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

Monday, November 24, 2014

NASA, the Drain Brain and Astro Samantha

Right now, on the International Space Station, the first female Italian astronaut, Samantha Cristoforetti, is settling into her new home.  Over the weekend, Cristoforetti left the earth's orbit from a rocket launch in Kazakhstan.  As she joins other international astronauts as part of Expedition 42/43, Cristoforetti will be conducting a major research experiment, using the technology developed by Dr. Paolo Zamboni.   This study, called Drain Brain, is a collaboration between NASA and the Italian Space Agency.  It will be using strain-gauge plethysmography (a neck collar which measures blood flow) to analyze cerebral drainage in space.  Here's why, as explained on the NASA site.

On Earth, blood flows down from a person’s brain back toward the heart thanks in part to gravity, but very little is known about how this flow happens without gravity’s effects.  Many crew members report headaches and other neurological symptoms in space, which may be related to the absence of gravity acting on blood flowing through the veins. Drain Brain uses a special neck collar to measure blood flow from the brain, to help researchers understand which physical processes in the body can compensate for the lack of gravity to ensure blood flows properly.

Space Applications
Drain Brain studies how blood returns to the heart from the brain through veins in an astronaut’s neck. This can help scientists better understand the mechanisms that ensure proper blood flow in microgravity. ISS Crewmembers report a variety of neurological symptoms that may be related to changes in this blood flow. The project also studies how blood flow changes in response to crewmember schedules in space, which do not follow the typical day-night schedule of most humans on Earth.
Earth Applications
The instrument developed for Drain Brain, called a strain-gauge plethysmograph, does not require any surgery or special knowledge, which could make it an ideal tool for monitoring patients with a wide range of heart or brain disorders. In previous research, the scientists who developed the instrument identified a possible link between some neurodegenerative disorders, such as multiple sclerosis, and blockage of veins that connect to the brain. Researchers are also interested in studying the connection between these brain-related veins and cognitive disorders, such as Alzheimer’s disease. Drain Brain’s novel system could be a new way to screen for this vein abnormality.
As NASA explains, Dr. Zamboni has been using this neck collar to study people with multiple sclerosis.  And he has found that in people with MS, when compared to healthy controls, there is marked delay in drainage of the brain when patients go from lying down to upright.  Dr. Zamboni, who also discovered Chronic Cerebrospinal Venous Insufficiency (CCSVI) in MS, believes that extracranial obstructions are causing this delay in blood leaving the brain to travel back to the heart.  

What I find particularly ironic in all of this, is the fact that NASA and the smartest rocket scientists on the planet are eager to use Dr. Zamboni's technology, to understand how zero gravity and delayed venous return is affecting the brains and eyes of their astronauts, yet neurologists won't even consider the correlation of slowed venous flow and MS.  
From the abstract of Dr. Zamboni's study:
The rate at which venous blood discharged in the vertical position (EG) was significantly faster in the controls (2.73 mL/second ± 1.63) compared with the patients with CCSVI (1.73 mL/second ± 0.94; P = .001). In addition, respectively, in controls and in patients with CCSVI, the following parameters were highly significantly different: FT 5.81 ± 1.99 seconds vs 4.45 ± 2.16 seconds (P = .003); FG 0.92 ± 0.45 mL/second vs 1.50 ± 0.85 mL/second (P < .001); RV 0.54 ± 1.31 mL vs 1.37 ± 1.34 mL (P = .005); ET 1.84 ± 0.54 seconds vs 2.66 ± 0.95 seconds (P < .001). Mathematical analysis demonstrated a higher variability of the dynamic process of cerebral venous return in CCSVI. Finally, ROC analysis demonstrated a good sensitivity of the proposed test with a percent concordant 83.8, discordant 16.0, tied 0.2 (C = 0.839).

CONCLUSIONS: 

Cerebral venous return characteristics of the patients with CCSVI were markedly different from those of the controls. In addition, our results suggest that cervical plethysmography has great potential as an inexpensive screening device and as a postoperative monitoring tool.

Some of the neurological issues being reported by astronauts living in zero gravity include loss of vision, fatigue and headaches,  possibly due to increased intracranial pressure.  One in five astronauts report changes in vision after returning to earth, and many problems involve the optic nerve, also an area of change in multiple sclerosis, which could be related to disturbed venous flow.  After five to six months in zero gravity, 20% of the astronauts are noting vision problems.
21 U.S. astronauts that have flown on the International Space Station for long flights (which tend to be five to six months) face visual problems. These include “hyperopic shift, scotoma, and choroidal folds to cotton wool spots, optic nerve sheath distension, globe flattening and edema of the optic nerve,” states the University of Houston, which is collaborating with NASA on a long-term study of astronauts while they’re in orbit. http://www.universetoday.com/114161/eye-problems-from-space-affect-at-least-21-nasa-astronauts-study/
"What we are seeing is flattening of the globe, swelling of the optic nerve, a far-sighted shift, and choroidal folds," said Dr. C. Robert Gibson, one of authors of the study published in the October 2011 issue of Ophthalmology, the journal of the American Academy of Ophthalmology. "We think it is intracranial pressure related, but we're not sure; it could also be due to an increase in pressure along the optic nerve itself or some kind of localized change to the back of the eyeball."
 

These black spots, swelling of the optic nerve, and changes to vision are seen in increased intracranial pressure, as well as multiple sclerosis.  My husband had all of these issues, and a loss of peripheral vision, as a child.  It would decades before he would be diagnosed with MS, and after that have a repair of his malformed venous system.

It will be interesting to learn what the Drain Brain study teaches us about venous return and the long terms affects of zero gravity. It is absurd to claim that slowed venous drainage does not matter to brain and eye health.

Here's to rocket scientists!  Here's to Samantha Cristoforetti!  You can follow her on twitter @AstroSamantha   Here's to Dr. Zamboni!  
Here's to answers.

Joan











Wednesday, November 19, 2014

How to remyelinate your own brain. New research

New research from the Karolinska Institute shows us, once again, that human and mouse brains are not the same.  Past assumptions about remyelination have been incorrect.  Attempting to model remyelination in the human brain using a mouse model simply does not work.

But there are things humans can do to remyelinate their own brains---and it's all about using the brain, and plasticity.

Here's the new research, which is calling into question all MS specialists thought they knew about myelin.
http://www.cell.com/cell/abstract/S0092-8674(14)01298-7



The brain's plasticity and its adaptability to new situations do not function the way researchers previously thought, according to a new study published in the journal Cell. Earlier theories are based on laboratory animals, but now researchers at Karolinska Institutet in Sweden have studied the human brain. The results show that a type of support cell, the oligodendrocyte, which plays an important role in the cell-cell communication in the nervous system, is more sophisticated in humans than in rats and mice - a fact that may contribute to the superior plasticity of the human brain. 

The learning process takes place partly by nerve cells creating new connections in the brain. Our nerve cells are therefore crucial for how we store new knowledge. But it is also important that nerve impulses travel at high speed and a special material called myelin plays a vital role. Myelin acts as an insulating layer around nerve fibres, the axons, and large quantities of myelin speed up the nerve impulses and improve function. When we learn something new, myelin production increases in the part of the brain where learning occurs. This interplay, where the brain's development is shaped by the demands that are imposed on it, is what we know today as the brain's plasticity. 

Myelin is made by cells known as oligodendrocytes. In the last few years, there has been significant interest in oligodendrocytes and numerous studies have been conducted on mice and rats. These studies have shown that when the nerve cells of laboratory animals need more myelin, the oligodendrocytes are replaced. This is why researchers have assumed that the same also applies in humans. Researchers at Karolinska Institutet and their international collaborators have shown that this is not the case. In humans, oligodendrocyte generation is very low but despite this, myelin production can be modulated and increased if necessary. In other words, the human brain appears to have a preparedness for it, while in mice and rats, increased myelin production relies on the generation of new oligodendrocytes.

In the study in question, researchers have studied the brains of 55 deceased people in the age range from under 1 to 92 years. They were able to establish that at birth most oligodendrocytes are immature. They subsequently mature at a rapid rate until the age of five, when most reach maturity. After this, the turnover rate is very low. Only one in 300 oligodendrocytes are replaced per year, which means that we keep most of these cells our whole lives. This was apparent when the researchers carbon-dated the deceased people's cells. The levels of carbon-14 isotopes rose sharply in the atmosphere after the nuclear weapons tests during the Cold War, and they provided a date mark in the cells. By studying carbon-14 levels in the oligodendrocytes, researchers have been able to determine their age. 

"We were surprised by this discovery. In humans, the existing oligodendrocytes modulate their myelin production, instead of replacing the cells as in mice. It is probably what enables us to adapt and learn faster. Production of myelin is vital in several neurological diseases such as MS. We now have new basic knowledge to build upon," says Jonas Frisén, PhD, Professor of Stem Cell Research at the Department of Cell and Molecular Biology at Karolinska Institutet.

Human and mice brains do not remyelinate in the same way.

That's right.  By keeping the mind active, learning new skills and firing your neurons, you can potentially remyelinate your own brain.  The problem is, there is no way for pharma to monetize this--so, you probably won't be hearing about this research in the mainstream press.  Because there is nothing to sell you.  No prescription.

After a comment below on how plasticity can't possibly remyelinate the MS brain, because it's "too easy" a solution--I've decided to add recent research that shows how plasticity has been noted in MS recovery.

Cortical plasticity predicts recovery from relapse in multiple sclerosis. http://www.ncbi.nlm.nih.gov/pubmed/24263385
Neuroplasticity and functional recovery in multiple sclerosis
http://www.nature.com/nrneurol/journal/v8/n11/full/nrneurol.2012.179.html

Increasingly sophisticated brain imaging techniques indicate that brain plasticity - the brain's ability to reorganize neural pathways based on new experiences - is the compensatory mechanism largely responsible for the clinical remissions that are typical of early stages of relapsing remitting MS. The adult brain is capable of both functional and structural plasticity - processes that are operational in normal brain development such as learning and memory5.
Interestingly, functional and structural changes can also take place in the brain after injury or damage, and brain plasticity is seen to act as an adaptive mechanism to compensate for a loss of function6. Following tissue damage, the structure and function of undamaged parts of the brain can be remodeled and shaped by the sensorimotor experiences of the individual in the weeks to months following injury7, 8.

Here's more on neuroplasticity from Dr. Norman Doidge on his research and book, "The Brain that Changes Itself."  Learning changes the connection between the neurons in our brain cells.  Activity changes and heals the brain.
https://www.youtube.com/watch?v=t3TQopnNXBU


Want to remyelinate your brain?  Learn a new language.  Take up a new, challenging hobby.  Paint a picture.  Do a crossword puzzle.  Read books about new topics.  Learn a musical instrument (which is especially helpful for the corpus callosum)   Move as much as you are able, and if you can,  combine a cardiovascular pursuit with learning--like taking a ballroom dancing class, learning a new sport, practicing yoga.  It's all possible.

Don't wait for your neurologist to tell you.
Do this for yourself, your brain.
And please let me know what new skill you're mastering---

be well!
Joan







Saturday, November 8, 2014

Genetics and MS

Every few months, there is a news story lauding the fact that researchers have finally verified that MS is autoimmune.  These stories have a similar theme.  MS is most certainly autoimmune, because the connections made between MS and genes are all found in the immune system.  

But that's because it is the only place researchers are looking.  The major histocompatilbility complex (MHC) region remains the area under exploration, now 40 years since its initial discovery.

And they continue to get research grants from pharmaceutical companies to continue to look at the same location, because making this connection to the autoimmune theory advances drug sales.

In fact, the connection to heretability and genetics in MS is rather slim.  In identical twins, genetic risk is less than 1/3 if one twin has MS.  

...there is a 2% to 4% elevated genetic risk in siblings of patients with MS and a 30% greater risk in identical twins.
http://www.medscape.com/viewarticle/833070



There was a recent story in the NY Times regarding research into a potential genetic link found in those who die due to Ebola infections.  Researchers Angela L. Rasmussen and Michael G. Katze of the University of Washington  found a problem with blood vessels, which were allowing immune cells open access and an overblown reaction to the virus. That's right.  Death from Ebola happens because of a break down of the endothelium, or the lining of blood vessels.  And there is a potential genetic link.
http://www.nytimes.com/2014/10/31/health/genes-influence-ebola-infections-in-mice-study-suggests.html?_r=1

About two-thirds of people who die from Ebola never develop the terrifying hemorrhages that appear in others a day or two before death, in which eyes turn fiery red, gums bleed, red dots emerge on the skin as blood seeps out of capillaries, and blood appears in vomit and diarrhea. Many mice, too, die of Ebola without hemorrhages.

The mouse studies indicate the animals that hemorrhage and — by implication, humans— die because their immune systems overreact to the virus. The result is an inflammatory response that makes cells leak fluids and white blood cells, and makes tissues and organs deteriorate. Many die at that point. In those mice — or humans — that survive long enough, the researchers propose, blood eventually starts to seep out of vessels.

In fact, researchers found a genetic link to two specific genes, which were allowing for the overblown inflammatory response.


The mouse studies showed that animals that died after bleeding had an overblown inflammatory response to the virus. They also had low activity of two genes, Tie1 and Tek, that made their blood vessels more permeable. The leaky vessels allowed white blood cells to stream out, escalating the inflammatory response and causing a chain reaction of damaging immune system chemicals that destroyed organs. 


She said that “a big take-home lesson from the paper” is that genetics plays a major role in determining the outcome of a mouse’s Ebola infection. By inference, she said, genetics probably plays the same role in humans.


(for those who enjoy learning more, here is a paper on how Tie1 and Tie2 (TEK) are involved in vascular permeability.)
http://www.bloodjournal.org/content/93/6/1969?sso-checked=true



An overblown inflammatory response due to a breakdown of the lining of the blood vessels.  Sounds like something MS researchers might want to investigate, especially considering the recent research of Dr. Yulin Ge of NYU.

At the ISNVD conference in February 2014, Dr. Yulin Ge discussed how 7T MRI technology is allowing us to see tiny hemorrhages in the MS brain which occur before demyelination.  This further elucidates the microvascular connection to MS.
From his abstract at the ISNVD:

Being the most common demyelinating disease of the central nervous system, multiple sclerosis (MS) MS has a significant microvascular pathological component as a consequence of the perivascular inflammation. The role of vascular pathology in MS was suggested long ago. Now there is accumulating evidence of a primary vascular pathogenesis in MS. In vivo studies of vascular and hemodynamic impairment in MS may provide insights into the etiology and pathophysiology of MS and offer the potential metrics for assessment of outcome of the disease. 

The definition of insanity is repeating the same act over and over and expecting different results.  Continually searching in the same place for a genetic link to MS is not bringing us any closer to understanding MS aetiology.  It's making money for research labs and drug companies, but it is not bringing health and healing to people with MS.

Thanks to the ISNVD, for looking beyond the autoimmune paradigm.
Joan