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Scientists claim that multiple sclerosis is not an autoimmune disease

 
, medical expert
Last reviewed: 17.10.2021
 
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12 January 2012, 17:31

Scientists suggest that multiple sclerosis, which has long been regarded as an autoimmune disease, is not really a disease of the immune system. Dr. Angelica Courtels, forensic anthropologist, and John J., a professor of the New York College of Criminal Justice, suggest that multiple sclerosis caused by lipid metabolism disorders is more similar in many respects to coronary atherosclerosis than to other autoimmune diseases.

Cortells believes that considering multiple sclerosis as a metabolic disorder, many of the mysterious aspects of the disease become understandable, in particular, why it affects more often women than men, and why recently there has been an increase in incidence across the world. She suggests that this hypothesis could help scientists develop new treatments and, ultimately, drugs for this disease.

At least 1.3 million people worldwide suffer from multiple sclerosis. Its main feature is systemic inflammation, resulting in scarring of tissues called myelin and which isolate the nerve tissue of the brain and spinal cord. Over time, these scars can lead to serious neurological damage. The scientists assumed that the immune system is to blame for the development of this disease, but no one could fully explain what exactly causes the disease. Genes, diet, pathogens or vitamin D deficiency - all of these factors can be associated with multiple sclerosis, but the evidence for these risk factors is inconsistent and even contradictory, frustrating scientists in seeking effective treatment.

"Every time the genetic factor showed a significant increase in the risk of developing multiple sclerosis in one population, it was found that in another population this did not really matter," says Kortaels. "It is impossible to explain the involvement of pathogens, including the Epstein-Barr virus, in the development of the disease, since genetically similar populations with similar pathogens sharply differ in the rate of disease development.Search for triggers of multiple sclerosis in the context of autoimmune disorders simply did not lead to general conclusions about the etiology of the disease" .

However, considering multiple sclerosis as a metabolic and not an autoimmune disease, one can see the common pathogenesis and the causes of the development of this disease.

Lipid hypothesis

Cortells believes that the main cause of multiple sclerosis can be transcription factors in the cell nuclei that control absorption, destruction, and the production of lipids (fats and other similar compounds) throughout the body. The breakdown of these proteins, known as peroxisome receptor proliferation activators (PPARs), causes the accumulation of a toxic byproduct - "bad" LDL cholesterol, forming plaques in the affected tissues. The accumulation of these plaques in turn induces an immune response, which ultimately leads to the formation of scars. This is essentially the same mechanism that is involved in the development of atherosclerosis, in which a deficiency of PPAR leads to the formation of plaques, an immune response and the appearance of scars in the coronary arteries.

"When lipid metabolism occurs in the arteries, you get atherosclerosis," explains Kortaels. "When this happens in the central nervous system, you get multiple sclerosis, but the main reason is the same."

The main risk factor for the development of violations of lipid homeostasis is a high level of LDL cholesterol. So, if PPARs were the basis for the development of multiple sclerosis, it would be understandable why in recent decades, cases of the disease have become increasingly recorded. "In general, people around the world consume more sugar and animal fats, which often lead to high levels of LDL cholesterol," said Cortells. "Thus, we would expect to see a higher incidence of diseases associated with lipid metabolism disorders such as heart disease and, in this case, multiple sclerosis, which also explains why statins that are used to treat high cholesterol have shown good efficacy in Multiple Sclerosis ".

The lipid hypothesis also sheds light on the link between multiple sclerosis and vitamin D deficiency. Vitamin D helps lower LDL cholesterol, and a lack of vitamin D increases the likelihood of the disease developing - especially in the context of a diet high in fat and carbohydrates.

Cortells also explains why multiple sclerosis is more common in women.

"Men and women differently digest fats," said Kortaels. "In men, PPAR disorders occur more often in vascular tissue, so they are more likely to have atherosclerosis." In connection with the reproductive role, women metabolize fats differently, and the violation of lipid metabolism in women is most likely affected by myelin production in the central nervous system. Way, multiple sclerosis develops more often in women, and atherosclerosis - in men. "

In addition to high cholesterol, there are other factors that disrupt the function of PPAR, including pathogenic microorganisms, for example the Epstein-Barr virus, injuries and some genetic profiles. In many cases, one of these risk factors is not enough to cause a collapse of lipid metabolism. But a combination of many factors can lead to a violation of lipid metabolism. For example, a genetically weakened PPAR system alone can not cause disease, but in combination with a pathogen or malnutrition can cause multiple sclerosis. This helps explain why different triggers of multiple sclerosis are important for some people and groups of people, but in others they are not significant.

Scientists intend to conduct additional studies to fully understand the role of PPARs in the development of multiple sclerosis, but Cortells hopes that this new understanding of the disease, ultimately, can lead to the emergence of new therapies and prevention measures.

"This new hypothesis gives hope for the sooner appearance of a drug for multiple sclerosis more than ever," said Kortaels.

trusted-source[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12]

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