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.

Plasma lathosterol measures rates of cholesterol synthesis and efficiency of dietary phytosterols in reducing the plasma cholesterol concentration.

OBJECTIVES: Because the plasma campesterol/cholesterol ratio does not differ between groups that absorb different amounts of cholesterol, the authors investigated whether the plasma Phytosterols (PS) relate to the body's cholesterol synthesis rate measured as non-cholesterol sterol precursors (lathosterol). METHOD: The authors studied 38 non-obese volunteers (58±12 years; Low-Density Lipoprotein Cholesterol ‒ LDL-C ≥ 130 mg/dL) randomly assigned to consume 400 mL/day of soy milk (Control phase) or soy milk + PS (1.6 g/day) for four weeks in a double-blind, cross-over study. PS and lathosterol were measured in plasma by gas chromatography coupled to mass spectrophotometry. RESULTS: PS treatment reduced plasma total cholesterol concentration (-5.5%, p < 0.001), LDL-C (-7.6%, p < 0.001), triglycerides (-13.6%, p < 0.0085), and apolipoprotein B (apo B) (-6.3%, p < 0.008), without changing high density lipoprotein cholesterol (HDL-C concentration), but plasma lathosterol, campesterol and sitosterol expressed per plasma cholesterol increased. CONCLUSIONS: The lathosterol-to-cholesterol plasma ratio predicted the plasma cholesterol response to PS feeding. The highest plasma lathosterol concentration during the control phase was associated with a lack of response of plasma cholesterol during the PS treatment period. Consequently, cholesterol synthesis in non-responders to dietary PS being elevated in the control phase indicates these cases resist to further synthesis rise, whereas responders to dietary PS, having in the control phase synthesis values lower than non-responders, expand synthesis on alimentary PS. Responders absorb more PS than non-responders, likely resulting from responders delivering into the intestinal lumen less endogenous cholesterol than non-responders do, thus facilitating greater intestinal absorption of PS shown as increased plasma PS concentration.

Interesterified Fats Induce Deleterious Effects on Adipose Tissue and Liver in LDLr-KO Mice.

Interesterified fats are being widely used by the food industry in an attempt to replace trans fatty acids. The effect of interesterified fats containing palmitic or stearic acids on lipid metabolism and inflammatory signaling pathways in adipose and hepatic tissues was evaluated. Male LDLr-KO mice were fed a high-fat diet containing polyunsaturated (PUFA), palmitic (PALM), palmitic interesterified (PALM INTER), stearic (STEAR), or stearic interesterified (STEAR INTER) fats for 16 weeks. The expression of genes and protein levels involved in lipid metabolism and inflammatory processes in liver and white adipose tissue was determined by quantitative RT-PCR and by Western blot, respectively. The infiltration of inflammatory cells in hepatic and adipose tissues was determined by eosin and hematoxylin, while liver collagen content was determined by Sirius Red staining. Both interesterified fats increased liver collagen content and JNK phosphorylation. Additionally, the STEAR INTER group developed nonalcoholic steatohepatitis (NASH) associated with higher neutrophil infiltration. PALM INTER induced adipose tissue expansion and enlargement of adipocytes. Furthermore, PALM INTER triggered increased IKK phosphorylation and TNFα protein content, conditions associated with the upstream activation of the NFkB signaling pathway. STEAR INTER induced NASH, while PALM INTER triggered hepatic fibrosis and adipocyte hypertrophy with inflammatory response in LDLr-KO mice.

Plasma lathosterol measures rates of cholesterol synthesis and efficiency of dietary phytosterols in reducing the plasma cholesterol concentration

Abstract Objectives Because the plasma campesterol/cholesterol ratio does not differ between groups that absorb different amounts of cholesterol, the authors investigated whether the plasma Phytosterols (PS) relate to the body's cholesterol synthesis rate measured as non-cholesterol sterol precursors (lathosterol). Method The authors studied 38 non-obese volunteers (58±12 years; Low-Density Lipoprotein Cholesterol ‒ LDL-C ≥ 130 mg/dL) randomly assigned to consume 400 mL/day of soy milk (Control phase) or soy milk + PS (1.6 g/day) for four weeks in a double-blind, cross-over study. PS and lathosterol were measured in plasma by gas chromatography coupled to mass spectrophotometry. Results PS treatment reduced plasma total cholesterol concentration (-5.5%, p < 0.001), LDL-C (-7.6%, p < 0.001), triglycerides (-13.6%, p < 0.0085), and apolipoprotein B (apo B) (-6.3%, p < 0.008), without changing high density lipoprotein cholesterol (HDL-C concentration), but plasma lathosterol, campesterol and sitosterol expressed per plasma cholesterol increased. Conclusions The lathosterol-to-cholesterol plasma ratio predicted the plasma cholesterol response to PS feeding. The highest plasma lathosterol concentration during the control phase was associated with a lack of response of plasma cholesterol during the PS treatment period. Consequently, cholesterol synthesis in non-responders to dietary PS being elevated in the control phase indicates these cases resist to further synthesis rise, whereas responders to dietary PS, having in the control phase synthesis values lower than non-responders, expand synthesis on alimentary PS. Responders absorb more PS than non-responders, likely resulting from responders delivering into the intestinal lumen less endogenous cholesterol than non-responders do, thus facilitating greater intestinal absorption of PS shown as increased plasma PS concentration.

Dietary interesterified fat enriched with palmitic acid induces atherosclerosis by impairing macrophage cholesterol efflux and eliciting inflammation.

Interesterified fats are currently being used to replace trans fatty acids. However, their impact on biological pathways involved in the atherosclerosis development was not investigated. Weaning male LDLr-KO mice were fed for 16weeks on a high-fat diet (40% energy as fat) containing polyunsaturated (PUFA), TRANS, palmitic (PALM), palmitic interesterified (PALM INTER), stearic (STEAR) or stearic interesterified (STEAR INTER). Plasma lipids, lipoprotein profile, arterial lesion area, macrophage infiltration, collagen content and inflammatory response modulation were determined. Macrophage cholesterol efflux and the arterial expression of cholesterol uptake and efflux receptors were also performed. The interesterification process did not alter plasma lipid concentrations. Although PALM INTER did not increase plasma cholesterol concentration as much as TRANS, the cholesterol enrichment in the LDL particle was similar in both groups. Moreover, PALM INTER induced the highest IL-1ß, MCP-1 and IL-6 secretion from peritoneal macrophages as compared to others. This inflammatory response elicited by PALM INTER was confirmed in arterial wall, as compared to PALM. These deleterious effects of PALM INTER culminate in higher atherosclerotic lesion, macrophage infiltration and collagen content than PALM, STEAR, STEAR INTER and PUFA. These events can partially be attributed to a macrophage cholesterol accumulation, promoted by apoAI and HDL2-mediated cholesterol efflux impairment and increased Olr-1 and decreased Abca1 and Nr1h3 expressions in the arterial wall. Interesterified fats containing palmitic acid induce atherosclerosis development by promoting cholesterol accumulation in LDL particles and macrophagic cells, activating the inflammatory process in LDLr-KO mice.

The impact of dietary fatty acids on macrophage cholesterol homeostasis.

The impact of dietary fatty acids in atherosclerosis development may be partially attributed to their effect on macrophage cholesterol homeostasis. This process is the result of interplay between cholesterol uptake and efflux, which are permeated by inflammation and oxidative stress. Although saturated fatty acids (SAFAs) do not influence cholesterol efflux, they trigger endoplasmic reticulum stress, which culminates in increased lectin-like oxidized LDL (oxLDL) receptor (LOX1) expression and, consequently, oxLDL uptake, leading to apoptosis. Unsaturated fatty acids prevent most SAFAs-mediated deleterious effects and are generally associated with reduced cholesterol efflux, although α-linolenic acid increases cholesterol export. Trans fatty acids increase macrophage cholesterol content by reducing ABCA-1 expression, leading to strong atherosclerotic plaque formation. As isomers of conjugated linoleic acid (CLAs) are strong PPAR gamma ligands, they induce cluster of differentiation (CD36) expression, increasing intracellular cholesterol content. Considering the multiple effects of fatty acids on intracellular signaling pathways, the purpose of this review is to address the role of dietary fat in several mechanisms that control macrophage lipid content, which can determine the fate of atherosclerotic lesions.

Dietary phytosterol does not accumulate in the arterial wall and prevents atherosclerosis of LDLr-KO mice.

SCOPE: There have been conflicting reports on the usefulness of phytosterols (PS) in preventing atherosclerosis. We evaluated the effects of dietary PS supplementation in LDLr-KO male mice on the plasma and aorta sterol concentrations and on atherosclerotic lesion development. METHODS AND RESULTS: Mice were fed a high fat diet (40% of energy) supplemented with or without PS (2% w/w, n = 10). Plasma and arterial wall cholesterol and PS concentrations, lesion area, macrophage infiltration, and mRNA expression from LOX-1, CD36, ABCA1 and ABCG1 in peritoneal macrophages were measured. After 16 weeks, the plasma cholesterol concentration in PS mice was lower than that in the controls (p = 0.02) and in the arterial wall (p = 0.03). Plasma PS concentrations were higher in PS-fed animals than in controls (p < 0.0001); however, the arterial wall PS concentration did not differ between groups. The atherosclerotic lesion area in the PS group (n = 5) was smaller than that in controls (p = 0.0062) and the macrophage area (p = 0.0007). PS correlates negatively with arterial lipid content and macrophage (r = -0.76; p < 0.05). PS supplementation induced lower ABCG1 mRNA expression (p < 0.05). CONCLUSIONS: Despite inducing an increase in PS plasma concentration, PS supplementation is not associated with its accumulation in the arterial wall and prevents atherosclerotic lesion development.

The role of dietary fatty acids in the pathology of metabolic syndrome.

Dysfunctional lipid metabolism is a key component in the development of metabolic syndrome, a very frequent condition characterized by dyslipidemia, insulin resistance, abdominal obesity and hypertension, which are related to an elevated risk for type 2 diabetes mellitus. The prevalence of metabolic syndrome is strongly associated with the severity of obesity; its physiopathology is related to both genetics and food intake habits, especially the consumption of a high-caloric, high-fat and high-carbohydrate diet. With the progress of scientific knowledge in the field of nutrigenomics, it was possible to elucidate how the majority of dietary fatty acids influence plasma lipid metabolism and also the genes expression involved in lipolysis and lipogenesis within hepatocytes and adipocytes. The aim of this review is to examine the relevant mechanistic aspects of dietary fatty acids related to blood lipids, adipose tissue metabolism, hepatic fat storage and inflammatory process, all of them closely related to the genesis of metabolic syndrome.

Cardiovascular risks in adolescents with different degrees of obesity.

BACKGROUND: There have been few studies on cardiovascular risk factors in adolescents with different degrees of obesity. OBJECTIVE: To evaluate metabolic effects associated with different degrees of obesity in adolescents and their impact on cardiovascular risks. METHODS: Cross-sectional study of 80 obese adolescents, divided in two groups: 22.5, classified as obese with lower or higher degree of obesity, respectively. Physical examination was carried out, as well as biochemical and body composition assessment. The statistical analysis was performed with t-Student and Chi-square tests, aiming at comparing both groups. A multiple logistic model was used to verify the associations between the biochemical variables and the degree of obesity. Risk scores were developed for cardiovascular disease, according to the number of alterations found in the following variables: fasting glycemia, triglycerides, HDL and blood pressure. Association between these scores and degree of obesity were verified. RESULTS: The two groups differed regarding weight, waist circumference, fasting glycemia and insulin, HOMA-IR, triglycerides, HDL, blood pressure (BP) and body composition measurements (p<0.05). The adolescents with the higher degree of obesity presented higher frequencies of alterations for glycemia, HOMA-IR, triglycerides, HDL and BP (p<0.05). The logistic model showed associations between the degree of obesity and the variables: HDL (OR=5.43), BP (OR=4.29), TG (OR=3.12). The risk score demonstrated that 57.7% of the adolescents with higher degrees of obesity had two or more metabolic alterations versus 16.7% from the other group (p<0.001). CONCLUSION: The degree of obesity influenced the onset of alterations that comprise the metabolic syndrome, increasing the cardiovascular risk.

Riscos cardiovasculares em adolescentes com diferentes graus de obesidade / Cardiovascular risks in adolescents with different degrees of obesity / Riesgos cardiovasculares en adolescentes con diferentes grados de obesidad

FUNDAMENTO: Há poucos estudos sobre riscos cardiovasculares em adolescentes com diferentes graus de obesidade. OBJETIVO: Avaliar repercussões metabólicas associadas a diferentes graus de obesidade em adolescentes e seu impacto nos riscos cardiovasculares. MÉTODOS: Estudo transversal com 80 adolescentes obesos, divididos em dois grupos: 2

BACKGROUND: There have been few studies on cardiovascular risk factors in adolescents with different degrees of obesity. OBJECTIVE: To evaluate metabolic effects associated with different degrees of obesity in adolescents and their impact on cardiovascular risks. METHODS: Cross-sectional study of 80 obese adolescents, divided in two groups: 2

FUNDAMENTO: Existen pocos estudios sobre riesgos cardiovasculares en adolescentes con diferentes grados de obesidad. OBJETIVO: Evaluar repercusiones metabólicas asociadas a diferentes grados de obesidad en adolescentes y su impacto en los riesgos cardiovasculares. MÉTODOS: Estudio transversal con 80 adolescentes obesos, divididos en dos grupos: 2

Sedentarismo e variáveis clínico-metabólicas associadas à obesidade em adolescentes / Inactivity and clinical and metabolic variables associated with adolescent obesity

OBJETIVO: Estudar a associação da obesidade com variáveis metabólicas, variáveis clínicas e sedentarismo, em adolescentes pós-púberes de escolas públicas de São Paulo. MÉTODOS: Estudo caso-controle com 128 adolescentes obesos (índice de massa corporal > percentil 95) e 151 adolescentes eutróficos (índice de massa corporal entre percentis 5 e 85). Foram realizados exame físico, avaliação bioquímica e de composição corporal. RESULTADOS Por meio da análise de variância, foi identificado um gradiente nos valores médios das variáveis metabólicas e clínicas com piora dessas variáveis em paralelo ao aumento do grau de sedentarismo, o que foi confirmado pelo teste qui-quadrado. Na análise bivariada de riscos para obesidade, os adolescentes obesos apresentaram maiores frequências de sedentarismo, de alterações nos níveis de lipoproteína de alta densidade e triglicérides, de hiperinsulinemia e homeostasis model assessment for insulin resistence alterado, e de pressão arterial alterada (p<0,05). O modelo logístico múltiplo mostrou associações entre obesidade e variáveis de sedentarismo (OR=2,23), lipoproteína de alta densidade reduzida (OR=3,05), pressão arterial alterada (OR=3,57), triglicerídeos aumentados (OR=4,13) e homeostasis model assessment for insulin resistence aumentado (OR=11,65). CONCLUSÃO: Sedentarismo, lipoproteína de alta densidade reduzida, hipertrigliceridemia, resistência insulínica e hipertensão estão fortemente associados com a obesidade em adolescentes. Estratégias para redução do peso corporal por meio de mudanças nos hábitos de vida devem fazer parte das políticas e programas de saúde pública, especialmente para essa faixa etária.

OBJECTIVE: This study investigated the association of obesity with metabolic and clinical variables and inactivity in post-pubertal adolescents attending public schools in São Paulo City. METHODS: This was a case-control study with 128 obese adolescents (body mass indices >the 95th percentile), and 151 normal weight adolescents (body mass indices between the 5th and 85th percentiles). Physical examination and biochemical and body composition assessments were done. A pretested questionnaire was administered, generating an inactivity score. Analysis of variance was performed with multiple comparison tests (Bonferroni and Pearson's chi-Square). A multiple regression model was used to ascertain the association among clinical variables, metabolic variables, inactivity score and nutritional status. RESULTS: Analysis of variance allowed the identification of a gradient of mean metabolic and clinical variables which worsened as activity decreased, confirmed by the chi-square test. In the bivariate analysis for obesity risk, obese adolescents were more frequently inactive, presented low high-density lipoprotein and high triglyceride levels, hyperinsulinemia, high homeostasis model assessment for insulin resistance, and high blood pressure (p<0.05). The multiple logistic model showed associations between obesity and inactivity (OR=2.23), low high-density lipoprotein levels (OR=3.05), high blood pressure (OR=3.57), high triglyceride levels (OR=4.13) and high homeostasis model assessment for insulin resistance (OR=11.65). CONCLUSION: Inactivity, low high-density lipoprotein, hypertriglyceridemia, insulin resistance and hypertension are strongly associated with obesity in adolescents. Strategies to reduce body weight by changing life habits should be part of public health programs and policies, especially for this age group.