The Ketogenic Diet & Multiple Sclerosis

Multiple Sclerosis (MS) is a neurological disease caused by demyelination or breakdown of the myelin coating around the nerve cells (1).   This is referred to as a neurodegeneration where the physical structure of the nerve is compromised, much like the coating around an electrical wire being chipped or stripped away. Common symptoms of MS are sensory symptoms in the extremities or face, unilateral visual loss, acute or subacute motor weakness of the muslces, diplopia (double vision), gait disturbance and balance problems, Lhermitte sign (electric shock-like sensations that run down the back and/or limbs upon flexion of the neck), vertigo, bladder problems, loss of control of a limb,  and pain.


Effects of Ketosis on Multiple Sclerosis

Initially, and for many years, the degeneration seen in multiple sclerosis (MS) was thought to occur because of an acute inflammatory attack on the cells by dis-regulated immune cells crossing the blood brain barrier.  However, treatments focused on modulating the inflammatory attack seem to have no effect on the degeneration and demyelination.  Thus, the actual definitive cause of this demyelination and neuro-degeneration has eluded us since 1868, when Jean-Martin Charcot first described it.

Recent studies point to evidence that this demyelation may be due to degeneration or breakdown of the nerve cell’s ability to use glucose as a primary fuel (2, 3).  It is now theorized that MS may be due to a combination of degeneration and localized inflammation related to poor glucose uptake causing the demyelination which is seen in a number of MS cases (4, 5, 6).

Demyelination of Nerve

A. Normal nerve cell with intact myelin sheath around the axon. B. Demyelinated axion nerve losing its ionic charge due to escape of potassium. C. Radio-labled tracer allowing visualization of demyelination on PET Scan

With this dual concept in mind, ketogenic diets have demonstrated some promising results when used with neurological diseases including MS.  Ketogenic diets have been used in the treatment of epilepsy since 500 B.C. and in the treatment of obesity since 1860.  It is now becoming apparent that ketogenic diets may play a very significant role in the treatment of neurological disease because of two-fold effects that arise when ketones become the primary fuel for the body.

First, when a person becomes keto-adapted and ketones are used as the primary fuel, instead of glucose, the body up-regulates mitochondria to use the ketones for fuel. As the ketone level rises,  the need for glucose diminishes.   This provides the nerve cell an alternative fuel source if glucose metabolism is impaired. It also decreases the need and production of insulin, a known hormone heavily involved in stimulating inflammation and inflammatory responses.

The second effect of a ketogenic diet is this favorable effect on inflammation.  It has been demonstrated that a ketogenic diet decreases reactive oxygen species, increased production of superoxide dismutase and catalayse, all of which notably decrease the inflammatory effects of oxidative stress (9,10, 11).  A ketogenic diet also is well known to raise glutithione levels, another anti-oxidant that decreases inflammation and oxidative stress (12-16).  This same anti-inflammatory and keto-adaptation effect can be obtained from intermittent fasting.

To date, studies in patients with neurologic diseases like MS, Alzheimer’s disease using ketogenic diets have had positive results in memory, cognition and diminished inflammation with evidence of halting or reversing the chronic demyelination (17,18, 19).  Still somewhat theoretical, the evidence points to effective dietary treatment and prevention for multiple sclerosis and other degenerative neurological diseases like Alzheimer’s Disease.



  1. J. M. Pearce, “Historical descriptions of multiple sclerosis,” European Neurology, vol. 1, no. 1, pp. 49–53, 2005.
  2. C.-A. Castellano, S. Nugent, N. Paquet et al., “Lower brain 18F-fluorodeoxyglucose uptake but normal 11C-acetoacetate metabolism in mild Alzheimer’s disease dementia,” Journal of Alzheimer’s Disease, vol. 43, no. 4, pp. 1343–1353, 2014.
  3. S. Nugent, S. Tremblay, K. W. Chen et al., “Brain glucose and acetoacetate metabolism: a comparison of young and older adults,” Neurobiology of Aging, vol. 35, no. 6, pp. 1386–1395, 2014.
  4. H. Lassmann, W. Brück, and C. F. Lucchinetti, “The immunopathology of multiple sclerosis: an overview,” Brain Pathology, vol. 17, no. 2, pp. 210–218, 2007.
  5. C. Confavreux and S. Vukusic, “Natural history of multiple sclerosis: a unifying concept,” Brain, vol. 129, no. 3, pp. 606–616, 2006.
  6. P. K. Stys, G. W. Zamponi, J. van Minnen, and J. J. G. Geurts, “Will the real multiple sclerosis please stand up?” Nature Reviews Neuroscience, vol. 13, no. 7, pp. 507–514, 2012.
  7. P. G. Nijland, I. Michailidou, M. E. Witte et al., “Cellular distribution of glucose and monocarboxylate transporters in human brain white matter and multiple sclerosis lesions,” Glia, vol. 62, no. 7, pp. 1125–1141, 2014.
  8. L. C. Costantini, L. J. Barr, J. L. Vogel, and S. T. Henderson, “Hypometabolism as a therapeutic target in Alzheimer’s disease,” BMC Neuroscience, vol. 9, supplement 2, article S16, 2008.
  9. P. G. Sullivan, J. E. Springer, E. D. Hall, and S. W. Scheff, “Mitochondrial uncoupling as a therapeutic target following neuronal injury,” Journal of Bioenergetics and Biomembranes, vol. 36, no. 4, pp. 353–356, 2004.
  10. P. G. Sullivan, N. A. Rippy, K. Dorenbos, R. C. Concepcion, A. K. Agarwal, and J. M. Rho, “The ketogenic diet increases mitochondrial uncoupling protein levels and activity,” Annals of Neurology, vol. 55, no. 4, pp. 576–580, 2004.
  11. T. Shimazu, M. D. Hirschey, J. Newman et al., “Suppression of oxidative stress by β-hydroxybutyrate, an endogenous histone deacetylase inhibitor,” Science, vol. 339, no. 6116, pp. 211–214, 2013.
  12. S. G. Jarrett, J. B. Milder, L.-P. Liang, and M. Patel, “The ketogenic diet increases mitochondrial glutathione levels,” Journal of Neurochemistry, vol. 106, no. 3, pp. 1044–1051, 2008.
  13. J. B. Milder, L.-P. Liang, and M. Patel, “Acute oxidative stress and systemic Nrf2 activation by the ketogenic diet,” Neurobiology of Disease, vol. 40, no. 1, pp. 238–244, 2010.
  14. N. Dupuis, N. Curatolo, J. F. Benoist, and S. Auvin, “Ketogenic diet exhibits anti-inflammatory properties,” Epilepsia, vol. 56, no. 7, pp. e95–e98, 2015.
  15. D. Y. Kim, J. Hao, R. Liu, G. Turner, F.-D. Shi, and J. M. Rho, “Inflammation-mediated memory dysfunction and effects of a ketogenic diet in a murine model of multiple sclerosis,” PLoS ONE, vol. 7, no. 5, Article ID e35476, 2012.
  16. Y.-H. Youm, K. Y. Nguyen, R. W. Grant et al., “The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome—mediated inflammatory disease,” Nature Medicine, vol. 21, no. 3, pp. 263–269, 2015.
  17. A. Ramm-Pettersen, K. O. Nakken, I. M. Skogseid et al., “Good outcome in patients with early dietary treatment of GLUT-1 deficiency syndrome: results from a retrospective Norwegian study,”Developmental Medicine and Child Neurology, vol. 55, no. 5, pp. 440–447, 2013.
  18. Y. Ito, H. Oguni, S. Ito, M. Oguni, and M. Osawa, “A modified Atkins diet is promising as a treatment for glucose transporter type 1 deficiency syndrome,” Developmental Medicine and Child Neurology, vol. 53, no. 7, pp. 658–663, 2011.
  19. M. Storoni and GT Plant, “The Therapeutic Potential of the Ketogenic Diet in Treating Progressive Multiple Sclerosis,” Multiple Sclerosis International, vol. 2015, Article ID 681289, 9 pages, 2015.

10 Comments on “The Ketogenic Diet & Multiple Sclerosis

  1. I am happy to see that this informaion is becoming more mainstream. I was diagnosed with RRMS in April 2012. I never took the drugs they offered me, and instead explored the science and studies in depth by myself. This brought me to follow a nutrient dense, gluten free, ketogenic diet. Since fully switching to this lifestyle, I have had no relapses and enjoy great health and high energy. In the early days, any indiscretions back to old eating habits, no matter how brief, always resulted in fatigue, a general feeling of malaise and often sensory symptoms, which was an always an abrupt reminder that I must stick to the ketogenic lifestyle for optimum health. Trust your instincts, there are alternatives to pharmaceuticals with unpleasant side effects, and for me, this diagnosis was the best thing that could have happened to me because it led me to improving my health exponentially.

    • I want this mind set. In newly diagnosed and that was purely accidental itself. Since starting injections 2 months ago I feel10X’s sicker and am now scheduled for yet another Mri Monday along with 3 days of iv steroids for some new out of the blue sensory issues.

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  4. My 34 yr. old daughter has MS. She won’t consider the possibility of eating a ketogenic diet at this time. But for over a year now she has cut sugar almost totally out of her life and tries to eat fresh produce every day. I ordered a couple of months worth of KETO OS for her to try, thinking it would help her possibly dip into ketosis once or twice a day without her having to cut carbs a whole lot. . BUT now I’m wondering if she would be able to eat a sandwich for lunch or a potato for dinner without it being a problem, as we’re not supposed to mix high fat WITH carbs. She does not eat HIGH carbs. But I’m wondering if she could safely eat a sandwich or a pasta meal at the same time she takes an exogenous ketone supplement? Would this be problematic? What carb level would be okay? I just wanted her to try KETO OS for a couple of months as an experiment to see if there would be any lessening in her MS symptoms. Do you think this is a problem?

    • Thank you for contacting me, however, due to the nature of medicine and without a formal face-to-face doctor patient relationship, I cannot answer any individual questions, make individual medical recommendations or give individual nutritional recommendations. To maintain the highest standards of medical compliance, clarity and accuracy for answers regarding these issues, you will need to schedule an appointment with me face-to-face in the office or take these questions directly to your personal physician. Thank you for your understanding.

      • I thought that could possibly be the case and totally understand. However I wonder if you would be able to — in general — speak to what level might be considered ‘high carb’ or ‘low carb’, not speaking specifically at all. Would 100g/day usually be considered a ‘low carb’ diet? 150g? 200g? I personally try to keep my carbs under abou 20g/day, so haven’t really paid attention when people talk about other levels. But I am very interested to know if….say…150 grams of carbs per day would usually be considered–by the low-carb community in general–as a low carb diet? Or is that considered moderate? What level would be considered ‘high carb’.

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  6. I started a Ketogenic Diet in October 2016. I have had MS for 30 yrs and the past 5 yrs have been a steady decline in mobility, gait and cognition. Since starting the diet all of my symptoms are gone. I feel like I did 25 yrs ago. It is amazing. I had to quit work 10 yrs ago and now I have an interview this week to start working again. I feel like it gave me my life back.

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