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Monday, May 21, 2018 6:09 AM | Venöse Multiple Sklerose, CVI & SVI, CCSVI Volg link
Effect of magnesium supplementation on endothelial function: A systematic review and meta-analysis of randomized controlled trials. https://www.atherosclerosis-journal.com/article/S0021-9150(18)30205-3/abstract
Effect of magnesium supplementation on endothelial function: A systematic review and meta-analysis of randomized controlled trials
Findings of past studies are inconsistent regarding the effects of magnesium (Mg) supplementation on endothelial function (EF). We performed this meta-analysis to examine the effects of magnesium supplementation on flow-mediated dilation (FMD) and carotid intima media thickness (CIMT) as markers of....
Monday, May 21, 2018 5:54 AM | Venöse Multiple Sklerose, CVI & SVI, CCSVI Volg link
Magnesium supplements show potential anti-inflammatory effects: Meta-analysis

08-Jun-2017 By Stephen Daniells

Dietary supplementation with magnesium may reduce levels of inflammatory biomarkers, says a new meta-analysis pooling data from 11 studies.

https://www.nutraingredients-usa.com/Article/2017/06/08/Magnesium-supplements-show-potential-anti-inflammatory-effects-Meta-analysis
Magnesium supplements show potential anti-inflammatory effects: Meta-analysis
Dietary supplementation with magnesium may reduce levels of inflammatory biomarkers, says a new meta-analysis pooling data from 11 studies.
Monday, May 21, 2018 4:29 AM | Venöse Multiple Sklerose, CVI & SVI, CCSVI Volg link
Meta-Analysis – The present meta-analysis of prospective cohorts suggests that higher magnesium intake is associated with reduced risk of total and ischaemic stroke.

Abstract:
BACKGROUND AND AIMS: Prospective cohort studies are inconsistent regarding the association between magnesium intake and the risk of stroke. The objective was to perform a meta-analysis to summarise the relationship between magnesium intake and risk of stroke in observational studies. METHODS AND RESULTS: We searched the PubMed and EMBASE databases for studies conducted from 1966 through August 2011. Prospective studies that provided relative risk (RR) estimates with 95% confidence intervals (CIs) for the association between magnesium intake and the risk of total stroke incidence or mortality were included. Data were independently abstracted by two investigators using a standardised protocol. Study-specific risk estimates were combined by using a random effects model. A total of eight studies, with 8367 stroke cases among 304,551 participants, were included in the meta-analysis. The summary RR indicated a significant association between the highest magnesium intake and reduced risk of total stroke (summary RR: 0.89; 95% CI: 0.82, 0.97); our dose-response analysis showed a borderline inverse association between magnesium intake and total stroke risk (an increment of 100 mg day(-1); summary RR: 0.98; 95% CI: 0.95, 1.00). Subgroup analyses suggested a significant inverse association between highest magnesium intake and the risk of ischaemic stroke (summary RR: 0.88; 95% CI: 0.80, 0.98). CONCLUSION: The present meta-analysis of prospective cohorts suggests that higher magnesium intake is associated with reduced risk of total and ischaemic stroke. However, well-designed randomised controlled trials are needed to draw a definitive conclusion.
Source: Nutr Metab Cardiovasc Dis. 2013 https://www.nmcd-journal.com/article/S0939-4753(12)00126-3/abstract
Magnesium intake and incidence of stroke: Meta-analysis of cohort studies
Prospective cohort studies are inconsistent regarding the association between magnesium intake and the risk of stroke. The objective was to perform a meta-analysis to summarise the relationship between magnesium intake and risk of stroke in observational studies.
Sunday, May 20, 2018 12:24 AM | The Vascular Connection to Multiple Sclerosis Volg link
"No matter what big pharma would like us to believe, ultimately, true health just doesn’t come in pill form — it comes from the things we do to promote our well-being. Though most of us know that spending time at the beach, in the woods or far beyond the city limits is a rejuvenating experience, it’s important to remember that nature has the power to heal — as long as we give it a chance — so get out there!" #ItsNotAPill
Get Out There: Nature's Healing Power
This modern hermetically-sealed lifestyle is turning many into indoor zombies — with dulled senses, suppressed immune systems, depressed spirits and sharply increased risk for illness and disease. One can hardly call that living — particularly when the healing power of nature is so close at hand...
Friday, May 18, 2018 10:38 PM | CCSVI Alliance Volg link
Additional reporting on our recent post (Wednesday, May 16, 2018) ......titled "How the Gut Influences Neurologic Disease"

“The beauty of this paper is that it provides a very detailed mechanistic understanding of how things work,” Jonathan Kipnis, a neuroscientist at the University of Virginia who did not participate in the study, tells The Scientist. Previous research linked the microbiome and the development of MS in mice, he says, but “we never understood how the gut communicates with the brain.”

https://www.the-scientist.com/?articles.view/articleNo/54592/title/Microbes-Affect-Brain-Cells--Activities-in-Mice-with-Multiple-Sclerosis/
Microbes Affect Brain Cells’ Activities in Mice with Multiple Sclerosis
Researchers find a link between molecules released by commensal bacteria and the degree of inflammation in a mouse model of MS.
Friday, May 18, 2018 3:26 AM | CCSVI Alliance Volg link
Check out Dr Paolo Zamboni's website
https://zambo850.wixsite.com/zambo
Home | Paolo Zamboni, MD
Home
Thursday, May 17, 2018 2:53 AM | CCSVI Alliance Volg link
Interesting study from Brigham Women's Hospital connecting the gut to neurological disease patterns including MS.
How the gut influences neurologic disease
A study published this week in Nature sheds new light on the connection between the gut and the brain, untangling the complex interplay that allows the byproducts of microorganisms living in the gut to influence the progression of neurodegenerative diseases. Investigators from Brigham and Women's Ho...
Wednesday, May 16, 2018 1:49 AM | Venöse Multiple Sklerose, CVI & SVI, CCSVI Volg link
How to test PROPERLY for Hormone D (aka Vitamin D) & Magnesium Deficiency

1. How to test properly for Hormone D deficiency?

Want to find out the true status of your storage AND active “Vitamin”-D and bypass BIG-Pharma ("Vitamin-D Council") brainwash?

Here we go. Please ask for these 4 blood tests before you take an insanely high dosage of a synthetic hormone called “Vitamin D” by the med. e$tablishment.

The 4 basic blood tests are:

1. Magnesium RBC (amount of Mg in red blood cell and NOT in blood serum!) 6.0 mg/dl is minimum & 6.5 is optimal
2. 25(OH)D (Storage form of Hormone-D), nothing over 21ng/dl has any clinical benefit.
3. 1,25(OH)2D3 (Active form of Hormone-D), should be no more the 1.5 to 2.0 times of 25(OH)D
4. "Ionized" Calcium blood test

If test No.1 is 6.0mg/dL (this is a sufficient amount of Mg in the body tissue needed for the production of Hormone D (aka "Vit.-D") because Mg-deficiency causes Hormone-D resistance/deficiency!) and test No.3 is low, and test No.4 is low too then and only then taking supplemental "D" (e.g. cod-liver oil) would be advised.

Test No.2 is essentially a distortion of reality and low "Calcidol" (storage form) is actually caused by too much Calcium in the blood means, there is too little Mg in the blood. Much better to know is the true status of your active hormone D and its mineral focus Calcium. Excess Calcium is the precursor to inflammation and more excess Calcium to Magnesium is the cause of hormonal imbalances, disease & death.

+++++++++++++++++++++++++++++++++++++++++++

2. How to test properly for Magnesium deficiency?

The right Magnesium test is called 'RBC Magnesium test' NOT! ‘serum Magnesium test’.
Serum Magnesium is worthless because only %1 of the body’s entire amount of Magnesium is circulating in the bloodstream the rest of this essential mineral is stored/hidden in your body tissue (bones/muscles/brain/teeth etc.) and your clever body will do EVERYTHING to keep that %1 Mg in your bloodstream in balance otherwise, you will die from a heart attack in seconds.
Months, weeks, days before such a fatal event takes place, your serum Magnesium level will even rise (body ‘steals’ it from the tissue and pumps it back in the bloodstream), which is kind of nature’s last attempt to allow the heart muscle to relax after every contraction it performs and to prevent a heart attack/death.

Get properly tested, people! In New Zealand such test is called Red Blood Cell (RBC) Magnesium tests and it cost ~NZ$ 25. You can order it directly at every "pathlab ltd." and you don't need a referral from a med. doctor! :)

Optimal RBC Magnesium values:

6.0 -7.0mg/dl
2.4-2.57 mol/L
3.37-5.77mEq/L
6.0/2.4/3.37 = minimum. Everything less is Magnesium deficiency.
Venöse Multiple Sklerose, CVI & SVI, CCSVI
Tuesday, May 15, 2018 12:23 AM | CCSVI Alliance shared Canadian Neurovascular Health Society's post. Volg link

Canadian Neurovascular Health Society
An overestimated study,
crippled by recruitment failure
and misleading conclusions

Bernhard H.J. Juurlink,1
Pietro M. Bavera,2 Salvatore Sclafani,3
Ivo Petrov,4 Donald B. Reid5

A recent study, published in JAMA
Neurology, examining whether using percutaneous
transluminal angioplasty (PTA) to
correct chronic cerebrospinal venous insufficiency
(CCSVI) in multiple sclerosis
(MS) patients concluded: Venous PTA has
proven to be a safe but largely ineffective
technique; the treatment cannot be recommended
in patients with MS. 1 This is rather
a bold statement for a study that was grossly
underpowered. Not surprisingly, given the
history of reaction to the idea that impairment
of venous return might influence the
progression of MS, the publication of this
study was followed by several editorials
that bemoaned the power of social media to
influence research on and treatment of disease.
2,3
The Brave Dreams clinical trial was a
multi-centre, randomized, sham-controlled
evaluation of the efficacy and safety of
venous PTA of extra-cranial and extra-vertebral
veins that contributed to CCSVI in
patients with MS.1 Involved were six centres
accredited by the Italian National
Health Service. Only physicians trained and
accredited in functional outcomes, operation
of Echo Colour Doppler (ECD) and
catheter venography with and without PTA
participated. Patients in the trial were
between 18 and 65 years old who had a
diagnosis of remitting relapsing (RR) or
secondary progressive (SP) MS with
Extended Disability Status Scale (EDSS)
score between 2 and 5.5, disease duration of 15 years or less, a stable neurology condition
for at least 30 days, CCSVI as determined
by ECD, not having received MSspecific
treatment for at least six months, no
prior PTA nor having a history on being on
certain medications such as fingolimod.
The primary outcomes measured at 12
months were a functional composite score
and MRI-detectable lesions. A new functional
composite score was developed based
upon commonly-experienced functional
impairments such as walking control, balance,
manual dexterity, post-void residual
urine volume, visual acuity, etc. Patients
were evaluated and placed into improved,
stable, worsened or mixed categories. MRI
analysis grouped patients into categories
having new and/or enlarged lesions compared
to baseline and those free of lesions.
Secondary outcomes included annualized
relapse rates, changes in EDSS score and
proportion of patients with restored venous
flow.A power analysis was performed that
determined that to detect 2.1 fewer lesions
in RR MS patients at 90% power (an a of
0.05) would require the enrollment of 423
patients and at an 80% power would require
enrollment of 300 patients. For SP MS
patients a 90% power would require recruiting
222 patients. How many patients were
actually enrolled in the clinical trial? Only
115 RR MS patients enrolled in the study, of
whom 112 completed the study while only
15 SP MS patients were enrolled. Herein
lies the major problem of the study: gross
underpowerment. This incomplete study
should not have been published, rather additional
centres should have been established
to ensure adequate patient enrolment.
What the study found was that there
were essentially no differences in functional
composite score between the PTA and Sham
groups of RR MS. However, 73% of the
PTA group had no new gadolinium-enhancing
lesions compared to 49% in the Sham
group (P=0.08). For secondary endpoints
the study showed that 23% of PTA had at
least one relapse (annualized rate of 0.32)
compared to 31% (annualized rate of 0.39)
of the Sham group but this was not a significant
difference.
With SP MS there were no differences
in composite functional score between the
two groups; however, 100% of the PTA
group (n=10) developed no new lesions as
opposed to 40% in the Sham group (n=5).
In summary, there was a trend for fewer
new lesions in both the RR and SP MS
groups if they had PTA and fewer relapses
in the PTA group of RR MS patients.
However, there were no differences noted
between the two groups for composite functional
and EDSS scores. About 41% of the RR improved compared to 49% of the
Sham while 12% of the RR and 19% of the
Sham worsened with the remaining patients
showing a mixed outcome. Curiously,
median EDSS scores decreased from a
median score of 2.5 to 2.0 in both the PTA
and Sham-treated groups.
What would the results have been if the
study was properly powered? We point out
that in a large study where 366 MS patients
who had PTA to correct for CCSVI were
followed up for 4 years, PTA resulted in significant
clinical improvement, especially in
the RR MS patient group.4,5 The patients
were divided into RR (264), Primary
Progressive (PP) and SP groups. All
patients underwent a Duplex exam and
filled out a Questionnaire that addressed the
following symptoms: diplopia, fatigue,
headache, upper limb numbness/mobility,
lower limb numbness/mobility, altered thermic
sensibility, bladder control, balance
coordination, quality of sleep, vertigo, mind
concentration and working activity. Patients
with CCSVI then underwent PTA and were
followed up for 4 years. It is important to
note that the researcher carrying out the
Duplex exams and analyzing the
Questionnaire data was completely independent
of the vascular surgeons carrying
out the PTA. This large study demonstrated
that in RR MS patients that venous blood
flow improvements were long-lasting when
the abnormalities were not so severe.
Further, improved venous outflow was associated with long-lasting improvements
in clinical symptoms with improvements in:
more than 90% with diplopia, fatigue,
headache, quality of sleep, vertigo and ability
to mentally concentrate; more than 80%
in balance control and upper and lower limb
functions; and more than 65% in bladder
control and thermic sensibility. In contrast,
although SP and PP MS patients showed
some initial clinical improvements following
angioplasty, these disappeared within 2-
12 weeks.
A problem with the Brave Dreams
study is that only about half of the patients
had improved venous blood flow following
PTA. Clearly, the reasons underlying this
surprising failure to improve blood flow in
almost 50% of the patients treated for
CCSVI must be investigated. The authors
are encouraged to publish a review of the
technical methodology and outcomes of
their study so that the techniques can be
analyzed and enhancement in technique be
considered. It is equally important to delineate
which subset of MS patients respond to
PTA. We point out that carotid endarterectomy,
which now is a well-accepted common
stroke prevention technique in a subset of
patients, was questioned as recently as
1984.6 The challenge in determining efficacy
of endarterectomy was to define which
subset of patients benefited from the
surgery. This has now been clarified.7 Those
who have performed angioplasty to correct
for CCSVI in MS patients have noted that
only a subset of patients benefits from treatment.
More research is needed to identify
the subset of MS patients with CCSVI that
can benefit from the treatment.
What also struck us was the lack of
composite functional endpoint analysis of
the subset of PTA-treated patients (54%)
where blood flow improved compared to
the patients where blood flow was not
improved? After all, one of the objectives of
PTA in treating CCSVI is improvement of
venous outflow and cerebrospinal fluid
drainage to ultimately enhance cerebrospinal
perfusion. And, as noted above, in
the Bavera follow-up study clinical
improvements were noted only if there were
improvements in venous outflow following
PTA.4,5 Further, why was no attention paid
to the fact that 38% of the sham-treated
group had improved blood flow, after all
improved blood flow regardless of treatment
is desired to improve symptoms of
MS. Improved blood flow following shamtreatment
is, at first glance, surprising; perhaps
valvular and other endoluminal alterations
resulting from catheterization itself
may improve flow. Moreover, there is some
evidence suggesting that PTA may improve
autonomic function which may itself improve blood flow.8,9 If this be the case
then it becomes important to know whether
improved venous blood flow, regardless of
treatment, improves outcomes. This was not
addressed in the paper.
The possibility of technical deficiencies
must be considered as a contributor to the
poor rate of flow restoration in the Brave
Dreams study. Reporting clinical outcomes
of a new operative procedure without also
reporting the technical parameters of the
procedure as was recommended by the
International Society for Neurovascular
Disease (ISNVD) and by the Society of
Interventional Radiology prevents real critique
of the procedure.10,11 Many aspects of
this therapy are dependent on the diagnostic
findings, such as use of intravascular ultrasound,
degree of stenosis, number of extrinsic
compressions, incidence of webs, divisum,
septum duplication and webs, transit
time, stagnation, reflux, and as well upon
technique, such as balloon size versus vessel
size, end point of angioplasty, pressure
of angioplasty, number of inflations, duration
of inflation, residual stenosis, incidence
of dissection. Without this information, proceduralists
cannot assess the validity of the
results, or learn why almost half of the
patients failed to have improved flow after
angioplasty, nor can they develop improvement
in techniques.
One firm conclusion from this randomized,
blinded study is that PTA to correct for
CCSVI is safe.1 This is not a new finding
since the safety of PTA to correct for
CCSVI had been described previously.12We
also note that if one combines the
Remitting-Relapsing and the Secondary
Progressive MS patients in the PTA (n=73
and n=10, respectively) and Sham (n=37
and n=5, respectively) and examines for
absence of new lesion formation, we find
that 56/83 PTA patients and 21/42 Sham
patients had no new lesions. A Chi Squared
analysis shows that the probability of the
PTA treatment having no effect is 0.058. As
noted this Brave Dreams study was greatly
underpowered and this statistical analysis
suggests that on this basis alone further
studies are well-warranted and we urge the
investigators to continue to enrol patients
into their clinical trial and to, especially, dig
deeper into the data. There is an abundance
of evidence that co-morbidities have an
effect on progression to disability in MS13
and it is, therefore, not unreasonable to
hypothesize that problems in venous outflow
from the CNS would affect progression
to disability.

References
1. Zamboni P, Tesio L, Galimberti L, et al.
Efficacy and safety of extracranial vein
angioplasty in Multiple Sclerosis. A randomized
clinical trial. JAMA Neurol
2018;75:35-43.
2. Green, AJ, Kamel H, Josephson, A.
Combating the spread of ineffective medical
procedures. A lesson learned from
Multiple Sclerosis. JAMA Neurol 2018;
75:15-7.
3. Zivadinov R, Weinstock-Guttman B.
Extracranial angioplasty is ineffective in
treating MS. Nature Rev Neurol 2018;
14:129-30.
4. Bavera PM. May symptoms of chronic
cerebrospinal venous insufficiency be
improved by venous angioplasty? An independent
4-year follow up on 366 cases.
Veins and Lymphatics 2015; 4:5400.
5. Bavera PM. Chronic Cerebrovascular Vein
Insufficiency (CCSVI): how and when can
Jugular Vein PTA Influence the most frequent
Symptoms and Disturbs in Multiple
Sclerosis. Acta Phleb 2016;17:27-32.
6. Barnett HJM, Plum F, Walton JN. Carotid
endarterectomy - an expression of concern.
Stroke 1984;15:941-43.
7. Easton JD. History of endarterectomy then
and now. Stroke 2014;45:e101-3.
8. Arata M, Sternberg Z. Transvascular autonomic
modulation: A modified balloon
angioplasty technique for the treatment of
autonomic dysfunction in Multiple
Sclerosis patients. J Endovasc Ther 2014;
21:417-28.
9. Sternberg Z, Grewal P, Cen S, et al. Blood
pressure normalization post-jugular
venous balloon angioplasty. Phlebol 2015;
30:280-7.
10. Simka M, Hubbard D, Siddiqui AH, et al.
Catheter venography for the assessment of
internal jugular veins and azygous vein:
Position statement by expert panel of the
International Society for Neurovascular
Disease. VASA 2013; 42:168-76.
11. Siskin, GP, Haskal ZJ, McLennan G, et al.
Development of a research agenda for
evaluation of interventional therapies for
chronic cerebrospinal venous insufficiency:
Proceedings from a multidisciplinary
research consensus panel. J Interv Radiol
2011;22:587-93.
12. Petrov I, Grozdinski L, Kaninski G, et al.
Safety profile of endovascular treatment
for chronic cerebrospinal venous insufficiency
in patients with multiple sclerosis. J
Endovasc Therap 2011; 18:314-23.
13. Zhang T, Tremlett H, Zhu F, et al. Effects
of physical comorbidities on disability progression
in Multiple Sclerosis. Neurol
2018 [Epub ahead of print].

http://www.pagepressjournals.org/index.php/vl/article/view/7340
Monday, May 14, 2018 11:55 PM | Venöse Multiple Sklerose, CVI & SVI, CCSVI shared The Vascular Connection to Multiple Sclerosis's post. Volg link
Brave Dreams: An overestimated study, crippled by recruitment failure and misleading conclusions
The Vascular Connection to Multiple Sclerosis
Brave Dreams: An overestimated study, crippled by recruitment failure and misleading conclusions
http://www.pagepressjournals.org/index.php/vl/article/view/7340
PDF: http://www.pagepressjournals.org/index.php/vl/article/download/7340/7175
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