Gut microbiota perturbation is associated with acute sleep disturbance among rectal cancer patients.

Cancer treatment-associated gut microbial perturbation/dysbiosis has been implicated in the pathobiology of sleep disturbance; however, evidence is scarce. Eighteen newly diagnosed rectal cancer patients (ages 52-81 years; 10 males) completed a sleep disturbance questionnaire and provided stool samples for 16s RNA gene sequencing during chemo-radiotherapy. Descriptive statistics, Wilcoxon test and regression analyses were computed. Regression analyses showed the Shannon's diversity index to be a significant factor associated with sleep disturbance. This preliminary work suggests that the biological "gut-brain axis" mechanism may be associated with symptoms of sleep disturbance.

Factors Affecting the Severity of Fatigue during Radiotherapy for Prostate Cancer; an Exploratory Study.

INTRODUCTION: Limited studies have examined potential risk factors associated with the fatigue experience of a sample of Puerto Rican men treated with radiotherapy for non-metastatic prostate cancer. Identifying these factors may provide initial information about targets for individualized interventions, leading to more effective management of fatigue in this population. PURPOSE: To examine the relationship of age, body max index, depressive symptoms, physical activity, and sleep disturbance with fatigue during radiotherapy for prostate cancer. METHODS: Twenty six participants completed five inventories: demographic intake, health form, the Functional Assessment of Cancer-Therapy-fatigue, Patient-Reported Outcome Measures Information System-Sleep disturbance, and the International Physical Activity Questionnaire-Short Form before, middle/days 19-21 and completion/days 38-42 of radiotherapy. The principal investigator rated the Hamilton depression scale. Descriptive statistics were performed. Interactions and influence of variables on fatigue were assessed using bivariate correlation and multiple linear regression, respectively. RESULTS: At each study time point, sleep disturbance and depressive symptoms were strongly correlated with each other and fatigue. The linear combination of sleep disturbance and depressive symptoms was significantly related to fatigue. CONCLUSION: Given the high association of sleep disturbance and depressive symptoms with fatigue, clinicians should assess and develop interventions to manage these symptoms altogether.

Association of Radiotherapy-Related Intestinal Injury and Cancer-related Fatigue: A Brief Review and Commentary.

Radiotherapy treatment-induced intestinal injury and gut microbial perturbation/dysbiosis have been implicated in the pathobiology of cancer-related fatigue. The objective of this brief review was to explore the available evidence of the relationship between intestinal injury and self-reported fatigue, especially among cancer patients. The scientific evidence-including our own-linking gut mucosal barrier dysfunction and gut microbial perturbation/dysbiosis induced by cancer treatment with worsening of cancer related fatigue (perhaps through the gut-brain axis) is limited but promising. Emerging data suggest that lifestyle interventions and the administration of specific probiotics may favorably modulate the gut microbiota and potentially mediate beneficial effects leading to improvements in fatigue.

Papel de la testosterona y el cortisol en el síndrome metabólico y la diabetes mellitus tipo 2 / Role of testosterone and cortisol in metabolic syndrome and type 2 diabetes mellitus

INTRODUCCIÓN: el síndrome metabólico y la diabetes mellitus tipo 2 son trastornos metabólicos que han sido ampliamente abordados en la literatura científica por su alta incidencia, así como la alta morbilidad y mortalidad que a ellos se asocia. En los últimos años se han explorado nuevos elementos de posible impacto en su fisiopatogenia, dentro de los que se destacan los esteroides sexuales y los glucocorticoides. En este trabajo se revisaron y comentaron los conocimientos más actuales sobre el papel de la testosterona y el cortisol en la fisiopatogenia del síndrome metabólico y de la diabetes mellitus tipo 2 en los hombres. DESARROLLO: la testosterona desempeña un papel importante en la modulación de la sensibilidad a la insulina y en la homeostasis de la glucosa, de manera que en los hombres, los niveles bajos de testosterona resultan un elemento predictor de la diabetes mellitus tipo 2 y del síndrome metabólico. Se ha establecido la existencia de una relación bidireccional y reversible entre la deficiencia de andrógenos y la adiposidad, así como entre la deficiencia de andrógenos y la resistencia a la insulina. Se sugiere que los niveles bajos de testosterona podrían predisponer a la obesidad abdominal, que provoca una alteración del metabolismo de los ácidos grasos, lo cual a la vez promovería la resistencia a la insulina. La secreción de cortisol y la de testosterona están interrelacionadas y tienen efectos inversos sobre la resistencia a la insulina. En la obesidad abdominal el eje hipotalámico-hipofisario-adrenal se hipersensibiliza lo cual provoca aumento frecuente de la secreción de cortisol y disminución de la secreción de esteroides sexuales. Por otro lado, un aumento desproporcionado de la respuesta fisiológica al estrés, induce un incremento de la secreción de cortisol que podría a su vez causar la aparición de la resistencia a la insulina y del síndrome metabólico. Uno de los mecanismos patogénicos de la resistencia a la insulina es el flujo aumentado de ácidos grasos que llega al hígado a partir del metabolismo de la grasa visceral. La relación cortisol/testosterona modula, entre otras hormonas, la acumulación de la grasa visceral; ha sido asociada, en hombres, a la mortalidad y la incidencia de enfermedades cardiovasculares isquémicas, a través de una alteración de los componentes del síndrome metabólico. Esta razón pudiera ser un indicador temprano de la resistencia a la insulina y del síndrome metabólico. Este elemento introduce una nueva dimensión dentro de la fisiopatogenia del síndrome metabólico que merece ser estudiada, con la finalidad de incrementar las potencialidades diagnósticas y terapéuticas en este campo(AU)

INTRODUCTION: metabolic syndrome and the type 2 diabetes mellitus are metabolic disorders fully approached in scientific literature due to its high incidence, as well as its association with a high morbidity and mortality. In past years new elements of potential impact in its physiopathology have been reviewed including the sexual steroids and the glucocorticoids. In present paper were reviewed and discussed the more current knowledges on the testosterone and cortisol role in the physiopathology of metabolic syndrome and type 2 diabetes mellitus in men. DEVELOPMENT: testosterone plays a significant role in modulation of sensitivity to insulin and in glucose homeostasis because of in men the low levels of testosterone are a predictor element of type 2 diabetes mellitus and of the metabolic syndrome. A bidirectional and reversible relation between androgen deficiency and the adiposity, as well as between the androgen deficiency and insulin resistance have been established. Authors suggest that low levels of testosterone could predispose to abdominal obesity provoking an alteration of fat acid metabolism, which at the same time will promote the insulin resistance. Cortisol and testosterone secretion are interrelated and have inverse effects on insulin resistance. In abdominal obesity the adrenal-hypophyseal-hypotalamic axis is hypersensitive leading to a frequent increase of cortisol secretion and a decrease of sexual steroids secretion. Besides, a disproportionate increase of stress-physiologic response induces a cortisol secretion increase which could at the same time, to provoke the insulin resistance and the metabolic syndrome. One of the pathogenic mechanisms of insulin resistance is the increased flow of fat acids arriving to liver from the visceral fat metabolism. The cortisol/testosterone relation modulates among other hormones the visceral fat accumulation has been associated in men, with mortality and with the incidence of ischemic cardiovascular diseases through an alteration of the metabolic syndrome components. This fact could be an early indicator of insulin resistance and of metabolic syndrome. This element introduces a new dimension within the metabolic syndrome physiopathology deserving be studied to increase the diagnostic and therapeutical potentials in this field(AU)