Barts-MS rose-tinted-odometer ★ ★ ★ ★ ★
Yawn! I am getting tired of the saying the same-old things on this blog. Is it time to retire and do something new?
We have done some modelling work and predict that ~20% of new or incident cases of MS could be prevented if we stop the population from smoking. The question is how do we achieve this? Taxation has worked to some extent in that we are seeing a fall in the number of current smokers, but the numbers of teenagers smoking looks as if it is quite resistant to change. The solution must be education, education, education and a war against the tobacco industry.
If social media is such a powerful tool to hack the brains of voters, why don’t public health departments use this technology to promote their agenda? What we need are companies like Cambridge Analytica to do some good in the world and to promote a ‘Don’t Start Smoking’ campaign.
We did try and get some insights into why teenage girls start smoking when Amy Sankey, a work experience student, did a survey in her school for us. Despite the almost universal awareness of the harms of smoking in terms of lung cancer, most girls, however, did not know that there is a link between smoking and autoimmunity. I suspect even if they knew about the link it would be unlikely to prevent them from starting to smoke.
We are interested in smoking as a risk factor for MS as it is telling us something about the cause of the disease. It appears that smoking must be acting via the lungs and is due to tobacco itself. Use of oral, non-smoked, tobacco is in fact associated with a reduced risk of getting MS, hence it is not tobacco exposure. Solvent exposure is also associated with an increased risk of getting MS, which supports the lung hypothesis of developing MS.
Lung hypothesis #1 argues that damage to the lung from smoking or solvents creates a pro-inflammatory environment that is sufficient to activate pre-existing autoreactive T-cells. In comparison, lung hypothesis #2 argues that smoking damages proteins by a process called post-translational modification and that these proteins stimulate an immune response that then cross-reacts with normal antigens to set-up autoimmunity. The argument for the latter in triggering rheumatoid arthritis, an autoimmune disease of joints, is quite compelling but is less compelling when it comes to MS. We hope to study whether post-translational modification of CNS antigens is relevant in MS via an ECTRIMS fellowship we have supported.
What is interesting is that smoking interacts with genetic risk factors for developing MS and with EBV infection suggesting that there is a critical gene-environment interaction that causes MS. Wouldn’t it be interesting to study and find out what these interactions are? We have an exceptionally bright and able young researcher, Ben Jacobs, who wants to do a PhD on this exact topic; gene-environment interactions. At the moment we are ruminating about the best approach he should take to address this question. It is not an easy experiment so if you have suggestions please feel free to contact us.
I would also like to remind you that smokers who have MS have a much poorer prognosis, which is why we recommend that you stop smoking if you can.
If you are interested in smoking and MS there is a new review that has just come out.
Rosso & Chitnis. Association Between Cigarette Smoking and Multiple Sclerosis: A Review. JAMA Neurol. 2019 Dec 16. doi: 10.1001/jamaneurol.2019.4271
IMPORTANCE: Cigarette smoking is a common environmental exposure and addiction, which has severe health consequences. Smoking is a risk factor for multiple sclerosis (MS); also, smoking has been associated with disease activity and overall prognosis for patients with MS.
OBSERVATIONS: Cigarette smoking is an irritative agent on the lungs, in which a proinflammatory cascade starts that culminates in autoimmunity. Inflammation may increase the risk of MS in some individuals, in a process driven by antigen cross-reactivity between lung antigens and myelin antigens. Genetics plays a central role in the individual predisposition to mounting an autoimmune reaction. Also, free radicals, cyanates, and carbon monoxide in cigarette smoke may be directly toxic to neurons. Patients with MS who smoke have higher rates of disease activity, faster rates of brain atrophy, and a greater disability burden. Some of the outcomes of smoking were found to be reversible, which makes counselling key.
CONCLUSIONS AND RELEVANCE: The pathways involved in cigarette smoking should be further analyzed to understand the mechanisms whereby smoking worsens MS prognosis. The proinflammatory and neurotoxic outcomes of cigarette smoking may be shared by other environmental exposures, such as pollution and organic solvents. From a global perspective, efforts should be made to diminish the prevalence of cigarette smoking in patients with MS.