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Good luck D W,this could be

Good luck D W,this could be the start of good things to come.

CPNi,capi oct 09,NAC2400mg,Doxyi 100mg,full sups,

Moving to dr Stratton protocol next month .

David you did an excellent

David you did an excellent work to get BBC corrected the text about vit D. As everything what you write is excellent. Now I like the text I can understand it clearly and I suppose everyone who reads it also does. There are no doubts about vit D. And now I also don't mind much the research on the genesi. Thanks also on behalf of everyone who reads it.

MSi for more than 30 years, WP since July 08, break Jan 09-March 09. NACi 2x600mg, Doxyi 2x100mg, Roxi 2x150mg, Entizol in pulzes, LDNi, supplementsi.Since May 2013 without abxi.

Goodness, excitement or

Goodness, excitement or what? ..................Sarah

A  Journey through Light and Shadow

Completed Stratton/Wheldon regime for aggressive secondary progressive MSi in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Well done, David!  That's

Well done, David!  That's great!  Fingers crossed for more great things to come.

Neuroi symptoms & many health problems from 1989. NACi+all supps(04/11) doxyi(05/11) roxi(06/11) few tinii pulses, amoxi(02/13) metroi pulses (02/14)

I have just received a very

I have just received a very pleasant reply from Helen Briggs, BBC Health Correspondent, who has revised the report "Genetic clues to what triggers MSi" to include a reference to Vitamin Di deficiency being a factor. http://www.bbc.co.uk/news/health-14475497< Ms Briggs also expressed an interest in the association of Chlamydia pneumoniae and MS. I did send her a link to my own MS pages.
D W - [Myalgia and hypertension">i (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazolei. No medication now. Morning BP typically 110/75]

OK...I did the alemtuzumab

OK...I did the alemtuzumab (2 rounds) over 2 years, the first was 5 days, second was 3 days...I did not feel any better...it could be that it held me here, but i had recorded a number of at least 3 exacerbations while in the study...2 others have had great results that were in my group of 3...unfortunately i was the one without results :(...Wheldon protocol since June (2011) waiting till september to pulse in flagyli...tolerating other antibioticsi quite well now...

Hi all,This is an

Hi all,

This is an interesting discussion.  It's unfortunate that when most of us hear the terms genesi or genetics, we think of something set in stone or something we are born with, rather than something that can be influenced positively or negatively by environmental factors.

As for the positive role that Vit D may play in certain diseasesi, here's a link to a recent study that found "2776 genomic positions occupied by the VDR and 229 genes with significant changes in expression in response to vitamin Di"

A ChIP-seq defined genome-wide map of vitamin D receptor binding: Associations with disease and evolution<

"This analysis highlighted a number of gene loci in which roles for vitamin D in gene regulation had not previously been proposed (Supplemental Table 7). We noted, for example, novel intronic VDR binding sites involving IRF8 (Fig. 4), which is associated with MS (De Jager et al. 2009), and in PTPN2 (Fig. 4), a gene locus strongly implicated in CD and T1D in recent GWAS (Barrett et al. 2008; Cooper et al. 2008). Both genes showed increased expression after calcitriol stimulation (∼1.5-fold induction for both; Supplemental Table 2). We validated these novel VDR binding sites by ChIP experiments in additional LCLs (Fig. 4) together with other novel sites we found in gene loci such as PTPN22 and CD226, which have been strongly associated with autoimmune disease susceptibility (Supplemental Fig. 4) (Bottini et al. 2004; Barrett et al. 2008; Baranzini 2009; Hafler et al. 2009). A systematic listing of gene loci implicated in a range of autoimmune diseases in which we identified VDR binding is provided in Supplemental Table 7. This includes genes such as IRF5, CLEC16A, CD40, CDKAL1, CTLA4, HLA-DRB1, HLA-DQA1, PRDM1, PTGER4, STAM, TNFAIP3, and TNFSF4."

You can find Table 7 by clicking on the "Supplemental Material" link toward the right in the article at the above link.

 

Hang in there all...

 

 

 

 

 

Treatment for Rosaceai<

  • CAPi:  01/06-07/07
  • High-Dose Vit D3, NACi:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

By the way, one of the main

By the way, one of the main campath researchers has recently been called to the church.  He is now a curate of St Andrews in Cambridge:  http://www.testoffaith.com/resources/resources.aspx?resource=true&catid=13&id=125<

My neurologist, also from Cambridge is a devout Methodist.  Since both have been involved in the study of motor lobe epilepsy you might care to take a look at this:

http://www.youtube.com/watch?v=qIiIsDIkDtg<   Perhaps  it isn’t just the patients but the neurologists who are often affected....................Sarah

A  Journey through Light and Shadow

Completed Stratton/Wheldon regime for aggressive secondary progressive MSi in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Well, David has just written

Well, David has just written to the BBC, asking them to correct the error.....................Sarah

A  Journey through Light and Shadow

Completed Stratton/Wheldon regime for aggressive secondary progressive MSi in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Sarah and David, I supposed

Sarah and David, I supposed that there may have been a mistake with vit D. But I do think the mistake like this can't be done when it is published. The message about vitD like this can be sent between two researchers when they know what they are talking about. Written like this for me as a common reader only means one thing - exposure to sunlight can cause MSi. If maybe 20 years ago I had an information that deficiency of vit D can trigger MS and the best way to get vit D is the sunlight I would do my best to take sunbathing as much as possible though I wasn't good after sunbathing. When I went to the seaside then the next year I was better. Wasn't it interesting? So I would go there every year if I knew this information. And if I read the information about vit D it isn't good I wouldn't go to the seaside at all. That's the reaction of a common person. But at that times the phobia of sun started.

 And in addition vitD was named in the article together with viruses and bacteria.

I know also the information about the genesi they are the ones that are connected with MS. I got this information mor than 30 years ago but I didn't care about it as there could be nothing done with it. But now it reminds me the autoimmunityi story. I am happy not being on CRABs. I don't know if there is a person on CRABs who has had MS for more than 30 years and is still on own legs. I would be interested in this much. 

And what's also interesting? Relapses are connected with a new respiratory infection. I can remember my neuroi always saying - just don't catch a cold. For maybe 25 years I had no new respiratory infection but I had 2 relapses a year regularly. My NMR confirms this - 58 lessions for 30 years. But in my childhood I had almost permanent respiratory infection.

And I am also afraid that when managing the genes there maybe something like managing the autoimmunity and the result could be the same. David, as you say, it's necessary to deal with the infection. You know it as the result of your amazing work. And I feel this from my young years that there has been something inside me that kills me but I should kill it. But the question was - WHAT? Now there is an answer which you also disclosed.

 

MSi for more than 30 years, WP since July 08, break Jan 09-March 09. NACi 2x600mg, Doxyi 2x100mg, Roxi 2x150mg, Entizol in pulzes, LDNi, supplementsi.Since May 2013 without abxi.

Jill, Vitamin Di deficiency

Jill, Vitamin Di deficiency may be not off the table in your case. I your vit D level weren't ok you may get MSi much sooner. I was really very curious whether you write about you vit D level. I supposed that you may not have vit D deficiency as where you live. I must be vit D deficient as I live where we don't have much sun and in addition from my childhood I was very bad after the exposure to sunlight. And I finished so bad with the sun that before the CAPi I couldn't stay outside at all while the sun was shinningl. I almost fainted. Now I enjoy exposing myself to the sun. Nobody has tested me for vitD level as it's expensive and there is no reason to test it.

MSi for more than 30 years, WP since July 08, break Jan 09-March 09. NACi 2x600mg, Doxyi 2x100mg, Roxi 2x150mg, Entizol in pulzes, LDNi, supplementsi.Since May 2013 without abxi.

P.S. Vitamin Di deficiency

P.S. Vitamin Di deficiency is completely off the table in my case. I've been tested, no deficiency there. Considering I live in Australia and have been a beach bum all my life it would seem pretty unlikely. But my sister tested positive for Vit D deficiency because she never walks out of the house without lathering sunscreen on! I, on the other hand, am very partial to sun worship. There is obviously a happy medium here though!

Jill

RRMSi diagnosed 1996. Many years of weird symptoms before this. Started CAPi around 6/11? Minoi 200mg daily, Roxyi 300mg daily, Tinii pulses started 11/11 (very tentatively!) Major problems with headaches 01/12, substitued mino with doxyi.&l

Could the fact that “80%

Could the fact that “80% of the genesi<i< that are implicated by the 57 ‘hits’ are immunological" be, in itself, idicative of an infective agent being the root cause of MSi? Could certain people be genetically predisposed to mounting an immunei response to cpni that is more destructive than other people? Is it inflammationi that causes the lesions and if so, is this an immune response? Excuse possible laymans terminology.

RRMSi diagnosed 1996. Many years of weird symptoms before this. Started CAPi around 6/11? Minoi 200mg daily, Roxyi 300mg daily, Tinii pulses started 11/11 (very tentatively!) Major problems with headaches 01/12, substitued mino with doxyi.&l

http://www.bbc.co.uk/news/hea

http://www.bbc.co.uk/news/health-13092524<

This paints a better picture regarding Vitamin Di deficiency.

I think D W should offer his services to the BBC,show them a thing or two about the real world!

CPNi,capi oct 09,NAC2400mg,Doxyi 100mg,full sups,

Moving to dr Stratton protocol next month .

I think it’s just badly

I think it’s just badly worded, Evita. Vitamin Di deficiency is thought to contribute to MSi.

“80% of the genesi that are implicated by the 57 ‘hits’ are immunological. This shouts out that this is an immunological disease at the beginning. This is a very important confirmation.”

Well, I suppose he would say that. His MS research unit is deeply into Campath (alemtuzumab) which is a monoclonal antibody directed against CD52, a glycoprotein on the surface of mature T lymphocytes. The effects of treatment were very curious. One must consider them carefully. Treatment with Campath resulted in a reduction of relapses in Relapsing-Remitting MS. In Secondary-Progressive disease, however, the results were very different. No new lesions appeared on MRI, but progression continued: “Patients with SPMSi showed sustained accumulation of disability due to uncontrolled progression marked by unrelenting cerebral atrophy, attributable to ongoing axonal loss. The rate of cerebral atrophy was greatest in patients with established cerebral atrophy and highest inflammatory lesion burden before treatment.” [The window of therapeutic opportunity in multiple sclerosis: evidence from monoclonal antibody therapy. Coles AJ, et al. J Neurol. 2006 Jan;253(1):98-108.]

These results give compelling evidence for a chronic, covert infection as the primary engine of pathology in MS. Campath causes prolonged T lymphocyte depletion. Relapses in RRMSi are probably due to immunei activation against a new respiratory infection [Buljevac D, et al. Chlamydia pneumoniae and the risk for exacerbation in multiple sclerosis patients. Ann Neurol. 2003 Dec;54(6):828-31.] Artificial paralysis of the immune response with a monoclonal antibody would indeed be expected to reduce the relapse rate in RRMS, while allowing the underlying infection to continue. This would account for the rapid deterioration found in persons with SPMS: the deterioration was in the form of cerebral atrophy. This surely points to untrammelled progression of infection. Indeed, serum antibodies to Chlamydia pneumoniae rise as the disease enters the progressive phase. [Munger KL, et al. Infection with Chlamydia pneumoniae and risk of multiple sclerosis. Epidemiology 2003 14:2 141-147].

A fitting metaphor might be that of a barking guard-dog. Silencing the guard-dog with a muzzle would certainly make for quieter nights. But all the time the burglars are silently making off with the silver.

 

D W - [Myalgia and hypertension">i (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazolei. No medication now. Morning BP typically 110/75]

I think that there is a

I think that there is a slight lapse of understanding by the script writer at the BBC here, with regards to vitamin Di.  There are lots of BBC posts extolling its virtue for MS.

As for genesi, it has long been known that some people are genetically more prone to develop MS than others.  The trigger is something else, most likely the ultra common clamydophila pneumoniae.  Even Compston, the main person behind this research doesn’t quite seem to have got that yet but he must be near to proper retirement, so perhaps he will undergo a Damascene conversion before he does!.....................Sarah

A  Journey through Light and Shadow

Completed Stratton/Wheldon regime for aggressive secondary progressive MSi in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Oh no! I can't believe this

Oh no! I can't believe this article. The one of the possible trigger of MSi is Vit D from the exposure to sunlight! So people should be forbidden to expose themselves to the sunlight and there will be the chance of more MSers and more money from the theoretical treatment. And the researchers are looking for other possible triggers among the genesi. This article seems to be the preparation for new cures as the present cure of immuno -suppresants is failing. Researchers are looking for another source of big money. Do they want to screw or cross the genes? MSers can't be cured seriously as their disease gives much profit. I hope this article stays just an idea.

MSi for more than 30 years, WP since July 08, break Jan 09-March 09. NACi 2x600mg, Doxyi 2x100mg, Roxi 2x150mg, Entizol in pulzes, LDNi, supplementsi.Since May 2013 without abxi.

Interesting. Thanks. 

Interesting. Thanks.

 

PPMSi-misdiagnosed 2001-diagnosed 2006. Probably caught cpni in birth canal but it didn't pass BBBi until my 40s. Minocycline 7 mos.- resulting bronchitis 5 months.Go to private m.d. out-of-plan. Wheldon CAPi 3/2/07 Stopped 12/12; resumed 12/13