Why would you NOT take meds?

If it's on your mind and it has to do with multiple sclerosis in any way, post it here.

Re: Why would you NOT take meds?

Postby NHE » Wed Jul 02, 2008 3:01 am

gwa wrote:I would not waste my time with any of the CRABS.

Well, although they're not an ideal treatment, they're not entirely worthless.

This paper demonstrated a reduction in brain atrophy in Avonex treated patients as well as an increase in the gray matter brain fraction.

Interferon beta-1a slows progression of brain atrophy in relapsing-remitting multiple sclerosis predominantly by reducing gray matter atrophy. Mult Scler. 2007 May;13(4):490-501.
    BACKGROUND: Brain atrophy, as assessed by magnetic resonance imaging (MRI), has been correlated with disability in patients with multiple sclerosis (MS). Recent evidence indicates that both white matter (WM) and gray matter (GM) are subject to atrophy in patients with MS. Although neurological deficiencies in MS are primarily due to loss of WM, the clinical significance of GM atrophy has not been fully explored in MS. METHODS: We have undertaken a three-year, open-label study, comparing 26 patients who elected to receive intramuscular interferon beta-1a (IFN beta-1a) therapy, with 28 patients who elected not to receive therapy. Both groups had quantitative cranial MRI scans at study entry and after three years, and standardized clinical assessments every six months. Brain parenchymal fraction (BPF), GM fraction (GMF), and WM fraction (WMF) percent changes were calculated, and T2- and T1-lesion volumes (LVs) assessed. RESULTS: After three years, mean percent (%) change in BPF favored the IFN beta-1a treatment group (IFN beta-1a -1.3% versus the control group -2.5%, P=0.009), as did the mean percent change in GMF (+0.2 versus -1.4%, P=0.014), and the mean percent change in T1-LV (-9.3 versus +91.6%, P=0.011). At the end of the study, there was a significant within-patient decrease in BPF for both groups (P=0.02 for the IFN beta-1a treatment group, and P<0.001 for the control group), a significant within-patient decrease in WMF for the IFN beta-1a treatment group (P=0.01), and a significant decrease in GMF for the control group (P=0.013) when compared with baseline. CONCLUSION: Over a three-year period, treatment with IFN beta-1a significantly slowed the progression of whole-brain and GM atrophy, and of T1-hypointense LV accumulation, when compared with the control group.

Moreover, this paper comparing Avonex to placebo showed that there was significantly less brain atrophy in the second year of Avonex use vs. placebo.

Brain atrophy in relapsing multiple sclerosis: relationship to relapses, EDSS, and treatment with interferon beta-1a.
Mult Scler. 2000 Dec;6(6):365-72.
    Brain atrophy is a relevant surrogate marker of the disease process in multiple sclerosis (MS) because it represents the net effect of various pathological processes leading to brain tissue loss. There are various approaches to quantifying central nervous system atrophy in MS. We have focused on a normalized measure of whole brain atrophy, the brain parenchymal fraction (BPF). BPF is defined as the brain parenchymal volume, divided by the volume within the surface of the brain. We applied this method to an MRI data set generated during a phase III clinical trial of interferon beta-1a (AVONEX). The purpose of the current study is to further explore clinical and MRI correlates of the BPF, particularly as they relate to relapse rate and Kurtzke's Expanded Disability Status Score (EDSS); and to further explore the therapeutic effects observed in interferon beta-1a recipients. Of all demographic and disease measures in the clinical trial data base, T2 lesion volume most closely correlated with BPF in cross sectional studies, and was the baseline factor most closely correlated with progressive brain atrophy in the subsequent 2 years. We also observed that change in T2 lesion volume was the disease measure most closely correlated with change in BPF during 2 years of observation. Of interest, relapse number and EDSS change during 2 years were only weakly correlated with BPF change during the same period. Disability progression, defined as sustained worsening of at least 1.0 EDSS points from baseline, persisting at least 6 months, was associated with significantly greater brain atrophy progression. We observed a therapeutic effect of interferon beta-1a in the second year of the clinical trial, and this beneficial effect was not accounted for by change in gadolinium enhanced lesion volume, or by corticosteroid medication within 40 days of the final MRI scan. The BPF is an informative surrogate marker for destructive pathological processes in relaping MS patients, and is useful in demonstrating treatment effects in controlled clinical trials. The significance of progressive brain atrophy during relapsing MS will be assessed by measuring clinical and MRI changes in prospective follow up studies.

Here's a data plot from the second paper...
    Image


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Postby jimmylegs » Wed Jul 02, 2008 8:23 am

hi folks, i don't really know anything about the drugs for this condition, except that in my early days of research i did decide my body could do the same thing on its own. i went looking into interferon again and i can't remember exactly what i had found or decided back then. i don't believe i was a member here yet so there wouldn't be a record unless i have something in one of my old planners.

anyway i read this from wikipedia...

Natural function and synthesis

Interferons in general have several effects in common. They are antiviral and possess antioncogenic properties, macrophage and natural killer lymphocyte activation, and enhancement of major histocompatibility complex glycoprotein classes I and II, and thus presentation of foreign (microbial) peptides to T cells. In a majority of cases, the production of interferons is induced in response to microbes such as viruses and bacteria and their products (viral glycoproteins, viral RNA, bacterial endotoxin, bacterial flagella, CpG sites), as well as mitogens and other cytokines, for example interleukin 1, interleukin 2, interleukin-12, tumor necrosis factor and colony-stimulating factor, that are synthesised in the response to the appearance of various antigens in the body. Their metabolism and excretion take place mainly in the liver and kidneys. They rarely pass the placenta but they can cross the blood-brain barrier.


it made me wonder why, when we have these overactive immune systems, that they need MORE of something that is typically generated in response to a foreign body.

i also picked up on the mention of natural killer cells... it's only a sliver of the interferon picture, but i remembered reading that there was a dip in the levels of these cells associated with relapse. i did a search and came up with these titles:

Clinical relapses of multiple sclerosis are associated with 'novel' valleys in natural killer cell functional activity.
http://www.ncbi.nlm.nih.gov/pubmed/14644036

A role for natural killer cells in the immunopathogenesis of multiple sclerosis.
http://www.ncbi.nlm.nih.gov/pubmed/9663557
Mean NK cell FA [functional activity] is significantly lower in MS patients, compared to controls (P < 0.001), while variability around the means is significantly greater (P < 0.01).


how to boost natural killer cells:

selenium
http://www.ncbi.nlm.nih.gov/pubmed/8811280

probiotics
http://www.ncbi.nlm.nih.gov/pubmed/11506196

EPA omega three fatty acid
http://www.ncbi.nlm.nih.gov/pubmed/2801 ... t=Abstract

those were just the easiest to find, can't get into it further this second but there are also things to be looked up pertaining to natural killers and
vitamin E, carotenoids, garlic, vitamin A, and laughter, for a start.

i think it would be interesting to look further into what each one of these drugs is doing, and how our body would ordinarily be doing it on its own.
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Postby gwa » Thu Jul 03, 2008 11:41 am

NHE

It is always difficult to find the real deal when looking at stats for clinical studies. I knew there was some recently published research for Avonex, but just now found it. One problem with the subjects in the trial that you posted is that is a very small study, which is a problem, according to other researchers claims.

This is the research, which is a much larger study, and which claims Avonex and Copaxone did not significantly differ from placebo in many endpoints.

http://www.ncbi.nlm.nih.gov/pubmed/18437041


Efficacy of disease-modifying therapies in relapsing remitting multiple sclerosis: a systematic comparison.
Freedman MS, Hughes B, Mikol DD, Bennett R, Cuffel B, Divan V, LaVallee N, Al-Sabbagh A.

Department of Medicine (Neurology), University of Ottawa, Ottawa, Ontario, Canada. mfreedman@ottawahospital.on.ca

The treatment of relapsing-remitting multiple sclerosis (RRMS) has become more effective over the last decade with the advent of the currently available disease-modifying therapies (DMTs). Pivotal clinical studies differ in many characteristics, such that cross-comparisons of relative risk reductions are of limited value and can be misleading. Our objective was to compare the clinical efficacy of currently approved first-line DMTs in patients with RRMS, applying an evidence-based medicine approach. We reviewed all phase III pivotal trials of DMTs. Six clinical trials of Avonex, Betaseron, Copaxone, Rebif and Tysabri in patients with RRMS were identified for analysis. Only randomized, placebo-controlled, double-blind studies were included. The clinical efficacy endpoints compared were: proportion of relapse-free patients at 1 and 2 years; annualized relapse rate at 2 years; proportion of progression-free patients at 2 years, and proportion of patients free of gadolinium-enhancing lesions at 1 year or 9 months. Based on these analyses, Betaseron, Rebif, and Tysabri show comparable effects, whereas for several endpoints Avonex or Copaxone did not significantly differ from placebo. In the absence of head-to-head studies for all products used to treat RRMS, it still may be possible to compare treatment effects by applying evidence-based medicine principles. (c) 2008 S. Karger AG, Basel."



If offered CRABS, there is still not one that I would take because I believe that, especially for RRMS, there are better alternatives, now and in the near future.

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Postby robbie » Thu Jul 03, 2008 12:30 pm

do you think there will ever just be a drug for ms or will it always be divided or the different types? i am still confused why a drug that helps rrms won't help the others.
Had ms for over 19 years now.
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Postby RuSmolikova » Thu Jul 03, 2008 10:45 pm

MS Research Update: The Great Debate--Inflammation vs Degeneration
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Postby Lyon » Fri Jul 04, 2008 5:21 am

..
Last edited by Lyon on Wed Jun 22, 2011 8:05 pm, edited 1 time in total.
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Postby MattB » Sun Aug 17, 2008 8:02 pm

It's discussions like these that make me feel like I shouldn't participate... but I like to anyhow. I had my only visible(well to me cause it was ON) exacerbation around the time the rest of this conversation ended. With the optical neuritis I was given dexamethasone by one doctor and prednisone by another--I didn't really notice a difference. My sight got only slightly better and that took a few months on it's own. I was finally given the official diagnosis(after many MRIs, a spinal(which was negative), many neuro visits, much research) in mid October.

I started taking Copaxone in mid March and in the time period between then and the dx I noticed no exacerbations. Now I know my case is extremely mild compared to some others but I'm just adding my personal input, which is what was asked for. Since then I've noticed absolutely no difference on the Copaxone. Once in a while it stings and sometimes if I hit a nerve or something it turns a little black and blue for a few days but never anything big. I only had one day where I think I may have had a flare up--I was at work and I was tons of stress from my job and from my ongoing relationship problem. I felt dizzy, weak, and generally unwell. I called my ex and asked her to come pick me up. After drinking some tea and laying down for a while I felt better. I can't attribute it to MS for sure because I had also lost 15 pounds and was sleeping very little but I sort of think it may have been a flare up.

That being said: Isn't there some type of scientific basis for Copaxone? I mean I've read things myself and it may help some people. I notice no side effects, need no liver enzyme tests, and am able to live an almost completely normal life while on Copaxone. In that case even if it may not be doing anything I have no reason to discontinue its use because it may be doing something. I know not everyone responds as well and I can completely understand not using the interferons because of the side effects but if you're able to find a drug that MAY be helping you and there are no side effects and you can afford it without great strain then I feel you should stay on it.

Everything I write on here turns into a book :oops:
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Postby cheerleader » Sun Aug 17, 2008 8:37 pm

Hey Matt...
it's good to see your name come up. Been concerned for you since the breakup. I hope you're finding your way on your own. Your period of not sleeping well and feeling bad could have been an exacerbation...hope you're sleeping and eating better.

You're absolutely right...the fact that you have not had a major exacerbation since your diagnosis could be due to the Copaxone, since that is what it was created to do....limit the number of exacerbations in RRMS. It's also been thought to repair nerve damage http://www.medicalnewstoday.com/articles/33735.php

if you're doing well on it...keep going, Matt!
best,
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby MattB » Tue Aug 19, 2008 3:43 pm

Thanks AC. It was a really rough period of time and I'm still dealing with a lot of the emotion issues. Luckily though I've been doing better eating and sleeping wise. I've gained back some of my weight and I've been getting almost normal sleep.

I plan on staying on Copaxone until something better comes along, which is what they always claim is going to happen within the next 2-3 years. Thanks for the encouragement!
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