Moderate alcohol consumption and stroke. The epidemiologic evidence

An extensive search of the English-language literature identified 62 epidemiologic studies that examined the relation between moderate alcohol consumption and risk of stroke. Moderate drinking (less than 60 g ethanol/day) and ischemic stroke have a complex association that might be explained by interaction with race; a J-shaped association has been found in predominantly white populations, while little (if any) association has been found among Japanese. By contrast, moderate drinking increases risk of both intracerebral and subarachnoid hemorrhage in diverse populations. There is insufficient epidemiologic evidence to conclude whether recent alcohol use affects risk of either ischemic or hemorrhagic stroke. These distinctive associations help explain contradictory reports on the relation between moderate alcohol consumption and risk of "stroke." The high prevalence of alcohol use throughout the world suggests opportunities for primary prevention and the importance of continued research in this area.     

Risk of stroke after bereavement—a systematic literature review

Several studies have suggested that psychological stress may increase the risk of stroke. However, this link remains a controversial issue because of conflicting findings. Bereavement, the loss of a close relative, is considered a severely stressful life event. Increased risk of stroke could thus be expected after bereavement if stress plays a causal role. We aimed to evaluate the association between bereavement and stroke by performing a systematic review of the existing literature. The literature search was conducted according to the PRISMA guidelines for systematic reviews. A search in Medline and Embase identified eligible studies, which were reviewed by two researchers independently according to specific inclusion criteria. We included six studies: five cohort studies and one case‐crossover study. Five studies found that loss of a first‐degree relative was associated with a 1.1‐ to 2.4‐fold higher risk of stroke. However, one study found a statistically significant overall risk only for women. Five studies evaluated the risk of stroke according to time since the loss; one study found no association, two studies indicated short‐term effect, one study indicated long‐term effect, and one study indicated both short‐term and long‐term effect. Three studies stratified their analysis by sex; two found higher association in bereaved women than men. Our systematic review suggests that bereavement‐related stress is associated with a higher risk of stroke. As relatively few studies were identified, new studies are needed to verify this association. These should aim to quantify the risk, describe the effect of time since bereavement, and identify risk‐modifying factors.     

Periodontal disease and stroke: a meta‐analysis of cohort studies

This review aimed to determine the association between periodontal disease and stroke incidence by a meta‐analysis of cohort studies. Cohort studies that evaluated the incidence of stroke (fatal or non‐fatal, ischaemic or haemorrhagic) and baseline periodontal status and calculated relative risk values were included. The quality of the included studies was assessed using an evaluation grid. The analyses were conducted separately for three outcomes: periodontitis, gingivitis and loss of teeth. Adjusted values of relative risk or of hazard ratio were used to assess risk values in each study. Random effects meta‐analyses were conducted when data could be pooled. From the 743 references retrieved, only nine cohort studies were suitable for inclusion in this review. Quality scores of the studies varied greatly. Three prospective studies, which used reliable indicators of periodontal disease, obtained the highest scores. Conversely, three studies that used a subjective evaluation of stroke incidence or diagnosed stroke without imaging obtained the lowest score. The results of the meta‐analyses varied depending on the outcome considered and the type of stroke. The risk of stroke was significantly increased by the presence of periodontitis [relative risk 1.63 (1.25, 2.00)]. Tooth loss was also a risk factor for stroke [relative risk 1.39 (1.13, 1.65)]. The risk of stroke did not vary significantly with the presence of gingivitis. This review shows that periodontitis and tooth loss are associated with the occurrence of stroke.     

A meta-analysis of coffee drinking,cigarette smoking,and the risk of Parkinson's disease

We conducted a systematic review to summarize the epidemiological evidence on the association between cigarette smoking, coffee drinking, and the risk of Parkinson's disease. Case-control and cohort studies that reported the relative risk of physician-confirmed Parkinson's disease by cigarette smoking or coffee drinking status were included. Study-specific log relative risks were weighted by the inverse of their variances to obtain a pooled relative risk and its 95% confidence interval (CI). Results for smoking were based on 44 case-control and 4 cohort studies, and for coffee 8 case-control and 5 cohort studies. Compared with never smokers, the relative risk of Parkinson's disease was 0.59 (95% CI, 0.54-0.63) for ever smokers, 0.80 (95% CI, 0.69-0.93) for past smokers, and 0.39 (95% CI, 0.32-0.47) for current smokers. The relative risk per 10 additional pack-years was 0.84 (95% CI, 0.81-0.88) in case-control studies and 0.78 (95% CI, 0.73-0.84) in cohort studies. Compared with non-coffee drinkers, relative risk of Parkinson's disease was 0.69 (95% CI, 0.59-0.80) for coffee drinkers. The relative risk per three additional cups of coffee per day was 0.75 (95% CI, 0.64-0.86) in case-control studies and 0.68 (95% CI, 0.46-1.00) in cohort studies. This meta-analysis shows that there is strong epidemiological evidence that smokers and coffee drinkers have a lower risk of Parkinson's disease. Further research is required on the biological mechanisms underlying this potentially protective effect.     

Smoking and Parkinson's and Alzheimer's disease: review of the epidemiological studies

The relationship between smoking and neurological diseases has always been controversial. Even the expected association between smoking and increased risk for cerebrovascular disease has been debated for years. It was at the end of the 1980s that smoking became definitively accepted as a risk factor for ischemic stroke. More recently, two other neurological diseases have been studied in relation to smoking: Parkinson's disease (PD) and Alzheimer's disease (AD). Many epidemiological studies have found a highly significant negative association between cigarette smoking and these two neurodegenerative disorders. The risk of AD or PD in nonsmokers has generally been about twice that of smokers. That is, patients with AD or PD are approximately 50% less likely to have smoked cigarettes during their lifetime than are age- and gender-matched controls. Alternatively, cigarette smokers are 50% less likely to have PD or AD than are age- and gender-matched nonsmokers. This statistically significant negative association has been interpreted as suggesting that cigarette smoking exerts an undefined, biologic, neuroprotective influence against the development of PD and AD. A review of all studies that either support or refute this hypothesis is presented separately for PD and AD.     

C-reactive protein gene polymorphisms and gene-environment interactions in ischaemic stroke

Abstract

Ischaemic stroke is a heterogeneous, multifactorial disease caused by the combination of certain risk factors and genetic factors. Several single nucleotide polymorphisms (SNPs) of C-reactive protein (CRP) have been reported to be associated with serum CRP levels. However, genetic association studies have produced conflicting results regarding the association between these SNPs and ischaemic stroke. In this paper, we conducted a population-based case-control study to determine whether two SNPs of CRP (rs1800947 and rs3093059) are associated with ischaemic stroke in Chinese Han population and to evaluate their interaction with environmental risk factors. We found that the rs1800947 GC genotype is significantly associated with the risk of ischaemic stroke, particularly the small-vessel disease and its subtype. Crossover analysis revealed that patients with the rs1800947 GC genotype and habits of smoking or drinking were more susceptible to ischaemic stroke. No association was found between the rs3093059 and ischaemic stroke.     

Migraine and the risk of stroke: an updated meta-analysis of prospective cohort studies

Dozens of observational studies and two meta-analyses have investigated the association of migraine with the risk of stroke, but their results are inconsistent. We aimed to quantitatively evaluate the relationship between migraine and stroke risk by performing a meta-analysis of prospective cohort studies. PubMed and Embase were searched through July 2016 to identify studies that met pre-stated inclusion criterion and reference lists of retrieved articles were also reviewed. Information on the characteristics of the included study, risk estimates, and control for possible confounding factors were extracted independently by two authors. The random-effects model was used to calculate the pooled risk estimates. Eleven prospective cohort studies involving 3371 patients with stroke and 2,221,888 participants were included in this systematic review. Compared with non-migraineurs, the pooled relative risks of total stroke, hemorrhagic stroke, and ischemic stroke for migraineurs were 1.55 [95% confidence interval (CI) 1.38–1.75], 1.15 (95% CI 0.85–1.56), and 1.64 (95% CI 1.22–2.20), respectively. Exception of any single study did not materially alter the combined risk estimate. Integrated epidemiological evidence supports that migraine should be associated with the increased risk of total stroke and ischemic stroke, but the relationship between migraine and the risk of hemorrhagic stroke is not of certainty.     

Aspirin use and risk of stroke in the elderly: the Rotterdam Study

The objective of the study was to assess the association between aspirin use and the risk of stroke in a population-based study in the elderly. The study was carried out within the framework of the Rotterdam Study, a prospective population-based cohort study. In the total study population there was a weak, nonsignificant association between aspirin use and the risk of stroke (adjusted relative risk 1.29, 95% CI 0.91-1.83). Stratification by history of vascular diseases revealed that aspirin considerably increased the risk of first-ever stroke in subjects free from vascular disease (adjusted relative risk 1.80; 95% CI 1.03-3.13). In persons with vascular disease, no association was observed between aspirin use and risk of stroke (adjusted relative risk 0.99, 95% CI 0.56-1.73). Our findings suggest that aspirin use may increase the risk of stroke in elderly subjects free from vascular disease.     

Exogenous risk factors in sporadic ALS: a review of the literature

The latest reviews of the literature devoted to the epidemiology of ALS all agree that exogenic risk factors play a role in sporadic ALS. Nevertheless, there is no convincing evidence demonstrating in a reproducible manner an association between an environmental risk factor and ALS. This discordance is mainly explained by methodological skews. Over the last ten years, exogenic factors have been analyzed within the framework of specific lifestyle factors such as place of residence, smoking or not, or certain eating practices. The most recent work suggests that interactions between genetic and environmental factors depend on the age at exposure and the duration of exposure. The objectives of this general review is: to analyze the principal case-control studies, historical cohort studies or mortality studies which looked at the associations between an environmental factor and ALS, to present main results of studies having analyzed lifestyles in relation to one or more exogenic factors, and to discuss the limitations of epidemiologic studies on ALS.     

Alzheimer's disease and smoking: bias in cohort studies

The discrepancy between cohort and case-control studies regarding the association between smoking and Alzheimer's disease (AD) has been attributed to the competing risk of early mortality of smokers. A simulation study was conducted to show that the bias favoring smokers acts also on cohort studies. In the model, individuals {grow older} and have smoking habits according to published year-age-gender-specific patterns, with morbidity and mortality according to their demographic and smoking profiles. Those individuals dying of smoking-related causes ("phantoms") remain at risk of AD and of death from other causes. Three scenarios were considered: no association of AD and smoking, increased risk for smokers, and decreased risk for smokers. For each simulation of a cohort study, two incidence density ratios (IDR) were computed: one including the phantoms that developed AD (thus ignoring smoking-related deaths) and another excluding them (thus mimicking real-life studies). For all scenarios, the simulations show that smoking-related death creates a bias, resulting in smokers having an understated risk of AD compared to non-smokers. The speculation that the conflicting results of case-control and cohort studies are solely due to the increased mortality in smokers thus appears unjustified. Other factors must also be considered to explain the discrepancy in results.     

Smoking and panic attacks: an epidemiologic investigation

BACKGROUND: Epidemiologic studies have reported a lifetime association between smoking and panic disorder. In this study, we examine potential explanations for this association. METHODS: Analysis was conducted on data from 2 epidemiologic studies, the Epidemiologic Study of Young Adults in southeast Michigan (N = 1007) and the National Comorbidity Survey Tobacco Supplement (n = 4411). Cox proportional hazards models with time-dependent covariates were used to estimate the risk for onset of panic attacks associated with prior smoking and vice versa, controlling for history of major depression. The role of lung disease in the smoking-panic attacks association was explored. RESULTS: Daily smoking signaled an increased risk for first occurrence of panic attack and disorder; the risk was higher in active than past smokers. No significant risk was detected for onset of daily smoking in persons with prior panic attacks or disorder. Exploratory analyses suggest that lung disease might be one of the mechanisms linking smoking to panic attacks. CONCLUSIONS: The evidence that the association between smoking and panic disorder might result primarily from an influence in one direction (i.e., from prior smoking to first panic attack) and the possibility of a higher risk in active than past smokers suggest a causal hypothesis for the smoking-panic attacks relationship.     

Smoking, snuff dipping and the risk of amyotrophic lateral sclerosis--a prospective cohort study

BACKGROUND: Little is known about the etiology of amyotrophic lateral sclerosis (ALS). The association between cigarette smoking, but not other types of smoking and snuff dipping, and the risk of ALS has been evaluated in several epidemiologic studies. The findings were inconclusive. METHODS: We studied the association of smoking and snuff dipping with the risk of ALS in the Swedish Construction Workers Cohort, which includes 280,558 male construction workers enrolled between 1978 and 1993 with detailed information on tobacco use. Incident cases of ALS were identified through cross-linkage to the Swedish Inpatient Register. Relative risks and their corresponding 95% confidence intervals (CIs) were estimated using the Cox proportional hazards regression model. RESULTS: After a mean follow-up duration of 19.6 years, we identified 160 incident cases of ALS through 2004. Compared with non-tobacco use, the relative risk of ALS was 0.8 (95% CI 0.6-1.1) for tobacco smoking and 0.6 (95% CI 0.3-1.5) for snuff dipping, respectively. For tobacco smoking, further stratified analyses of smoking status or types of tobacco smoking did not reveal any excess risks in any strata. CONCLUSIONS: Our study provides no evidence that smoking or snuff dipping is associated with an increased ALS risk among men.     

Prospective study of phobic anxiety and risk of Parkinson's disease.

Anxiety disorders are common in Parkinson's disease (PD). However, the risk of PD among people with anxiety has not been examined in a prospective cohort study. We examined this relation prospectively within the Health Professionals Follow-Up Study, a cohort of US male health professionals. In 1988, anxiety was assessed using the Crown-Crisp phobic anxiety index in 35,815 men without PD, stroke, or cancer at baseline. There were 189 incident cases of PD during 12 years of follow-up. After adjusting for age, smoking, and caffeine intake, the relative risk of PD among men with the highest level of anxiety (Crown-Crisp index scores of 4 and above) was 1.5 (95% CI = 1.0-2.1; P-trend = 0.01) compared to men with the lowest level of anxiety. This positive association persisted after excluding cases of PD with onset in the first 2 years of follow-up. Use of anxiolytic medication was also associated with an elevated risk of PD (RR= 1.6; 95% CI = 0.9-3.1), but adjusting for this potential confounder did not materially affect the association between anxiety and risk of PD. Our results suggest that anxiety is a risk factor for PD. Whether this association is causal or the result of shared underlying biology remains a question.     

The association between smoking and Alzheimer's disease: effects of study design and bias.

In epidemiologic studies, unrecognized bias can contribute to observed results, causing them to be inaccurate. Analytic study designs, such as the case-control and cohort designs, each carry potential for specific forms of bias. The cohort design is not susceptible to many forms of bias that are experienced by case-control studies. A consistent "protective" effect of smoking on Alzheimer's disease was documented by many case-control studies. However, the potential effect of biases cannot be separated from the results. Cohort studies now show that smoking may either be unrelated to Alzheimer's disease onset or possibly generate a modest increased risk. In this review the results and comparisons of various studies and potential biases are discussed.     

The role of cardiac diseases in the comorbidity between migraine and stroke

Neurological Sciences - Several case-control and cohort studies have suggested an association between migraine and stroke. A significantly higher risk for stroke was found in women under the age of...     

Epidemiology of classical risk factors in stroke patients in the Middle East

The Middle East (ME) is an ethnically and economically diverse region. A systematic review of all stroke studies conducted in the ME was carried out, with the aim of determining the prevalence of classic vascular risk factors (CRFs) across this region. Additionally, the prevalence of CRFs in the ME was compared to that of a US cohort. Prospective and retrospective ME stroke studies published from 1994 to 2014 were searched for that specifically reported on the prevalence of CRFs. The Z test for proportions was used to determine the significance of differences in CRF rates between the ME and non‐ME studies. A total of 21 724 stroke patients from 13 nations in the ME were included. The prevalence rates for CRFs in the ME stroke population were hypertension, 62.1%; diabetes, 33.1%; dyslipidaemia, 36.8%; ischaemic heart disease, 24.6%; smoking, 19.3%; and atrial fibrillation, 13.6%. Compared to the US cohort, ME patients had a lower prevalence of all CRFs except diabetes (P < 0.0001) and smoking (P = 0.05). Compared with stroke patients in the USA, those in the ME have a significantly higher prevalence of diabetes and smoking. Education and lifestyle modification is perhaps the most effective strategy in reducing the risk of stroke in this population.     

Association of smoking with risk of multiple sclerosis: a population-based study

Genetic and environmental factors have important roles in multiple sclerosis (MS) susceptibility. Several studies have shown an association between smoking and MS risk. Here, in a population-based Canadian cohort, we investigate the relationship between personal and maternal smoking exposure and the risk of MS. Using the longitudinal Canadian database, 3,157 MS cases and 756 spouse controls were administered questionnaires on active and passive smoking history. Mothers of cases and controls were also asked about their smoking exposure during pregnancy. The MS cases were more likely to have smoked than spouse controls (odds ratio 1.32, 95 % confidence interval 1.10–1.60, p = 0.003). This association was driven by an excess of ever-smokers in male MS cases. No association was seen with maternal active or passive smoking exposure during pregnancy. Ever-smoking is associated with increased MS risk in males. Further work is needed to understand the mechanism underlying this association.     

Tobacco smoking,epilepsy, and seizures

Tobacco smoking is considered the greatest risk factor for death caused by noncommunicable diseases. In contrast to extensive research on the association between tobacco smoking and diseases such as heart attack, stroke, and cancers, studies on the association between tobacco smoking and seizures or epilepsy are insufficient. The exact roles tobacco smoking and nicotine use play in seizures or epilepsy have not been well reviewed.We reviewed available literature and found that 1) there are vast differences between tobacco smoke and nicotine based on their components and their effects on seizures or epilepsy; 2) the seizure risk in acute active tobacco smokers, women who smoke during pregnancy, electronic cigarette smokers, and the role of smoking in sudden unexplained/unexpected death in epilepsy remain unclear; 3) seizure risks are higher in acute secondhand smokers, chronic active smokers, and babies whose mothers smoke; 4) tobacco smoke protects against seizures in animal models whereas nicotine exerts mixed effects in animals; and 5) tobacco smoking agents can be noneffective, proconvulsant, or anticonvulsant. Finally, the opportunities for future research on this topic is discussed.     

Epidemiology of cerebrovascular accidents]

Recent studies concerning secular trends in stroke incidence and mortality and identification of independent risk factors for stroke are reviewed. Stroke mortality has declined in many industrialized countries in recent decades. In France, it has been declining by more than 30% between 1968 and 1982 in all age groups and in both sexes except for women under 40 years. The decline in stroke mortality seems to be partly real and partly apparent. In the community-based study of Rochester, Minnesota, stroke incidence decreased by 54% between 1945-49 and 1975-79. Recent data from Rochester, however, suggest that the incidence of stroke may no longer be declining. Survival after stroke has also apparently been improving but several sources of potential bias may also have influenced the decrease in reported survival rates. Hypertension is a major risk factor for stroke. Prolonged differences in "usual" diastolic blood pressure of 5 to 10 mmHg are associated with about 40% difference in stroke incidence. Recent analysis suggests that stroke incidence reduction could arise rapidly after hypertension control and that a lower blood pressure should confer a lower risk of vascular disease, even in individuals conventionally considered as "normotensive". There is evidence that cigarette smoking is an important risk factor for stroke with an overall relative risk of 1.5 and that the risk of stroke declines rapidly after the cessation of smoking. A cardiac condition may be a marker for another risk factor or the primary substrate for cerebral embolism. In patients with atrial fibrillation, the risk of stroke is increased through both of these mechanisms. Diabetes mellitus, chronic alcohol consumption (> 3 drinks/day), and high fibrinogen levels are other independent risk factors for stroke. While high levels of cholesterol may be associated with ischemic stroke, an inverse association of the serum cholesterol with the occurrence of intracerebral hemorrhage in men has been reported. In patients with asymptomatic internal carotid stenosis, higher degrees of stenosis convey a higher risk of stroke. However, far from all these strokes are due to thromboembolism from an atheromatous plaque in the ipsilateral internal carotid artery. The relative risk of stroke during the first 5 years following a transient ischemic attack is 7 times that in persons without transient ischemic attack. More than a third of the subsequent strokes occur in a vascular territory different from that of the incident TIA. While the use of oral contraceptives may increase the relative risk of stroke, postmenopausal estrogen treatment may have a protective effect on the risk of vascular diseases.     

NINJ2 polymorphism is associated with ischemic stroke in Chinese Han population

Recently, a genome-wide association study reported an association between two single nucleotide polymorphisms (SNPs) rs11833579 and rs12425791 near NINJ2 gene and ischemic stroke in Caucasians. Therefore, NINJ2 gene is an important candidate locus in the prevalence of ischemic stroke. We performed a hospital based genetic association study in Chinese Han subjects to investigate the relationship between NINJ2 gene and ischemic stroke. We genotyped 14 tagging single nucleotide polymorphisms (tSNP) in 749 ischemic stroke subjects and 924 control subjects and conducted the association between these tSNPs and ischemic stroke. We detected a tSNP rs10849373 in the first intron of the NINJ2 gene significantly associated with ischemic stroke (both genotype and allelic p=0.0001). The minor A allele increased the risk of ischemic stroke with a per-allele OR of 1.37 for the additive genetic model in univariate analysis (p=0.0001). The significance remained after adjustment for the covariates of age, gender, BMI, cigarette smoking, alcohol drinking, hypertension, and diabetes. Therefore, we report a new genetic variant, rs10849373, located in the first intron of the NINJ2 gene, conferring risk of ischemic stroke in Chinese Han subjects. Further genetic association and functional studies are required to search the causal functional variant in linkage disequilibrium with this polymorphism.