I've been researching this a lot, since I'm still trying to decide whether to inject myself with these drugs.
As FJLhawk pointed out, at least one major study showed interferon does not reduce time to disability.
The reasons I'm still considering this, in spite of my needle phobia, are:
1. Interferon Beta is an antiviral drug, and the viral theory is an alternate theory of MS.
2. Interferon Beta calms systemic inflammation and inflammation is apparently a mechanism of the damage done to our nervous system.
3. There is an ugly mortality study written by Professor Douglas Goodin of the University of California San Francisco, neurologist and professor at the local MS center. I'm not sure how much to trust it, since the professor was paid by Bayer, but he showed that a group people treated with Betaseron in an early trial of the drug were less likely to die of MS related causes than the controls in the same experiment who did not receive interferon treatment. It isn't an easy or cheerful read.
All of this suggests to me that difference in time to disability is not the only important variable in measuring the effect of a drug for MS. Reduction in relapses has its own value. Calming inflammation and reducing oxidative stress is an important task to accomplish by whatever method.
I am not yet personally taking interferon beta. I am considering it. I don't fully understand the statistics around reduction in relapses, so I don't know how much benefit is provided. I also don't trust the conflicts of interest around the big drug companies. I'm not sure how reliable the Goodin study is.
Having said that, here is a very small subset of the research being done around interferon beta and beneficial effects on harmful inflammation, both in MS and in other conditions.
Interferon-β attenuates lung inflammation following experimental subarachnoid hemorrhage
Pieter M Cobelens, Ivo ACW Tiebosch, Rick M Dijkhuizen, Peter H van der Meide, René Zwartbol, Cobi J Heijnen, Jozef Kesecioglu, Walter M van den Bergh
Crit Care. 2010; 14(4): R157. Published online 2010 August 23. doi: 10.1186/cc9232
Suppression of Inflammation in Ulcerative Colitis by Interferon-β-1a Is Accompanied by Inhibition of IL-13 Production
Peter J. Mannon, Ronald L. Hornung, Zhiqiong Yang, Chuli Yi, Catherine Groden, Julia Friend, Michael Yao, Warren Strober, Ivan J. Fuss
Gut. Author manuscript; available in PMC 2012 August 30.
Published in final edited form as: Gut. 2011 April; 60(4): 449–455. Published online 2010 October 22. doi: 10.1136/gut.2010.226860
Interferon-β treatment in multiple sclerosis attenuates inflammatory gene expression through inducible activity of the phosphatase SHP-1
George P. Christophi, Michael Panos, Chad A. Hudson, Chriso Tsikkou, Cornelia Mihai, Luis J. Mejico, Burk Jubelt, Paul T. Massa
Clin Immunol. Author manuscript; available in PMC 2010 October 1.
PEGylated interferon-β modulates the acute inflammatory response and recovery when combined with forced exercise following cervical spinal contusion injury
Harra R. Sandrow-Feinberg, Victoria Zhukareva, Lauren Santi, Kassi Miller, Jed S. Shumsky, Darren P. Baker, John D. Houle
Exp Neurol. Author manuscript; available in PMC 2011 June 1
J Inflamm Res. 2010; 3: 25–31..
Injectable interferon beta-1b for the treatment of relapsing forms of multiple sclerosis
Slobodan M Jankovic
Multiple sclerosis (MS) is chronic inflammatory and demyelinating disease with either a progressive (10%–15%)
or relapsing-remitting (85%–90%) course. The pathological hallmarks of MS are lesions of both white and grey matter
in the central nervous system. The onset of the disease is usually around 30 years of age.
The patients experience an acute focal neurologic dysfunction which is not characteristic,
followed by partial or complete recovery. Acute episodes of neurologic dysfunction with
diverse signs and symptoms will then recur throughout the life of a patient, with periods of
partial or complete remission and clinical stability in between. Currently, there are
several therapeutic options for MS with disease-modifying properties. Immunomodulatory therapy
with interferon beta-1b (IFN-β1b) or -1a, glatiramer and natalizumab shows similar efficacy;
in a resistant or intolerant patient, the most recently approved therapeutic option is mitoxantrone.
IFN-β1b in patients with MS binds to specific receptors on surface of immune cells,
changing the expression of several genes and leading to a decrease in quantity of
cell-associated adhesion molecules, inhibition of major histocompatibility complex
class II expression and reduction in inflammatory cells migration into the central nervous system.
After 2 years of treatment, IFN-β1b reduces the risk of development of clinically
defined MS from 45% (with placebo) to 28% (with IFN-β1b). It also reduces relapses for 34%
(1.31 exacerbations annually with placebo and 0.9 with higher dose of IFN-β1b) and
makes 31% more patients relapse-free. In secondary-progressive disease annual rate of
progression is 3% lower with IFN-β1b. In recommended doses IFN-β1b causes the following
frequent adverse effects: injection site reactions (redness, discoloration,
inflammation, pain, necrosis and non-specific reactions), insomnia, influenza-like syndrome,
asthenia, headache, myalgia, hypoesthesia, nausea, paresthesia, myasthenia, chills and depression.
Efficacy of IFN-β1b in relapsing-remitting MS is higher than that of IFN-β1a, and
similar to the efficacy of glatiramer acetate. These facts promote IFN-β1b as
one of the most important drugs in the spectrum of immunological therapies for this debilitating disease.