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Mult Scler. 2013 Jan 14. [Epub ahead of print]
Nicotine might have a protective effect in the etiology of multiple sclerosis.
Hedström A, Hillert J, Olsson T, Alfredsson L.
Source
Institute of Environmental Medicine, Karolinska Institutet, Sweden.
Abstract
OBJECTIVE:
The use of moist snuff is common in Sweden and leads to exposure to high doses of nicotine. Recent studies indicate that exposure to nicotine could modulate immune responses. The aim of this study was to investigate the influence of snuff use on the risk of developing multiple sclerosis (MS), taking smoking habits into consideration.
METHODS:
In two Swedish population-based, case-control studies (7883 cases, 9437 controls), subjects with different snuff use habits were compared regarding MS risk, by calculating odds ratios (ORs) with 95% confidence intervals (CIs).
RESULTS:
Snuff-takers have a decreased risk of developing MS compared with those who have never used moist snuff (OR 0.83, 95% CI 0.75-0.92), and we found clear evidence of an inverse dose-response correlation between cumulative dose of snuff use and the risk of developing the disease. We further observed that subjects who combined smoking and snuff use had a significantly lower risk for MS than smokers who had never used moist snuff, also after adjustment for amount of smoking.
CONCLUSIONS:
Our results add evidence to the hypothesis that nicotine exerts anti-inflammatory and immune-modulating effects in a way that might decrease the risk of developing MS.

Conclusions: Smokers of both sexes run an increased risk of developing multiple sclerosis (MS), and the risk increases with cumulative dose of smoking. However, the use of Swedish snuff is not associated with elevated risk for MS, which may indicate that nicotine is not the substance responsible for the increased risk of developing MS among smokers.

Snus, Swedish Match's main product, is banned everywhere in the EU except Sweden which has lobbied to get the ban overturned. Swedish daily Aftonbladet reported that the businessman had asked Swedish Match for 10 million euros in advance and another 50 million once the legislation was changed.

In 2000, a study performed at Stanford revealed surprising results about nicotine's effects on blood vessels. Contrary to popular opinion, the study showed that nicotine actually boosts the growth of new blood vessels

In 1999, my laboratory group was examining factors that interfere with therapeutic angiogenesis. As a specialist in vascular medicine, I was interested to know why some individuals are not capable of generating an adequate angiogenic response to coronary or peripheral arterial obstruction. I asked one of the students in the laboratory (James Jang) to help me test the hypothesis that nicotine could interfere with angiogenesis. This hypothesis was based on the observation that smokers have an impairment of endothelial vasodilator function, possibly related to decreased bioactivity or synthesis of nitric oxide (NO) and prostacyclin (PGI2) (Celermajer et al, 1993; Reinders et al, 1986). This is significant because endothelium derived NO and PGI2 are critically involved in a number of angiogenic processes including endothelial cell survival, proliferation and migration. Indeed, we had previously shown that the endogenous NO synthase inhibitor, asymmetric dimethylarginine (ADMA) was anti-angiogenic (Jang et al, 2000). Notably, ADMA is elevated in disease states associated with impaired angiogenesis such as hypercholesterolemia (Cooke, 2004). Thus, we hypothesized that tobacco smoking may elevate plasma ADMA levels, and thus impair endothelium dependent vasodilation and angiogenesis.

There are over 4,000 different chemicals in tobacco smoke (U.S. Department of Health and Human Services, 1989), which makes it difficult to determine the individual effects of these agents on angiogenesis. Accordingly, we focused on nicotine, the major bioactive component of tobacco. We hypothesized that nicotine would impair the NO synthase pathway, and inhibit angiogenesis. Indeed, other workers had suggested that nicotine could be toxic to endothelial cells (Suzuki et al, 1994). However, these observations were made using doses of nicotine that were above clinically relevant concentrations.

To determine the effect of nicotine on angiogenesis, we first used a disc angiogenesis assay. A pellet of polyvinyl alcohol sponge was loaded with nicotine solution, coated with a copolymer for slow elution, and placed into a sponge disc, with filter paper backing on each side. When the disk is placed subcutaneously in mice, vessels enter through the rim of the disk. To our great surprise, in the nicotine-treated disk, fibrovascular growth was accelerated. The angiogenic effect of nicotine was equipotent to basic fibroblast growth factor (FGF) in this model (Heeschen et al, 2001). These observations caused us to consider what role nicotine-induced angiogenesis might play in tobacco-related disease.

I really don't think I could take up a snuff habit. Just, no. But I'd be ok with nicotine gum if it turned out to be good for us.

I think there is also an inverse relationship between Cancer and MS. Cancer being characterized by mutant angiogenesis and uncontrolled blood supply characteristic of precancerous cells becoming malignant. S'nuff said.

But it is a different possibility to consider the explanation to be reduced angiogenesis in people with MS.