Position statement on nutrition therapy for overweight and obesity: nutrition department of the Brazilian association for the study of obesity and metabolic syndrome (ABESO-2022).

Obesity is a chronic disease resulting from multifactorial causes mainly related to lifestyle (sedentary lifestyle, inadequate eating habits) and to other conditions such as genetic, hereditary, psychological, cultural, and ethnic factors. The weight loss process is slow and complex, and involves lifestyle changes with an emphasis on nutritional therapy, physical activity practice, psychological interventions, and pharmacological or surgical treatment. Because the management of obesity is a long-term process, it is essential that the nutritional treatment contributes to the maintenance of the individual's global health. The main diet-related causes associated with excess weight are the high consumption of ultraprocessed foods, which are high in fats, sugars, and have high energy density; increased portion sizes; and low intake of fruits, vegetables, and grains. In addition, some situations negatively interfere with the weight loss process, such as fad diets that involve the belief in superfoods, the use of teas and phytotherapics, or even the avoidance of certain food groups, as has currently been the case for foods that are sources of carbohydrates. Individuals with obesity are often exposed to fad diets and, on a recurring basis, adhere to proposals with promises of quick solutions, which are not supported by the scientific literature. The adoption of a dietary pattern combining foods such as grains, lean meats, low-fat dairy, fruits, and vegetables, associated with an energy deficit, is the nutritional treatment recommended by the main international guidelines. Moreover, an emphasis on behavioral aspects including motivational interviewing and the encouragement for the individual to develop skills will contribute to achieve and maintain a healthy weight. Therefore, this Position Statement was prepared based on the analysis of the main randomized controlled studies and meta-analyses that tested different nutrition interventions for weight loss. Topics in the frontier of knowledge such as gut microbiota, inflammation, and nutritional genomics, as well as the processes involved in weight regain, were included in this document. This Position Statement was prepared by the Nutrition Department of the Brazilian Association for the Study of Obesity and Metabolic Syndrome (ABESO), with the collaboration of dietitians from research and clinical fields with an emphasis on strategies for weight loss.

Effects of resveratrol on inflammation and oxidative stress induced by the uremic toxin indoxyl sulfate in Murine macrophage-like RAW 264.7.

Indoxyl sulfate (IS) is a uremic toxin produced by the gut microbiota that commonly accumulates in patients with chronic kidney disease (CKD) and can be harmful. Resveratrol is a polyphenol with properties that attenuate oxidative stress and inflammation. This study aims to evaluate the effect of resveratrol against the damage caused by IS in RAW 264.7 murine macrophages. Cells were treated with 0, 250, 500 and 1000 µmol/L of IS, in the presence of 50 µmol/L of resveratrol. The mRNA and protein expressions of erythroid-related nuclear factor 2 (Nrf2) and nuclear factor kappa-B (NF-κB) were measured using rt-PCR and Western blot analysis, respectively. Malondialdehyde (MDA) and reactive oxygen species (ROS) levels were also analyzed. As a result, it was demonstrated that resveratrol induces the activation of the Nrf2 pathway that enhances cytoprotective response. IS upregulated the NF-κB expression and downregulated the Nrf2 expression. In contrast, resveratrol treatment significantly reduced the MDA and ROS production and inhibited the IS-induced expression of NF-κB in macrophage-like RAW 264.7. In conclusion, resveratrol can mitigate inflammation and oxidative stress caused by uremic toxins produced by the gut microbiota, such as IS.

Can Resveratrol Supplementation Reduce Uremic Toxin Plasma Levels From the Gut Microbiota in Nondialyzed Patients With Chronic Kidney Disease?

OBJECTIVES: Uremic toxins such as indoxyl sulfate (IS), p-cresyl sulfate (pCS), and indole-3-acetic acid (IAA) produced by the gut microbiota are recognized as risk factors for many comorbidities, including cardiovascular diseases. Patients with chronic kidney disease (CKD) have an accumulation of these toxins, and nutritional strategies have been proposed to mitigate gut dysbiosis and, consequently, reduce these toxins. This study aimed to evaluate the effects of resveratrol supplementation on the plasma levels of IS, pCS, and IAA in nondialyzed patients with CKD. METHODS: In this placebo-controlled crossover study, twenty nondialyzed patients were randomly divided into two groups: they received either one capsule/day containing 500 mg of trans-resveratrol (63 ± 7.5 years, glomerular filtration rate [GFR]: 34 ± 14 mL/min, body mass index: 26.8 ± 5.6 kg/m2) or a placebo containing 500 mg wheat flour (62 ± 8.4 years, GFR: 34 ± 13 mL/min, body mass index: 28.6 ± 4.4 kg/m2) during 4 weeks. After 8 weeks of washout (no supplementation), another 4 weeks of supplementation with crossover was initiated. IS, IAA, and pCS plasma levels were quantified by the reverse phase high-efficiency liquid chromatography method with fluorescent detection. The mRNA expression of nuclear factor erythroid 2-related factor 2 and nuclear factor kappa B in peripheral blood mononuclear cells was evaluated by polymerase chain reaction. C-reactive protein plasma levels were also evaluated. RESULTS: As expected, the uremic toxin levels were negatively correlated with the GFR, but no effect of trans-resveratrol supplementation was found on levels of IS, IAA, and pCS. There was a positive correlation between IS and nuclear factor erythroid 2-related factor 2 (r = 0.24, P = .03) and also between IS and C-reactive protein (r = 0.21, P = .05). CONCLUSION: Supplementation with trans-resveratrol did not reduce the plasma levels of IS, pCS, and IAA in nondialyzed patients with CKD. The interactions among uremic toxins and anti-inflammatory and proinflammatory pathways deserve more studies.

Effects of Resveratrol Supplementation in Nrf2 and NF-κB Expressions in Nondialyzed Chronic Kidney Disease Patients: A Randomized, Double-Blind, Placebo-Controlled, Crossover Clinical Trial.

INTRODUCTION: Resveratrol is a phenolic compound that has demonstrated anti-inflammatory and antioxidant effects, resulting from enhanced antioxidant enzymes production and modulating nuclear factors involved in the inflammation-oxidative stress cycle, as nuclear erythroid 2-related factor 2 (Nrf2) and nuclear factor-κB (NF-κB). OBJECTIVE: The study aim was to evaluate the effects of resveratrol supplementation on Nrf2 and NF-κB expression in nondialyzed chronic kidney disease (CKD) patients. MATERIALS AND METHODS: A randomized, double-blind, crossover trial was performed in 20 nondialyzed CKD patients (62.0 ± 8.0 years old, 45% men, body mass index of 27.7 ± 1.2 kg/m2, estimated glomerular filtration rate of 34.0 ± 13.0 mL/minute). Eleven patients were randomly allocated to "placebo first" (4 weeks placebo; 8 weeks washout, 4 weeks 500 mg of resveratrol/day) and 9 to "resveratrol first" (4 weeks 500 mg of resveratrol/day, 8 weeks washout, 4 weeks placebo). The peripheral blood mononuclear cells were isolated and processed for expression Nrf2 and NF-κB by quantitative real-time polymerase chain reaction. Proinflammatory cytokines and antioxidant enzymes were also measured. RESULTS: The effect size of Nrf2 supplementation (-0.13, P = .29) and NF-κB (0.09, P = .31) was not significant. There was no difference in proinflammatory biomarkers or antioxidant biomarkers after resveratrol supplementation. CONCLUSION: In this pilot study, 500 mg of resveratrol supplementation for 4 weeks had no antioxidant and anti-inflammatory effect in nondialyzed CKD patients. Additional studies with differing doses and/or time of treatment should be conducted to better elucidate the effects of the resveratrol supplementation in CKD patients.

Determination of the binding properties of the uremic toxin phenylacetic acid to human serum albumin.

Uremic toxins are compounds normally excreted in urine that accumulate in patients with chronic kidney disease as a result of decreased renal clearance. Phenylacetic acid (PAA) has been identified as a new protein bound uremic toxin. The purpose of this study was to investigate in vitro the interaction between PAA and human serum albumin (HSA) at physiological and pathological concentrations. We used ultrafiltration to show that there is a single high-affinity binding site for PAA on HSA, with a binding constant on the order of 3.4 × 10(4) M(-1) and a maximal stoichiometry of 1.61 mol per mole. The PAA, at the concentration reported in end-stage renal patients, was 26% bound to albumin. Fluorescent probe competition experiments demonstrated that PAA did not bind to Sudlow's site I (in subdomain IIA) and only weakly bind to Sudlow's site II (in subdomain IIIA). The PAA showed no competition with other protein-bound uremic toxins such as p-cresyl-sulfate or indoxyl sulfate for binding to serum albumin. Our results provide evidence that human serum albumin can act as carrier protein for phenylacetic acid.

The uremic toxin indoxyl sulfate exacerbates reactive oxygen species production and inflammation in 3T3-L1 adipose cells.

Inflammation and oxidative stress are common features of patients with chronic kidney disease (CKD) and many uremic solutes retained in these patients could be involved in these processes, among which protein-bound solutes such as indoxyl sulfate (IS). White adipose tissue recently gained attention as an important source of inflammation and oxidative stress. To examine the effect of IS on adipocytes, 3T3-L1 adipose cells were incubated with IS to mimic the conditions encountered in uremic patients. Incubation of adipose cells with IS increased reactive oxygen species production generated mainly through activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase since it was prevented by the NADPH oxidase inhibitor apocynin. Exposure to IS furthermore exacerbated the secretion of tumor necrosis factor-α and interleukin-6 by adipose cells. This inflammatory response was prevented by NADPH oxidase inhibition pinpointing the pivotal role of intracellular oxidative stress. IS induces adipocyte perturbation and promotes inflammatory state mainly through induction of oxidative stress. IS, a uremic toxin, accumulates in CKD patients could, therefore, be an important mediator of adipocyte dysfunction in these patients.

NRF2 and NF-κB mRNA expression in chronic kidney disease: a focus on nondialysis patients.

PURPOSE: To evaluate nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor-kappaB (NF-κB) mRNA expression in nondialysis chronic kidney disease (CKD) patients, comparing with data from hemodialysis (HD) patients and healthy individuals. METHODS: Twenty nondialysis CKD patients (62.0 ± 8.1 years old, 11 men, estimated glomerular filtration rate of 36.8 ± 13.6 mL/min/1.73 m(2)), twenty HD patients (55.0 ± 15.2 years old, 13 men, and dialysis vintage of 76.5 ± 46.3 months) and eleven healthy individuals (50.9 ± 8.0 years old, 6 men) were enrolled in the study. The peripheral blood mononuclear cells were isolated and processed for the evaluation of expression of NF-κB and Nrf2 by quantitative real-time polymerase chain reaction. RESULTS: Nrf2 mRNA expression was significantly higher in nondialysis (1.12 ± 0.57) when compared to HD patients (0.58 ± 0.35, p = 0,006) but similar to healthy individuals (1.13 ± 0.64). Inversely, NF-κB mRNA expression was lower in nondialysis (1.21 ± 0.71) when compared to HD patients (2.08 ± 0.7, p < 0.0001) and similar to healthy individuals (1.04 ± 0.22). Nrf2 mRNA was positively correlated with NF-κB mRNA expression in nondialysis CKD patients (r = 0.52, p = 0.02) and healthy individuals (r = 0.77, p < 0.006). By contrast, Nrf2 mRNA was inversely correlated with NF-κB mRNA expression (r = -0.65, p = 0.003) in HD patients. CONCLUSION: Nondialysis CKD patients may conserve regular homeostatic balance between Nrf2 and NF-κB expressions, being comparable to healthy individuals. However, HD patients seem to have Nrf2 downregulation and NF-κB upregulation. Thus, the association among Nrf2 and NF-κB expressions and nutritional status, kidney disease progression or immune deregulation deserve further investigation.

Cardiovascular Mortality in Chronic Kidney Patients: the Role of Uremic Toxins / Mortalidade Cardiovascular em Pacientes Renais Crônicos: o Papel das Toxinas Urêmicas

A doença cardiovascular (DCV) é a maior causa de morte nos pacientes com doença renal crônica (DRC) nomundo. Vários fatores estão associados a essa elevada mortalidade e, recentemente, as toxinas urêmicas produzidas pela microbiota intestinal têm recebido bastante atenção, já que a falência renal cursa com o acúmulo dessas toxinas no plasma. Essas toxinas têm relação com estresse oxidativo, inflamação, disfunção endotelial e induçãoda aterosclerose e, recentes estudos têm observado que pacientes com elevados níveis de tais toxinas têm aumento na mortalidade por DCV. Assim, o objetivo da presente revisão foi discutir o papel das toxinas urêmicasprovenientes da microbiota intestinal e seu impacto na mortalidade cardiovascular em pacientes renais crônicos, bem como as possíveis perspectivas terapêuticas que podem ser elucidadas a partir do conhecimento aprofundado do tema...

The cardiovascular disease (CVD) is the leading cause of death in patients with chronic kidney disease (CKD) in the world. Several factors are associated with this high mortality. Recently, the uremic toxins produced by intestinal microbiota have received extensiveattention from researchers, since kidney failure evolves with the accumulation of these toxins in the plasma. These toxins are related to oxidative stress, inflammation, endothelial dysfunction, and induction of atherosclerosis, and recent studies have noted thatpatients with high levels of these toxins have increased mortality due to CVD. Therefore, the purpose of this review was to discuss the role of uremic toxins from the intestinal microbiota and their impact on cardiovascular mortality in CKD patients, as well as the possible therapeutic perspectives that can be explained based on an in-depth understanding of the subject...

Resveratrol: why is it a promising therapy for chronic kidney disease patients?

Resveratrol, a phenolic compound found in various plants, including grapes, berries, and peanuts, shows promise for the treatment of cancer, aging, type 2 diabetes, and cardiovascular diseases. Resveratrol can promote transcription factor nuclear factor-erythroid 2-related factor 2 (Nrf2) activation, increase the expression level of SIRT-1, which is a sirtuin family protein, and reduce mTOR pathway signaling. This compound has anti-inflammatory properties in that it inhibits or antagonizes the nuclear factor-κB (NF-κB) activity, which is a redox-sensitive transcription factor that coordinates the inflammatory response. Inflammation and oxidative stress, which are common features in patients with chronic kidney disease (CKD), are interrelated and associated with cardiovascular disease and the progression of CKD itself. Because of the modulation of the mechanisms involved in the inflammatory-oxidative stress cycle, resveratrol could play an important role in controlling CKD-related metabolic derangements. Although resveratrol supplementation in theory is a promising therapy in this patient group, there are no studies evaluating its effects. Thus, the present review aims to describe the role of resveratrol in inflammation and oxidative stress modulation and its possible benefits to patients with CKD.

Enamel matrix derivative versus guided tissue regeneration in the presence of nicotine: a histomorphometric study in dogs.

AIM: The goal of this histometric study was to compare the healing process of dehiscence-type defects treated by enamel matrix derivative (EMD) or guided tissue regeneration (GTR) under the effect of nicotine in the dog model. MATERIALS AND METHODS: Eight mongrel dogs were used. Buccal osseous dehiscences were surgically created on the mesial roots of the mandibular third and fourth pre-molars. The defects were exposed to plaque accumulation for 3 months. After this period, the defects were randomly assigned to one of the treatments: open flap debridement (OFD), EMD or GTR with a resorbable membrane. During 4 months, the dogs received subcutaneous administration of nicotine (2 mg/kg twice a day with a 12 h interval between the applications). After this period, the animals were killed and the blocks were processed. The histometric parameters evaluated included gingival recession, epithelial length, connective tissue adaptation, new cementum and new bone. RESULTS: A superior length of new cementum was observed in the sites treated by EMD in comparison with OFD (p< or =0.05). No statistically significant differences were observed between GTR and the other groups. CONCLUSIONS: In the presence of nicotine, EMD may promote more new cementum formation than OFD while GTR failed to provide a significant difference.

Smoking may affect the alveolar process dimensions and radiographic bone density in maxillary extraction sites: a prospective study in humans.

PURPOSE: Loss of ridge width and height typically occur after tooth extraction. This study aimed to investigate whether smoking would effect alveolar ridge remodeling after tooth extraction. MATERIALS AND METHODS: Twenty-one individuals (11 nonsmokers, 10 smokers) requiring a nonmolar extraction in the upper jaw were selected. Radiographs were taken 7 and 180 days after surgery, and the following parameters obtained: alveolar process height (AH), alveolar process width (AW), radiographic bone density in the postextraction socket (BDS), and in the pre-existing bone apically (BDPB). RESULTS: Six months after surgery, intragroup analysis showed that both groups presented a significant reduction in AH, while only smokers had a significant reduction in AW, BDS, and BDPB (P < .05). Furthermore, intergroup analysis showed that smokers presented lower BDS (91.45 pixels +/- 26.62 and 59.53 pixels +/- 19.99, for nonsmokers and smokers, respectively; P = .006) and continued to present lower BDPB (129.34 pixels +/- 42.10 and 89.29 pixels +/- 29.96, for nonsmokers and smokers, respectively; P = .023). Additionally, smokers presented a tendency for lower AH and AW than nonsmokers, but this was not statistically significant. CONCLUSION: Within the limits of the present study, smoking may lead to a more significant dimensional reduction of the residual alveolar ridge and postpone postextraction socket healing.

Coronally positioned flap with or without acellular dermal matrix graft in gingival recessions: a histometric study.

PURPOSE: To evaluate, histometrically, the healing of gingival recession treated by coronally positioned flaps (CPF) with or without acellular dermal matrix (ADM) as a subepithelial graft. METHODS: Gingival recessions were created on the upper cuspids of six dogs and were randomly assigned to: CPF+ADM (ADM group) or CPF alone (CPF group). After 4 months, the dogs were sacrificed, and the histometric measurements were performed. RESULTS: The epithelial length was 2.28 + 0.92 mm and 2.10 + 0.46 mm for the ADM and CPF groups, respectively (P=0.74). The connective tissue adaptation was 0.05 + 0.08 mm for the ADM group and 0.06 + 0.08 mm for the CPF group (P=0.36). The new cementum was 2.35 + 1.55 mm and 2.90 + 0.96 mm in the ADM and CPF groups, respectively (P=0.53). The new bone was 0.60 + 1.36 mm for the ADM group and 0.35 + 0.82 mm for the CPF group (P=0.53). The gingival recession was -0.88 + 1.33 mm in the ADM group and -0.21 + 0.22 mm in the CPF group (P=0.21). The gingival thickness was 1.63 + 0.28 mm in the ADM group and 1.16 + 0.20 mm in the CPF group (P=0.002).

Irrigação subgengival com clorexidina. Quais os benefícios? / Subgingival irrigation with chlorhexidine. Which are the benefits?

Diante da associação da placa bacteriana com o desenvolvimento da gengivite e progressão da periodontite, agentes químicos de controle de placa têm sido empregados na prevenção da doença periodontal e no seu tratamento. A clorexidina tem sido considerada o gold standard dos agentes antiplaca, porém seus efeitos colaterais limitam seu uso prolongado para prevenção. Sabendo-se da dificuldade dos antimicrobianos atingirem as porções mais profundas das bolsas periodontais através de meios conven¬cionais, como escovação e bochechos, grande interesse foi dado à aplicação de clorexidina diretamente no interior das bolsas periodontais. Logo, o objetivo deste trabalho é apresentar uma revista bibliográfica com os estudos que utilizaram a clorexidina para irrigação subgengival, como método coadjuvante da terapia mecânica convencional, avaliando seus possíveis benefícios.

Histologic evaluation of the effect of nicotine administration on bone regeneration: a study in dogs

O objetivo do presente estudo foi avaliar histometricamente a influência da nicotina sobre a regeneração óssea de defeitos criados cirurgicamente em rebordos alveolares edêntulos de cães. Defeitos ósseos foram criados cirurgicamente em um dos lados da mandíbula de dezesseis cães e foram deixados para que curassem espontanea-mente. Os animais foram aleatoriamente designados para um dos seguintes grupos: Grupo 1 - controle (n = 8) e Grupo 2 - administração subcutânea de nicotina (2 mg/kg) duas vezes ao dia durante 4 meses (n = 8). Os animais foram sacrificados, e secções semi-seriadas descalcificadas, obtidas. Os parâmetros histométricos avaliados foram altura, largura, área e densidade do tecido ósseo neoformado. A análise intergrupos (Mann-Whitney "rank sum test") demonstrou que a administração de nicotina não influenciou altura, largura e área de tecido ósseo neoformado (p > 0,05). Entretanto, a administração de nicotina influenciou significativamente a densidade do tecido ósseo neoformado (p < 0,001). Dentro dos limites do presente estudo, pode-se concluir que a nicotina pode afetar, mas não impedir a regeneração de defeitos ósseos criados cirurgicamente em mandíbulas edêntulas de cães.

Enamel matrix derivative and guided tissue regeneration in the treatment of dehiscence-type defects: a histomorphometric study in dogs.

BACKGROUND: The goal of this investigation was to histologically and histometrically evaluate the healing process of dehiscence-type defects treated by enamel matrix derivative (EMD) and/or guided tissue regeneration (GTR). METHODS: Seven mongrel dogs were used. Buccal osseous dehiscences were surgically created on the mesial roots of the mandibular third and fourth premolars. The defects were exposed to plaque accumulation for 3 months. After this period, the defects were randomly assigned to one of the treatments: open flap debridement (OFD), enamel matrix derivative (EMD), GTR with bioabsorbable membrane (GTR), and the combination of both procedures (EMD + GTR). After 4 months of healing, the dogs were sacrificed and the blocks were processed. The histometric parameters evaluated included gingival recession, epithelial length, connective tissue adaptation, new cementum, and new bone. RESULTS: A superior length of new cementum was observed in the sites treated by EMD (3.7 mm) and EMD + GTR (3.8 mm) in comparison with OFD (2.4 mm) (P < 0.05). No statistically significant differences were found in the remaining histometric parameters. CONCLUSIONS: Within the limits of this study, it can be concluded that EMD alone or in combination with GTR barriers may effectively promote new cementum formation. The combination of both therapies may not provide additional benefits.

Guided bone regeneration may be negatively influenced by nicotine administration: a histologic study in dogs.

BACKGROUND: A series of animal and in vitro data confirms that nicotine impairs bone healing, diminishes osteoblast function, and causes autogenous bone graft morbidity. Therefore, this study aimed to investigate the impact of nicotine on the healing of bone defects treated by the guided bone regeneration (GBR) principle. METHODS: Sixteen mongrel dogs were used. One defect was surgically created bilaterally and randomly assigned as an expanded polytetrafluoroethylene (ePTFE) membrane site or a non-membrane control site. The animals were randomly assigned to one of the following groups: group 1, placebo (n = 8) and group 2, subcutaneous administration of nicotine (2 mg/kg) twice daily (n = 8). After 4 months, the animals were sacrificed and the specimens routinely processed for semi-serial decalcified sections. The evaluated parameters were bone height, bone width, bone density, and bone area of newly formed bone. RESULTS: Intergroup analysis (Kruskal-Wallis) showed that membrane-protected defects in the placebo group demonstrated an increased bone area when compared to membrane-protected defects in the nicotine group and non-membrane sites, regardless of nicotine administration (P < 0.05). In addition, nicotine administration significantly affected bone density in membrane- and non-membrane-protected sites (P < 0.05). CONCLUSIONS: Within the limits of the present study, nicotine might affect, but not prevent, bone healing in defects treated by guided bone regeneration. The mechanisms of this effect should be investigated further.

Histologic evaluation of the effect of nicotine administration on bone regeneration. A study in dogs.

The objective of this study was to investigate the histometric impact of nicotine on bone regeneration of surgically created alveolar ridge defects in dogs. Sixteen mongrel dogs were used. One defect was surgically created unilaterally in the mandible, and left to heal spontaneously. The animals were randomly assigned to one of the following groups: Group 1--control (n = 8) and Group 2--subcutaneous nicotine administration (2 mg/kg) twice a day (n = 8). After 4 months, the animals were sacrificed and the specimens routinely processed for semi-serial decalcified sections. Bone height (BH), bone width (BW), bone density (BD), and bone area (BA) of the newly-formed bone were evaluated. Intergroup analysis (Mann-Whitney rank sum test) showed that regardless of the presence of nicotine, no significant differences were observed regarding bone width (BW), bone area (BA) and bone height (BH) (p > 0.05). On the other hand, it was demonstrated that nicotine administration significantly influenced the proportion of mineralized tissue within the limits of the newly-formed bone (BD) (p < 0.001). Within the limits of the present study, it can be concluded that nicotine might affect but not prevent bone healing in defects left to heal spontaneously.