Beverage consumption in Auckland primary school children : a thesis presented in partial fulfilment of the requirements for the degree of Master of Science in Nutrition and Dietetics at Massey University, Albany, New Zealand

Background: The New Zealand (NZ) Ministry of Health advises that plain water and plain low-fat milk should be consumed daily and that if children are to drink sugar-sweetened beverages (SSB) they should be limited. The latest comprehensive NZ beverage intake data in 8 to 12 year old children was published in 2008, however, fizzy drink intake data is updated annually. This means that NZ is lacking a full picture of children’s beverage consumption. SSB intake has been associated with weight gain in some studies. However, most of these studies calculate adiposity using body mass index (BMI) and few measure body fat percentage (BF%). International and limited national evidence has identified home availability, parental encouragement, socioeconomic status, and knowledge in children as factors associated with SSB intake. Many NZ schools have become ‘water-only’ schools (WOS) to try to reduce SSB consumption. Aim: To investigate beverage consumption in 8 to 12 year old Auckland primary school children. Methods: This cross-sectional study evaluated beverage intake and associated factors using self-administered questionnaires. SSB consumption measurements consisted of 17 types of beverages, and different combinations of these. Body composition was measured using bioelectrical impedance analysis (BIA). Chi squared and Mann-Whitney tests were used to examine the associations between SSB consumption and the factors associated with it. Results: Children (n=695, 9.9±0.7 years, 44.8% male) were recruited from 6 schools (4 WOS). Plain water and plain milk were consumed less than once per day by 11.6% and 54.7% of the children, respectively. Soft drink and fruit juice were consumed more than once per week by 30.6% and 39% of the children, respectively. SSBs (p<0.001), including fruit juice (p=0.021), had a positive relationship with BF% in girls. There was an increased likelihood of consuming beverages at least once per week if they were usually available at home. Receiving a lot of encouragement for healthy beverage intake from parents or school had an inverse relationship with SBB intake (p<0.001). Low socioeconomic status was inversely associated with SSB intake (p<0.001). WOS had a higher consumption of SSBs compared to non-WOS (p<0.001). Conclusions: Too many children in this cohort were not meeting the NZ Ministry of Health recommendations for plain water and milk consumption. Thus, they may benefit from increasing their intake, whilst decreasing their SSB intake. If parents limited SSB home availability and encouraged intake of healthy beverages it may contribute to a decrease in their children’s SSB consumption. Our findings support a recommendation to include fruit juice in any public health actions to discourage SSB consumption. More research is needed to assess school water-only policies and their effect on SSB consumption

Interaction between cardiac sympathetic drive and heart rate in heart failure Modulation by adrenergic receptor genotype

ObjectivesIn the present study, we aimed to evaluate the effect of adrenergic receptor polymorphisms on the response of myocardium to measured levels of cardiac adrenergic drive, and to evaluate whether polymorphisms of presynaptic adrenoceptors modified the rate of cardiac and systemic release of norepinephrine.BackgroundHeightened sympathetic activity plays an important pathophysiologic role in congestive heart failure (CHF). Recently several functionally relevant polymorphisms of the α2-, β1-, and β2-adrenoceptors have been identified, and specific genotypes have been associated with the incidence or clinical severity of CHF. These adrenoceptors are known to be located both pre-synaptically (α2and β2) and post-synaptically (β1and β2), raising the possibility that their association with clinical measures in CHF could be mediated either by modulation of the cardiac response to a given level of adrenergic drive or by altering norepinephrine release from sympathetic nerve terminals.MethodsWe determined the β1-, β2-, and α2C-adrenoceptor genotype in 60 patients with severe CHF in conjunction with measurement of cardiac and systemic sympathetic activity using the radiotracer norepinephrine spillover method.ResultsWe showed a strong relationship (r = 0.67, p < 0.001) between heart rate and the level of cardiac adrenergic drive, and heart rate for a given level of cardiac adrenergic drive was substantially greater in patients with the Arg/Arg16 β2-adrenoceptor polymorphism (p = 0.02), whereas no such relationship existed for polymorphisms of the β1-adrenoceptor. The genotype of the α2C- and β2-adrenoceptors showed no relationship to the rate of norepinephrine release from cardiac sympathetic nerves.ConclusionsFor the first time, we show that β2-adrenoceptor polymorphisms significantly influence the relationship between heart rate and cardiac adrenergic drive in CHF, but do not affect the rate of norepinephrine release from sympathetic nerve terminals

Arterial Pressure, Cardiac Output and Systemic Resistance before and after Pithing in Normotensive and Spontaneously Hypertensive Rats

After complete cardiovascular denervation mean arterial pressure (MAP) falls to almost equally low levels in spontaneously hypertensive rats (SHR) and normotensive control rats (NCR). This has earlier been suggested to indicate a dominance of neurogenic mechanisms in established SHR hypertension.–In the present study, total peripheral resistance (TPR) remains, however, some 35 per cent higher in adult SHR than in NCR after pithing while cardiac output (CO), and stroke volume, is 35 per cent lower in SHR. These opposite differences in TPR and CO after denervation, resulting in equal MAP levels in SHR and NCR, seem rather to be a consequence of the rapidly established structural adaptation that affects all SHR high-pressure cardiovascular sections. Thus, the SHR precapillary resistance vessels display thick- ened walls and luminal narrowing, which keeps TPR higher than in NCR even during maximal vaso- dilatation. Due to hypertrophy, the SHR left ventricle exhibits a reduced myocardial stretch for a given filling pressure and stroke volume is consequently reduced more than in NCR after complete denervation.–Paradoxically, therefore, rather than reflecting any dominance of neurogenic mechanisms in established SHR hypertension the MAP equalization in SHR and NCR after cardiovascular denervation emphasizes the hemodynamic importance of cardiovascular structural changes present in hypertension.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66147/1/j.1748-1716.1975.tb05897.x.pd

The dropout problem in antihypertensive treatment : A pilot study of social and emotional factors influencing a patient's ability to follow antihypertensive treatment

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/32818/1/0000192.pd

Is near basal blood pressure a more accurate predictor of cardiorenal manifestations of hypertension than casual blood pressure?

Measurement of casual and near basal systolic and diastolic blood pressures were correlated with the severity of cardiorenal manifestations of hypertension in 471 patients. There was a significant association of each of the four blood pressure measurements with each other (P All four blood pressure measurements were significantly associated (r &gt;= 0.78, P The level of blood pressure is the important correlate of these manifestations of hypertension. This is equally true whether systolic, diastolic, casual or near basal measurements are used. Near basal blood pressure does not correlate better with the cardiorenal manifestations of hypertension than casual blood pressure, neither does diastolic blood pressure correlate better with these manifestations than systolic blood pressure.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/22749/1/0000304.pd

The contribution of refractoriness to arrhythmic substrate in hypokalemic Langendorff-perfused murine hearts

The clinical effects of hypokalemia including action potential prolongation and arrhythmogenicity suppressible by lidocaine were reproduced in hypokalemic (3.0 mM K(+)) Langendorff-perfused murine hearts before and after exposure to lidocaine (10 μM). Novel limiting criteria for local and transmural, epicardial, and endocardial re-excitation involving action potential duration (at 90% repolarization, APD(90)), ventricular effective refractory period (VERP), and transmural conduction time (Δlatency), where appropriate, were applied to normokalemic (5.2 mM K(+)) and hypokalemic hearts. Hypokalemia increased epicardial APD(90) from 46.6 ± 1.2 to 53.1 ± 0.7 ms yet decreased epicardial VERP from 41 ± 4 to 29 ± 1 ms, left endocardial APD(90) unchanged (58.2 ± 3.7 to 56.9 ± 4.0 ms) yet decreased endocardial VERP from 48 ± 4 to 29 ± 2 ms, and left Δlatency unchanged (1.6 ± 1.4 to 1.1 ± 1.1 ms; eight normokalemic and five hypokalemic hearts). These findings precisely matched computational predictions based on previous reports of altered ion channel gating and membrane hyperpolarization. Hypokalemia thus shifted all re-excitation criteria in the positive direction. In contrast, hypokalemia spared epicardial APD(90) (54.8 ± 2.7 to 60.6 ± 2.7 ms), epicardial VERP (84 ± 5 to 81 ± 7 ms), endocardial APD(90) (56.6 ± 4.2 to 63.7 ± 6.4 ms), endocardial VERP (80 ± 2 to 84 ± 4 ms), and Δlatency (12.5 ± 6.2 to 7.6 ± 3.4 ms; five hearts in each case) in lidocaine-treated hearts. Exposure to lidocaine thus consistently shifted all re-excitation criteria in the negative direction, again precisely agreeing with the arrhythmogenic findings. In contrast, established analyses invoking transmural dispersion of repolarization failed to account for any of these findings. We thus establish novel, more general, criteria predictive of arrhythmogenicity that may be particularly useful where APD(90) might diverge sharply from VERP

Origin and insertion of the medial patellofemoral ligament: a systematic review of anatomy.

PURPOSE: The medial patellofemoral ligament (MPFL) is the major medial soft-tissue stabiliser of the patella, originating from the medial femoral condyle and inserting onto the medial patella. The exact position reported in the literature varies. Understanding the true anatomical origin and insertion of the MPFL is critical to successful reconstruction. The purpose of this systematic review was to determine these locations. METHODS: A systematic search of published (AMED, CINAHL, MEDLINE, EMBASE, PubMed and Cochrane Library) and unpublished literature databases was conducted from their inception to the 3 February 2016. All papers investigating the anatomy of the MPFL were eligible. Methodological quality was assessed using a modified CASP tool. A narrative analysis approach was adopted to synthesise the findings. RESULTS: After screening and review of 2045 papers, a total of 67 studies investigating the relevant anatomy were included. From this, the origin appears to be from an area rather than (as previously reported) a single point on the medial femoral condyle. The weighted average length was 56 mm with an 'hourglass' shape, fanning out at both ligament ends. CONCLUSION: The MPFL is an hourglass-shaped structure running from a triangular space between the adductor tubercle, medial femoral epicondyle and gastrocnemius tubercle and inserts onto the superomedial aspect of the patella. Awareness of anatomy is critical for assessment, anatomical repair and successful surgical patellar stabilisation. LEVEL OF EVIDENCE: Systematic review of anatomical dissections and imaging studies, Level IV