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A study of cleft lip and cleft palate was carried out in order to determine whether or not any differences in incidence between Europeans and Polynesians were accompanied by differences in recurrence risks, and to test the genetic hypotheses currently favoured as explanations of familial agggregation of these disorders. An incidence study vas undertaken on all live births in the Auckland urban area for the years 1960 to 1976.Family information was obtained from these probands and from other affected persons or their close relatives, by interview at the cleft palate clinic at Middlemore Hospital. The ascertainment probability for cleft 1ip and cleft palate probands was about 95% and was not correlated with any of the demographic characteristics measured on the probands. After correction for ascertainment, the incidence of cleft palate in Maoris was estimated to be 1.867/1000 1lve births. For Europeans the estimate was 0.643/1000. The corresponding figures for cleft lip with or without cleft palate were 0.397/1000 and 1.195/1000. The sex ratio for cleft palate was 0.485 with heterogeneity between the races. For cleft lip the sax ratio was 0.649 overall. There were no secular or seasonal trends in the incidence of facial clefts and no significant effects of maternal age, or paternal age. The mean birth rank for probands with cleft lip with or without cleft palate was higher than expected. For probands with cleft palate, mean birth rank was not significantly elevated. The pattern of additional malformations in these probands was similar to those reported in similar studies from other centres. The recurrence risk for cleft palate was 1.8% overall. Although it was s1ightly higher in polynesian families than in European families, the difference was nowhere near statistical significance. For cleft lip the recurrence risk was 2.6% overall, with the risk being slightly higher in Polynesian families, but again not significantly higher than in European families. Using current analytical techniques, no discrimination was possible between a generalized single autosomal locus model and a multifactoriar threshold model. A consideration of the parameter estimates for both models suggests that the multifactorial threshold model is the more appropriate one to use for the calculation of recurrence risks in complicated family situations. It is concluded that further family studies of this nature would no longer be warranted unless hypotheses can realistically be tested on the samples available. However, incidence studies in special populations will remain important for hypothesis testing. Following on the work using animal models, a study of face shape within and among races in New Zealand may provide clues to the aetiology of facial clefts, particularly isoleted cleft palate. It will be important to follow changes in incidence over time and discover what effects intermarriage and cultural changes might have on the incidence of facial clefts.

The primary aim of the study was to validate the short and long form of the recently-created NZ physical activity questionnaires (NZPAQ-SF and NZPAQ-LF, respectively) in a multi-ethnic sample in Auckland. An international physical activity questionnaire (IPAQ-long) was also validated and compared to the NZ instruments. Objective PA measures were used to create a NZ compendium of PA intensities, providing baseline data for culturally-specific PAs. Secondary aims included an examination of the relationship between PA and CRF, and their associations with cross-sectional measures of cardiovascular (CV) risk factors. The study sample consisted of 186 apparently healthy males (n=90) and females (n=96) aged 19-86 yrs, classified as European/Other (n=60), Māori (n=61), and Pacific (n=65). Heart rate monitoring (HRM) with individual calibration was used to objectively measure the duration, frequency, and intensity of at least moderate-intensity PAs performed over 3 consecutive days. Type of PA and the context in which it was performed was simultaneously recorded by participants on daily PA logs. Correlations between HRM and self-reported levels of brisk walking, moderate-intensity, vigorousintensity, were poor for each questionnaire, and correlations were lower for Māori and Pacific ethnic groups than for European/Other. The NZPAQ-SF (r=0.3, p<0.001) and NZPAQ-LF (r=0.3, p<0.001) performed better than the IPAQ-long (r=0.1, p=0.37). The culturally-specific list of PA intensities showed strong correlation (R2=0.68) to an internationally-accepted compendium of PA intensities, and provided baseline energy cost data for 13 PAs performed by Māori and Pacific people in NZ. CRF levels were primarily influenced by gender, ethnicity, obesity, and performing at least 15 min/day of vigorous-intensity PA, and showed stronger associations with fasting blood lipids and glucose, while PA was more strongly related to SBP and DBP. The validated NZPAQs are acceptable for measuring population level PA prevalence in NZ adults, although accuracy is lower for Māori and Pacific people. However, the availability of a culturallyspecific list of PA intensities could potentially increase the accuracy of self-reported PA by Māori and Pacific people. Results from this study highlight the importance of vigorous-intensity PA for CV health, and identifies NZ Pacific people as high risk in terms of PA, obesity, and CRF.

The risk of developing type 2 diabetes is four fold higher in New Zealand(NZ) Polynesians compared to Caucasians. Hence diabetes is more prevalent in Maori (16.5% of the general population) and Pacific Island people (10.1%) compared to NZ Caucasians (9.3%). It is generally accepted that type 2 diabetes has major genetic determinants and heterozygous mutations in a number of genes have previously been identified in some subsets of type 2 diabetes and certain ethnic groups. The high prevalence of diabetes in NZ Polynesians, when compared with NZ Caucasians, after controlling for age, income and body mass index (BMI), suggest that genes may be important in this population. Therefore, the prevalence of allelic variations in the genes encoding amylin and insulin promoter factor-1 (IPF-1), and exon 2 of the hepatocyte nuclear factor-1α (HNF-1α) gene in NZ Polynesians with type 2 diabetes was determined. These genes are known to produce type 2 diabetes in other populations. The genes investigated were screened for mutations by PCR amplification and direct sequencing of promoter regions, exons and adjacent intronic sequences from genomic DNA. DNA was obtained from 146 NZ Polynesians (131 Maori and 15 Pacific Island) with type 2 diabetes and 387 NZ Polynesian non-diabetic control subjects (258 Maori and 129 Pacific Island). Sequences were compared to previously published sequences in the National Centre for Biotechnology Information database. Allelic variations in IPF-1 and exon 2 of the HNF-1α gene were not associated with type 2 diabetes in NZ Polynesians. However, in the amylin gene, two new and one previously described allele was identified in the Maori population including: two alleles in the promoter region (-132G>A and -215T>G), and a missense mutation in exon 3 (QlOR). The -215T>G allele was observed in 5.4% and l% of type 2 diabetic and non-diabetic Maori respectively, and predisposed the carrier to diabetes with a relative risk of 7.23. The -215T>G allele was inherited with a previously described amylin promoter polymorphism(-230A>C) in 3% of Maori with type 2 diabetes, which suggests linkage equilibrium exists between these two alleles. Both Q10R and -132G>A were observed in 0.76% of type 2 diabetic patients and were absent in non-diabetic subjects. Together these allelic variations may account for approximately 7% of type 2 diabetes in Maori. These results suggest that the amylin gene maybe an important candidate marker gene for type 2 diabetes in Maori.

Cardiovascular disease is the leading cause of mortality in New Zealand. The most current evidence indicates that the burden of cardiovascular disease is greatest among Maori and Pacific peoples and Pacific peoples have the highest mortality rate for cerebrovascular disease [1]. There is substantial scientific evidence that cardiovascular disease has its origin early in life and that a person's risk of cardiovascular disease is determined by the synergistic effect of all the cardiovascular risk factors over time. The Auckland High School Heart Survey (AHHS) is an epidemiological survey designed to determine the prevalence of risk factors for cardiovascular disease in an adolescent high school population in New Zealand. It takes a 'lifecourse' and primary prevention approach to reducing the incidence of cardiovascular disease. The aims of the study were to determine cardiovascular risk factor levels in, and compare the cardiovascular and diabetes risk factor levels between, Pacific and European students and the main Pacific communities (Samoan, Cook Islands, Tongan, and Niuean). The AHHS was a school-based cross-sectional survey of 2,549 adolescent students, across 10 Auckland High Schools. A cluster sampling technique was used to obtain the target of 1000 Pacific participants, to enable Pacific ethnic-specific analysis. The study specifically aimed to determine ethnic-specific differences in lifestyle, intermediate and outcome variables that have been established as cardiovascular risks. Lifestyle variables included: smoking, alcohol consumption, leisure-time physical activity (LTPA), television exposure and sun exposure. The intermediate variables analysed included: body mass index (BMI), waist to hip ratio (WHR), percentage body fat (PBF) and physical work capacity 170 (PWC170). The outcome variables included: total cholesterol (TC), high density lipoprotein cholesterol (HDLC), ratio of total cholesterol to high density lipoprotein cholesterol (TC:HDLC), low density lipoprotein cholesterol (LDLC), triglycerides (TG), fasting blood glucose (FG), urinary micro albumin (UA), systolic and diastolic blood pressure (SBP & DPB). Demographic variables analysed included: sex, age, ethnic group, school, socio-economic status and growth development and maturation. The AHHS study results showed that demographic variables were strongly associated with both intermediate and outcome variables. The findings showed that there were significant ethnic variations between the four main ethnic groups (Pacific, Maori, Asian and European) in risk factors for cardiovascular disease. Pacific participants had the highest BMI and PBF. Pacific participants had the lowest levels of PWC170. With regard to outcome variables, Pacific adolescents had lower levels of TC, HDLC and LDLC compared to Europeans. However, Pacific participants had higher levels of TC:HDLC, FG, TG and DPB. To a lesser degree, lifestyle variables were also associated with other variables. However, the weaker association was likely due to measurement error. The findings of the AHHS study show that ethnic differences present in the adult population are already established among adolescents [2]. Some significant differences were also found between the Pacific ethnic groups (Samoan, Cook Islands, Tongan and Niuean). Among Pacific participants, Cook Islands participants also had the highest level of adjusted mean PWC170. With regard to outcome variables (lipids, fasting glucose and blood pressure), Tongan participants had lower TC, LDLC and TC:HDLC compared to Samoans. However, Tongan participants had significantly higher levels of TG compared to Samoans. For Pacific participants, Cook Islands participants significantly differed from Samoan in smoking, alcohol consumption and PWC170. Cook Islands participants were more likely to have tried smoking for the first time and at an earlier age. They were also more likely to smoke daily and to smoke higher amounts than the other Pacific ethnic groups. Cook Islands participants were more likely to have tried alcohol and at an earlier age. They were also more likely to be drinking alcohol weekly or more often when compared to Samoans. The AHHS study is one of the first pieces of epidemiological research undertaken in New Zealand that provides evidence that there are significant differences between Pacific ethnic groups for this age group. The AHHS study was also able to identify the determinant that explains ethnic differences in outcome variables. BMI was the most significant variable in determining the ethnic differences in outcome variables (lipids, blood pressure and fasting glucose). The AHHS study results showed that Pacific participants had the highest BMI levels of all the ethnic groups, followed by Maori. Television watching was the one lifestyle risk factor that was positively associated with BMI. The most effective variable in terms of decreasing mean difference in BMI was PWC170. PWC170 was significantly lower in Pacific, Asian, and Maori participants compared with European participants. Pacific participants had the lowest levels of PWC170 compared to all other ethnic groups. The AHHS findings support early interventions and programmes targeted to adolescents to reduce the incidence of cardiovascular disease. The findings which show that there are significant differences between Pacific ethnic groups for this age group, may warrant some specific public health initiatives being targeted directly to Pacific ethnic-specific groups. In addition, interventions and programmes that target reducing BMI and improving physical fitness should have an impact on a number of important cardiovascular risk factor outcome variables in adolescents, including: blood pressure, lipids and fasting glucose.

This thesis traces the public health debate about venereal disease in New Zealand from 1920, when the first venereal disease clinics were established, to 1980 before the first AIDS/HIV cases emerged. Studies of venereal disease in New Zealand have concentrated on issues of morality and on the political and social debates; this thesis focuses on treatment procedures and Health Department campaigns. The thesis explores the role of doctors in relation to venereal disease. While advancements in drug therapy benefited patients, medical authority was undermined by demanding and defaulting patients, inadequate medical education, and a low status of the profession. The medical profession developed epidemiological studies and defined 'at risk' groups in post-war decades. Despite claims to be 'scientific', the assessments were informed by stereotypes which had changed little over time. The thesis evaluates the scope of preventative health campaigns. Defined as a public health issue by the 1920s, venereal disease was seen as an individual responsibility by the 1960s. During this time the use of legislation declined, and education and contact tracing increased. The control of infection was limited owing to financial and administrative problems, defaulters and opposition from doctors. Those deemed most at risk were not reached by government educational campaigns, leaving much to the work of welfare groups and individual doctors. The health campaigns targeted groups like Maori and servicemen. The historiography has tended to overlook Maori, and, when military campaigns are discussed, to focus on females. This thesis attempts to redress the balance. Maori had, at least until the 1950s, different treatment experiences from non-Maori patients, although this did not necessarily imply discrimination. The military did attempt to control servicemen, though each Service had different experiences. This thesis stresses the complexity of the gender issue. There was a change from blaming females for infection in the early twentieth century to increasingly pointing to male responsibility. Despite these changes, even with the concept of individual risk pattern by the 1960s, and the understanding that men could be asymptomatic carriers, women were persistently seen as the 'reservoir'. A gender bias persisted. / Note: Thesis now published. (2007) Kampf, Antje. Mapping Out the Venereal Wilderness: Public Health and STD in New Zealand, 1920-1980. Berlin: Lit-Verlag. http://www.lit-verlag.de/isbn/3-8258-9765-9. Whole Document not available at the request of the author.

A study of cleft lip and cleft palate was carried out in order to determine whether or not any differences in incidence between Europeans and Polynesians were accompanied by differences in recurrence risks, and to test the genetic hypotheses currently favoured as explanations of familial agggregation of these disorders. An incidence study vas undertaken on all live births in the Auckland urban area for the years 1960 to 1976.Family information was obtained from these probands and from other affected persons or their close relatives, by interview at the cleft palate clinic at Middlemore Hospital. The ascertainment probability for cleft 1ip and cleft palate probands was about 95% and was not correlated with any of the demographic characteristics measured on the probands. After correction for ascertainment, the incidence of cleft palate in Maoris was estimated to be 1.867/1000 1lve births. For Europeans the estimate was 0.643/1000. The corresponding figures for cleft lip with or without cleft palate were 0.397/1000 and 1.195/1000. The sex ratio for cleft palate was 0.485 with heterogeneity between the races. For cleft lip the sax ratio was 0.649 overall. There were no secular or seasonal trends in the incidence of facial clefts and no significant effects of maternal age, or paternal age. The mean birth rank for probands with cleft lip with or without cleft palate was higher than expected. For probands with cleft palate, mean birth rank was not significantly elevated. The pattern of additional malformations in these probands was similar to those reported in similar studies from other centres. The recurrence risk for cleft palate was 1.8% overall. Although it was s1ightly higher in polynesian families than in European families, the difference was nowhere near statistical significance. For cleft lip the recurrence risk was 2.6% overall, with the risk being slightly higher in Polynesian families, but again not significantly higher than in European families. Using current analytical techniques, no discrimination was possible between a generalized single autosomal locus model and a multifactoriar threshold model. A consideration of the parameter estimates for both models suggests that the multifactorial threshold model is the more appropriate one to use for the calculation of recurrence risks in complicated family situations. It is concluded that further family studies of this nature would no longer be warranted unless hypotheses can realistically be tested on the samples available. However, incidence studies in special populations will remain important for hypothesis testing. Following on the work using animal models, a study of face shape within and among races in New Zealand may provide clues to the aetiology of facial clefts, particularly isoleted cleft palate. It will be important to follow changes in incidence over time and discover what effects intermarriage and cultural changes might have on the incidence of facial clefts.

The primary aim of the study was to validate the short and long form of the recently-created NZ physical activity questionnaires (NZPAQ-SF and NZPAQ-LF, respectively) in a multi-ethnic sample in Auckland. An international physical activity questionnaire (IPAQ-long) was also validated and compared to the NZ instruments. Objective PA measures were used to create a NZ compendium of PA intensities, providing baseline data for culturally-specific PAs. Secondary aims included an examination of the relationship between PA and CRF, and their associations with cross-sectional measures of cardiovascular (CV) risk factors. The study sample consisted of 186 apparently healthy males (n=90) and females (n=96) aged 19-86 yrs, classified as European/Other (n=60), Māori (n=61), and Pacific (n=65). Heart rate monitoring (HRM) with individual calibration was used to objectively measure the duration, frequency, and intensity of at least moderate-intensity PAs performed over 3 consecutive days. Type of PA and the context in which it was performed was simultaneously recorded by participants on daily PA logs. Correlations between HRM and self-reported levels of brisk walking, moderate-intensity, vigorousintensity, were poor for each questionnaire, and correlations were lower for Māori and Pacific ethnic groups than for European/Other. The NZPAQ-SF (r=0.3, p<0.001) and NZPAQ-LF (r=0.3, p<0.001) performed better than the IPAQ-long (r=0.1, p=0.37). The culturally-specific list of PA intensities showed strong correlation (R2=0.68) to an internationally-accepted compendium of PA intensities, and provided baseline energy cost data for 13 PAs performed by Māori and Pacific people in NZ. CRF levels were primarily influenced by gender, ethnicity, obesity, and performing at least 15 min/day of vigorous-intensity PA, and showed stronger associations with fasting blood lipids and glucose, while PA was more strongly related to SBP and DBP. The validated NZPAQs are acceptable for measuring population level PA prevalence in NZ adults, although accuracy is lower for Māori and Pacific people. However, the availability of a culturallyspecific list of PA intensities could potentially increase the accuracy of self-reported PA by Māori and Pacific people. Results from this study highlight the importance of vigorous-intensity PA for CV health, and identifies NZ Pacific people as high risk in terms of PA, obesity, and CRF.

The risk of developing type 2 diabetes is four fold higher in New Zealand(NZ) Polynesians compared to Caucasians. Hence diabetes is more prevalent in Maori (16.5% of the general population) and Pacific Island people (10.1%) compared to NZ Caucasians (9.3%). It is generally accepted that type 2 diabetes has major genetic determinants and heterozygous mutations in a number of genes have previously been identified in some subsets of type 2 diabetes and certain ethnic groups. The high prevalence of diabetes in NZ Polynesians, when compared with NZ Caucasians, after controlling for age, income and body mass index (BMI), suggest that genes may be important in this population. Therefore, the prevalence of allelic variations in the genes encoding amylin and insulin promoter factor-1 (IPF-1), and exon 2 of the hepatocyte nuclear factor-1α (HNF-1α) gene in NZ Polynesians with type 2 diabetes was determined. These genes are known to produce type 2 diabetes in other populations. The genes investigated were screened for mutations by PCR amplification and direct sequencing of promoter regions, exons and adjacent intronic sequences from genomic DNA. DNA was obtained from 146 NZ Polynesians (131 Maori and 15 Pacific Island) with type 2 diabetes and 387 NZ Polynesian non-diabetic control subjects (258 Maori and 129 Pacific Island). Sequences were compared to previously published sequences in the National Centre for Biotechnology Information database. Allelic variations in IPF-1 and exon 2 of the HNF-1α gene were not associated with type 2 diabetes in NZ Polynesians. However, in the amylin gene, two new and one previously described allele was identified in the Maori population including: two alleles in the promoter region (-132G>A and -215T>G), and a missense mutation in exon 3 (QlOR). The -215T>G allele was observed in 5.4% and l% of type 2 diabetic and non-diabetic Maori respectively, and predisposed the carrier to diabetes with a relative risk of 7.23. The -215T>G allele was inherited with a previously described amylin promoter polymorphism(-230A>C) in 3% of Maori with type 2 diabetes, which suggests linkage equilibrium exists between these two alleles. Both Q10R and -132G>A were observed in 0.76% of type 2 diabetic patients and were absent in non-diabetic subjects. Together these allelic variations may account for approximately 7% of type 2 diabetes in Maori. These results suggest that the amylin gene maybe an important candidate marker gene for type 2 diabetes in Maori.

Cardiovascular disease is the leading cause of mortality in New Zealand. The most current evidence indicates that the burden of cardiovascular disease is greatest among Maori and Pacific peoples and Pacific peoples have the highest mortality rate for cerebrovascular disease [1]. There is substantial scientific evidence that cardiovascular disease has its origin early in life and that a person's risk of cardiovascular disease is determined by the synergistic effect of all the cardiovascular risk factors over time. The Auckland High School Heart Survey (AHHS) is an epidemiological survey designed to determine the prevalence of risk factors for cardiovascular disease in an adolescent high school population in New Zealand. It takes a 'lifecourse' and primary prevention approach to reducing the incidence of cardiovascular disease. The aims of the study were to determine cardiovascular risk factor levels in, and compare the cardiovascular and diabetes risk factor levels between, Pacific and European students and the main Pacific communities (Samoan, Cook Islands, Tongan, and Niuean). The AHHS was a school-based cross-sectional survey of 2,549 adolescent students, across 10 Auckland High Schools. A cluster sampling technique was used to obtain the target of 1000 Pacific participants, to enable Pacific ethnic-specific analysis. The study specifically aimed to determine ethnic-specific differences in lifestyle, intermediate and outcome variables that have been established as cardiovascular risks. Lifestyle variables included: smoking, alcohol consumption, leisure-time physical activity (LTPA), television exposure and sun exposure. The intermediate variables analysed included: body mass index (BMI), waist to hip ratio (WHR), percentage body fat (PBF) and physical work capacity 170 (PWC170). The outcome variables included: total cholesterol (TC), high density lipoprotein cholesterol (HDLC), ratio of total cholesterol to high density lipoprotein cholesterol (TC:HDLC), low density lipoprotein cholesterol (LDLC), triglycerides (TG), fasting blood glucose (FG), urinary micro albumin (UA), systolic and diastolic blood pressure (SBP & DPB). Demographic variables analysed included: sex, age, ethnic group, school, socio-economic status and growth development and maturation. The AHHS study results showed that demographic variables were strongly associated with both intermediate and outcome variables. The findings showed that there were significant ethnic variations between the four main ethnic groups (Pacific, Maori, Asian and European) in risk factors for cardiovascular disease. Pacific participants had the highest BMI and PBF. Pacific participants had the lowest levels of PWC170. With regard to outcome variables, Pacific adolescents had lower levels of TC, HDLC and LDLC compared to Europeans. However, Pacific participants had higher levels of TC:HDLC, FG, TG and DPB. To a lesser degree, lifestyle variables were also associated with other variables. However, the weaker association was likely due to measurement error. The findings of the AHHS study show that ethnic differences present in the adult population are already established among adolescents [2]. Some significant differences were also found between the Pacific ethnic groups (Samoan, Cook Islands, Tongan and Niuean). Among Pacific participants, Cook Islands participants also had the highest level of adjusted mean PWC170. With regard to outcome variables (lipids, fasting glucose and blood pressure), Tongan participants had lower TC, LDLC and TC:HDLC compared to Samoans. However, Tongan participants had significantly higher levels of TG compared to Samoans. For Pacific participants, Cook Islands participants significantly differed from Samoan in smoking, alcohol consumption and PWC170. Cook Islands participants were more likely to have tried smoking for the first time and at an earlier age. They were also more likely to smoke daily and to smoke higher amounts than the other Pacific ethnic groups. Cook Islands participants were more likely to have tried alcohol and at an earlier age. They were also more likely to be drinking alcohol weekly or more often when compared to Samoans. The AHHS study is one of the first pieces of epidemiological research undertaken in New Zealand that provides evidence that there are significant differences between Pacific ethnic groups for this age group. The AHHS study was also able to identify the determinant that explains ethnic differences in outcome variables. BMI was the most significant variable in determining the ethnic differences in outcome variables (lipids, blood pressure and fasting glucose). The AHHS study results showed that Pacific participants had the highest BMI levels of all the ethnic groups, followed by Maori. Television watching was the one lifestyle risk factor that was positively associated with BMI. The most effective variable in terms of decreasing mean difference in BMI was PWC170. PWC170 was significantly lower in Pacific, Asian, and Maori participants compared with European participants. Pacific participants had the lowest levels of PWC170 compared to all other ethnic groups. The AHHS findings support early interventions and programmes targeted to adolescents to reduce the incidence of cardiovascular disease. The findings which show that there are significant differences between Pacific ethnic groups for this age group, may warrant some specific public health initiatives being targeted directly to Pacific ethnic-specific groups. In addition, interventions and programmes that target reducing BMI and improving physical fitness should have an impact on a number of important cardiovascular risk factor outcome variables in adolescents, including: blood pressure, lipids and fasting glucose.