Nutritional Ergogenic Aids in Combat Sports: A Systematic Review and Meta-Analysis

Nutritional ergogenic aids (NEAs) are substances included within the group of sports supplements. Although they are widely consumed by athletes, evidence-based analysis is required to support training outcomes or competitive performance in specific disciplines. Combat sports have a predominant use of anaerobic metabolism as a source of energy, reaching peak exertion or sustained effort for very short periods of time. In this context, the use of certain NEAs could help athletes to improve their performance in those specific combat skills (i.e., the number of attacks, throws and hits; jump height; and grip strength, among others) as well as in general physical aspects (time to exhaustion [TTE], power, fatigue perception, heart rate, use of anaerobic metabolism, etc.). Medline/PubMed, Scopus and EBSCO were searched from their inception to May 2022 for randomised controlled trials (RCTs). Out of 677 articles found, 55 met the predefined inclusion criteria. Among all the studied NEAs, caffeine (5–10 mg/kg) showed strong evidence for its use in combat sports to enhance the use of glycolytic pathways for energy production during high-intensity actions due to a greater production of and tolerance to blood lactate levels. In this regard, abilities including the number of attacks, reaction time, handgrip strength, power and TTE, among others, were improved. Buffering supplements such as sodium bicarbonate, sodium citrate and beta-alanine may have a promising role in high and intermittent exertion during combat, but more studies are needed in grappling combat sports to confirm their efficacy during sustained isometric exertion. Other NEAs, including creatine, beetroot juice or glycerol, need further investigation to strengthen the evidence for performance enhancement in combat sports. Caffeine is the only NEA that has shown strong evidence for performance enhancement in combat sports.     

Spontaneous regression of a breast carcinoma: a case report

Spontaneous regression of malignant tumors is a rare event. It is defined as partial or total disappearance of a proven malignant tumor without adequate medical treatment. The causes of this phenomenon are various. Nevertheless, malignant tumors do regress occasionally for no apparent reason, as evidenced by many clinical observations. We report a case of a 68-year-old woman, who was presented with a several-month history of a painless firm lump, initially of 1 cm in diameter and growing to a large solid regular tumor of 2.5 x 2.5 cm in size, in the upper outer quadrant of her right breast. Preoperative histopathological diagnosis revealed ductal invasive carcinoma. Later on, while awaiting surgical treatment, she suffered an arm injury requiring a 1-month delay of surgery. After recovery, on the date of surgery the tumor disappeared, and, in addition, it was not found in tissue specimens obtained from quadrantectomy. After 78 months of follow-up there was no evidence of relapse. In this report, we discuss clinical and histopathological findings, patient management and possible mechanisms of cancer regression.     

Human teratogens and evidence-based teratogen risk counseling: the Motherisk approach

There are only a limited number of drugs proven to be human teratogens including thalidomide, isotretinoin, coumarin derivates, valproic acid, and folate antagonists. In some cases, the combination of 2 drugs may increase the teratogenic risk. The risk of birth defects may also vary with the time at which the drug is administered during pregnancy and the dose. There are some examples of drugs in which the dose has proven to be a major determinant of their teratogenicity in humans. There is more safety information for older than for newer drugs. Proactive teratogen risk counseling should include a critical appraisal of all available data including the consequences of the untreated maternal condition.     

Evaluation of Liver and Renal Toxicity in Peptide Receptor Radionuclide Therapy for Somatostatin Receptor Expressing Tumors: A 2-Year Follow-Up

BackgroundPeptide receptor radionuclide therapy (PRRT) with radiolabeled somatostatin receptor (SSR) analogs is now an established systemic treatment for neuroendocrine tumors (NET). However, more short- and long-term data about renal and hepatotoxicity is needed. Here we present our experience in this clinical scenario.MethodsEighty-six patients with progressive SSR-expressing malignancies underwent PRRT with Lu-177 Dotatate and were followed up for up to 2 years. Laboratory tests were done 1 week before each cycle and every 2 months at follow-up. Hepatic and renal toxicity was determined based on NCI CTCAE V5.0.Results55/86 (64%) patients completed all 4 cycles of PRRT; 18/86 (20.9%) are currently being treated; 13/86 (15.1%) had to discontinue PRRT: 4/13 (31%) due to hematologic toxicity, 9/13 (69%) due to non-PRRT-related comorbidities. Out of the patients who finished treatment, only transient grade 2 toxicities were observed during PRRT: hypoalbuminemia in 5.5% (3/55), and renal toxicity (serum creatinine and estimated glomerular filtration rate) in 1.8% (1/55). No grade 3 or 4 liver and renal toxicity occurred. Patients presenting with impaired liver or renal function prior to PRRT, either improved or had stable findings. No deterioration was observed.ConclusionPeptide receptor radionuclide therapy does not have a negative impact on liver and renal function, even in patients with pre-existing impaired parameters. No grade 3 or 4 hepatic or renal toxicity was identified. Only transient grade 2 hypoalbuminemia in 5.5% and nephrotoxicity in 1.8% of patients were seen during PRRT.     

Coordination of hypothalamic and pituitary T3 production regulates TSH expression

Type II deiodinase (D2) activates thyroid hormone by converting thyroxine (T4) to 3,5,3′-triiodothyronine (T3). This allows plasma T4 to signal a negative feedback loop that inhibits production of thyrotropin-releasing hormone (TRH) in the mediobasal hypothalamus (MBH) and thyroid-stimulating hormone (TSH) in the pituitary. To determine the relative contributions of these D2 pathways in the feedback loop, we developed 2 mouse strains with pituitary- and astrocyte-specific D2 knockdown (pit-D2 KO and astro-D2 KO mice, respectively). The pit-D2 KO mice had normal serum T3 and were systemically euthyroid, but exhibited an approximately 3-fold elevation in serum TSH levels and a 40% reduction in biological activity. This was the result of elevated serum T4 that increased D2-mediated T3 production in the MBH, thus decreasing Trh mRNA. That tanycytes, not astrocytes, are the cells within the MBH that mediate T4-to-T3 conversion was defined by studies using the astro-D2 KO mice. Despite near-complete loss of brain D2, tanycyte D2 was preserved in astro-D2 KO mice at levels that were sufficient to maintain both the T4-dependent negative feedback loop and thyroid economy. Taken together, these data demonstrated that the hypothalamic-thyroid axis is wired to maintain normal plasma T3 levels, which is achieved through coordination of T4-to-T3 conversion between thyrotrophs and tanycytes.