Pub Date : 2025-01-01Epub Date: 2024-12-12DOI: 10.1080/01635581.2024.2437833
Jessica Abene, Sherilyn Tyburski, Tanja V E Kral, Ryan Quinn, Jie Deng
This review analyzed existing literature regarding the relationship between different diets and chemotherapy toxicities, as well as the quality of life (QOL) among patients undergoing treatment. It aims to identify the most advantageous diet for cancer patients. PubMed, CINAHL, and Embase were used to select randomized control trials (RCTs) assessing the relationship between a specific diet and chemotherapy toxicities and/or QOL in patients as of October 2023. Out of 1,419 records, 11 RCTs were included. Analyses were stratified by diet type. Pooled odds ratios and 95% confidence intervals (CI) were obtained from the random-effect model using STATA. We included 7 studies testing fasting variations; 1 testing a ketogenic diet; 1 testing a Mediterranean diet; 1 testing a plant-based, high-protein diet; and 1 testing an anti-inflammatory diet. Four fasting studies were in the meta-analysis. The random-effects meta-analysis showed no significant difference in the incidence of chemotherapy toxicities between fasting and non-fasting patients. There is insufficient evidence to determine which dietary intervention is the most advantageous, however, there is evidence that all the diets examined may complement conventional cancer therapy by helping to reduce chemotherapy toxicities. No intervention can be ruled out. More research is needed in this field.
{"title":"Diet as an Adjunct Therapy in Reducing Chemotherapy Toxicities and Improving Patients Quality of Life: A Systematic Review and Meta-Analysis.","authors":"Jessica Abene, Sherilyn Tyburski, Tanja V E Kral, Ryan Quinn, Jie Deng","doi":"10.1080/01635581.2024.2437833","DOIUrl":"10.1080/01635581.2024.2437833","url":null,"abstract":"<p><p>This review analyzed existing literature regarding the relationship between different diets and chemotherapy toxicities, as well as the quality of life (QOL) among patients undergoing treatment. It aims to identify the most advantageous diet for cancer patients. PubMed, CINAHL, and Embase were used to select randomized control trials (RCTs) assessing the relationship between a specific diet and chemotherapy toxicities and/or QOL in patients as of October 2023. Out of 1,419 records, 11 RCTs were included. Analyses were stratified by diet type. Pooled odds ratios and 95% confidence intervals (CI) were obtained from the random-effect model using STATA. We included 7 studies testing fasting variations; 1 testing a ketogenic diet; 1 testing a Mediterranean diet; 1 testing a plant-based, high-protein diet; and 1 testing an anti-inflammatory diet. Four fasting studies were in the meta-analysis. The random-effects meta-analysis showed no significant difference in the incidence of chemotherapy toxicities between fasting and non-fasting patients. There is insufficient evidence to determine which dietary intervention is the most advantageous, however, there is evidence that all the diets examined may complement conventional cancer therapy by helping to reduce chemotherapy toxicities. No intervention can be ruled out. More research is needed in this field.</p>","PeriodicalId":54701,"journal":{"name":"Nutrition and Cancer-An International Journal","volume":" ","pages":"341-359"},"PeriodicalIF":2.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142814674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-10-09DOI: 10.1080/01635581.2024.2408775
Renhua Na, Christina M Nagle, Stefanie Bartsch, Torukiri I Ibiebele, Merran Williams, Peter Grant, Michael L Friedlander, Penelope M Webb
The use of dietary supplements by cancer patients is common but contentious, particularly during chemotherapy. Few studies have investigated this for ovarian cancer. In a prospective study of women with ovarian cancer, dietary supplement use was collected through questionnaires. Data on the use of supplements were available for 421 women before diagnosis, during chemotherapy, and after chemotherapy completion. Predictors of changes in supplement use were investigated using logistic regression. The use of ≥1 supplement pre-diagnosis, during, and after chemotherapy completion was reported by 72%, 57%, and 68% of women, respectively. Multivitamins, vitamin D, and fish oils were the most commonly used supplements at all time points. The supplements most commonly discontinued during treatment were fish oils (69% of pre-diagnosis users) and multivitamins (53% of users); while 9%-10% of pre-diagnosis non-users initiated vitamin D and multivitamins. Predictors of supplement initiation during chemotherapy included pre-diagnosis use of medications, such as statins (Odds Ratio, OR = 4.12, 95% confidence interval, CI = 1.28-13.3), antidepressants (5.39, 1.18-24.7), acetaminophen (3.13, 1.05-9.33), and NSAIDs (2.15, 0.81-5.72). Other factors included younger age, university education, neoadjuvant chemotherapy, and/or experiencing fatigue during treatment, although not statistically significant. In conclusion, a high proportion of women with ovarian cancer reported using supplements at all time points.
癌症患者使用膳食补充剂很常见,但也存在争议,尤其是在化疗期间。有关卵巢癌的研究很少。在一项针对卵巢癌妇女的前瞻性研究中,通过问卷调查收集了膳食补充剂的使用情况。421名妇女在确诊前、化疗期间和化疗结束后使用补充剂的数据。采用逻辑回归法研究了营养补充剂使用变化的预测因素。据报告,在诊断前、化疗期间和化疗结束后,分别有 72%、57% 和 68% 的妇女使用了≥1 种补充剂。多种维生素、维生素 D 和鱼油是所有时间点最常使用的补充剂。治疗期间最常停用的补充剂是鱼油(占诊断前使用者的 69%)和多种维生素(占使用者的 53%);而 9%-10% 的诊断前非使用者开始服用维生素 D 和多种维生素。化疗期间开始服用补充剂的预测因素包括诊断前使用的药物,如他汀类药物(Odds Ratio,OR = 4.12,95% 置信区间,CI = 1.28-13.3)、抗抑郁药(5.39,1.18-24.7)、对乙酰氨基酚(3.13,1.05-9.33)和非甾体抗炎药(2.15,0.81-5.72)。其他因素包括年龄较小、大学教育程度、新辅助化疗和/或在治疗期间感到疲劳,但无统计学意义。总之,患有卵巢癌的妇女中有很高比例的人在所有时间点都使用过保健品。
{"title":"Use of Dietary Supplements Before, During and After Treatment for Ovarian Cancer: Results from the Ovarian Cancer Prognosis and Lifestyle (OPAL) Study.","authors":"Renhua Na, Christina M Nagle, Stefanie Bartsch, Torukiri I Ibiebele, Merran Williams, Peter Grant, Michael L Friedlander, Penelope M Webb","doi":"10.1080/01635581.2024.2408775","DOIUrl":"10.1080/01635581.2024.2408775","url":null,"abstract":"<p><p>The use of dietary supplements by cancer patients is common but contentious, particularly during chemotherapy. Few studies have investigated this for ovarian cancer. In a prospective study of women with ovarian cancer, dietary supplement use was collected through questionnaires. Data on the use of supplements were available for 421 women before diagnosis, during chemotherapy, and after chemotherapy completion. Predictors of changes in supplement use were investigated using logistic regression. The use of ≥1 supplement pre-diagnosis, during, and after chemotherapy completion was reported by 72%, 57%, and 68% of women, respectively. Multivitamins, vitamin D, and fish oils were the most commonly used supplements at all time points. The supplements most commonly discontinued during treatment were fish oils (69% of pre-diagnosis users) and multivitamins (53% of users); while 9%-10% of pre-diagnosis non-users initiated vitamin D and multivitamins. Predictors of supplement initiation during chemotherapy included pre-diagnosis use of medications, such as statins (Odds Ratio, OR = 4.12, 95% confidence interval, CI = 1.28-13.3), antidepressants (5.39, 1.18-24.7), acetaminophen (3.13, 1.05-9.33), and NSAIDs (2.15, 0.81-5.72). Other factors included younger age, university education, neoadjuvant chemotherapy, and/or experiencing fatigue during treatment, although not statistically significant. In conclusion, a high proportion of women with ovarian cancer reported using supplements at all time points.</p>","PeriodicalId":54701,"journal":{"name":"Nutrition and Cancer-An International Journal","volume":" ","pages":"200-209"},"PeriodicalIF":2.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142395334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Isoquercitrin possesses anti-tumor activity in several types of cancers, however, its effects and underlying mechanisms on lung cancer have not been reported. Human lung cancer cell lines as well as normal lung epithelial BEAS-2B cells were treated with isoquercitrin. The influences of isoquercitrin in vitro were evaluated by determining cell viability, apoptosis, pyroptosis, and ferroptosis. Additionally, A549 tumor-bearing mice were generated to explore the anti-cancer effect of isoquercitrin in vivo. We found that isoquercitrin dose-dependently reduced lung cancer cells' viability, with no toxicity against BEAS-2B cells. Isoquercitrin at 40 μM and 80 μM was used in vitro. Isoquercitrin increased apoptosis, elevated NLRP3 inflammasome activation-mediated pyroptosis, and promoted ferroptosis in lung cancer cells. NLRP3 knockdown and caspase-1 selective inhibitor VX-765 attenuated isoquercitrin-induced pyroptosis and ferroptosis, but not apoptosis. Furthermore, isoquercitrin accelerated ROS generation, while ROS inhibitor N-acetylcysteine abrogated isoquercitrin-induced apoptosis, NLRP3 related-pyroptosis and ferroptosis. In vivo, isoquercitrin (1 mg/kg and 5 mg/kg) inhibited tumor growth, increased apoptosis, NLRP3-related pyroptosis, ferroptosis and ROS generation in tumors. Taken together, isoquercitrin inhibits lung cancer growth by triggering ROS/NLRP3-mediated pyroptosis and ferroptosis, with ROS also directly inducing apoptosis. This suggests that isoquercitrin might be a potential therapeutic agent for lung cancer.
{"title":"Isoquercitrin Inhibits Lung Cancer Cell Growth Through Triggering Pyroptosis and Ferroptosis.","authors":"Haiyin Fan, Pengfei Xu, Bin Zou, Huanyuan Wang, Chao Li, Jian Huang","doi":"10.1080/01635581.2024.2416246","DOIUrl":"10.1080/01635581.2024.2416246","url":null,"abstract":"<p><p>Isoquercitrin possesses anti-tumor activity in several types of cancers, however, its effects and underlying mechanisms on lung cancer have not been reported. Human lung cancer cell lines as well as normal lung epithelial BEAS-2B cells were treated with isoquercitrin. The influences of isoquercitrin <i>in vitro</i> were evaluated by determining cell viability, apoptosis, pyroptosis, and ferroptosis. Additionally, A549 tumor-bearing mice were generated to explore the anti-cancer effect of isoquercitrin <i>in vivo</i>. We found that isoquercitrin dose-dependently reduced lung cancer cells' viability, with no toxicity against BEAS-2B cells. Isoquercitrin at 40 μM and 80 μM was used <i>in vitro</i>. Isoquercitrin increased apoptosis, elevated NLRP3 inflammasome activation-mediated pyroptosis, and promoted ferroptosis in lung cancer cells. NLRP3 knockdown and caspase-1 selective inhibitor VX-765 attenuated isoquercitrin-induced pyroptosis and ferroptosis, but not apoptosis. Furthermore, isoquercitrin accelerated ROS generation, while ROS inhibitor N-acetylcysteine abrogated isoquercitrin-induced apoptosis, NLRP3 related-pyroptosis and ferroptosis. <i>In vivo</i>, isoquercitrin (1 mg/kg and 5 mg/kg) inhibited tumor growth, increased apoptosis, NLRP3-related pyroptosis, ferroptosis and ROS generation in tumors. Taken together, isoquercitrin inhibits lung cancer growth by triggering ROS/NLRP3-mediated pyroptosis and ferroptosis, with ROS also directly inducing apoptosis. This suggests that isoquercitrin might be a potential therapeutic agent for lung cancer.</p>","PeriodicalId":54701,"journal":{"name":"Nutrition and Cancer-An International Journal","volume":" ","pages":"299-310"},"PeriodicalIF":2.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142481157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-11-03DOI: 10.1080/01635581.2024.2422637
Rong Hu, Zi-Tan Peng, Hui Liu
Ferroptosis plays an important role in the pathogenesis of neuronal damage, generally mediated by iron and lipid peroxidation. In the present study, we measured the protective effects of puerarin against corticosterone-induced neuronal injury via PI3K/AKT-mediated activation of nuclear factor erythroid 2-related factor 2 (Nrf2). After exposing corticosterone-treated PC12 cells to indicated compounds, we measured the key regulators of ferroptosis (ferritin, SLC7A11, and Ptgs2), ferroptosis events (levels of iron, ROS, MDA, and GSH), and the PI3K/AKT/Nrf2 axis. Corticosterone induced ferroptosis in PC12 cells, evidenced by reduced levels of ferritin, SLC7A11, and GSH and increased levels of iron, ROS, and MDA. These effects were reversed by inhibiting ferroptosis with ferrostatin-1. Puerarin-mediated activation of Nrf2 repressed ferroptosis in corticosterone-treated PC12 cells by upregulating ferritin and SLC7A11 expression. Moreover, the protective effects of puerarin on ferroptosis in corticosterone-treated cells relied on the activation of the PI3K/AKT pathway though the upregulation of nuclear Nrf2. These findings indicate that ferroptosis plays an essential role in corticosterone-induced neuronal damage, and puerarin protects against ferroptosis in corticosterone-treated cells via PI3K/AKT-mediated activation of Nrf2.
{"title":"Puerarin Ameliorates Ferroptosis in Neuronal Injury Through the PI3K/AKT Signaling Pathway.","authors":"Rong Hu, Zi-Tan Peng, Hui Liu","doi":"10.1080/01635581.2024.2422637","DOIUrl":"10.1080/01635581.2024.2422637","url":null,"abstract":"<p><p>Ferroptosis plays an important role in the pathogenesis of neuronal damage, generally mediated by iron and lipid peroxidation. In the present study, we measured the protective effects of puerarin against corticosterone-induced neuronal injury <i>via</i> PI3K/AKT-mediated activation of nuclear factor erythroid 2-related factor 2 (Nrf2). After exposing corticosterone-treated PC12 cells to indicated compounds, we measured the key regulators of ferroptosis (ferritin, SLC7A11, and Ptgs2), ferroptosis events (levels of iron, ROS, MDA, and GSH), and the PI3K/AKT/Nrf2 axis. Corticosterone induced ferroptosis in PC12 cells, evidenced by reduced levels of ferritin, SLC7A11, and GSH and increased levels of iron, ROS, and MDA. These effects were reversed by inhibiting ferroptosis with ferrostatin-1. Puerarin-mediated activation of Nrf2 repressed ferroptosis in corticosterone-treated PC12 cells by upregulating ferritin and SLC7A11 expression. Moreover, the protective effects of puerarin on ferroptosis in corticosterone-treated cells relied on the activation of the PI3K/AKT pathway though the upregulation of nuclear Nrf2. These findings indicate that ferroptosis plays an essential role in corticosterone-induced neuronal damage, and puerarin protects against ferroptosis in corticosterone-treated cells <i>via</i> PI3K/AKT-mediated activation of Nrf2.</p>","PeriodicalId":54701,"journal":{"name":"Nutrition and Cancer-An International Journal","volume":" ","pages":"424-432"},"PeriodicalIF":2.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142565349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-10-21DOI: 10.1080/01635581.2024.2418607
Fan Jiang, Zhiju Chen, Xiang Wang, Chuangyu Huang, Yiwei Li, Ning Liu
Glucose is an important energy source for tumors, however the molecular mechanisms by which tumor cells regulate glucose uptake remain unclear. In this study, we aimed to investigate the regulation mechanism of the WNT7B/β-catenin pathway for glucose transporter 1 (GLUT1)-mediated glucose metabolism in colorectal cancer. Here, we found that WNT7B expression levels were significantly increased in colorectal cancer tissues and closely associated with the clinical stage and lymph node metastasis in patients with colorectal cancer. Next, we confirmed that WNT7B significantly increased the glucose consumption and lactic acid levels in SW480 cells by overexpressing WNT7B. Additionally, gene and protein levels of GLUT1 were increased in WNT7B-overexpressing SW480 cells. However, WNT7B knockdown reversed these effects. WNT7B also enhanced GLUT1-mediated cell proliferation, invasion, and migration. WNT7B overexpression inhibited the effect of glucose deprivation on apoptosis. The WNT/β-catenin signaling pathway inhibitor, LGK974, inhibited WNT7B secretion, leading to GLUT1 levels downregulation and promotion of cell apoptosis. Ectopic tumor xenograft model experiments revealed that WNT7B promoted tumor progression in mice. Overall, our results suggest that WNT7B promotes β-catenin entry into the nucleus to initiates GLUT1 transcription, increases glucose transport and consumption, and enhances aerobic glycolysis, thus promoting tumor progression in colorectal cancer cells.
{"title":"Activation of the WNT7B/β-Catenin Pathway Initiates <i>GLUT1</i> Expression and Promotes Aerobic Glycolysis in Colorectal Cancer Cells.","authors":"Fan Jiang, Zhiju Chen, Xiang Wang, Chuangyu Huang, Yiwei Li, Ning Liu","doi":"10.1080/01635581.2024.2418607","DOIUrl":"10.1080/01635581.2024.2418607","url":null,"abstract":"<p><p>Glucose is an important energy source for tumors, however the molecular mechanisms by which tumor cells regulate glucose uptake remain unclear. In this study, we aimed to investigate the regulation mechanism of the WNT7B/β-catenin pathway for glucose transporter 1 (GLUT1)-mediated glucose metabolism in colorectal cancer. Here, we found that WNT7B expression levels were significantly increased in colorectal cancer tissues and closely associated with the clinical stage and lymph node metastasis in patients with colorectal cancer. Next, we confirmed that WNT7B significantly increased the glucose consumption and lactic acid levels in SW480 cells by overexpressing WNT7B. Additionally, gene and protein levels of GLUT1 were increased in WNT7B-overexpressing SW480 cells. However, WNT7B knockdown reversed these effects. WNT7B also enhanced GLUT1-mediated cell proliferation, invasion, and migration. WNT7B overexpression inhibited the effect of glucose deprivation on apoptosis. The WNT/β-catenin signaling pathway inhibitor, LGK974, inhibited WNT7B secretion, leading to GLUT1 levels downregulation and promotion of cell apoptosis. Ectopic tumor xenograft model experiments revealed that WNT7B promoted tumor progression in mice. Overall, our results suggest that WNT7B promotes β-catenin entry into the nucleus to initiates GLUT1 transcription, increases glucose transport and consumption, and enhances aerobic glycolysis, thus promoting tumor progression in colorectal cancer cells.</p>","PeriodicalId":54701,"journal":{"name":"Nutrition and Cancer-An International Journal","volume":" ","pages":"311-323"},"PeriodicalIF":2.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142481154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Coconut milk contains plant-based saturated fat and phytochemicals with antioxidant activities. However, its role in breast cancer risk remains unclear. A case-control study was conducted on 244 participants to study the association. The Case group includes 61 newly diagnosed breast cancer patients receiving < 6 months of therapies. The Control group includes 183 healthy people with matched characteristics. A new questionnaire was developed, validated, and used in this study to estimate the frequency of coconut milk-containing food intake. Results show that the questionnaire has satisfactory content validity, test-retest reliability, and criterion-related validity. From the case-control study, either consuming 1-3 or 4-6 times/week of coconut-milk-containing curry or consuming 4-6 times/week of coconut milk-topped desserts are associated with increased risk of breast cancer (OR = 5.23, 5.6, and 2.6 respectively, p < 0.01). Consuming less than half of coconut milk liquid in desserts correlated with a reduced risk (OR = 0.43, p < 0.05). The findings suggest that moderate (less than half of a serving) and infrequent (less than once a week) consumption of coconut milk may be beneficial for breast cancer prevention. A larger scale study is warranted to confirm the findings and provide evidence for dietary recommendations.
{"title":"Coconut Milk Consumption and Breast Cancer Risk in Thai Women: A Case-Control Study.","authors":"Phornsawan Leechanavanicpan, Pakkapong Phucharoenrak, Phenphop Phansuea, Dunyaporn Trachootham","doi":"10.1080/01635581.2024.2390202","DOIUrl":"10.1080/01635581.2024.2390202","url":null,"abstract":"<p><p>Coconut milk contains plant-based saturated fat and phytochemicals with antioxidant activities. However, its role in breast cancer risk remains unclear. A case-control study was conducted on 244 participants to study the association. The Case group includes 61 newly diagnosed breast cancer patients receiving < 6 months of therapies. The Control group includes 183 healthy people with matched characteristics. A new questionnaire was developed, validated, and used in this study to estimate the frequency of coconut milk-containing food intake. Results show that the questionnaire has satisfactory content validity, test-retest reliability, and criterion-related validity. From the case-control study, either consuming 1-3 or 4-6 times/week of coconut-milk-containing curry or consuming 4-6 times/week of coconut milk-topped desserts are associated with increased risk of breast cancer (OR = 5.23, 5.6, and 2.6 respectively, <i>p</i> < 0.01). Consuming less than half of coconut milk liquid in desserts correlated with a reduced risk (OR = 0.43, <i>p</i> < 0.05). The findings suggest that moderate (less than half of a serving) and infrequent (less than once a week) consumption of coconut milk may be beneficial for breast cancer prevention. A larger scale study is warranted to confirm the findings and provide evidence for dietary recommendations.</p>","PeriodicalId":54701,"journal":{"name":"Nutrition and Cancer-An International Journal","volume":" ","pages":"51-61"},"PeriodicalIF":2.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141918119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-10-09DOI: 10.1080/01635581.2024.2411763
Koji Amano, Rony Dev, Tateaki Naito, Egidio Del Fabbro
ABSTRACTA self-reported electronic questionnaire to advocate for a consensus definition of nutrition impact symptoms (NISs) was conducted in a diverse group of international healthcare providers. The questionnaire had 2 components: the definition of NISs and the relevance of each symptom as a NIS. Agreement on the tentative definition and 24 symptoms were evaluated using a seven-point Likert scale. For the factor validity and internal consistency of symptoms, an exploratory factor analysis was employed, and Cronbach's alpha coefficients (Cronbach's α) were calculated in each domain. A total of 66 healthcare providers responded. Regarding the tentative definition of NISs, the percentages of the number of participants with agree and strongly agree were 40.9% and 42.4%. Three conceptual groups were extracted as follows: 1) symptoms that interfere with patients' ability to ingest or digest nutrients, 2) symptoms that compromise patients' desire to eat and take nutrients, and 3) symptoms that indirectly compromise patients' food and nutrient intake. The values of Cronbach's α were 0.91, 0.92, and 0.87. We proposed a new definition - NISs are symptoms that compromise patients' desire or ability to eat, interfering with their nutritional needs and increasing the risk for malnutrition, loss of lean body mass, and impaired QOL.
{"title":"International Survey on Consensus Definition on Nutrition Impact Symptoms in Patients with Cancer.","authors":"Koji Amano, Rony Dev, Tateaki Naito, Egidio Del Fabbro","doi":"10.1080/01635581.2024.2411763","DOIUrl":"10.1080/01635581.2024.2411763","url":null,"abstract":"<p><p><u>ABSTRACT</u>A self-reported electronic questionnaire to advocate for a consensus definition of nutrition impact symptoms (NISs) was conducted in a diverse group of international healthcare providers. The questionnaire had 2 components: the definition of NISs and the relevance of each symptom as a NIS. Agreement on the tentative definition and 24 symptoms were evaluated using a seven-point Likert scale. For the factor validity and internal consistency of symptoms, an exploratory factor analysis was employed, and Cronbach's alpha coefficients (Cronbach's α) were calculated in each domain. A total of 66 healthcare providers responded. Regarding the tentative definition of NISs, the percentages of the number of participants with agree and strongly agree were 40.9% and 42.4%. Three conceptual groups were extracted as follows: 1) symptoms that interfere with patients' ability to ingest or digest nutrients, 2) symptoms that compromise patients' desire to eat and take nutrients, and 3) symptoms that indirectly compromise patients' food and nutrient intake. The values of Cronbach's α were 0.91, 0.92, and 0.87. We proposed a new definition - <i>NISs are symptoms that compromise patients' desire or ability to eat, interfering with their nutritional needs and increasing the risk for malnutrition, loss of lean body mass, and impaired QOL.</i></p>","PeriodicalId":54701,"journal":{"name":"Nutrition and Cancer-An International Journal","volume":" ","pages":"210-220"},"PeriodicalIF":2.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142395333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-12-27DOI: 10.1080/01635581.2024.2435079
Juliana Priebe Steffens, Caroline Abud Drumond Costa
Acute lymphoblastic leukemia is the most prevalent form of leukemia in children and adolescents. Despite high survival rates due to advanced treatments, these therapies often result in significant treatment-related adverse effects. This scoping review explores dietary supplementation strategies for managing these adverse effects in pediatric leukemia patients. Twelve studies were included, involving participants aged between 0.8 and 21 years, all undergoing chemotherapy at various treatment phases. Chemotherapy-related adverse effects identified in this review included gastrointestinal symptoms, cardiometabolic risk factors, hepatotoxicity, osteopathies, neuro-psychiatric effects, hematological disorders, and changes in body composition. The dietary supplements evaluated for managing these effects were probiotics, ginger, glutamine, omega-3, vitamin D, calcium, potassium, honey, chamomile, and medium-chain triglyceride. Most of these supplements showed promising outcomes in reducing or preventing adverse effects. However, there is a demand for more rigorous clinical trials with larger sample sizes and standardized protocols to validate the efficacy of these interventions. Further research to identify optimal dosages, better understand long-term effects, and develop evidence-based guidelines for the use of dietary supplements in managing treatment-related adverse effects in children and adolescents with leukemia is needed.
{"title":"The Use of Dietary Supplements for the Management of Adverse Effects of Treatment in Children and Adolescents with Leukemia: A Scoping Review.","authors":"Juliana Priebe Steffens, Caroline Abud Drumond Costa","doi":"10.1080/01635581.2024.2435079","DOIUrl":"10.1080/01635581.2024.2435079","url":null,"abstract":"<p><p>Acute lymphoblastic leukemia is the most prevalent form of leukemia in children and adolescents. Despite high survival rates due to advanced treatments, these therapies often result in significant treatment-related adverse effects. This scoping review explores dietary supplementation strategies for managing these adverse effects in pediatric leukemia patients. Twelve studies were included, involving participants aged between 0.8 and 21 years, all undergoing chemotherapy at various treatment phases. Chemotherapy-related adverse effects identified in this review included gastrointestinal symptoms, cardiometabolic risk factors, hepatotoxicity, osteopathies, neuro-psychiatric effects, hematological disorders, and changes in body composition. The dietary supplements evaluated for managing these effects were probiotics, ginger, glutamine, omega-3, vitamin D, calcium, potassium, honey, chamomile, and medium-chain triglyceride. Most of these supplements showed promising outcomes in reducing or preventing adverse effects. However, there is a demand for more rigorous clinical trials with larger sample sizes and standardized protocols to validate the efficacy of these interventions. Further research to identify optimal dosages, better understand long-term effects, and develop evidence-based guidelines for the use of dietary supplements in managing treatment-related adverse effects in children and adolescents with leukemia is needed.</p>","PeriodicalId":54701,"journal":{"name":"Nutrition and Cancer-An International Journal","volume":" ","pages":"334-340"},"PeriodicalIF":2.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142900541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Previous cohort studies have shown conflicting findings on the associations between obesity and the risk of thyroid cancer. This meta-analysis aimed to investigate the associations between them by using a meta-analysis of cohort studies. PubMed and EMBASE were searched using keywords from inception until November 2023 to identify relevant studies on this topic. Two authors independently reviewed and selected relevant studies according to the predefined criteria. Out of 475 studies searched from the databases, a total of 22 cohort studies were included in the final analysis. In a random-effects meta-analysis, obesity was significantly associated with an increased risk of thyroid cancer [odds ratio (OR), relative risk (RR), or hazard ratio (HR) = 1.33; 95% confidence interval (CI) 1.24 - 1.43]. Obesity was consistently associated with the increased risk of thyroid cancer in the subgroup meta-analyses by various factors such as study type (prospective or retrospective cohort study), gender (male or female), continent (America, Europe, or Asia), and study quality (high or low). This meta-analysis of cohort studies suggests that obesity increases the risk of thyroid cancer.
{"title":"Associations Between Obesity and Risk of Thyroid Cancer: A Meta-Analysis of Cohort Studies.","authors":"Urfa Khairatun Hisan, Seung-Kwon Myung, Giap Viet Nguyen","doi":"10.1080/01635581.2024.2419488","DOIUrl":"10.1080/01635581.2024.2419488","url":null,"abstract":"<p><p>Previous cohort studies have shown conflicting findings on the associations between obesity and the risk of thyroid cancer. This meta-analysis aimed to investigate the associations between them by using a meta-analysis of cohort studies. PubMed and EMBASE were searched using keywords from inception until November 2023 to identify relevant studies on this topic. Two authors independently reviewed and selected relevant studies according to the predefined criteria. Out of 475 studies searched from the databases, a total of 22 cohort studies were included in the final analysis. In a random-effects meta-analysis, obesity was significantly associated with an increased risk of thyroid cancer [odds ratio (OR), relative risk (RR), or hazard ratio (HR) = 1.33; 95% confidence interval (CI) 1.24 - 1.43]. Obesity was consistently associated with the increased risk of thyroid cancer in the subgroup meta-analyses by various factors such as study type (prospective or retrospective cohort study), gender (male or female), continent (America, Europe, or Asia), and study quality (high or low). This meta-analysis of cohort studies suggests that obesity increases the risk of thyroid cancer.</p>","PeriodicalId":54701,"journal":{"name":"Nutrition and Cancer-An International Journal","volume":" ","pages":"288-298"},"PeriodicalIF":2.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142513129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-12-20DOI: 10.1080/01635581.2024.2443260
Song Wang, Deli Tan
Objective: This study aimed to investigate the causal relationship between diet compositions and lung cancer (LC) risk.
Methods: A two-sample Mendelian randomization (MR) analysis was performed to assess the causal relationship between diet and LC risk, including three LC subtypes. Instrumental variables (IVs) for three diet compositions were selected from genome-wide association studies (GWAS). Summary statistics for LC and its subtypes came from the largest meta-analysis. The inverse-variance weighted (IVW) method was used as the main MR analysis, with sensitivity analyses to ensure result robustness. Then, we conducted an observational study using data from National Health and Nutrition Examination Survey (NHANES) to verify the relationship.
Results: Our results showed significant evidence that fat intake was correlated with the lower risk of lung adenocarcinoma. There were also suggestive correlations between fat intake and overall LC. However, no significant associations were found between other macronutrients and LC risk. NHANES data further showed that higher polyunsaturated fatty acid (PUFA) intake was linked to better outcomes in LC patients.
Conclusion: PUFA intake may have a protective effect against LC. Adjusting dietary proportions could potentially help in the primary prevention of LC.
{"title":"Investigating Causal Associations of Diet Compositions with the Risk of Lung Cancer.","authors":"Song Wang, Deli Tan","doi":"10.1080/01635581.2024.2443260","DOIUrl":"10.1080/01635581.2024.2443260","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the causal relationship between diet compositions and lung cancer (LC) risk.</p><p><strong>Methods: </strong>A two-sample Mendelian randomization (MR) analysis was performed to assess the causal relationship between diet and LC risk, including three LC subtypes. Instrumental variables (IVs) for three diet compositions were selected from genome-wide association studies (GWAS). Summary statistics for LC and its subtypes came from the largest meta-analysis. The inverse-variance weighted (IVW) method was used as the main MR analysis, with sensitivity analyses to ensure result robustness. Then, we conducted an observational study using data from National Health and Nutrition Examination Survey (NHANES) to verify the relationship.</p><p><strong>Results: </strong>Our results showed significant evidence that fat intake was correlated with the lower risk of lung adenocarcinoma. There were also suggestive correlations between fat intake and overall LC. However, no significant associations were found between other macronutrients and LC risk. NHANES data further showed that higher polyunsaturated fatty acid (PUFA) intake was linked to better outcomes in LC patients.</p><p><strong>Conclusion: </strong>PUFA intake may have a protective effect against LC. Adjusting dietary proportions could potentially help in the primary prevention of LC.</p>","PeriodicalId":54701,"journal":{"name":"Nutrition and Cancer-An International Journal","volume":" ","pages":"397-404"},"PeriodicalIF":2.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142866425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}