Effects of a free school breakfast programme on children's attendance, academic achievement and short-term hunger: results from a stepped-wedge, cluster randomised controlled trial.

BACKGROUND: Free school breakfast programmes (SBPs) exist in a number of high-income countries, but their effects on educational outcomes have rarely been evaluated in randomised controlled trials. METHODS: A 1-year stepped-wedge, cluster randomised controlled trial was undertaken in 14 New Zealand schools in low socioeconomic resource areas. Participants were 424 children, mean age 9±2 years, 53% female. The intervention was a free daily SBP. The primary outcome was children's school attendance. Secondary outcomes were academic achievement, self-reported grades, sense of belonging at school, behaviour, short-term hunger, breakfast habits and food security. RESULTS: There was no statistically significant effect of the breakfast programme on children's school attendance. The odds of children achieving an attendance rate <95% was 0.76 (95% CI 0.56 to 1.02) during the intervention phase and 0.93 (95% CI 0.67 to 1.31) during the control phase, giving an OR of 0.81 (95% CI 0.59 to 1.11), p=0.19. There was a significant decrease in children's self-reported short-term hunger during the intervention phase compared with the control phase, demonstrated by an increase of 8.6 units on the Freddy satiety scale (95% CI 3.4 to 13.7, p=0.001). There were no effects of the intervention on any other outcome. CONCLUSIONS: A free SBP did not have a significant effect on children's school attendance or academic achievement but had significant positive effects on children's short-term satiety ratings. More frequent programme attendance may be required to influence school attendance and academic achievement. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry (ANZCTR)-ACTRN12609000854235.

Effects of a free school breakfast programme on school attendance, achievement, psychosocial function, and nutrition: a stepped wedge cluster randomised trial.

BACKGROUND: Approximately 55,000 children in New Zealand do not eat breakfast on any given day. Regular breakfast skipping has been associated with poor diets, higher body mass index, and adverse effects on children's behaviour and academic performance. Research suggests that regular breakfast consumption can improve academic performance, nutrition and behaviour. This paper describes the protocol for a stepped wedge cluster randomised trial of a free school breakfast programme. The aim of the trial is to determine the effects of the breakfast intervention on school attendance, achievement, psychosocial function, dietary habits and food security. METHODS/DESIGN: Sixteen primary schools in the North Island of New Zealand will be randomised in a sequential stepped wedge design to a free before-school breakfast programme consisting of non-sugar coated breakfast cereal, milk products, and/or toast and spreads. Four hundred children aged 5-13 years (approximately 25 per school) will be recruited. Data collection will be undertaken once each school term over the 2010 school year (February to December). The primary trial outcome is school attendance, defined as the proportion of students achieving an attendance rate of 95% or higher. Secondary outcomes are academic achievement (literacy, numeracy, self-reported grades), sense of belonging at school, psychosocial function, dietary habits, and food security. A concurrent process evaluation seeks information on parents', schools' and providers' perspectives of the breakfast programme. DISCUSSION: This randomised controlled trial will provide robust evidence of the effects of a school breakfast programme on students' attendance, achievement and nutrition. Furthermore the study provides an excellent example of the feasibility and value of the stepped wedge trial design in evaluating pragmatic public health intervention programmes. TRIAL REGISTRATION NUMBER: Australian New Zealand Clinical Trials Registry (ANZCTR) - ACTRN12609000854235.

The environment and physical activity: The influence of psychosocial, perceived and built environmental factors.

UNLABELLED: : This study sought to integrate perceived and built environmental and individual factors into the Theory of Planned Behavior (TPB) model to better understand adolescents' physical activity. METHODS: Participants (n = 110) aged 12 to 17 years (M = 14.6 +/- 1.55) were recruited from two large metropolitan high schools in Auckland, New Zealand, were included in the analysis. Participants completed measures of the revised TPB and the perceived environment. Individual factors such as ethnicity and level of deprivation were also collected. Geographical Information Systems (GIS) software was used to measure the physical environment (walkability, access to physical activity facilities). Physical activity was assessed using the ActiGraph accelerometer and the Physical Activity Questionnaire for Adolescents (PAQ-A). Data from the various sources were combined to develop an integrated model integrated for statistical analysis using structural equation modeling. RESULTS: The TPB model variables (intention and perceived behavioral control) explained 43% of the variance of PAQ-A. Unique and individual contributions were made by intention and PBC and home ownership of home equipment. The model explained 13% of time spent in moderate and vigorous physical activity (Actigraph). Unique and individual contribution was made by intention. CONCLUSION: Social cognitive variables were better predictors of both subjective and objective physical activity compared to perceived environmental and built environment factors. Implications of these findings are discussed.

Ethnic disparities in nutrition-related mortality in New Zealand: 1997-2011.

AIMS: To estimate the mortality due to non-optimal levels of systolic blood pressure, total blood cholesterol, body mass index (BMI), and vegetable and fruit intake amongst Maori and non-Maori in New Zealand in 1997. In addition, to estimate the ethnic-specific burden of disease that could potentially be avoided in 2011 if exposure to these risk factors were reduced. METHODS: The study uses comparative risk assessment methodology, a systematic approach to estimating both attributable and avoidable burden of disease developed by the World Health Organization. RESULTS: About 47% of deaths among Maori and 39% of deaths among non-Maori were estimated to be due to the selected risk factors. Age-standardised mortality rates for attributable ischaemic heart disease burden were consistently higher in Maori for individual risk factors. Age standardised mortality attributable to BMI was relatively higher for Maori, especially diabetes mortality. Estimates of avoidable mortality suggest that the health gains for Maori would be relatively greater than for non-Maori across all risk factors, but particularly with improvements in BMI. CONCLUSIONS: Non-optimal levels of systolic blood pressure, cholesterol, BMI, and to a lesser extent vegetable and fruit intake are major modifiable causes of death in New Zealand. Small changes in risk factor levels could have a major impact on population health within a decade, with relatively greater health gains for Maori.

Non-fatal disease burden associated with excess body mass index and waist circumference in New Zealand adults.

OBJECTIVE: To describe the relationship between two measures of body fat and selected non-fatal health conditions in the New Zealand adult population in 2003. METHOD: Data were obtained from the 2002/03 New Zealand Health Survey. A total of 10,026 adults aged 25 years and over were classified according to measured body mass index (BMI) and waist circumference (WC). BMI classes were 18.5-24.9, 25.0-29.9, 30.0-34.9, > or = 35.0 kg/m2. WC classes were < 94, 94-102, > 102 centimetres (cm) for males and < 80, 80-88, > 88 cm for females. Prevalence rate ratio estimates for selected self-reported health conditions were calculated for males and females separately, adjusting for age, ethnicity, deprivation and smoking using logistic regression. RESULTS: Increasing BMI or WC class was associated with increasing prevalence of cardiovascular disease, diabetes, high blood pressure, high blood cholesterol, osteoarthritis, asthma and sleep disorders in both males and females. The association with depression was not statistically significant in either gender. Associations were strongest for diabetes and blood pressure, with adults in the highest BMI or WC class at least 3.5 times more likely to have diabetes and 2-3 times more likely to have high blood pressure compared with those in the lowest classes. CONCLUSIONS: Increasing body fatness, defined by either BMI or WC, was associated with increased prevalence of many important health conditions. If the obesity epidemic is not halted or reversed, the impact on both the New Zealand population and health system will be considerable.

Cardiovascular mortality attributable to high blood cholesterol in New Zealand.

OBJECTIVE: To estimate mortality attributable to higher-than-optimal blood cholesterol in New Zealand in 1997, and the mortality burden that could be potentially avoided in 2011 if modest reductions in mean population blood cholesterol concentrations were achieved. DESIGN: Comparative risk assessment methodology was used to estimate the attributable and avoidable mortality due to higher-than-optimal total blood cholesterol (> 3.8 mmol/L). Disease outcomes assessed were deaths from ischaemic heart disease (IHD) and ischaemic stroke. RESULTS: Overall, higher-than-optimal blood cholesterol contributed to 4,721 deaths in New Zealand in 1997 (17% of all deaths). This included 4,096 IHD deaths (64%) and 625 ischaemic stroke deaths (38%). Modest reductions in mean population blood cholesterol concentrations (e.g. 0.1 mmol/L) could potentially prevent 300 deaths (261 IHD and 39 ischaemic stroke) each year from 2011. CONCLUSIONS: Higher-than-optimal blood cholesterol concentrations are a leading cause of mortality in New Zealand. Modest reductions in blood cholesterol levels could have a major impact on population health within a decade.

Vegetable and fruit intake and mortality from chronic disease in New Zealand.

OBJECTIVE: To estimate mortality attributable to inadequate vegetable and fruit intake in New Zealand in 1997, and the burden of disease that could be avoided in 2011 if modest increases in vegetable and fruit intake were to occur. METHODS: Comparative risk assessment methodology was used to estimate both attributable and avoidable mortality due to inadequate vegetable and fruit consumption (< 600 g/day). Vegetables and fruit were defined as all fresh, frozen, canned, dried or juiced vegetables and fruit, except potatoes, nuts, seeds and pulses. Disease outcomes assessed were mortality from ischaemic heart disease, ischaemic stroke, and lung, oesophageal, stomach and colorectal cancers. RESULTS: In 1997, mean vegetable and fruit intake was 420 g/day in males and 404 g/day in females. Inadequate vegetable and fruit intake is estimated to have contributed to 1,559 deaths (6% of all deaths) in that year, including 1,171 from ischaemic heart disease, 179 from ischaemic stroke and 209 from cancer. Modest increases in vegetable and fruit intake (40 g/day above the historic trend) could prevent 334 deaths each year from 2011, mostly from ischaemic heart disease. CONCLUSIONS: Inadequate vegetable and fruit intake is an important cause of mortality in New Zealand. Small increases in vegetable and fruit intake could have a major impact on population health within a decade.

Debunking the 'only 50%' myth: prevalence of established risk factors in New Zealanders with self-reported ischaemic heart disease.

OBJECTIVE: To estimate the prevalence of established risk factors for ischaemic heart disease (IHD) in New Zealand adults and compare the prevalence in adults with and without this disease. DESIGN: Data were obtained from the 2002/03 New Zealand Health Survey. Risk factor prevalence was determined by: self-reported doctor diagnosis of high blood pressure, high cholesterol and diabetes; self-report of smoking and physical inactivity; and measurement of obesity. Presence of IHD was based on self-report of heart disease (doctor diagnosed at age 25 years or over) together with current medical or past surgical treatment for this disease. Multiple logistic regression was used to determine prevalence rate ratios (PRRs) for males and females separately, adjusting for age, ethnicity and deprivation. RESULTS: The overall prevalence of IHD was 8%. Overall risk factor prevalences were in the range of 20-25% for each of high blood pressure, high cholesterol, smoking, obesity and physical inactivity, and approximately 5% for diabetes. Overall, 94-97% of adults with IHD had at least one risk factor (depending on how smoking was defined). The PRRs of IHD were highest for cholesterol (about 4.5), followed by blood pressure (about 2.3), with all other risk factors around 1.5. PAF estimates indicate that 80-85% of IHD was attributable to the presence of at least one risk factor for all age, gender and ethnic groups. CONCLUSIONS: Established risk factors account for 80-85% of the non-fatal burden of IHD in New Zealand. Limited research resources would be better used to evaluate which interventions are effective and efficient at reducing exposure of all population groups to known risk factors, rather than on identification of additional risk factors.

Nutrition and the burden of disease in New Zealand: 1997-2011.

OBJECTIVE: To estimate the burden of disease due to selected nutrition-related risk factors (high total blood cholesterol, high systolic blood pressure, high body mass index (BMI) and inadequate vegetable and fruit intake) in 1997, as well as the burden that could potentially be avoided in 2011 if small, favourable changes in the current risk factor distribution were to occur. DESIGN: Data on risk factor levels, disease burden and risk associations were combined using comparative risk assessment methodology, a systematic approach to estimating both attributable and avoidable burden of disease. Disease outcomes assessed varied according to risk factor and included ischaemic heart disease, stroke, type 2 diabetes mellitus and selected cancers. SETTING: New Zealand. RESULTS: Approximately 4500 deaths (17% of all deaths) in 1997 were attributable to high cholesterol, 3500 (13%) to high blood pressure, 3000 (11%) to high BMI and 1500 (6%) to inadequate vegetable and fruit intake. Taking prevalence overlap into account, these risk factors were estimated jointly to contribute to approximately 11 000 (40%) deaths annually in New Zealand. Approximately 300 deaths due to each risk factor could potentially be avoided in 2011 if modest changes were made to each risk factor distribution. CONCLUSIONS: High cholesterol, blood pressure and BMI, as well as inadequate vegetable and fruit intake, are major modifiable causes of death in New Zealand. Small changes in the population distribution of these risk factors could have a major impact on population health within a decade.

Mortality attributable to higher-than-optimal body mass index in New Zealand.

OBJECTIVES: To estimate the burden of mortality in New Zealand due to higher-than-optimal body mass index (BMI) in 1997, as well as mortality that could be avoided in 2011 with feasible changes in mean population BMI. SETTING: New Zealand. DESIGN: Comparative risk assessment methodology was used to estimate the attributable and avoidable mortality due to high BMI. Outcomes assessed were ischaemic heart disease (IHD), ischaemic stroke, type 2 diabetes mellitus, colorectal cancer and postmenopausal breast cancer. RESULTS: In 1997, 3154 deaths (11% of all deaths) in New Zealand were due to higher-than-optimal BMI (>21 kg m(-2)). This amounted to 83% of diabetes deaths, 24% of IHD deaths, 15% of ischaemic stroke deaths and 4% of all cancer deaths. If the projected increase in mean population BMI by 2011 was limited to 1.0 kg m(-2) rather than 1.3 kg m(-2), approximately 385 deaths could be prevented annually, mainly from diabetes. CONCLUSIONS: These results quantify the importance of higher-than-optimal BMI as a major modifiable cause of premature death in New Zealand. Intervention policies that would have only modest effects on slowing the rate of increase in mean population BMI by 2011 could still prevent hundreds of deaths annually.

Causes of death classified by risk and condition, New Zealand 1997.

OBJECTIVE: To classify causes of death in New Zealand by risk factor (in addition to condition) as a planning tool for health promotion. METHOD: Deaths occurring in New Zealand in 1997 were classified by 20 prevalent risk factors using a combination of categorical attribution (rule-based) and counterfactual modelling (population-attributable risk-based) approaches. RESULTS: Approximately 30% of deaths were attributed to the joint effect of dietary factors. Tobacco consumption was responsible for 18% of deaths and insufficient physical activity for almost 10%. Less important behavioural risk factors included alcohol consumption (3%), illicit drug use (0.5%) and unsafe sex (0.5%). Among biological risk factors, higher than optimal total blood cholesterol, systolic blood pressure and body mass index accounted for 17%, 15% and 12% of deaths respectively. Deprivation contributed to 17% of deaths, and adverse in-hospital events to 6%. Among environmental exposures, microbes accounted for 6.5% of deaths, air pollution 3.5% and occupational diseases and injuries 0.5%. Among injury hazards, risk factors related to road traffic were responsible for 2% of deaths, while violence accounted for 2.5% of deaths, mostly through suicide. Cross-classifying deaths by both condition and risk factor, 90% of ischaemic heart disease and 80% of stroke, but only 30% of cancer deaths, could be attributed to specific risk factors. CONCLUSIONS: This is the first comprehensive ranking of causes of death at the level of risk factors available for New Zealand and should prove useful as a planning tool, especially for disease prevention and health promotion.

Ethnic differences in diet and associations with clinical markers of prostate disease in New Zealand men.

OBJECTIVE: To examine ethnic differences in diet and dietary associations with clinical markers of prostate disease in New Zealand men. MATERIALS AND METHODS: A total of 1031 males (616 New Zealand European, 230 Maori and 185 Pacific Islands) aged 40-69 years, with no history of prostate cancer, completed a questionnaire covering diet. A serum prostate specific antigen (PSA) blood analysis was also undertaken. Regression models were developed to examine the ethnic-specific levels of selected dietary components, and their relationship with PSA and urinary symptom scores. RESULTS: The results confirmed previously found ethnic differences in the New Zealand diet. Combined tomato intake was positively-correlated with free PSA and % free PSA (p=0.021, r=0.197 and p=0.011, r=0.096 respectively). Beer intake was negatively-correlated with total PSA (p=0.028, r=-0.071) and free PSA (p=0.004, r=-0.094). CONCLUSION: Ethnic differences found in the consumption of foods (associated with prostate cancer) highlight the possible importance of dietary interactions for ethnic prostate cancer risk. Associations between specific foods and PSA warrant further investigation.

Economic cost of community-acquired pneumonia in New Zealand adults.

AIMS: The aim of this study was to evaluate the economic cost of community-acquired pneumonia (CAP) in New Zealand adults. Although this is an important illness, there is little published information on the national costs of treatment. Without such information, new treatment options cannot be evaluated in economic terms. METHODS: Costs were estimated from a societal perspective for the adult population (aged 15 years and over) using New Zealand age-specific hospital admission rates (average of 2000-2002), population data (2003), and unit costs (2003) in combination with international data on the proportion of pneumonia cases hospitalised. Univariate and multivariate sensitivity analyses were used to determine the major cost drivers and evaluate uncertainty in the estimates. RESULTS: It was estimated that in 2003 there were 26,826 episodes of pneumonia in adults; a rate of 859 per 100,000 people. The annual cost was estimated to be 63 million dollars, (direct medical costs of 29 million dollars; direct non-medical costs of 1 million dollars; lost productivity of 33 million dollars). CONCLUSIONS: The major generators of costs for community-acquired pneumonia are the number of hospitalisations (particularly for the group aged 65 years and over) and loss of productivity. Intensified prevention and effective community treatment programmes focussing on the 65 years and older age groups should be investigated (as they have the greatest potential to reduce healthcare costs).