Efficacy of Poria Cocos Extract on Sleep Quality Enhancement: A Clinical Perspective with Implications for Functional Foods.

BACKGROUND: Since the outbreak of the pandemic started, an increase in the number of sleep disorders, including insomnia and poor sleep quality, has been seen. The pattern will probably continue. METHODS: This study focuses on the preparation and clinical testing of Poria cocos extract in treating suboptimal sleep quality. The optimal extraction method utilized a 75% ethanol concentration, and the clinical investigation involved subjects with defined poor sleep taking 800 mg of the extract nightly, assessed using the Sleep Questionnaire and polysomnography. The non-parametric Wilcoxon signed-rank test was used for statistical analysis due to the non-normal distribution of the collected data. RESULTS: The study involved 21 insomnia sufferers with a mean age of 55 who were administered Poria cocos extracts. The findings of the study indicate a statistically significant rise in the overall duration of sleep (from 327.395 ± 43.2 min to 356.516 ± 63.21 min, p = 0.014). Additionally, there was a notable decrease in the level of arousal during sleep (from 76.316 ± 44.78 min to 47.989 ± 42.38 min, p = 0.009), and an improvement in the sleep severity index of the sleep questionnaire test. CONCLUSIONS: Poria cocos as a natural substance could improve quality of sleep, based on the findings. The study investigates Pachymic acid, a substance found in Poria cocos, as a potential indicator for the development of sleeping aids.

The Positive Effects of Poria cocos Extract on Quality of Sleep in Insomnia Rat Models.

Sleep disorders may have various causes and can incur mental and/or physical symptoms, and affect an individual's quality of life. In this study, we confirm that the Poria cocos extract (PCET) can improve sleep quality and structure by promoting inhibitory neurotransmission via the γ-aminobutyric acid (GABA) type A (GABAA) receptors based on the mechanisms revealed in the experiment with superior cervical ganglion neurons. Pentobarbital-induced sleep tests were conducted in order to determine whether the PCET extract improves the sleep quality and structure in normal ICR mice. Sleep latency and duration were checked with the righting reflex. To simulate the state of awakening as well as a normal sleep state, caffeine was administered orally before the PCET diet. After oral gavage of PCET, sleep latency was decreased, and total sleep duration was increased in normal and caffeine-induced sleep disturbance state. In the ACTH-induced sleep disturbed models, administration of PCET significantly reduced the sleep latency and increased the non-REM sleep duration, which was analyzed in real-time EEG by implanting wireless electrodes in SD rats. PCET was found to improve the sleep quality under a normal sleep state through the GABAA receptor; it also promoted and improved the sleep quality and sleep structure in both the arousal activation state and stress-based sleep disturbance.

Effect of Forest Therapy for Menopausal Women with Insomnia.

Female hormone changes during menopause can affect the autonomic nervous system, circadian rhythm, and secretion of cortisol/melatonin, resulting in a vulnerability to insomnia. In this light, therapy has been gaining attention as a way to reduce stress hormones by stabilizing the autonomic nervous system. Thus, this study aims to objectively and scientifically analyze the impact of forest therapy in postmenopausal insomnia patients. The forest therapy program lasted 6 days, wherein 35 postmenopausal women performed activities such as trekking, leg massages, stretches, and bathing in warm and cold water. They also underwent serologic tests, participated in polysomnography (PSG), and answered sleep questionnaires before and after the program. Further, a statistical analysis compared the results. Serologic tests showed a significant reduction of cortisol from 10.2 ± 3.79 to 7.75 ± 2.81, while PSGs showed how sleep efficiency increased to 89.3 ± 4.3% (p < 0.01), and how waking after sleep onset reduced to 47.4 ± 22.3 min (p < 0.01). The total sleep time also increased to 428.5 min and sleep latency was 11.1 ± 11.0 min. Despite its limitations, forest therapy could be a good alternative to nonpharmacological treatment for mitigating insomnia in postmenopausal women.

An Exploratory Study on the Effects of Forest Therapy on Sleep Quality in Patients with Gastrointestinal Tract Cancers.

The improvement of sleep quality in patients with cancer has a positive therapeutic effect on them. However, there are no specific treatment guidelines for treating sleep disturbance in cancer patients. We investigated the effect of forest therapy on the quality of sleep in patients with cancer. This study was conducted on nine patients (one male, eight female; mean age, 53.6 ± 5.8 years) with gastrointestinal tract cancer. All patients participated in forest therapy for six days. They underwent polysomnography (PSG) and answered questionnaires on sleep apnea (STOP BANG), subjective sleep quality (Pittsburgh Sleep Quality Index, PSQI), sleepiness (Stanford and Epworth Sleepiness Scales), and anxiety and depression (Hospital Anxiety and Depression Scale) to evaluate the quality of sleep before and after forest therapy. Sleep efficiency from the PSG results was shown to have increased from 79.6 ± 6.8% before forest therapy to 88.8 ± 4.9% after forest therapy (p = 0.027) in those patients, and total sleep time was also increased, from 367.2 ± 33.4 min to 398 ± 33.8 min (p = 0.020). There was no significant difference in the STOP BANG score, PSQI scores, daytime sleepiness based on the results of the Stanford and Epworth Sleepiness Scales, and depression and anxiety scores. Based on the results of this study, we suggest that forest therapy may be helpful in improving sleep quality in patients with gastrointestinal cancers.

Poststroke restless legs syndrome and lesion location: anatomical considerations.

Several case studies have reported on restless legs syndrome (RLS) associated with stroke. In this study, we investigated the prevalence and the lesion topography of poststroke RLS. There were 137 patients with ischemic stroke included in this study. The diagnosis of RLS was made 1 month after the index stroke using the criteria established by the International RLS Study Group. All patients enrolled underwent magnetic resonance imaging within 7 days of the onset of the stroke. The prevalence of stroke-related RLS was calculated, and the topography of the associated ischemic lesions was analyzed. Among 137 patients, 17 patients (12.4%) were diagnosed with RLS after a stroke. Stroke-related RLS was found in 10 out of 33 patients with a basal ganglia/corona radiata infarct (30.3%), 1 out of 8 patients with an internal capsular infarct (12.5%), and 1 out of 7 patients with a thalamic infarct (14.3%). In addition, one out of 54 with a cortical lesion with/without subcortical involvement (1.9%), and 4 out of 18 patients with a pontine lesion (22.2%) had RLS. The analysis of the lesions in the cortical and subcortical group showed only 1 patient in the cortical group had stroke-related RLS, whereas 16 in the subcortical group had stroke-related RLS. The results of this study suggest that lesions of the subcortical brain areas such as the pyramidal tract and the basal ganglia-brainstem axis, which are involved in motor functions and sleep-wake cycles, may lead to RLS symptoms in patients after an ischemic stroke.

Protective effect of epigallocatechin gallate on brain damage after transient middle cerebral artery occlusion in rats.

Epigallocatechin gallate (EGCG), a major constituent of green tea, is a potent free radical scavenger. The purpose of this study was to verify whether EGCG reduces focal ischemia/reperfusion-induced brain injury in a rat model. Male Sprague-Dawley rats were anesthetized with chloral hydrate (400 mg/kg, i.p.) and subjected to a middle cerebral artery 2 h occlusion and then a 24-h reperfusion. The EGCG (25 mg and 50 mg/kg, i.p.) or vehicle was administered immediately after reperfusion. Twenty-four hours after reperfusion, infarction size, levels of oxidative stress markers (malondialdehyde and oxidized/total glutathione ratio) in the brain and neurological deficits were evaluated. The dose of 50 mg/kg of EGCG significantly reduced the infarction volume (9.9+/-3.2%) as compared to those (45.6+/-5.3%, 34.5+/-7.8%) of the control group and the EGCG 25 mg/kg treated group (p<0.01). The dose of 50 mg/kg of EGCG significantly reduced the neurological deficit total score (5.2+/-1.7) as compared to those (9.5+/-1.2, 8.5+/-2.5) of the control group and the EGCG 25 mg/kg treated group (p<0.05). The dose of 50 mg/kg of EGCG significantly attenuated the level of malondialdehyde and the level of oxidized/total glutathione ratio (281+/-66 nmol/g and 0.48+/-0.03) as compared to the those (415+/-46 nmol/g and 0.64+/-0.05, 381+/-51 nmol/g and 0.61+/-0.06) of the control group and the EGCG 25 mg/kg treated group (p<0.05). These results demonstrate the anti-oxidant effects of EGCG (50 mg/kg) in a rat model of transient focal ischemia, which is a likely explanation for EGCG's neuroprotective effects.