Multiple Sclerosis (MS) is a chronic autoimmune condition impacting the central nervous system. In MS, the body’s immune system mistakenly attacks myelin, the protective sheath surrounding nerve fibers, disrupting communication between the brain and the rest of the body. This damage can lead to various symptoms affecting vision, movement, sensation, and cognitive function. While there is currently no guaranteed method to prevent MS, scientific research has identified several factors that can significantly influence a person’s risk of developing the condition.
Established Risk Factors for Multiple Sclerosis
The development of multiple sclerosis involves a complex interplay of genetic and environmental factors. Genetics play a role, as having a first-degree relative with MS, such as a parent or sibling, increases an individual’s risk. Specific genes within the human leukocyte antigen (HLA) complex, particularly HLA-DRB115:01, are strongly associated with a heightened risk of MS. This genetic predisposition influences how the immune system interacts with its environment.
A geographical pattern shows MS is more common in areas farther from the equator. Conversely, populations living closer to the equator generally have lower rates of MS. This trend suggests that environmental factors, possibly related to sunlight exposure, play a role in MS prevalence. Moving from a high-risk to a low-risk area before the age of 15 may reduce one’s risk, while moving in the opposite direction can increase it, further supporting an environmental link.
Beyond genetics and geography, other demographic factors also contribute to MS risk. The condition is diagnosed most commonly between 20 and 40 years of age. Women are two to three times more likely than men to develop relapsing-remitting MS, indicating a potential role for hormonal influences.
Vitamin D’s Protective Role
Vitamin D plays a role in regulating the immune system, extending beyond its known function in bone health. The active form of vitamin D, calcitriol, interacts with the vitamin D receptor (VDR) found in various immune cells. This interaction can induce immunological tolerance in T cells and lessen inflammatory responses, which are implicated in MS development.
There is substantial evidence linking low levels of vitamin D and reduced sun exposure to a higher risk of developing MS. Studies have shown that individuals with vitamin D deficiency may have more than double the risk of MS compared to those with sufficient levels. Low sun exposure appears to increase MS risk both directly and indirectly by affecting vitamin D status, suggesting both vitamin D-dependent and independent pathways are involved in the protective effect of sun exposure.
The primary source of vitamin D for most people is sensible sun exposure. During summer months, sun exposure can produce significant amounts of vitamin D. Dietary sources also provide vitamin D, including fatty fish like salmon and mackerel, cod liver oil, and egg yolks. Fortified foods also contribute. While the evidence for supplementation effectively preventing MS is still being researched, maintaining adequate vitamin D levels, often through a combination of sun exposure, diet, and potentially supplements under medical guidance, is considered a way to modify disease risk.
Actionable Lifestyle Modifications
Smoking
Cigarette smoking is recognized as a significant and causal risk factor for developing MS. The harmful chemicals present in tobacco smoke can enter the bloodstream, potentially contributing to inflammation and damaging myelin in the central nervous system. People who smoke have a higher risk of MS compared to non-smokers. Research suggests a substantial portion of MS cases could be prevented by avoiding tobacco smoking.
Smoking also exacerbates the disease course for individuals already diagnosed with MS, leading to more frequent relapses, faster disease progression, and worse cognitive symptoms. It is associated with increased MS lesion volume and a higher risk of brain atrophy. Quitting smoking can improve the outlook for individuals with MS, with some research suggesting that the risk may eventually align with that of never-smokers.
Obesity
Obesity, particularly during childhood and adolescence, is an independent risk factor for developing multiple sclerosis. Studies indicate that being overweight in youth is associated with an increased risk of MS in females. This association persists even after accounting for other known genetic and environmental factors.
Childhood and adolescent obesity is linked to a significantly higher risk of MS compared to the general population, although the overall risk remains low. This heightened risk is thought to be partly due to the low-grade chronic inflammation associated with obesity, which can influence immune system regulation.
Diet
Dietary patterns can influence the body’s inflammatory processes. Adopting an anti-inflammatory diet rich in fruits, vegetables, whole grains, and healthy fats is generally recommended. Such a diet may help reduce inflammation and improve overall health, indirectly benefiting those at risk for MS. Foods like fatty fish provide omega-3 fatty acids, which have been shown to reduce inflammatory markers.
Emerging research highlights the role of gut health and the microbiome—the collection of microorganisms in the digestive tract—in immune regulation and MS. An unhealthy diet, particularly one low in fiber and high in fat, may contribute to imbalances in the gut microbiome. Consuming a diverse diet rich in fiber can support the growth of beneficial gut bacteria and potentially reduce inflammation. While specific dietary guidelines for MS prevention are still being developed, promoting gut health through dietary choices is an area of ongoing study.
The Viral Link to MS Development
Compelling evidence points to a strong connection between certain viral infections and the risk of developing multiple sclerosis. The Epstein-Barr virus (EBV), a common herpesvirus that infects over 90% of the global population, is now considered a near-necessity for MS development. While most people infected with EBV never develop MS, studies have shown that the risk of MS increases significantly after EBV infection.
Studies revealed that the risk of MS increased 32-fold after infection with EBV, a finding that cannot be explained by other known MS risk factors. This suggests a causal link, with EBV infection preceding the onset of MS symptoms and nerve damage. The proposed mechanism involves “molecular mimicry,” where a protein from EBV resembles a protein found in the brain and spinal cord. This resemblance can trick the immune system into attacking the body’s own nervous system while fighting the virus.
EBV infection alone is not sufficient to cause MS; rather, it acts as a trigger in genetically susceptible individuals. The vast majority of people infected with EBV remain healthy, indicating that other genetic and environmental factors must also be present for MS to develop. Research continues to explore the complex interplay between EBV, genetic predisposition, and other environmental influences.