Omega-3 polyunsaturated fatty acids (n-3 PUFAs) are known to help resolve inflammation through generation of anti-inflammatory eicosanoids and specialized pro-resolving mediators, including resolvins, protectins, and maresins. Through binding to the GPR120/FFAR4 receptor, their beneficial effects result from phospholipid membrane remodeling, impairment of inflammatory signaling molecules clustering, subsequent inhibition of NF-κB and inflammasome activation, and a reduction in oxidative stress. Obesity, a chronic inflammatory disease that contributes to metabolic disorders, is alleviated by n-3 PUFAs. In the adipose tissue (AT) of individuals with obesity, n-3 PUFAs counteract hypoxia, inhibit immune cell infiltration and AT inflammation, improve insulin sensitivity, and reduce fat mass. Beyond AT, n-3 PUFAs also alleviate other metabolic disorders such as metabolic-associated steatotic liver disease (MASLD), gut dysbiosis, and/or renal dysfunction. In cardiovascular disease (CVD), they are mainly recommended as a secondary prevention for patients with coronary heart disease risks. This review provides an in-depth analysis of the benefits of n-3 PUFAs in obesity and related metabolic diseases, examining both the mechanistic and clinical aspects. Additionally, it also explores the effects of n-3 PUFAs in obesity-related chronic inflammatory conditions, including inflammatory bowel disease, psoriasis, rheumatoid arthritis, osteoarthritis, and multiple sclerosis, by targeting specific pathophysiological mechanisms. Clinical applications and limitations of n-3 PUFAs are discussed based on findings from human clinical trials.

Polyphenol supplementation during early life has been associated with a reduction of oxidative stress and neuroinflammation in diseases caused by oxygen deprivation, including cerebral palsy, hydrocephaly, blindness, and deafness. Evidence has shown that perinatal polyphenols supplementation may alleviate brain injury in embryonic, fetal, neonatal, and offspring subjects, highlighting its role in modulating adaptative responses involving phenotypical plasticity. Therefore, it is reasonable to infer that the administration of polyphenols during the early life period may be considered a potential intervention to modulate the inflammatory and oxidative stress that cause impairments in locomotion, cognitive, and behavioral functions throughout life. The beneficial effects of polyphenols are linked with several mechanisms, including epigenetic alterations, involving the AMP-activated protein kinase (AMPK), nuclear factor kappa B (NF-κB), and phosphoinositide 3-kinase (PI3K) pathways. To highlight these new perspectives, the objective of this systematic review was to summarize the understanding emerging from preclinical studies about polyphenol supplementation, its capacity to minimize brain injury caused by hypoxia-ischemia in terms of morphological, inflammatory, and oxidative parameters and its repercussions for motor and behavioral functions.

Quercetin supplementation during pregnancy and lactation has been linked to a lower risk of maternal cardio-metabolic disorders such as gestational diabetes mellitus (GDM), dyslipidemia, preeclampsia, attenuation of malnutrition-related conditions, and gestational obesity in animal studies. Pre-clinical studies have shown that maternal supplementation with quercetin reduces cardio-metabolic diseases in dams and rodents’ offspring, emphasizing its role in modifying phenotypic plasticity. In this sense, it could be inferred that quercetin administration during pregnancy and lactation is a viable strategy for changing cardio-metabolic parameters throughout life. Epigenetic mechanisms affecting the AMP-activated protein kinase (AMPK), nuclear factor-kappa B (NF-κB), and phosphoinositide 3-kinase (PI3 K) pathways could be associated with these changes. To highlight these discoveries, this review outlines the understanding from animal studies investigations about quercetin supplementation and its capacity to prevent or decrease maternal and offspring cardio-metabolic illnesses and associated comorbidities.

Objective: To analyze the association between ultra-processed food (UPF) consumption and cardiometabolic, biochemical, and inflammatory risk factors in children in a metropolis in Northeast Brazil. Methods: A cross-sectional study using baseline data from a community-based controlled trial was carried out with 151 children from public schools in João Pessoa, Paraíba, Brazil aged 7 to 10 years. Dietary consumption was assessed using 24 h food recall, and UPF consumption was estimated using the NOVA classification system. Anthropometry (BMI for age), blood pressure, biochemical parameters (ALT, AST, GGT, cholesterol, LDL-c, HDL-c, triglycerides, fasting glucose, HbA1c, HOMA-IR, creatinine, urea, hs-CRP), and cytokines (IL-2, IL-4, IL-6, IL-10, IL-17a, IFN-γ, and TNF-α) were also assessed. Results: Children in the third tertile (highest UPF consumption) had higher serum concentrations of LDL-c (p-value = 0.04) and ALT (p-value = 0.01), with a trend towards higher AST (p-value = 0.06). Total energy (p-value = 0.01), trans fatty acid (p-value = 0.02), and sodium (p-value = 0.04) intakes were higher in the highest tertile, whereas protein (p-value < 0.01) and fiber (p-value < 0.01) intakes were lower. Concentrations of IL-17A (p-value = 0.01) and IL-10 (p-value = 0.04) were significantly higher in the second tertile. Multiple linear regression showed that UPF consumption was significantly associated with increased LDL-c, ALT, and AST concentrations. Conclusions: High intake of UPFs was associated with dyslipidemia, elevated liver enzymes, and inflammatory changes in children. Dietary interventions are needed to reduce UPF consumption and prevent cardiometabolic and liver disease in childhood.

Evaluate autonomic function and low-grade inflammation and characterize the correlation between these variables in schoolchildren with obesity living in the Brazilian northeast region. 84 children with obesity and 41 with normal weight were included in this cross-sectional study. Anthropometry, body composition, blood pressure (BP), inflammatory biomarkers, and heart rate variability (HRV) indexes were analyzed in children aged 7 to 11 years. children with obesity had increased systolic (p = 0.0017) and diastolic (p = 0.0131) BP and heart rate (p = 0.0022). The children with obesity displayed significantly lower SDNN, RMSSD, NN50, HF (ms), HF (nu), SD1, SD2, and higher LF (ms), LF (nu), LF/HF, SD1/SD2, DFA-α1, and DFA-α2, compared to normal weight. A lower and higher capacity for producing IL-10 (p = 0.039) and IL-2 (p = 0.009), respectively, were found in children with obesity compared to children with normal weight. Although IL-2, IL-4 and IL17A did not correlate with HRV parameters, IL-6 was positively correlated with SDNN, LF (ms) and SD2, TNF-α was positively correlated with LF/HF and SD1/SD2 ratio, and IFN-γ was positively correlated with SDNN, RMMSSD, NN50, LF (ms), HF (ms), SD1, and SD2. The findings suggest that children with obesity have impaired autonomic function and systemic low-grade inflammation compared to children within the normal weight range, the inflammatory biomarkers were correlated with HRV parameters in schoolchildren living in the northeastern region of Brazil.

Background/Objectives: Depression, anxiety, and stress are highly prevalent mental disorders worldwide, and food consumption can change in individuals with these conditions. We aimed to assess the food consumption of women with depressive symptoms and compare it to a control without symptoms. Methods: A cross-sectional study was conducted with 96 women, aged 18–59, allocated into two groups: control (n = 62) or depressive symptoms (n = 34). The participants underwent an anthropometric assessment, and food consumption was evaluated using a 24 h food recall and the NOVA classification. Depressive symptoms, anxiety, and stress were measured using the DASS-21 questionnaire. Results: Anthropometric parameters did not differ between the groups. Women with depressive symptoms consumed fewer calories (p = 0.006), carbohydrates (p = 0.014), proteins (p = 0.036), and lipids (0.011) from unprocessed and minimally processed foods (UMPF) compared to the control women. A negative correlation was found between the dietary consumption energy of UMPF and symptoms of depression (r = −0.337; p = 0.001), anxiety (r = −0.262; p = 0.014), and stress (r = −0.260; p = 0.014), as well as a positive correlation between energy intake from ultra-processed foods (UPF) and symptoms of depression (r = 0.218; p = 0.042) and stress (r = 0.227; p = 0.034). Regression analysis showed that depressive symptoms accounted for 7.6% of the lower energy consumption from UMPF. Conclusions: Women with depressive symptoms displayed lower UMPF consumption, and this was negatively correlated with symptoms of depression, anxiety, and stress. Professional dietary advice can improve health status in these patients.