Aa
NYT Article on MS and Interferon Beta
http://www.nytimes.com/2012/07/18/health/research/multiple-sclerosis-drug-doesnt-stop-disability-study-finds.html
I don't really know what to make of this, having been on Betaseron since February. It just seems all sorts of discouraging. I pride myself on being optimistic and hopeful but then I read things like this and the negative thoughts come rushing in, mainly... am I being naive when I plan for a future that doesn't involve disability? Or am I just taking the wrong DMD?
I don't really know what to make of this, having been on Betaseron since February. It just seems all sorts of discouraging. I pride myself on being optimistic and hopeful but then I read things like this and the negative thoughts come rushing in, mainly... am I being naive when I plan for a future that doesn't involve disability? Or am I just taking the wrong DMD?
Points I took away from the NYT write up to announce research finding about interferon beta and MS disability progression.
All remarks in quotations are taken from the online article:
http://www.nytimes.com/2012/07/18/health/research/multiple-sclerosis-drug-doesnt-stop-disability-study-finds.html
The GOOD NEWS:
(FYI: Some of this was easy to miss. News reports sometimes have a way of making good news sound bad. Besides, most of this good news didn’t make it into the lead paragraph or two…. or six. You had to go pretty deep.)
1.) CONFIRMATION was given that interferon beta DOES help reduce the development of brain lesions and DOES limit the frequency of MS relapses.
There you go. All is not lost.
2.) Helen Tremlett, PhD, study report author and associate professor of neurology at the University of British Columbia, “cautioned against” a fear I’ve seen expressed here in our own MS community forum.
She asked people to remember that interferon beta is NOT useless. Did anyone else notice that?
Personally, I don’t believe ANY of the disease modifying drugs are useless and see no reason to stop taking the only drugs we have that offer a sliver of hope for diminishing disease presence.
3.) I was pleased to read Dr. Tremlett’s comments affirming, “These drugs were licensed because they reduce relapse and have a better outcome with lesions. That has not changed.”
See? She thinks so too :)
4.) Following a disclaimer type listing of study limitations the article eased toward its end with this statement, “But after controlling for sex, age at onset, disease duration, relapse rate and other factors, they could find no association between taking interferon beta and any reduction in progression to disability.”
To which Dr. Tremlett remarks, “Relapses and brain lesions do not, apparently, drive disability.”
Ahhh, what did she say???
Wondering why I consider this good news?
Read it again please.
She said, RELAPSES AND BRAIN LESIONS DO NOT, APPARENTLY, DRIVE DISABILITY!
I consider that to be a HUGE statement. I hadn’t thought there was an expert who would CONSIDER such a thing let alone say it OUT LOUD!
MANY of us little people (the ones living with MS) have asked again and again for an explanation of WHY we experience new symptoms in the absence of new lesions. It seems someone other than us has FINALLY asked our question. If so, perhaps a new chapter in the search for answers AND solutions can be opened. And maybe, just maybe some of the lesion counting can be stopped.
At a minimum, that qualifies as potential good news.
5.) The very last paragraph makes the boldest good news proclamation of all (even though I’d guess the reporter never realized it). The entire content is contained in three sentences so I’ll quote it in full.
“There may be other processes at work,” she [Dr. Tremlett] added. “In an ideal world, we want drugs that target whatever is driving long-term disability. We need other drugs aiming at other targets in the brain.”
Other processes Dr. Tremlett? Other drugs with other targets? Like DMD twins maybe? DMD-1 to modify disease and DMD-2 to modify disability? Ohhhh, I like it. Here’s to a future of help and hope for the younger-than-me generation of PwMS.
The BAD NEWS:
(AKA: Facts that sometimes take on a big, bad life of their own when stated in isolation.)
1.) This study concluded that PwMS “who took interferon beta were no less likely to suffer long-term disability than those who took none.”
Thank you. It’s been suspected and suggested all along. It doesn’t mean PwMS shouldn’t appreciate some freedom from the short-to-moderate-term disability associated with exacerbations.
2.) You can’t have Dr. Tremlett as your MS doctor. She holds a staff position in the Division of Neurology, Department of Medicine, The University of British Columbia with a PhD in Pharmacy and Pharmacology.
3.) I didn’t actually find any certifiable bad news (but I guess that’s good news…).
3. (revised) I can’t pretend I was pleased to see Eeyore type responses attributed to two MS experts who represent major university affiliated hospitals here in the U.S.A.
In the end, I AM REMINDED that:
1.) When the media presents MS research reports (anything, actually) they seem to enjoy painting a dark and ugly picture of the disease. In truth, MS isn’t a very attractive disease (if such a thing exists). But after the initial fear and some time to adjust, living on the inside of the diagnosis usually isn’t quite as bleak as those on the outside seem to imagine.
I’m glad that after using long ugly brushstrokes to create a dark word picture, NYT writer Nicholas Bakalar chose to attach a disclaimer that “many people live with the disease for decades, still able to walk and work with minimal disability.” Well then, maybe we will be okay after all - WITH or WITHOUT so much immediate worry about the long-term.
2.) The reported findings don’t change much of anything for those of us presently living in the trenches. In fact, I heard to similar arguments leveled against my own DMD of choice (Copaxone) before I ever started using it to replace the money in my pockets. Hadn’t I read the company’s printed insert?! Didn’t I know ‘they’ had admitted ‘in their own words’ that there was no ‘proof’ Copaxone could stop or delay disability progression?!
Maybe it’s true (even if I never did find it in print). It just wasn’t enough to stop me from trying Copaxone then. And now, nothing is convincing me I’d be better off giving it up. I hope others aren’t going to give up either.
3.) I’m okay accepting a risk of long-term disability that equals the risk of PwMS who don’t take advantage of disease modifiers. Why? Because impacting long-term ability would be great but a less-than-perfect possibility is still far better than hopeless.
I’m willing to ‘settle’ for reaping the benefits of having my MS served up with fewer unpredictable and ill-timed flares. It’s a lot better than the choices we had a decade or two ago. Call me crazy but I choose to avoid the rigors and lost time even ONE additional flare will demand in exchange for a bid to (maybe) return to baseline.
Well, that and I’m secretly hoping to gain a little extra…. ahhh, something. Something as yet unproven - perhaps even unsuspected - by researchers…. or reporters.
~~~~~~~~~~~~~~~~~
[That’s my take. It is my intention to post this in multiple threads containing statements of concern about the matter. This is for the benefit of any search engine that randomly pulls one topic over others. Feel free to ignore duplicates and/or the original if you wish but voicing my observations is somehow more important than I care to explain further.]
All remarks in quotations are taken from the online article:
http://www.nytimes.com/2012/07/18/health/research/multiple-sclerosis-drug-doesnt-stop-disability-study-finds.html
The GOOD NEWS:
(FYI: Some of this was easy to miss. News reports sometimes have a way of making good news sound bad. Besides, most of this good news didn’t make it into the lead paragraph or two…. or six. You had to go pretty deep.)
1.) CONFIRMATION was given that interferon beta DOES help reduce the development of brain lesions and DOES limit the frequency of MS relapses.
There you go. All is not lost.
2.) Helen Tremlett, PhD, study report author and associate professor of neurology at the University of British Columbia, “cautioned against” a fear I’ve seen expressed here in our own MS community forum.
She asked people to remember that interferon beta is NOT useless. Did anyone else notice that?
Personally, I don’t believe ANY of the disease modifying drugs are useless and see no reason to stop taking the only drugs we have that offer a sliver of hope for diminishing disease presence.
3.) I was pleased to read Dr. Tremlett’s comments affirming, “These drugs were licensed because they reduce relapse and have a better outcome with lesions. That has not changed.”
See? She thinks so too :)
4.) Following a disclaimer type listing of study limitations the article eased toward its end with this statement, “But after controlling for sex, age at onset, disease duration, relapse rate and other factors, they could find no association between taking interferon beta and any reduction in progression to disability.”
To which Dr. Tremlett remarks, “Relapses and brain lesions do not, apparently, drive disability.”
Ahhh, what did she say???
Wondering why I consider this good news?
Read it again please.
She said, RELAPSES AND BRAIN LESIONS DO NOT, APPARENTLY, DRIVE DISABILITY!
I consider that to be a HUGE statement. I hadn’t thought there was an expert who would CONSIDER such a thing let alone say it OUT LOUD!
MANY of us little people (the ones living with MS) have asked again and again for an explanation of WHY we experience new symptoms in the absence of new lesions. It seems someone other than us has FINALLY asked our question. If so, perhaps a new chapter in the search for answers AND solutions can be opened. And maybe, just maybe some of the lesion counting can be stopped.
At a minimum, that qualifies as potential good news.
5.) The very last paragraph makes the boldest good news proclamation of all (even though I’d guess the reporter never realized it). The entire content is contained in three sentences so I’ll quote it in full.
“There may be other processes at work,” she [Dr. Tremlett] added. “In an ideal world, we want drugs that target whatever is driving long-term disability. We need other drugs aiming at other targets in the brain.”
Other processes Dr. Tremlett? Other drugs with other targets? Like DMD twins maybe? DMD-1 to modify disease and DMD-2 to modify disability? Ohhhh, I like it. Here’s to a future of help and hope for the younger-than-me generation of PwMS.
The BAD NEWS:
(AKA: Facts that sometimes take on a big, bad life of their own when stated in isolation.)
1.) This study concluded that PwMS “who took interferon beta were no less likely to suffer long-term disability than those who took none.”
Thank you. It’s been suspected and suggested all along. It doesn’t mean PwMS shouldn’t appreciate some freedom from the short-to-moderate-term disability associated with exacerbations.
2.) You can’t have Dr. Tremlett as your MS doctor. She holds a staff position in the Division of Neurology, Department of Medicine, The University of British Columbia with a PhD in Pharmacy and Pharmacology.
3.) I didn’t actually find any certifiable bad news (but I guess that’s good news…).
3. (revised) I can’t pretend I was pleased to see Eeyore type responses attributed to two MS experts who represent major university affiliated hospitals here in the U.S.A.
In the end, I AM REMINDED that:
1.) When the media presents MS research reports (anything, actually) they seem to enjoy painting a dark and ugly picture of the disease. In truth, MS isn’t a very attractive disease (if such a thing exists). But after the initial fear and some time to adjust, living on the inside of the diagnosis usually isn’t quite as bleak as those on the outside seem to imagine.
I’m glad that after using long ugly brushstrokes to create a dark word picture, NYT writer Nicholas Bakalar chose to attach a disclaimer that “many people live with the disease for decades, still able to walk and work with minimal disability.” Well then, maybe we will be okay after all - WITH or WITHOUT so much immediate worry about the long-term.
2.) The reported findings don’t change much of anything for those of us presently living in the trenches. In fact, I heard to similar arguments leveled against my own DMD of choice (Copaxone) before I ever started using it to replace the money in my pockets. Hadn’t I read the company’s printed insert?! Didn’t I know ‘they’ had admitted ‘in their own words’ that there was no ‘proof’ Copaxone could stop or delay disability progression?!
Maybe it’s true (even if I never did find it in print). It just wasn’t enough to stop me from trying Copaxone then. And now, nothing is convincing me I’d be better off giving it up. I hope others aren’t going to give up either.
3.) I’m okay accepting a risk of long-term disability that equals the risk of PwMS who don’t take advantage of disease modifiers. Why? Because impacting long-term ability would be great but a less-than-perfect possibility is still far better than hopeless.
I’m willing to ‘settle’ for reaping the benefits of having my MS served up with fewer unpredictable and ill-timed flares. It’s a lot better than the choices we had a decade or two ago. Call me crazy but I choose to avoid the rigors and lost time even ONE additional flare will demand in exchange for a bid to (maybe) return to baseline.
Well, that and I’m secretly hoping to gain a little extra…. ahhh, something. Something as yet unproven - perhaps even unsuspected - by researchers…. or reporters.
~~~~~~~~~~~~~~~~~
[That’s my take. It is my intention to post this in multiple threads containing statements of concern about the matter. This is for the benefit of any search engine that randomly pulls one topic over others. Feel free to ignore duplicates and/or the original if you wish but voicing my observations is somehow more important than I care to explain further.]
What all these DMDs fail to address is that MS is not just relapse and recovery - it's an ongoing degenerative process. Axons in the brain are breaking even without lesion formation.
Supposedly Copaxone helps to slow that - unfortunately I'm allergic to it. What I'd hoped is that betaseron also helps to slow the invisible damage of MS, but it sounds as if it does not.
Supposedly Copaxone helps to slow that - unfortunately I'm allergic to it. What I'd hoped is that betaseron also helps to slow the invisible damage of MS, but it sounds as if it does not.
I struggled to understand what they were saying. I have not yet read Lulu's article. I'm not sure what the difference is between relapse & lesions v. disability. Isn't disability caused by lesions? Are they just talking about the progression of existing disability?
Kyle
Kyle
One of the quotes that needs scruitinizing is this....
"We know that this class of drugs is very helpful in reducing relapses, which can be important to patients."
CAN be important? Really?
Ok, (to me) this goes back to the definition of "relapse." Relapses are defined in more than one way, however, two main ones are practiced, and that is clinically identified relapse, and imaging, that is, a true break in the blood brain barrier as seen by way of MRI.
So, utilizing those two identifiers ...
My thoughts are that reducing relapse can, and does indeed prolong progression. That is not to say there is not progression from existing damage. Some experience this progression from the initial attack.
But, for those with stable damage by way of imaging, dealing with chronic problems are far better off than those who experience a "continued" attack through the blood brain barrier, and increasing damage to the CNS as a result of that continued attack.
Have you noticed this has me fired up? lol
"We know that this class of drugs is very helpful in reducing relapses, which can be important to patients."
CAN be important? Really?
Ok, (to me) this goes back to the definition of "relapse." Relapses are defined in more than one way, however, two main ones are practiced, and that is clinically identified relapse, and imaging, that is, a true break in the blood brain barrier as seen by way of MRI.
So, utilizing those two identifiers ...
My thoughts are that reducing relapse can, and does indeed prolong progression. That is not to say there is not progression from existing damage. Some experience this progression from the initial attack.
But, for those with stable damage by way of imaging, dealing with chronic problems are far better off than those who experience a "continued" attack through the blood brain barrier, and increasing damage to the CNS as a result of that continued attack.
Have you noticed this has me fired up? lol
Seems these articles are creating doubt in treatment many are taking. Shame on the NYT for not reporting all the facts.
We've said, as the trials do that there are those percentages of folks who do not respond to interferon, or peptide (copax), etc. This is where the biomarkers being identified, (specifically interlukin (sp?) for interferon) that will help gauge who will respond to each med. It's going to be awhile until we can benefit from these findings, but for future MSers, this will be helpful where therapy is concerned.
But, to get back to the point. I'm discouraged more-so how the reporting did not include positive evidence of years of trial and reporting and success.
I'm disappointed that the media once again creates fear, doubt, for so many. What we need is confidence to inject and take our meds to cease this disease best we can whether that requires a med change or not.
I seriously hope the drug manufacturers stand behind their medicine that has helped so many, and strongly counter this bunk.
I'm still going to take interferon, there are so many anti-viral properties. And, I know it's served me well.
-shell
We've said, as the trials do that there are those percentages of folks who do not respond to interferon, or peptide (copax), etc. This is where the biomarkers being identified, (specifically interlukin (sp?) for interferon) that will help gauge who will respond to each med. It's going to be awhile until we can benefit from these findings, but for future MSers, this will be helpful where therapy is concerned.
But, to get back to the point. I'm discouraged more-so how the reporting did not include positive evidence of years of trial and reporting and success.
I'm disappointed that the media once again creates fear, doubt, for so many. What we need is confidence to inject and take our meds to cease this disease best we can whether that requires a med change or not.
I seriously hope the drug manufacturers stand behind their medicine that has helped so many, and strongly counter this bunk.
I'm still going to take interferon, there are so many anti-viral properties. And, I know it's served me well.
-shell
I'm sorry this link is so long - but here is the medical take on this report on the beta interferons.
http://www.medpagetoday.com/clinical-context/MultipleSclerosis/33790?utm_content=&utm_medium=email&utm_campaign=DailyHeadlines&utm_source=WC&eun=g421114d0r&userid=421114&email=***@****&mu_id=5520442
http://www.medpagetoday.com/clinical-context/MultipleSclerosis/33790?utm_content=&utm_medium=email&utm_campaign=DailyHeadlines&utm_source=WC&eun=g421114d0r&userid=421114&email=***@****&mu_id=5520442
I saw this late last night and am trying to process this news. You are asking the right questions - stay tuned.
You are reading content posted in the Multiple Sclerosis Community
Top Neurology Answerers
Australia
ON
Queensland, Australia
Queen Creek, AZ
Find out how beta-blocker eye drops show promising results for acute migraine relief.
In this special Missouri Medicine report, doctors examine advances in diagnosis and treatment of this devastating and costly neurodegenerative disease.
Here are 12 simple – and fun! – ways to boost your brainpower.
Discover some of the causes of dizziness and how to treat it.
Discover the common causes of headaches and how to treat headache pain.
Two of the largest studies on Alzheimer’s have yielded new clues about the disease
