**4. Causes of ethnic differences**

There are several factors that contribute to the development of dyslipidaemia (2001), including genetic factors (Cohen et al. 1994) and acquired factors (Chait and Brunzell 1990; Devroey et al. 2004; Ruixing et al. 2008) such as overweight and obesity (Denke et al. 1993; Denke et al. 1994; Brown et al. 2000), physical inactivity (Berg et al. 1997; Hardman 1999), cigarette smoking (Criqui et al. 1980; Cade and Margetts 1989; Umeda et al. 1998; Fisher et al. 2000; Wu et al. 2001; Maeda et al. 2003; Mammas et al. 2003; Venkatesan et al. 2006; Grant and Meigs 2007; Arslan et al. 2008; Batic-Mujanovic et al. 2008), high fat intake (Hennig et al. 2001; Millen et al. 2002; Tanasescu et al. 2004), very high carbohydrate diets (> 60 percent of total energy) (McNamara and Howell 1992) and certain drugs (Lehtonen 1985; Fogari et al. 1988; Roberts 1989; Middeke et al. 1990; Stone 1994) (such as beta-blockers, anabolic steroids, progestational agents, et al.). Excess alcohol intake is also documented as a risk factor (Umeda et al. 1998; Wu et al. 2001; Mammas et al. 2003) despite that moderate alcohol consumption may have a beneficial effect on improving HDL-C concentrations (De Oliveira et al. 2000; Shai et al. 2004). In addition, glycaemic control is an important determinant of dyslipidaemia in patients with diabetes (Ismail et al. 2001; Grant and Meigs 2007; Ahmed et al. 2008; Gatti et al. 2009). Among these acquired factors, overweight, obesity and physical inactivity appear to be most important (Denke et al. 1993; Denke et al. 1994; Berg et al. 1997; Hardman 1999; Brown et al. 2000). They are also the most important lifestyle variables that decrease insulin action and increase the risk of diabetes.

The causes of ethnic difference in cardiovascular risk profile are complex. Possible contributors include genetic, environmental, psychosocial, cultural and unmeasured factors and many are not well clarified (Zaninotto et al. 2007). It is clear that the observed ethnic differences in lipid profiles cannot be explained by genetics alone and may be more indicative of lifestyle-related factors such as dietary pattern and physical activity (Ruixing et al. 2008; McNaughton et al. 2009; Sisson et al. 2009). To what extent is ethnic-specific lifestyle pattern associated with different lipid profiles deserves further investigation.

#### **4.1 Genetic factors**

An adverse lipid profile in Asian Indians has been reported to be associated with the greater susceptibility to insulin resistance (Tan et al. 1999; Anand et al. 2000; Bhalodkar et al. 2005; Palaniappan et al. 2007), and a higher percentage of body fat for the same BMI as compared with Whites (McKeigue et al. 1991), which may contribute to the high prevalence of CVD

ethnic groups in the UK (Zaninotto et al. 2007), the prevalence of low HDL-C was highest in south Asian groups such as Bangladeshi, Indian and Pakistani, followed by Chinese, Irish and those from the general population living in private households; In contrast, the lowest prevalence was seen in Black Caribbean. Similar finding was reported in another study where the comparison was made between non-South-Asians and South Asians (France et al. 2003). In addition, African Americans have been reported to have less adverse lipid profiles than Whites or Hispanics despite the presence of diabetes (Werk et al. 1993; Cowie et al. 1994; Sharma and Pavlik 2001). The causes of ethnic difference in levels of CVD risk factor are complex and may include genetic, environmental and cultural factors (Zaninotto et al. 2007). However, little is known about such ethnic differences in lipid profiles at comparable

There are several factors that contribute to the development of dyslipidaemia (2001), including genetic factors (Cohen et al. 1994) and acquired factors (Chait and Brunzell 1990; Devroey et al. 2004; Ruixing et al. 2008) such as overweight and obesity (Denke et al. 1993; Denke et al. 1994; Brown et al. 2000), physical inactivity (Berg et al. 1997; Hardman 1999), cigarette smoking (Criqui et al. 1980; Cade and Margetts 1989; Umeda et al. 1998; Fisher et al. 2000; Wu et al. 2001; Maeda et al. 2003; Mammas et al. 2003; Venkatesan et al. 2006; Grant and Meigs 2007; Arslan et al. 2008; Batic-Mujanovic et al. 2008), high fat intake (Hennig et al. 2001; Millen et al. 2002; Tanasescu et al. 2004), very high carbohydrate diets (> 60 percent of total energy) (McNamara and Howell 1992) and certain drugs (Lehtonen 1985; Fogari et al. 1988; Roberts 1989; Middeke et al. 1990; Stone 1994) (such as beta-blockers, anabolic steroids, progestational agents, et al.). Excess alcohol intake is also documented as a risk factor (Umeda et al. 1998; Wu et al. 2001; Mammas et al. 2003) despite that moderate alcohol consumption may have a beneficial effect on improving HDL-C concentrations (De Oliveira et al. 2000; Shai et al. 2004). In addition, glycaemic control is an important determinant of dyslipidaemia in patients with diabetes (Ismail et al. 2001; Grant and Meigs 2007; Ahmed et al. 2008; Gatti et al. 2009). Among these acquired factors, overweight, obesity and physical inactivity appear to be most important (Denke et al. 1993; Denke et al. 1994; Berg et al. 1997; Hardman 1999; Brown et al. 2000). They are also the most important lifestyle variables that

The causes of ethnic difference in cardiovascular risk profile are complex. Possible contributors include genetic, environmental, psychosocial, cultural and unmeasured factors and many are not well clarified (Zaninotto et al. 2007). It is clear that the observed ethnic differences in lipid profiles cannot be explained by genetics alone and may be more indicative of lifestyle-related factors such as dietary pattern and physical activity (Ruixing et al. 2008; McNaughton et al. 2009; Sisson et al. 2009). To what extent is ethnic-specific lifestyle

An adverse lipid profile in Asian Indians has been reported to be associated with the greater susceptibility to insulin resistance (Tan et al. 1999; Anand et al. 2000; Bhalodkar et al. 2005; Palaniappan et al. 2007), and a higher percentage of body fat for the same BMI as compared with Whites (McKeigue et al. 1991), which may contribute to the high prevalence of CVD

pattern associated with different lipid profiles deserves further investigation.

glucose tolerance status.

**4.1 Genetic factors** 

**4. Causes of ethnic differences** 

decrease insulin action and increase the risk of diabetes.

(Kuller 2004) and diabetes (Ramachandran et al. 2008; Snehalatha and Ramachandran 2009) in this ethnic group. In addition, it may also reflect the genetic variation, for example, at the apoE locus (Tan et al. 2003) and an excess of other risk factors such as homocysteine, Lp(a) or dietary fat (France et al. 2003).
