Dietary recalls have been used previously to identify food sources of iodine in Australian schoolchildren. Dietary assessment can provide information on the relative contributions of individual food groups which can be related to a robust objective measure of daily intake (24-h urinary iodine excretion (UIE)). In Australia, the government has mandated the use of iodised salt in breadmaking to address iodine deficiency. The aim of this study was to determine the dietary intake and food sources of iodine to assess their contribution to iodine excretion (UIE) in a sample of Australian schoolchildren. In 2011–2013, UIE was assessed using a single 24-h urine sample and dietary intake was assessed using one 24-h dietary recall in a convenience sample of primary schoolchildren from schools in Victoria, Australia. Of the 454 children with a valid recall and urine sample, 55 % were male (average age 10·1 (1·3 (sd) years). Mean UIE and dietary iodine intake were 108 (sd 54) and 172 (sd 74) μg/d, respectively. Dietary assessment indicated that bread and milk were the main food sources of iodine, contributing 27 and 25 %, respectively, to dietary iodine. Milk but not bread intake was positively associated with UIE. Multiple regression (adjusted for school cluster, age and sex) indicated that for every 100 g increase in milk consumption, there was a 3 μg/d increase in UIE (β = 4·0 (se 0·9), P < 0·001). In conclusion, both bread and milk were important contributors to dietary iodine intake; however, consumption of bread was not associated with daily iodine excretion in this group of Australian schoolchildren.

Higher intakes of Na may contribute to weight gain. The primary aim of this systematic review and meta-analysis was to examine the relationship between dietary Na intake and measures of adiposity in children and adults. Given the previous link between Na intake and the consumption of sugar-sweetened beverages (SSB), which are a known risk factor for obesity, a secondary aim examining the relationship between Na intake and SSB consumption was assessed. A systematic literature search identified cross-sectional and longitudinal studies and randomised controlled trials (RCT) which reduced dietary Na (≥3 months). Meta-analysis was performed for outcomes with ≥3 studies. Cross-sectionally higher Na intakes were associated with overweight/obesity in adults (five studies; n 11 067; OR 1·74; 95 % CI 1·43, 2·13) and in children (three studies; n 3625, OR 3·29; 95 % CI 2·25, 4·80), and abdominal obesity (five studies; n 19 744; OR 2·04; 95 % CI 1·72, 2·42) in adults. Overall, associations remained in sensitivity analyses which adjusted for energy. Findings from longitudinal studies were inconsistent. RCT in adults indicated a trend for lower body weight on reduced-Na compared with control diets (fifteen studies; n 5274; −0·29 kg; 95 % CI −0·59, 0·01; P = 0·06); however, it is unclear if energy intakes were also altered on reduced-Na diets. Among children higher Na intakes were associated with higher intake of SSB (four studies, n 10 329, b = 22, 16 and 26 g/d); no studies were retrieved for adults. Overall, there was a lack of high-quality studies retrieved. While cross-sectional evidence indicates Na intake was positively associated with adiposity, these findings have not been clearly confirmed by longitudinal studies or RCT.

In Victoria, Australia, a statewide salt reduction partnership was launched in 2015. The aim was to measure Na intake, food sources of Na (level of processing, purchase origin) and discretionary salt use in a cross-section of Victorian adults prior to a salt reduction initiative. In 2016/2017, participants completed a 24-h urine collection (n 338) and a subsample completed a 24-h dietary recall (n 142). Participants were aged 41·2 (sd 13·9) years, and 56 % were females. Mean 24-h urinary excretion was 138 (95 % CI 127, 149) mmol/d for Na. Salt equivalent was 8·1 (95 % CI 7·4, 8·7) g/d, equating to about 8·9 (95 % CI 8·1, 9·6) g/d after 10 % adjustment for non-urinary losses. Mean 24-h intake estimated by diet recall was 118 (95 % CI 103, 133) mmol/d for Na (salt 6·9 (95 % CI 6·0, 7·8 g/d)). Leading dietary sources of Na were cereal-based mixed dishes (12 %), English muffins, flat/savoury/sweet breads (9 %), regular breads/rolls (9 %), gravies and savoury sauces (7 %) and processed meats (7 %). Over one-third (38 %) of Na consumed was derived from discretionary foods. Half of all Na consumed came from ultra-processed foods. Dietary Na derived from foods was obtained from retail stores (51 %), restaurants and fast-food/takeaway outlets (28 %) and fresh food markets (9 %). One-third (32 %) of participants reported adding salt at the table and 61 % added salt whilst cooking. This study revealed that salt intake was above recommended levels with diverse sources of intake. Results from this study suggest a multi-faceted salt reduction strategy focusing on the retail sector, and food reformulation would most likely benefit Victorians and has been used to inform the ongoing statewide salt reduction initiative.

Fatty acid taste (FAT) perception is involved in the regulation of dietary fat intake, where impaired FAT is associated with increased fatty food intake. There are a number of FAT receptors identified on human taste cells that are potentially responsible for FAT perception. Manipulating dietary fat intake, and in turn FAT perception, would elucidate the receptors that are associated with long-term regulation of FAT perception. The present study aimed to assess associations between diet-mediated changes to FAT receptors and FAT perception in humans. A co-twin randomised controlled trial was conducted, where each matching twin within a pair were randomly allocated to either an 8-week low-fat (LF; <20 % energy fat) or an 8-week high-fat (HF; >35 % energy fat) diet. At baseline and week 8, fungiform papillae were biopsied in the fasted state and FAT receptor gene expressions (cluster of differentiation 36 (CD36), free fatty acid receptor 2 (FFAR2), FFAR4, G protein-coupled receptor 84 (GPR84) and a delayed rectifying K+ channel (K+ voltage-gated channel subfamily A member 2; KCNA2)) were measured using RT-PCR; and FAT threshold (FATT) was assessed using three-alternate forced choice methodology. Linear mixed models were fitted, adjusting for correlation between co-twins. Intake was compliant with the study design, with the LF and HF groups consuming 14·8 and 39·9 % energy from fat, respectively. Expression of FFAR4 increased by 38 % in the LF group (P = 0·023; time–diet interaction P = 0·063). ΔFFAR4 (Δ, week 8–baseline) was associated with Δfat intake (g) ( = −159·4; P < 0·001) and ΔFATT ( = −8·8; P = 0·016). In summary, FFAR4 is involved in long-term diet-mediated changes to FAT perception. Manipulating dietary fat intake, and therefore FFAR4 expression, might aid in reducing taste-mediated passive overconsumption of fatty foods.

Vitamin D deficiency is recognised as a public health problem globally, and a high prevalence of deficiency has previously been reported in Australia. This study details the prevalence of vitamin D deficiency in a nationally representative sample of Australian adults aged ≥25 years, using an internationally standardised method to measure serum 25-hydroxyvitamin D (25(OH)D) concentrations and identifies demographic and lifestyle factors associated with vitamin D deficiency. We used data from the 2011–2013 Australian Health Survey (n 5034 with complete information on potential predictors and serum 25(OH)D concentrations). Serum 25(OH)D concentrations were measured by a liquid chromatography-tandem MS that is certified to the reference measurement procedures developed by the National Institute of Standards and Technology, Ghent University and the US Centers for Disease Control and Prevention. Vitamin D deficiency and insufficiency were defined as serum 25(OH)D concentrations <50 nmol/l and 50 to <75 nmol/l, respectively. Overall, 20 % of participants (19 % men; 21 % women) were classified as vitamin D deficient, with a further 43 % classified as insufficient (45 % men; 42 % women). Independent predictors of vitamin D deficiency included being born in a country other than Australia or the main English-speaking countries, residing in southern (higher latitude) states of Australia, being assessed during winter or spring, being obese, smoking (women only), having low physical activity levels and not taking vitamin D or Ca supplements. Given our increasingly indoor lifestyles, there is a need to develop and promote strategies to maintain adequate vitamin D status through safe sun exposure and dietary approaches.

High Na intake and chronically elevated cortisol levels are independently associated with the development of chronic diseases. In adults, high Na intake is associated with high levels of urinary cortisol. We aimed to determine the association between urinary Na and K and urinary cortisol in a cross-sectional sample of Australian schoolchildren and their mothers. Participants were a sample of Australian children (n 120) and their mothers (n 100) recruited through primary schools. We assessed Na, K, free cortisol and cortisol metabolites in one 24 h urine collection. Associations between 24 h urinary electrolytes and 24 h urinary cortisol were assessed using multilevel mixed-effects linear regression models. In children, urinary Na was positively associated with urinary free cortisol (β=0·31, 95 % CI 0·19, 0·44) and urinary cortisol metabolites (β=0·006, 95 % CI 0·002, 0·010). Positive associations were also observed between urinary K and urinary free cortisol (β=0·65, 95 % CI 0·23, 1·07) and urinary cortisol metabolites (β=0·02, 95 % CI 0·03, 0·031). In mothers, urinary Na was positively associated with urinary free cortisol (β=0·23, 95 % CI 0·01, 0·50) and urinary cortisol metabolites (β=0·008, 95 % CI 0·0007, 0·016). Our findings show that daily Na and K intake were positively associated with cortisol production in children and their mothers. Investigation of the mechanisms involved and the potential impact of Na reduction on cortisol levels in these populations is warranted.

Significant experimental evidence supports fat as a taste modality; however, the associated peripheral mechanisms are not well established. Several candidate taste receptors have been identified, but their expression pattern and potential functions in human fungiform papillae remain unknown. The aim of this study is to identify the fat taste candidate receptors and ion channels that were expressed in human fungiform taste buds and their association with oral sensory of fatty acids. For the expression analysis, quantitative RT-PCR (qRT-PCR) from RNA extracted from human fungiform papillae samples was used to determine the expression of candidate fatty acid receptors and ion channels. Western blotting analysis was used to confirm the presence of the proteins in fungiform papillae. Immunohistochemistry analysis was used to localise the expressed receptors or ion channels in the taste buds of fungiform papillae. The correlation study was analysed between the expression level of the expressed fat taste receptors or ion channels indicated by qRT-PCR and fat taste threshold, liking of fatty food and fat intake. As a result, qRT-PCR and western blotting indicated that mRNA and protein of CD36, FFAR4, FFAR2, GPR84 and delayed rectifying K+ channels are expressed in human fungiform taste buds. The expression level of CD36 was associated with the liking difference score (R −0·567, β=−0·04, P=0·04) between high-fat and low-fat food and FFAR2 was associated with total fat intake (ρ=−0·535, β=−0·01, P=0·003) and saturated fat intake (ρ=−0·641, β=−0·02, P=0·008).

Resistance training (RT) and increased dietary protein are recommended to attenuate age-related muscle loss in the elderly. This study examined the effect of a lean red meat protein-enriched diet combined with progressive resistance training (RT+Meat) on health-related quality of life (HR-QoL) in elderly women. In this 4-month cluster randomised controlled trial, 100 women aged 60–90 years (mean 73 years) from self-care retirement villages participated in RT twice a week and were allocated either 160 g/d (cooked) lean red meat consumed across 2 meals/d, 6 d/week or ≥1 serving/d (25–30 g) carbohydrates (control group, CRT). HR-QoL (SF-36 Health Survey questionnaire), lower limb maximum muscle strength and lean tissue mass (LTM) (dual-energy X-ray absorptiometry) were assessed at baseline and 4 months. In all, ninety-one women (91 %) completed the study (RT+Meat (n 48); CRT (n 43)). Mean protein intake was greater in RT+Meat than CRT throughout the study (1·3 (sd 0·3) v. 1·1 (sd 0·3) g/kg per d, P<0·05). Exercise compliance (74 %) was not different between groups. After 4 months there was a significant net benefit in the RT+Meat compared with CRT group for overall HR-QoL and the physical component summary (PCS) score (P<0·01), but there were no changes in either group in the mental component summary (MCS) score. Changes in lower limb muscle strength, but not LTM, were positively associated with changes in overall HR-QoL (muscle strength, β: 2·2 (95 % CI 0·1, 4·3), P<0·05). In conclusion, a combination of RT and increased dietary protein led to greater net benefits in overall HR-QoL in elderly women compared with RT alone, which was because of greater improvements in PCS rather than MCS.

Emerging evidence indicates that dietary Na may be linked to obesity; however it is unclear whether this relationship is independent of energy intake (EI). The aim of this study was to assess the association between Na intake and measures of adiposity, including BMI z score, weight category and waist:height ratio (WHtR), in a sample of Australian schoolchildren. This was a cross-sectional study of schoolchildren aged 4–12 years. Na intake was assessed via one 24-h urine collection. BMI was converted to age- and sex-specific z scores, and WHtR was used to define abdominal obesity. In children aged ≥8 years, EI was determined via one 24-h dietary recall. Of the 666 children with valid urine samples 55 % were male (average age 9·3 (sd 1·8) years). In adjusted models an additional 17 mmol/d of Na was associated with a 0·10 higher BMI z score (95 % CI 0·07, 0·13), a 23 % (OR 1·23; 95 % CI 1·16, 1·31) greater risk of being overweight/obese and a 15 % (OR 1·15; 95 % CI 1·09, 1·23) greater risk of being centrally obese. In the subsample of 8–12-year-old children (n 458), adjustment for EI did not markedly alter the associations between Na and adiposity outcomes. Using a robust measure of daily Na intake we found a positive association between Na intake and obesity risk in Australian schoolchildren, which could not be explained by total energy consumption. To determine whether this is a causal relationship, longitudinal studies, with high-quality measures of Na and EI, are required.

This meta-analysis of randomised controlled trials assessed the effect of Ca on body weight and body composition through supplementation or increasing dairy food intake. Forty-one studies met the inclusion criteria (including fifty-one trial arms; thirty-one with dairy foods (n 2091), twenty with Ca supplements (n 2711). Ca intake was approximately 900 mg/d higher in the supplement groups compared with control. In the dairy group, Ca intake was approximately 1300 mg/d. Ca supplementation did not significantly affect body weight (mean change ( − 0·17, 95 % CI − 0·70, 0·37) kg) or body fat (mean change ( − 0·19, 95 % CI − 0·51, 0·13) kg) compared to control. Similarly, increased dairy food intake did not affect body weight ( − 0·06, 95 % CI − 0·54, 0·43) kg or body fat change ( − 0·36, 95 % CI − 0·80, 0·09) kg compared to control. Sub-analyses revealed that dairy supplementation resulted in no change in body weight (nineteen studies, n 1010) ( − 0·32, 95 % CI − 0·93, 0·30 kg, P= 0·31), but a greater reduction in body fat (thirteen studies, n 564) ( − 0·96, 95 % CI − 1·46, − 0·46 kg, P < 0·001) in the presence of energy restriction over a mean of 4 months compared to control. Increasing dietary Ca intake by 900 mg/d as supplements or increasing dairy intake to approximately 3 servings daily (approximately 1300 mg of Ca/d) is not an effective weight reduction strategy in adults. There is, however, an indication that approximately 3 servings of dairy may facilitate fat loss on weight reduction diets in the short term.

It has been proposed that low birth weight is associated with high levels of blood pressure in later life. The aim of this study was to assess the relationship of blood pressure to birth weight and current body size during growth and adulthood. A total of 711 female multiple births, with one group of 244 in their growth phase mean age 12.0 (2.3)(SD) years and the other of 467 adults (mean age 35.2 (12.6) years), had height, weight and both systolic (SBP) and diastolic (DBP) blood pressures measured, and self-reported their birth weight. Regression analyses were performed to assess the cross-sectional and within-pair associations of blood pressure to birth weight, with and without adjustments for current body size. Within-pair analysis was based on 296 twin pairs. Cross-sectionally, a reduction in birth weight of 1 kg was associated with 2 to 3 mm Hg higher age-adjusted SBP, which was of marginal significance and explained about 2% of the population variance. Adjustment for body mass index did not significantly change this association. Within-pair analyses found no association between birth weight and SBP or DBP, even after adjusting for current body size. After age, current body size was the strongest predictor of systolic BP. The weak association of blood pressure to birth weight cross-sectionally is of interest, but any within-pair effect of birth weight on blood pressure must be minimal compared with the effect of current body size.

The average reported dietary Na intake of children in Australia is high: 2694 mg/d (9–13 years). No data exist describing food sources of Na in Australian children's diets and potential impact of Na reduction targets for processed foods. The aim of the present study was to determine sources of dietary Na in a nationally representative sample of Australian children aged 2–16 years and to assess the impact of application of the UK Food Standards Agency (FSA) Na reduction targets on Na intake. Na intake and use of discretionary salt (note: conversion of salt to Na, 1 g of NaCl (salt) = 390 mg Na) were assessed from 24-h dietary recall in 4487 children participating in the Australian 2007 Children's Nutrition and Physical Activity Survey. Greatest contributors to Na intake across all ages were cereals and cereal-based products/dishes (43 %), including bread (13 %) and breakfast cereals (4 %). Other moderate sources were meat, poultry products (16 %), including processed meats (8 %) and sausages (3 %); milk products/dishes (11 %) and savoury sauces and condiments (7 %). Between 37 and 42 % reported that the person who prepares their meal adds salt when cooking and between 11 and 39 % added salt at the table. Those over the age of 9 years were more likely to report adding salt at the table (χ2 199·5, df 6, P < 0·001). Attainment of the UK FSA Na reduction targets, within the present food supply, would result in a 20 % reduction in daily Na intake in children aged 2–16 years. Incremental reductions of this magnitude over a period of years could significantly reduce the Na intake of this group and further reductions could be achieved by reducing discretionary salt use.

Identifying dietary modifications that potentiate the blood pressure (BP)-lowering effects of antihypertensive medications and that are practical for free-living people may assist in achieving BP reduction goals. We assessed whether two dietary patterns were effective in lowering BP in persons on antihypertensive therapy and in those not on therapy. Ninety-four participants (38/56 females/males), aged 55·6 (sd 9·9) years, consumed two 4-week dietary regimens in random order (Dietary Approaches to Stop Hypertension (DASH)-type diet and low-Na high-K (LNAHK) diet) with a control diet before each phase. Seated home BP was measured daily for the last 2 weeks in each phase. Participants were grouped based on antihypertensive drug therapy. The LNAHK diet produced a greater fall in systolic BP (SBP) in those on antihypertensive therapy ( − 6·2 (sd 6·0) mmHg) than in those not on antihypertensive therapy ( − 2·8 (sd 4·0) mmHg) (P = 0·036), and this was greatest for those on renin–angiotensin system (RAS) blocker therapy ( − 9·5 (sd 6·4) mmHg) (interaction P = 0·007). The fall in SBP on the DASH-type diet, in those on therapy (overall − 1·1 (sd 6·2) mmHg; renin–angiotensin blocker therapy − 4·2 (sd 4·7) mmHg), was not as marked as that observed on the LNAHK diet. Dietary modifications are an important part of all hypertension management regimens, and a low-Na and high-K diet enhances the BP-lowering effect of antihypertensive medications, particularly those targeting the RAS.

Psychological stress is a common feature of modern day societies, and contributes to the global burden of disease. It was proposed by Henry over 20 years ago that the salt intake of a society reflects the level of stress, and that stress, through its effect on increasing salt intake, is an important factor in the development of hypertension. This review evaluates the evidence from animal and human studies to determine if stress does induce a salt appetite and increase salt consumption in human subjects. Findings from animal studies suggest that stress may drive salt intake, with evidence for a potential mechanism via the sympatho-adrenal medullary system and/or the hypothalamo–pituitary–adrenal axis. In contrast, in the few laboratory studies conducted in human subjects, none has found that acute stress affects salt intake. However, one study demonstrated that life stress (chronic stress) was associated with increased consumption of snack foods, which included, but not specifically, highly salty snacks. Studies investigating the influence of chronic stress on eating behaviours are required, including consumption of salty foods. From the available evidence, we can conclude that in free-living, Na-replete individuals, consuming Na in excess of physiological requirements, stress is unlikely to be a major contributor to salt intake.

A randomised, parallel-design dietary intervention study was conducted in women (aged 45–75 years) with prehypertension or stage 1 hypertension. The aim was to compare the effects on bone turnover of a low-Na base-producing (LNAB) Dietary Approaches to Stop Hypertension (DASH)-type diet (including six serves lean red meat/week) with a high-carbohydrate low-fat (HCLF) diet with a higher acid load (both >800 mg dietary Ca/d). Fasting serum bone markers (baseline and week 14) and 24 h urinary electrolyte excretion (baseline, weeks 4, 8, 12 and 14) were measured. After the intervention period, the LNAB group (n 46) had a fall of 26 (sem 6) % (P < 0·0001) in urinary Na, an increase in K excretion (6·8 (sem 3·6) mmol/d; P = 0·07) and, compared with the HCLF group (n 49), a greater reduction in urinary Ca excretion by 0·7 (sem 0·3) mmol/d. Serum 25-hydroxyvitamin D, intact parathyroid hormone and osteocalcin did not change, and both groups had a similar increase of 23 (sem 5) % (P < 0·0001) in C-terminal telopeptide of type I collagen. The HCLF group had an 11 (sem 4) % increase (P = 0·003) in N-terminal propeptide, type I procollagen, which could indicate an increased rate of bone turnover. The fall in urinary Ca with the lower-Na lower-acid load diet is likely to have long-term beneficial effects on bone. As bone resorption was not different between the two dietary patterns with relatively high Ca intake, the effect on bone health of a dietary pattern with a lower acid load warrants further study on a lower Ca intake.

Dietary therapies are routinely recommended to reduce disease risk; however, there is concern they may adversely affect mood. We compared the effect on mood of a low-sodium, high-potassium diet (LNAHK) and a high-calcium diet (HC) with a moderate-sodium, high-potassium, high-calcium Dietary Approaches to Stop Hypertension (DASH)-type diet (OD). We also assessed the relationship between dietary electrolytes and cortisol, a stress hormone and marker of hypothalamic–pituitary–adrenal (HPA) axis activity. In a crossover design, subjects were randomized to two diets for 4 weeks, the OD and either LNAHK or HC, each preceded by a 2-week control diet (CD). Dietary compliance was assessed by 24 h urine collections. Mood was measured weekly by the Profile of Mood States (POMS). Saliva samples were collected to measure cortisol. The change in mood between the preceding CD and the test diet (LNAHK or HC) was compared with the change between the CD and OD. Of the thirty-eight women and fifty-six men (mean age 56·3 (sem 9·8) years) that completed the OD, forty-three completed the LNAHK and forty-eight the HC. There was a greater improvement in depression, tension, vigour and the POMS global score for the LNAHK diet compared to OD (P < 0·05). Higher cortisol levels were weakly associated with greater vigour, lower fatigue, and higher levels of urinary potassium and magnesium (r 0·1–0·2, P < 0·05 for all). In conclusion, a LNAHK diet appeared to have a positive effect on overall mood.