Aim: A high ponderal index at birth has been associated with later obesity and it has been suggested that intervention to prevent obesity and its sequela should consider the antenatal period. In this context, we investigated the association between maternal nutrition and birth anthropometry. Design: We analyzed data on 1040 mother-infant pairs collected during the Tasmanian Infant Health Survey (TIHS), Tasmania, 1988Tasmania, -1989. Maternal dietary intake during pregnancy was measured by food frequency questionnaire (FFQ) applied soon after birth. Outcomes of interest were birth weight, birth length, head circumference, ponderal index, head circumference -toponderal index ratio, placenta-to-birth weight ratio and head circumference-to-birth length index. Results: In multiple regression model, an increase of 10 g of absolute protein intake/day was associated with a reduction in birth weight of 17.8 g (95% CI: À32.7, À3.0; P ¼ 0.02). Protein intake was also associated negatively with ponderal index (b ¼ À0.01; 95% CI: À0.02, À0.00; P ¼ 0.01). A 1 % increase in carbohydrate intake resulted in a 1% decline in placental weight relative to birth weight. Higher protein intake in the third trimester was associated with a reduced ponderal index among large birth weight infants but not low birth weight infants. Conclusions: This raises the possibility that any effect of high protein in altering infant anthropometry at birth may involve changes in body composition and future work to examine how a high-protein diet influences body composition at birth is warranted.

Objective: To quantify Indigenous mortality in the Northern Territory by remoteness of residence. Design, setting and participants: Australian Bureau of Statistics mortality data were used to compare rates of death from chronic disease in the NT Indigenous population with rates in the general Australian population over the period 1998–2003. Rates were evaluated by categories of remoteness based on the Accessibility/Remoteness Index of Australia: outer regional areas (ORAs), remote areas (RAs) and very remote areas (VRAs). Main outcome measures: Mortality from cardiovascular disease, diabetes and renal disease; standardised mortality ratios (SMRs); percentage change in annual death rates; changes in mortality between 1998–2000 and 2001–2003. Results: In 1998–2000, SMRs for all‐cause mortality were 285% in ORAs, 875% in RAs and 214% in VRAs. In 2001–2003, corresponding SMRs were 325%, 731% and 208%. For the period 1998–2003, percentage changes in annual all‐cause mortality were 4.4% (95% CI, –2.2%, 11.5%) in ORAs, –5.3% (95% CI, –9.6%, –0.8%) in RAs, and 1.1% (95% CI, –7.2%, 11.3%) in VRAs. In 2001–2003, compared with 1998–2000, changes in the number of Indigenous deaths were +35 in ORAs, –37 in RAs and +32 in VRAs. Similar patterns were observed for cardiovascular mortality. Conclusions: Compared with mortality in the general Australian population, Indigenous mortality was up to nine times higher in RAs, three times higher in ORAs and two times higher in VRAs. The fact that rates were lowest in VRAs runs contrary to claims that increasing remoteness is associated with poorer health status. Despite the high death rate in RAs, there was a downward trend in mortality in RAs over the study period. This was partly attributable to a fall in the absolute number of deaths.

We have demonstrated a differential effect of fish intake for sensitization to different aeroallergens. This may be due to the different timing of allergen exposure during early life. Further investigation of the causes of atopic disease should take into account allergen-specific subgroups.

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BackgroundDespite the well-recognised Indigenous-non-Indigenous health disparity, some reports suggest improvements in Indigenous mortality. Our aim was to quantify Indigenous mortality in Outer Regional (OR), Remote (R), and Very Remote (VR) areas in New South Wales, Queensland, South Australia, Western Australia, and the Northern Territory and changes in mortality from 1998 to 2005.MethodsWe calculated rates, standardized mortality ratios (SMRs) and percentage change in annual rates of Indigenous cardiovascular, diabetes and renal mortality mentioned anywhere on the death certificate by using ICD-10 codes and the 2001 total Australian population as the reference population.ResultsIn 1998-2001, Indigenous SMRs for all-cause mortality were 241%, 421% and 220% in OR, R and VR, respectively. In 2001-03, corresponding SMRs were 202%, 331% and 176%. Percentage changes (95% confidence interval) in annual all-cause mortality were -3.0% (-5.3%, -0.7%) in OR, -4.2% (-7.4%, -0.9%) in R and -0.5 (-9.1%, -0.7%) in VR. In 2002-2005, compared with 1998-2001, changes in the number of Indigenous deaths were -147, -195, and -197 in OR, R and VR, respectively. Similar patterns and trends were observed for cardiovascular mortality.ConclusionsMortality was elevated about 2-fold in OR, 4-fold in R and 2-fold in VR areas. The downward trend in mortality regardless of remoteness of residence was partly attributable to a decrease in the absolute number of deaths. These patterns were observed for each of the states/territories individually.

The Indigenous population in Queensland has elevated rates of renal deaths compared with the non-Indigenous population. This disparity increases markedly with increasing remoteness of residence. Reliance on underlying causes of death alone greatly underestimates the association of renal disease with deaths in this population.

Studies on the role of non-milk fluids in the development of child atopic disease are scarce. We had a unique opportunity to investigate prospective association between the introduction of fruit syrup, orange juice, sterilized water, vitamins and honey at 1 month and the development of child atopic disease. The exposure of interest was measured by parental report of non-milk fluids introduction to infants aged 1 month at the Tasmanian Infant Health Survey, 1988-89, Tasmania. Data on the outcomes of interest (atopic sensitization, asthma, eczema and hay fever) were collected during the 1997 Childhood Allergy and Respiratory Health Study when children were 8 yr old. Relative risks were derived from generalized linear model with a log link function and binomial error structure. None of the non-milk fluids appeared to be a significant predictor of atopic sensitization. Only sterilized water was a significant risk factor for asthma (adjusted relative risk = 1.59; 95% confidence intervals: 1.14-2.22), which may be partly because of associated overall better hygienic conditions and decreased exposure to early infections in the household. In summary, we were unable to find evidence for an association between introduction of non-milk fluids in infancy and childhood atopic disease.

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