Behavioral and metabolic risk factors associated with periodontitis in Brazil, 1990-2019: a multidimensional analysis for the Global Burden of Disease Study 2019.

OBJECTIVES: Periodontitis is a non-communicable disease (NCD) that may be linked to other NCDs through shared risk factors. Accordingly, we analyzed the relationship between periodontitis and behavioral and metabolic risks common to NCDs in Brazilian adults over three decades. METHODS: Indicators of periodontitis, behavioral risks (smoking, alcohol use, sugar-sweetened beverages (SSB), and physical activity), and metabolic risks (overweight/obesity, dyslipidemia, hyperglycemia, and hypertension) in Brazilian adults (25-49 y-old) between 1990 to 2019 were obtained from the Global Burden of Disease Study 2019. Data were adjusted for Gini index. Fixed-effects and Prais-Winsten regressions were performed (p < 0.05). RESULTS: The prevalence of periodontitis has increased among Brazilians since 2005. High-SSB diet, alcohol use, and metabolic risks increased between 1990-2019, whereas smoking decreased. In crude models, periodontitis prevalence increased with alcohol use (2545.1; 95%CI: 2307.9-2782.3), high-SSB diet (365.5; 95%CI: 322.5-408.4), low physical activity (1784.4; 95%CI: 763.7-2805.0), overweight/obesity (172.3; 95%CI: 156.3-188.4), dyslipidemia (734.5; 95%CI: 624.7-844.2), and hyperglycemia (1774.3; 95%CI: 1555.9-1992.7). After adjustment for the Gini index, periodontitis prevalence raised with a high-SBB diet (1416.0; 95%CI: 1120.2-1711.8), overweight/obesity (629.9; 95%CI: 573.1-686.8), dyslipidemia (2035.8; 95%CI: 1728.1-2343.5), and hyperglycemia (8918.1; 95%CI: 7979.8-9856.3). CONCLUSIONS: Periodontitis has increased in Brazil since 2005, despite the smoking reduction. Sugar-sweetened beverage was the behavioral risk that mostly accompanied the periodontal trend. CLINICAL RELEVANCE: Our results support upstream strategies targeting commercial, social, political, and structural determinants to tackle NCDs and reduce oral health inequities.

Determining the Arterial Occlusion Pressure for Blood Flow Restriction: Pulse Oximeter as a New Method Compared With a Handheld Doppler.

ABSTRACT: Lima-Soares, F, Pessoa, KA, Torres Cabido, CE, Lauver, J, Cholewa, J, Rossi, FE, and Zanchi, NE. Determining the arterial occlusion pressure for blood flow restriction: Pulse oximeter as a new method compared with a handheld Doppler. J Strength Cond Res 36(4): 1120-1124, 2022-In laboratorial and clinical settings, the use of Doppler ultrasound equipment has been considered the gold standard method to determine arterial occlusion pressure (AOP). However, the use of Doppler equipment is inherently limited to the technical expertise needed to perform AOP measurements. To overcome the technical difficulties of the use of Doppler equipment use in the determination of AOP, a simpler and less subjective methodology would be helpful for blood flow restriction (BFR) practitioners. In this regard, portable pulse oximetry has been largely used in clinical practice for measuring systolic pressures, as well as loss or recovery of pulse, with results similar to those observed with the use of Doppler equipment. For such purposes, the AOP from young male and female subjects was evaluated after different body positions (standing, seated, and supine positions). Loss of capillary blood flow or AOP was readily determined by simple visual inspection for the pulse oximeter and loss of sound for the Doppler equipment. The results presented herein strongly suggest the use of the portable pulse oximetry equipment as reliable, when compared with the handheld Doppler (seated k = 0.962, standing k = 0.845, and supine k = 0.963 and seated rs = 0.980, standing rs = 0.958, and supine rs = 0.955). Because AOP measurement by pulse oximetry is relatively easier to perform and financially more accessible than handheld Doppler equipment, BFR practitioners may benefit from this new methodology to measure AOP, thus determining individualized restriction pressures.

Effects of dietary sports supplements on metabolite accumulation, vasodilation and cellular swelling in relation to muscle hypertrophy: A focus on "secondary" physiological determinants.

Increased blood flow via vasodilation, metabolite production, and venous pooling contribute to the hyperemia and cellular swelling experienced during resistance training. It has been suggested that these effects play a role in hypertrophic adaptations. Over the past 2 decades, sport supplement products have been marketed to promote exercise hyperemia and intracellular fluid storage, thereby enhancing hypertrophy via acute swelling of myocytes. The three main classes of supplements hypothesized to promote exercise-induced hyperemia include vasodilators, such as nitric oxide precursor supplements; anaerobic energy system ergogenic aids that increase metabolite production, such as ß-alanine and creatine; and organic osmolytes, such as creatine and betaine. Previous studies indicated that these dietary supplements are able to improve muscle performance and thus enhance muscle hypertrophy; however, recent evidences also point to these three classes of supplements affecting "secondary" physiological determinants of muscle mass accretion such as vasodilation, metabolite accumulation, and muscle cellular swelling. Although we recognize that the literature is relatively scarce regarding these topics, a better comprehension and discussion of these determinants can lead to increased knowledge and might guide further research regarding the proposed mechanisms of action of the identified compounds. In this case, increased knowledge may contribute to the development of improved efficacy, new products, or direct new research to specifically investigate those secondary effects. The aim of this review was to bring into focus new perspectives associated with secondary physiological effects induced by supplementation and to determine their relevance.

Targeting Inflammation and Downstream Protein Metabolism in Sarcopenia: A Brief Up-Dated Description of Concurrent Exercise and Leucine-Based Multimodal Intervention.

Sarcopenia is defined as the progressive loss of muscle mass with age, and poses a serious threat to the physiological and psychological health of the elderly population with consequential economic and social burdens. Chronic low-grade inflammation plays a central role in the development of sarcopenia such that it alters cellular protein metabolism to favor proteolysis over synthesis, and thereby accelerates muscular atrophy. The purpose of this review is to highlight how exercise and nutrition intervention strategies can attenuate or treat sarcopenia. Resistance exercise increases not only muscle mass but also muscle strength, while aerobic exercise is able to ameliorate the age-related metabolic disorders. Concurrent exercise training integrates the advantages of both aerobic and resistance exercise, and may exert a significant synergistic effect in the aging organism. Higher protein intakes rich in the amino acid leucine appear to restore skeletal muscle protein metabolism balance by rescuing protein synthesis in older adults. There is good reason to believe that a multimodal treatment, a combination of exercise and increased leucine consumption in the diet, can combat some of the muscle loss associated with aging. Future research is needed to consolidate these findings to humans, and to further clarify to what extent and by which mechanisms protein metabolism might be directly involved in sarcopenia pathogenesis and the multimodal treatment responses.

Dietary proteins and amino acids in the control of the muscle mass during immobilization and aging: role of the MPS response.

Dietary proteins/essential amino acids (EAAs) are nutrients with anabolic properties that may increase muscle mass or attenuate muscle loss during immobilization and aging via the stimulation of muscle protein synthesis (MPS). An EAA's anabolic threshold, capable to maximize the stimulation of MPS has been hypothesized, but during certain conditions associated with muscle loss, this anabolic threshold seems to increase which reduces the efficacy of dietary EAAs to stimulate MPS. Preliminary studies have demonstrated that acute ingestion of dietary proteins/EAA (with a sufficient amount of leucine) was capable to restore the postprandial MPS during bed rest, immobilization or aging; however, whether these improvements translate into chronic increases (or attenuates loss) of muscle mass is equivocal. For example, although free leucine supplementation acutely increases MPS and muscle mass in some chronic studies, other studies have reported no increases in muscle mass following chronic leucine supplementation. In contrast, chronically increasing leucine intake via the consumption of an overall increase in dietary protein appears to be the most effective dietary intervention toward increasing or attenuating lean mass during aging; however, more research investigating the optimal dose and timing of protein ingestion is necessary. Several studies have demonstrated that decreases in postprandial MPS as a result of increased circulating oxidative and inflammatory are more responsible than muscle protein breakdown for the decreases in muscle mass during disuse and health aging. Therefore, nutritional interventions that reduce oxidation or inflammation in conjunction with higher protein intakes that overcome the anabolic resistance may enhance the MPS response to feeding and either increase muscle mass or attenuate loss. In preliminary studies, antioxidant vitamins and amino acids with antioxidant or anti-inflammatory properties show potential to restore the anabolic response associated with protein ingestion. More research, however, is required to investigate if these nutrients translate to increases in MPS and, ultimately, increased lean mass in aging humans. The purpose of the present review is to discuss the role of protein/EAA intake to enhance postprandial MPS during conditions associated with muscle loss, and bring new perspectives and challenges associated nutritional interventions aimed to optimize the anabolic effects of dietary protein/EAAs ingestion.