Since my diagnosis in 2003, I've only tried copaxone for about a year (due to it having the least side effects), which didn't help at all in any way.
Since then I made the decision to combat the disease without the medication being offered by my neuro as they were seemingly just suppressing the immune system (which I strongly disagreed with) when I thoroughly believed there was nothing wrong with the immune system in the first place.
I felt then and still do today believe the immune system is simply doing what it has been designed to do by acting on a problem in the body which of course was then unknown.
So suppressing the immune system I didn't feel was the answer.
My Peru experience only strengthened my belief as the question had to be asked..
If ms is an auto immune disease.. what is it that caused the immune system to back off at altitude?
There was something definitely there which the immune system agreed with.
Low and behold.. ccsvi is discovered!
So medication mimicking what can be achieved naturally without chemicals is a no from me ( not to mention the side effects).
I think the discovery of ccsvi is the best discovery for ms sufferers..
since sliced bread.. lol
Do you mind if I ask you Jugular..
Do you work for a Pharmaceutical?
vg440 wrote:Dear Jugular,
I'm uncertain if your for or against high altitude and the fantastic testimonials from ms sufferers of almost instantaneous symptom relief.
Everspring has actually relocated to the high altitudes of The Rocky Mountains for the benefit of altitude and she is doing wonderful!
What I'm confused with is your recent post at the subject of 'Altitude and blood flow' in which you suggest trying the drug Fampridine which you say works much the same way as high altitude.
You may be interested in a new drug called Fampridine that’s just been approved by the FDA (to be sold in the US under the trade name AMPYRA by Acorda Pharmaceuticals) .
It apparently works much the same way as high altitude by blocking potassium channels on nerve fibres. I believe Biogen have marketing rights to it outside the US and may have applied for approval in Oz. Perhaps all the benefits of high altitude without having to leave home?
Perhaps the discussion of 'Altitude and blood flow' might be of interest, especially to those ms sufferers who've been at altitude and felt the benefits.
The Haleakala National Park ranges through 5 distinctly different climates zones. The road to the Haleakala summit holds the world record for climbing to the highest elevation in the shortest distance (38 miles). The dormant volcano's vast moonlike crater floor with its towering cindercones is a geological wonder. From the 10,023 foot summit, the Big Island of Hawaii can be seen.
Mult Scler. 2008 Jun;14(5):602-8. Epub 2008 Apr 11.
The role of iron dysregulation in the pathogenesis of multiple sclerosis:
Abo-Krysha N, Rashed L.
Department of Neurology, Cairo University, Cairo, Egypt. firstname.lastname@example.org
BACKGROUND: Iron is essential for virtually all types of cells and organisms. The significance of iron for brain function is reflected by the presence of receptors for transferrin on brain capillary endothelial cells. Iron imbalance is associated with proinflammatory cytokines and oxidative stress, which have been implicated in the pathogenesis of multiple sclerosis (MS). Transferrin receptor (TfR) is the major mediator of iron uptake. Its expression is increased to facilitate iron entrance into the cell. The increased serum level of soluble transferrin receptor (sTfR) may indicate an abnormal intracellular distribution of iron and a decrease in the cytoplasmic compartment. OBJECTIVE: Our objective is to assess the possible role of iron metabolism dysfunction in the pathogenesis of MS. METHODS: Thirty subjects were selected from the Neurology Department of Kasr El-Aini hospital, Cairo University: 20 MS patients, where nine patients were relapsing and progressive (secondary progressive (SP) of which six were secondary progressive active (SP-A) and three were secondary progressive stable (SP-S)), seven were relapsing-remitting active (RR-A) and four were primary progressive (PP); and 10 control subjects matched in age and sex. Each patient was subjected to a thorough general medical and neurological examination, Kurtzke MS rating scales, laboratory assessment, neuro-imaging, evoked potentials and quantitative determination of the indices of iron metabolism, such as serum iron and sTfR. RESULTS: The serum level of sTfR was significantly higher in our MS patients compared with the control group (p = 0.0001). The levels were significantly higher in SP-A (p = 0.001), SP-S (p = 0.01), RR-A (p = 0.0001) and PP (p = 0.003) patients than in controls. Iron values were within normal limits in all patients. The increased serum sTfR level in non-anemic MS patients with active disease reflects the increased iron turnover. The elevation of sTfR levels in stable patients may indicate active inflammation with ongoing oxidative damage that is not detectable by history or examination. CONCLUSIONS: Iron overload and upregulation of iron-handling proteins, such as TfR, in the MS brain can contribute to pathogenesis of Multiple Sclerosis and iron imbalance is associated with a pro-oxidative stress and a proinflammatory environment, this suggest that iron could be a target for MS therapy to improve neuronal iron metabolism.
PMID: 18408021 [PubMed - indexed for MEDLINE]
Bethr wrote:They had increased transferrin saturation, just like I did when I got my one and only lesion. All my symptoms are gone now as I have lowered it by phlebotomy.
There are many iron rich vegetarian diets, such as the typical East Indian diet. Many nuts, seeds, legumes and green vegetables are all sources of iron. I don't know a lot about the Swank diet, but if it includes many of these foods than it is not designed to reduce iron intake.
Hemochromatosis C282Y gene mutation increases the risk of venous leg ulceration
Presented at the Seventeenth Annual Meeting of the American Venous Forum, San Diego, Calif, Feb 10–13, 2005.
Paolo Zamboni, MD, Silvia Tognazzo, BS, Marcello Izzo, MD, Francesca Pancaldi, MD, Gian L. Scapoli, MD, Alberto Liboni, MD, Donato Gemmati, BS
Received 3 February 2005; accepted 1 April 2005.
Chronic venous disease (CVD) is the most common vascular disorder, progressing in approximately 10% of cases toward chronic venous leg ulceration, whereas the hemochromatosis gene (HFE) C282Y mutation is the most common recognized genetic defect in iron metabolism. Because CVD leads to local iron overload in the affected legs, we investigated whether two common HFE mutations could increase the risk of chronic venous leg ulceration.
This was a case-control study at the Vascular Diseases Center, University of Ferrara, Italy. From a cohort of 980 consecutive patients affected by severe CVD (CEAP clinical classes C4 to C6) we selected 238 cases with the exclusion of any other comorbidity factor potentially involved in wound etiology (group A). They were subdivided into group B, including 137 patients with ulcer (classes C5 and C6: 98 primary and 39 postthrombotic cases), and group C, including 101 cases with no skin lesions (class C4). They were completely matched for sex, age, and geographic origin with 280 healthy controls (group D). A total of 518 subjects were polymerase chain reaction genotyped for HFE mutations (C282Y and H63D). We assessed the risk of ulceration by comparing the prevalence of ulcer in homogenous cases with and without the HFE variants. Other main outcome measures were the sensitivity, specificity, and predictive values of the genetic test in CVD cases.
C282Y mutation significantly increases the risk of ulcer in primary CVD by almost seven times (odds ratio, 6.69; 95% confidence interval, 1.45–30.8; P = .01). Application of the HFE test in primary CVD demonstrated increased specificity and positive predictive values (98% and 86%, respectively), with negligible sensitivity and negative predictive values.
The overlap of primary CVD and the C282Y mutation consistently increases the risk of developing venous leg ulceration. These data, which have been confirmed in other clinical settings, suggest new strategies for preventing and treating primary CVD.
The number of patients affected by primary CVD is so great that the vast majority of ulcers are also related to this common problem. On the other hand, there is not a reliable way for identifying in advance, from the broad base of primary CVD patients (20–40% of the general population), the high risk minority (10% of primary CVD cases) who will develop a venous ulcer. In such cases, a simple C282Y blood genetic test demonstrated an elevated specificity in predicting ulcer development (98%, CI 95%, 92.8–99.7). The genetic test could be applied starting from the C2 class, varicose veins, the most common situation observed in clinical practice. In perspective, the presence of the C282Y mutation would strengthen the indications and priorities for surgical correction of superficial venous insufficiency.
Inter-Departmental Vascular Disease Center, University of Ferrara.
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