Kuwait didn't wait.....

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Postby sbr487 » Fri Apr 23, 2010 1:32 am

Ruthless67 wrote:
In Kuwait the MS patient is increasing and it is estimated about 3000 – 6000 patients.

In conclusion, the incidence and prevalence of MS in Kuwait has increased between the early and late 1990s with no signs of leveling off.


So my question is why the increase? And it’s not just Kuwait seeing this increase.

Our results so far shows strong link between CCSVI and M.S.

It has also been established that CCSVI is a congenital disorder and precedes the development of MS.


OK, so what starts all this congenital disorder? How do we get to the bottom of that? What is X if: X = congenital disorder = MS

I can’t believe it’s just genetic and passed by our genes. That wouldn’t explain it’s rapid increase.

I’m thinking it’s organic in origin. Because MS has been with us for quite a while.

More like a lack of something in parents diet like Vitamin D or because, starting with our parents generation, we don’t cook with bones anymore, so we get much less collagen in our diets.

Or maybe it’s the pesticides used in farming since the 40’s that we’ve all been ingesting like PCB, DDT etc; or the fertilizers, or pollution in general. But wait, MS has been around much longer than these things, so again,

I’m thinking it’s organic in origin. But again, something that’s been present all along, just getting stronger in nature over the last few years.

I think maybe it’s something naturally occurring but in an overgrowth state such as Candida albicans where the mother has this condition and in the womb the fetus then has the same condition and it effects the vascular system during it’s developmental stage.


The truncular venous malformation (VM) represents an embryologically defective vein where developmental arrest has occurred during the vascular trunk formation period in the 'later stage' of the embryonic development.


I can’t find it, but I’m pretty sure Dr. Zamboni eluded to something along these lines in his research. I believe I read it paraphrased on another thread.

Or it could be fungal, even parasitic in nature that follows the same scenario as above. Kind of like what they learned about the origin of ulcers.

But if it is organic in origin, why the increase now? What has changed?

The increasing cases of MS have been steady, but these documented stats regarding this 7 year period, 1993 - 2000, in Kuwait is very powerful.


As we get closer to answers, there are so many questions…………I believe it is a puzzle!


Ruth, dont forget the gene mutation that might be playing a role. It takes generation of mutations to result in bad genes. So for generations we might be getting mutated genes. And we will pass on these bad genes to our children ...
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Postby hwebb » Fri Apr 23, 2010 4:18 am

Ruthless,

it's interesting you point out
The increasing cases of MS have been steady, but these documented stats regarding this 7 year period, 1993 - 2000, in Kuwait is very powerful.


When studying the incidence of MS in the Faroe Islands after WWII, John F. Kurtzke speculated that an infectious agent with an incubation time of approximately 7.2 years may play a role in the development of MS:

http://www.stanford.edu/~siegelr/rnorris.html
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Postby sbr487 » Fri Apr 23, 2010 5:43 am

Now the usual suspects (especially that Colin Rose) will pick up spelling mistakes in the report to bash it, as if there is a direct co-relation between spelling & intellectual ability.
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Postby cheerleader » Fri Apr 23, 2010 6:20 am

...and how many other languages would "he who shall not be named" speak, anyway? I cannot make out one character of the Arabic language... I put no stock in anything that man vomits into cyberspace...

Changes to the endothelial lining of the blood vessels can happen in months ...doesn't take a generation for our veins and arteries to narrow. We see this in Crp levels of inflammation--which are now occurring in healthy people.

Remember, nitric oxide disruption creates vasoconstriction and inflammation- and disrupts the blood brain barrier-- here is the mechanism in stroke--

Background and Purpose— Increased mortality after stroke is associated with brain edema formation and high plasma levels of the acute phase reactant C-reactive protein (CRP). The aim of this study was to examine whether CRP directly affects blood–brain barrier stability and to analyze the underlying signaling pathways.

Methods— We used a cell coculture model of the blood–brain barrier and the guinea pig isolated whole brain preparation.

Results— We could show that CRP at clinically relevant concentrations (10 to 20 µg/mL) causes a disruption of the blood–brain barrier in both approaches. The results of our study further demonstrate CRP-induced activation of surface Fc receptors CD16/32 followed by p38-mitogen-activated protein kinase-dependent reactive oxygen species formation by the NAD(P)H-oxidase. The resulting oxidative stress increased myosin light chain kinase activity leading to an activation of the contractile machinery. Blocking myosin light chain phosphorylation prevented the CRP-induced blood–brain barrier breakdown and the disruption of tight junctions.

Conclusions— Our data identify a previously unrecognized mechanism linking CRP and brain edema formation and present a signaling pathway that offers new sites of therapeutic intervention.


http://stroke.ahajournals.org/cgi/conte ... /40/4/1458

I think the answers will come when we start looking at CCSVI as a chronic venous micro- stroke--

-and what changes nitric oxide distribution and creates endothelial disruption, raising Crp levels? Viruses (EBV), bacteria (cpn), low vitamin D, saturated fats, heavy metals (mercury), oxidative stress (low amounts of antioxidants from fruits and veg), Diesel fuel exhaust, pcbs in plastics, smoking (which makes MS worse, even though it dampens the immune system)....the list of nitric oxide disrupters is a veritable laundry list of modern, industrialized living. Which is what has happened to Kuwait.
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby sbr487 » Fri Apr 23, 2010 6:34 am

Cheer, are you a teacher by any chance? because, every time we digress, you beat us back onto track.

BTW, just wanted to know if you are accepting any donations for CCSVI Alliance?
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Postby cheerleader » Fri Apr 23, 2010 6:43 am

sbr487 wrote:Cheer, are you a teacher by any chance? because, every time we digress, you beat us back onto track.

BTW, just wanted to know if you are accepting any donations for CCSVI Alliance?


My late father taught public school music for 40 years, my Mom is a retired high school English teacher, but I'm just a no-good chick singer :)
I just think the pieces are starting to fit together, and it's exciting to me. Maybe I need to get out more?

The CCSVI Alliance is accepting donations...although we haven't launched officially, -contact the treasurer at http://www.ccsvi.org/
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Last edited by cheerleader on Fri Apr 23, 2010 6:45 am, edited 2 times in total.
Husband dx RRMS 3/07
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http://ccsviinms.blogspot.com
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Postby costumenastional » Fri Apr 23, 2010 6:44 am

NO NO!!!!
Dont!!!!

:)

Nice weekend to all of us.
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Postby Johnson » Fri Apr 23, 2010 11:57 am

the list of nitric oxide disrupters is a veritable laundry list of modern, industrialized living.


But it makes me wonder what those disruptors may have been in pre-modern, pre-industrial times. Think Halldora circa 1000 AD, Creuvhalier in the 1860s, etc. I think that the pathogenesis is more mundane, but the exacerbating factors more varied - can't point to smoking, Epstein-Barr in non-smokers, or in those negative for EB. Smoking and EB are disparate suspects to boot.

So, MS/CCSVI has been around for a very long time, but seems to be picking up in prevalence. Kuwait is interesting because of the marked increase since Gulf War I (17 years is a short window for "natural" mutations). Thinking of genetic mutation, what could cause such a rapid mutation in Kuwait? Depleted uranium? Anthrax vaccines?

Bah! I may know how to spell, but my intellect is definitely suffering - I forget where I was, and where I was trying to get too. My three year old is not helping me to concentrate.
My name is not really Johnson. MSed up since 1993
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Postby babiezuique » Fri Apr 23, 2010 12:53 pm

As everyday those medical sources are helping me rebuilt my cheesy brain! I feel so bless... to be a part of what you are diong here;)

Love you all!
have a nice and cool weekend;)
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Postby cheerleader » Fri May 07, 2010 7:21 am

Wow....I think we may have a partial answer as to the rising MS rates in Kuwait. They've been "super sized"----

In Kuwait, at family gatherings and social events, food is always at the top of the menu.
Friends meet at restaurants two or three times a week and if you don't want to go out, Western fast food chains like Burger King will deliver tasty, high-fat meals to your front door.
At family occasions, the more opulent the spread the greater the social status conferred. Tables groan under the weight of multi-course banquets laid on by competitive hostesses, often aided by maids.
But, in the oil-rich Gulf state where scorching summers keep people indoors, this appetite for excess is taking its toll. Kuwait is one of the fattest nations on earth -- and it is affecting people's health.
Just over 74 percent of the population is overweight, according to the World Health Organization (WHO) and this "obesity epidemic" is contributing to a rise in heart disease and diabetes.

WHO says around 14 percent of Kuwaitis currently suffer from diabetes and it is on the rise.
"[Being] overweight and obesity have been gradually increasing for the past 15 years," Nawal Al Hamad, Head of Nutrition at Kuwait's Ministry of Health, told CNN.
The underlying causes are complex, but an abundance of food and sedentary lifestyles are major factors, according to Hamad.


In the venous paradigm of MS, saturated fats, lack of vitamin D, lack of exercise and obesity are vasoconstrictors and endothelial disrupters....could certainly make MS worse (as well as other autoimmune disorders) This is so sad...our global community needs to deal with this epidemic.
link to article

cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby cah » Fri May 07, 2010 8:20 am

There are numerous studies which indicate a link between obesity and CVI, for example: http://www.schattauer.de/en/magazine/su ... /show.html

Now why should this only affect the legs?

Then again, this would be a contradiction to the theory that CCSVI is congenital. But there are so many different signs of CCSVI... so the assumption that there are different reasons for venous obstructions all leading to CCSVI makes sense.
"There is only one good, knowledge, and one evil, ignorance." Socrates
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Postby cheerleader » Fri May 07, 2010 8:26 am

Cah-
Thanks for the CVI/obesity links...
I believe you can have a congenital venous malformation, and environmental/lifestyle factors will make stenosis and reflux even worse....just as you can have a genetic predisposition to high cholesterol or stroke. These malformations may start out "baby sized" and grow, due to vasoconstriction and endothelial disruption. This may be why we are seeing higher rates of, not only MS, but all autoimmune diseases.
cheer
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dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby frodo » Fri May 07, 2010 9:10 am

What is there is simply no increase in real incidence but in reported incidence? Some years ago there was no possible diagnosis before death, and at that time it really didn't matter. What if we are only seeing an advance in diagnosis?
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Postby cheerleader » Fri May 07, 2010 9:17 am

frodo wrote:What is there is simply no increase in real incidence but in reported incidence? Some years ago there was no possible diagnosis before death, and at that time it really didn't matter. What if we are only seeing an advance in diagnosis?


Possible...but this has happened VERY quickly (in the last 10 years) and there was diagnosis in place in Kuwait, as evidenced by the published research.
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dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby cah » Fri May 07, 2010 10:11 am

cheerleader wrote:Cah-
Thanks for the CVI/obesity links...
I believe you can have a congenital venous malformation, and environmental/lifestyle factors will make stenosis and reflux even worse....just as you can have a genetic predisposition to high cholesterol or stroke. These malformations may start out "baby sized" and grow, due to vasoconstriction and endothelial disruption. This may be why we are seeing higher rates of, not only MS, but all autoimmune diseases.
cheer


That's intriguing! If it was only a question of lifestyle, the main age of MS onset was contradictory to that. MS would be seen much more in older patients, as in other "livestyle" diseases like stroke or diabetes. So the congenital factor must be strong. But if it was only the congenital issue, the average MS onset would be earlier. But with some sort of interference of both, it fits perfectly. That is, at least to my laypersons mind...
"There is only one good, knowledge, and one evil, ignorance." Socrates
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