Improving sleep health management in primary care: A potential role for community nurses?

AIMS: To explore community nurses sleep health practices and their perspectives on improving sleep health care provision. DESIGN: An exploratory study utilizing the qualitative description methodology. METHODS: Semi-structured interviews were conducted with community nurses from May 2019 - October 2021. Interviews were audio-recorded, transcribed, and subjected to an inductive thematic analysis using a constructivist-interpretive paradigm. RESULTS: Twenty-three Australian community nurses were interviewed. Participants frequently encountered sleep disturbances/disorders in their patients. Data analysis yielded three main themes: (1) Sleep health in the community serviced, (2) sleep health awareness and management, and (3) community nurses' A to Z of improving sleep health. The most common sleep disorder presentations were insomnia and sleep apnea. Although most community sleep apnea cases were appropriately managed, insomnia was often mismanaged. Participants described their sleep health knowledge as deficient, with the majority advocating for increased sleep-related education tailored to their profession. Other important factors needed for improving sleep health provision were standardized patient treatment/referral pathways, increased interprofessional collaboration, and sufficient time for patient consults. CONCLUSION: Community nurses service a patient population that requires increased sleep health care. However, they are currently underequipped to do so, leading to suboptimal treatment provision. Providing community nurses with the appropriate resources, such as increased sleep-related education and standardized treatment frameworks, could enable them to better manage sleep disturbance/disorder presentations, such as insomnia. IMPACT: Little is known about how community nurses care for patients with sleep disturbance/sleep disorders. This study found that contemporary sleep health care was lacking due to knowledge deficits, competing challenges, and a need for standardized care pathways. These findings can inform the development of targeted education/training and standardized guidelines for community nurses providing sleep health care to patients as well as the design of future practice models of care provision. PATIENT OR PUBLIC CONTRIBUTION: Previous research by authors has involved extensive engagement with patients and health professionals, such as community pharmacists, general practitioners, and naturopaths who play a role in sleep health in the primary health care sector. These previous research projects built a significant understanding of the patient and health practitioner experience and have provided the background to the concept and design of this study.

The Effect of Light Therapy on Electroencephalographic Sleep in Sleep and Circadian Rhythm Disorders: A Scoping Review.

Light therapy is used to treat sleep and circadian rhythm disorders, yet there are limited studies on whether light therapy impacts electroencephalographic (EEG) activity during sleep. Therefore, we aimed to provide an overview of research studies that examined the effects of light therapy on sleep macro- and micro-architecture in populations with sleep and circadian rhythm disorders. We searched for randomized controlled trials that used light therapy and included EEG sleep measures using MEDLINE, PubMed, CINAHL, PsycINFO and Cochrane Central Register of Controlled Trials databases. Five articles met the inclusion criteria of patients with either insomnia or delayed sleep−wake phase disorder (DSWPD). These trials reported sleep macro-architecture outcomes using EEG or polysomnography. Three insomnia trials showed no effect of the timing or intensity of light therapy on total sleep time, wake after sleep onset, sleep efficiency and sleep stage duration compared to controls. Only one insomnia trial reported significantly higher sleep efficiency after evening light therapy (>4000 lx between 21:00−23:00 h) compared with afternoon light therapy (>4000 lx between 15:00−17:00 h). In the only DSWPD trial, six multiple sleep latency tests were conducted across the day (09:00 and 19:00 h) and bright light (2500 lx) significantly lengthened sleep latency in the morning (09:00 and 11:00 h) compared to control light (300 lx). None of the five trials reported any sleep micro-architecture measures. Overall, there was limited research about the effect of light therapy on EEG sleep measures, and studies were confined to patients with insomnia and DSWPD only. More research is needed to better understand whether lighting interventions in clinical populations affect sleep macro- and micro-architecture and objective sleep timing and quality.

Safety of higher doses of melatonin in adults: A systematic review and meta-analysis.

Melatonin is commonly used for sleep and jetlag at low doses. However, there is less documentation on the safety of higher doses, which are being increasingly used for a wide variety of conditions, including more recently COVID-19 prevention and treatment. The aim of this review was to investigate the safety of higher doses of melatonin in adults. Medline, Scopus, Embase and PsycINFO databases from inception until December 2019 with convenience searches until October 2020. Randomised controlled trials investigating high-dose melatonin (≥10 mg) in human adults over 30 years of age were included. Two investigators independently abstracted articles using PRISMA guidelines. Risk of bias was assessed by a committee of three investigators. 79 studies were identified with a total of 3861 participants. Studies included a large range of medical conditions. The meta-analysis was pooled data using a random effects model. The outcomes examined were the number of adverse events (AEs), serious adverse events (SAEs) and withdrawals due to AEs. A total of 29 studies (37%) made no mention of the presence or absence of AEs. Overall, only four studies met the pre-specified low risk of bias criteria for meta-analysis. In that small subset, melatonin did not cause a detectable increase in SAEs (Rate Ratio = 0.88 [0.52, 1.50], p = .64) or withdrawals due to AEs (0.93 [0.24, 3.56], p = .92), but did appear to increase the risk of AEs such as drowsiness, headache and dizziness (1.40 [1.15, 1.69], p < .001). Overall, there has been limited AE reporting from high-dose melatonin studies. Based on this limited evidence, melatonin appears to have a good safety profile. Better safety reporting in future long-term trials is needed to confirm this as our confidence limits were very wide due to the paucity of suitable data.

The efficacy of combined bright light and melatonin therapies on sleep and circadian outcomes: A systematic review.

The aim of this systematic review was to investigate the effects of combined melatonin and bright light therapies on improved sleep and circadian outcomes. We conducted a systematic review that resulted in a total of eight papers meeting criteria. Four papers investigated the effectiveness of combined therapy in inducing a circadian phase shift on healthy participants. Combined therapy outperformed single light and melatonin therapies in phase advancing, but not in delaying, dim light melatonin onset (DLMO). The other four papers investigated the effect of combined therapy on sleep outcomes. Two of them were performed in elderly populations suffering from cognitive decline and two in delayed sleep-wake phase disorder (DSWPD) patients. While combined therapy was more beneficial than single therapy in elderly populations it did not show any benefit in DSWPD patients. The reported adverse effects of melatonin in elderly populations must be carefully considered. Future studies should investigate the separate and combined effect of melatonin and bright light on sleep and circadian outcomes in different target populations.

Feasibility of 3-month melatonin supplementation for brain oxidative stress and sleep in mild cognitive impairment: protocol for a randomised, placebo-controlled study.

INTRODUCTION: Melatonin has multiple proposed therapeutic benefits including antioxidant properties, synchronisation of the circadian system and lowering of blood pressure. In this protocol, we outline a randomised controlled trial to assess the feasibility, acceptability and tolerability of higher dose (25 mg) melatonin to target brain oxidative stress and sleep disturbance in older adults with mild cognitive impairment (MCI). METHODS AND ANALYSIS: The study design is a randomised double-blind, placebo-controlled, parallel group trial. Forty individuals with MCI will be recruited from the Healthy Brain Ageing Clinic, University of Sydney and from the community, and randomised to receive either 25 mg oral melatonin or placebo nightly for 12 weeks. The primary outcomes are feasibility of recruitment, acceptability of intervention and adherence to trial medication at 12 weeks. Secondary outcomes will include the effect of melatonin on brain oxidative stress as measured by magnetic resonance spectroscopy, blood pressure, blood biomarkers, mood, cognition and sleep. Outcomes will be collected at 6 and 12 weeks. The results of this feasibility trial will inform a future conclusive randomised controlled trial to specifically test the efficacy of melatonin on modifiable risk factors of dementia, as well as cognition and brain function. This will be the first trial to investigate the effect of melatonin in the population with MCI in this way, with the future aim of using this approach to reduce progression to dementia. ETHICS AND DISSEMINATION: This protocol has been approved by the Sydney Local Health District Ethics Committee (X18-0077). This randomised controlled trial will be conducted in compliance with the protocol published in the registry, the International Conference for Harmonisation on Good Clinical Practice and all other applicable regulatory requirements. The findings of the trial will be disseminated via conferences, publications and media, as applicable. Participants will be informed of results of the study at the conclusion of the trial. Eligible authors will include investigators who are involved in the conception and design of the study, the conduct of the trial, the analysis of the results, and reporting and presentation of study findings. TRIAL REGISTRATION NUMBER: Australian and New Zealand Clinical Trials Registry (ANZCTRN 12619000876190). PROTOCOL VERSION: V.8 15 October 2020.

Case report of sudden death in a twin infant given melatonin supplementation: A challenging interpretation of postmortem toxicology.

Melatonin (MEL) is a neurohormone in humans produced in a number of locations. Starting with the amino acid tryptophan, MEL is produced through a number of enzymatic steps that includes serotonin as an intermediate compound. The primary production of MEL is in the pineal gland located in the brain. It is directly associated with the the suprachiasmatic nucleus (SCN) located in the hypothalamus. In young and adult humans, the blood levels of MEL are typically in the picogram levels and produced in a cyclic schedule highly regulated by light detected in the retina by intrinsically photosensitive retinal ganglion cells (ipRGCs), resulting in production primarily during periods of darkness. During periods of light, MEL levels are typically very low or undetectable. Basal levels of MEL in infants have been observed to be either undetectable or also in the picogram levels, although some medical treatment has involved administration of exogenous MEL resulting in peak levels in the nanogram range. MEL is considered to be well tolerated and there have been limited reports of toxicity. In this case, an infant was found unresponsive and cause of death was ruled as Undetermined. Melatonin was detected in the peripheral blood at a concentration of 1,400ng/mL.

The efficacy of biofeedback for the treatment of insomnia: a critical review.

BACKGROUND: The popularity of biofeedback as a non-pharmacological treatment option for insomnia has increased in recent times despite inconsistent empirical evidence for its therapeutic efficacy. OBJECTIVE: The purpose of the current review was to systematically assess the efficacy of using biofeedback to treat insomnia. METHODS AND RESULTS: A search of electronic databases (PubMED, MEDLINE, OvidSP, Ovid EMBASE, PsychInfo, The Cochrane Library including Cochrane Reviews), clinical trials databases and registries (Clinical Trials Database [US], Australian New Zealand Clinical Trials Registry [ANZCTR]) and online journal (eg, SLEEP, Sleep Medicine) identified 92 studies. Of these, 50 publications were descriptive or review papers about use of biofeedback for the treatment of insomnia, while an additional 37 did not meet the detailed inclusion criteria (ie not original research, participants do not meet the diagnostic criteria for insomnia). Six full-text articles met inclusion criteria and were included in this review. Methodological flaws including poor study design (small sample size, lack of control group) limit the validity of the body of work in this field to date and fail adequately to account for other unspecified factors likely to drive the observed changes, such as care and attention of those administering the treatment, as well as the expectations and motivations of the patient. CONCLUSION: There is an urgent need for future studies to clarify the role of unspecific placebo effects when reporting biofeedback effects for the treatment of insomnia.

Energy reallocation to breeding performance through improved nest building in laboratory mice.

Mice are housed at temperatures (20-26 °C) that increase their basal metabolic rates and impose high energy demands to maintain core temperatures. Therefore, energy must be reallocated from other biological processes to increase heat production to offset heat loss. Supplying laboratory mice with nesting material may provide sufficient insulation to reduce heat loss and improve both feed conversion and breeding performance. Naïve C57BL/6, BALB/c, and CD-1 breeding pairs were provided with bedding alone, or bedding supplemented with either 8 g of Enviro-Dri, 8 g of Nestlets, for 6 months. Mice provided with either nesting material built more dome-like nests than controls. Nesting material improved feed efficiency per pup weaned as well as pup weaning weight. The breeding index (pups weaned/dam/week) was higher when either nesting material was provided. Thus, the sparing of energy for thermoregulation of mice given additional nesting material may have been responsible for the improved breeding and growth of offspring.

Thermoregulatory, behavioral, and metabolic responses to heatstroke in a conscious mouse model.

The typical core temperature (T(c)) profile displayed during heatstroke (HS) recovery consists of initial hypothermia followed by delayed hyperthermia. Anecdotal observations led to the conclusion that these T(c) responses represent thermoregulatory dysfunction as a result of brain damage. We hypothesized that these T(c) responses are mediated by a change in the temperature setpoint. T(c) (+/- 0.1 degrees C; radiotelemetry) of male C57BL/6J mice was monitored while they were housed in a temperature gradient with ambient temperature (T(a)) range of 20-39 degrees C to monitor behaviorally selected T(a) (T(s)) or an indirect calorimeter (T(a) = 25 degrees C) to monitor metabolism (V(O(2))) and calculate respiratory exchange ratio (RER). Responses to mild and severe HS (thermal area 249.6 +/- 18.9 vs. 299.4 +/- 19.3 degrees C.min, respectively) were examined through 48 h of recovery. An initial hypothermia following mild HS was associated with warm T(s) (approximately 32 degrees C), approximately 35% V(O(2)) decrease, and RER approximately 0.71 that indicated reliance on fatty acid oxidation. After 24 h, mild HS mice developed hyperthermia associated with warm T(s) (approximately 32 degrees C), approximately 20% V(O(2)) increase, and RER approximately 0.85. Severe HS mice appeared poikilothermic-like in the temperature gradient with T(c) similar to T(s) (approximately 20 degrees C), and these mice failed to recover from hypothermia and develop delayed hyperthermia. Cellular damage (hematoxylin and eosin staining) was undetectable in the hypothalamus or other brain regions in severe HS mice. Overall, decreases and increases in T(c) were associated with behavioral and autonomic thermoeffectors that suggest HS elicits anapyrexia and fever, respectively. Taken together, T(c) responses of mild and severe HS mice suggest a need for reinterpretation of the mechanisms of thermoregulatory control during recovery.

A multianalyte profile of serum proteins to screen for toxicological effects of anticholinesterase insecticides in the rat.

The development of high throughput biochemical screens could be useful to assess the broad spectrum of physiological effects of environmental toxicants. To explore the prospect of using a screen in an in vivo exposure scenario, we applied a commercially available multianalyte profile (MAP) of 58 serum biomarkers to rats exposed acutely to two anticholinesterase insecticides, chlorpyrifos (CHP) and carbaryl (CAR). Male, Long-Evans rats were dosed orally with 30 mg/kg CHP, 75 mg/kg CAR or the corn oil vehicle. Doses were selected based on their equivalent physiological effects (hypothermia and reduced motor activity). The animals were terminated 24h or 7 days after dosing. Serum was collected and analyzed for 58 biomarkers consisting primarily of cytokines, chemokines, and a few hormones. There were changes in six analytes (four up, two down) following CHP and eight analytes (five up, three down) following CAR at 24h. There were significant changes in only two biomarkers when measured 7 days after dosing with CHP. Overall, the MAP detected a broad spectrum of unique effects for CHP and CAR. It is concluded that the MAP is a useful tool to screen for in vivo effects of environmental toxicants and its use could lead to the discovery of novel mechanisms of action.