The findings included confirmation that up to 50% of the disability accumulation in adult patients with relapse-remitting multiple sclerosis (RRMS) was not associated with “overt relapses.” What Dr. Frank Lublin and colleagues noted in the published study, “How patients with MS acquire disability” was that disease progression independent of relapse activity (PIRA) started in the early disease stage, occurred in all phenotypes or groups, and was identified as the primary factor in disability accumulation in the progressive phase of the disease.
Early treatment with disease-modifying therapies (DMTs) appears to provide the most effective course of action. Using the Expanded Disability Status Scale (EDSS), the study found that for placebo recipients, it took nearly nine (8.95) years for greater limitations in walking ability (EDSS 4) to manifest and 18.48 years to require walking assistance (EDSS 6). But treating patients with DMTs earlier delayed these times significantly by 3.51 years and by 3.09 years respectively.1
One excellent resource is the use of Neuroquant® technology, which provides an excellent means of following volume loss long before it is evident on standard magnetic resonance imaging (MRI). Also important, Neuroquant can detect high levels of neuroinflammation that tell us that the current treatment may be failing.
As we’ve previously written, NeuroQuant is FDA-approved software that analyzes a neurological MRI and provides critical details about changes in certain brain structures. You can read more about its complementary benefits in a total treatment protocol at: https://www.suzannegazdamd.com/blog---ms-in-the-news/what-a-neuroquantr-image-can-tell-us-about-ms
We need to employ every avenue of treatment, including diet and modifiable lifestyle changes, in order to prevent disease progression. In our practice, we aim for vitamin D levels between 60 and 80 ng/mL and there is much research that points to the efficacy of this often-deficient nutrient and its value in MS approaches. Studies also show that vitamin D deficiency can be linked to impaired cognitive function even in the early stages of the disorder.
Can other supplements be of value?
While we typically think of melatonin as a readily available sleep aid, it also has been shown to be helpful for overall brain health. In the peer-reviewed journal Revue Neurologique, researchers reported that the natural hormone melatonin showed great potential to prevent and possibly even alleviate neurodegenerative diseases, such as MS as well as Alzheimer’s and Parkinson’s disease.2 In fact, the impressed scientists even concluded that “melatonin may be the solution we have been looking for."
They stated that the neuroprotective effects of melatonin can be attributed to many factors. Melatonin appears to cushion the brain from the effects of “stress” hormones, such as epinephrine, cortisol, and norepinephrine, all of which can impair memory among other deleterious effects. Melatonin can also increases levels of a protein known as a brain-derived neurotrophic factor (BDNF), which increases the formation of neurons, which are the fundamental units of our brain and nerve system. So, it stands to reason that providing any level of protection for these critical cells is integral to maintaining our brain health. And both vitamin D and melatonin are widely available for optimum patient access.
Our blog archives have a number of articles relevant to MS and current therapies, so be sure to check out these and other titles:
And please let us know if you have any questions or would like to schedule a visit – we’re here to help!
In hope and healing,
Dr. Suzanne Gazda
1 Fred D. Lublin, Dieter A. Häring, Habib Ganjgahi, Alex Ocampo, Farhad Hatami, Jelena Čuklina, Piet Aarden, Frank Dahlke, Douglas L. Arnold, Heinz Wiendl, Tanuja Chitnis, Thomas E. Nichols, Bernd C. Kieseier, Robert A. Bermel, How patients with multiple sclerosis acquire disability, Brain, 2022;, awac016, https://doi.org/10.1093/brain/awac016
1 Gunata M, Parlakpinar H, Acet HA. Melatonin: A review of its potential functions and effects on neurological diseases. Rev Neurol (Paris). 2020;176(3):148-165. doi:10.1016/j.neurol.2019.07.025