Background The gut microbiota can impact older adults’ health, especially in patients with frailty syndrome. Understanding the association between the gut microbiota and frailty syndrome will help to explain the etiology of age-related diseases. Low-grade systemic inflammation is a factor leading to geriatric disorders, which is known as “inflammaging”. Intestinal dysbiosis has a direct relationship with low-grade systemic inflammation because when the natural gut barrier is altered by age or other factors, some microorganisms or their metabolites can cross this barrier and reach the systemic circulation. Objectives This review had two general goals: first, to describe the characteristics of the gut microbiota associated with age-related diseases, specifically frailty syndrome. The second aim was to identify potential interventions to improve the composition and function of intestinal microbiota, consequently lessening the burden of patients with frailty syndrome. Methods A search of scientific evidence was performed in PubMed, Science Direct, and Redalyc using keywords such as “frailty”, “elderly”, “nutrient interventions”, “probiotics”, and “prebiotics”. We included studies reporting the effects of nutrient supplementation on frailty syndrome and older adults. These studies were analyzed to identify novel therapeutic alternatives to improve gut microbiota characteristics as well as subclinical signs related to this condition. Results The gut microbiota participates in many metabolic processes that have an impact on the brain, muscles, and other organs. These processes integrate feedback mechanisms, comprising their respective axis with the intestine and the gut microbiota. Alterations in these associations can lead to frailty. We report a few interventions that demonstrate that prebiotics and probiotics could modulate the gut microbiota in humans. Furthermore, other nutritional interventions could be used in patients with frailty syndrome. Conclusion Probiotics and prebiotics may potentially prevent frailty syndrome or improve the quality of life of patients with this disorder. However, there is not enough information about their appropriate doses and periods of administration. Therefore, further investigations are required to determine these factors and improve their efficacy as therapeutic approaches for frailty syndrome.

Introduction. Breast cancer is the most frequently diagnosed malignancy in women, and comorbidities like hypertension and obesity diminish their quality of life and negatively affect their response to chemotherapy. Furthermore, inulin supplementation is associated with the reduction of cardiovascular diseases (CVD) risk. Objective. To determine whether inulin supplementation prevents the elevation of blood pressure in women with breast cancer undergoing neoadjuvant therapy with cyclophosphamide and doxorubicin. Methods. This was a randomized, double-blind placebo controlled trial which included women with early-stage breast cancer undergoing neoadjuvant therapy (n=38). Patients were randomly assigned to participate in two different groups to receive either 15 g of inulin or 15 g of placebo (maltodextrin) for 21 days. Body composition and blood pressure were evaluated before and after the supplementation period. Results. Women in the inulin group showed a lower systolic blood pressure (SBP) after the supplementation (-4.21 mmHg, p<0.001). However, SBP increased in the placebo supplemented group. Diastolic blood pressure (DBP) nonsignificantly decreased in the inulin group. Inulin supplementation also increased BMI (p<0.001) but reduced BFP (p=0.288). Furthermore, confounding variables, such as BMI, baseline fasting glucose, age, menopause status, vomiting, constipation, and chronic medication did not have a statistical influence over the inulin effect on SBP. Conclusion. Inulin supplementation reduces SBP and prevents increases in DBP in women with breast cancer. This could be an innovative nutraceutical approach to prevent hypertension present in women with this type of cancer at an early stage and may improve the quality of life of the patients and their prognostic development through chemotherapy. Trial Registration Number. This trial is registered with ACTRN12616001532493.

Phthalates and bisphenols are ubiquitous environmental pollutants with the ability to perturb different systems. Specifically, they can alter the endocrine system, and this is why they are also known as endocrine-disrupting compounds (EDCs). Interestingly, they are related to the development and progression of breast cancer (BC), but the threshold concentrations at which they trigger that are not well established. Objectives: The aim of this study was to compare the concentration measures of parent EDCs in three groups of women (without BC, with BC, and BC survivors) from two urban populations in Mexico, to establish a possible association between EDCs and this disease. We consider the measure of the parent compounds would reflect the individual’s exposure. Methods: The levels of di-ethyl-hexyl-phthalate (DEHP), butyl-benzyl-phthalate (BBP), di-n-butyl phthalate (DBP) and di-ethyl-phthalate (DEP), bisphenol A (BPA) and bisphenol S (BPS) were determined by gas chromatograph-mass spectrometry in 102 subjects, including 37 women without any pathological disease, 46 patients with BC and 19 women survivals of BC of Mexico and Toluca City. Results: All phthalates were detected in 100% of women, two of them were significantly higher in patients with different BC subtypes in Mexico City. Differential increases were observed mainly in the serum concentration of phthalates in women with BC compared to women without disease between Mexico and Toluca City. In addition, when performing an analysis of the concentrations of phthalates by molecular type of BC, DEP and BBP were found mainly in aggressive and poorly differentiated types of BC. It should be noted that female BC survivors treated with anti-hormonal therapy showed lower levels of BBP than patients with BC. BPA and BPS were found in most samples from Mexico City. However, BPS was undetectable in women from Toluca City. Discussion: The results of our study support the hypothesis of a positive association between exposure to phthalates and BC incidence.

Our objective was to study hypertension induced by chronic administration of synthetic glucocorticoid, dexamethasone (DEX), under non-stressful conditions and examine the role of catecholamine biosynthesis. To achieve this, 1) we used radiotelemetry to record mean arterial pressure (MAP) and heart rate (HR) in freely moving rats, and 2) administered different doses of DEX in drinking water. To evaluate the involvement of tyrosine hydroxylase (TH), the rate-limiting step in catecholamine biosynthesis, we treated rats with the TH inhibitor, α-methyl-para-tyrosine (α-MPT), for 3 days prior to administration of DEX, and assessed TH mRNA and protein expression by qPCR and Western blot in the adrenal medulla. We observed a dose-dependent elevation in blood pressure with a DEX dose of 0.3 mg/kg administered for 10 days significantly increasing MAP by +15.0 ± 1.1 mm Hg, while concomitantly reducing HR. Although this DEX treatment also significantly decreased body weight, pair-fed animals that showed similar decreases in body weight due to lowered food intake were not hypertensive, suggesting that body weight changes may not account for DEX-induced hypertension. Chronic DEX treatment significantly increased the TH mRNA and protein levels in the adrenal medulla, and α-MPT administration not only reduced DEX pressor effects, but also inhibited TH (Serine⁴⁰)-phosphorylation. Our study thus validates a novel model to study hypertension induced by chronic intake of DEX in freely moving rats not subject to the confounding factors of previous models, and establishes its dependence on concomitant activation of peripheral catecholamine biosynthesis.