What's the difference between nitrous oxide and nitric oxide?

January 30, 2012 at 2:53pm

I get this question a lot.  Thought I'd take the time to break it down in English (as opposed to chemistry talk, which still makes my head spin.) 

Nitric Oxide (NO) is NOT the same as Nitrous Oxide (N2O).

Nitric Oxide is one molecule of nitrogen, one of oxygen.

Nitrous Oxide has 2 molecules of nitrogen, and one of oxygen.

And that extra molecule of nitrogen changes the gas completely.

Nitrous Oxide (N2O) has been getting some press recently, since Demi Moore was hospitalized for inhaling canned Nitrous Oxide (in a form called "whippets") and having a seizure.  Nitrous oxide is used in aerosol cans, to propel whipped cream or cooking spray out of the bottle.

Nitrous Oxide (N20) is what they give you at the dentist's office, also called "laughing gas."  I had my wisdom teeth out on Nitrous Oxide, and it made me so loopy, I was laughing while the oral surgeon was sawing into my jawbone to remove my impacted wisdom teeth.  It's powerful stuff.  And should not be used recreationally.

What I started writing about and investigating for Jeff's health was nitric oxide.

Nitric Oxide (NO) is a tiny, 2 atom gas that is the hallmark of healthy vascular function.  It is the signaling factor that controls the body's vascular tone, and levels of inflammation, coagulation and oxidation.  It controls the endothelium, or the lining of all of our blood vessels.  It's good for you.

NO has been show to protect the heart, stimulate the brain, and kill bacteria, thus playing a pivotal role in a wide variety of diseases and conditions.

If the lining of our blood vessels become damaged and the NO levels become imbalanced, cells which should remain in the blood can leak through blood vessels and into adjacent body tissue. Some of the leaked cells can include proteins, such as the C-reactive protein, which is produced by the liver and causes inflammation. When NO in inhibited, endothelial signaling can become impaired, and disease may result. 

The Endothelial Health program discusses ways to enhance nitric oxide bioavailability in our bodies, and to maintain healthy immune systems and vascular systems.  This does not mean taking nitric oxide supplements....it means healthy living for healthy blood vessels.

Here's the program I created for Jeff, for those who may not have checked it out yet---

http://www.ccsvi.org/index.php/helping-myself/endothelial-health

Chemistry is important...one extra molecule can make a big difference!

Joan

Vascular inflammation in MS

January 24, 2012 at 11:42am

The Buffalo team has recently published a study on Lp-PLA2 levels in the blood of people with MS.

Lp-PLA2 is an enzyme that circulates in the blood and attaches to cholesterol in the blood stream.  It is an important marker of inflammation, just like C reactive protein.

Here's more information on Lp-PLA2

http://www.c-reactive-protein.com/103.htm

Lp-PLA2 is also an important marker in endothelial dysfunction.  This means that the lining of the blood vessels is breaking down and inflamed.

What the Buffalo researchers found is that this enzyme shows up in the blood of pwMS---and levels are significantly higher than in controls.

Lp-PLA2: Inflammatory Biomarker of Vascular Risk in Multiple Sclerosis.

A member of the A2 phospholipase superfamily, the enzyme lipoprotein-associated phospholipase A2 (Lp-PLA2), is involved in atherogenic processes. Lp-PLA2 mass and activity were measured by the enzyme-linked immunosorbent assay and by a colorimetric method, respectively, and compared among 63 multiple sclerosis (MS) patients and 47 age-matched healthy controls (HCs). Lp-PLA2 plasma levels were significantly higher in MS patients (236.7 ± 10 ng/ml) compared to HCs (197.0 ± 7 ng/ml) (p = 0.003)

http://www.ncbi.nlm.nih.gov/pubmed/22246459

Here is a study of plasma levels of Lp-PLA2 in those with coronary disease and normals.  Lp-PLA2 is a marker of endothelial dysfunction. ( Note that pwMS had a 236.7 ng/ml level, and those with coronary arterial disease had a 246.2 ng/ml level.  Normals have around a 200 ng/ml level.)

Hypoxia reactivates latent EBV

January 22, 2012 at 10:06am

Perhaps researchers need to look more closely at hypoperfusion, or slowed cerebral blood flow, in MS.  Lower levels of oxygen can affect the brain in many ways.

There has been much made about the connection of the Epstein Barr virus (EBV) and MS.  Most people carry the latent, or dormant version of this virus.  Nearly 95% of all adults carry the EBV virus.

A recent post mortem study showed reactivated EBV cells in active MS lesions.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118531/

In the seven MS patients' postmortem brain tissue studied, active MS lesions all contained Epstein-Barr virus infected cells.

Such cells weren't unique to MS, but were also detected in CNS tissue from two control patients with stroke, which the researchers pointed out is also a disease in which inflammation plays an important role.

Notably, Epstein-Barr virus-positive cells were present in much higher numbers in active MS lesions than expected in peripheral blood B cells, "which suggests that these cells are recruited to or accumulate in CNS infiltrates," Lünemann noted.

http://www.everydayhealth.com/multiple-sclerosis/0103/latent-virus-sparks-inflammation-in-ms.aspx

What might reactivate this virus and cause it to replicate in the B cells?

Why were these cells also in the brains of stroke patients?  It's not just about inflammation or the immune system.

Hypoxia.  Lack of oxygen reactivates EBV infection.  The ischemic injury of slowed blood flow, caused be stroke or CCSVI,  could reactivate EBV cells.

EBV in latent infection can be activated to lytic infection by hypoxia treatment.

http://www.journalofclinicalvirology.com/article/S1386-6532(06)00244-7/abstract

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC419879/

In fact, researchers have found a link between pwMS who smoke, and the levels of EBV antigens, or ENBA titers. 

Perspective

January 9, 2012 at 11:27am

In reading postings on the internet, checking in on the CCSVI advocacy groups, and trying to assess what's going on, it's easy to be discouraged these days.

The science and investigation of venous malformations in MS is moving too slowly for many.  People with MS have to deal with their progressive disease and time limitations.  The language of many MS specialists and neurologists is inflammatory and negative towards this research.  There are misguided and badly researched stories in the media.  Or complete oblivion of the vascular research and cheerleading for the pharmaceutical industry in the media.  There are allegations made between groups of people who should be working to help others. There are medical and tourism organizations looking for ways to make money off CCSVI.  Calls of quackery, angry words, hateful speech, negativity.  Lots of drama going on.

and it's discouraging.

But underneath all of the commotion, there is actual progress being made in understanding multiple sclerosis.

I want to try and focus on the progress and the positive today, and give some perspective, for my own spirit, as well as for others.  Because MS is our common enemy.  It is why we're here.  Life has enough drama.

Here is the explanation of the importance of the upcoming International Society for Neurovascular Disease (ISNVD) convention from the program--

 The meeting as a whole will primarily focus on advancing understanding of the recently described condition called CCSVI and its relationship to multiple sclerosis, other neurologic disorders and aging. A great amount of fresh and original information will be presented on this condition. Included are 5 scientific sessions on CCSVI that will further discuss the role of imaging techniques, diagnostic guidelines and standard consensuses to be used for diagnosing CCSVI.

Of particular interest is the session reporting first postmortem study results that assessed jugular and azygos venous pathology. Dr. Fox from the Cleveland Clinic will present some of his recent findings. Basic scientific and hemodynamic contributions, lectures and abstracts on the CCSVI hypothesis are sure to generate a significant level of interest among the participants. In particular, the session about computational fluid dynamics and measuring flow is aimed at attracting most of the conference attendees.

Iron and gray matter - What do we know?

January 3, 2012 at 8:52am

As more and more MS reseachers come forward and explain how MS appears to be a disease of the gray matter first---before white matter lesions appear---it is vital that we look at gray matter structures in the MS brain, to see what is different in the MS brain when compared to normal brains.

This post will be long, but I believe it's important to understand MS research as it stands today, the beginning of 2012.

Last month, University of Texas researchers published in the Journal of Neuroscience--reporting that the thalamus, the deep gray matter of the brain, is smaller and atrophied in people with MS when compared to normal brains, and that this loss of deep gray matter tissue happens at the beginning of the disease, early on and before any white matter lesions are detected.

http://health.usnews.com/health-news/family-health/brain-and-behavior/articles/2011/12/30/multiple-sclerosis-may-cause-changes-in-thalamus-study

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

A recent paper from Hubbard, Haacke, et al shows how stenotic veins creates slowed jugular return of blood in pwMS.  Blood flow thru the brains of pwMS is much less than those with non-stenotic veins.  This may be an indication of hypoperfusion and decreased oxygenation, and we'll be hearing more about that from the Hubbard Foundation later this year.

Dr. E. Haacke has also noted an early change in the gray matter of MS brains--abnormally high iron content.

Dr. E. Mark Haacke has been looking at the gray matter in MS brains for almost a decade.  He is one of the inventors of SWI technology, an imagery system that can visualize iron deposed into brain tissue.

This is from his new paper is published in the American Journal of Neuroradiology--

Fifty-two patients with MS were recruited to assess abnormal iron content in their basal ganglia and thalamas (THA) structures. One hundred twenty-two healthy subjects were recruited to establish a baseline of normal iron content in deep gray matter (GM) structures.

RESULTS: A clear separation between iron content in healthy subjects versus patients with MS was seen. For healthy subjects 13% and for patients with MS 65% showed an iron-weighting factor.

The results for those patients younger than 40 years are even more impressive. In these cases, only 1% of healthy subjects and 67% of patients with RRMS showed abnormally high iron content.

Currently, there is an increased interest in studying how GM is affected and particularly deep GM involvement in MS when iron deposition has been observed.  

Brain iron accumulation in neurodegenerative diseases, including MS, is not new and has been shown histologically in the past.  In MS, its source is likely due to myelin or oligodendrocyte debris, concentrated iron in the macrophages, or as a product of local microhemorrhages following venule wall damage.  As the wall breaks down, free iron may escape outside the vessel. This process has typically been seen in the basal ganglia, neurons, oligodendrocytes, macrophages, and microglia.6 Generally, free iron is known to lead to the formation of highly reactive hydroxyl radicals that can trigger cell membrane dysfunction and chronic microglial activation. Thus, iron from any of the above-mentioned sources could lead to inflammation and a further buildup of iron, causing the system to be self-sustainable.  

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

What Dr. Haacke is explaining is that we've known about iron in gray matter tissue in MS brains and other neurodegenerative diseases for awhile.   This is not new information.   Dr. Haacke explains that there are three possible causes of this iron in the MS brain.  The iron could come from one, two, or all three of these sources.