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Lifestyle And Risk Factor Management

5th Edition
December 2014

The Canadian Stroke Best Practice Recommendations for the Secondary Prevention of Stroke, 5th Edition 2014 module is published in the International Journal of Stroke (IJS) (Online Open‑Access available December 2014; Printed Journal scheduled for April 2015).

To access the specific recommendations for Lifestyle And Risk Factor Management and all other sections of the Secondary Prevention of Stroke module, please click on this URL which will take you to the recommendations online in the IJS:  http://onlinelibrary.wiley.com/doi/10.1111/ijs.12439/full. For the French version of these recommendations, open the appendix at this link : http://onlinelibrary.wiley.com/store/10.1111/ijs.12439/asset/supinfo/ijs12439-sup-0001-si.pdf?v=1&s=b0ed4fff1d7fc435cf4e2a83ccbcbffbdad767de.

All other supporting information, including performance measures, implementation resources, evidence summaries and references, remain available through www.strokebestpractices.ca, and not through the IJS.  Please click on the appropriate sections below for this additional content.


A healthy lifestyle reduces the risk of an initial stroke and the risk of a subsequent stroke for patients with a prior stroke. Hypertension is the single most important modifiable risk factor for stroke. Current research reports estimate that reducing sodium in foods would abolish high blood pressure for almost one in three Canadians. Furthermore, this evidence suggests that lowering sodium consumption to adequate intake levels could reduce the incidence of stroke and heart disease by as much as 30 percent, and has a significant impact on lowering blood pressure. There is a growing concern for obesity in the Canadian population, especially in younger adults and this must be addressed with all patients with stroke or at risk. Regular exercise also reduces the risk of stroke and other vascular diseases.5   Research has demonstrated an increased risk of thrombosis with estrogen-based hormone therapy (both oral contraceptives and hormone-replacement therapy).

Although causes of stroke are generally different for children, lifestyle management issues as described above are equally as important for the paediatric population, particularly as the long-term risk of recurrence for children is much higher.

System Implications
  • Health promotion efforts that contribute to the prevention of stroke in all communities (integrated with existing chronic disease prevention initiatives) must be established.
  • Coordinated and comprehensive stroke prevention should be offered by primary care providers, and a mechanism in place to ensure that stroke risk is addressed during encounters with healthcare professionals throughout the continuum of care.
  • Public focus on cerebrovascular health for paediatric cases–such as diet, sodium and sugar intake, exercise, non-smoking, avoidance of drugs that increase stroke risk.
  • National and international efforts to reduce sodium intake by working with governments and changing the food supply.
  • Increase public awareness and knowledge about the risks of sodium through targeted and population based campaigns.
  • Access to risk factor management programs (such as hypertension and smoking cessation programs) in all communities, primary healthcare settings and workplaces.
  • Government action at all levels of government to reduce tobacco use.
  • Coordinated efforts among stakeholders such as the Heart and Stroke Foundation, public health agencies, ministries of health and care providers across the continuum to produce patient, family and caregiver education materials with consistent information and messages on risk factor management.
  • Coordinated processes for ensuring access to and awareness of educational materials, programs, activities and other media related to risk factor management by healthcare professionals, patients and caregivers, including promotion of educational material and effective dissemination mechanisms.
  • Access to culturally and ethnically appropriate educational resources in multiple languages for patients with aphasia.
  • Access to healthy living programs, educational materials and healthcare professionals for persons living in rural and remote locations, including innovative use of technology.
Performance Measures
  1. Proportion of the population with major risk factors for stroke, including hypertension, obesity, history of smoking, low fruit and vegetable consumption, low physical activity, hyperlipidemia, diabetes, and atrial fibrillation (core).
  2. Annual occurrence rates for stroke in each province and territory by stroke type (core).
  3. Stroke mortality rates across provinces and territories, including in-hospital or 30-day rate and one-year rate (core).
  4. Percentage of the population who can identify the major risk factors for stroke, including hypertension, sodium intake, diet, weight, exercise, smoking and alcohol intake.
  5. The annual readmission rate for a recurrent stroke or TIA event in patients with previous stroke or transient ischemic attack.

Measurement notes

  • For performance measures 1, 2 and 3: self-reported data can be extracted from provincial and national health surveys. These data should be standardized to the most current national census data for age and sex.
  • Performance measures 4: administrative data are available at the local, provincial and national levels.
  • Mortality rates should be risk adjusted for age, sex, stroke severity and comorbidities.
Implementation Resources and Knowledge Transfer Tools

Health Care Provider Information

Patient Information

Summary of the Evidence, Evidence Tables and References

Lifestyle Management Evidence Tables and Reference List

Lifestyle and Risk Factor Management

Examining the relationship between stroke risk and diet is challenging, in large part due to the limitations in methods for collecting information of long-term dietary intake. The results of studies evaluating individual dietary components (fruit/vegetable consumption, fats, dairy products and whole grains) and dietary patterns of eating have yielded ambiguous results. In a cohort study including 175,000 participants, Sharma et al. (2013) reported no protective effect of consuming fruit or vegetables in either men or women during 8 years of follow-up. The mean number of servings of fruit and vegetables servings between those who died of stroke was similar to all others, assessed by determining whether participants were compliant with the USDA’s food pyramid. In a case-control study O’Donnell et al. (2010) reported an increased consumption of fruits was associated with a decreased risk of stroke (adj OR of tertiles 1 vs. T3=0.61, 95% CI 0.66-0.91), while increased consumption of vegetables was not (adj OR of T3 vs. T1=0.91, 95% CI 0.75-1.00). A meta-analysis of fruit and vegetable consumption and stroke, which included eight studies and 257,551 individuals followed over a 13-year period, showed that increasing consumption was associated with a lower risk of stroke (He et al. 2006). Compared with individuals who had fewer than three servings of fruit and vegetables per day, the risk of stroke was decreased significantly for those consuming three to five servings per day (adjusted RR=0.89, 95% CI 0.83-0.97), and for those who consumed >5 servings/day, the risk was even lower (adjusted RR=0.74, 95% CI 0.69-0.79).

The role of dietary fat as a risk factor for stroke remains unclear. Siri-Tarino et al. (2010) conducted a systematic review & meta-analysis that included the results of 21 prospective cohort studies, of which stroke was the outcome in 8 studies (n=179,436). The mean follow-up periods ranged from 8-23 years. There was no increased risk of stroke associated with the highest intakes of saturated fat compared with the lowest (adjusted RR=0.81, 95% CI 0.62-1.05, p=0.11). He et al. (2003) did not find associations between amount of total fat, source of fat (animal or vegetable), type of fat (saturated, unsaturated, monounsaturated, polyunsaturated, trans fat or cholesterol) or source of fat (red meat, high-fat dairy products, nuts or eggs) and incidence of ischemic or hemorrhagic stroke, in a prospective cohort study including the results from 43,732 men aged 40-75 years included in the Health Professionals’ follow-up study who were free of cardiovascular disease and diabetes at baseline.

Larsson et al. (2012) reported that consumption of low-fat dairy products was associated with a decreased risk of all stroke (RR=0.88, 95% CI 0.80-0.97) and ischemic stroke (RR=0.87, 95% CI 0.78-0.98) in a cohort study including 74,961 Swedish men and women, aged 45-83 years without a history of stroke.

In terms of reductions in stroke risk associated with different dietary patterns, Agnoli et al. (2011) compared adherence to four commonly-recognized diet regimes and their impact on stroke risk, including Healthy Eating Index 2005 (HEI-2005), Dietary Approaches to Stop Hypertension (DASH), Greek Mediterranean Index, and the Italian Mediterranean Index. There was an inverse relationship between adherence to each of the regimens and stroke occurrence. Overall, the Italian Mediterranean Index was the most protective (HR = 0.37, 95% CI = 0.19–0.70). A systematic review & meta-analysis was conducted by Psaltopoulou et al. (2013) to examine the protective effects associated with adherence to the Mediterranean diet. Of the 11 studies that were included that assessed stroke as an outcome, high adherence to a Mediterranean diet was associated with reduced risk of total stroke and ischemic stroke (total stroke: RR=0.71, 95% CI 0.57-0.89; ischemic stroke: RR=0.52, 95% CI 0.28-0.96). A systematic review and meta-analysis authored by Soedamah-Muthu et al. (2013) also provide evidence of the reduced risk of stroke associated with the DASH style diet. High adherence was protective for the development of cardiovascular disease (RR=0.80, 95% CI 0.74-0.86). The randomized controlled trial PREDIMED, evaluated the benefits of 2 types of Mediterranean diet types, one emphasizing increased consumption of extra-virgin olive oil and the other, mixed nuts, compared with a control group, in which participants were advised to follow a low-fat diet (Estruch et al. 2013). After a median follow-up of 4.8 years, the two Mediterranean diets were associated with 30% reductions in the primary outcome, a composite of myocardial infarction, stroke, or death from cardiovascular causes. The majority of this protective effect was driven by a reduction in stroke events.

It is well documented that a consistently high dietary sodium intake is associated with elevated blood pressure, while modest decreases may lower blood pressure and reduce stroke risk. (Joffres et al. 2007, Penz et al. 2008, Strazzullo et al. 2009). Canadians consume about 3400 mg of sodium each day, which is higher than the upper limit of 2000 mg, currently recommended by both the Canadian Best Practice Recommendations for Stroke Care and the 2014 Canadian Hypertension Education Program recommendations.

In a Cochrane review, He et al. (2013) examined 34 RCTs (n=3230) comparing the effect of moderately restricted sodium intake (2.3-7.0 g/day or 40-120 mmol/day urinary sodium excretion) for a minimum of 4 weeks with usual intake over the same duration. The mean difference in sodium intake between groups was 1,955 mg per day, which was associated with a significant decrease in SBP (-4.18 mmHg, 95% CI -5.18 to -3.18; p<0.001) and DBP (-2.06 mmHg, 95% CI -2.67 to -1.45; p<0.001). In a subgroup analysis of 22 trials that included 990 patients with hypertension, the results were similar. Reduced intake was associated with a significant reduction in SBP (-5.39 mmHg, 95% CI -4.15 to -6.62; p<0.001) and DBP -2.82 mmHg, 95% CI -2.11 to -3.54; p<0.001). Abuerto et al. (2013) identified 36 RCTs (n=5,508; n with hypertension=1,478) also comparing the effects of decreased sodium vs. higher sodium intake. The mean between group difference in sodium intake was ≥40 mmol/day. Reduced sodium intake was associated with a mean SBP reduction of 3.39 mm Hg (95% CI 2.46 to 4.31) in all participants and a mean SBP reduction of 4.06 mm Hg (95% CI 2.96 to 5.15) in participants with hypertension. In trials where the relative sodium reduction of subjects in the intervention group was <1/3 of the control group, there were significant reduction in both SBP (MD= -1.45, 95% CI -2.29 to -0.60) and DBP (MD= -0.74, 95% CI -1.28 to -0.19). In trials where the relative sodium reduction of subjects in the intervention group was ≥1/3 of the control group, the reductions in both SBP and DBP were even greater (SBP: MD= -3.79, 95% CI -4.82 to -2.75 and DBP: MD= -1.68, 95% CI -2.34 to -1.02).

Physical activity is an important modifiable lifestyle factor that can influence both the primary and secondary prevention of stroke. A large prospective cohort study including 30,239 US residents, aged ≥45 years, the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study (McDonnell et al. 2013), reported that compared with persons exercising ≥4x/week, the risk of stroke was increased in persons who engaged in no physical activity (HR= 1.20, 95% CI, 1.02–1.42). In the INTERSTROKE case-control study, O’Donnell et al. (2010) reported that regular physical activity was associated with a reduced risk of total and ischemic stroke (total stroke: OR=0.69, 95% CI 0.53-0.90, ischemic stroke: OR=0.68, 95% CI 0.51-0.91). While Sattelmair et al. (2010) reported that increasing amount of time spent engaged in physical activity was not associated with decreased total stroke risk in 39,315 healthy women who had been participants of the Women’s Health Study (1992-1995), those who walked ≥2 hours per week had a 30% lower risk of any stroke than women who did not walk (RR=0.70 95% CI, 0.52 to 0.94). Additionally, women who reported walking at a brisk pace (4.8 km/hour) had a 37% lower risk (RR=0.63, 95% CI, 0.44 to 0.91) compared with women who did not walk. Lee et al. (2003) published a meta-analysis of 23 studies published between 1983 and 2002 examining the association between physical activity and stroke incidence or mortality and reported a dose-response relationship. Highly active individuals had a 27% lower risk of stroke than individuals who were designated as “low active.” Individuals who were designated as moderately active also had a significantly reduced risk of ischemic and hemorrhagic strokes when compared with low active individuals (RR = 0.80, 95% CI 0.69-0.91< 0.001).

Evidence suggests there is an increased risk of stroke associated with being overweight or obese. Saito et al. (2011) compared stroke risk in 32,847 men and 38,875 Japanese women, aged 45–74 years, with no history of cardiovascular disease who were of normal weight (BMI 23.0-24.9 kg/m2) with persons who had high BMIs (27.0 to 29.9 and ≥ 30.0). The risk of stroke was significantly increased with increasing BMI (HR= 1.09 and 1.25 for men, and HR=1.29 and 2.16 for women, respectively, relative to healthy weight). In addition, in women a weight increase of greater than 10% over the previous five years was also associated with increased stroke risk. Bazzano et al. (2010) reported similar findings in a study of 154,736 Chinese men and women ≥ 40 years. The risk for stroke increased significantly for persons considered overweight (BMI 25.0 to 29.9, HR=1.43, 95% CI 1.36-1.52) and for those who were obese (BMI≥ of 30, HR= or 1.72, 95% CI 1.55-1.91). In the INTERSTROKE case-control study, O’Donnell et al. (2010) reported that increasing weight-to-hip ratio was associated with increased risk of stroke. Waist-to-hip ratio was expressed in tertiles, based on participants in the control group. Cut-off points used were 0.91 and 0.96, for men and 0.86 and 0.93, in women. In comparisons of tertiles 1 vs. 2 and 1 vs. 3, the risk of total stroke, ischemic stroke and hemorrhagic stroke were all significantly elevated. For example, the ORs for (all) stroke were 1.42, 95% CI 1.18-1.71 (T1 vs. T2) and 1.65, 95% CI 1.39-1.99 (T1 vs. T3). Hu et al. (2007) studied 49,996 men and women, aged 25-74 years, with no history of stroke or coronary heart disease. BMI, waist circumference and waist-hip measures were obtained at baseline and stroke risk assessed after an average follow up of 9.5 years. The risk of all stroke and ischemic stroke were increased in both men and women with increasing BMI, while increased waist circumference and waist-to-hip ratio were risk factors for total and ischemic stroke in men, but not women.

Alcohol Consumption
Using the results from 26 studies Patra et al. (2010) reported a dose-response relationship that was linear for hemorrhagic stroke with increasing risk associated with increasing consumption, whereas there was a curvilinear relationship for ischemic stroke, with a protective effect of alcohol for low to moderate consumption, and increased risk for higher exposure. Women who consumed more 3 or more drinks on average/day, had higher risks than men. O’Donnell et al. (2010) reported that moderate alcohol consumption (1-30 drinks/month) was associated with reduced risk of ischemic stroke (OR=0.79, 95% CI 0.63-1.00), but with an increased risk of hemorrhagic stroke (OR=1.52, 95% CI 1.07-2.16) compared with never/former drinkers while >30 drinks/month or binge drinking was associated with an increased risk of ischemic and hemorrhagic stroke compared with never/former drinkers. A meta-analysis including 35 observational studies examining the effects of alcohol consumption on stroke risk over a follow-up period of 4-30 years revealed a J-shaped relationship between the amounts of alcohol consumed per day and the risk of ischemic stroke (Reynolds et al. 2003). Individuals who consumed <12 grams of alcohol per day had the lowest risk for ischemic stroke (RR = 0.80, 95% CI 0.67-0.96), while those having more than 60 grams/day had the highest risk (RR = 1.69, 95% CI 1.34-2.15) when compared with a group of abstainers. Jemenez et al (2012) studied 83,578 women aged 30-55 years, who were participants of the Nurses’ Health Study and found that compared to non-drinkers, moderate alcohol consumption (>0 to 14.9 g/day) was associated with a significant reduction in total stroke risk.

Birth control/Hormone Replacement Therapy
Women taking oral contraceptive or hormone replacement therapy (HRT) may be at an increased risk of stroke. Bath &Gray (2005) conducted a meta-analysis including the results from 28 RCTs and found that HRT was associated with significant increases in the risk of total stroke (OR =1.29, 95% CI 1.13 to 1.47), non-fatal stroke (OR=1.23, 1.06 to 1.44), stroke leading to death or disability (OR=1.56, 1.11 to 2.20), and ischaemic stroke (OR=1.29, 1.06 to 1.56). They also reported that hormone replacement therapy was not associated with hemorrhagic stroke (OR=1.07, 0.65 to 1.75) or transient ischaemic attack (OR=1.02, 0.78 to 1.34). Similarly, Renoux et al. (2010) reported that, compared to non-users, women using oral hormone replacement therapy within the previous year had a higher risk of stroke (RR= 1.28, 1.15-1.42). Use of oral HRT for >1 year was associated with increased risk of stroke (RR=1.35, 95% CI 1.20-1.52), but not for a duration of ≤1 year. High dose transdermal patch use was associated with an increased risk of stroke (RR=1.89, 95% CI 1.15-3.11), although low- dose patches were not (RR=0.95, 0.75-1.20).

In terms of elevated risk of stroke associated with hormonal forms of birth control, the evidence is equivocal. In a large cohort study including the results of over 1.6 million women between the ages of 15 and 49 years, Lidegaard et al. (2012) reported that current use of ethinyl estradiol at doses of 20 to 50 μg was associated with an increased risk of thrombotic stroke, compared with nonusers, while current use of progestin only was not. In a large cohort study of 49, 259 Swedish women aged 30-49, Yang et al. (2009) reported that the risk of fatal or nonfatal ischemic or hemorrhagic stroke was not significantly increased. The associations were not influenced by age at menarche nor with parity status.

Recreational Drug Use
The most commonly-used illicit drugs associated with increased stroke risk are cocaine, amphetamines, Ecstasy, heroin/opiates, phencyclidine (PCP), lysergic acid diethylamide (LSD), and cannabis/marijuana. These drugs may increase the risk for stroke through a variety of mechanisms including hypertensive surges, vasospasm, enhanced platelet aggregation, vasculitis, accelerated atherosclerosis and cardioebolism. Kaku & Lowenstein (1990) reported that the risk ratio for (any) drug abuse was 6.5 (95% CI 3.1-13.6) compared with non-drug users. There was a strong temporal relationship whereby the risk was highest during the first 6 hours after use and decreased over time. Westover et al. (2007) reviewed the records of 1,935 patients aged 18-44 years discharged from hospitals with a diagnosis of stroke and found that cocaine abuse was associated with an increased risk of both ischemic and hemorrhagic stroke. In the same study, amphetamine use was associated with an increase in the risk of hemorrhagic stroke (OR=4.95, 95% CI 3.24-7.55) and an increased risk of hemorrhagic stroke resulting in death (OR=2.63, 95% CI 1.07-6.50). The association between cannabis use and stroke does not appear to be as strong. While cannabis use was associated with an increased risk of ischemic stroke (OR=1.76, 95% CI 1.15-2.71) but not hemorrhagic stroke (OR=1.36, 95% CI 0.90-2.06) in one study (Westover et al. 2007), after adjusting for age, sex, ethnicity and current tobacco use, Barber et al. (2013) reported there was no association between stroke and cannabis use (OR=1.59, 95% CI 0.71-3.70).