The various types of CVD share a range of common risk factors, working through an underlying pathway that leads to atherosclerosis and vessel damage.
The risk factors for the development of CVD can be categorised in various ways, e.g. classical/traditional CVD risk factors, including behavioural/lifestyle factors such as nutrition/diet, physical inactivity, tobacco exposure or perinatal exposures, versus non-traditional risk factors through pathways such as adipocyte dysfunction in brown adipose tissue (23), and changes in adipokines such as adiponectin (24). Here we use the categorisation into modifiable or non-modifiable risk factors, as is used in the GBD studies. Among the non-modifiable risk factors, the effect of ethnicity is shown by the varying incidence of CVD across different ethnic groups (25, 26). This will be carefully discussed in the following sections, since there may also be modifiable elements in “ethnicity”. The modifiable risk factors can also be separated into two main categories (with clear links between them): behavioural factors and biomedical factors. The behavioural factors include physical inactivity and smoking, while the biomedical risk factors include high blood pressure, high fasting plasma glucose, dyslipidaemia and, according to some evidence, vitamin D deficiency (27).
According to the Global Burden of Disease and Injury Study (2010) the top eight modifiable risk factors of the CVD disease burden in DALYs were high blood pressure, smoking, high body mass index (BMI), high total cholesterol, high fasting plasma glucose, insufficient physical activity, alcohol use, and dietary factors (5). East Asian populations share the same common major modifiable CVD risk factors as other populations. A study using nationally representative data from 10 Asian countries found a substantial proportion of the CVD burden could be attributed to 5 major modifiable risk factors: high blood pressure, smoking, high BMI, high total cholesterol and diabetes (28). However, the prevalence of modifiable risk factors such as smoking, physical activity and dietary habits may vary considerably among different ethnic groups, affecting biomedical factors and further exaggerating the effect of ethnicity on CVD incidence.
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In the remainder of this section, I will briefly address these risk factors except for smoking and vitamin D deficiency. I have chosen to focus on these two risk factors as particular considerations of this thesis.
Smoking accounts for a major proportion of IHD DALYs (31%) (29) and is one risk factor where the prevalence has changed dramatically in Western populations but has been slower to change in Asian populations over time.
Vitamin D deficiency was an emerging novel risk factor for CVD when this thesis was being developed. Although clinical trials have not supported an independent role of vitamin D status in CVD, vitamin D deficiency can also be considered as a marker of multiple CVD risk factors, such as low physical activity, low time outdoors, and high BMI. These risk factors are the key determinants of serum 25(OH)D level. This means that these two risk factors are useful to examine the broad scope of modifiable risk factors, with a high likelihood of seeing changes with acculturation. More detailed sections on these risk factors are presented separately.
High blood pressure
The WHO definition for hypertension is having any of the following: a systolic blood pressure (SBP) of 140 mm Hg or more; a diastolic blood pressure (DBP) of 90 mm Hg or more; taking antihypertensive medication. According to data from the AHS, the prevalence of hypertension was 32% in Australian adults in 2011-2012 (30).
Hypertension is the leading risk factor for CVD according to the Global Burden of Disease and Injury Study 2010. Fifty-three per cent of IHD DALYs was attributable to high blood pressure worldwide in 2010 (5).
Evidence suggests that hypertension is associated with increased risk of a range of CVD outcomes. In a large-scale prospective study of 1.25 million people, modest associations were found between hypertension and intracerebral haemorrhage (hazard ratio (HR) 1.44 (95% CI 1.32-1.58)), and stable angina (HR: 1.41 (1.36-1.46)) (31).
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Controlling or reducing hypertension reduces the risk of CVD. A meta-analysis of randomised controlled trials from the Blood Pressure Lowering Treatment Trialists’ Collaboration reported that blood pressure-lowering treatment reduced the risk of cardiovascular events (including stroke, heart attack, heart failure, or cardiovascular death) by 13%-18% for people in different categories of baseline 5-year CVD risk (32).
High body mass index (BMI)
The WHO definition for overweight and obesity based on BMI is: underweight BMI < 18.5, healthy weight BMI ≥ 18.5 and BMI < 25, overweight BMI ≥ 25 and BMI < 30, obese BMI ≥ 30. According to the 2011–12 National Health Measures Survey, 35% of Australian adults were overweight and 28% were obese (30). WHO recommends additional cut-off points to define higher BMI in Asian populations. The suggested categories are: BMI 23–27·5 kg/m2 for overweight and > 27·5 kg/m2 for
obesity (33).
Higher BMI has been shown to be associated with an increased risk of a range of CVD events and CVD mortality across diverse populations. A meta-analysis of 57 prospective cohort studies reported that each 5kg/m2 increase in BMI was associated with a 40% increase in CVD mortality (HR: 1.41 (1.37-1.45)) (34). A recently published meta-analysis of 95 cohorts with a total of 1.2 million participants reported that the age-adjusted HR of coronary heart disease for those overweight was 1.20 (1.12–1.29) in women and 1.22 (1.12–1.32) in men; and for those obese 1.61 (1.42– 1.82) in women and 1.60 (1.43–1.79) in men (35). A meta-analysis of 25 prospective studies including 2 million participants reported that the relative risk (RR) of ischaemic stroke was 1.22 (1.05-1.41) in the overweight and 1.64 (1.36-1.99) in the obese. There was a non-significant association with haemorrhagic stroke (RR for overweight: 1.01 (0.88-1.17); RR for obesity: 1.24 (0.99-1.54)) (36).
Dyslipidaemia
The Australian National Heart Foundation defines dyslipidaemia as a disorder of lipoprotein metabolism that consists of one or more of the following abnormalities in serum lipid concentrations: high total cholesterol (TC ≥ 5.5 mmol/L); high low-
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density lipoprotein cholesterol (LDL-C ≥ 3.5 mmol/L); high triglycerides (TG ≥ 2.0 mmol/L); low high-density lipoprotein cholesterol (HDL-C < 1.0 mmol/L for men, and < 1.3 mmol/L for women) (37). According to data from the AHS, 33% of Australian adults had high LDL-C, 23% had low HDL-C cholesterol and 14% had high TG in 2011-2012 (30).
Abnormality of LDL-C has been reported to increase the risk of developing atherosclerosis resulting in IHD, angina, and stroke (37-39). High LDL-C is the primary target for CVD prevention. Evidence from large-scale meta-analysis of 27 randomised trials suggested that, in individuals with low risk of CVD, for each 1 mmol/L reduction in LDL-C, the RR for major vascular events (including major coronary events, strokes, and coronary revascularisation procedures) was 0.79 (0.77- 0.81) (40).There is no evidence to support interventions that increase the levels of HDL-C to reduce CVD incidence or CVD mortality (41).
High fasting plasma glucose
WHO defines impaired fasting glucose (IFG) as a fasting plasma glucose concentration between 6.1 mmol/l and 6.9 mmol/l, with a diabetic level defined as 7.0 mmol/L or higher (42). “High fasting plasma glucose” includes both IFG and diabetes. In 2011–12, the estimated prevalence for high fasting plasma glucose was 8.2% in Australian adults, based on self-reported data, HbA1c results, and test results of fasting plasma glucose (5.1% for diabetes, and 3.1% for IFG) (30).
In a meta-analysis of 102 prospective studies, the risk for a wide range of CVD outcomes in individuals with diabetes was around twice that of those without diabetes (HRs: IHD, 2.00, 95% CI (1.83–2.19); ischaemic stroke, 2.27 (1.95–2.65); haemorrhagic stroke, 1.56 (1.19–2.05)). In the same study, in people without diabetes, HRs for IHD were 1.17 (1.08–1.26) for those with IFG, compared to those with fasting blood glucose concentrations in the normal range (3.90–5.59 mmol/L) (43). According to recent findings in a randomised controlled trial, intensive glycaemic control in people with type 2 diabetes significantly reduced the risk of major cardiovascular events (defined as heart attack, stroke, new or worsening congestive heart failure, amputation for ischaemic gangrene, or cardiovascular-related death) (HR: 0.83 (0.70–0.99)) (44). A meta-analysis of thirteen randomised-controlled trials
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reported a 20% AMI risk reduction associated with intensive glucose lowering treatment in people with type 2 diabetes (45). However, that evidence suggests intensive glycaemic control has little effect on reducing CVD mortality (44-46). Physical inactivity
Sufficient physical activity is defined as ‘accumulate 150 to 300 minutes of moderate intensity physical activity or 75 to 150 minutes of vigorous intensity physical activity, or an equivalent combination of both moderate and vigorous activities (where vigorous physical activity is weighted by two) each week, according to Australia’s Physical Activity and Sedentary Behaviour Guidelines (47). In 2011–12, 56% of the adult population did not meet this physical activity recommendation (30).
Physical inactivity is implicated in increased risk of a range of CVD outcomes from IHD and stroke, to peripheral vascular disease. In addition to the direct effect of insufficient physical activity on cardiovascular health, it also contributes to other CVD risk factors such as overweight or obesity, hypertension, and dyslipidaemia. On the other hand, regular physical activity has a protective effect on decreasing the risk of CVD and other more proximal CVD risk factors. A meta-analysis of prospective cohort studies reported a dose-response relationship between physical activity and risk of IHD. In comparison with those without leisure-time physical activity, the relative risk (RR) of IHD was 0.86 (0.77-0.96) in those engaged in the equivalent of 150 min/week of moderate-intensity leisure-time physical activity. For higher physical activity levels (i.e. 300 min/week of moderate-intensity leisure-time physical activity) the RR of IHD was 0.80 (0.74-0.88) (48). Another meta-analysis reported that, compared with inactivity, moderately intense physical activity had a protective effect on total stroke (with RR ranging from 0.64 (0.48-0.87) to 0.85 (0.78-0.93)) (49).
Dietary risk factors
Dietary risk factors include diets low in fruits, vegetables, nuts, seeds, whole grains, sea food, omega-3 fatty acids, and diets high in sodium. In the GBD 2010 Study, the largest proportion (10%) of global DALYs was attributable to poor diet (22).
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The 2013 Australian Dietary Guidelines provide minimum daily intake for five food groups including vegetables, fruit, dairy food , lean meat and grains (50). The guideline also recommends that intake of intake of foods containing saturated fat, added salt, added sugars and alcohol is limited (50). The Australian Health Survey 2011-2013 reported that most Australians failed to meet recommended daily intakes of any of the five food groups (51) and over half of Australians exceeded the
recommended free sugar intake (less than 10% of dietary energy) (52).
Observational studies suggested insufficient intake of nutritious foods and consumption of foods high in saturated fat, added salt, added sugars are associated with a range of CVD outcomes (53-55). However, there is no strong evidence from randomised controlled trials that supports the benefits of changing intake of these dietary risk factors.