Pub Date : 2024-06-01DOI: 10.1016/j.advnut.2024.100238
Nicole U. Stoffel, Hal Drakesmith
Vaccines can prevent infectious diseases, but their efficacy varies, and factors impacting vaccine effectiveness remain unclear. Iron deficiency is the most common nutrient deficiency, affecting >2 billion individuals. It is particularly common in areas with high infectious disease burden and in groups that are routinely vaccinated, such as infants, pregnant women, and the elderly. Recent evidence suggests that iron deficiency and low serum iron (hypoferremia) not only cause anemia but also may impair adaptive immunity and vaccine efficacy. A report of human immunodeficiency caused by defective iron transport underscored the necessity of iron for adaptive immune responses and spurred research in this area. Sufficient iron is essential for optimal production of plasmablasts and IgG responses by human B-cells in vitro and in vivo. The increased metabolism of activated lymphocytes depends on the high-iron acquisition, and hypoferremia, especially when occurring during lymphocyte expansion, adversely affects multiple facets of adaptive immunity, and may lead to prolonged inhibition of T-cell memory. In mice, hypoferremia suppresses the adaptive immune response to influenza infection, resulting in more severe pulmonary disease. In African infants, anemia and/or iron deficiency at the time of vaccination predict decreased response to diphtheria, pertussis, and pneumococcal vaccines, and response to measles vaccine may be increased by iron supplementation. In this review, we examine the emerging evidence that iron deficiency may limit adaptive immunity and vaccine responses. We discuss the molecular mechanisms and evidence from animal and human studies, highlight important unknowns, and propose a framework of key research questions to better understand iron–vaccine interactions.
疫苗可以预防传染病,但其功效各不相同,而且影响疫苗功效的因素仍不明确。缺铁是最常见的营养素缺乏症,影响人数超过 20 亿。在传染病高发地区以及婴儿、孕妇和老年人等常规疫苗接种人群中,缺铁症尤为常见。最新证据表明,缺铁和血清铁过低(低铁血症)不仅会导致贫血,还可能损害适应性免疫和疫苗功效。一份关于铁转运缺陷导致人类免疫缺陷的报告强调了铁对适应性免疫反应的必要性,并激发了这一领域的研究。充足的铁对人体 B 细胞在体外和体内产生最佳的浆细胞和 IgG 反应至关重要。活化淋巴细胞新陈代谢的增加有赖于铁的获取,而低铁血症,尤其是在淋巴细胞扩增期间发生的低铁血症,会对适应性免疫的多个方面产生不利影响,并可能导致 T 细胞记忆的长期抑制。在小鼠中,低铁血症会抑制对流感感染的适应性免疫反应,导致更严重的肺部疾病。在非洲婴儿中,接种疫苗时贫血和/或缺铁会降低对白喉、百日咳和肺炎球菌疫苗的反应,而对麻疹疫苗的反应可通过补铁而提高。在本综述中,我们研究了铁缺乏可能限制适应性免疫和疫苗反应的新证据。我们讨论了来自动物和人体研究的分子机制和证据,强调了重要的未知因素,并提出了一个关键研究问题框架,以更好地理解铁与疫苗的相互作用。
{"title":"Effects of Iron Status on Adaptive Immunity and Vaccine Efficacy: A Review","authors":"Nicole U. Stoffel, Hal Drakesmith","doi":"10.1016/j.advnut.2024.100238","DOIUrl":"10.1016/j.advnut.2024.100238","url":null,"abstract":"<div><p>Vaccines can prevent infectious diseases, but their efficacy varies, and factors impacting vaccine effectiveness remain unclear. Iron deficiency is the most common nutrient deficiency, affecting >2 billion individuals. It is particularly common in areas with high infectious disease burden and in groups that are routinely vaccinated, such as infants, pregnant women, and the elderly. Recent evidence suggests that iron deficiency and low serum iron (hypoferremia) not only cause anemia but also may impair adaptive immunity and vaccine efficacy. A report of human immunodeficiency caused by defective iron transport underscored the necessity of iron for adaptive immune responses and spurred research in this area. Sufficient iron is essential for optimal production of plasmablasts and IgG responses by human B-cells in vitro and in vivo. The increased metabolism of activated lymphocytes depends on the high-iron acquisition, and hypoferremia, especially when occurring during lymphocyte expansion, adversely affects multiple facets of adaptive immunity, and may lead to prolonged inhibition of T-cell memory. In mice, hypoferremia suppresses the adaptive immune response to influenza infection, resulting in more severe pulmonary disease. In African infants, anemia and/or iron deficiency at the time of vaccination predict decreased response to diphtheria, pertussis, and pneumococcal vaccines, and response to measles vaccine may be increased by iron supplementation. In this review, we examine the emerging evidence that iron deficiency may limit adaptive immunity and vaccine responses. We discuss the molecular mechanisms and evidence from animal and human studies, highlight important unknowns, and propose a framework of key research questions to better understand iron–vaccine interactions.</p></div>","PeriodicalId":7349,"journal":{"name":"Advances in Nutrition","volume":"15 6","pages":"Article 100238"},"PeriodicalIF":9.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2161831324000723/pdfft?md5=6d1b5af6bdcc9c4fda732d0f0067a131&pid=1-s2.0-S2161831324000723-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140905254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-31DOI: 10.1016/j.advnut.2024.100251
Cydne A Perry , Tammy A Butterick
{"title":"Biotin","authors":"Cydne A Perry , Tammy A Butterick","doi":"10.1016/j.advnut.2024.100251","DOIUrl":"10.1016/j.advnut.2024.100251","url":null,"abstract":"","PeriodicalId":7349,"journal":{"name":"Advances in Nutrition","volume":"15 7","pages":"Article 100251"},"PeriodicalIF":9.3,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2161831324000851/pdfft?md5=254011c905fce7411a8de00716c8af50&pid=1-s2.0-S2161831324000851-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141201416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-10DOI: 10.1016/j.advnut.2024.100241
Gwen M Chodur, Francene M Steinberg
Because of their role in regulating and fine-tuning gene expression in the posttranscriptional period, microRNA (miRNA) may represent a mediating factor that connects diet and metabolic regulation. Given the vast number of miRNAs and that modulations in miRNA happen in response to a variety of stimuli, a comprehensive registry of miRNAs impacted by diet and the food items that modulate them, would have utility in the identification of miRNA complements for analysis of diet interventions and in helping to establish linkages between the specific impacts of diet components. A scoping literature search of online databases (PubMed, SCOPUS, EMBASE, and Web of Science) was performed. Only studies in human populations, those that used a diet intervention or meal challenge, and those that measured miRNA profiles in the same subject at multiple time points were included. Of the 6167 studies screened, only 25 met the study criteria and were included in the review. Seven studies examined miRNA following a meal challenge, whereas 18 investigated miRNA following a sustained diet intervention. The results demonstrated that miRNA are modulated following a variety of diet interventions and that intensity of miRNA response is greater in metabolically healthy subjects. Heterogeneity in the intensity and length of the diet intervention, the study populations being observed, and the methodology through which target miRNA are identified contribute to a lack of comparability across studies. The findings of this review highlight the need for more study of miRNA responsiveness to intake and provide recommendations for future research.
{"title":"Human MicroRNAs Modulated by Diet: A Scoping Review","authors":"Gwen M Chodur, Francene M Steinberg","doi":"10.1016/j.advnut.2024.100241","DOIUrl":"10.1016/j.advnut.2024.100241","url":null,"abstract":"<div><p>Because of their role in regulating and fine-tuning gene expression in the posttranscriptional period, microRNA (miRNA) may represent a mediating factor that connects diet and metabolic regulation. Given the vast number of miRNAs and that modulations in miRNA happen in response to a variety of stimuli, a comprehensive registry of miRNAs impacted by diet and the food items that modulate them, would have utility in the identification of miRNA complements for analysis of diet interventions and in helping to establish linkages between the specific impacts of diet components. A scoping literature search of online databases (PubMed, SCOPUS, EMBASE, and Web of Science) was performed. Only studies in human populations, those that used a diet intervention or meal challenge, and those that measured miRNA profiles in the same subject at multiple time points were included. Of the 6167 studies screened, only 25 met the study criteria and were included in the review. Seven studies examined miRNA following a meal challenge, whereas 18 investigated miRNA following a sustained diet intervention. The results demonstrated that miRNA are modulated following a variety of diet interventions and that intensity of miRNA response is greater in metabolically healthy subjects. Heterogeneity in the intensity and length of the diet intervention, the study populations being observed, and the methodology through which target miRNA are identified contribute to a lack of comparability across studies. The findings of this review highlight the need for more study of miRNA responsiveness to intake and provide recommendations for future research.</p></div>","PeriodicalId":7349,"journal":{"name":"Advances in Nutrition","volume":"15 6","pages":"Article 100241"},"PeriodicalIF":9.3,"publicationDate":"2024-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2161831324000759/pdfft?md5=6ae2d4b4151b5dc38ffdabdaca438a78&pid=1-s2.0-S2161831324000759-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140909673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-10DOI: 10.1016/j.advnut.2024.100240
Qing Jiang
The vitamin E family contains α-tocopherol (αT), βT, γT, and δT and α-tocotrienol (TE), βTE, γTE, and δTE. Research has revealed distinct roles of these vitamin E forms in prostate cancer (PCa). The ATBC trial showed that αT at a modest dose significantly decreased PCa mortality among heavy smokers. However, other randomized controlled trials including the Selenium and Vitamin E Cancer Prevention Trial (SELECT) indicate that supplementation of high-dose αT (≥400 IU) does not prevent PCa among nonsmokers. Preclinical cell and animal studies also do not support chemopreventive roles of high-dose αT and offer explanations for increased incidence of early-stage PCa reported in the SELECT. In contrast, accumulating animal studies have demonstrated that γT, δT, γTE, and δTE appear to be effective for preventing early-stage PCa from progression to adenocarcinoma in various PCa models. Existing evidence also support therapeutic roles of γTE and its related combinations against advanced PCa. Mechanistic and cell-based studies show that different forms of vitamin E display varied efficacy, that is, δTE ≥ γTE > δT ≥ γT >> αT, in inhibiting cancer hallmarks and enabling characteristics, including uncontrolled cell proliferation, angiogenesis, and inflammation possibly via blocking 5-lipoxygenase, nuclear factor κB, hypoxia-inducible factor-1α, modulating sphingolipids, and targeting PCa stem cells. Overall, existing evidence suggests that modest αT supplement may be beneficial to smokers and γT, δT, γTE, and δTE are promising agents for PCa prevention for modest-risk to relatively high-risk population. Despite encouraging preclinical evidence, clinical research testing γT, δT, γTE, and δTE for PCa prevention is sparse and should be considered.
{"title":"Different Roles of Tocopherols and Tocotrienols in Chemoprevention and Treatment of Prostate Cancer","authors":"Qing Jiang","doi":"10.1016/j.advnut.2024.100240","DOIUrl":"10.1016/j.advnut.2024.100240","url":null,"abstract":"<div><p>The vitamin E family contains α-tocopherol (αT), βT, γT, and δT and α-tocotrienol (TE), βTE, γTE, and δTE. Research has revealed distinct roles of these vitamin E forms in prostate cancer (PCa). The ATBC trial showed that αT at a modest dose significantly decreased PCa mortality among heavy smokers. However, other randomized controlled trials including the Selenium and Vitamin E Cancer Prevention Trial (SELECT) indicate that supplementation of high-dose αT (≥400 IU) does not prevent PCa among nonsmokers. Preclinical cell and animal studies also do not support chemopreventive roles of high-dose αT and offer explanations for increased incidence of early-stage PCa reported in the SELECT. In contrast, accumulating animal studies have demonstrated that γT, δT, γTE, and δTE appear to be effective for preventing early-stage PCa from progression to adenocarcinoma in various PCa models. Existing evidence also support therapeutic roles of γTE and its related combinations against advanced PCa. Mechanistic and cell-based studies show that different forms of vitamin E display varied efficacy, that is, δTE ≥ γTE > δT ≥ γT >> αT, in inhibiting cancer hallmarks and enabling characteristics, including uncontrolled cell proliferation, angiogenesis, and inflammation possibly via blocking 5-lipoxygenase, nuclear factor κB, hypoxia-inducible factor-1α, modulating sphingolipids, and targeting PCa stem cells. Overall, existing evidence suggests that modest αT supplement may be beneficial to smokers and γT, δT, γTE, and δTE are promising agents for PCa prevention for modest-risk to relatively high-risk population. Despite encouraging preclinical evidence, clinical research testing γT, δT, γTE, and δTE for PCa prevention is sparse and should be considered.</p></div>","PeriodicalId":7349,"journal":{"name":"Advances in Nutrition","volume":"15 7","pages":"Article 100240"},"PeriodicalIF":9.3,"publicationDate":"2024-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2161831324000747/pdfft?md5=25b4c7a217e74acaec417f60ba2f9faf&pid=1-s2.0-S2161831324000747-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140909658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-01DOI: 10.1016/j.advnut.2024.100215
Clay T Cohen, Jacquelyn M Powers
Iron deficiency (ID) is a common and challenging problem in adolescence. In order to prevent, recognize, and treat ID in this age range, it is critical to understand the recommended daily intake of iron in relation to an adolescent’s activity, dietary habits, and basal iron losses. Adolescents following vegetarian or vegan diets exclusively rely on plant-based, nonheme iron, which has decreased bioavailability compared with heme iron and requires increased total iron intake. Individuals with disordered eating habits, excessive menstrual blood loss, and certain chronic health conditions (including inflammatory bowel disease and heart failure) are at high risk of ID and the development of symptomatic iron deficiency anemia (IDA). Adolescent athletes and those with sleep and movement disorders may also be more sensitive to changes in iron status. Iron deficiency is typically treated with oral iron supplementation. To maximize iron absorption, oral iron should be administered no more than once daily, ideally in the morning, while avoiding foods and drinks that inhibit iron absorption. Oral iron therapy should be provided for ≥3 mo in the setting of ID to reach a ferritin of 20 ng/mL before discontinuation. Intravenous iron is being increasingly used in this population and has demonstrated efficacy and safety in adolescents. It should be considered in those with persistent ID despite a course of oral iron, severe and/or symptomatic IDA, and chronic inflammatory conditions characterized by decreased gastrointestinal iron absorption.
缺铁(ID)是青少年时期的一个常见且具有挑战性的问题。为了预防、识别和治疗这一年龄段的缺铁症,了解与青少年的活动量、饮食习惯和基础铁流失量相关的每日推荐铁摄入量至关重要。采用素食或纯素饮食的青少年完全依赖植物性非血红素铁,这种铁的生物利用率比血红素铁低,因此需要增加铁的总摄入量。饮食习惯紊乱、月经失血过多和患有某些慢性疾病(包括炎症性肠病和心力衰竭)的人患 ID 和症状性缺铁性贫血 (IDA) 的风险很高。青少年运动员以及患有睡眠和运动障碍的人对铁状态的变化也可能更为敏感。缺铁通常通过口服铁剂来治疗。为了最大限度地促进铁的吸收,口服铁剂每天不应超过一次,最好在早晨服用,同时避免食用抑制铁吸收的食物和饮料。在 ID 的情况下,口服铁剂治疗应持续至少三个月,以达到铁蛋白 20 纳克/毫升,然后再停止治疗。静脉注射铁剂在这一人群中的应用越来越广泛,在青少年中的疗效和安全性已得到证实。在口服铁剂后仍有持续性 ID 的患者、严重和/或有症状的 IDA 患者,以及胃肠道铁吸收减少的慢性炎症患者中,应考虑使用静脉注射铁剂。
{"title":"Nutritional Strategies for Managing Iron Deficiency in Adolescents: Approaches to a Challenging but Common Problem","authors":"Clay T Cohen, Jacquelyn M Powers","doi":"10.1016/j.advnut.2024.100215","DOIUrl":"10.1016/j.advnut.2024.100215","url":null,"abstract":"<div><p>Iron deficiency (ID) is a common and challenging problem in adolescence. In order to prevent, recognize, and treat ID in this age range, it is critical to understand the recommended daily intake of iron in relation to an adolescent’s activity, dietary habits, and basal iron losses. Adolescents following vegetarian or vegan diets exclusively rely on plant-based, nonheme iron, which has decreased bioavailability compared with heme iron and requires increased total iron intake. Individuals with disordered eating habits, excessive menstrual blood loss, and certain chronic health conditions (including inflammatory bowel disease and heart failure) are at high risk of ID and the development of symptomatic iron deficiency anemia (IDA). Adolescent athletes and those with sleep and movement disorders may also be more sensitive to changes in iron status. Iron deficiency is typically treated with oral iron supplementation. To maximize iron absorption, oral iron should be administered no more than once daily, ideally in the morning, while avoiding foods and drinks that inhibit iron absorption. Oral iron therapy should be provided for ≥3 mo in the setting of ID to reach a ferritin of 20 ng/mL before discontinuation. Intravenous iron is being increasingly used in this population and has demonstrated efficacy and safety in adolescents. It should be considered in those with persistent ID despite a course of oral iron, severe and/or symptomatic IDA, and chronic inflammatory conditions characterized by decreased gastrointestinal iron absorption.</p></div>","PeriodicalId":7349,"journal":{"name":"Advances in Nutrition","volume":"15 5","pages":"Article 100215"},"PeriodicalIF":9.3,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2161831324000498/pdfft?md5=a278348293c9d74795b6429e875b119b&pid=1-s2.0-S2161831324000498-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140332360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-01DOI: 10.1016/j.advnut.2024.100221
Kelly E LeBlanc , Sara Baer-Sinnott , Kristie J Lancaster , Hannia Campos , Ka Hei Karen Lau , Katherine L Tucker , Lawrence H Kushi , Walter C Willett
The Mediterranean diet is a well-studied cultural model of healthy eating, yet research on healthy models from other cultures and cuisines has been limited. This perspective article summarizes the components of traditional Latin American, Asian, and African heritage diets, their association with diet quality and markers of health, and implications for nutrition programs and policy. Though these diets differ in specific foods and flavors, we present a common thread that emphasizes healthful plant foods and that is consistent with high dietary quality and low rates of major causes of disability and deaths. In this perspective, we propose that nutrition interventions that incorporate these cultural models of healthy eating show promise, though further research is needed to determine health outcomes and best practices for implementation.
{"title":"Perspective: Beyond the Mediterranean Diet—Exploring Latin American, Asian, and African Heritage Diets as Cultural Models of Healthy Eating","authors":"Kelly E LeBlanc , Sara Baer-Sinnott , Kristie J Lancaster , Hannia Campos , Ka Hei Karen Lau , Katherine L Tucker , Lawrence H Kushi , Walter C Willett","doi":"10.1016/j.advnut.2024.100221","DOIUrl":"10.1016/j.advnut.2024.100221","url":null,"abstract":"<div><p>The Mediterranean diet is a well-studied cultural model of healthy eating, yet research on healthy models from other cultures and cuisines has been limited. This perspective article summarizes the components of traditional Latin American, Asian, and African heritage diets, their association with diet quality and markers of health, and implications for nutrition programs and policy. Though these diets differ in specific foods and flavors, we present a common thread that emphasizes healthful plant foods and that is consistent with high dietary quality and low rates of major causes of disability and deaths. In this perspective, we propose that nutrition interventions that incorporate these cultural models of healthy eating show promise, though further research is needed to determine health outcomes and best practices for implementation.</p></div>","PeriodicalId":7349,"journal":{"name":"Advances in Nutrition","volume":"15 5","pages":"Article 100221"},"PeriodicalIF":9.3,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2161831324000553/pdfft?md5=bc1fdd69d00d1384bf39f36aae958451&pid=1-s2.0-S2161831324000553-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140801435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-20DOI: 10.1016/j.advnut.2024.100232
Noha Sulaimani , Michael J Houghton , Maxine P Bonham , Gary Williamson
Circadian clocks regulate metabolic homeostasis. Disruption to our circadian clocks, by lifestyle behaviors such as timing of eating and sleeping, has been linked to increased rates of metabolic disorders. There is now considerable evidence that selected dietary (poly)phenols, including flavonoids, phenolic acids and tannins, may modulate metabolic and circadian processes. This review evaluates the effects of (poly)phenols on circadian clock genes and linked metabolic homeostasis in vitro, and potential mechanisms of action, by critically evaluating the literature on mammalian cells. A systematic search was conducted to ensure full coverage of the literature and identified 43 relevant studies addressing the effects of (poly)phenols on cellular circadian processes. Nobiletin and tangeretin, found in citrus, (–)-epigallocatechin-3-gallate from green tea, urolithin A, a gut microbial metabolite from ellagitannins in fruit, curcumin, bavachalcone, cinnamic acid, and resveratrol at low micromolar concentrations all affect circadian molecular processes in multiple types of synchronized cells. Nobiletin emerges as a putative retinoic acid–related orphan receptor (RORα/γ) agonist, leading to induction of the circadian regulator brain and muscle ARNT-like 1 (BMAL1), and increased period circadian regulator 2 (PER2) amplitude and period. These effects are clear despite substantial variations in the protocols employed, and this review suggests a methodological framework to help future study design in this emerging area of research.
{"title":"Effects of (Poly)phenols on Circadian Clock Gene–Mediated Metabolic Homeostasis in Cultured Mammalian Cells: A Scoping Review","authors":"Noha Sulaimani , Michael J Houghton , Maxine P Bonham , Gary Williamson","doi":"10.1016/j.advnut.2024.100232","DOIUrl":"10.1016/j.advnut.2024.100232","url":null,"abstract":"<div><p>Circadian clocks regulate metabolic homeostasis. Disruption to our circadian clocks, by lifestyle behaviors such as timing of eating and sleeping, has been linked to increased rates of metabolic disorders. There is now considerable evidence that selected dietary (poly)phenols, including flavonoids, phenolic acids and tannins, may modulate metabolic and circadian processes. This review evaluates the effects of (poly)phenols on circadian clock genes and linked metabolic homeostasis in vitro, and potential mechanisms of action, by critically evaluating the literature on mammalian cells. A systematic search was conducted to ensure full coverage of the literature and identified 43 relevant studies addressing the effects of (poly)phenols on cellular circadian processes. Nobiletin and tangeretin, found in citrus, (–)-epigallocatechin-3-gallate from green tea, urolithin A, a gut microbial metabolite from ellagitannins in fruit, curcumin, bavachalcone, cinnamic acid, and resveratrol at low micromolar concentrations all affect circadian molecular processes in multiple types of synchronized cells. Nobiletin emerges as a putative retinoic acid–related orphan receptor (<em>RORα/γ</em>) agonist, leading to induction of the circadian regulator brain and muscle ARNT-like 1 (<em>BMAL1)</em>, and increased period circadian regulator 2 (<em>PER2)</em> amplitude and period. These effects are clear despite substantial variations in the protocols employed, and this review suggests a methodological framework to help future study design in this emerging area of research.</p></div>","PeriodicalId":7349,"journal":{"name":"Advances in Nutrition","volume":"15 6","pages":"Article 100232"},"PeriodicalIF":9.3,"publicationDate":"2024-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2161831324000668/pdfft?md5=f945a9b50d04cb25bbfc399aad5148c0&pid=1-s2.0-S2161831324000668-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140755890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-11DOI: 10.1016/j.advnut.2024.100228
Amanda V Montana , Alison Mildon , Allison I Daniel , Michael A Pitino , Jo-Anna B Baxter , Megan R Beggs , Sharon L Unger , Deborah L O’Connor , Kathryn Walton
Maternal adiposity impacts lactation performance, but the pathways are unclear. We conducted a systematic review to understand whether maternal adiposity (body mass index [BMI] or percentage fat mass) is associated with onset of lactogenesis II (copious milk; hours), human milk production (expressed volume/24 h), and infant consumption of mother’s own milk (volume/24 h). We used random-effects standard meta-analyses to compare the relative risk (RR) of delayed lactogenesis II (>72 h) between mothers classified as underweight (BMI <18.5 kg/m2), healthy weight (BMI, 18.5–24.9 kg/m2), and overweight/obese (BMI ≥25 kg/m2) and random-effects meta-regressions to examine associations with hours to lactogenesis II and infant milk consumption. The certainty of evidence was assessed using the Grading of Recommendations, Assessment, Development and Evaluation approach. We included 122 articles. Mothers with underweight (RR: 0.64; 95% CI: 0.49, 0.83; I2 = 39.48%; 8 articles/data points) or healthy weight status (RR: 0.67; 95% CI: 0.57, 0.79; I2 = 70.91%; 15 articles/data points) were less likely to experience delayed lactogenesis II than mothers with overweight/obesity. We found no association between maternal BMI and time to onset of lactogenesis II (β: 1.45 h; 95% CI: −3.19, 6.09 h; P = 0.52, I2 = 0.00%; 8 articles, 17 data points). Due to limited data, we narratively reviewed articles examining BMI or percentage fat mass and milk production (n = 6); half reported an inverse association and half no association. We found no association between maternal BMI (β: 6.23 mL; 95% CI: −11.26, 23.72 mL; P = 0.48, I2 = 47.23%; 58 articles, 75 data points) or percentage fat mass (β: 7.82 mL; 95% CI: −1.66, 17.29 mL; P = 0.10, I2 = 28.55%; 30 articles, 41 data points) and infant milk consumption. The certainty of evidence for all outcomes was very low. In conclusion, mothers with overweight/obesity may be at risk of delayed lactogenesis II. The available data do not support an association with infant milk consumption, but the included studies do not adequately represent mothers with obesity.
{"title":"Is Maternal Body Weight or Composition Associated with Onset of Lactogenesis II, Human Milk Production, or Infant Consumption of Mother’s Own Milk? A Systematic Review and Meta-Analysis","authors":"Amanda V Montana , Alison Mildon , Allison I Daniel , Michael A Pitino , Jo-Anna B Baxter , Megan R Beggs , Sharon L Unger , Deborah L O’Connor , Kathryn Walton","doi":"10.1016/j.advnut.2024.100228","DOIUrl":"10.1016/j.advnut.2024.100228","url":null,"abstract":"<div><p>Maternal adiposity impacts lactation performance, but the pathways are unclear. We conducted a systematic review to understand whether maternal adiposity (body mass index [BMI] or percentage fat mass) is associated with onset of lactogenesis II (copious milk; hours), human milk production (expressed volume/24 h), and infant consumption of mother’s own milk (volume/24 h). We used random-effects standard meta-analyses to compare the relative risk (RR) of delayed lactogenesis II (>72 h) between mothers classified as underweight (BMI <18.5 kg/m<sup>2</sup>), healthy weight (BMI, 18.5–24.9 kg/m<sup>2</sup>), and overweight/obese (BMI ≥25 kg/m<sup>2</sup>) and random-effects meta-regressions to examine associations with hours to lactogenesis II and infant milk consumption. The certainty of evidence was assessed using the Grading of Recommendations, Assessment, Development and Evaluation approach. We included 122 articles. Mothers with underweight (RR: 0.64; 95% CI: 0.49, 0.83; <em>I</em><sup>2</sup> = 39.48%; 8 articles/data points) or healthy weight status (RR: 0.67; 95% CI: 0.57, 0.79; <em>I</em><sup>2</sup> = 70.91%; 15 articles/data points) were less likely to experience delayed lactogenesis II than mothers with overweight/obesity. We found no association between maternal BMI and time to onset of lactogenesis II (β: 1.45 h; 95% CI: −3.19, 6.09 h; <em>P</em> = 0.52, <em>I</em><sup>2</sup> = 0.00%; 8 articles, 17 data points). Due to limited data, we narratively reviewed articles examining BMI or percentage fat mass and milk production (<em>n</em> = 6); half reported an inverse association and half no association. We found no association between maternal BMI (β: 6.23 mL; 95% CI: −11.26, 23.72 mL; <em>P</em> = 0.48, <em>I</em><sup>2</sup> = 47.23%; 58 articles, 75 data points) or percentage fat mass (β: 7.82 mL; 95% CI: −1.66, 17.29 mL; <em>P</em> = 0.10, <em>I</em><sup>2</sup> = 28.55%; 30 articles, 41 data points) and infant milk consumption. The certainty of evidence for all outcomes was very low. In conclusion, mothers with overweight/obesity may be at risk of delayed lactogenesis II. The available data do not support an association with infant milk consumption, but the included studies do not adequately represent mothers with obesity.</p><p>This study was registered in PROSPERO as 285344.</p></div>","PeriodicalId":7349,"journal":{"name":"Advances in Nutrition","volume":"15 6","pages":"Article 100228"},"PeriodicalIF":9.3,"publicationDate":"2024-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2161831324000620/pdfft?md5=b292e1b5e5bda42dace342b17326789c&pid=1-s2.0-S2161831324000620-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140788334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-08DOI: 10.1016/j.advnut.2024.100219
Camilla Christensen , Andrea Knudsen , Erik K Arnesen , Jan Gunnar Hatlebakk , Ida Sofie Sletten , Lars T Fadnes
Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), contributes to substantial morbidity. Understanding the intricate interplay between dietary factors and the incidence and progression of IBD is essential for developing effective preventative and therapeutic strategies. This umbrella review comprehensively synthesizes evidence from systematic reviews and meta-analyses to evaluate these complex associations. Dietary factors associated with an increased incidence and/or progression of IBD include a high intake of red and processed meat, other processed foods, and refined sugars, together with a low intake of vegetables, fruits, and fiber. For most other food groups, the results are mixed or indicate no clear associations with IBD, CD, and UC. Some differences seem to exist between UC and CD and their risk factors, with increased intake of dietary fiber being inversely associated with CD incidence but not clearly associated with UC. Dietary fiber may contribute to maintaining the gut epithelial barrier and reduce inflammation, often through interactions with the gut microbiota. This seems to play an important role in inflammatory mechanisms in the gut and in IBD incidence and progression. Diets low in fermentable saccharides and polyols can alleviate symptom burden, but there are concerns regarding their impact on the gut microbiota and their nutritional adequacy. Mediterranean diets, vegetarian diets, and a diet low in grains, sugars, and lactose (specific carbohydrate diet) are also associated with lower incidence and/or progression of IBD. The associations of dietary patterns are mirrored by inflammatory biomarkers. IBD is typically treated pharmaceutically; however, many patients have a suboptimal response to medical treatments. The findings from this umbrella review could provide evidence for nutritional counseling and be a valuable addition to traditional treatment plans for IBD.
This systematic review was registered at PROSPERO as CRD440252.
{"title":"Diet, Food, and Nutritional Exposures and Inflammatory Bowel Disease or Progression of Disease: an Umbrella Review","authors":"Camilla Christensen , Andrea Knudsen , Erik K Arnesen , Jan Gunnar Hatlebakk , Ida Sofie Sletten , Lars T Fadnes","doi":"10.1016/j.advnut.2024.100219","DOIUrl":"https://doi.org/10.1016/j.advnut.2024.100219","url":null,"abstract":"<div><p>Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), contributes to substantial morbidity. Understanding the intricate interplay between dietary factors and the incidence and progression of IBD is essential for developing effective preventative and therapeutic strategies. This umbrella review comprehensively synthesizes evidence from systematic reviews and meta-analyses to evaluate these complex associations. Dietary factors associated with an increased incidence and/or progression of IBD include a high intake of red and processed meat, other processed foods, and refined sugars, together with a low intake of vegetables, fruits, and fiber. For most other food groups, the results are mixed or indicate no clear associations with IBD, CD, and UC. Some differences seem to exist between UC and CD and their risk factors, with increased intake of dietary fiber being inversely associated with CD incidence but not clearly associated with UC. Dietary fiber may contribute to maintaining the gut epithelial barrier and reduce inflammation, often through interactions with the gut microbiota. This seems to play an important role in inflammatory mechanisms in the gut and in IBD incidence and progression. Diets low in fermentable saccharides and polyols can alleviate symptom burden, but there are concerns regarding their impact on the gut microbiota and their nutritional adequacy. Mediterranean diets, vegetarian diets, and a diet low in grains, sugars, and lactose (specific carbohydrate diet) are also associated with lower incidence and/or progression of IBD. The associations of dietary patterns are mirrored by inflammatory biomarkers. IBD is typically treated pharmaceutically; however, many patients have a suboptimal response to medical treatments. The findings from this umbrella review could provide evidence for nutritional counseling and be a valuable addition to traditional treatment plans for IBD.</p><p>This systematic review was registered at PROSPERO as CRD440252.</p></div>","PeriodicalId":7349,"journal":{"name":"Advances in Nutrition","volume":"15 5","pages":"Article 100219"},"PeriodicalIF":9.3,"publicationDate":"2024-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S216183132400053X/pdfft?md5=0f7ad3d148265474db100f553fd19158&pid=1-s2.0-S216183132400053X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140644609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-05DOI: 10.1016/j.advnut.2024.100218
Karina M Tonon, Somchai Chutipongtanate, Ardythe L Morrow, David S Newburg
In infants worldwide, respiratory syncytial virus (RSV) is the leading cause of lower respiratory infections, including bronchiolitis, which is a major source of infant mortality. Bronchiolitis is the most common lower respiratory infection and the major cause of hospitalization in the first 6 mo of life. Infant responses to RSV infection are highly diverse, with symptoms varying from asymptomatic or mild to so severe as to require mechanical ventilation. Breastfed infants present a lower incidence and less severe forms of RSV lower respiratory infections. Among the multitude of human milk bioactive compounds, human milk oligosaccharides (hMOSs) are strong candidates for having a protective effect against RSV. hMOS reduces the viral load and the inflammatory signaling in cultured RSV-infected respiratory human cells. In addition to this direct effect, indirect mechanisms, notably gut microbiota composition and metabolism, have been proposed to mediate the protective effect of hMOS. Intake of infant formula containing synthetic hMOS has been shown to increase Bifidobacterium abundance and that of its metabolites, especially acetate, in infant feces and to reduce lower respiratory tract infections during the first year of life. Breastfeeding and the use of hMOS are promising approaches to protect against and treat RSV disease. Here, we review current evidence on the role of hMOS with regard to RSV infection and disease, attending to knowledge gaps and future research directions.
{"title":"Human Milk Oligosaccharides and Respiratory Syncytial Virus Infection in Infants","authors":"Karina M Tonon, Somchai Chutipongtanate, Ardythe L Morrow, David S Newburg","doi":"10.1016/j.advnut.2024.100218","DOIUrl":"10.1016/j.advnut.2024.100218","url":null,"abstract":"<div><p>In infants worldwide, respiratory syncytial virus (RSV) is the leading cause of lower respiratory infections, including bronchiolitis, which is a major source of infant mortality. Bronchiolitis is the most common lower respiratory infection and the major cause of hospitalization in the first 6 mo of life. Infant responses to RSV infection are highly diverse, with symptoms varying from asymptomatic or mild to so severe as to require mechanical ventilation. Breastfed infants present a lower incidence and less severe forms of RSV lower respiratory infections. Among the multitude of human milk bioactive compounds, human milk oligosaccharides (hMOSs) are strong candidates for having a protective effect against RSV. hMOS reduces the viral load and the inflammatory signaling in cultured RSV-infected respiratory human cells. In addition to this direct effect, indirect mechanisms, notably gut microbiota composition and metabolism, have been proposed to mediate the protective effect of hMOS. Intake of infant formula containing synthetic hMOS has been shown to increase <em>Bifidobacterium</em> abundance and that of its metabolites, especially acetate, in infant feces and to reduce lower respiratory tract infections during the first year of life. Breastfeeding and the use of hMOS are promising approaches to protect against and treat RSV disease. Here, we review current evidence on the role of hMOS with regard to RSV infection and disease, attending to knowledge gaps and future research directions.</p></div>","PeriodicalId":7349,"journal":{"name":"Advances in Nutrition","volume":"15 6","pages":"Article 100218"},"PeriodicalIF":9.3,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2161831324000528/pdfft?md5=1060f9a6c16bf3ccaa0d2a61cae23cb4&pid=1-s2.0-S2161831324000528-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140769964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}