Infusion timing and sleep habits of adults receiving home parenteral and enteral nutrition: A patient-oriented survey study.

BACKGROUND: The emerging field of chrononutrition investigates the effects of the timing of nutritional intake on human physiology and disease pathology. It remains largely unknown when patients receiving home nutrition support routinely administer home parenteral nutrition (HPN) and/or home enteral nutrition (HEN). METHODS: The present descriptive study included data collected from a patient-oriented survey designed to assess the timing of infusions and sleep habits of patients receiving HPN and HEN in the United States. RESULTS: A total of 100 patients were included. Patients had a mean age of 44.1 years and 81% were female. Among 73 patients supported with HPN and 27 patients supported with HEN, 86% and 44% reported overnight infusions, respectively. The median start and end times of overnight infusions were 2100 (interquartile range [IQR] = 1900-2200) and 0800 (IQR = 0700-1000), respectively, for HPN and 2000 (IQR = 1845-2137) and 0845 (IQR = 0723-1000), respectively, for HEN. Overnight infusions started 2.0 h (IQR = 1.1-3.0) and 2.0 h (IQR = 0.6-3.3) before bedtime for HPN and HEN, respectively, and stopped 12.9 min (IQR = -21.3 to 29.1) and 30.0 min (IQR = -17.1 to 79.3) after wake time for HPN and HEN, respectively. Sleep disruption because of nutrition support or urination was most common among patients receiving infusions overnight compared with those receiving infusions continuously or during the daytime. CONCLUSIONS: Our survey study focusing on a novel and medically relevant dimension of nutrition found that most HPN-dependent and HEN-dependent patients receive infusions overnight while asleep. Our findings suggest that overnight infusions coinciding with sleep may result in sleep and circadian disruption.

Sleep patterns of patients receiving home parenteral nutrition: A home-based observational study.

BACKGROUND: Patients supported with home parenteral nutrition (HPN) often report poor sleep; however, limited research has been conducted to objectively measure sleep patterns of HPN-dependent patients. METHODS: We aimed to characterize the sleep patterns of patients receiving HPN through 7-day actigraphy in a home-based observational study. Sleep measures of clinical importance were derived from actigraphy, including sleep duration, sleep efficiency, sleep onset latency, and wake after sleep onset. Participants also completed validated sleep surveys. RESULTS: Twenty participants completed all study procedures (mean [SD]: age = 51.6 [13.9] years, body mass index = 21.4 [4.6], and 80% female). The population median (IQR) for sleep duration, sleep efficiency, sleep onset latency, and wake after sleep onset was 6.9 (1.1) h, 83.3% (7.8%), 11.8 (7.1) min, and 57.2 (39.9) min, respectively, and 55%, 60%, 35%, and 100% of participants did not meet the recommendations for these measures from the National Sleep Foundation. Sixty-five percent of participants reported napping at least once during the 7-day period. Based on the Insomnia Severity Index, 70% of participants were classified as having subthreshold or more severe insomnia. Based on the Pittsburgh Sleep Quality Index, 85% were classified as having significant sleep disturbance. CONCLUSION: Most HPN-dependent patients likely have disrupted sleep largely driven by difficulty maintaining sleep. The extent to which HPN contributed to poor sleep cannot be elucidated from this observational study. Addressing known factors that contribute to sleep disruption and considering sleep interventions may improve the overall quality of life of patients receiving HPN.

Acute sleep deprivation upregulates serotonin 2A receptors in the frontal cortex of mice via the immediate early gene Egr3.

Serotonin 2A receptors (5-HT2ARs) mediate the hallucinogenic effects of psychedelic drugs and are a key target of the leading class of medications used to treat psychotic disorders. These findings suggest that dysfunction of 5-HT2ARs may contribute to the symptoms of schizophrenia, a mental illness characterized by perceptual and cognitive disturbances. Indeed, numerous studies have found that 5-HT2ARs are reduced in the brains of individuals with schizophrenia. However, the mechanisms that regulate 5-HT2AR expression remain poorly understood. Here, we show that a physiologic environmental stimulus, sleep deprivation, significantly upregulates 5-HT2AR levels in the mouse frontal cortex in as little as 6-8 h (for mRNA and protein, respectively). This induction requires the activity-dependent immediate early gene transcription factor early growth response 3 (Egr3) as it does not occur in Egr3 deficient (-/-) mice. Using chromatin immunoprecipitation, we show that EGR3 protein binds to the promoter of Htr2a, the gene that encodes the 5-HT2AR, in the frontal cortex in vivo, and drives expression of in vitro reporter constructs via two EGR3 binding sites in the Htr2a promoter. These results suggest that EGR3 directly regulates Htr2a expression, and 5-HT2AR levels, in the frontal cortex in response to physiologic stimuli. Analysis of publicly available post-mortem gene expression data revealed that both EGR3 and HTR2A mRNA are reduced in the prefrontal cortex of schizophrenia patients compared to controls. Together these findings suggest a mechanism by which environmental stimuli alter levels of a brain receptor that may mediate the symptoms, and treatment, of mental illness.