A new paper published in Science (online before it is available in print), one of the highest impact scientific journals in the world, announced it has found compelling evidence that infection with Epstein Barr virus (EBV) is a trigger for development of multiple sclerosis (MS).¹ The scientists used frozen serum from 10,000,000 men and women in the military, collected over a 20-year period. Within that group and time period, 801 individuals developed multiple sclerosis. At the initial blood draw, 35 were negative for a prior EBV infection, and 34 developed EBV in the military. The scientists report that 800 of the 801 MS cases had antibodies to EBV in the serum after diagnosis of MS. No additional details are provided about the clinical course of the veterans diagnosed with MS, nor are there any details about the circumstances of the veterans before or after diagnosis. This paper is getting a lot of attention and it does reinforce what we have known for a very long time: having EBV increases the risk of developing multiple sclerosis and other autoimmune conditions. But how does EBV do the damage?

The scientists discuss the potential mechanisms of how a virus that infects B cells may lead to MS and other autoimmune diseases. They discuss the concept of molecular mimicry where amino acid sequences in EBV share similar sequences to myelin, basic protein, and other central nervous system structures.

The scientists noted that 95% of the 10,000,000 samples were positive for EBV antibodies, but only 800 out of 10,000,000 developed multiple sclerosis. In other words, only 0.008% of those who were positive for EBV antibodies developed multiple sclerosis. Yes, this study identifies EBV infection as an important step, but it does not lead to multiple sclerosis for 99.992% of those are infected. Why? What makes the 0.008% vulnerable? Science happens because of the questions asked. Unfortunately, these are the questions these scientists should have asked but did not.

The scientists discussed other factors, including genetic vulnerability, which contributes to the development of molecular mimicry. They also discussed B-cell depleting treatments, vaccines, and antivirals. But there was no discussion of the environmental factors that prevent a person’s immune system from properly containing EBV.

Immunosenescence is the scientific term for how immune cells become less effective as we age. Ongoing severe psychological stress, physical stress, sedentary behavior, and/or a diet high in sugar and processed foods can make us more likely to experience accelerated aging. Those with immunosenescence have higher rates of infection-related illness and cancers.^2,3

Unfortunately, the scientists did not discuss literature that implicates other infectious agents in the development of MS and other autoimmune diseases ^4,5 which include chlamydia pneumoniae, staph aureus, HIV, human herpes virus, human endogenous retrovirus, coronavirus, HIV and Lyme ^4,5

We have known for many years that multiple sclerosis results from the combination of genetic vulnerability, infectious exposure (probably), and the interaction of a lifetime of environmental and modifiable lifestyle factors. Insufficient sleep compromises immune function and accelerates immunosenescence. ^6,7 So do tobacco use and air pollution. ^8,9 What is in the past we cannot change, but we can influence our choices about our future exposures. Improving diet and getting regular exercise can improve immune function and reverse immunosenescence.^10,11

Nearly all of us have been infected with several of the microbes that are associated with increased risk for developing an autoimmune disease. While other scientists are thinking about patentable drugs and vaccines, I am thinking about what each of us can do to help our immune cells keep all the various microbes we have in our body under proper surveillance and control. To me, the solution is as simple as teaching ourselves the power of our choices: what we feed ourselves and our family, how much time we spend with loved ones, how much time we spend sitting and moving, how well and how much we sleep. I teach these concepts in my online course, Autoimmune Intervention Mastery. There is so much you can do to make sure your immune cells are healthy enough to prevent the conversion to an autoimmune disease. Sign up today and protect yourself from the infections that are waiting for you to develop immunosenescence so they can do their dirty work.

1. Robinson WH, Steinman L. Epstein-Barr virus and multiple sclerosis. Science. 2022:eabm7930.

2. de Araujo AL, Silva LC, Fernandes JR, Benard G. Preventing or reversing immunosenescence: can exercise be an immunotherapy? Immunotherapy. 2013;5(8):879-893.

3. De la Fuente M, Gimenez-Llort L. Models of aging of neuroimmunomodulation: strategies for its improvement. Neuroimmunomodulation. 2010;17(3):213-216.

4. Marrodan M, Alessandro L, Farez MF, Correale J. The role of infections in multiple sclerosis. Mult Scler. 2019;25(7):891-901.

5. De Chiara G, Marcocci ME, Sgarbanti R, et al. Infectious agents and neurodegeneration. Mol Neurobiol. 2012;46(3):614-638.

6. Besedovsky L, Lange T, Haack M. The Sleep-Immune Crosstalk in Health and Disease. Physiol Rev. 2019;99(3):1325-1380.

7. Gamaldo CE, Shaikh AK, McArthur JC. The sleep-immunity relationship. Neurol Clin. 2012;30(4):1313-1343.

8. Perricone C, Versini M, Ben-Ami D, et al. Smoke and autoimmunity: The fire behind the disease. Autoimmun Rev. 2016;15(4):354-374.

9. Prisco LC, Martin LW, Sparks JA. Inhalants other than personal cigarette smoking and risk for developing rheumatoid arthritis. Curr Opin Rheumatol. 2020;32(3):279-288.

10. Davison G, Kehaya C, Wyn Jones A. Nutritional and Physical Activity Interventions to Improve Immunity. Am J Lifestyle Med. 2016;10(3):152-169.

11. 11. Weyh C, Kruger K, Strasser B. Physical Activity and Diet Shape the Immune System during Aging. Nutrients. 2020;12(3).