Smoking and MS

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Multiple Sclerosis - Smoking may contribute to progression

21 Apr 2005

 

 

 

 

 

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? "

 

The research was funded by a grant from the National Multiple

Sclerosis Society.

 

Harvard School of Public Health is dedicated to advancing the

public's health through learning, discovery, and communication. More

than 300 faculty members are engaged in teaching and training the 900-

plus student body in a broad spectrum of disciplines crucial to the

health and well being of individuals and populations around the

world. Programs and projects range from the molecular biology of AIDS

vaccines to the epidemiology of cancer; from risk analysis to

violence prevention; from maternal and children's health to quality

of care measurement; from health care management to international

health and human rights.

 

Contact: Robin Herman

rherman

617-432-4752

Harvard School of Public Health

http://www.hsph.harvard.edu