endothelin 1" this "endothelin1" can cause fibrosis ( stiffness) and hypertrophy (thickening) of vessels (arteries and veins) especially valves. So from birth this may cause the veins/ valves to get worse CCSVI over time.

3. Endothelin1 is found in much higher levels in people with MS. It would be interesting to see if they could test if the level goes down after CCSVI angioplasty and normal cerebral venous outflow?

4.could a high level of Endothelin1 influence restenosis/ resumption of reflux after angioplasty?

http://www.ncbi.nlm.nih.gov/pubmed/19946214

Cell Cycle. 2009 Dec 15;8(24):4079-84. Epub 2009 Dec 21.
Sex steroid-mediated reprogramming of vascular smooth muscle cells to stem cells and neurons: possible utilization of sex steroid combinations for regenerative treatment without utilization of in vitro developed stem cells.

Bukovsky A.
a_buko@comcast.net

Unlike OSE cells, the vascular SMC accompany as pericytes all vessels, including CNS microvasculature. We also observed that sex steroid combinations could produce SMC stem type cells which differentiated within a few days back to mature vascular SMC. This is of potential interest for the vascular regenerative medicine. Altogether, our observations suggest that sex steroid combinations could induce in vivo improvement of neurodegenerative, traumatic and ischemic neurological disorders and vascular diseases via their effect on resident pluripotent vascular SMC, i.e., without a need of in vitro developed stem cells.

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http://www.ncbi.nlm.nih.gov/pubmed/20376198

J Cardiovasc Transl Res. 2010 Apr;3(2):103-13.
Gender dimorphisms in progenitor and stem cell function in cardiovascular disease.
Herrmann JL, Abarbanell AM, Weil BR, Manukyan MC, Poynter JA, Wang Y, Coffey AC, Meldrum DR.
Department of Surgery, Indiana University School of Medicine, Indianapolis, IN, USA.

This review discusses (1) the cardiovascular effects of sex steroids (specifically estradiol and testosterone); (2) the therapeutic potentials of endothelial progenitor cells, mesenchymal stem cells, and embryonic stem cells; and (3) the direct effect of sex steroids on these cell types.
PMID: 20376198 [PubMed - indexed for MEDLINE]PMCID: PMC2850109 [Available on 2011/4/1]

Endothelin-1 (ET-1), a potent vasoconstrictor, has been implicated in the pathogenesis of collagen accumulation.

http://www.ncbi.nlm.nih.gov/pubmed/21169360

J Biol Chem. 2010 Dec 17. [Epub ahead of print]
Endothelin-1 increases collagen accumulation in renal mesangial cells by stimulating a chemokine and cytokine autocrine signaling loop.
Simonson MS, Ismail-Beigi F.
Case Western Reserve University, United States.

Endothelin-1 (ET-1), a potent vasoconstrictor, has been implicated in the pathogenesis of collagen accumulation, extracellular matrix remodeling, and renal and cardiac fibrosis in diabetes. ……Taken together, these results demonstrate that an autocrine signaling loop involving MCP-1 and IL-6 contributes to ET-1-induced collagen accumulation.

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http://www.ncbi.nlm.nih.gov/pubmed/21239258

Trends Cardiovasc Med. 1992 Jul-Aug;2(4):129-33.
Genetic regulation of endothelin-1 in vascular endothelial cells.
Hilkert RJ, Lee ME, Quertermous T.
Cardiovascular Institute, Boston University, Boston, MA 02118 USA.

Endothelin-1 (ET-1) is a potent vasoconstrictor and smooth muscle cell mitogen synthesized and secreted by endothelial cells. This vasoactive peptide is genetically regulated by many of the cytokines, hormones, and physical forces that are involved in vascular disease processes.

I wish I understood all this but props for those of you that do. I am going to get a basic vascular textbook one of these days. (Any recommendations?)

Could changes in hormones as women age affect MS for the worse? If 2/3rds of MSers are women, this is relevant to a whole lot of us.

Before treatment of 10/12/10 my blood oxygen level was below normal now normal at 97

Bumping this one up.

Therapeutic Testosterone Administration Preserves Excitatory Synaptic Transmission in the Hippocampus during Autoimmune Demyelinating Disease

http://www.jneurosci.org/content/32/36/12312.long

Over 50% of multiple sclerosis (MS) patients experience cognitive deficits, and hippocampal-dependent memory impairment has been reported in >30% of these patients. While postmortem pathology studies and in vivo magnetic resonance imaging demonstrate that the hippocampus is targeted in MS, the neuropathology underlying hippocampal dysfunction remains unknown. Furthermore, there are no treatments available to date to effectively prevent neurodegeneration and associated cognitive dysfunction in MS. We have recently demonstrated that the hippocampus is also targeted in experimental autoimmune encephalomyelitis (EAE), the most widely used animal model of MS. The objective of this study was to assess whether a candidate treatment (testosterone) could prevent hippocampal synaptic dysfunction and underlying pathology when administered in either a preventative or a therapeutic (postdisease induction) manner. Electrophysiological studies revealed impairments in basal excitatory synaptic transmission that involved both AMPA receptor-mediated changes in synaptic currents, and faster decay rates of NMDA receptor-mediated currents in mice with EAE. Neuropathology revealed atrophy of the pyramidal and dendritic layers of hippocampal CA1, decreased presynaptic (Synapsin-1) and postsynaptic (postsynaptic density 95; PSD-95) staining, diffuse demyelination, and microglial activation. Testosterone treatment administered either before or after disease induction restores excitatory synaptic transmission as well as presynaptic and postsynaptic protein levels within the hippocampus. Furthermore, cross-modality correlations demonstrate that fluctuations in EPSPs are significantly correlated to changes in postsynaptic protein levels and suggest that PSD-95 is a neuropathological substrate to impaired synaptic transmission in the hippocampus during EAE. This is the first report demonstrating that testosterone is a viable therapeutic treatment option that can restore both hippocampal function and disease-associated pathology that occur during autoimmune disease.

Although, addressing the underlying cause is prudent....a vascular condition warrants vascular treatment and the EAE model is not vascular based. CCSVI is real.