940 resultados para Diet-induced obesity


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To examine socioeconomic differences in the frequency and types of takeaway foods consumed. Cross-sectional postal survey. Participants were asked about their usual consumption of overall takeaway food (< four times a month, or ≥ four times a month) and 22 specific takeaway food items (< once a month, or ≥ once a month): these latter foods were grouped into “healthy” and “less healthy” choices. Socioeconomic position was measured using education and equivalised household income and differences in takeaway food consumption were assessed by calculating prevalence ratios using log binomial regression. Adults aged 25–64 years from Brisbane, Australia were randomly selected from the electoral roll (N = 903, 63.7% response rate). Compared with their more educated counterparts, the least educated were more regular consumers of overall takeaway food, fruit/vegetable juice, and less regular consumers of sushi. For the “less healthy” items, the least educated more regularly consumed potato chips, savoury pies, fried chicken, and non-diet soft drinks; however, the least educated were less likely to consume curry. Household income was not associated with overall takeaway consumption. The lowest income group were more regular consumers of fruit/vegetable juice compared with the highest income group. Among the “less healthy” items, the lowest income group were more regular consumers of fried fish, ice-cream, and milk shakes, while curry was consumed less regularly. The frequency and types of takeaway foods consumed by socioeconomically disadvantaged groups may contribute to inequalities in overweight/obesity and chronic disease.

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Purpose: Parenting style and early feeding practices have been linked to child intake, eating behaviour and weight status. The purpose of this study was to examine associations between general maternal parenting behaviours and feeding beliefs in Australian mothers of 11-17 month-old children. Methods: This cross-sectional analysis included 223 first-time mothers and their children (49% male, mean age 14 [sd 1] months) enrolled in the control group of the NOURISH trial. Mothers self-reported their feeding beliefs and parenting behaviours (overprotection, irritability, warmth, autonomy-encouraging) using modified questions from the Infant Feeding Questionnaire (Baughcum, 2001) and the Longitudinal Study of Australian Children. Multiple regression analyses were conducted, using feeding beliefs (four factors) as dependent and parenting behaviours as independent variables while adjusting for child gender, age, weight-for-age z-score and maternal age, education level, feeding mode (breast vs. non-breast), and perception of own pre-pregnancy and child weight status. Results/Findings: Two of four parenting behaviours were significantly associated with feeding beliefs. Maternal warmth was inversely associated with concerns that the child would become underweight (β=-0.156, p=0.022) and positively associated with mothers’ awareness of child’s hunger/satiety cues (β=0.303, p<0.001). Mothers’ overprotection was positively associated with concerns that the child would become underweight (β=0.213, p=0.001); become overweight (β=0.174, p=0.005); and mother’s responsive feeding (β=0.135, p=0.057). Weight-for-age z-score, mothers’ perception of their child and own weight status, education, feeding mode, and child’s age were significant covariates. Conclusions: Feeding occurs within the broader parenting context. Improving early feeding beliefs and practices may require addressing mother’s approaches to parenting, especially warmth and overprotection.

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The growth of solid tumours beyond a critical size is dependent upon angiogenesis, the formation of new blood vessels from an existing vasculature. Tumours may remain dormant at microscopic sizes for some years before switching to a mode in which growth of a supportive vasculature is initiated. The new blood vessels supply nutrients, oxygen, and access to routes by which tumour cells may travel to other sites within the host (metastasize). In recent decades an abundance of biological research has focused on tumour-induced angiogenesis in the hope that treatments targeted at the vasculature may result in a stabilisation or regression of the disease: a tantalizing prospect. The complex and fascinating process of angiogenesis has also attracted the interest of researchers in the field of mathematical biology, a discipline that is, for mathematics, relatively new. The challenge in mathematical biology is to produce a model that captures the essential elements and critical dependencies of a biological system. Such a model may ultimately be used as a predictive tool. In this thesis we examine a number of aspects of tumour-induced angiogenesis, focusing on growth of the neovasculature external to the tumour. Firstly we present a one-dimensional continuum model of tumour-induced angiogenesis in which elements of the immune system or other tumour-cytotoxins are delivered via the newly formed vessels. This model, based on observations from experiments by Judah Folkman et al., is able to show regression of the tumour for some parameter regimes. The modelling highlights a number of interesting aspects of the process that may be characterised further in the laboratory. The next model we present examines the initiation positions of blood vessel sprouts on an existing vessel, in a two-dimensional domain. This model hypothesises that a simple feedback inhibition mechanism may be used to describe the spacing of these sprouts with the inhibitor being produced by breakdown of the existing vessel's basement membrane. Finally, we have developed a stochastic model of blood vessel growth and anastomosis in three dimensions. The model has been implemented in C++, includes an openGL interface, and uses a novel algorithm for calculating proximity of the line segments representing a growing vessel. This choice of programming language and graphics interface allows for near-simultaneous calculation and visualisation of blood vessel networks using a contemporary personal computer. In addition the visualised results may be transformed interactively, and drop-down menus facilitate changes in the parameter values. Visualisation of results is of vital importance in the communication of mathematical information to a wide audience, and we aim to incorporate this philosophy in the thesis. As biological research further uncovers the intriguing processes involved in tumourinduced angiogenesis, we conclude with a comment from mathematical biologist Jim Murray, Mathematical biology is : : : the most exciting modern application of mathematics.

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PURPOSE. To assess whether there are any advantages of binocular over monocular vision under blur conditions. METHODS. We measured the effect of defocus, induced by positive lenses, on the pattern reversal Visual Evoked Potential (VEP) and on visual acuity (VA). Monocular (dominant eye) and binocular VEPs were recorded from thirteen volunteers (average age: 28±5 years, average spherical equivalent: -0.25±0.73 D) for defocus up to 2.00 D using positive powered lenses. VEPs were elicited using reversing 10 arcmin checks at a rate of 4 reversals/second. The stimulus subtended a circular field of 7 degrees with 100% contrast and mean luminance 30 cd/m2. VA was measured under the same conditions using ETDRS charts. All measurements were performed at 1m viewing distance with best spectacle sphero-cylindrical correction and natural pupils. RESULTS. With binocular stimulation, amplitudes and implicit times of the P100 component of the VEPs were greater and shorter, respectively, in all cases than for monocular stimulation. Mean binocular enhancement ratio in the P100 amplitude was 2.1 in-focus, increasing linearly with defocus to be 3.1 at +2.00 D defocus. Mean peak latency was 2.9 ms shorter in-focus with binocular than for monocular stimulation, with the difference increasing with defocus to 8.8 ms at +2.00 D. As for the VEP amplitude, VA was always better with binocular than with monocular vision, with the difference being greater for higher retinal blur. CONCLUSIONS. Both subjective and electrophysiological results show that binocular vision ameliorates the effect of defocus. The increased binocular facilitation observed with retinal blur may be due to the activation of a larger population of neurons at close-to-threshold detection under binocular stimulation.

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It is frequently reported that the actual weight loss achieved through exercise interventions is less than theoretically expected. Amongst other compensatory adjustments that accompany exercise training (e.g., increases in resting metabolic rate and energy intake), a possible cause of the less than expected weight loss is a failure to produce a marked increase in total daily energy expenditure due to a compensatory reduction in non-exercise activity thermogenesis (NEAT). Therefore, there is a need to understand how behaviour is modified in response to exercise interventions. The proposed benefits of exercise training are numerous, including changes to fat oxidation. Given that a diminished capacity to oxidise fat could be a factor in the aetiology of obesity, an exercise training intensity that optimises fat oxidation in overweight/obese individuals would improve impaired fat oxidation, and potentially reduce health risks that are associated with obesity. To improve our understanding of the effectiveness of exercise for weight management, it is important to ensure exercise intensity is appropriately prescribed, and to identify and monitor potential compensatory behavioural changes consequent to exercise training. In line with the gaps in the literature, three studies were performed. The aim of Study 1 was to determine the effect of acute bouts of moderate- and high-intensity walking exercise on NEAT in overweight and obese men. Sixteen participants performed a single bout of either moderate-intensity walking exercise (MIE) or high-intensity walking exercise (HIE) on two separate occasions. The MIE consisted of walking for 60-min on a motorised treadmill at 6 km.h-1. The 60-min HIE session consisted of walking in 5-min intervals at 6 km.h-1 and 10% grade followed by 5-min at 0% grade. NEAT was assessed by accelerometer three days before, on the day of, and three days after the exercise sessions. There was no significant difference in NEAT vector magnitude (counts.min-1) between the pre-exercise period (days 1-3) and the exercise day (day 4) for either protocol. In addition, there was no change in NEAT during the three days following the MIE session, however NEAT increased by 16% on day 7 (post-exercise) compared with the exercise day (P = 0.32). During the post-exercise period following the HIE session, NEAT was increased by 25% on day 7 compared with the exercise day (P = 0.08), and by 30-33% compared with the pre-exercise period (day 1, day 2 and day 3); P = 0.03, 0.03, 0.02, respectively. To conclude, a single bout of either MIE or HIE did not alter NEAT on the exercise day or on the first two days following the exercise session. However, extending the monitoring of NEAT allowed the detection of a 48 hour delay in increased NEAT after performing HIE. A longer-term intervention is needed to determine the effect of accumulated exercise sessions over a week on NEAT. In Study 2, there were two primary aims. The first aim was to test the reliability of a discontinuous incremental exercise protocol (DISCON-FATmax) to identify the workload at which fat oxidation is maximised (FATmax). Ten overweight and obese sedentary male men (mean BMI of 29.5 ¡Ó 4.5 kg/m2 and mean age of 28.0 ¡Ó 5.3 y) participated in this study and performed two identical DISCON-FATmax tests one week apart. Each test consisted of alternate 4-min exercise and 2-min rest intervals on a cycle ergometer. The starting work load of 28 W was increased every 4-min using 14 W increments followed by 2-min rest intervals. When the respiratory exchange ratio was consistently >1.0, the workload was increased by 14 W every 2-min until volitional exhaustion. Fat oxidation was measured by indirect calorimetry. The mean FATmax, ƒtV O2peak, %ƒtV O2peak and %Wmax at which FATmax occurred during the two tests were 0.23 ¡Ó 0.09 and 0.18 ¡Ó 0.08 (g.min-1); 29.7 ¡Ó 7.8 and 28.3 ¡Ó 7.5 (ml.kg-1.min-1); 42.3 ¡Ó 7.2 and 42.6 ¡Ó 10.2 (%ƒtV O2max) and 36.4 ¡Ó 8.5 and 35.4 ¡Ó 10.9 (%), respectively. A paired-samples T-test revealed a significant difference in FATmax (g.min-1) between the tests (t = 2.65, P = 0.03). The mean difference in FATmax was 0.05 (g.min-1) with the 95% confidence interval ranging from 0.01 to 0.18. Paired-samples T-test, however, revealed no significant difference in the workloads (i.e. W) between the tests, t (9) = 0.70, P = 0.4. The intra-class correlation coefficient for FATmax (g.min-1) between the tests was 0.84 (95% confidence interval: 0.36-0.96, P < 0.01). However, Bland-Altman analysis revealed a large disagreement in FATmax (g.min-1) related to W between the two tests; 11 ¡Ó 14 (W) (4.1 ¡Ó 5.3 ƒtV O2peak (%)).These data demonstrate two important phenomena associated with exercise-induced substrate oxidation; firstly, that maximal fat oxidation derived from a discontinuous FATmax protocol differed statistically between repeated tests, and secondly, there was large variability in the workload corresponding with FATmax. The second aim of Study 2 was to test the validity of a DISCON-FATmax protocol by comparing maximal fat oxidation (g.min-1) determined by DISCON-FATmax with fat oxidation (g.min-1) during a continuous exercise protocol using a constant load (CONEX). Ten overweight and obese sedentary males (BMI = 29.5 ¡Ó 4.5 kg/m2; age = 28.0 ¡Ó 4.5 y) with a ƒtV O2max of 29.1 ¡Ó 7.5 ml.kg-1.min-1 performed a DISCON-FATmax test consisting of alternate 4-min exercise and 2-min rest intervals on a cycle ergometer. The 1-h CONEX protocol used the workload from the DISCON-FATmax to determine FATmax. The mean FATmax, ƒtV O2max, %ƒtV O2max and workload at which FATmax occurred during the DISCON-FATmax were 0.23 ¡Ó 0.09 (g.min-1); 29.1 ¡Ó 7.5 (ml.kg-1.min-1); 43.8 ¡Ó 7.3 (%ƒtV O2max) and 58.8 ¡Ó 19.6 (W), respectively. The mean fat oxidation during the 1-h CONEX protocol was 0.19 ¡Ó 0.07 (g.min-1). A paired-samples T-test revealed no significant difference in fat oxidation (g.min-1) between DISCON-FATmax and CONEX, t (9) = 1.85, P = 0.097 (two-tailed). There was also no significant correlation in fat oxidation between the DISCON-FATmax and CONEX (R=0.51, P = 0.14). Bland- Altman analysis revealed a large disagreement in fat oxidation between the DISCONFATmax and CONEX; the upper limit of agreement was 0.13 (g.min-1) and the lower limit of agreement was ¡V0.03 (g.min-1). These data suggest that the CONEX and DISCONFATmax protocols did not elicit different rates of fat oxidation (g.min-1). However, the individual variability in fat oxidation was large, particularly in the DISCON-FATmax test. Further research is needed to ascertain the validity of graded exercise tests for predicting fat oxidation during constant load exercise sessions. The aim of Study 3 was to compare the impact of two different intensities of four weeks of exercise training on fat oxidation, NEAT, and appetite in overweight and obese men. Using a cross-over design 11 participants (BMI = 29 ¡Ó 4 kg/m2; age = 27 ¡Ó 4 y) participated in a training study and were randomly assigned initially to: [1] a lowintensity (45%ƒtV O2max) exercise (LIT) or [2] a high-intensity interval (alternate 30 s at 90%ƒtV O2max followed by 30 s rest) exercise (HIIT) 40-min duration, three times a week. Participants completed four weeks of supervised training and between cross-over had a two week washout period. At baseline and the end of each exercise intervention,ƒtV O2max, fat oxidation, and NEAT were measured. Fat oxidation was determined during a standard 30-min continuous exercise bout at 45%ƒtV O2max. During the steady state exercise expired gases were measured intermittently for 5-min periods and HR was monitored continuously. In each training period, NEAT was measured for seven consecutive days using an accelerometer (RT3) the week before, at week 3 and the week after training. Subjective appetite sensations and food preferences were measured immediately before and after the first exercise session every week for four weeks during both LIT and HIIT. The mean fat oxidation rate during the standard continuous exercise bout at baseline for both LIT and HIIT was 0.14 ¡Ó 0.08 (g.min-1). After four weeks of exercise training, the mean fat oxidation was 0.178 ¡Ó 0.04 and 0.183 ¡Ó 0.04 g.min-1 for LIT and HIIT, respectively. The mean NEAT (counts.min-1) was 45 ¡Ó 18 at baseline, 55 ¡Ó 22 and 44 ¡Ó 16 during training, and 51 ¡Ó 14 and 50 ¡Ó 21 after training for LIT and HIIT, respectively. There was no significant difference in fat oxidation between LIT and HIIT. Moreover, although not statistically significant, there was some evidence to suggest that LIT and HIIT tend to increase fat oxidation during exercise at 45% ƒtV O2max (P = 0.14 and 0.08, respectively). The order of training treatment did not significantly influence changes in fat oxidation, NEAT, and appetite. NEAT (counts.min-1) was not significantly different in the week following training for either LIT or HIIT. Although not statistically significant (P = 0.08), NEAT was 20% lower during week 3 of exercise training in HIIT compared with LIT. Examination of appetite sensations revealed differences in the intensity of hunger, with higher ratings after LIT compared with HIIT. No differences were found in preferences for high-fat sweet foods between LIT and HIIT. In conclusion, the results of this thesis suggest that while fat oxidation during steady state exercise was not affected by the level of exercise intensity, there is strong evidence to suggest that intense exercise could have a debilitative effect on NEAT.

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Prevention and safety promotion programmes. Traditionally, in-depth investigations of crash risks are conducted using exposure controlled study or case-control methodology. However, these studies need either observational data for control cases or exogenous exposure data like vehicle-kilometres travel, entry flow or product of conflicting flow for a particular traffic location, or a traffic site. These data are not readily available and often require extensive data collection effort on a system-wide basis. Aim: The objective of this research is to propose an alternative methodology to investigate crash risks of a road user group in different circumstances using readily available traffic police crash data. Methods: This study employs a combination of a log-linear model and the quasi-induced exposure technique to estimate crash risks of a road user group. While the log-linear model reveals the significant interactions and thus the prevalence of crashes of a road user group under various sets of traffic, environmental and roadway factors, the quasi-induced exposure technique estimates relative exposure of that road user in the same set of explanatory variables. Therefore, the combination of these two techniques provides relative measures of crash risks under various influences of roadway, environmental and traffic conditions. The proposed methodology has been illustrated using Brisbane motorcycle crash data of five years. Results: Interpretations of results on different combination of interactive factors show that the poor conspicuity of motorcycles is a predominant cause of motorcycle crashes. Inability of other drivers to correctly judge the speed and distance of an oncoming motorcyclist is also evident in right-of-way violation motorcycle crashes at intersections. Discussion and Conclusions: The combination of a log-linear model and the induced exposure technique is a promising methodology and can be applied to better estimate crash risks of other road users. This study also highlights the importance of considering interaction effects to better understand hazardous situations. A further study on the comparison between the proposed methodology and case-control method would be useful.

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The induction of apoptosis in thymocytes by the glucocorticoid dexamethasone was used as a model system to investigate whether there are changes in 20 S and 26 S proteasome activities during apoptosis. We observed that thymocytes contain high concentrations of proteasomes and that following treatment with dexamethasone, cell extracts showed a decrease in proteasome chymotrypsin-like activity which correlated with the degree of apoptosis observed. The decrease in chymotrypsin-like activity of 20 S and 26S proteasomes was still apparent after these complexes had been partially puri®ed from apoptotic thymocyte extracts and was therefore not due to competition resulting from a general increase in protein turnover. The trypsin-like and peptidylglutamylpeptide hydrolase activities of proteasome complexes were also observed to decrease during apoptosis, but these decreases were reversed by the inhibition of apoptosis by the caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp(OMe)-¯uoromethylketone. However, the chymotrypsin-like activity of proteasomes decreased further in the presence of the apoptosis inhibitor. Val-Ala-Asp-¯uoromethylketone was found to inhibit the chymotrypsin- and trypsin-like activity of 26 S proteasomes in .itro. The decrease in proteasome activities in apoptosis did not appear to be due to a decrease in the concentration of total cellular proteasomes. Thus, the early decreases in 20 S and 26 S proteasome activities during apoptosis appear to be due to a down-regulation of their proteolytic activities and not to a decrease in their protein concentration. These data suggest that proteasomes may be responsible, in thymocytes, for the turnover of a protein that functions as a positive regulator of apoptosis.

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Presently, global rates of skin cancers induced by ultraviolet radiation (UVR) exposure are on the rise. In view of this, current knowledge gaps in the biology of photocarcinogenesis and skin cancer progression urgently need to be addressed. One factor that has limited skin cancer research has been the need for a reproducible and physiologically-relevant model able to represent the complexity of human skin. This review outlines the main currently-used in vitro models of UVR-induced skin damage. This includes the use of conventional two-dimensional cell culture techniques and the major animal models that have been employed in photobiology and photocarcinogenesis research. Additionally, the progression towards the use of cultured skin explants and tissue-engineered skin constructs, and their utility as models of native skin's responses to UVR are described. The inherent advantages and disadvantages of these in vitro systems are also discussed.

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Studies show that in 3-11 year-olds, parental feeding style is directly associated with child weight [1] and also moderates the association between feeding practices and weight [2]. This cross-sectional study aimed to examine these relationships in younger children. Data from 331 of 698 first-time mothers of healthy term children (151 boys, mean age 24±1 months) enrolled in the NOURISH RCT included (a) measured child weight, (b) self-reported feeding styles and controlling feeding practices, and (c) maternal and child covariates. ANCOVA compared mean child weight-for-age z-score (cWAZ) across 4 feeding styles. Regression examined the associations between cWAZ and 5 controlling feeding practices. Moderated multiple regression analysis was planned to examine effects of feeding style on relationships between feeding practices and cWAZ. Feeding style (indulgent = 38.6%, authoritarian = 35.8%, authoritative = 13.1%, uninvolved = 12.5%) was not independently associated with cWAZ. However, ’pressure to eat’ was negatively associated with cWAZ (�=-0.131, p<0.05) higher pressure associated with lower cWAZ. Given feeding style was not associated with cWAZ, moderation analysis was not performed. Contrary to findings in older children, cWAZ in 2-year-olds was not associated with maternal feeding style. However, the negative association between child weight and pressure feeding found in 6-11year-olds [2] appears to hold in toddlers. Educating mothers about potentially detrimental long-term effects of pressure feeding in early childhood, may be more practical and effective in promoting healthy weight than targeting the less concrete concept of feeding styles. References: [1] Hughes, Appetite, 2005;44:83-92. [2] Hennessy, Appetite, 2010;54:369-377.

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Poor nutritional status in chronic obstructive pulmonary disease (COPD) is associated with increased mortality independently of disease-severity (Collins et al).1 Epidemiological studies have suggested a protective role of obesity against mortality in COPD (Vestbo et al)2 which is contrary to data from the general population where obesity is associated with decreased life expectancy. This relationship has been referred to as the ‘obesity paradox’ and has been demonstrated in a number of chronic wasting conditions (Kalantar-Zadeh et al).3 This study investigated the existence of the obesity paradox in outpatients with COPD by examining the effect of body mass index (BMI) on 1-year healthcare use and clinical outcome in terms of hospital admission rates, length of hospital stay, outpatient appointments and mortality. BMI was assessed in 424 outpatients with COPD, with measurements performed by specialist respiratory nurses during outpatient clinics. 1-year healthcare use was retrospectively collected from the date of BMI measurement. Abstract S163 Table 1 Patients classified as overweight (25.0–29.9 kg/m2) or obese (>30 kg/m2) experienced significantly fewer emergency hospital admissions, as well as a reduced length of hospital stay, in comparison to normal weight (20.0–24.9 kg/m2) or underweight (<20 kg/m2) outpatients. There was a significant negative trend between BMI classification and mortality. This study supports the existence of the ‘obesity paradox’ in COPD, not only in relation to reduced 1 year mortality rates but also in terms of reduced emergency hospital admissions and reduced length of hospital stay.

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Human activity-induced vibrations in slender structural sys tems become apparent in many different excitation modes and consequent action effects that cause discomfort to occupants, crowd panic and damage to public infrastructure. Resulting loss of public confidence in safety of structures, economic losses, cost of retrofit and repairs can be significant. Advanced computational and visualisation techniques enable engineers and architects to evolve bold and innovative structural forms, very often without precedence. New composite and hybrid materials that are making their presence in structural systems lack historical evidence of satisfactory performance over anticipated design life. These structural systems are susceptible to multi-modal and coupled excitation that are very complex and have inadequate design guidance in the present codes and good practice guides. Many incidents of amplified resonant response have been reported in buildings, footbridges, stadia a nd other crowded structures with adverse consequences. As a result, attenuation of human-induced vibration of innovative and slender structural systems very ofte n requires special studies during the design process. Dynamic activities possess variable characteristics and thereby induce complex responses in structures that are sensitive to parametric variations. Rigorous analytical techniques are available for investigation of such complex actions and responses to produce acceptable performance in structural systems. This paper presents an overview and a critique of existing code provisions for human-induced vibration followed by studies on the performance of three contrasting structural systems that exhibit complex vibration. The dynamic responses of these systems under human-induced vibrations have been carried out using experimentally validated computer simulation techniques. The outcomes of these studies will have engineering applications for safe and sustainable structures and a basis for developing design guidance.

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OBJECTIVE: To evaluate a universal obesity prevention intervention, which commenced at infant age 4-6 months, using outcome data assessed 6-months after completion of the first of two intervention modules and 9 months from baseline. DESIGN: Randomised controlled trial of a community-based early feeding intervention. SUBJECTS AND METHODS: 698 first-time mothers (mean age 30±5 years) with healthy term infants (51% male) aged 4.3±1.0 months at baseline. Mothers and infants were randomly allocated to self-directed access to usual care or to attend two group education modules, each delivered over three months, that provided anticipatory guidance on early feeding practices. Outcome data reported here were assessed at infant age 13.7±1.3 months. Anthropometrics were expressed as z-scores (WHO reference). Rapid weight gain was defined as change in weight-for-age z-score (WAZ) > +0.67. Maternal feeding practices were assessed via self-administered questionnaire. RESULTS: There were no differences according to group allocation on key maternal and infant characteristics. At follow up (n=598 [86%]) the intervention group infants had lower BMIZ (0.42±0.85 vs 0.23±0.93, p=0.009) and infants in the control group were more likely to show rapid weight gain from baseline to follow up (OR=1.5 CI95%1.1-2.1, p=0.014). Mothers in the control group were more likely to report using non- responsive feeding practices that fail to respond to infant satiety cues such as encouraging eating by using food as a reward (15% vs 4%, p=0.001) or using games ( 67% vs 29%, p<0.001). CONCLUSIONS: These results provide early evidence that anticipatory guidance targeting the ‘when, what and how’ of solid feeding can be effective in changing maternal feeding practices and, at least in the short term, reducing anthropometric indicators of childhood obesity risk. Analyses of outcomes at later ages are required to determine if these promising effects can be sustained.

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1. Both dietary magnesium depletion and potassium depletion (confirmed by tissue analysis) were induced in rats which were then compared with rats treated with chlorothiazide (250 mg/kg diet) and rats on a control synthetic diet. 2. Brain and muscle intracellular pH was measured by using a surface coil and [31P]-NMR to measure the chemical shift of inorganic phosphate. pH was also measured in isolated perfused hearts from control and magnesium-deficient rats. Intracellular magnesium status was assessed by measuring the chemical shift of β-ATP in brain. 3. There was no evidence for magnesium deficiency in the chlorothiazide-treated rats on tissue analysis or on chemical shift of β-ATP in brain. Both magnesium and potassium deficiency, but not chlorothiazide treatment, were associated with an extracellular alkalosis. 4. Magnesium deficiency led to an intracellular alkalosis in brain, muscle and heart. Chlorothiazide treatment led to an alkalosis in brain. Potassium deficiency was associated with a normal intracellular pH in brain and muscle. 5. Magnesium depletion and chlorothiazide treatment produce intracellular alkalosis by unknown mechanism(s).

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Changing sodium intake from 70-200 mmol/day elevates blood pressure in normotensive volunteers by 6/4 mmHg. Older people, people with reduced renal function on a low sodium diet and people with a family history of hypertension are more likely to show this effect. The rise in blood pressure was associated with a fall in plasma volume suggesting that plasma volume changes do not initiate hypertension. In normotensive individuals the most common abnormality in membrane sodium transport induced by an extra sodium load was an increased permeability of the red cell to sodium. Some normotensive individuals also had an increase in the level of a plasma inhibitor that inhibited Na-K ATPase. These individuals also appeared to have a rise in blood pressure. Sodium intake and blood pressure are related. The relationship differs in different people and is probably controlled by the genetically inherited capacity of systems involved in membrane sodium transport.