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The Marshall Protocol Study Site > PROF. MARSHALL'S PERSPECTIVE > Prof. Marshall's Perspective > Antibiotic use increases the risk of Multiple Sclerosis


Antibiotic use increases the risk of Multiple Sclerosis
 Moderated by: Prof Trevor Marshall
 

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Prof Trevor Marshall
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 Posted: Wed Nov 23rd, 2011 14:20

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A new paper concludes "underlying infections may be causally associated with MS," although I had expected them to incorrectly conclude that antibiotic over-use was the cause :) :) I am getting somewhat cynical these days :) :)


"Use of penicillin and other antibiotics and risk of multiple sclerosis: a population-based case-control study"

http://www.ncbi.nlm.nih.gov/pubmed/21920946

"A 2006 study from the United Kingdom found that penicillin use may decrease the risk of multiple sclerosis (MS). To confirm this finding, the authors conducted a nationwide case-control study in Denmark, using the Danish Multiple Sclerosis Registry to identify 3,259 patients with MS onset from 1996 to 2008, and selected 10 population controls per case (n = 32,590), matched on sex and age. Through the National Prescription Database, prescriptions for antibiotics redeemed from 1995 to 2008 and before the date of first MS symptom/index date were identified. Conditional logistic regression analysis was used to compute odds ratios associating antibiotic use with MS occurrence. In total, 1,922 patients (59%) redeemed penicillin prescriptions before the index date and 2,292 (70%) redeemed any type of antibiotic prescription. Penicillin use was associated with an increased risk of MS (odds ratio = 1.21, 95% confidence interval: 1.10, 1.27). Use of any type of antibiotic was similarly associated with an increased risk of MS (odds ratio = 1.41, 95% confidence interval: 1.29, 1.53). The odds ratios for different types of antibiotics ranged between 1.08 and 1.83. Thus, this study found that penicillin use and use of other antibiotics were similarly associated with increased risk of MS, suggesting that the underlying infections may be causally associated with MS."

..Trevor..
 

seanlane
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 Posted: Wed Nov 23rd, 2011 14:51

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I thought that it was both....that antibiotics like penicillin promoted the formation of l-form bacteria from the bacteria targeted?



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Aunt Diana
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 Posted: Wed Nov 23rd, 2011 19:10

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I'm not sure I understand the article but if it is saying that the use of penicillin may curtail the incidence of MS this only makes sense to me.

My reasoning is this: The only reason Lyme disease was brought to the public's attention was one mother who had noticed that the children in one school district in Lyme, Conn. who were prone to "rheumatoid arthritis" were given antibiotics but the children in the other school district were not.
The children from the other school had no such benefit since the doctor did not prescribe antibiotics to the children. The children who were not given abx went on to become disabled with crippling arthritis.

The doctor for one school regularly prescribed antibiotics to his patients who exhibited those symptoms, while the other school district doctor did not.

So I can see why prescribing penicillin at the onset of a bacterial infection would lead to lesser incidence of chronic disease.



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seanlane
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 Posted: Wed Nov 23rd, 2011 20:47

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I believe that the older study in 2006 is implying that treatment with penicillin is associated with fewer incidents of MS.

The newer study here claims the opposite...(which I am more inclined to agree with:))

Last edited on Wed Nov 23rd, 2011 21:10 by seanlane



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ChrisMavo
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 Posted: Thu Nov 24th, 2011 00:07

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Very interesting study that fits perfectly with my suspicions that the use of penicillin may have caused my ALS decades later!  If this correlation of penicillin use was found for MS, it most likely is also true for ALS.   It has been proven that penicillin generates l-form bacteria and that is what I believe is the root cause of ALS.  When I was younger I got chronic tonsillitis and my family doctor did not believe in removing the tonsils.  So I was given a penicillin many times up until my mid-20's when the tonsillitis ceased to bother me.  Dr Blaney also feels this may have been a contributing factor to my ALS later in life. 

I told my neurologist this about penicillin and she kind of looked at me in a way that I thought she did not believe it at all.  When I show her this study she may take this possibility more seriously. 



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Limburg
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 Posted: Thu Nov 24th, 2011 00:47

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I never had antibiotics before I started MP.



:?



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 Posted: Thu Nov 24th, 2011 00:53

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Thanks Annemarie ... and important point. 

However this study does not indicate the ONLY way to get MS is by antibiotic use... merely that it seems to increase the chances. 

I wonder what they would find if they did a similar study for ALS. 



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 Posted: Thu Nov 24th, 2011 01:05

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Ofcourse Chris, but there are many hypotheses from studies suggesting causes in MS, if you ask me this is just one more....

Sometimes I think it is little things in the build-up of the studies that have big influence on the outcome.Sometimes I suspect a studie gets written towards the target....

Difficult to prove in an irrefutable and objective manner.....

Maybe I sound too negative, because I also think it's good we have studies, otherwise we couldn't learn at all...



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 Posted: Thu Nov 24th, 2011 06:55

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In my opinion, it could be a myriad of reasons why the bacteria grow into L forms.  Antibiotic use, environmental reasons, stress, wounds, etc.  But the bugs are there in the first place, and humanity has been grappling with how to deal with them for eons.

Until the MP.

Sherry



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 Posted: Sat Dec 3rd, 2011 08:56

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As you know, penicillin is a beta lactam.   I have been working in the Biotechnology Lab at Collin College on a personal project related to my observations of E. coli when treated with sub-inhibitory concentrations of the beta lactam antibiotic, Cefsulodin.  What I saw was that E coli cells continued to divide but were unable to form a septum resulting in long filaments of cell wall material (peptidoglycan) that included the membrane cells inside.

The forming of the septum is one of the last steps in the prokaryote cell division pathway. So, when the cell is disturbed by a sub inhibitory beta lactam antibiotic concentration, the membrane cells actually will form inside the filaments but the cell cannot divide (form the septum to divide). Some of these membrane cells were able to burst out of the filaments and I later observed what appeared to be cell division of these membrane cells. 

In this experiment, it was the osmotic pressure of the medium that the cells were grown in that determined if they could expand and burst out of the filament.  Membrane cells have no wall to confine them so they will expand or contract based on the osmotic pressure of the environment they are in.
 
 Last March I presented this hypothesis as a poster at the Texas Academy of Science and I have included my abstract below.  I continue to work on this project and plan to present a paper once I have confirmed my observations.

  If you want more information on this experiment send me a PM.

 Gene

 ABSTRACT
Inhibitory doses of beta-lactam antibiotics are often prescribed to treat infections caused by gram negative bacteria.  These antibiotics interfere with formation of the bacteria cell wall preventing cell division.  However little is known about bacteria cell morphology when exposed to sub-inhibitory concentrations of these antibiotics.  Transient sub-inhibitory concentrations may occur over time within different areas of the patient’s body as the drug concentration changes relative to dosage and timing.  These experiments demonstrate that under low antibiotic conditions, there are significant morphology differences in E coli compared with normal prokaryote growth.  Filaments form indicating that the antibiotic is inhibitory to septum formation, but not cell division.  The cell wall continues to grow, forming a filament, and appears to stop growing in a dose-dependent manner. This results in multiple protoplasts within a cell wall filament.  These growing cells eventually break out from the peptidoglycan shell becoming independent “cell wall deficient” cells also known as “L form” bacteria, which are capable of autonomous division.  We are investigating the ability of these “L form” membrane cells to revert back to the parent cell wall morphology.  These “L forms” may play a role in persistent chronic infection in humans.  We have demonstrated that the “L form” of  E coli can be induced by low dose cefsulodin.  Future studies will investigate the nature of this dimorphism.
 



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Prof Trevor Marshall
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 Posted: Sat Dec 3rd, 2011 09:38

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Great work, Gene :)
 

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 Posted: Mon Dec 12th, 2011 04:34

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http://onlinelibrary.wiley.com/doi/10.1002/ana.22678/abstract

ms & cyp27b



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Prof Trevor Marshall
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 Posted: Mon Dec 12th, 2011 06:45

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Remember that they way they are measuring Gene defects does not allow for the presence of pathogens, and thus the 'genetic' changes they are seeing could very well just be elements of the microbiota.

We explained this error in our Metagenomics book chapter

..Trevor..

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 Posted: Mon Dec 12th, 2011 07:54

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Of course the people doing this study aren't taking into account that all those  who took antibiotics, had infections in the first place. Otherwise, they wouldn't have taken antibiotics. Why would anyone do a study on this? I hope evryone sees the humour, or the waste of time and money on such a study.

 Bevin Black



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Prof Trevor Marshall
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 Posted: Mon Dec 12th, 2011 08:11

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Bevin,
The last time I tried to have a discussion with the lead author of that study, George Ebers, at a conference, he ended up accusing me of "being an evolution denier, like all the other Americans."  It is really tough to read the minds of people like this :X Best to wait until they retire, I think.

..Trevor..
 

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 Posted: Mon Dec 12th, 2011 13:17

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http://onlinelibrary.wiley.com/doi/10.1002/ana.22678/abstract

ms & cyp27b


My take home message from the report is " More evidence that lowering VDR activity is associated with the development of chronic disease."



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 Posted: Tue Dec 13th, 2011 10:03

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Cholecalciferol supplementation wouldnt work in these patients due to lack of conversion by CYP27B1, but a VDR agonist would be interesting.

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 Posted: Tue Dec 20th, 2011 00:17

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http://www.bbc.co.uk/news/uk-scotland-16255661

Looks like he wants to make his mark here before he retires! If cyp27B is a smoking gun, how come the 25D/1,25D ratio is skewed the other way in MS?



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Prof Trevor Marshall
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 Posted: Tue Dec 20th, 2011 04:41

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"It came not only from Prof Ebers but from a group of world experts in multiple sclerosis and vitamin D who met in Glasgow."

I was there. There was no such consensus, no such resolution, and no such conclusion. This guy is delusional and dangerous to UK health...

"He says the Scottish government could face legal action from people who go on to develop MS in future"

Hmm. Those are pretty strong words, and any legal action would require more definitive epidemiological studies than those which are on the books right now. Remember that the Canadian MS study was a failure - finally realizing that innate immunosuppression was resulting from the Vitamin D doses in that study. The Australian study found Vit D was harmful in MS.

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 Posted: Tue Dec 20th, 2011 10:27

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Dr Trevor Marshall wrote:
"He says the Scottish government could face legal action from people who go on to develop MS in future"

I've never heard of any legal precedent in Scotland that dictates the government is responsible for doctoring nutritional supplementation of the population, and I very much doubt he has either.



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 Posted: Fri Dec 30th, 2011 18:49

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Add vitamin D to Scotland's food – experts, Dosing whole population would help cut levels of multiple sclerosis, say scientists The following is a letter from Professor Stewart Fleming, University of Dundee to the Guardian in regard to above article:

guardian.co.uk, Wednesday 28 December 2011 16.00 EST Article history

sclerosis" TARGET="_blank">Your report
(24 December) on the proposal that there should be artificial supplementation of Scotland's food by vitamin D to reduce the frequency of sclerosis" TARGET="_blank">multiple sclerosis did not address the two main questions of whole-population interventions. Is it effective? Is it safe?

Current evidence strongly supports a role for low levels of vitamin D in the development of MS, as your article says. However, other factors are also involved. There are no population-based clinical trials supporting the effectiveness of artificial dietary supplementation by vitamin D in lowering the frequency of MS.

On the matter of safety, vitamin D supplementation should have no adverse effect on healthy individuals. However, whole-population medication also affects the frail, elderly and ill. There are a number of illnesses in which vitamin D supplementation is potentially harmful. These are diseases associated with elevated blood calcium and include hyperparathyroidism, myeloma, lymphoma, tuberculosis and sarcoidosis.


How common are these conditions? In Scotland hyperparathyroidism alone affects 6 per 1,000 of the population – it is several times more frequent than MS. So while we need to examine this issue carefully, mass medication with no published evidence of benefit, and with the risk that more people could be harmed than are likely to benefit, would be irresponsible.”


Professor Stewart Fleming 
University of Dundee

http://www.guardian.co.uk/science/2011/dec/28/vitamin-d-ms-medical-research?newsfeed=true




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 Posted: Fri Dec 30th, 2011 19:39

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Good find Gene!



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 Posted: Sat Dec 31st, 2011 08:25

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Frenchie wrote: Dr Trevor Marshall wrote:
"He says the Scottish government could face legal action from people who go on to develop MS in future"

I've never heard of any legal precedent in Scotland that dictates the government is responsible for doctoring nutritional supplementation of the population, and I very much doubt he has either.

I think the Scots have enough challenges with their diet without supplementing anything. (I speak from from 20years experience of living on that diet..)



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 Posted: Sat Dec 31st, 2011 11:46

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Oh, aye, I can relate to that!  :P

Happy Hogmanay, but let's skip the haggis on Rabbie Burns' Night!



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