BCAA 6000mg - 240 Comprimidos

Aims: The purpose of this review was to examine how five commonly used supplements, including creatine, citrulline, L-arginine, beta-alanine, and branched-chain amino acids (BCAAs), affect physical performance and kidney health. These compounds are widely consumed in the context of athletic training, yet their long-term safety with respect to renal function remains insufficiently defined. Methodology: Relevant literature published between 1990 and 2024 was identified using PubMed, Scopus, and Google Scholar. The selection included studies describing the physiological effects and potential renal impact of each supplement. State of Knowledge: Analysis of the available research suggests that creatine does not impair kidney function in healthy individuals. Citrulline is considered metabolically safe and may support renal health in specific contexts, although elevated concentrations in patients with reduced kidney function could indicate metabolic imbalance. L-arginine may be beneficial in acute clinical settings but shows potentially harmful effects when used long term, especially in older or chronically ill individuals. Beta-alanine has demonstrated safety and antioxidant properties that could protect kidney cells. In contrast, high or prolonged intake of BCAAs may contribute to insulin resistance and worsen renal outcomes in people with diabetes or hereditary kidney disorders. Conclusions: When used appropriately by healthy individuals, these supplements are generally safe for kidney function. However, individual health status, dosage, and duration of use can significantly affect renal outcomes. BCAA supplementation, in particular, should be approached with caution in at-risk populations. More long-term studies are needed to fully assess the renal safety of these compounds in both athletic and clinical settings.

Cancer and cardiovascular diseases (CVDs) are global health challenges. In cancer patients, CVDs is the second leading cause of death following disease progression. There are few specialized services for cardio-oncology patients worldwide currently. Branched-chain amino acids (BCAAs) are essential amino acids and promote protein synthesis and energy homeostasis. The disruption of BCAAs metabolism facilitates the development of cancer and CVDs while the benefit of BCAAs supplement is full of controversy. In this review, we summarized BCAA-related studies in cardiometabolism, cancer and chemotherapy-induced cardiotoxicity, and provided our perspectives on the roles of BCAAs in cardio-oncology research. We find that supplementation of BCAAs presents protective effects in cardiometabolic diseases, while the influence on cancer is intricate and varies across different types. Large-scale clinical studies are needed to understand the long-term effects of BCAA intake and its impact on different disease stages. BCAAs have potential to mitigate chemotherapy-induced cardiotoxicity such as doxorubicin (DOX) and 5-fluorouracil (5-FU). Continued research is still essential to understand the precise mechanisms, determine optimal usage, and assess the effectiveness of BCAAs supplement.

Background: Sustainable, dual-action ergogenic strategies are underexplored; most products target a single pathway and rarely upcycle seafood sidestreams. We therefore tested an upcycled formulation combining grouper bone hydrolysate and Undaria pinnatifida extract (GU) for ergogenic and microbiota effects in mice. We tested the ergogenic and microbiota modulating effects of GU in mice versus a vehicle and a BCAA control. Methods: GU was prepared via enzymatic hydrolysis of marine by-products and administered to male ICR mice for 4 weeks. Mice were divided into five groups (n = 7/group), receiving a vehicle control, a branched-chain amino acid (BCAA) supplement, or GU at three dose levels (1X, 2X, 3X) based on human-equivalent conversion. Exercise performance was assessed via grip strength and treadmill tests. Biochemical markers of fatigue, body composition, and safety indicators were also analyzed. Gut microbiota was evaluated using 16S rRNA sequencing and constrained principal coordinates analysis (CPCoA). Results: Four weeks of GU supplementation significantly enhanced exercise performance [(treadmill time ↑ Δ = 10.2–11.7 min versus vehicle (q ≤ 0.0002), grip strength ↑ Δ = 40.4–48.5 g (q ≤ 0.05)] and lean body mass [FFM ↑ at GU-1X (Δ = +0.80%, q = 0.0123)], surpassing the commercial BCAA control. Biochemical analyses indicated reduced exercise-induced lactate accumulation [(post-exercise lactate ↓ Δ = −2.71/−2.18 mmol·L−1, q = 0.0006)]. Gut microbiota profiling revealed distinct shifts in community composition in GU-treated groups, notably with an increased abundance of beneficial taxa such as Lactobacillus and Muribaculum. These alterations reflect the prebiotic activity of seaweed-derived polysaccharides, promoting a healthier gut microbial profile. Notably, GU improved metabolic markers (aspartate aminotransferase, [AST]; lactate dehydrogenase, [LDH]) without inducing toxicity. Conclusions: These findings indicate that GU functions as a dual-action supplemen

Autism spectrum disorders (ASD) are a group of heterogeneous, behaviorally defined neurodevelopmental conditions influenced by both genetic and environmental factors. Here, we show that nutrients—an important environmental factor—can modulate synaptic proteomes, reconfigure neural ensembles, and improve social behaviors in ASD mouse genetic models. We analyzed Tbr1+/− mice, a well-established model of ASD, using proteomic approaches and in vivo calcium imaging. Synaptic and metabolic proteomes were found to be sensitive to Tbr1 haploinsufficiency. Our results also revealed that Tbr1 haploinsufficiency promotes hyperactivation and hyperconnectivity of basolateral amygdala (BLA) neurons, enhancing the activity correlation between individual neurons and their corresponding ensembles. Zinc, branched-chain amino acids (BCAA), and serine—all nutrients known to regulate synapse formation and activity—were then combined into supplement cocktails and administered to Tbr1+/− mice. This treatment altered synaptic and metabolic proteomes and normalized the activity and connectivity of the BLA in Tbr1+/− mice during social interactions. We further show that although a low dose of individual nutrients did not alter social behaviors, treatment with supplement cocktails containing low-dose individual nutrients improved social behaviors and associative memory of Tbr1+/− mice, implying a synergistic effect of combining low-dose zinc, BCAA, and serine. Moreover, the supplement cocktails also improved social behaviors in Nf1+/− and Cttnbp2+/M120I mice, two additional ASD mouse models. Thus, our findings reveal aberrant neural connectivity in the BLA of Tbr1+/− mice and indicate that dietary supplementation with zinc, BCAA, and/or serine offers a safe and accessible approach to mitigate neural connectivity and social behaviors across multiple ASD models.