And while we do have a wide variety of drug resources that address inflammation, these drugs do not restore myelin, the protective sheath that surrounds nerves. In order to stop MS from progressing, we desperately need treatments that can potentially support the repair of damaged myelin.
 
A 2023 study shows some very promising results with n-acetyl glucosamine or NAG (also referenced as GLcNAc), an accessible dietary supplement derived from the outer shells of shellfish; vegetarian/vegan forms (non-animal derived) are also available.
 
While NAG has regularly been included as part of a treatment protocol in conditions like osteoarthritis and inflammatory bowel disease, researchers were able to demonstrate its ability to help the brain as well!
 
The study, “N-acetylglucosamine inhibits inflammation and neurodegeneration markers in multiple sclerosis: a mechanistic trial,” concluded that by suppressing damaging autoimmune responses, NAG may contribute to restoring neurological function in some MS patients.
 
Some of the science.
 
NAG is a triple modulator of inflammation, myelination, and neurodegeneration. In mice subjects, it crosses the blood-brain barrier (BBB). This results in an increase in N-glycan branching, suppression of inflammatory demyelination by T and B cells, and triggering stem/progenitor cell mediated myelin repair.
 
N-glycan branching independently regulates five critical pathogenic mechanisms in MS: T-cell hyperactivity; B cell innate function; microglia; myelination, and neurodegeneration.
 
(Note: if you keep these brief explanations below in italics, I see it as an image/graphic so it’s distinct from the content, just to clarify the terms above)
 
Good to know…
 
T-cell hyperactivity: when these white cells are overworked, we may become more susceptible to diseases of an overactive immune response.
 
B cell innate function: B cells, another white cell, protect us from infection through the production of antibodies.
 
Microglia: the resident immune cells of the brain, microglia act as regulators against pathogens.
 
Myelination: the formation of the protective sheath around nerves.
 
Neurodegeneration: the process whereby structures or functions of neurons or nerve cells are impaired, leading to neurodegenerative disease.
                                                             
The study design.
 
Methods comprised an open label, dose-escalation mechanistic trial of oral NAG at 6 g (n = 18) and 12 g (n = 16) for 4 weeks. The study was conducted in MS patients, who at the time were on glatiramer acetate and not in relapse, from March 2016 to December 2019. Researchers sought to assess any changes in serum NAG, lymphocyte N-glycosylation and inflammatory markers and clinical response via the Expanded Disability Status Scale or EDSS, a standardized test used in research settings to measure MS-related disease outcomes.
 
The findings.
 
Oral NAG dose-dependently reduced serum levels of the anti-inflammatory cytokine IL-10, which is increased in the brain of MS patients. Thirty percent of treated patients displayed confirmed improvement in neurological disability, with an average EDSS score decrease of 0.52 points. A reduction in neurofilament light chain (NfL) levels was also observed; neurofilament light chain (NfL) is a blood biomarker that can provide clinically useful information about prognosis and therapeutic efficacy in MS.
 
The benefits.
 
Researchers noted that in addition to its novel mechanism of action that targets both immune and neural stem cells, NAG has several advantages over some existing therapies. It’s generally affordable, historically safe, and well tolerated with few, if any, side effects (i.e., minimal and limited gastrointestinal discomfort). And as an over-the-counter dietary supplement, it’s also widely available.
 
Summing up…
 
As reported by the researchers, the findings from this study are certainly encouraging and warrant additional investigations to determine the full efficacy of NAG supplementation. The scientific team also concluded that the results and the focus on N-glycan branching may also be applicable in future exploratory trials of other neurodegenerative and autoimmune disorders with microglia-associated inflammation, such as Alzheimer’s and Parkinson’s.
 
As with any dietary supplement, our practice ALWAYS recommends choosing a high quality, third-party tested product; if desired, patients may purchase the same supplement used in the study here or at several online retailers.
 
Stay informed, stay curious, and stay on top of your own health plan - understanding your options is incredibly important to your wellbeing today and tomorrow. So please let us know how we can help or answer any of your questions. We are here for you!
 
In hope and healing,
Dr. Suzanne Gazda
 
References:
 
Sy, M., Newton, B.L., Pawling, J. et al. N-acetylglucosamine inhibits inflammation and neurodegeneration markers in multiple sclerosis: a mechanistic trial. J Neuroinflammation 20, 209 (2023). https://doi.org/10.1186/s12974-023-02893-9
 
Mazzuli, J. Development of GlCNAc as disease modifing treatment for Parkinson’s Disease. Northwestern University. 2019. https://www.scholars.northwestern.edu/en/projects/development-of-glcnac-as-disease-modifying-treatment-for-parkinso-3
 
Paharia, P. The association between regular glucosamine use and risk of dementia. News Medical Life Sciences. 2023. https://www.news-medical.net/news/20230403/The-association-between-regular-glucosamine-use-and-risk-of-dementia.aspx
 
Lee, B.E., Suh, PG. & Kim, JI. O-GlcNAcylation in health and neurodegenerative diseases. Exp Mol Med 53, 1674–1682 (2021). https://doi.org/10.1038/s12276-021-00709-5
 
Brandt AU, Sy M, Bellmann-Strobl J, et al. Association of a Marker of N-Acetylglucosamine With Progressive Multiple Sclerosis and Neurodegeneration. JAMA Neurol. 2021;78(7):842–852. doi:10.1001/jamaneurol.2021.1116 https://jamanetwork.com/journals/jamaneurology/fullarticle/2779917
 
Starossom SC, Mascanfroni ID, Imitola J, Cao L, Raddassi K, Hernandez SF, et al. Galectin-1 deactivates classically activated microglia and protects from inflammation-induced neurodegeneration. Immunity. 2012;37(2):249–63.

With numerous symptoms that challenge their lives every day, multiple sclerosis (MS) patients also appear to suffer almost twice as many migraine events as their healthy counterparts. According to a soon-to-be-published study, this represents nearly 24% of individuals with a MS diagnosis.

First, some basic facts about migraine: it’s one of the most common chronic diseases in the United States and around the world, affecting roughly 15% and 14% of the populations respectively. Migraines are thought to be the result of interactions occurring between neurons, glial cells (which are the cells that help support, connect, and protect the neurons of the central and peripheral nervous systems), vasculature or the arrangement of blood vessels, and inflammatory signaling. Symptoms may include but are not limited to:

• Recurrent, unilateral headaches that may last anywhere from a few hours to a few days.
• Nausea
• Light and noise sensitivity
• Dizziness
• Fatigue, mood changes, and other issues.

 
Read more about migraine in our previous blog at: https://www.suzannegazdamd.com/blog/migraines-the-science-causes-and-treatment-options
 
MS is a neurological autoimmune disorder that has over the last 30 years become increasingly prevalent worldwide, which may be due in part to more sophisticated diagnostic tools, socioeconomic factors, and geographic influences. We have written extensively about the disorder, its potential treatments, and much more at https://www.suzannegazdamd.com/blog---ms-in-the-news.
 
The National Multiple Sclerosis Society explains “Multiple sclerosis is a disease that impacts the brain, the spinal cord, and optic nerves, which make up the central nervous system and controls everything we do. The exact cause of MS is unknown, but we do know that something triggers the immune system to attack the CNS. The resulting damage to myelin, the protective layer insulating wire-like nerve fibers, disrupts signals to and from the brain. This interruption of communication signals causes unpredictable symptoms such as numbness, tingling, mood changes, memory problems, pain, fatigue, blindness and/or paralysis. Everyone’s experience with MS is different and these losses may be temporary or long lasting.”
 
More evidence regarding a link.
 
MS patients have a much higher risk of experiencing migraine symptoms than the general population. Additionally, migraine and MS patients share similar demographics, with the highest incidence among young, female patients with no history of another established condition.
 
Many decades ago, studies began reporting on the MS/migraine connection. In 1952, Compston described a possible association, noting that 2% of patients develop migraine within three months of the onset of MS.
 
The strongest evidence to date for an association between migraine and MS comes from a cohort study within the Nurses’ Health Study II.  A 2012 study found that women with migraines prior to their diagnosis of MS had a 39% higher risk of developing MS when compared to the participants without migraines.
 
What are the pathophysiological mechanisms between migraine and MS and MS and migraine?
 
Some of the mechanisms contributing to the link between the disorders:

1. Dysfunction of the brain circuitry modulating the peripheral nociceptive stimuli (areas of the brain networks for pain stimuli and pain suppression). 
2. Migraines may occur due to direct MS-related damage to certain brain structures or due to changes in metabolic activity. An increasing amount of evidence, much of it clinical, suggests that migraine is a response to cerebral energy deficiency or oxidative stress levels that exceed antioxidant capacity and that the attack itself helps to restore brain energy homeostasis and reduces harmful oxidative stress levels.
3. Neuroinflammation: Brain imaging studies show white matter lesions in both MS and migraine patients. Neuroinflammatory mechanisms likely play a key role in downstream effects.
4. Geography: One theory is that the headaches of MS are attributable to the geography of demyelinating lesions or where the lesions are such as the brain stem and periaqueductal gray matter. The periaqueductal gray (PAG)s implicated in multiple functions, such as pain, analgesia, fear, anxiety, and cardiovascular responses and is believed to be a central hub for the integration of the pain experience.
5. Cortical Spreading Depression (CSD): Another potential mechanism is that migraine, and specifically migraine with aura, may lead to subtle increase in permeability of the blood–brain barrier and neuroinflammation. Migraine is thought to generate from CSD and the aura phase that precedes migraine headache in about 20–30% of migraineurs may be a direct consequence of the events of CSD; the role of CSD in migraine patients without aura is not well understood and as such the relationship cannot yet be explained.

 
CSD, a slowly propagated wave of depolarization followed by suppression of brain activity, is a remarkably complex event that involves dramatic changes in neural and vascular function.
 
This electrophysiologic event underlying migraine and an attack trigger may be a crucial factor for promoting MS onset by facilitating contact between peripheral immune cells and the usually privileged CNS structures. CSD may increase factors that influence the integrity of the blood–brain barrier permeability, thereby initiating neuroinflammation.

In summary…
 
There are many environmental factors that may lead to the onset of migraine and multiple sclerosis – clearly, more research is needed to better understand the corresponding links between these disorders.
 
As we have continually stressed in previous writings and in our clinical practice, lifestyle modifications also can be helpful not only in promoting general health and wellness, but in patients living with nearly any chronic disease. That’s why we also continue to encourage patients to be informed about your or your loved ones’ conditions and to be aware of all available resources!
 
The American Migraine Foundation has a wealth of helpful literature regarding the disorder and potentially helpful lifestyle approaches to consider:
 
https://americanmigrainefoundation.org/resource-library/lifestyle-changes-for-migraine/
 
And please visit our blog library as well for other related reading, including:
 
https://www.suzannegazdamd.com/blog/study-shows-that-dietary-intervention-could-aid-migraine-sufferers
 
https://www.suzannegazdamd.com/blog/migraine-remedies-can-a-drug-for-ms-or-natural-treatments-help
 
https://www.suzannegazdamd.com/blog/what-if-there-was-another-way-to-treat-neuropathic-pain
 
If you have questions or need to schedule a visit, please reach out to our offices – we’re here to help!
 
In hope and health,
Dr. Suzanne Gazda
 
References:
 
Mohammadi, M. et al. The association between multiple sclerosis and migraine: A meta-analysis. Multiple Sclerosis and Related Disorders. Volume 79, 2023.
https://doi.org/10.1016/j.msard.2023.104954.
https://www.sciencedirect.com/science/article/abs/pii/S2211034823004558
 
Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018;38(1):1-211. doi:10.1177/0333102417738202
 
Stovner, L.J., Hagen, K., Linde, M. et al. The global prevalence of headache: an update, with analysis of the influences of methodological factors on prevalence estimates. J Headache Pain 23, 34 (2022). https://doi.org/10.1186/s10194-022-01402-2

Reports of improved neurologic disability, fatigue, and depression along with a “heightened quality of life” were just a few of the positive impacts of following a ketogenic diet (KD).
 
So, I was particularly interested in a new study published in Clinical Nutrition that sought to better understand the tolerability and clinical efficacy of this dietary approach – in other words, while many patient-reported and clinical benefits are noted, what is the sustainability of these diets outside of a clinical trial? What factors would increase the likelihood that the diet would be continued and to what degree?
 
The study enrolled 64 subjects with diagnosed RRMS and all followed the same diet that included restriction of net carbohydrates to <20 g/day with a subsequent increase healthy fat intake; there was no caloric restriction.
 
The results were indeed promising: of the ~89% of original enrollees who completed the six-month study, many patients perceived an improvement in MS symptoms such as:

• Paresthesia (burning and/or prickling sensations) and pain often felt in the extremities.
• Numbness
• Balance
• Frequency or severity of headaches
• A subset of subjects was able (with physician guidance) to reduce and/or discontinue previously prescribed medications that had been used for symptomatic relief.

 
Three months following the study conclusion, those patients who cited weight loss and concurrent reduction in body-mass index (BMI) were most likely to have continued the KD program; even those participants who chose to follow a similar but less restrictive diet subsequently shifted their dietary patterns to include more protein, fewer carbohydrates, and less sugar. Those individuals who ceased the diet entirely reported worse concentration (30%), sleep problems (23%), and ongoing MS symptoms.
 
More about dietary influences.
 
Dr. Terry Wahls recently shared the results of a small trial in MS patients utilizing intermittent fasting. This studyshowed a marked increase in both brain volume measurement and improved cerebral blood flow as measured using magnetic resonance imaging (MRI).
 
One of our earlier blogs also looked at the effects of dietary restriction and intermittent fasting and presented evidence from 2021 that noted significant benefits relevant to a healthier gut microbiome and commensurate reduced inflammation – which we know is not only associated with MS, but all autoimmune diseases as well.
 
The major takeaway: dietary guidance is important for EVERYONE and, as we’ve continually emphasized, it should be the first step of the healing journey! Even if you do not have MS or any other identified disorder, what we eat (or don’t eat) can truly play a huge role in our present and future wellbeing.
 
We encourage you to please take some time to read and learn more about the impact of dietary choices on our brain and general health:
 
What does gut health have to do with MS?
https://www.suzannegazdamd.com/blog---ms-in-the-news/what-does-gut-health-have-to-do-with-ms-research-shows-it-could-be-significant
 
Diet and managing MS.
https://www.suzannegazdamd.com/blog---ms-in-the-news/what-do-studies-tell-us-about-diet-and-managing-ms
 
Does all disease begin in the gut?
https://www.suzannegazdamd.com/blog/does-all-disease-begin-in-the-gut
 
How we eat now and our future brain health.
https://www.suzannegazdamd.com/blog/what-how-we-eat-now-could-determine-our-future-brain-health
 
And of course, feel free to reach out to our offices if we can answer any questions or schedule a visit. We’re here to help!
 
In hope and healing,
Dr. Suzanne Gazda
 
References:
 
Gazda, S. A low carb, high fat diet may improve symptoms in MS patients. suzannegazdamd.com. (May 2022). https://www.suzannegazdamd.com/blog---ms-in-the-news/a-low-carb-high-fat-diet-may-improve-symptoms-in-ms-patients
 
Wetmore, E. et al. Ketogenic diet in relapsing multiple sclerosis: Patient perceptions, post-trial diet adherence & outcomes. Clinical Nutrition. (August 2023). https://www.sciencedirect.com/science/article/abs/pii/S0261561423002145
 
Wahls, T. The Impact On Brain Volume And Biomarkers In The Setting Of MS Using Intermittent Fasting. terrywahls.com. (June 2023). https://terrywahls.com/the-impact-on-brain-volume-and-biomarkers-in-the-setting-of-ms-using-intermittent-fasting/
 
Gazda, S. Intermittent fasting and dietary restriction for MS. suzannegazdamd.com. (March 2021). https://www.suzannegazdamd.com/blog---ms-in-the-news/intermittent-fasting-and-dietary-restriction-for-ms

The gut microbiome refers to microbes or the bacteria, fungi, etc. that live mostly in the small and large intestines and act almost as another functioning organ. Not only is the gut microbiome critical to digestion, but we’re also learning that it affects the wellbeing of our immune health as well.
 
We know a there’s essentially a direct route between our gut and our brain – so we’d expect that the state of our microbiome could affect our neurological wellness too. 
 
Recently we read an article that explores the fascinating connection between the microbiome and MS, noting the many studies which have found patients with the disease have a gut microbiome that is very different than people who do not have the disease – but what causes this isn’t fully understood. What is known, however, is that to a large degree, we really are what we eat. And diet whether we have a known disorder or not can certainly influence how we feel and how well our immune system protects us.

Immune system modulation.
 
In a review published in Nature, scientists did find that “modulation of the microbiome could be therapeutically beneficial,” presenting evidence from trials conducted in mice and humans that these effects of the gut microbiota on the immune system are important in the development and course of MS. Additionally, they looked at strategies for manipulating the microbiome status and whether it could be used to influence disease-related immune dysfunction, such as we see with MS, and may potentially result in novel therapeutics.
 
Another study concluded that “diet is able to influence the composition of the intestinal bacterial flora and indirectly favor the development of autoimmune inflammatory diseases such as MS.” The investigators stated that while the cause of MS is not always known and depends on heterogeneous factors (both genetic and environmental) that determine the RISK of disease, our eating habits, lifestyle, and other modifiable risk factors can influence the COURSE of the condition.

Extensive research suggests that certain dietary patterns may indeed have an impact on disease progression and symptom management. Our colleague and friend, Dr. Terry Wahls, who following her MS diagnosis from over 20 years ago designed and adhered to a unique protocol that includes dietary controls, recently wrote about the benefits of intermittent fasting and caloric restriction as a tool for disease management.
​
In her June blog, she spotlighted the results of a small trial that used intermittent caloric restriction over a period of 12 weeks, following this physician- and dietitian-supervised regimen: The intervention was to reduce calories to about 25% of usual intake (< 500 calories) on two non-consecutive days each week and to not compensate for the reduced intake on the other days. On the reduced calorie days, participants were to eat salads with steamed vegetables and a light dressing. 
 
Exciting results emerged at the end of the study period – participants showed a marked increase in brain volume measurement as determined by MRIs, as well as improved blood flow. Dr. Wahls noted too that previous trials in animal models had shown intermittent caloric restriction to enhance blood flow and cognition, as well as reducing oxidative stress and inflammation. 
 
More research is forthcoming as the scientific community continues to pursue the potential benefits of these and similar approaches to MS as well as other immune-mediated disorders.

Our recommendation for all patients – and even if you aren’t challenged by a neuroimmune or other diagnosis – is, when possible, to choose fresh over processed foods, preferably organic and non-GMO products. There are also certain foods to avoid, such as:

Dairy
Breads (e.g., wheat, rye, white, sourdough, etc.) 
Cereals and many grains (i.e., barley, most commercial oatmeal)
Wheat or semolina pastas
Crackers, cookies (any prepared or baked goods that use flours other than rice or another acceptable gluten-free starch)
Processed foods (soups, frozen meals, etc.)
Beer (derived from problematic grains)
 
Following a healthy diet can help also help in addressing obesity, a known factor at the root of many diseases including MS. In fact, obesity in childhood has been shown to increase the risk of MS developing in young adults and later in life.
 
Depending on your particular health needs and if there are no contraindications with any medicines, there are foods to consider including as part of a healthy diet, like fermented items (i.e., kimchi), sauerkraut) and probiotics; fiber-rich foods like fresh vegetables and fruits; lean proteins; olive oil; high quality vitamin D supplements, and more.
 
Importantly, never change or add anything to your diet without consulting your physician, whether it’s a new supplement and certainly if you are interested in intermittent fasting and caloric restriction…this should only be undertaken with medical supervision.
 
Of course, while diet alone cannot replace disease-modifying or other medically prescribed treatments, it can play a positive, complementary role in managing the condition and promoting overall wellbeing. Be sure to check our blog archives for more related reading and let us know if we can help!
 
In hope and healing,
Dr. Suzanne Gazda
 
References:
 
Gazda, S. Does all disease begin in the gut
Weiss, K. Can gut health affect multiple sclerosis? Everyday Health. (2022) https://www.everydayhealth.com/multiple-sclerosis/can-gut-health-affect-multiple-sclerosis/
 
Schepici G, Silvestro S, Bramanti P, Mazzon E. The Gut Microbiota in Multiple Sclerosis: An Overview of Clinical Trials. Cell Transplant. 2019;28(12):1507-1527. doi:10.1177/0963689719873890
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6923550/
 
Correale, J., Hohlfeld, R. & Baranzini, S.E. The role of the gut microbiota in multiple sclerosis. Nat Rev Neurol 18, 544–558 (2022). https://doi.org/10.1038/s41582-022-00697-8.
 
Wahls, T. The Impact On Brain Volume And Biomarkers In The Setting Of MS Using Intermittent Fasting. terrywahls.com. (2023)
https://terrywahls.com/the-impact-on-brain-volume-and-biomarkers-in-the-setting-of-ms-using-intermittent-fasting/
 
Gazda, S. Intermittent fasting and dietary restriction for MS. suzannegazdamd.com. (2021)
https://www.suzannegazdamd.com/blog---ms-in-the-news/intermittent-fasting-and-dietary-restriction-for-ms
 
Gazda, S. Childhood obesity linked to higher risk of MS. suzannegazdamd.com. (2020)
https://www.suzannegazdamd.com/blog/childhood-obesity-linked-to-higher-risk-of-ms
 
Gazda, S. Upset stomach? Your brain may be trying to tell you something. suzannegazdamd.com. (2021)
https://www.suzannegazdamd.com/blog---ms-in-the-news/upset-stomach-your-brain-may-be-trying-to-tell-you-something

As recently reported, multiple sclerosis patients in the U.S. (age 22+) can with a prescription now obtain the portable neuromodulation stimulator (PoNS) device, which could improve walking ability in individuals with mild to moderate disease activity.1

We wrote about the PoNS device last year when it was approved by the Food and Drug Administration, but until last month it was not as yet available commercially in this country, although it has been in use in Canada and Australia.
 
Developers Helius Technologies found that with short term therapy the device can enhance mobility, decrease the degree of disability, and additionally provide quality of life improvements through its neuromodulation and neuroplasticity mode of operation. Noninvasive and portable, the PoNS device has been tested in several clinical trials with no identified side effects to date. 
 
The opportunity to use neuromodulation to potentially encourage the creation of new neural connections is a significant boon to patient treatment options that could offer more hope in the fight against MS.

Please read our previous article that fully details how the PoNS device works and learn more about its mechanisms: https://www.suzannegazdamd.com/blog---ms-in-the-news/scientific-advances-are-helping-to-heal-the-brain
 
And to find out more about neuroplasticity and how it affects brain health, see:
https://www.suzannegazdamd.com/blog/novelty-as-a-neuroplasticity-tool
 
If you have specific questions regarding whether this innovation may be appropriate for your condition, please talk to your healthcare provider and, of course, don’t hesitate to reach out to our offices if you’d like to schedule a visit. We are here to help!
 
In hope and healing,
Dr. Suzanne Gazda 

References:
 
1 Shapiro, L., PhD. PoNS Device for MS-associated Gait Problems Now Available in US. MS News Today. (April 29, 2022). https://multiplesclerosisnewstoday.com/news-posts/2022/04/29/pons-brain-stimulating-device-multiple-sclerosis-gait-problems-now-available-us/

​Once again, there’s more clinical evidence that dietary interventions can positively impact the course of many autoimmune diseases, including multiple sclerosis (MS). 

In a recent study at the University of Virginia, researchers found that following a low-carbohydrate, high-fat protocol like the “keto diet” reduced the symptoms of neurologic disability, fatigue, and depression in patients with relapsing-remitting MS. Additionally, the study participants noted a “heightened overall quality of life,” reporting that their performance also improved on select physical endurance testing.1
 
Results were monitored in the laboratory at the start of the trial and again at three and six months; tests confirmed adherence to the diet by measuring the ketones, which is a metabolite that the body produces when it is burning fats – a hallmark of a keto-type diet. A total of 83% of the original 65 participants adhered to the diet for the full term of the study period. Scientists also found that study participants had less body fat at the end of the trial as well as decrease in depression and fatigue, with an improvement in disability scores. And laboratory testing showed a reduction in inflammatory markers in subjects’ blood samples.2
 
The basics of a keto diet.

The keto diet is founded upon these guidelines and has been shown to be beneficial in reducing blood sugar levels in patients with diabetes, which is also an inflammatory-based condition.
​
Patients, with their doctor’s guidance, may enjoy a variety of:

• Lean proteins such as fish, chicken, eggs, and limited red meats (red meat can cause inflammation in some patients).
• Healthy fats including olive oil, avocados and avocado oil, some butter and cream although we often recommend limiting dairy consumption.
• Fresh, leafy greens such as spinach and lettuces, broccoli, celery, asparagus and similar produce. 
• Nuts and seeds (excluding prepared items like trail mix or packaged granolas)

 
There are additional tenets of a keto diet that may or may not be appropriate when following this type of plan in the management of a disorder like MS – so it’s doubly important to talk to your practitioner before eliminating any foods or making drastic dietary changes! But keto or other monitored protocols may be helpful as part of a total therapeutic approach only if you eliminate the detrimental things like highly processed, commercially prepared snacks and foods that typically contain saturated fat, excess sodium, preservatives, chemical additives, and a lot of “empty” calories.

While additional research is definitely warranted to learn how keto diets may be a helpful tool in MS protocols, this latest study does present with very interesting and hopeful findings. If you have questions or need to schedule an appointment, just reach out to our offices – we’re here to help!
 
In health and healing,
Dr. Suzanne Gazda

References:
 
1 University of Virginia, UVAHealth (March 8, 2022)
https://makingofmedicine.virginia.edu/2022/03/08/big-benefits-for-keto-diet-for-people-with-ms/
 
2 Neuroscience News (March 2022)
https://neurosciencenews.com/ketogenic-diet-multiple-sclerosis-20142/

One recent investigation explored the link between cow’s milk proteins and the prevalence of multiple sclerosis (MS). The environmental influences involved in the pathophysiology of autoimmune diseases like MS includes the very things we eat, drink, and are exposed to on a regular basis.We’ve long thought that milk from cows, which contains the protein casein and derivative products, has been shown to negatively affect MS patients.1 
 
In this new study, the scientists also looked at the role of antibodies and how these could exacerbate symptoms in a subset of patients. Their findings demonstrated that “a high percentage of MS patients harbor antibodies to bovine casein but also that antibody cross-reactivity between cow’s milk and CNS antigens can exacerbate demyelination.” 
 
Additionally, the authors stated a belief that consuming cow’s milk in some patients who have previously experienced a loss of tolerance to bovine casein could indeed aggravate the disease. They concluded that the data suggest these patients with antibodies to the cow’s milk protein could benefit from restricting dairy consumption and also expand clinician’s understanding of how diet influences MS in order to identify the most individualized and beneficial diet plans along with disease-modifying treatments (DMTs).
 
In addition to dairy, we often recommend our MS patients limit or avoid altogether foods containing gluten, just some of which include:
 

• Breads (e.g., wheat, rye, white, sourdough, etc.) 
• Cereals and many grains (e.g. barley, most commercial oatmeal)
• Wheat or semolina pastas
• Crackers, cookies (any prepared or baked goods that use flours other than rice or another acceptable gluten-free starch)
• Processed foods (soups, frozen meals, etc.) – become a label reader!
• Beer

 
We know – the list can be long! But there is a great deal of research that shows how gluten can incite inflammation in autoimmune disease and may be a factor in MS.
 
There also are studies that have provided preclinical data suggesting that a keto diet (KD), which restricts foods that typically contain gluten, and a fasting diet (FD) may “modulate immunity, reduce disease severity, promote remyelination” as observed in studies using mice models.3 And as reported in MS News Today, a recent small study found that short-term ketogenic diet resulted in significant improvements in people with relapsing-remitting multiple sclerosis (RRMS). 
 
You can find additional related reading in our blog archives about the role of diet in MS as well as other neurodegenerative diseases, including:
 
https://www.suzannegazdamd.com/blog---ms-in-the-news/intermittent-fasting-and-dietary-restriction-for-ms
 
https://www.suzannegazdamd.com/blog/new-study-shows-lower-risk-of-ms-relapse-with-the-prudent-diet
 
Or let us know if you have any questions or need to schedule a visit – we’re always here to help!
 
In hope and healing,
Dr. Suzanne Gazda 
 
References:
 
1 Malosse, D & Hervé, Perron & Sasco, Annie & Seigneurin, J. (1992). Correlation between Milk and Dairy Product Consumption and Multiple Sclerosis Prevalence: A Worldwide Study. Neuroepidemiology. 11. 304-12. 10.1159/000110946.
 
2 Chunder, R., Weier, A., Mäurer, H., Luber, N. et al. Antibody cross-reactivity between casein and myelin-associated glycoprotein results in central nervous system demyelination. (2022) Proceedings of the National Academy of Sciences (PNAS).https://doi.org/10.1073/pnas.2117034119
https://multiplesclerosisnewstoday.com/news-posts/2022/03/08/immune-response-casein-cow-milk-protein-may-explain-ms-diary-link/
 
3 Bahr LS, Bock M, Liebscher D, et al. Ketogenic diet and fasting diet as Nutritional Approaches in Multiple Sclerosis (NAMS): protocol of a randomized controlled study. Trials. 2020;21(1):3. Published 2020 Jan 2. doi:10.1186/s13063-019-3928-9

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:
 
https://www.suzannegazdamd.com/blog---ms-in-the-news/understanding-the-implications-in-cognitive-dominant-ms
 
https://www.suzannegazdamd.com/blog/ms-and-contrast-mris-is-there-another-option
 
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
 
References:
 
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

In treating patients with any neurological disease, it’s important to look at each case on an individual basis – what is helpful for one person may not be valuable in another, based on any number of variables. 

With multiple sclerosis (MS), the issue of de-escalating therapies, or transitioning patients from high efficacy treatments with greater risks to approaches that may be safer but have lower efficacy, is always a question that requires careful consideration. And in older individuals, this can be a particularly worrisome issue.
 
We know that as patients age, there can be a concern that the high-efficacy MS medications could increase the potential for illnesses such as the John Cunningham virus (JCV) and subsequently progressive multifocal leukoencephalopathy (PML), other infections, or certain malignancies. So, knowing when to de-escalate or even discontinue a particular treatment is critical to the patient’s neurological and general wellbeing. 
 
The John Cunningham virus, or JC virus (JCV) causes PML. JC virus is also known as human polyomavirus.  2 Most people have been infected with this virus in childhood although it rarely causes symptoms. However, people with a weakened immune system, due to either disease and/or the effects of immunosuppressant therapies are at greater risk of developing PML.1
 
PML is a disease of the white matter of the brain, caused by a virus infection that targets cells that make myelin, which is the material that insulates nerve cells or neurons.
 
A recent study regarding de-escalation.
 
In this study, scientists looked at the key question of de-escalation as it pertains to patient age and disease progression or instances of relapse. The authors reanalyzed data from a retrospective, real-world cohort of MS patients to model disease activity and impact of certain disease-modifying therapies (DMTs) along with patient age. 
 
The results: “In a real-world cohort of relapsing MS patients, high efficacy DMTs had less benefit with aging but were associated with increased risks. This cohort helps overcome some limitations of trials where older patients were excluded. To better balance benefits/risks, we propose a DMT de-escalation approach for aging MS patients.”
 
Researchers also noted that DMTs are typically more effective early in the disease course and are therefore more justified at that stage; patient ages are also younger earlier in the disease course and there is less disability, so there is a lower risk of adverse events.
 
Their recommendations included considering whether de-escalating therapies as patients approach 40 to 55 years of age would be most appropriate. Patient disability, especially in those who required bilateral support or who are wheelchair bound, and DMT-specific factors that could increase infection risk should also be considered. If after de-escalation the patient is clinically stable, then discontinuing the therapy might be an option and with any proposed change in prescribed treatments, the patient and their family should always be part of the decision process. 
 
In our practice, we approach MS and treatment for any disorder on a patient-specific basis and always review clinical status throughout any therapeutic course. It’s critical to examine the “risk vs. benefit” in making these choices and looking at all the factors that can affect disease progression. And studies like this are extremely valuable in reaffirming clinical practices for the most appropriate guidance. 
 
If you have any questions or would like to consult with our team, please reach out to our offices – we are here to help!
 
In hope and healing,
Dr. Suzanne Gazda  
 
References: 
 
1 Medline Plus, National Library of Medicine
https://medlineplus.gov/ency/article/000674.htm
 
2 Vollmer BL, Wolf AB, Sillau S, Corboy JR and Alvarez E (2022) Evolution of Disease Modifying Therapy Benefits and Risks: An Argument for De-escalation as a Treatment Paradigm for Patients With Multiple Sclerosis. Front. Neurol. 12:799138. doi: 10.3389/fneur.2021.799138