Welcome! This blog contains research, information on lifestyle, nutrition, dietary supplements and health for those with MS, as well as continuing information on the understanding of CCSVI and cerebral hypoperfusion. This blog is informative only--all medical decisions should be discussed with your own physicians.

The posts are searchable---simply type in your topic of interest in the search box at the top left.

Almost all of MS research is initiated and funded by pharmaceutical companies. This maintains the EAE mouse model and the immune paradigm of MS, and continues the 15 billion dollar a year MS treatment industry. But as we learn more about slowed blood flow, gray matter atrophy, and environmental links to MS progression and disability--all things the current drugs do not address--we're discovering more about how to help those with MS.

To learn how this journey began, read my first post from August, 2009. Be well! Joan

Thursday, December 31, 2009

Hypoperfusion (decreased blood flow) in MS


December 31, 2009 at 10:53am

Before 2009 comes to a close, I'd like to share more research on the decrease of blood flow in the MS brain. There are many researchers around the globe using new MRI technology to study slowed perfusion in MS brains.

I would like to break down this one medical research paper for you, to show you how these researchers' findings can be linked what Dr. Zamboni has discovered.  I will quote sections from the paper- and then we will discuss.

Hypoperfusion of the cerebral white matter in multiple sclerosis: possible mechanisms and pathophysiological significance
This work was supported by MS Anders (Amsterdam, The Netherlands).
Jacques De Keyser1,2, Christel Steen2, Jop P Mostert2 and Marcus W Koch2
1Department of Neurology, Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel,Brussels, Belgium
2Department of Neurology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands


from the abstract:

"A number of recent studies using perfusion magnetic resonance imaging in both relapsing and progressive forms of MS have shown a decreased perfusion of the NAWM, which does not appear to be secondary to axonal loss."


This means that in normal appearing white matter (NAWM) in MS brains, there is a slowing of blood flow which does not appear to be caused by axonal death. Something else is causing the slowed blood flow FIRST-because it shows up before we see lesions.

"The classic teaching is that MS is a T-cell-mediated autoimmune disorder of the central nervous system. However, a number of pathophysiological observations cannot be simply explained on the basis of autoimmune mechanisms. First, the progressive (neurodegenerative) component of the disease continues despite intense immunosuppressive interventions that effectively stop inflammatory disease activity (Coles et al, 1999; Metz et al, 2007; Roccatagliata et al, 2007; Samijn et al, 2006). Second, pathologic studies have shown that some demyelinating lesions develop without a preceding inflammatory reaction (Barnett and Prineas, 2004; Gay, 2007, 2006; Guseo and Jellinger, 1975; Lucchinetti et al, 2000). Third, another intriguing finding difficult to explain by autoimmune phenomena is the finding of a diffuse cerebral white matter hypoperfusion, which is the subject of this review."


The prior thought has been that MS is a t-cell mediated disease, autoimmune..we've all heard this. HOWEVER, the researchers wonder, how can the autoimmune hypothesis explain what we (many other researchers) are observing?
1. Even when suppressing the immune system, damage continues in the MS brain
2. Demyelinating lesions appear BEFORE inflammation
3, There is a slowing down of blood flow in cerebral white matter in MS brains

Wednesday, December 30, 2009

Vascular white matter lesions are 50-500 times more likely than MS


December 30, 2009 at 2:57pm


Neurologists refer to the "unique" presentation of MS as an autoimmune disease- with oligoclonal banding in CSF showing myelin degradation and perivenous (or around the veins) white matter lesions on MRI.

But these features are not unique to MS. Most of these signs are also found as result of hypoxic injuries to the brain: including (but not limited to) stroke, diffuse cerebral hypoxia, dementia and vascular insufficiency- in which the immune system is similarly activated.  What makes MS unique are the perivenous lesions, shown on MRI.  MS is diagnosed as MS because of the location of the lesions, age of the patient and their symptoms.

Here is research from a radiology web site, authored by Dr. Barkhof, on white matter lesions in MRI.

MS vs. Vascular findings
Consequently, it is not wise to put MS in the differential diagnosis, if the clinician does not suspect the patient of having MS and on the MR incidental white matter lesions (WML) are found.  The odds are against the diagnosis of MS, because vascular WMLs are 50-500 times more likely than MS plaques.

MS is a diagnosis of exclusion.  It can be 500 times more likely that someone has a vascular disorder.  Diagnosticians can also exclude those patients who are old, who have had a stroke, who have been poisoned by carbon monoxide, who have high blood pressure- even though these patients may have MRIs that look strikingly similar to an MS patient. When the mode of brain injury is apparent, the diagnosis is easier. MS researchers have here-to-fore not had an explanation for injury, and so the autoimmune theory was employed.  Even though the main issues for these lesions are predominantly vascular.

Dr. Zamboni is now showing us that there is a mode of brain injury in MS patient- chronic cerebrospinal venous insufficiency created by venous stenosis and reflux, which is directly linked to the slowed perfusion and hypoxic-like lesions found in the MS brain-as well as the degradation of gray matter due to iron deposition.

Please consider the following research:

Hypoxia-like tissue injury as a component of multiple sclerosis lesions.
Lassmann H.
http://www.ncbi.nlm.nih.gov/pubmed/12559509

Ischemic Demylination:
Recent studies have looked at lesion load in a fashion analogous to that seen with multiple sclerosis. A particularly relevant clinical model for white matter disease is cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) which combines the potential components of small vessel disease, resulting in progressive neurological deficit, with a common association with migraine which can also be associated with white matter lesions. However, the most common pathogenic factor associated with the microangiopathy, which appears to be at the heart of ischemic demyelination, continues to be hypertension. 
http://www.ingentaconnect.com/content/maney/nres/2006/00000028/00000003/art00018

Multiple Sclerosis: The Role of MR Imaging
Y. Ge From Department of Radiology/Center for Biomedical Imaging, New York University Medical Center, New York, NY

commentary on this research:
Ischemia and Multiple Sclerosis: Perfusion MR Imaging Provides Insight into an Underexplored Pathophysiology
Jack Simon, Guest Editorialist
a University of Colorado Health Sciences Center

Deep white matter ischemia


Sunday, December 13, 2009


EGCG (green tea): metal chelator, anti-inflammatory, and super anti-oxidant

December 13, 2009 at 3:54pm

Recent studies on the usage of EGCG (green tea extract) in Multiple Sclerosis patients have shown a benefit as a neuroprotective agent and an effective antioxidant.  

EGCG is also a known chelator of iron and is capable of removing iron and metals from the brain, since it passes through the blood brain barrier, even if taken orally.

Consider this wonderful, natural, inexpensive and non-toxic supplement or just drink the tea.  Something you can do today.

Neuroprotective molecular mechanisms of (-)-epigallocatechin-3-gallate: a reflective outcome of its antioxidant, iron chelating and neuritogenic properties.

Tea, the major source of dietary flavonoids, particularly the epicatechins, signifies the second most frequently consumed beverage worldwide, which varies its status from a simple ancient cultural drink to a nutrient component, endowed possible beneficial neuro-pharmacological actions. Accumulating evidence suggests that oxidative stress, resulting in reactive oxygen species generation, plays a pivotal role in neurodegenerative diseases, supporting the implementation of radical scavengers and metal chelating agents, such as natural tea polyphenols, for therapy. Vast epidemiology data indicate a correlation between occurrence of neurodegenerative disorders, such as Parkinson's and Alzheimer's diseases, and green tea consumption. In particular, recent literature strengthens the perception that diverse molecular signaling pathways, participating in the neuroprotective activity of the major green tea polyphenol, (-)-epigallocatechin-3-gallate (EGCG), renders this natural compound as potential agent to reduce the risk of various neurodegenerative diseases. In the current review, we discuss the studies concerning the mechanisms of action implicated in EGCG-induced neuroprotection and discuss the vision to translate these findings into a lifestyle arena.

http://forschungsberichte.charite.de/FOB_2006-2007/deutsch/PJ/PJ28373.html

Charite University in Berlin is currently conducting a clinical trial of EGCG in MS.  

http://clinicaltrials.gov/ct2/show/NCT00525668

EGCG and neuroprotection --

EGCG, has emerged as a potent neuroprotective agent for treatment of several neuropathological states associated with damaging effects of reactive oxygen species (ROS). EGCG has an inhibitory effect both on inflammation, by influencing T cell proliferation and inhibiting the activation of NF- B, and on neurodegeneration through its antioxidative potency as a free radical scavenger. In the present study we aim to evaluate the safety and neuroprotective effects of orally administered epigallocatechin-gallate in patients with relapsing-remitting MS in a multicentre, double-blind, randomised, stratified, placebo-controlled prospective 2-arm study. As a result of its anti-inflammatory and neuroprotective potency, EGCG should be significantly more effective than placebo in reducing the development of new contrast enhancing and T2 lesions on the one hand, but also in their conversion into T1-hypointense lesions ( black holes ), and in arresting the disease dependent acceleration of brain atrophy, and neuronal loss or dysfunction.

http://forschungsberichte.charite.de/FOB_2006-2007/deutsch/PJ/PJ28373.html

EGCG and metal chelation-

Evidence to link abnormal metal (iron, copper, mercury and zinc) metabolism and handling with Parkinson’s and Alzheimer’s diseases pathology has frequently been reported. The capacity of free iron to enhance and promote the generation of toxic reactive oxygen radicals has been discussed numerous times.

Metal chelation has the potential to prevent iron-induced oxidative stress and aggregation of alpha-synuclein and beta-amyloid peptides. The efficacy of iron chelators depends on their ability to penetrate the subcellular compartments and cellular membranes where iron dependent free radicals are generated. Thus, natural, non-toxic, brain permeable neuroprotective drugs, are preferentially advocated for “ironing out iron” from those brain areas where it preferentially accumulates in neurodegenerative diseases. This review will discuss the most recent findings from in vivo and in vitro studies concerning the transitional metal (iron and copper) chelating property of green tea and its major polyphenol, (−)-epigallocatechin-3-gallate with respect to their potential for the treatment of neurodegenerative diseases.

http://www.ncbi.nlm.nih.gov/pubmed/17447435


Jeff's been doing well with EGCG, going on five years now.  Ask your doctor or naturopath if it might be good for you, too.  Remember, I'm not a doctor, but I want to bring you the recent studies in MS.
Joan