Study links cigarette smoking with progression of multiple sclerosis

First modifiable risk factor for disease advancement identified

Researchers from the Harvard School of Public Health (HSPH) recently discovered that cigarette smoking may contribute to the progression of multiple sclerosis (MS), suggesting that quitting smoking could limit or delay central nervous system deterioration. This is the first time that a modifiable risk factor for MS progression has been identified, providing a new strategy for patients hoping to control neurological damage from the disease. Study results appear in the March 9, 2005 issue of Brain.
Miguel Hernán, lead author of the study and an assistant professor of epidemiology at HSPH, noted that “the findings are interesting because no modifiable risk factors for the progression of MS are known. This was the first prospective study that identified a potential intervention (quitting smoking) for reducing the risk of progression of MS.”

Analyzing over 2,000 medical records in the General Practice Research Database (GPRD), researchers identified 179 British patients who were originally diagnosed with relapsing-remitting MS, a form of the disease in which symptoms fade and recur in unpredictable patterns. Patients who were current or past smokers were 3.6 times as likely as patients who had never smoked to develop secondary progressive MS, a later stage of the disease marked by steady deterioration of the central nervous system. This disease progression also occurred more quickly in patients who were identified as current or past smokers. The study also supported earlier research showing that smoking may increase the risk of initial MS diagnosis. Current and past smokers were 30% more likely to be diagnosed with MS than those who had never smoked.

While more research is needed to understand the mechanisms behind these findings, Hernán and his colleagues speculate that nitrous oxide, a chemical present in cigarette smoke, may play a role in hastening the degeneration of nerve fibers. Alternatively, chemicals in cigarette smoke could damage the cells that create myelin, a protective coating for neurons, or may predispose smokers to autoimmune responses.

According to Hernán, “Our findings raise a number of other questions that future research needs to address. Does a dose-response relation between cumulative exposure to tobacco and risk exist? How long does the tobacco effect last? Is second-hand smoking associated with an increased risk as well?”