Altitude and blood flow

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Altitude and blood flow

Postby vg440 » Tue Jan 26, 2010 11:01 pm

Altitude doesn't discriminate the physiological changes in the body selecting one over the other.
Logic would suggest that many factors take place at altitude and seemingly the combination of both IBT at altitude would be Awesome.

Reason being ..
the improvements felt by IBT at sea level occur over a period of time where as improvements felt at altitude is almost instantaneous.

I'm glad to see you acknowledge now that the amazing improvements are experienced at altitude due to the physiological changes Jugular!
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Altitude and blood flow

Postby vg440 » Tue Jan 26, 2010 11:55 pm

Jugular,

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?
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Mountain man proves CCSVI theory

Postby vg440 » Wed Jan 27, 2010 2:32 am

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.
re: Quote

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?[/quote]

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.
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Re: Altitude and blood flow

Postby AndrewKFletcher » Wed Jan 27, 2010 2:58 am

vg440 wrote:Jugular,

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?


The best discovery since sliced bread is the bread machine!

The best discovery for ms, is the Inclined Bed!

CCSVI is a lable placed upon a venous anomoly.

I can just se the Pharma Boardroom with someone reverberating these old words: "If Mohammed won't come to the mountain, the mountain must come to Mohammed" In the form of a tablet. Now where have we heard this before?

Blocking potassium channels is a very dangerous game! Prediction side effects: Massive edema problems! Heart palpatations, circulatory collapse, stroke and deaths, linked to Fampridine. 27/01/2010 Andrew K Fletcher
Find us on Facebook.com/InclinedBedTherapy
IBT website: http://inclinedbedtherapy.com
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Re: Mountain man proves CCSVI theory

Postby Jugular » Wed Jan 27, 2010 8:36 am

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.
re: Quote

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.


Nope, I’m not a shill for a pharmaceutical company. I try to avoid drugs if I can, but will take them if needed. I went off immuno suppressants years ago, but think they helped me when my symptoms were on a slippery slope. As for Acorda, I happen to like them. I would classify them as small pharma. They are focused on the remyelination side of things and have some interesting drugs in their pipeline in that regard. If stents help fix the attack mechanism of MS, we are still left with damaged nerves in need of repair.

I am interested in reading some reviews of Ampyra before seriously thinking about trying it. Andrew, the side effects about which you warn are not on the monogram so I don't think I described its mode of action properly. That said, it’s not a benign drug and does not repair myelin.

As for high altitude, not having experienced the benefits myself, I only have the few testimonials to go off in this thread as I couldn't locate any studies. Researchers seem to have studied the effect of altitude on everything else so I think this would make for a good research project.

Like anything, positives have to be weighed against negatives. The positives may be temporary improved damaged nerve function and increase in red blood cell production. The negatives would appear to be impaired mental acuity, impaired muscle motor function, risk of stroke and brain damage. Generally, I'm not excited about starving myself of oxygen to get some abatement of my symptoms.

You were wondering about places to vacation. I have the ideal spot for you - Maui. You can spend time at the top of a dormant volcano, Haleakala, with an elevation of 10,000 feet. They rent cabins at the summit and it is easy to get to and get around once you’re there (yes, I’ve been there).

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.


For this reason, I think Maui would be the ideal place to study the effects of altitude on MS symptoms. In the span of 38 miles you can test 5 different climate zones from a moist tropical oxygen rich environment to a barren, arid, high altitude one. If you can get some funding I'm prepared to be in the test group that has to spend time on the humid oxygen dense beaches of Maui drinking Mai Tai's and you can be in the test group at Haleakula’s summit. We can compare notes after a week or so. I am prepared to volunteer for such punishment, for science!
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Altitude and blood flow

Postby vg440 » Wed Jan 27, 2010 9:53 am

Certainly sounds like punishment!.. lol

I was just reading up on Leadville in Colorado.
Also at 9000+ ft and most probably wheelchair friendly too.
The Maui beaches within reach would be nice though. Will have a look at that.

My feelings on the current data on the dangers of altitude is that it's focus has been only on the negatives, which may occur occasionally and perhaps rarely

But not to all.. or even to most at common altitude destinations.
Few and far between it seems as I didn't see any evidence of this ill health at 11,000ft in Cusco where the numerous tourist were thriving
(except for the initial altitude sickness which passes anyway and forgotten)

No doubt care has to taken when traveling to altitude but it's certainly not as traumatic to the body as data has described.

I'm wondering if the data is referring to the extremes of very high altitudes in which I definitely would not advise.

Otherwise I tend to look at the positives and work toward it with the risk factor in consideration.. if any.
Nothing ventured, nothing gained!.. within reason of course.
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Postby Bethr » Wed Jan 27, 2010 12:21 pm

I reckon the importance is the reduction in iron levels in the blood.
This is the effect of going up to high altitudes. Transferrin saturation halved in the study.
I have no symptoms at all at the moment after one phlebotomy. My iron levels were never much past the "normal" values, so it was never assumed I was iron-overloaded. I am, I have the signs on my forearms and I have been seriously fatigued and asleep for 2-3 years, and i developed a lesion on the brain.

Instantly fixed for me! It was miraculous.

My sister has been dxed with MS since the late 1980's.
She is going to have a phlebotomy on Monday, so we will see if she gets relief too. She is clinically within the safe limits of iron levels, but on the high side. She also has the marks of iron-overload on her forearms.

Why go to the heights, when you can get the same effect in 30 minutes.

I would be interested to hear from any MS women who felt better after blood loss from giving birth. That kept me well for five years. I only figured that out when I looked back over my history.

Does any period of blood loss make you feel better?
I noticed it during menstruation, a very slight improvement. Quite amazing energy and no sleeping for four days after an decent sized blood test. This was how I was diagnosed, I figured it out for myself. The doctors and neurologists were oblivious.

Can anyone else here relate to that. Maybe after a big surgical operation for something else?
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Postby Bethr » Wed Jan 27, 2010 12:47 pm

Try this abstract for size:

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. nhtaha@yahoo.com

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]



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.

Transferrin saturation will not show up on a normal iron test your doctor may do. My doctor ignored mine. She's old and behind the times. A young doctor more conversant with iron-overload and the fact that ferritin may still be normal, as may iron levels immediately picked it up. (Thank God!).
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Postby Bethr » Wed Jan 27, 2010 1:01 pm

Another interesting point (a bit embarrasing for me, so I haven't mentioned it before).
I have had a bleeding vein in my rectum for at least eight years.
If I strain it bleeds, it is especially active before my menstruation when my iron levels were at their highest.
I even noted the monthly cycle of the bleeding about 6 years ago when I was sent to a gastroenteroligist to check it out. He said he's never heard that one before. :lol:

The amazing things is, since the blood draw I've been a bit constipated and the vein which gets a a bit sore sometimes is totally inactive. No bleeding, no pain, no swelling since phlebotomy. I'll keep you updated on this. It's a link to veins and iron I think. The effect was immediate.
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Postby Zeureka » Wed Jan 27, 2010 2:16 pm

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.

I was very puzzled when heard the iron theory of Zamboni, as I remembered well that my blood test in June 2005 was normal, except for iron: "Sideremia 180 mcg/dl" - reference value D 37-145.

I had the blood test done since felt abnormally tired and had light instability. I was not diagnosed for MS yet. My generalist was astonished, since he expected the contrary (dizziness for doctors = low iron). He could neither explain the high blood iron level, nor my symptoms and then just ignored it...

One month later (on 17 July 2005) I then woke up in the morning with my second unknown MS relapse!
I had such strong instability/balance problems that I was unable to walk: had to use a wheelchair in the hospital... Fortunately, lucky me, I do not need it anymore!

Does the Swank diet maybe also for this iron reason help to stay relapse-free? I do not eat any red meat = full of iron!
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Postby foreignlesion » Wed Jan 27, 2010 2:59 pm

Zeureka,

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.
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Postby Bethr » Wed Jan 27, 2010 3:14 pm

There are plenty of vegetarians with iron overload. Just go the the hemachromatosis forums and you will hear about them. It's not the problem of ingestion of iron as much as the iron metabolism.
Your body regulates iron by ceasing to gather it from the gut. In people with the crook genes, this regulation doesn't work so well and you keep absorbing iron and storing it away.

Zeureka, that's exactly what happened to me, I had my one and only lesion when my Transferrin Saturation was high, well actually the month after the blood test I got to see why I was so fatigued and sleepy.
I don't recognise the word Sideremia, is that ferritin? If it is, mine was never above 175, yet I am iron overloaded.


My iron levels have fallen since then, maybe that's why I had no further events after than single one. But the fatigue and stiff joints and daytime sleeping never went away. Until now!!!!!!!!! :D :D
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Postby Zeureka » Wed Jan 27, 2010 3:34 pm

foreignlesion wrote:Zeureka,
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.

Dr. Swank began studying the correlation between diet and MS in the late 1940's. He then developed a diet for MS and also recommended the same diet for cardiovascular disease. I feel very good on this diet + many other diets recommended for MS have now taken over Swank's ideas. I think it combines well with IBT and getting treatment for CCSVI to feel better :wink: !

"My 50 years of research and working with approximately 5,000 people, just like you, have proven that this protocol works to slow progression of the disease as well as benefit overall health."
— Roy L. Swank M.D., Ph.D. (Montreal Neurological Clinic)

QUICK REFERENCE of low-fat diet, very low in saturated fats and higher in fish and poly-unsaturated fat consumption (eg via seed oils).

Saturated fat should not exceed 15 grams per day.
Unsaturated fat (oils) should be kept to 20-50 grams per day.
No red meat for the first year. Lots of fish and only cooking with sunflower/olive oil
After the first year, 3 oz. of red meat is allowed once per week.
Dairy products must contain 1% or less butterfat unless otherwise noted (no butter/cream/fatty cheese).
No processed foods containing saturated fat.
Cod liver oil (1 tsp. or equivalent capsules) recommended daily.
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Postby Bethr » Wed Jan 27, 2010 3:48 pm

I read that one phlebotomy takes out the iron equal of 750 meals. You need to get the iron levels right down to almost anemic, then the body starts to draw the iron out of storage areas, such as the liver and hopefully brain.

I'd rather get rid of this stuff quick, as I feel I am being damaged while it is still there.
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Postby Bethr » Wed Jan 27, 2010 4:18 pm

Amazingly I've just found that Zamboni has this abstract in 2005 on Hemochromatosis and the C282Y gene (the one that I have) and vein problems in the legs caused by iron overloaders. Maybe that's why my problem veins mentioned above have ceased to be a problem.
Another interesting link though.

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.

Objective
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.

Methods
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.

Results
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.

Conclusions
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.

Clinical Relevance
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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