This Is MS Multiple Sclerosis Community: Knowledge & Support

hot off the presses, cheer

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my approach: no meds so far - just balanced whole foods (partial 'paleo', much less outright elimination), science, supplements, & bloodwork
my regimen - www.thisisms.com/ftopict-2489.html
www.whfoods.com, www.nutritiondata.com

new information on the endothelium?
Just buy my book, JL...oh, wait.
You don't have to
carry on, all

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Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS

Annesse, I hope you continue to post here. I really like the way you present your information.

Thank you Bethr~
I have been so busy lately. We STILL do not have our 2nd edition out. I am not very good at multi-tasking, so I have been trying to stay focused on getting the next edition out. I thought I could post some information on the lung involvement in MS.


Here is some information on the lung dysfunction found in MS.

http://ms.about.com/od/signssymptoms/a/ ... ry_gen.htm

I can make some additional posts on the reason for this in the next few days.

Hi,

I'm a little bit cautious about the conclusion about lung function this article comes to. Around the time that I was diagnosed with MS and had some quite bad attacks I had a constant hacking cough, laryngitis and constant problems breathing. The doctors all said I had some unusual "rare" form of asthma and prescribed some very powerful cough mixtures that were quite dangerous.
As it turned out, I was mouth breathing due to a deviated septum which caused tonsilitis, rhinitis, sinusitis and breathing problems. I required a septoplasty, tonsilectomy and a partial resection of the soft palette to fix me up. The ENT surgeon said my tonsils were just bags of pus.
The line I follow is that B Cells that are in the same tissue are infected with EBV and that leads to a cascade resulting in MS. Maybe the surgery I had alleviated my MS (which still required other treatment) because it removed infected tissue.
The article doesn't establish in my mind that the relationship between MS and breathing has been properly established and other causes have been correctly discounted. My own view is infected tonsil tissue could lead to breathing difficulties and the infection may have a basis involving EBV but the article jumps to conclusions. In my own case the lungs were unaffected but the doctors consistently misdiagnosed. All they had to do was send me to an ENT specialist.
I would be interested in knowing if others have breathing problems because that is worth knowing.
I love your work Annesse but I don't like this article based on the really rough experience I had years ago.

Regards

Hi Scott1~I can really understand where you are coming from. I was just using the article to introduce the topic of lung dysfunction in MS. Here is a study that connects MS and COPD. As the authors state, "The study was undertaken to investigate any possible comorbidity of COPD and MS, thus indicating common inflammatory vulnerability." The conclusion states that, "COPD and MS have an inflammatory vulnerability in common."

http://www.ncbi.nlm.nih.gov/pubmed/18351419

Hi Annesse,

I think I'll remain the sceptic on this avenue. I've not really heard of a strong relationship between MS and lung dysfunction before and the link you gave doesn't fill me with confidence that it's on the right track. I think they are too casual about what they are looking at. COPD is predominately a smokers disease. Autopsies have found scarring on the brain as a sign of MS but they didn't find lung damage as a reliable marker of MS. I would accept something relating inflammation of tonsil tissues and lymph node as you can get convulsive coughing from that but I don't think lungs are going to be a reliable marker.

Good luck with the book launch.

Regards

Hi Scott1~Do you have a take on the white matter lesions found in COPD?

http://jnnp.bmj.com/content/75/5/733.abstract

I agree with your comment on the lungs not being a reliable marker. I am just trying to show that all of these diseases share common features. The study authors believe that MS and COPD share an inflammatory component. I believe they do too. I am going to be posting more evidence on this soon.

Hi Annesse,

You would need to test the pathology of the lesions on a decent sized sample to start to draw a conclusion but they are also associated with age, cardiovascular disease, strokes and injury which would all need to be identified and discounted. Migranes also pop up with an association.
Oxygen deprivation could cause plaques and different pathogens could play a role as well.
I spent two years visiting a hypobaric chamber which I felt did reverse some plaque accumulation and I presume gave anaerobic infections a bad time. The advantage of that process is it will lead to revascularisation but it does cure MS depite what it's proponents say.

Regards

Here are some additional studies on MS and lung involvement.

Respiratory Involvement In Multiple Sclerosis
Howard RS; Wiles CM; Hirsch NP; Loh L; Spencer GT; Newsom-Davis J
Brain 1992 Apr;115 ( Pt 2):479-94
National Hospital for Neurology and NeuroSurgery, Batten/Harris Unit, London, UK
--------------------------------------------------------------------------------
IS - 0006-8950, UI - 92298187
Abstract

The abstract states, "Respiratory complications occur in advanced Multiple Sclerosis (MS) but may also complicate acute relapses earlier in the disease."

We present 19 patients with MS who developed Respiratory Complications at a mean of 5.9 (range 1-12) yrs after the onset of Neurological symptoms.

Fourteen patients developed Severe Respiratory Insufficiency presenting with a combination of reduced Forced Vital Capacity (FVC), Hypoxaemia or Hypercapnia (12 patients) and Respiratory Arrest (four patients).


Hi Scott1~ Once again, I agree, but why are white matters lesions associated with COPD? I think the next study will show the connection to COPD, MS, white matter lesions and the inflammatory component the other study researchers believe is common to both diseases.

It is entitled, " Hyperhomocysteinaemia and poor vitamin B status in chronic obstructive pulmonary disease." The researchers found that COPD patients had low vitamin B12 and as a consequence, increased homocysteine. These are common denominators between these two diseases. Lack of B12 will lead to white matter lesions and high homocysteine is a potent inflammatory.

http://www.ncbi.nlm.nih.gov/pubmed/19282159

Hi Annesse,

I still think there are too many variables to draw the conclusion. Have a look at this article using a large sample that looked at serum B12, folic acid etc and smokers and you would almost be forgiven for concluding that smoking was good for your B12 level!

http://journals.cambridge.org/article_S1368980003000922

To get to the true relationship the researchers need to eliminate the extraneous variables and I don't see that they have.

Regards

Hi Scott1~This information is from the study. I think they did adjust for smoking.

We performed a case-control, cross-sectional study of 42 patients with COPD and 29 control subjects. Folate, vitamin B12, vitamin B6, tHcy, renal function, C-reactive protein, blood gases and lipids were measured in patients and controls. COPD patients had higher plasma tHcy (median: 13.9mumol/l, interquantile range [IQR]: 12.1-18.5 versus 11.5, IQR: 10.1-14, p=0.002) and lower circulating folate (median: 2.5ng/ml, IQR: 1.2-3.3 versus 2.8, IQR: 2.1-4 of controls, p=0.03) than controls had. Compared to the control group, COPD was associated with higher tHcy concentrations also after adjusting for smoking, heart failure, renal function and C-reactive protein with logistic regression analysis (OR 1.36, 95% CI 1.06-1.72, p=0.01). In the COPD group, low levels of folate (beta=-0.27, p=0.02) and vitamin B12 (beta=-0.24, p=0.04), and hypertriglyceridaemia (beta=0.580, p<0.0001) were independent predictors of the presence of high tHcy concentrations in a multiple linear regression model (adjusted R(2)=0.522).

Also, there are additional studies that confirm high homocysteine in COPD. Here is one.

Plasma Homocysteine is Elevated in COPD Patients and is Related to COPD Severity
Seemungal, T.A., J.C. Lun, G. Davis, C. Neblett, N. Chinyepi, C. Dookhan, S. Drakes, E. Mandeville, F. Nana, S. Sethake, C.P. King, L. PintoPereira, J. Delisle, T.M. Wilkenson, J.A. Wedzicha. 2007. Int J Chron Obstruct Pulmon Dis 2(3):313-

Here is the conclusion from the study.

Conclusions: Plasma homocysteine is significantly elevated in COPD patients relative to age and sex-matched controls and is related to serum CRP and COPD severity.

Hi Annesse,

Lets agree to disagree. I still don't like the way they draw the conclusion they come to.

I found this interesting article today. The Australian Institute they refer to (Walter and Eliza Hall)would be in the top 10 worldwide. I noticed there is a company working on an MS drug based on this active compound. Have you covered this in your work to date?

http://www.lifescientist.com.au/article ... andidate_/

Regards

Hi Scott1~No, I have not heard of it. I don't use extracts, just whole herbs.

Two other diseases that are associated with MS also have an association with COPD. They are RA and diabetes.
We have already discussed the overlap between MS and RA. Reporting in the May 2006 issue of the Journal of Rheumatology, researchers identified an association between rheumatoid arthritis and MS. They state, "Since a great proportion of our patients developed MS first and subsequently RA, the best explanation for these cases is a predispositon in MS patients to develop another autoimmune disease with common etiologic cofactors."

RA patients also have low B12 and white matter lesions.
They also have high homocysteine.
And they also have an association with COPD.

Abnormal Homocysteine Metabolism in Rheumatoid Arthritis
Roubenoff, R., P. Dellaripa, M.R. Nadeau, L.W. Abad, B.A. Muldoon, J. Selhub, I.H.
Rosenberg IH. 1997. Arthritis Rheum. 40(4):718-22.
Objective: Assess total homocysteine (tHcy) metabolism in patients with rheumatoid
arthritis (RA).
Methods: Assessments were performed to determine the fasting levels of tHcy and
the increase in tHcy in response to methionine (Met) challenge in blood samples from
28 patients with RA and 20 healthy age-matched control subjects.

Conclusion: Elevated tHcy levels occur commonly in patients with RA, and may
explain some of the increased cardiovascular mortality seen in such patients. Studies
of the prevalence and mechanism of hyperhomocysteinemia in RA are warranted.

Here is some book info.

"Now, a new study presented at the EULAR 2011 Annual Congress
(European League Against Rheumatism) has confirmed a link between
rheumatoid arthritis and COPD. An article on this study in News-Medical
states, “Patients with rheumatoid arthritis are two times more likely to
have COPD than healthy controls. The study of 15,766 patients with RA
and 15,340 controls found that the prevalence of COPD was significantly
higher in RA patients than healthy controls. Interestingly, the link was still
significant after risk factors common in both RA and COPD patients, such
as smoking, obesity and socioeconomic status, were controlled for,” (News-
Medical, 2011). The large, population-based study was performed using the
patient database of Israel’s largest healthcare provider, Clalit Health Services.
The researchers concluded, “We know that similar changes in core
physiological processes cause symptoms in RA and COPD…..”
COPD and RA share a common link. This link would explain the “similar
changes in core physiological processes” between RA and COPD. The link
is homocysteine."

Patients with lupus and scleroderma also have lung involvement associated with elevated levels of homocysteine.

The following study from the Journal of Rheumatology states, “In patients with scleroderma the homocysteine concentration was significantly higher than in controls. We found a significant association between plasma homocysteine concentration and severity of lung involvement …” The researchers believe that elevated homocysteine may worsen injury of the endothelium. They concluded, “Our data support the hypothesis that homocysteine could be involved in the pathogenetic process of scleroderma pulmonary lung involvement.”
Homocysteine Plasma Concentration is Related to Severity of Lung Impairment in Scleroderma
Caramaschi, P., N. Martinelli, D. Biasi, A. Carletto, G. Faccini, A. Volpe, M. Ferrari, C. Scambi, L.M. Bambara. 2003. J Rheumatol 30(2):298-304.
Objective: To investigate the correlation between plasma concentration of total homocysteine and pulmonary involvement in patients with limited or diffuse scleroderma (systemic sclerosis, SSc).
Conclusion: High level of homocysteinemia is associated with an increased risk of pulmonary disease in patients with scleroderma. We hypothesize that hyperhomocysteinemia may worsen injury of the endothelium, a key lesion in scleroderma disease, favoring the development of lung involvement. “Our data support the hypothesis that homocysteine could be involved in the pathogenetic process of scleroderma pulmonary involvement”. (J Rheumatol 2003;30:298-304).