lin therapy is begun (Brody, 2003). Catalano (2003) suggested that insulin therapy is one of the most suitable treatments. It is claimed that this regimen can reduce fetal macrosomia, but more studies to show the effect on maternal and neonatal health outcomes are needed (Brody, 2003). Association between perinatal mortality and morbidity and abnormal GTT or GDM has Risk factors for GDM may be classified into two types: modifiable and unmodifiable (Dornhorst and Rossi, 1998). Risk factors over which a woman has no control include maternal age of above 25 years, ethnicity (e.g. Aboriginal Canadians, African-American, Asian, Hispanic, Indian, Native American and Pima Indians, and probably other indigenous groups), weight prior to pregnancy, parity, and personal and family history of diabetes. Risk factors which are potentially modifiable include obesity (a body mass index (BMI) more than 27 kg/m2) and further weight gain (American Diabetes Association, 2004; Jones and Stone, 1998; Ostlund, 2003; Scott, 2002). BMI is calculated by dividing weight in kilograms by the height in meters squared.

Other risk factors include a prior low birth weight baby (less than 2,500 g), impaired glucose tolerance, impaired fasting glucose, poor diet, sedentary life style, smoking, hypertension and other cardiovascular risk factors, and genetic problems (e.g. glucokinase and hepatic nuclear disorder) (Capes and Anand, 2001; Scott, 2002).

There is disagreement about the treatment of GDM, and particularly about the management of minor degrees of glucose elevation or glucose intolerance (Scott, 2002). There is more than one treatment for women with GDM, including diet control, insulin therapy, and exercise. An appropriate diet may accomplish physiologic glucose homeostasis. If dietary modification fails to achieve this, then insulin therapy is begun (Brody, 2003). Catalano (2003) suggested that insulin therapy is one of the most suitable treatments. It is claimed that this regimen can reduce fetal macrosomia, but more studies to show the effect on maternal and neonatal health outcomes are needed (Brody, 2003). Association between perinatal mortality and morbidity and abnormal GTT or GDM has b

pregnancy, parity, and personal and family history of diabetes. Risk factors which are potentially modifiable include obesity (a body mass index (BMI) more than 27 kg/m2) and further weight gain (American Diabetes Association, 2004; Jones and Stone, 1998; Ostlund, 2003; Scott, 2002). BMI is calculated by dividing weight in kilograms by the height in meters squared.

Other risk factors include a prior low birth weight baby (less than 2,500 g), impaired glucose tolerance, impaired fasting glucose, poor diet, sedentary life style, smoking, hypertension and other cardiovascular risk factors, and genetic problems (e.g. glucokinase and hepatic nuclear disorder) (Capes and Anand, 2001; Scott, 2002).

There is disagreement about the treatment of GDM, and particularly about the management of minor degrees of glucose elevation or glucose intolerance (Scott, 2002). There is more than one treatment for women with GDM, including diet control, insulin therapy, and exercise. An appropriate diet may accomplish physiologic glucose homeostasis. If dietary modification fails to achieve this, then insulin therapy is begun (Brody, 2003). Catalano (2003) suggested that insulin therapy is one of the most suitable treatments. It is claimed that this regimen can reduce fetal macrosomia, but more studies to show the effect on maternal and neonatal health outcomes are needed (Brody, 2003). Association between perinatal mortality and morbidity and abnormal GTT or GDM has

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Other risk factors include a prior low birth weight baby (less than 2,500 g), impaired glucose tolerance, impaired fasting glucose, poor diet, sedentary life style, smoking, hypertension and other cardiovascular risk factors, and genetic problems (e.g. glucokinase and hepatic nuclear disorder) (Capes and Anand, 2001; Scott, 2002).

There is disagreement about the treatment of GDM, and particularly about the management of minor degrees of glucose elevation or glucose intolerance (Scott, 2002). There is more than one treatment for women with GDM, including diet control, insulin therapy, and exercise. An appropriate diet may accomplish physiologic glucose homeostasis. If dietary modification fails to achieve this, then insulin therapy is begun (Brody, 2003). Catalano (2003) suggested that insulin therapy is one of the most suitable treatments. It is claimed that this regimen can reduce fetal macrosomia, but more studies to show the effect on maternal and neonatal health outcomes are needed (Brody, 2003). Association between perinatal mortality and morbidity and abnormal GTT or GDM has

t the treatment of GDM, and particularly about the management of minor degrees of glucose elevation or glucose intolerance (Scott, 2002). There is more than one treatment for women with GDM, including diet control, insulin therapy, and exercise. An appropriate diet may accomplish physiologic glucose homeostasis. If dietary modification fails to achieve this, then insulin therapy is begun (Brody, 2003). Catalano (2003) suggested that insulin therapy is one of the most suitable treatments. It is claimed that this regimen can reduce fetal macrosomia, but more studies to show the effect on maternal and neonatal health outcomes are needed (Brody, 2003). Association between perinatal mortality and morbidity and abnormal GTT or GDM has lin therapy is begun (Brody, 2003). Catalano (2003) suggested that insulin therapy is one of the most suitable treatments. It is claimed that this regimen can reduce fetal macrosomia, but more studies to show the effect on maternal and neonatal health outcomes are needed (Brody, 2003). Association between perinatal mortality and morbidity and abnormal GTT or GDM has been overemphasized (Hunter and Keirse, 1989). Hunter and Keirse (1989) found no evidence that insulin therapy improves neonatal outcome and decreases macrosomia in the infant.