My dad the Gravity Doctor

If it's on your mind and it has to do with multiple sclerosis in any way, post it here.

Postby harry1 » Sun Feb 07, 2010 9:07 am

Wilfy

Well it think that's cool how you look out for your dad like that :) and there's nothing wrong with thinking ''outside the box'' when there are currently no cure(s) for MS, Parkinson's, ALS, Alzheimer's, Motor Neuropathies etc.. and after 14 years of having this disease with no medication that has helped me i'm now looking at different alternative options including diet and supplements etc.

I'll research this more online and thanks again for the info.

harry
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Postby jackD » Mon Feb 08, 2010 6:49 pm

AndrewKFletcher wrote:
jackD wrote:I just knew I was doing something wrong, because I sleep with my legs elevated about 6 inches!!!


jackD


Why would you choose to sleep this way Jack?


I suffer from "Chronic Venous Insufficiency" in ONE LEG!!!!

This condition was caused by numerous, too numerous to count unnecessary surgeries done to my right leg!!!

I have some moderate edema in my foot and lower leg.

I have been researching Blood Pressure Medications for both positive and negative effects and have found some truly remarkable results in Pub-Med.

One of the things I discovered is that some Calcium Channel Blocker drugs may have a potent neuron protective benefit.

My doctor (the cardiologist) wants me to take that class of BP drugs. The problem is those drugs cause edema(pedal edema) and after trying two different ones I called it quits because my edema became so severe that my foot hurt all-the-time and was quite swollen.

I still want to take a Calcium Channel Blocker so I got one of those $6,000 leg squeezing pumps and sleep with my right leg elevated.

I am interested in NIFEDIPINE and think I may have solved the edema problem because I found this abstract that says that one of my favorite supplements -PINE BARK EXTRACT - "PYCNOGENOL" has been shown to prevent this specific medication from causing this specific kind of edema.

jackD


Clin Appl Thromb Hemost. 2006 Oct;12(4):440-4.

Control of edema in hypertensive subjects treated with calcium antagonist (nifedipine) or angiotensin-converting enzyme inhibitors with Pycnogenol.

Belcaro G, Cesarone MR, Ricci A, Cornelli U, Rodhewald P, Ledda A, Di Renzo A, Stuard S, Cacchio M, Vinciguerra G, Gizzi G, Pellegrini L, Dugall M, Fano F.

Department of Biomedical Sciences, Irvine2 Vasc Lab, G D'annunzio University. Cardres@abol.it

The presence of edema in different phases and stages of essential hypertension may be due to antihypertensive treatment.

Some drugs may cause edema by inducing vasodilatation, increasing the capillary exchange surface and capillary filtration.

Pycnogenol has an important anti-edema effect in diabetic microangiopathy and chronic venous insufficiency.

This 8-week study evaluated capillary filtration in 2 comparable treatment groups with hypertension treated with a calcium antagonist (nifedipine) or angiotensin-converting enzyme inhibitor to define its efficacy in preventing edema caused by antihypertensives.

A significant decrease in filtration was observed in the Pycnogenol groups.

Pycnogenol controls this type of edema, it helps to prevent and limit long-term damage in the microcirculation in hypertensive patients, and allows the dose of anti-hypertensive drugs to be reduced in most patients.

PMID: 17000888 [PubMed - indexed for MEDLINE]
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.
Angiology. 2006 Oct-Nov;57(5):569-76.

Rapid relief of signs/symptoms in chronic venous microangiopathy with pycnogenol: a prospective, controlled study.
Cesarone MR, Belcaro G, Rohdewald P, Pellegrini L, Ledda A, Vinciguerra G, Ricci A, Gizzi G, Ippolito E, Fano F, Dugall M, Acerbi G, Cacchio M, Di Renzo A, Hosoi M, Stuard S, Corsi M.

Irvine2 Vascular Lab and Physiology, Department of Biomedical Sciences, G 'Annunzio, Chieti-Pescara University, San Valentino Vascular Screening Project, Faculty of Motory Sciences, L'Aquila University, Italy.

Erratum in:

Angiology. 2008 Jun-Jul;59(3):385.

The aim of this study was to investigate the clinical efficacy of oral Pycnogenol (Horphag Research Ltd, UK) in patients with severe chronic venous insufficiency. Patients with severe venous hypertension (chronic venous insufficiency, ankle swelling) and history of venous ulcerations were treated with Pycnogenol.

Patients received oral Pycnogenol (50 mg capsules, 3 times daily for a total of 150 mg daily) for 8 weeks. A group of 21 patients was included in the treatment group and 18 equivalent patients were observed as controls (no treatment during the observation period). All 21 patients (age 53 years; range, 42-60 years; M:F=11:10) in the treatment group completed the 8-week study. Also the 18 controls completed the follow-up period. There were no drop-outs. The average ambulatory venous pressure was 59.3 (SD 7.2; range 50-68) with a refilling time shorter than 10 seconds (average 7.6; SD 3). There were no differences in ambulatory venous pressure or refilling time between the treatment and control patients. The duration of the disease-from the first signs/symptoms-was on average 5.7 years (SD 2.1).

At 4 and 8 weeks, in all Pycnogenol-treated subjects, microcirculatory and clinical evaluations indicated a progressive decrease in skin flux, indicating an improvement in the level of microangiopathy; a significant decrease in capillary filtration; a significant improvement in the symptomatic score; and a reduction in edema.

There were no visible effects in controls.

In conclusion, this study confirms the fast clinical efficacy of Pycnogenol in patients with chronic venous insufficiency and venous microangiopathy.

The study indicates the significant clinical role of Pycnogenol in the management, treatment and control of this common clinical problem. The treatment may be also useful to prevent ulcerations by controlling the level of venous microangiopathy.

PMID: 17067979 [PubMed - indexed for MEDLINE]
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Postby jimmylegs » Mon Feb 08, 2010 7:16 pm

why were the surgeries unnecessary, if i may ask?

ran across these, not sure if they contribute anything useful:
A New Method for the Assessment of Tissue Hemoglobin Oxygenation in Patients with Chronic Venous Insufficiency

Abstract
Venous incompetence often leads to ulceration of the skin of the lower limb due to a disturbance of skin microcirculation. We investigated 10 healthy subjects and 18 patients with chronic venous insufficiency by means of a fast scanning reflection photometer and determined noninvasively the hemoglobin oxygen saturation (SHB) and the relative concentration of hemoglobin (CHB) in the skin of the forefoot and at the calf, 10 cm proximal of the inner malleolus during positional changes. In supine position no significant differences were found. During sitting and standingSHBdropped and was significantly lower in patients at both locations (calf, standing, patients 22.2 ± 10.6% vs controls 48.2 ± 13.5%,P< 0.001).CHBincreased in patients during standing from 0.71 to 2.13 ± 0.33 aU (in controls from 0.69 to 1.49 ± 0.28 aU,P< 0.001). Activation of the muscle pump decreasedCHBand increasedSHBin patients and in controls. After the movements were stopped,SHBdecreased again and fell to the initial low values eight times faster in patients (7.4 ± 5.3 vs 57.5 ± 19.6 sec,P< 0.001).CHBincreased four times faster in patients (7.2 ± 6.1 vs 29.9 ± 13.6 sec). In sitting and standing positions hemoglobin oxygenation in the skin of the lower limb was markedly reduced in patients, but normal perfusion conditions were restored in supine position, indicating reversibility of the changes. Reflection oxymetry seems a valuable tool for the assessment of chronic venous insufficiency. The substantially reduced oxygenation of dermal hemoglobin in standing patients may contribute to the development of venous ulcers.
Microvasc Res. 2000 Jan;59(1):99-106.
Local oxygen content in the skin is increased in chronic venous incompetence.

In skin lesions of chronic venous incompetence (CVI) transcutaneous oxygen pressure (tcpO(2)) at the ankle is often reduced. However, in some CVI patients the tcpO(2) during suprasystolic occlusion remains significantly higher than in healthy subjects. The aim of the present study was to investigate which kind of CVI patients develop this phenomenon and whether the higher tcpO(2) during occlusion is caused by a smaller oxygen consumption of the skin or by an increased local oxygen content. The oxygen consumption of the skin was measured by the pO(2) decrease (DeltatcpO(2)/Deltat) after stopping the arterial oxygen supply when the hemoglobin was saturated by oxygen inhalation, i.e., at tcpO(2) values above 120-130 mmHg. By multiplying the tcpO(2) with the mean oxygen solubility coefficient of the skin the content of physically dissolved oxygen is obtained. The decrease of tcpO(2) in the 55- to 45-mmHg range indicates the consumption of oxygen physically dissolved and chemically bound to hemoglobin. It gave a parameter for estimating the local hemoglobin content of the skin. These values and the minimal tcpO(2) after a 5-min arterial occlusion were measured in 14 healthy subjects, in 13 patients with varicose veins, but no skin lesions, in 10 patients with CVI lesions like white atrophy and lipodermatosclerosis and in 16 CVI patients with open venous ulcers. During suprasystolic occlusion tcpO(2) at the ankle remained significantly higher in CVI patients with skin lesions than in the healthy control subjects (25.6 +/- 18.9 versus 8.0 +/- 7.0 mmHg). The steepness of the tcpO(2) decrease caused by cutaneous oxygen consumption in healthy subjects was not significantly different from the CVI patients. In contrast, the decrease of tcpO(2) at the ankle between 55 and 45 mmHg was 1.9 +/- 2.0 mmHg/s in the control group and 0.7 +/- 0.5 mmHg/s in the group with open venous ulcers. These results indicate a higher hemoglobin content in the skin of the CVI patients than in healthy subjects. Obviously, the hemoglobin bound oxygen content in the skin of CVI patients is increased. Thus, a lack of oxygen is unlikely to be the primary reason for the development of skin lesions in CVI
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Postby jackD » Mon Feb 08, 2010 8:40 pm

QUOTE:-why were the surgeries unnecessary, if i may ask?QUOTE-->jimmylegs



I had an Infantile Hemangioma which required at least 5 operations on my leg, two of which removed a major amount of leg tissue (my veins).

It has been discovered that it can be treated (removed) without any surgery by several high dose steroids treatments with no problems.

This is a great discovery because many of these Infantile Hemangiomas are on the face or neck.

The surgeons charged me 1(one) dollar for each removal attempt. They were trying to develop a procedure that worked and found my thigh a great place to practice

jackD
Last edited by jackD on Mon Feb 08, 2010 9:29 pm, edited 1 time in total.
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Postby jackD » Mon Feb 08, 2010 8:48 pm

here is a very recent abstract that helps me think that a GOOD Calcium Channel Blocker may be a good idea for MS folks.

http://home.ix.netcom.com/~jdalton/ms-two-stages.pdf

jackD
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Ann Neurol. 2009 Feb;65(2):151-9.

Glutamate receptors on myelinated spinal cord axons: I. GluR6 kainate receptors.
Ouardouz M, Coderre E, Basak A, Chen A, Zamponi GW, Hameed S, Rehak R, Yin X, Trapp BD, Stys PK.

Ottawa Health Research Institute, University of Ottawa, Ontario, Canada.

Comment in:

Ann Neurol. 2009 Feb;65(2):120-1.

OBJECTIVE: The deleterious effects of glutamate excitotoxicity are well described for central nervous system gray matter. Although overactivation of glutamate receptors also contributes to axonal injury, the mechanisms are poorly understood. Our goal was to elucidate the mechanisms of kainate receptor-dependent axonal Ca(2+) deregulation.

METHODS: Dorsal column axons were loaded with a Ca(2+) indicator and imaged in vitro using confocal laser-scanning microscopy.

RESULTS: Activation of glutamate receptor 6 (GluR6) kainate receptors promoted a substantial increase in axonal [Ca(2+)]. This Ca(2+) accumulation was due not only to influx from the extracellular space, but a significant component originated from ryanodine-dependent intracellular stores, which, in turn, depended on activation of L-type Ca(2+) channels: ryanodine, nimodipine, or nifedipine blocked the agonist-induced Ca(2+) increase. Also, GluR6 stimulation induced intraaxonal production of nitric oxide (NO), which greatly enhanced the Ca(2+) response: quenching of NO with intraaxonal (but not extracellular) scavengers, or inhibition of neuronal NO synthase with intraaxonal Nomega-nitro-L-arginine methyl ester, blocked the Ca(2+) increase. Loading axons with a peptide that mimics the C-terminal PDZ binding sequence of GluR6, thus interfering with the coupling of GluR6 to downstream effectors, greatly reduced the agonist-induced axonal Ca(2+) increase. Immunohistochemistry showed GluR6/7 clusters on the axolemma colocalized with neuronal NO synthase and Ca(v)1.2.

INTERPRETATION: Myelinated spinal axons express functional GluR6-containing kainate receptors, forming part of novel signaling complexes reminiscent of postsynaptic membranes of glutamatergic synapses. The ability of such axonal "nanocomplexes" to release toxic amounts of Ca(2+) may represent a key mechanism of axonal degeneration in disorders such as multiple sclerosis where abnormal accumulation of glutamate and NO are known to occur.
PMID: 19224535 [PubMed - indexed for MEDLINE]
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Postby jackD » Mon Feb 08, 2010 9:22 pm

Additional reading for the preverted few...

The Second Stage of MS is "The Degererative Stage" in which "excess Glutamate" runs wild on a killing spree. First phase, of course, is the "Inflammatory Stage".

Here is how it is done..mass murder of poor little neurons
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The Glutamate <--> Calcium Connection
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http://www.psychiatrist.com/pcc/brainstorm/br5806.htm

jackD

additional info

http://www.psychiatrist.com/pcc/brainstorm/br5904.htm

http://www.psychiatrist.com/pcc/brainstorm/br5906.htm
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