2021 Assessment of New Zealand district health boards' institutional healthy food and drink policies: the HealthY Policy Evaluation (HYPE) study.

AIM: To assess adoption of the voluntary National Healthy Food and Drink Policy (NHFDP) and the alignment of individual institutional healthy food and drink policies with the NHFDP. METHOD: All 20 district health boards (DHBs) and two national government agencies participated. Policies of those organisations that had not fully adopted the NHFDP were assessed across three domains: nutrition standards; promotion of a healthy food and beverages environment; and policy communication, implementation and evaluation. Three weighted domain scores out of 10, and a total score out of 30 were calculated. RESULTS: Nine of the 22 organisations reported adopting the NHFDP in full. Of the remaining 13, six referred to the NHFDP when developing their institutional policy and three were working toward full adoption of the NHFDP. Mean scores (SD) were 8.7 (1.0), 6.1 (2.6) and 3.8 (2.2) for the three domains, and 18.6 (4.8) in total. Most individual institutional policies were not as comprehensive as the NHFDP. However, some contained stricter/additional clauses that would be useful to incorporate into the NHFDP. CONCLUSION: Since a similar policy analysis in 2018, most DHBs have adopted the NHFDP and/or strengthened their own nutrition policies. Regional inconsistency remains and a uniform mandatory NHFDP should be implemented that incorporates improvements identified in individual institutional policies.

Central sensitisation in chronic fatigue syndrome and fibromyalgia; a case control study.

INTRODUCTION: Chronic fatigue syndrome (CFS) and fibromyalgia (FM) are both complex conditions that are challenging to treat. This may be related to an incomplete understanding of their pathophysiology, itself obfuscated by their heterogeneity. The symptomatic overlap between them and their common comorbidity suggests a shared vulnerability, which might be explained by central sensitisation. METHODS: 19 CFS cases, 19 FM cases and 20 age and sex matched healthy controls (HC) were recruited primarily from secondary care clinics in London. Those with other pain disorders, psychiatric diagnoses and those taking centrally acting or opiate medications were excluded. Participants were asked to abstain from alcohol and over the counter analgaesia 48 h prior to assessment by static and dynamic quantitative sensory tests, including measures of temporal summation (TS) and conditioned pain modulation (CPM). RESULTS: CS, as defined by the presence of both enhanced TS and inefficient CPM, was present in 16 (84%) CFS cases, 18 (95%) FM cases, and none of the HC (p < 0.001). Pressure pain thresholds were lower in CFS (Median222kPaIQR 146-311; p = 0.04) and FM cases (Median 189 kPa; IQR 129-272; p = 0.003) compared to HC (Median 311 kPa; IQR 245-377). FM cases differed from HC in cold-induced (FM = 22.6 °C (15.3-27.7) vs HC = 14.2 °C (9.0-20.5); p = 0.01) and heat-induced (FM = 38.0 °C (35.2-44.0) vs HC = 45.3 °C (40.1-46.8); p = 0.03) pain thresholds, where CFS cases did not. CONCLUSION: Central sensitisation may be a common endophenotype in chronic fatigue syndrome and fibromyalgia. Further research should address whether central sensitisation is a cause or effect of these disorders.

The Scottish police caution: do individuals with intellectual disabilities understand a verbally presented police caution, and can comprehension be improved?

This study considers comprehension of the Scottish police caution amongst people with an intellectual disability (n = 30). It applies techniques to the caution that are suggested to increase its 'listenability', to examine whether this could be a successful method of improving understanding. These techniques include providing instructions, further explanations and listing information. Half of the participants were assessed using the original version and half the modified version. Participants were assessed using an abbreviated IQ assessment, a measure of working memory and measure of state anxiety to consider potential predictors of performance. The modified version did not improve performance, with no participants judged to have adequate understanding in either version.

Cost and greenhouse gas emissions of current, healthy, flexitarian and vegan diets in Aotearoa (New Zealand).

OBJECTIVE: To compare the costs and climate impact (greenhouse gas emissions) associated with current and healthy diets and two healthy and environmentally friendly dietary patterns: flexitarian and vegan. DESIGN: Modelling study. SETTING: Aotearoa (New Zealand). MAIN OUTCOME MEASURES: The distribution of the cost and climate impact (kgCO2e/kg of food per fortnight) of 2 weekly current, healthy, vegan and flexitarian household diets was modelled using a list of commonly consumed foods, a set of quantity/serves constraints for each, and constraints for food group and nutrient intakes based on dietary guidelines (Eating and Activity Guidelines for healthy diets and EAT-Lancet reference diet for vegan and flexitarian diets) or nutrition survey data (current diets). RESULTS: The iterative creation of 210-237 household dietary intakes for each dietary scenario was achieved using computer software adapted for the purpose (DIETCOST). There were stepwise differences between diet scenarios (p<0.001) with the current diet having the lowest mean cost in New Zealand Dollars (NZ$584 (95% CI NZ$580 to NZ$588)) per fortnight for a family of four) but highest mean climate impact (597 kgCO2e (95% CI 590 to 604 kgCO2e)), followed by the healthy diet (NZ$637 (95% CI NZ$632 to NZ$642), 452 kgCO2e (95% CI 446 to 458 kgCO2e)), the flexitarian diet (NZ$728 (95% CI NZ$723 to NZ$734), 263 kgCO2e (95% CI 261 to 265 kgCO2e)) and the vegan diet, which had the highest mean cost and lowest mean climate impact (NZ$789, (95% CI NZ$784 to NZ$794), 203 kgCO2e (95% CI 201 to 204 kgCO2e)). There was a negative relationship between cost and climate impact across diets and a positive relationship within diets. CONCLUSIONS: Moving from current diets towards sustainable healthy diets (SHDs) will reduce climate impact but generally at a higher cost to households. The results reflect trade-offs, with the larger constraints placed on diets, the greater cost and factors such as nutritional adequacy, variety, cost and low-emissions foods being considered. Further monitoring and policies are needed to support population transitions that are country specific from current diets to SHD.

The effect of surfactant on the dissolution of porcine pulpal tissue by sodium hypochlorite solutions.

INTRODUCTION: A previous study of the relative dental pulp-dissolving abilities of Milton brand of sodium hypochlorite (NaOCl) and other surfactant-containing NaOCl solutions produced specifically for endodontic treatment showed a markedly better performance of the surfactant-containing product that was not explained by differences in active chlorine content. This study investigated whether the presence of surfactant in the NaOCl solutions was responsible for the difference in dissolution times seen in the previous study. METHODS: Circular samples 2.5 mm in diameter were punched out of the pulps of mandibular incisor teeth from young pigs. The 4 NaOCl solutions tested were Hypochlor 1% and Hypochlor 4% forte, which contained surfactant, and 2 identical solutions without surfactant. Twenty pulp specimens were immersed in 20 individual 25-mL aliquots of each of the 4 NaOCl solutions and observed while stirring until dissolution was complete. The time to dissolution of each sample was determined by stopwatch. Dissolution times for each solution were averaged and compared statistically in R (version 2.12.0) by using multiple regression with nominal active chlorine content as a covariate. RESULTS: No statistical difference was detected between the dissolution times for either of the Hypochlor solutions with and without surfactant. CONCLUSIONS: The addition of surfactant alone does not appear to improve the abilities of NaOCl to dissolve dental pulp tissue.

Arthritis and pain. Current approaches in the treatment of arthritic pain.

Current evidence suggests that although persistent arthritic pain is initiated and maintained by articular pathology, it is also heavily influenced by a range of other factors. Strategies for treating arthritic pain are therefore different from those adopted for acute pain. Although published guidelines offer general assistance, the complexity of underlying mechanisms requires that measures designed to relieve pain must take into account individual biological, psychological and societal factors. It follows that a combination of both pharmacological and non-pharmacological approaches offers the best opportunity for therapeutic success, although determining the effectiveness of such complex interventions remains difficult. Pharmacological therapy is often prolonged, and safety and tolerability issues become as important as efficacy over time.

The differential contribution of tumour necrosis factor to thermal and mechanical hyperalgesia during chronic inflammation.

Therapies directed against tumour necrosis factor (TNF) are effective for the treatment of rheumatoid arthritis and reduce pain scores in this condition. In this study, we sought to explore mechanisms by which TNF contributes to inflammatory pain in an experimental model of arthritis. The effects of an anti-TNF agent, etanercept, on behavioural pain responses arising from rat monoarthritis induced by complete Freund's adjuvant were assessed and compared with expression of TNF receptors (TNFRs) by dorsal root ganglion (DRG) cells at corresponding time points. Etanercept had no effect on evoked pain responses in normal animals but exerted a differential effect on the thermal and mechanical hyperalgesia associated with rat arthritis induced by complete Freund's adjuvant (CFA). Joint inflammation was associated with increased TNFR1 and TNFR2 expression on DRG cells, which was maintained throughout the time course of the model. TNFR1 expression was increased in neuronal cells of the DRG bilaterally after arthritis induction. In contrast, TNFR2 expression occurred exclusively on non-neuronal cells of the macrophage-monocyte lineage, with cell numbers increasing in a TNF-dependent fashion during CFA-induced arthritis. A strong correlation was observed between numbers of macrophages and the development of mechanical hyperalgesia in CFA-induced arthritis. These results highlight the potential for TNF to play a vital role in inflammatory hyperalgesia, both by a direct action on neurons via TNFR1 and by facilitating the accumulation of macrophages in the DRG via a TNFR2-mediated pathway.

Chronic upper limb pain: an exploration of the biopsychosocial model.

OBJECTIVE: To model pain intensity and consequent disability by independent physical, psychological, and social variables in a group of patients with chronic upper limb pain. METHODS: We studied a group of 73 hospital outpatients with either chronic work related diffuse upper limb pain or carpal tunnel syndrome. We assessed pain intensity, disability, and personality by self-rated questionnaires; and psychiatric morbidity by a standardized interview. We measured illness behavior by assessing coping strategies, illness beliefs, financial benefits, and movements of the most affected limb. RESULTS: In both pain conditions, disability was positively correlated with present pain intensity, depression, helpless coping style, and receipt of state financial benefits; and was negatively correlated with age. This explained 43% of the variance and correctly classified 85% of all patients. Present pain intensity was positively correlated with both depression and the number of arm movements at night. This model explained 15% of the variance and correctly classified 75% of all patients. Inclusion of diagnostic group has no effect on these models. CONCLUSION: The correlations between disability and pain intensity with both psychosocial and physical factors support the biopsychosocial model of disability in particular, and pain to a lesser extent, irrespective of the diagnosis.

Pain related behaviour in two models of osteoarthritis in the rat knee.

Osteoarthritis (OA) is a major healthcare burden, with increasing incidence. Pain is the predominant clinical feature, yet therapy is ineffective for many patients. While there are considerable insights into the mechanisms underlying tissue remodelling, there is poor understanding of the link between disease pathology and pain. This is in part owing to the lack of animal models that combine both osteoarthritic tissue remodelling and pain. Here, we provide an analysis of pain related behaviours in two models of OA in the rat: partial medial meniscectomy and iodoacetate injection. Histological studies demonstrated that in both models, progressive osteoarthritic joint pathology developed over the course of the next 28 days. In the ipsilateral hind limb in both models, changes in the percentage bodyweight borne were small, whereas marked mechanical hyperalgesia and tactile allodynia were seen. The responses in the iodoacetate treated animals were generally more robust, and these animals were tested for pharmacological reversal of pain related behaviour. Morphine was able to attenuate hyperalgesia 3, 14 and 28 days after OA induction, and reversed allodynia at days 14 and 28, providing evidence that this behaviour was pain related. Diclofenac and paracetamol were effective 3 days after arthritic induction only, coinciding with a measurable swelling of the knee. Gabapentin varied in its ability to reverse both hyperalgesia and allodynia. The iodoacetate model provides a basis for studies on the mechanisms of pain in OA, and for development of novel therapeutic analgesics.

The role of inflammatory mediators on nociception and pain in arthritis.

Pain is the most common complaint of individuals with osteoarthritis but the cause of symptoms in this disorder remains unclear. Quantitative sensory testing reveals that in patients with chronic joint disease there is diffuse and persistent alteration of nociceptive (pain) pathways, irrespective of the level of activity of the underlying disease. Inflammatory mediators contribute to this plasticity either by directly activating high threshold receptors or more commonly by sensitizing nociceptive neurons to subsequent everyday stimuli. This involves early post-translational modification of receptors/ion channels and later, longer-lasting transcription-dependent mechanisms involving changes to the chemical phenotype of the neuron. Included amongst these changes are the increased production and release of various pro- and anti-inflammatory neuropeptides which have diverse actions on both circulating and resident cell populations. These neurally derived mediators act synergistically with cytokines and growth factors to contribute to ongoing tissue injury. It is becoming apparent that the interaction between a damaged joint and the sensory nervous system is far from straightforward and that activity arising from such interactions may produce not only pain but may also influence the subsequent course of the underlying disease.

Inhibition of inflammation and hyperalgesia in NK-1 receptor knock-out mice.

We sought to characterise the contribution of the neuropeptide substance P to the outcome of two models of footpad inflammation of differing severity. In an intense inflammatory model produced by intra-plantar Mycobacterium tuberculosus (10 mg/ml) substantial reductions in footpad swelling, histological outcome and mechanical hyperalgesia were observed from early time points in mice lacking the neurokin-1 receptor for substance P compared with wild-type controls. Conversely, in a less intense model (M. tuberculosus 1 mg/ml) no differences were observed other than for a reduction in mechanical hyperalgesia at later time points (day 9 onwards). The results point to a previously unrecognised influence of substance P on peripheral tissue injury and the maintenance of hyperalgesia during more severe or more chronic phases of inflammatory disease.

Enhancement of angiogenesis by endogenous substance P release and neurokinin-1 receptors during neurogenic inflammation.

Early angiogenesis is a key step in the transition from acute to persistent inflammation. The nervous system has long been known to play a role in inflammation, in part through the release of substance P from peripheral nerve terminals (neurogenic inflammation). Application of substance P can stimulate vessel growth in a variety of angiogenesis assays, although it was previously not known whether endogenous substance P released from sensory nerves could modulate angiogenesis. We hypothesized that endogenous substance P can initiate angiogenesis during acute neurogenic inflammation. Here we show that 10 nmol of substance P can stimulate angiogenesis within the rat knee synovium, as shown by increased endothelial cell proliferation index [PCNA index, 19% (95% confidence interval (CI), 17 to 20%)] compared with saline injected knees [6% (95% CI, 4% to 8%), p < 0.05]. Moreover, this was prevented by coadministration of an antagonist of the neurokinin-1 (NK1) subtype of neurokinin receptor SR140333 (nolpitantium), 1 micro mol [8% (95% CI, 5% to 11%)]. Capsaicin 0.5%, which stimulates release of endogenous substance P from sensory nerves, was also found to enhance synovial angiogenesis, [PCNA index 17% (95% CI, 14% to 19%)] compared with saline injected control knees [2% (95% CI, 1% to 3%), p < 0.05], and this also was inhibited by 1 micro mol of SR140333 [11% (95% CI, 8 to 16%)]. Inhibition of capsaicin-enhanced angiogenesis was incomplete, and this may indicate a contribution of other neuropeptides, in addition to substance P-NK1 receptor interactions, in capsaicin-enhanced angiogenesis. NK1 receptor antagonists could have therapeutic potential in conditions where neurogenic angiogenesis contributes to disease.

Illness behavior and psychosocial factors in diffuse upper limb pain disorder: a case-control study.

OBJECTIVE: To compare behavioral and other psychosocial factors in patients with diffuse upper limb pain disorder (ULPD) and patients with carpal tunnel syndrome (CTS). METHODS: We compared 37 hospital outpatients with diffuse ULPD with 36 hospital outpatients with CTS, matched by sex, pain intensity, and duration of illness. We assessed psychiatric morbidity by a standardized interview, and both symptoms and personality by self-rated questionnaires. We measured illness behavior by assessing financial benefits and compensation, coping strategies, illness beliefs, treatments received, and 24 hours of monitoring movements of the most affected arm and the body as a whole. RESULTS: There were no significant differences in the prevalence of either current or premorbid psychiatric disorders, personality scores, symptom amplification, disability, or treatments received. Subjects with ULPD had significantly lower self-rated scores for depression, somatic distress, sleep disturbance, and physical fatigue than subjects with CTS, although there were more than normal levels of anxiety, fatigue, and sleep disturbance in both groups. There were no significant differences in the numbers of arm or body movements by day and night. Significantly more ULPD subjects had been involved in litigation, but litigating patients were a minority. CONCLUSION: The primary etiology of endemic diffuse ULPD, presenting in secondary care, is no more psychiatric, psychological, behavioral, or related to personality than is the case with a similarly chronic and painful condition of known pathology. We cannot exclude either a specific role for psychosocial factors at work, or a more general role for psychosocial factors in maintaining disability in patients with chronic pain.

Disease modifying and anti-nociceptive effects of the bisphosphonate, zoledronic acid in a model of bone cancer pain.

Inoculation of syngeneic MRMT-1 mammary tumour cells into one tibia of female rats produced tumour growth within the bone associated with a reduction in bone mineral density (BMD) and bone mineral content (BMC), severe radiological signs of bone destruction, together with the development of behavioural mechanical allodynia and hyperalgesia. Histological and radiological examination showed that chronic treatment with the bisphosphonate, zoledronic acid (30 microg/kg, s.c.), for 19 days significantly inhibited tumour proliferation and preserved the cortical and trabecular bone structure. In addition, BMD and BMC were preserved and a dramatic reduction of tartrate resistant acid phosphatase-positive polykaryocytes (osteoclasts) was observed. In behavioural tests, chronic treatment with zoledronic acid but not the significantly less effective bisphosphonate, pamidronate, or the selective COX-2 inhibitor, celebrex, attenuated mechanical allodynia and hyperalgesia in the affected hind paw. Zoledronic acid also attenuated mechanical hyperalgesia associated with chronic peripheral neuropathy and inflammation in the rat. In contrast, pamidronate or clodronate did not have any anti-hyperalgesic effect on mechanical hyperalgesia in the neuropathic and inflammatory pain models. We conclude that zoledronic acid, in addition to, or independent from, its anti-metastatic and bone preserving therapeutic effects, is an anti-nociceptive agent in a rat model of metastatic cancer pain. This unique property of zoledronic acid amongst the bisphosphonate class of compounds could make this drug a preferred choice for the treatment of painful bone metastases in the clinic.

How does neuropathophysiology affect the signs and symptoms of spinal disease?

A complex relationship exists between back pain and the presence of spinal disease. Particularly in chronic situations, back pain and its behavioural and emotional consequences are as likely to reflect the influence of psychosocial factors as any underlying spinal pathology. Nevertheless, physical factors are clearly important and it is significant that whereas in normal discs only the outer third of the annulus fibrosus is innervated, a much more extensive innervation develops in the presence of degeneration. Inflammation, as evidenced by leukocyte infiltration and expression of inflammatory mediators, is associated with disc degeneration and serves to alter the neural responses resulting in local and referred pain. It is probable that similar inflammatory processes, as well as direct root compression, contribute to radicular symptoms following disc herniation. An appreciation of these mechanisms encourages the search for novel treatments and permits a more rational and effective use of existing strategies for relieving pain.

Oral anti-hyperalgesic and anti-inflammatory activity of NK(1) receptor antagonists in models of inflammatory hyperalgesia of the guinea-pig.

The oral analgesic and anti-inflammatory activity of NK(1) antagonists with species preference for the human receptor were assessed in (1) the carrageenan-induced inflammatory hyperalgesia and (2) Freund's complete adjuvant (FCA)-induced extravasation in the knee joint models of the guinea-pig, respectively. Mechanical hyperalgesia was determined by measuring the withdrawal threshold to a noxious mechanical stimulus applied to the paw and thermal hyperalgesia as the withdrawal latency to a noxious thermal stimulus applied to the plantar surface. A concentration of 1.0% carrageenan (intraplantar) reduced mechanical thresholds from 124+/-5 to 63+/-3 g and thermal latencies from 19+/-0.4 to 4.7+/-0.9 s as determined 4 h after injection. The hyperalgesia persisted for over 24 h. The NK(1) receptor antagonists, SDZ NKT 343, RPR100893 and SR140333, reduced mechanical hyperalgesia by 68, 36 and 27% at a dose of 30 mg kg(-1) p.o., respectively. No further reduction was noted at higher doses (maximum 100 mg kg(-1) p.o.). The anti-hyperalgesic effect of SDZ NKT 343 and RPR100893 peaked at 3 h while SR140333 produced maximal reversal at 1 h after oral administration. D(30) values indicated significant differences between the potency of these compounds. SDZ NKT 343 was by far the most potent anti-hyperalgesic agent (D(30): 1.1 mg kg(-1)). The D(30) values for RPR100893 and SR140333 were estimated to be 17 and >100 mg kg(-1), respectively. In thermal hyperalgesia, SDZ NKT 343 produced a significantly weaker anti-hyperalgesic effect with a peak of 25% reversal. The D(30) value for SDZ NKT 343 was 3.89 mg kg(-1). For comparison, morphine inhibited the carrageenan-induced mechanical and thermal hyperalgesia with an ED(50) of 1.85 and 2.51 mg kg(-1) s.c., respectively. When tested up to 300 mg kg(-1) p.o., aspirin reduced carrageenan-induced mechanical and thermal hyperalgesia by 55.0 and 45.2%, respectively. In addition to the anti-hyperalgesic effects of NK(1) receptor antagonists, the effects of SDZ NKT 343 and RPR100893 on plasma protein extravasation were measured in the FCA-treated knee joint of the guinea-pig. SDZ NKT 343 reversed plasma protein extravasation 2 h after administration by 60% at the oral dose of 30 mg kg(-1). RPR100893 was significantly less effective with a maximum reversal of 30% at 100 mg kg(-1). In comparison, indomethacin produced a 50% reversal at a 10 mg kg(-1) dose. These experiments indicate that the carrageenan-induced hyperalgesia in the guinea-pig may be predictive of analgesic activity of NK(1) receptor antagonists in man. NK(1) receptor antagonists are active anti-hyperalgesic drugs in both mechanical and thermal hyperalgesia in the guinea-pig. In addition they inhibit plasma protein extravasation in the same species. The variability of in vivo potency and efficacy of the NK(1) receptor antagonists in the mechanical hyperalgesia model is difficult to interpret as all compounds are highly effective at blocking the NK(1) receptor in guinea-pig tissues. Amongst several possibilities, differences in pharmacokinetics may explain discrepancies.