We know that cigarette smoking is bad for our health. The Centers for Disease Control and Prevention (CDC) states that more than 16 million Americans suffer from a disease caused by smoking,
such as cancer, heart disease, stroke, lung diseases, or diabetes. In
the United States, cigarette smoking is responsible for more than
480,000 deaths per year, including an estimated 41,000 deaths in persons
exposed to secondhand smoke. Worldwide, tobacco use kills more than 5
million people annually with numbers growing each year.
Epidemiological
studies have reported that cigarette smoking increases the risk of
developing multiple sclerosis and accelerates disease progression
(Sundstrom, 2008). A recent study demonstrated that in a large
population of MS patients in England, current smoking behavior was associated with more than 2.5-fold increased risk of death.
In addition, the life expectancy of current smokers with MS was reduced
by about 10 years as compared to non-smokers with MS (Manouchehrinia,
2014).
It is logical that smokers who understand the
increased risk of tobacco would want to do what they can to limit their
exposure to nicotine or other harmful chemicals while smoking. Hence the
tobacco industry has developed “reduced exposure” or “light” products
containing lower levels of nicotine, nitrosamines, or other chemicals
deemed to be potentially toxic. However, these ultralow nicotine or
tobacco-free cigarettes may be worse than their full flavor versions.
Researchers
comparing the effects of exposure to full flavor, nicotine-free, or
ultralow nicotine products on the integrity of the blood-brain-barrier
(BBB) found that nicotine-free and ultralow nicotine cigarettes are potentially more harmful
to the BBB endothelium than regular tobacco products. This study
demonstrates that the detrimental effect of tobacco smoke on the BBB is
strongly correlated to the tar and nitric oxide levels in the cigarettes
rather than the nicotine content (Naik, 2014).
Meanwhile,
a different team of researchers have assessed the effects of nicotine
and non-nicotine components of cigarette smoke on experimental
autoimmune encephalomyelitis (EAE), a form of MS induced in mice. They
found that nicotine significantly improved the severity of EAE,
as shown by reduced demyelination, increased body weight, and
attenuated microglial activation. Nicotine administration after the
development of EAE symptoms prevented further disease exacerbation,
suggesting that it might be useful as an EAE/MS therapeutic agent (Gao,
2014).
Read this post in its entirety:
Could Nicotine Be Used to Treat MS Someday?
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