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\"Instead of helping in the aftermath of loss, many of the books and strategies meant to guide us through grief only add to the sadness. No one understands the need for a new approach more than Michelle Steinke-Baumgard, who lost her husband in a tragic plane accident and became a widow overnight. In the darkest moment of her life, the mother of two young children found solace and hope in the unlikeliest of places: exercise. She recorded her journey in her blog, One Fit Widow, and soon had a huge community of devoted followers. Now, Michelle offers her revolutionary solution to grief to everyone struggling with their own loss. Healthy Healing addresses the physical, mental, and emotional effects of grief in a way that no other book in the category has ever done, offering a 12-week plan that empowers you to work through loss by using the power of exercise and endorphins, and rediscovering happiness by strengthening body, mind and spirit through fitness. And the benefits don't end there: Exercise helps with poor sleep--a common side effect of trauma--and proper nutrition boosts immunity and fuels you through a busy, stressful time. Michelle dispels common myths about grief and replaces them with relatable advice and actionable inspiration, including: Starting with baby steps such as taking a walk or being in nature Learning to be comfortable with alone time and rediscovering your strength Pairing your exact circumstances with the right form of exercise, whether it's gentle yoga to release trapped sadness or intense kickboxing to work through anger[bullet] Embracing community and surrounding yourself with support This book is an exercise plan, nutrition guide, and, most importantly, a compassionate companion during the most difficult time in your life. With Healthy Healing, you'll learn how to channel your pain into something productive--and use tragedy as a catalyst for inspired change\"-- Provided by publisher.

The aim of this study was to evaluate the influence of β-endorphins and serotonin on the course of treatment, disease-free time, and overall survival of patients with ovarian cancer. This study may contribute to the identification of modifiable factors that may influence the treatment of ovarian cancer. The research was carried out in a group of 162 patients of which 139 respondents were included in the research; ovarian cancer was diagnosed in 78 of these patients. The study consisted of three stages. In the first stage of diagnostics, a survey among the patients was carried out. In the second stage—5 mL of blood was collected from each patient (n = 139) in the preoperative period to determine the concentration of β-endorphin and serotonin. In the third stage—blood samples were collected from those patients who had completed chemotherapy treatment or had surgery. Concentrations of β-endorphin and serotonin were measured by the Luminex method, using the commercial Luminex Human Discovery Assay kit. The average age of the patients was 62.99 years. The level of β-endorphin significantly differs among patients diagnosed with ovarian cancer and among patients in the control group (202.86; SD—15.78 vs. 302.00; SD—24.49). A lower level of β-endorphins was found in the patients with a recurrence of the neoplastic process compared to those without recurrence (178.84; SD—12.98 vs. 205.66; SD—13.37). On the other hand, the level of serotonin before chemotherapy was higher in the group of people with disease recurrence compared to those without recurrence (141.53; SD—15.33 vs. 134.99; SD—10.08). Statistically significantly positive correlations were found between the level of β-endorphin and both disease-free time (β-endorphin levels before chemotherapy: rho Spearman 0.379, p < 0.027; β-endorphin levels after chemotherapy: rho Spearman 0.734 p < 0.001) and survival time (β-endorphin levels before chemotherapy: rho Spearman 0.267, p < 0.018; β-endorphin levels after chemotherapy: rho Spearman 0.654 p < 0.001). 1. The levels of serotonin and β-endorphin levels are significantly related to ovarian cancer and change during treatment. 2. High mean preoperative concentrations of β-endorphins were significantly related to overall survival and disease-free time.

β-Endorphins are peptides that exert a wide variety of effects throughout the body. Produced through the cleavage pro-opiomelanocortin (POMC), β-endorphins are the primarily agonist of mu opioid receptors, which can be found throughout the body, brain, and cells of the immune system that regulate a diverse set of systems. As an agonist of the body’s opioid receptors, β-endorphins are most noted for their potent analgesic effects, but they also have their involvement in reward-centric and homeostasis-restoring behaviors, among other effects. These effects have implicated the peptide in psychiatric and neurodegenerative disorders, making it a research target of interest. This review briefly summarizes the basics of endorphin function, goes over the behaviors and regulatory pathways it governs, and examines the variability of β-endorphin levels observed between normal and disease/disorder affected individuals.

Aim This study aimed to investigate the regulation of pain hypersensitivity induced by the spinal synaptic transmission mechanisms underlying interleukin (IL)‐10 and glucagon‐like peptide 1 receptor (GLP‐1R) agonist exenatide‐induced pain anti‐hypersensitivity in neuropathic rats through spinal nerve ligations. Methods Neuropathic pain model was established by spinal nerve ligation of L5/L6 and verified by electrophysiological recording and immunofluorescence staining. Microglial expression of β‐endorphin through autocrine IL‐10‐ and exenatide‐induced inhibition of glutamatergic transmission were performed by behavioral tests coupled with whole‐cell recording of miniature excitatory postsynaptic currents (mEPSCs) and miniature inhibitory postsynaptic currents (mIPSCs) through application of endogenous and exogenous IL‐10 and β‐endorphin. Results Intrathecal injections of IL‐10, exenatide, and the μ‐opioid receptor (MOR) agonists β‐endorphin and DAMGO inhibited thermal hyperalgesia and mechanical allodynia in neuropathic rats. Whole‐cell recordings of bath application of exenatide, IL‐10, and β‐endorphin showed similarly suppressed enhanced frequency and amplitude of the mEPSCs in the spinal dorsal horn neurons of laminae II, but did not reduce the frequency and amplitude of mIPSCs in neuropathic rats. The inhibitory effects of IL‐10 and exenatide on pain hypersensitive behaviors and spinal synaptic plasticity were totally blocked by pretreatment of IL‐10 antibody, β‐endorphin antiserum, and MOR antagonist CTAP. In addition, the microglial metabolic inhibitor minocycline blocked the inhibitory effects of IL‐10 and exenatide but not β‐endorphin on spinal synaptic plasticity. Conclusion This suggests that spinal microglial expression of β‐endorphin mediates IL‐10‐ and exenatide‐induced inhibition of glutamatergic transmission and pain hypersensitivity via presynaptic and postsynaptic MORs in spinal dorsal horn. Schematic diagram shows the role of microglial expression of β‐endorphin in IL‐10‐ and specific GLP‐1 receptor agonist exenatide‐induced inhibition of spinal excitatory synaptic transmission and pain hypersensitivity in neuropathic pain. Following activation of GLP‐1 receptors, IL‐10 is released and then activates IL‐10 receptors via a microglial autocrine mechanism. Afterward, the β‐endorphin is released to microglial neuronal synapses and activates neuronal presynaptic and postsynaptic μ‐opioid receptors (MORs) to inhibit the enhanced glutamatergic transmission, leading to pain anti‐hypersensitivity.

Physical exercise may affect drug use by balancing neurohormonal system mechanisms. Cortisol and β-endorphin, associated with stress, mood, and pleasure feelings, can be affected by exercise and act as regulators of withdrawal symptoms associated with drug use during short-term abstinence. The present study investigated the effect of a supervised, two-month moderate-intensity aerobic exercise program on salivary cortisol and β-endorphin levels in patients with an opioid use disorder (OUD) and on a substitution treatment during a short-term, 24–36 h withdrawal phase from methadone/buprenorphine medication. Ninety opioid users (41 females) in methadone and buprenorphine substitution treatment were randomly divided into four groups: (a) buprenorphine exercise (BEX) (n = 26; age (mean ± SD): 41.9 ± 6.1 yrs), (b) buprenorphine control (BCON) (n = 25; age: 41.9 ± 5.6 yrs), (c) methadone exercise (MEX) (n = 20; age: 46.7 ± 6.6 yrs), and (d) methadone control (MCON) (n = 19; age: 46.1 ± 7.5 yrs). The exercise intervention groups (BEX and MEX) followed a training program on a treadmill for 20 min at 70% HRmax, 3 days/week for 8 weeks. The responses of cortisol and β-endorphin were measured before (t0) and immediately after an exercise session (t20) on different days (i.e., the 1st, 12th, and 24th session) corresponding to the beginning, middle, and end of the training program. A significant increase in β-endorphin levels was observed after the completion of the training intervention (24th exercise session) in both exercise groups (BEX before: 63.8 ± 33; BEX after: 185.6 ± 182.8 pg/mL; MEX before: 115 ± 211; MEX after: 262.3 ± 505.7 pg/mL), whereas β-endorphin was decreased in the control groups (BCON before: 34.7 ± 20.1; BCON after: 24.2 ± 8.8 pg/mL; MCON before: 129.7 ± 185.7; MCON after: 84.9 ± 104.3 pg/mL) (p < 0.05). Inversely, cortisol decreased in both exercise groups post-intervention (BEX before: 9.5 ± 5.9; BEX after: 2.8 ± 1.5 ng/mL; MEX before: 9.3 ± 6.6; MEX after: 3.1 ± 1.5 ng/mL) and increased in control groups (BCON before: 6.3 ± 2.5; BCON after: 10.1 ± 5.4 ng/mL; MCON before: 7.5 ± 3.2; MCON after: 12.5 ± 4.3 ng/mL) (p < 0.05). Moderate-intensity aerobic exercise can beneficially influence β-endorphin and cortisol levels in individuals undergoing treatment for OUD. By increasing endogenous opioid levels and reducing stress hormones, exercise emerges as a promising adjunctive strategy for alleviating withdrawal symptoms, enhancing emotional regulation, and potentially reducing the risk of relapse. The inverse relationship between β-endorphin and cortisol highlights the role of physical activity as a long-term modulator of neuroendocrine function in the context of substance use recovery. Future research should prioritize longitudinal studies extending beyond two months and involving larger, more diverse populations. Additionally, investigating the integration of exercise with non-pharmacological interventions—and its effects on relapse rates, mental health outcomes, and overall quality of life—would provide further insight into its therapeutic value in addiction recovery.

In the pituitary gland, hormones are stored in a functional amyloid state within acidic secretory granules before they are released into the blood. To gain a detailed understanding of the structure–function relationship of amyloids in hormone secretion, the three-dimensional (3D) structure of the amyloid fibril of the human hormone β-endorphin was determined by solid-state NMR. We find that β-endorphin fibrils are in a β-solenoid conformation with a protonated glutamate residue in their fibrillar core. During exocytosis of the hormone amyloid the pH increases from acidic in the secretory granule to neutral level in the blood, thus it is suggested—and supported with mutagenesis data—that the pH change in the cellular milieu acts through the deprotonation of glutamate 8 to release the hormone from the amyloid. For amyloid disassembly in the blood, it is proposed that the pH change acts together with a buffer composition change and hormone dilution. In the pituitary gland, peptide hormones can be stored as amyloid fibrils within acidic secretory granules before release into the blood stream. Here, we use solid-state NMR to determine the 3D structure of the amyloid fiber formed by the human hormone β-endorphin. We find that β-endorphin fibrils are in a β-solenoid conformation that is generally reminiscent of other functional amyloids. In the β-endorphin amyloid, every layer of the β-solenoid is composed of a single peptide and protonated Glu8 is located in the fibrillar core. The secretory granule has an acidic pH but, on exocytosis, the β-endorphin fibril would encounter neutral pH conditions (pH 7.4) in the blood; this pH change would result in deprotonation of Glu8 to release the hormone peptide from the amyloid. Analyses of β-endorphin variants carrying mutations in Glu8 support the role of the protonation state of this residue in fibril disassembly, among other environmental changes.The solid-state NMR structure of an amyloid fiber formed by human hormone β-endorphin reveals a protonated Glu8 in the fibrillar core. Under neutral conditions, deprotonation of Glu8 would contribute to fibril disassembly and hormone peptide release.

The purpose of this exploratory study was to examine the effects of Tai Chi on blood levels of beta endorphin (β-endorphin) and inflammatory markers in older adults with chronic pain. Forty community-dwelling older adults with chronic pain were randomized to Tai Chi or light physical exercise, and each offered twice weekly for 12 weeks. Following the 12-week intervention, neither Tai Chi nor light physical exercise changed levels of β-endorphin and inflammatory markers. However, in older adults who completed 70% or more classes, Tai Chi significantly lowered levels of β-endorphin (p < 0.05), whereas light physical exercise did not change levels of β-endorphin. The results suggest that Tai Chi may reduce levels of β-endorphin in older adults with chronic pain. Future studies are needed to better understand the role of the opioid analgesic system and immune system in regulating pain with aging and the long-term effects of Tai Chi on pain-related biomarkers.

The use of alternative interventions, such as gluten-free and casein-free (GFCF) diets, is frequent due to limited therapies for Autism Spectrum Disorder (ASD). Our aims were to determine the influence of a GFCF diet on behavior disorders in children and adolescents diagnosed with ASD and the potential association with urinary beta-casomorphin concentrations. Thirty-seven patients were recruited for this crossover trial. Each patient consumed a normal diet (including gluten and casein) for 6 months and a GFCF diet for another 6 months. The order of the intervention (beginning with normal diet or with GFCF diet) was assigned randomly. Patients were evaluated at three time-points (at the beginning of the study, after normal diet and after GFCF diet). Questionnaires regarding behavior and autism and dietary adherence were completed and urinary beta-casomorphin concentrations were determined at each time-point. No significant behavioral changes and no association with urinary beta-casomorphin concentrations were found after GFCF diet. A 6-month GFCF diet do not induce significant changes in behavioral symptoms of autism and urinary beta-casomorphin concentrations. Further studies with a long follow-up period similar to ours and including placebo and blinding elements are needed to identify better those respondents to GFCF diets.

Background Cows’ milk generally contains two types of β-casein, A1 and A2 types. Digestion of A1 type can yield the peptide β-casomorphin-7, which is implicated in adverse gastrointestinal effects of milk consumption, some of which resemble those in lactose intolerance. This study aimed to compare the effects of milk containing A1 β-casein with those of milk containing only A2 β-casein on inflammation, symptoms of post-dairy digestive discomfort (PD3), and cognitive processing in subjects with self-reported lactose intolerance. Methods Forty-five Han Chinese subjects participated in this double-blind, randomized, 2 × 2 crossover trial and consumed milk containing both β-casein types or milk containing only A2 β-casein. Each treatment period was 14 days with a 14-day washout period at baseline and between treatment periods. Outcomes included PD3, gastrointestinal function (measured by smart pill), Subtle Cognitive Impairment Test (SCIT), serum/fecal laboratory biomarkers, and adverse events. Results Compared with milk containing only A2 β-casein, the consumption of milk containing both β-casein types was associated with significantly greater PD3 symptoms; higher concentrations of inflammation-related biomarkers and β-casomorphin-7; longer gastrointestinal transit times and lower levels of short-chain fatty acids; and increased response time and error rate on the SCIT. Consumption of milk containing both β-casein types was associated with worsening of PD3 symptoms relative to baseline in lactose tolerant and lactose intolerant subjects. Consumption of milk containing only A2 β-casein did not aggravate PD3 symptoms relative to baseline (i.e., after washout of dairy products) in lactose tolerant and intolerant subjects. Conclusions Consumption of milk containing A1 β-casein was associated with increased gastrointestinal inflammation, worsening of PD3 symptoms, delayed transit, and decreased cognitive processing speed and accuracy. Because elimination of A1 β-casein attenuated these effects, some symptoms of lactose intolerance may stem from inflammation it triggers, and can be avoided by consuming milk containing only the A2 type of beta casein. Trial registration ClinicalTrials.gov/NCT02406469

Background Preterm neonates undergo many painful procedures as part of their standard care in the neonatal intensive care unit. However, pain treatment is inadequate in many of these routine procedures. In the present study, we investigated the impact and mechanism of combined music and touch intervention (CMT) on the pain response in premature infants. Methods Sixty-two preterm neonates (gestational age of <37 weeks) were randomly assigned to either the experimental or control group. Infants in the experimental group underwent painful procedures with CMT, and those in the control group underwent painful procedures without CMT. Blood samples were collected from all infants at the beginning of hospitalization and 2 weeks later to assess the cortisol and β-endorphin concentrations. Differences in the levels of cortisol and β-endorphin between two groups were examined using analysis of covariance (ANCOVA). Results In total, 3707 painful procedures were performed on 62 neonates during their hospitalization. The average number of painful procedures in the control group ( n  = 35.5) was higher than that in the experimental group ( n  = 29.0) during hospitalization, although no significant difference was reached ( P  > 0.05). After 2 weeks, the Premature Infant Pain Profile scores were significantly higher in the control group than experimental group (13.000 ± 0.461 vs 10.500 ± 0.850, respectively; P  < 0.05). The cortisol concentration was not significantly different between the control and experimental groups either at the beginning of hospitalization (131.000 ± 18.190 vs 237.200 ± 43.860, respectively; P  > 0.05) or 2 weeks later (162.400 ± 23.580 vs 184.600 ± 21.170, respectively; P  > 0.05). However, the serum β-endorphin concentration was higher in the experimental group than in the control group both at the beginning of hospitalization (1.640 ± 0.390 vs 1.179 ± 0.090, respectively; P  < 0.05) and 2 weeks later (2.290 ± 0.740 vs 1.390 ± 0.410, respectively; P  < 0.05). Conclusions CMT might decrease the pain response of preterm neonates by significantly improving the β-endorphin concentration, but not the blood cortisol concentration. Trial registration Current Controlled Trials ISRCTN14131492 . Registered on 01 Aug 2016.