Search

Background and Aims: Chronic Kidney Disease (CKD) is characterized by slow, progressive, and irreversible kidney function loss and the disease itself and hemodialysis treatment can predispose an inflammatory state that increased cardiovascular complications, being one of major mortality causes in kidney patients. The study purpose was to evaluate nutritional profile and impacts of w-3 fatty acid supplementation on inflammatory parameters and cardiovascular events risk in patients with CKD undergoing hemodialysis treatment., Methods: Non-randomized clinical trial, patients with CKD were randomly grouped into a control (n = 29) and supplemented (n = 30) group. Supplemented group patients were instructed to consume two w-3 capsules a day (2g/day) for 8 weeks for further analysis of pre- and post-supplementation C-reactive protein (CRP) and other blood parameters. To nutritional status assessment, anthropometric and bioelectrical impedance data were measured, carried out close to supplementation start., Results: 59 patients were evaluated, 49.1% (n = 29) were overweight and 70.7% (n = 41) had high percentage of body fat. Comparing control versus supplemented groups after supplementation serum CRP levels have reduced, no differences were observed (p = 0.716) nevertheless there was reduction in cardiovascular events risk according to C-reactive protein classification (p = 0.004). Ferritin levels have improved in all groups. Changes in the levels of other biochemical markers hemoglobin, hematocrit, urea, creatinine, and Kt/v have happened. However, group that received w-3 showed an improvement in serum albumin levels (p = 0.014), in addition to demonstrating greater adequacy classification of albumin after supplementation (p = 0.022)., Conclusion: Omega-3 supplementation have caused an improvement in albumin plasma levels suitableness in Chronic Kidney Disease patients, however, it did not demonstrate statistical effects to reducing CRP levels, although this helped to reduce cardiovascular risk., Competing Interests: Declaration of competing interest The authors have no conflicts of interest, or other relationships with people or organizations that could influence the present article., (Copyright © 2023 European Society for Clinical Nutrition and Metabolism. Published by Elsevier Ltd. All rights reserved.)

Purpose of Review: Systemic cancer therapy-associated skeletal muscle wasting is emerging as a powerful impetus to the overall loss of skeletal muscle experienced by patients with cancer. This review explores the clinical magnitude and biological mechanisms of muscle wasting during systemic cancer therapy to illuminate this adverse effect. Emerging strategies for mitigation are also discussed., Recent Findings: Clinical findings include precise, specific measures of muscle loss over the course of chemotherapy, targeted therapy and immunotherapy. All these therapeutic classes associate with quantitatively important muscle loss, independent of tumor response. Parallel experimental studies provide understanding of the specific molecular basis of wasting, which can include inhibition of protein synthesis, proliferation and differentiation, and activation of inflammation, reactive oxygen species, autophagy, mitophagy, apoptosis, protein catabolism, fibrosis and steatosis in muscle. Strategies to mitigate these muscle-specific adverse effects of cancer therapy remain in the earliest stages of development., Summary: The adverse side effect of cancer therapy on skeletal muscle has been largely ignored in the development of cancer therapeutics. Given the extent to which loss of muscle mass and function can bear on patients' function and quality of life, protection/mitigation of these side effects is a research priority., (Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)

This research aimed to evaluate the interdisciplinary educational intervention effects on knowledge of eating, nutrition, and physical activity in elementary-school students. Participants were 368 school children enrolled in public schools. The research was organized in three stages: pre-intervention, intervention and post-intervention. In pre-intervention, children were evaluated regarding their nutritional status. They also answered questionnaires related to eating and nutrition and physical activity. In the intervention stage, educational interventions were carried out on the same topics for a period of five months; in post-intervention, children answered the same questionnaires applied in pre-intervention. Despite most children having normal nutritional status (58.2%), a high number of students were overweight (38%). In the initial phase, it was found that most children had excellent knowledge of eating, nutrition, and good physical activity knowledge (p-value < 0.05). Educational health intervention significantly increased children’s knowledge of eating, nutrition, and physical activity, when evaluated in the post-intervention period. Both boys and girls increased their knowledge of eating, nutrition, and physical activity after the application of interdisciplinary interventions (p-value < 0.05). A similar effect was observed for children with different nutritional status. It is concluded that interdisciplinary educational interventions carried out for children in an elementary-school environment are effective for improving knowledge of eating, nutrition, and in physical activity, promoting healthier habits among children.

Background and Aims: Weight loss is present in most cancer patients, being even more frequent in gastrointestinal tract tumors (GIT). Malnourished patients may be at greater toxicity risk during treatment, which may interfere with survival. Tumor-triggered hypercatabolism can lead to impaired nutritional status. In addition, other factors such as the presence of nutritional impact symptoms (NIS) can lead to decrease food consumption, influencing weight loss. The purpose of this study was verify nutritional status and understand which factors are related to survival and weight loss in patients with gastrointestinal tract cancers., Methods: This study is a retrospective cross-sectional, with data collected from patient's medical records with the gastrointestinal tract cancers, between the years 2012-2019. Data were classified of tumor location, disease staging, weight change, number of nutritional impact symptoms and diet at the treatment beginning. Survival was calculated using the start of treatment and death dates., Results: A total of 388 medical patient's records were analyzed, most of which presented weight loss (82.5%) with an average weight loss of 9.0 kg representing 12.2% of body weight. The main NIS presented by the patients were dry mouth, abdominal pain, constipation and esophagitis. According to predetermined groups, the highest weight loss percentages were for patients with stomach and pancreatic cancer, Stage 4, the presence of 3 or more NIS and enteral diet. The lowest survival and highest death risk were observed at the univariable analysis to patients that have the presence of 3 or more NIS 8.3 months and HR 1.51 (IC95% 1.1-2.1) and to the multivariable analysis, for patients with pancreatic cancer 4.8 months HR 3.13 (IC95% 1.9-5.2), stage IV 9.8 months and HR 4.8 (IC95% 1.7-13.2)., Conclusion: Tumor location, cancer stage and the presence of nutritional impact symptoms influenced weight loss and survival of oncologic patients., Competing Interests: Declaration of competing interest The authors have no conflicts of interest, or other relationships with people or organizations that could influence the present article., (Copyright © 2022 European Society for Clinical Nutrition and Metabolism. Published by Elsevier Ltd. All rights reserved.)

Cancer patients are highly vulnerable to weight loss and malnutrition, before chemotherapy, thus reducing overall survival (OS). The objective was assessing weight loss and OS prognostication in gastric cancer patients at baseline of chemotherapy treatment. Observational retrospective study with patients who were treating in cancer public clinic in Brazil, was evaluated weight loss and cachexia. It was evaluated by sex, BMI, grade system classification (GSC) and stage the OS by Kaplan-Meier method and Cox proportional hazards model. Ninety-two patients, 73.9% were male. At baseline chemotherapy patients have presented 15.3% of body weight loss, 28.3% were malnourished, 86.8% classified witch cachexia, 80.3% were grade 3-4 in GSC and 86.9% at cancer stage 3-4. OS was lower for male (15.9 mo.), malnourished (12.0 mo.), GCS-4 (16.3 mo.) and Stage 4 (13.3 mo.) patients. GSC grade four and BMI classification to underweight comparing obesity are associated with reduced OS, together to male sex and cancer stage 4, have gotten together shown that seems to confer a survival disadvantage to other patients in these parameters too. Cox regression analysis have not shown statistical significance for sex, Initial BMI Class, GSC, cancer stage. Gastric cancer patients at chemotherapy treatment outset present high weight loss, cachexia prevalence and OS reduction.

Some endocrine-disrupting chemicals (EDCs) can affect the endocrine system through covalent interactions with specific sites, leading to deregulation of physiological homeostasis. The acrylamide (AA) present in some fried or baked foods is an example of an electrophile molecule that is able to form adducts with nucleophilic regions of nervous system proteins leading to neurological defects. A positive correlation between increased urinary AA metabolite concentration and reduced levels of thyroid hormones (TH) was described in adolescents and young adults. Thus, this study aimed to evaluate whether AA affects the physiology of the hypothalamus-pituitary-thyroid (HPT) axis and the possible repercussions in peripheral TH-target systems. For this, male Wistar rats were exposed to doses of 2.5 or 5.0 mg AA/Kg/day, based on the LOAEL (Lowest Observed Adverse Effect Level) during prepubertal development. The expression of molecular markers of HPT functionality was investigated in the hypothalamus, pituitary, thyroid, heart and liver, as well as the hormonal and lipid profiles in blood samples. Herein, we showed that AA acts as EDCs for thyroid gland function, increasing the transcript expression of several proteins related to TH synthesis and altering hypothalamus-pituitary-thyroid axis homeostasis, an effect evidenced by the higher levels of THs in the serum. Compensatory mechanisms were observed in TH-target tissues, such as an increase in Dio3 mRNA expression in the liver and a reduction in Mct8 transcript content in the hearts of AA-treated rats. Together, these results pointed out an allostatic regulation of the HPT axis induced by AA and suggest that chronic exposure to it, mainly associated with food consumption, might be related to the higher prevalence of thyroid dysfunctions., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2020 The Author(s).)

The increase in human infertility prevalence due to male reproductive disorders has been associated with extensive endocrine-disrupting chemical (EDC) exposure. Acrylamide (AA) is a compound formed spontaneously during heat processing of some foods that are mainly consumed by children and adolescents. In this study, we evaluated the prepubertal AA exposure effects on male adult reproductive physiology using a prepubertal experimental model to analyze the pubertal development, spermatogenesis hormones levels and genes expression involved in male reproductive function. This study is the first one to use the validated protocol to correlate the AA exposure with puberty development, as well as the AA-induced endocrine disrupting effects on reproductive axis. AA did not affect the age at puberty, the reproductive organ's weight and serum hormonal levels. AA reduces spermatogenesis, induces morphological and functional defects on sperm and alters transcript expression of sexual hormone receptors (Ar and Esr2), the transcript expression of Tnf, Egr2, Rhcg and Lrrc34. These findings suggest that excessive AA consumption may impair their reproductive capacity at adulthood, despite no changes in hormonal profile being observed., Competing Interests: Declaration of Competing Interest All authors declare that they have no conflicts of interest., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Cancer-associated malnutrition is driven by reduced dietary intake and by underlying metabolic changes (such as inflammation, anabolic resistance, proteolysis, lipolysis and futile cycling) induced by the tumour and activated immune cells. Cytotoxic and targeted chemotherapies also elicit proteolysis and lipolysis at the tissue level. In this review, we summarise specific mediators and chemotherapy effects that provoke excess proteolysis in muscle and excess lipolysis in adipose tissue. A nutritionally relevant question is whether and to what degree these catabolic changes can be reversed by nutritional therapy. In skeletal muscle, tumour factors and chemotherapy drugs activate intracellular signals that result in the suppression of protein synthesis and activation of a transcriptional programme leading to autophagy and degradation of myofibrillar proteins. Cancer nutrition therapy is intended to ensure adequate provision of energy fuels and a complete repertoire of biosynthetic building blocks. There is some promising evidence that cancer- and chemotherapy-associated metabolic alterations may also be corrected by certain individual nutrients. The amino acids leucine and arginine provided in the diet at least partially reverse anabolic suppression in muscle, while n-3 PUFA inhibit the transcriptional activation of muscle catabolism. Optimal conditions for exploiting these anabolic and anti-catabolic effects are currently under study, with the overall aim of net improvements in muscle mass, functionality, performance status and treatment tolerance.

Objective: Polyunsaturated fatty acids n-3 (PUFA n-3) have shown effects in reducing tumor growth, in particular eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) abundantly present in fish oil (FO). When these fatty acids are provided in the diet, they alter the functions of the cells, particularly in tumor and immune cells. However, the effects of α-linolenic fatty acid (ALA), which is the precursor of EPA and DHA, are controversial. Thus, our objective was to test the effect of this parental fatty acid., Methods: Non-tumor-bearing and tumor-bearing Wistar rats (70 days) were supplemented with 1 g/kg body weight of FO or Oro Inca® (OI) oil (rich in ALA). Immune cells function, proliferation, cytokine production, and subpopulation profile were evaluated., Results: We have shown that innate immune cells enhanced phagocytosis capacity, and increased processing and elimination of antigens. Moreover, there was a decrease in production of pro-inflammatory cytokines (tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6)) by macrophages. Lymphocytes showed decreased proliferation capacity, increased cluster of differentiation 8 (CD8 + ) subpopulation, and increased TNF-α production., Conclusions: Oil rich in ALA caused similar immune modulation in cancer when compared with FO.

Fish oil (FO) has been shown to affect cancer cachexia, tumor mass, and immunity cell. n-3 PUFA, specifically α-linolenic fatty acid (ALA), has controversial effects. We investigated this in nontumor-bearing Wistar rats fed regular chow (C), fed regular chow and supplemented with FO or Oro Inca oil (OI), and Walker 256 tumor-bearing rats fed regular chow (W), fed regular chow and supplemented with FO (WFO) or OI (WOI). Rats were supplemented (1g/kg body weight/day) during 4 wk and then the groups tumor-bearing were inoculated with Walker 256 tumor cells suspension and 14 days later the animals were killed. WFO increased EPA fivefold and DHA 1.5-fold in the tumor tissue compared to W (P < 0.05). OI supplementation increased of threefold of ALA when compared to W (P < 0.05). Tumor mass in WFO and OI was of 2.3-fold lower, as well as tumor cell proliferation of 3.0-fold tumor tissue lipoperoxidation increased of 76.6% and cox-2 expression was 20% lower. Cachexia parameters were attenuate, blood glucose (25% higher), Triacylglycerolemia (50% lower), and plasma TNF-α (65% lower; P < 0.05) and IL-6 (62.5% lower). OI, rich in ALA, caused the same effect on cancer as those seen in FO.

We investigated the effect of fish oil (FO) supplementation on tumor growth, cyclooxygenase 2 (COX-2), peroxisome proliferator-activated receptor gamma (PPARγ), and RelA gene and protein expression in Walker 256 tumor-bearing rats. Male Wistar rats (70 days old) were fed with regular chow (group W) or chow supplemented with 1 g/kg body weight FO daily (group WFO) until they reached 100 days of age. Both groups were then inoculated with a suspension of Walker 256 ascitic tumor cells (3 × 10(7) cells/mL). After 14 days the rats were killed, total RNA was isolated from the tumor tissue, and relative mRNA expression was measured using the 2(-ΔΔCT) method. FO significantly decreased tumor growth (W=13.18 ± 1.58 vs WFO=5.40 ± 0.88 g, P<0.05). FO supplementation also resulted in a significant decrease in COX-2 (W=100.1 ± 1.62 vs WFO=59.39 ± 5.53, P<0.001) and PPARγ (W=100.4 ± 1.04 vs WFO=88.22 ± 1.46, P<0.05) protein expression. Relative mRNA expression was W=1.06 ± 0.022 vs WFO=0.31 ± 0.04 (P<0.001) for COX-2, W=1.08 ± 0.02 vs WFO=0.52 ± 0.08 (P<0.001) for PPARγ, and W=1.04 ± 0.02 vs WFO=0.82 ± 0.04 (P<0.05) for RelA. FO reduced tumor growth by attenuating inflammatory gene expression associated with carcinogenesis.

Background: Obesity is commonly associated with diabetes, cardiovascular diseases and cancer. The purpose of this study was to determinate the effect of a lower dose of fish oil supplementation on insulin sensitivity, lipid profile, and muscle metabolism in obese rats., Methods: Monosodium glutamate (MSG) (4 mg/g body weight) was injected in neonatal Wistar male rats. Three-month-old rats were divided in normal-weight control group (C), coconut fat-treated normal weight group (CO), fish oil-treated normal weight group (FO), obese control group (Ob), coconut fat-treated obese group (ObCO) and fish oil-treated obese group (ObFO). Obese insulin-resistant rats were supplemented with fish oil or coconut fat (1 g/kg/day) for 4 weeks. Insulin sensitivity, fasting blood biochemicals parameters, and skeletal muscle glucose metabolism were analyzed., Results: Obese animals (Ob) presented higher Index Lee and 2.5 fold epididymal and retroperitoneal adipose tissue than C. Insulin sensitivity test (Kitt) showed that fish oil supplementation was able to maintain insulin sensitivity of obese rats (ObFO) similar to C. There were no changes in glucose and HDL-cholesterol levels amongst groups. Yet, ObFO revealed lower levels of total cholesterol (TC; 30%) and triacylglycerol (TG; 33%) compared to Ob. Finally, since exposed to insulin, ObFO skeletal muscle revealed an increase of 10% in lactate production, 38% in glycogen synthesis and 39% in oxidation of glucose compared to Ob., Conclusions: Low dose of fish oil supplementation (1 g/kg/day) was able to reduce TC and TG levels, in addition to improved systemic and muscle insulin sensitivity. These results lend credence to the benefits of n-3 fatty acids upon the deleterious effects of insulin resistance mechanisms.