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Little is known about Se intakes and status in very young New Zealand children. However, Se intakes below recommendations and lower Se status compared with international studies have been reported in New Zealand (particularly South Island) adults. The Baby-Led Introduction to SolidS (BLISS) randomised controlled trial compared a modified version of baby-led weaning (infants feed themselves rather than being spoon-fed), with traditional spoon-feeding (Control). Weighed 3-d diet records were collected and plasma Se concentration measured using inductively coupled plasma mass spectrometry (ICP-MS). In total, 101 (BLISS n 50, Control n 51) 12-month-old toddlers provided complete data. The OR of Se intakes below the estimated average requirement (EAR) was no different between BLISS and Control (OR: 0·89; 95 % CI 0·39, 2·03), and there was no difference in mean plasma Se concentration between groups (0·04 μmol/l; 95 % CI −0·03, 0·11). In an adjusted model, consuming breast milk was associated with lower plasma Se concentrations (–0·12 μmol/l; 95 % CI −0·19, −0·04). Of the food groups other than infant milk (breast milk or infant formula), ‘breads and cereals’ contributed the most to Se intakes (12 % of intake). In conclusion, Se intakes and plasma Se concentrations of 12-month-old New Zealand toddlers were no different between those who had followed a baby-led approach to complementary feeding and those who followed traditional spoon-feeding. However, more than half of toddlers had Se intakes below the EAR.
Charitable food aid has become a first line of response for addressing rising rates of hunger in many high-income countries such as the United States (US), Canada, Australia and the United Kingdom (UK). This can be seen in the soaring numbers of food banks, alongside other charitable projects such as community kitchens, resourced through volunteer labour and food donations from corporate retailers. In the US and Canada, food banks have been an institutionalised response to food poverty for 35 years, and in the UK they can be traced back to the introduction of economic austerity measures implemented in response to the 2008 financial crisis (Lambie-Mumford, 2019). In the UK, where 8.4 million people live in food poverty, the largest national food bank provider, The Trussell Trust, has grown its network from 65 food banks in 2011 to more than 1,200 in 2019 (Sosenko et al, 2019). Australia's largest food relief organisation, Foodbank, reports that during the 12 months leading up to 2019, the need for food relief increased by 22 per cent, with more than one in five people experiencing food insecurity. The organisation works with 2,400 charities to provide food relief but only 37 per cent reported that they were meeting the needs of those they assist (Foodbank, 2019).
Critical voices in research, policy and advocacy argue that charitable food aid forms part of the retrenchment of the welfare state, allowing governments to devolve their responsibilities onto the charitable sector and community groups (Lambie-Mumford and Dowler, 2014; Barbour et al, 2016). While alleviating the symptoms of food insecurity, food aid fails to address the structural causes, such as stagnating wages, welfare reforms and austerity policies. In March 2019, these concerns culminated in researchers and poverty campaigners publishing an open letter declaring that charitable food aid in the UK and US is ‘a sticking plaster on a gaping wound of systemic inequality in our societies’.
The global COVID-19 pandemic has amplified the connections between food and social inequality further. The wake of the pandemic attuned us to the dysfunctionality of a food aid system reliant on corporate philanthropy, with food aid donations dwindling due to the disruption of fragile just-in-time food supply chains caused by consumer stockpiling (Beacham and Willatt, 2020). The economic insecurities created by loss of income and employment have led to soaring rates of food insecurity.
As discussed in Chapters 1 and 2, one of the central tenets of the HSCA 2012 was the desirability of increasing the involvement of GPs (and other clinicians) in the commissioning of services for their patients. This ideological commitment – based upon belief and founded, in part at least, upon an implicit denigration of managerial work (in order to increase control over the NHS and commissioners), had far-reaching consequences in the design of the reforms. For example, the initial separation of responsibility for commissioning primary care services from secondary and community services was deemed necessary because of the potential for conflicts of interest, whilst the creation of CCGs as ‘membership organisations’ had, as seen in Chapter 3, significant implications for their organisation and governance. The initial White Paper, ‘Equity and Excellence’ (Department of Health, 2010a: 9) was relatively non-specific about the expected benefits of clinical leadership of commissioning. It was argued that:
The headquarters of the NHS will not be in the Department of Health or the new NHS Commissioning Board but instead, power will be given to the front-line clinicians and patients. The headquarters will be in the consulting room and clinic. The Government will liberate the NHS from excessive bureaucratic and political control, and make it easier for professionals to do the right things for and with patients, to innovate and improve outcomes.
The document suggested that the proposals would: ‘liberate professionals and providers from top down control’; shift decision making closer to patients; enable better dialogue between primary and secondary care practitioners; and ensure that service development had real clinical involvement. However, the mechanisms underlying these perceived benefits were unstated. Furthermore, it was claimed that, whilst previous incarnations of GP-led commissioning (which in the UK go back to the creation of ‘GP fundholding’ in the 1990s) had delivered some benefits, these had been limited by the failure to give those involved complete autonomy and real budgets. The creation of CCGs, it was argued, would remedy these problems and ‘liberate’ clinicians to significantly improve care.
Despite significant needs, patients with chronic obstructive pulmonary disease (COPD) make limited use of palliative care, in part because the current models of palliative care do not address their key concerns.
Our aim was to develop a tailored model of palliative care for patients with COPD and their family caregivers.
Based on information gathered within a program of studies (qualitative research exploring experiences, a cohort study examining service use), an expert advisory committee evaluated and integrated data, developed responses, formulated principles to inform care, and made recommendations for practice. The informing studies were conducted in two Australian states: Victoria and South Australia.
A series of principles underpinning the model were developed, including that it must be: (1) focused on patient and caregiver; (2) equitable, enabling access to components of palliative care for a group with significant needs; (3) accessible; and (4) less resource-intensive than expansion of usual palliative care service delivery. The recommended conceptual model was to have the following features: (a) entry to palliative care occurs routinely triggered by clinical transitions in care; (b) care is embedded in routine ambulatory respiratory care, ensuring that it is regarded as “usual” care by patients and clinicians alike; (c) the tasks include screening for physical and psychological symptoms, social and community support, provision of information, and discussions around goals and preferences for care; and (d) transition to usual palliative care services is facilitated as the patient nears death.
Significance of results:
Our proposed innovative and conceptual model for provision of palliative care requires future formal testing using rigorous mixed-methods approaches to determine if theoretical propositions translate into effectiveness, feasibility, and benefits (including economic benefits). There is reason to consider adaptation of the model for the palliative care of patients with other nonmalignant conditions.
Epidemiological studies have identified increased colorectal cancer (CRC) risk with high red meat (HRM) intakes, whereas dietary fibre intake appears to be protective. In the present study, we examined whether a HRM diet increased rectal O6-methyl-2-deoxyguanosine (O6MeG) adduct levels in healthy human subjects, and whether butyrylated high-amylose maize starch (HAMSB) was protective. A group of twenty-three individuals consumed 300 g/d of cooked red meat without (HRM diet) or with 40 g/d of HAMSB (HRM+HAMSB diet) over 4-week periods separated by a 4-week washout in a randomised cross-over design. Stool and rectal biopsy samples were collected for biochemical, microbial and immunohistochemical analyses at baseline and at the end of each 4-week intervention period. The HRM diet increased rectal O6MeG adducts relative to its baseline by 21 % (P< 0·01), whereas the addition of HAMSB to the HRM diet prevented this increase. Epithelial proliferation increased with both the HRM (P< 0·001) and HRM+HAMSB (P< 0·05) diets when compared with their respective baseline levels, but was lower following the HRM+HAMSB diet compared with the HRM diet (P< 0·05). Relative to its baseline, the HRM+HAMSB diet increased the excretion of SCFA by over 20 % (P< 0·05) and increased the absolute abundances of the Clostridium coccoides group (P< 0·05), the Clostridiumleptum group (P< 0·05), Lactobacillus spp. (P< 0·01), Parabacteroides distasonis (P< 0·001) and Ruminococcus bromii (P< 0·05), but lowered Ruminococcus torques (P< 0·05) and the proportions of Ruminococcus gnavus, Ruminococcus torques and Escherichia coli (P< 0·01). HRM consumption could increase the risk of CRC through increased formation of colorectal epithelial O6MeG adducts. HAMSB consumption prevented red meat-induced adduct formation, which may be associated with increased stool SCFA levels and/or changes in the microbiota composition.
The beneficial effects of green tea catechins, such as the proposed improvement in endothelial function, may be influenced by phase II metabolism during and after absorption. The methylation enzyme, catechol-O-methyltransferase (COMT), has a missense mutation rs4680 (G to A), proposed to result in a 40 % reduction in enzyme activity. In the present pilot study, twenty subjects (ten of each homozygous COMT genotype) were recruited. Green tea extract capsules (836 mg green tea catechins) were given in a fasted state, and a high-carbohydrate breakfast was given after 60 min. Blood samples and vascular function measurements were taken at regular intervals. The change in digital volume pulse stiffness index (SI) from baseline was shown to be different between genotype groups at 120 and 240 min, with a lower SI in the GG individuals (P ≤ 0·044). The change in blood pressure from baseline also differed between genotype groups, with a greater increase in systolic (P = 0·023) and diastolic (P = 0·034) blood pressure at 120 min in the GG group. The AA group was shown to have a greater increase in insulin concentrations at 120 min (P = 0·019) and 180 min (P = 0·008) compared with baseline, despite similar glucose profiles. No genotypic differences were found in vascular reactivity measured using laser Doppler iontophoresis, total nitrite, lipids, plasma total antioxidant capacity or inflammatory markers after ingestion of the green tea extract. In conclusion, SI and insulin response to the glucose load differed between the COMT genotype groups, and this may be suggestive of a green tea extract and genotype interaction.
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