Smoking and Disease Progression in Multiple Sclerosis

Healy, Brian C.; Ali, Eman N.; Guttmann, Charles R.G.; Chitnis, Tanuja; Glanz, Bonnie I.; Buckle, Guy J.; Houtchens, Maria K.; Stazzone, Lynn; Moodie, Jennifer; Berger, Annika; Yang, Dan; Bakshi, Rohit; Khoury, Samia J.; Weiner, Howard L.; Ascherio, Alberto

doi:10.1001/archneurol.2009.122

Cited by 202 publications

(176 citation statements)

References 55 publications

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“…Smoking significantly speeds conversion from CIS to confirmed MS [Di Pauli et al 2008] and usually from RRMS to SPMS, also increasing the rate of accumulation of disability in established progressive forms of MS [Hernan et al 2005;Healy et al 2009;Pittas et al 2009]. However, there was an exception to such worsening effects in one study and only a trend for smoking to increase the risk of SPMS in a meta-analysis .…”

Section: Genetic Risk Factors For Multiple Sclerosis Possibly Involvimentioning

confidence: 99%

Contribution of vitamin D insufficiency to the pathogenesis of multiple sclerosis

Pierrot‐Deseilligny

Souberbielle

2013

Ther Adv Neurol Disord

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Abstract:The contribution of vitamin D insufficiency to the pathogenesis of multiple sclerosis (MS) is reviewed. Among the multiple recently discovered actions of vitamin D, an immunomodulatory role has been documented in experimental autoimmune encephalomyelitis and in humans. This action in the peripheral immune system is currently the main known mechanism through which vitamin D might influence MS, but other types of actions could be involved within the central nervous system. Furthermore, vitamin D insufficiency is widespread in temperate countries and in patients with MS at the earliest stages of the disease, suggesting that the deleterious effects related to vitamin D insufficiency may be exerted in these patients. In fact, many genetic and environmental risk factors appear to interact and contribute to MS. In genetics, several human leukocyte antigen (HLA) alleles (more particularly HLA-DRB1*1501) could favour the disease whereas some others could be protective. Some of the genes involved in vitamin D metabolism (e.g. CYP27B1) also play a significant role. Furthermore, three environmental risk factors have been identified: past Epstein-Barr virus infection, vitamin D insufficiency and cigarette smoking. Interactions between genetic and environmental risk or protective factors may occur during the mother's pregnancy and could continue during childhood and adolescence and until the disease is triggered in adulthood, therefore possibly modulating the MS risk throughout the first decades of life. Furthermore, some clinical findings already strongly suggest that vitamin D status influences the relapse rate and radiological lesions in patients with MS, although the results of adequately powered randomized clinical trials using vitamin D supplementation have not yet been reported. While awaiting these incontrovertible results, which might be long in coming, patients with MS who are currently in vitamin D insufficiency should be supplemented, at least for their general health status, using moderate doses of the vitamin.

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Section: Genetic Risk Factors For Multiple Sclerosis Possibly Involvimentioning

confidence: 99%

Contribution of vitamin D insufficiency to the pathogenesis of multiple sclerosis

Pierrot‐Deseilligny

Souberbielle

2013

Ther Adv Neurol Disord

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“…Like other autoimmune disorders, MS is considered to be triggered by environmental factors in individuals with a genetic predisposition, and smoking has been considered one of the most established environmental risk factors for this illness (Mandia et al., 2014; Ramanujam et al., 2015). The relative risk of developing MS among smokers is almost twice that of never‐smokers, and patients with MS who smoke exhibit a more severe disease course and a faster disability progression rate (Correale & Farez, 2015; Fragoso, 2014; Healy et al., 2009; Manouchehrinia et al., 2013; Zhang et al., 2016). …”

Section: Introductionmentioning

confidence: 99%

The lack of association between angiotensin‐converting enzyme gene insertion/deletion polymorphism and nicotine dependence in multiple sclerosis

et al. 2016

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ObjectiveBlood‐borne angiotensin II is generated from angiotensinogen via cleavage by renin and angiotensin‐converting enzyme (ACE), an enzymatic cascade known as the renin–angiotensin system (RAS). Several lines of evidence indicate that ACE, beyond its classical role of mediating blood pressure regulation, might contribute to the etiology of substance addictions by influencing dopaminergic signaling. A functional insertion/deletion (I/D) polymorphism of the ACE gene was associated with risk for being a smoker among individuals with depression and with smoking severity in studies comprising patients with depression and healthy controls. Several reports have described significantly increased ACE activity in cerebrospinal fluid and serum among MS patients. Furthermore, in our previous work with MS patients from Croatian and Slovenian populations, we demonstrated that the ACE‐I/D polymorphism contributes to an elevated MS risk among male patients. Here we investigated whether the ACE‐I/D polymorphism might influence smoking behavior among patients with MS.Patients and MethodsGenotyping was performed in 521 patients (males/females: 139/382) using polymerase chain reaction.ResultsWe revealed no significant differences in ACE genotype and allele frequencies between smokers and nonsmokers and no significant association between the ACE‐I/D polymorphism and either pack‐year smoking history or number of cigarettes smoked daily (p > .05, respectively).ConclusionThe ACE‐I/D polymorphism does not contribute either to risk for nicotine dependence or to smoking severity among MS patients. In the context of reports on the ACE‐I/D polymorphism and nicotine dependence among healthy controls and patients with depression, we may speculate that the mechanism by which this polymorphism influences nicotine dependence risk differs in MS compared to depression, although not compared to a healthy population. In addition to angiotensin II, other potential ACE substrates, such as substance P and neurotensin, which also influence dopaminergic neurotransmission (and are proposed to be associated with MS), may deserve study in future.

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“…15,16 Current smokers had significantly worse MS disability at baseline than never-smokers, as measured by the Expanded Disability Severity Scale (EDSS) and MS Severity Scale, as well as a 64% and 34% increased risk of reaching EDSS 4 and 6 compared with non-smokers and former smokers, respectively. Smoking among PwMS has been shown to be associated with decreased whole brain volume and increased T2 lesion volume, increased contrast enhancing lesions, and T1 lesion volume on MRI.…”

Section: Smokingmentioning

confidence: 99%

A Review of Vascular Disease Risk Factors and Multiple Sclerosis

Kannan¹,

Yadav²

2017

US Neurology

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Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system and the most common non-traumatic cause of disability in young adults. Recent research shows that vascular disease risk factors (VDRFs) such as obesity, smoking, hyperlipidemia, hypertension, type II diabetes mellitus, and metabolic syndrome, can influence MS on its onset, disease activity, progression, and resultant disability. This review evaluates the current knowledge on the role of VDRFs on outcomes among people with MS (PwMS) and shows that while VDRF prevalence may or may not be higher among PwMS compared with the general population, its presence can influence MS in myriad ways. Management of VDRFs through early detection and treatment may be a promising approach to improving outcomes in PwMS. KeywordsMultiple sclerosis, smoking, obesity, dyslipidemia, hypertension, type II diabetes, metabolic syndrome Compliance with Ethics:This study involves a review of the literature and did not involve any studies with human or animal subjects performed by any of the authors.Authorship: All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship of this manuscript, take responsibility for the integrity of the work as a whole, and have given final approval for the version to be published.Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any noncommercial use, distribution, adaptation, and reproduction provided the original author(s) and source are given appropriate credit. Multiple sclerosis (MS) is the most common inflammatory demyelinating disease of the central nervous system and the most common non-traumatic cause of disability in young adults. MS affects nearly 400,000 people in the US and 2.5 million people worldwide. While the precise etiology of MS is unknown, it is suspected that the disease causation is multifactorial, in which exposure to environmental factors triggers an autoimmune response among genetically susceptible individuals.1 Recent research suggests an important plausible role of vascular disease risk factors (VDRFs) such as smoking, obesity, hyperlipidemia, hypertension, diabetes, and metabolic syndrome on MS pathogenesis. It is estimated that nearly 50% of people with MS (PwMS) have at least one VDRF at the time of their MS diagnosis, and are more likely than healthy controls to have more than one VDRF.2,3 The presence of VDRFs among PwMS appears to be associated not only with ongoing radiographic disease activity and progression on magnetic resonance imaging (MRI), but also with increased risk of clinical disability progression.3-5 The purpose of this paper is to examine the current literature on the relationship between these potentially modifiable factors that affect MS onset, activity, progression, and disability, and identify potential targets for improving clinical outcome among PwMS. SmokingThe association between smoking and MS susceptibility has been investigated extensively over...

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Smoking and Disease Progression in Multiple Sclerosis

Cited by 202 publications

References 55 publications

Contribution of vitamin D insufficiency to the pathogenesis of multiple sclerosis

Contribution of vitamin D insufficiency to the pathogenesis of multiple sclerosis

The lack of association between angiotensin‐converting enzyme gene insertion/deletion polymorphism and nicotine dependence in multiple sclerosis

A Review of Vascular Disease Risk Factors and Multiple Sclerosis

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