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Clinical symptoms and markers of disease mechanisms in adolescent chronic fatigue following Epstein-Barr virus infection: An exploratory cross-sectional study.
Kristiansen, MS, Stabursvik, J, O'Leary, EC, Pedersen, M, Asprusten, TT, Leegaard, T, Osnes, LT, Tjade, T, Skovlund, E, Godang, K, et al
Brain, behavior, and immunity. 2019;80:551-563
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Epstein-Barr virus (EBV) can trigger chronic fatigue (CF) and chronic fatigue syndrome (CFS) in individuals who are predisposed. However, how fatigue develops and how infections may trigger this is not fully understood. This exploratory cross-sectional study of 200 fatigued and non-fatigued adolescents 6 months after EBV aimed to understand symptoms and potential markers for disease. The results showed that all symptoms (not just fatigue) were more pronounced in those individuals suffering from fatigue, despite no increases in viral load. Those with fatigue only had slight changes in immune, nerve and hormonal markers and none correlated with severity of symptoms. It was concluded that there is a discrepancy between symptoms and viral load and alterations to several markers were only marginal. This study could be used by healthcare professionals to understand the possible limitations of using several biomarkers as a diagnostic tool for CF and CFS.
Abstract
INTRODUCTION Acute Epstein-Barr virus (EBV) infection is a trigger of chronic fatigue (CF) and Chronic Fatigue Syndrome (CFS). The aim of this cross-sectional study was to explore clinical symptoms as well as markers of disease mechanisms in fatigued and non-fatigued adolescents 6 months after EBV-infection, and in healthy controls. MATERIALS AND METHODS A total of 200 adolescents (12-20 years old) with acute EBV infection were assessed 6 months after the initial infectious event and divided into fatigued (EBV CF+) and non-fatigued (EBV CF-) cases based on questionnaire score. The EBV CF+ cases were further sub-divided according to case definitions of CFS. In addition, a group of 70 healthy controls with similar distribution of sex and age was included. Symptoms were mapped with a questionnaire. Laboratory assays included EBV PCR and serology; detailed blood leukocyte phenotyping and serum high-sensitive C-reactive protein; and plasma and urine cortisol and catecholamines. Assessment of autonomic activity was performed with continuous, non-invasive monitoring of cardiovascular variables during supine rest, controlled breathing and upright standing. Differences between EBV CF+ and EBV CF- were assessed by simple and multiple linear regression adjusting for sex as well as symptoms of depression and anxiety. A p-value ≤ 0.05 was considered statistically significant. This study is part of the CEBA-project (Chronic fatigue following acute Epstein-Barr virus infection in adolescents). RESULTS The EBV CF+ group had significantly higher scores for all clinical symptoms. All markers of infection and most immune, neuroendocrine and autonomic markers were similar across the EBV CF+ and EBV CF- group. However, the EBV CF+ group had slightly higher serum C-reactive protein (0.48 vs 0.43 mg/L, p = 0.031, high-sensitive assay), total T cell (CD3+) count (median 1573 vs 1481 × 106 cells/L, p = 0.012), plasma norepinephrine (1420 vs 1113 pmol/L, p = 0.01) and plasma epinephrine (363 vs 237 nmol/L, p = 0.032); lower low-frequency:high frequency (LF/HF) ratio of heart rate variability at supine rest (0.63 vs 0.76, p = 0.008); and an attenuated decline in LF/HF ratio during controlled breathing (-0.11 vs -0.25, p = 0.002). Subgrouping according to different CFS diagnostic criteria did not significantly alter the results. Within the EBV CF+ group, there were no strong correlations between clinical symptoms and markers of disease mechanisms. In a multiple regression analysis, serum CRP levels were independently associated with serum cortisol (B = 4.5 × 10-4, p < 0.001), urine norepinephrine (B = 9.6 × 10-2, p = 0.044) and high-frequency power of heart rate variability (B = -3.7 × 10-2, p = 0.024). CONCLUSIONS In adolescents, CF and CFS 6 months after acute EBV infection are associated with high symptom burden, but no signs of increased viral load and only subtle alterations of immune, autonomic, and neuroendocrine markers of which no one is strongly correlated with symptom scores. A slight sympathetic over parasympathetic predominance is evident in CF and might explain slightly increased CRP levels.
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Plant-Based Diets Are Associated With a Lower Risk of Incident Cardiovascular Disease, Cardiovascular Disease Mortality, and All-Cause Mortality in a General Population of Middle-Aged Adults.
Kim, H, Caulfield, LE, Garcia-Larsen, V, Steffen, LM, Coresh, J, Rebholz, CM
Journal of the American Heart Association. 2019;8(16):e012865
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Plant based diets have been associated with better health outcomes, however mixed results have been shown on their relationship with death by any cause and death due to heart disease. This cohort study of 15792 middle aged people aimed to determine if plant-based diets are associated with a lower risk of heart disease, death due to heart disease or death due to any cause and whether this was on a sliding scale depending on adherence to a healthful plant-based diet. The results showed that individuals following a plant-based diet had a 16% lower risk of heart disease, 32% lower risk of death due to heart disease and a 25% lower risk of death by any cause and individuals who followed a healthier plant-based diet were at an even lower risk of heart disease, death due to heart disease and death due to any cause. Interestingly when margarine was included in an individual’s diet, the decreased risk of heart disease was attenuated. It was concluded that higher adherence to a healthy plant-based diet was associated with a lower risk of heart disease, death due to heart disease and death by any cause. This study could be used by healthcare practitioners to recommend a plant-based diet to those at an increased risk of heart disease.
Abstract
Background Previous studies have documented the cardiometabolic health benefits of plant-based diets; however, these studies were conducted in selected study populations that had narrow generalizability. Methods and Results We used data from a community-based cohort of middle-aged adults (n=12 168) in the ARIC (Atherosclerosis Risk in Communities) study who were followed up from 1987 through 2016. Participants' diet was classified using 4 diet indexes. In the overall plant-based diet index and provegetarian diet index, higher intakes of all or selected plant foods received higher scores; in the healthy plant-based diet index, higher intakes of only the healthy plant foods received higher scores; in the less healthy plant-based diet index, higher intakes of only the less healthy plant foods received higher scores. In all indexes, higher intakes of animal foods received lower scores. Results from Cox proportional hazards models showed that participants in the highest versus lowest quintile for adherence to overall plant-based diet index or provegetarian diet had a 16%, 31% to 32%, and 18% to 25% lower risk of cardiovascular disease, cardiovascular disease mortality, and all-cause mortality, respectively, after adjusting for important confounders (all P<0.05 for trend). Higher adherence to a healthy plant-based diet index was associated with a 19% and 11% lower risk of cardiovascular disease mortality and all-cause mortality, respectively, but not incident cardiovascular disease (P<0.05 for trend). No associations were observed between the less healthy plant-based diet index and the outcomes. Conclusions Diets higher in plant foods and lower in animal foods were associated with a lower risk of cardiovascular morbidity and mortality in a general population.
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Inflammatory Bowel Diseases and Food Additives: To Add Fuel on the Flames!
Marion-Letellier, R, Amamou, A, Savoye, G, Ghosh, S
Nutrients. 2019;11(5)
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Inflammatory Bowel Diseases (IBDs), such as Crohn’s disease (CD) and Ulcerative Colitis (UC) are becoming increasingly common. Diet is thought to play a role in the development of IBDs. The consumption of Ultra Processed Food (UPF) is increasing and has been associated with a higher risk of some chronic diseases. Food additives may be an aspect of UPF responsible for its harmful effects. This literature review examined the role of food additives in the development and severity of IBDs. The authors discuss how common food additives such as salt, emulsifiers, stabilisers, bulking agents, sweeteners, and food colouring may promote inflammation and disrupt gut bacteria. Metals and compounds found in food packaging such as aluminium and bisphenol A (BPA) may trigger intestinal permeability and increase inflammatory markers. Much of the evidence available is based on clinical trials on animals, whilst epidemiological studies on food additives and IBD risk are still limited. The authors concluded that the majority of food consumed by IBD patients should be home-cooked in order to reduce exposure to additives in the diet.
Abstract
Inflammatory bowel diseases (IBDs) develop in genetically predisposed individuals in response to environmental factors. IBDs are concomitant conditions of industrialized societies, and diet is a potential culprit. Consumption of ultra-processed food has increased over the last decade in industrialized countries, and epidemiological studies have found associations between ultra-processed food consumption and chronic diseases. Further studies are now required to identify the potential culprit in ultra-processed food, such as a poor nutritional composition or the presence of food additives. In our review, we will focus on food additives, i.e., substances from packaging in contact with food, and compounds formed during production, processing, and storage. A literature search using PubMed from inception to January 2019 was performed to identify relevant studies on diet and/or food additive and their role in IBDs. Manuscripts published in English from basic science, epidemiological studies, or clinical trials were selected and reviewed. We found numerous experimental studies highlighting the key role of food additives in IBD exacerbation but epidemiological studies on food additives on IBD risk are still limited. As diet is a modifiable environmental risk factor, this may offer a scientific rationale for providing dietary advice for IBD patients.
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Gut microbial metabolites in depression: understanding the biochemical mechanisms.
Caspani, G, Kennedy, S, Foster, JA, Swann, J
Microbial cell (Graz, Austria). 2019;6(10):454-481
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Major depressive disorder is a leading cause of disability and is linked to shortened life expectancy and suicide. Despite its prevalence, for near to a third of patients, long-term treatment options are ineffective. In addition to the primary presentation of persistent low mood, other emotional and physiological symptoms, researchers have also identified alterations in metabolism, hormones and the immune system. Furthermore, increasing evidence suggests that depression and depressive behaviour is also influenced by divergences in gut health and gut bacteria composition. With insights from animal and human research, this review highlights how the gut and gut bacteria-derived metabolites can directly or indirectly influence mood. Described are the pathways of how the gut and its microorganism communicate with the brain, the essential role the immune system has as part of the gut-brain communication, and the impact of low-grade, chronic inflammation on neurofunction. Comprehensive summaries are dedicated to how several metabolites or by-products from gut bacteria can influence the nervous system and gene expression in relation to depression. These include substances like neurotransmitters, short-chain fatty acids, tryptophan metabolites, lactate, bile acids, choline metabolites and folate. This article yields a detailed overview of how gut health and microbiota can influence neurofunction and mental health. The authors promote the idea of the gut as a suitable target for the management of depressive disorders, whilst also eluding to the current limitations and need for further research.
Abstract
Gastrointestinal and central function are intrinsically connected by the gut microbiota, an ecosystem that has co-evolved with the host to expand its biotransformational capabilities and interact with host physiological processes by means of its metabolic products. Abnormalities in this microbiota-gut-brain axis have emerged as a key component in the pathophysiology of depression, leading to more research attempting to understand the neuroactive potential of the products of gut microbial metabolism. This review explores the potential for the gut microbiota to contribute to depression and focuses on the role that microbially-derived molecules - neurotransmitters, short-chain fatty acids, indoles, bile acids, choline metabolites, lactate and vitamins - play in the context of emotional behavior. The future of gut-brain axis research lies is moving away from association, towards the mechanisms underlying the relationship between the gut bacteria and depressive behavior. We propose that direct and indirect mechanisms exist through which gut microbial metabolites affect depressive behavior: these include (i) direct stimulation of central receptors, (ii) peripheral stimulation of neural, endocrine, and immune mediators, and (iii) epigenetic regulation of histone acetylation and DNA methylation. Elucidating these mechanisms is essential to expand our understanding of the etiology of depression, and to develop new strategies to harness the beneficial psychotropic effects of these molecules. Overall, the review highlights the potential for dietary interventions to represent such novel therapeutic strategies for major depressive disorder.
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Tryptophan Metabolism in Inflammaging: From Biomarker to Therapeutic Target.
Sorgdrager, FJH, Naudé, PJW, Kema, IP, Nollen, EA, Deyn, PP
Frontiers in immunology. 2019;10:2565
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Inflammation is a normal physiological process activated by the immune system in response to injury or infection. As we age, the immune system changes and the balance between pro- and anti-inflammatory agents can shift. This causes a chronic inflammatory state referred to as inflammaging. The rate of inflammaging is strongly associated with age-related disability, disease and mortality. The way in which the essential amino acid tryptophan (Trp) is broken down affects inflammation. If it is converted to kynurenine (Kyn) and its metabolites, inflammation is modulated. Studies have shown that the Kyn/Trp ratio, measured in blood, is strongly associated with ageing in humans. It could therefore be a useful marker to predict the onset of age-related diseases. This review discusses the metabolism of Trp and the links to inflammation. The authors hypothesize how intervening in these pathways could impact health- and lifespan. Future studies are needed to confirm the value of Trp metabolism as a biomarker for (un)healthy ageing and as drug target for inflammaging-related disease.
Abstract
Inflammation aims to restore tissue homeostasis after injury or infection. Age-related decline of tissue homeostasis causes a physiological low-grade chronic inflammatory phenotype known as inflammaging that is involved in many age-related diseases. Activation of tryptophan (Trp) metabolism along the kynurenine (Kyn) pathway prevents hyperinflammation and induces long-term immune tolerance. Systemic Trp and Kyn levels change upon aging and in age-related diseases. Moreover, modulation of Trp metabolism can either aggravate or prevent inflammaging-related diseases. In this review, we discuss how age-related Kyn/Trp activation is necessary to control inflammaging and alters the functioning of other metabolic faiths of Trp including Kyn metabolites, microbiota-derived indoles and nicotinamide adenine dinucleotide (NAD+). We explore the potential of the Kyn/Trp ratio as a biomarker of inflammaging and discuss how intervening in Trp metabolism might extend health- and lifespan.
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Does weight-related stigmatisation and discrimination depend on educational attainment and level of income? A systematic review.
Bernard, M, Fankhänel, T, Riedel-Heller, SG, Luck-Sikorski, C
BMJ open. 2019;9(11):e027673
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Obesity is a global health issue due to its association with many chronic diseases, including type 2 diabetes, cardiovascular disease and certain cancers. Stigmatisation and discrimination against people with obesity has increased over the past few decades. According to the “Theory of class” a person’s “habitus”, that is their general attitude, lifestyle and even body shape, can be seen as a metaphor for social status. The aim of this systematic review of 17 studies was to investigate whether socioeconomic status is associated with “weight bias”, that is stigmatising and discriminating attitudes towards people with obesity. 11 of the 17 studies found a significant association between educational attainment and/or income with stigmatising and/or discriminatory attitudes, but results were mixed, with some studies showing that people with higher education and/or income level were more likely to display stigmatising and/or discriminating attitudes, whilst other studies showed the opposite. The authors conclude that the findings have to be discussed in the cultural context, including cultural and governmental differences.
Abstract
OBJECTIVES Obesity is considered a global health issue, because of its health-related consequences and also because of its impact on social status as a result of stigma. This study aims to review the quantitative state of research regarding socioeconomic characteristics' influence on weight-related stigmatisation and discrimination. Based on Bourdieu's Theory of Class and his concept of 'habitus', it is assumed that people with a higher level of education and income show stronger negative attitudes towards people with obesity. METHOD A narrative systematic literature review was conducted in 2017 using PubMed, PsychINFO, Web of Science and the Cochrane Library. Seventeen studies that measured weight bias and either educational attainment or level of income were included in the analysis. RESULTS The results of the studies included were inconsistent: six of these studies were found to support the hypothesis, whereas two of the studies contradicted it. The remaining seven studies did not show any significant correlation between weight bias and either education or income. CONCLUSION In light of the inconsistent and heterogeneous results of the studies that report a significant association between weight bias and socioeconomic variables, the findings must be discussed concerning their cultural context, that is, cultural and governmental differences. Furthermore, educational attainment seems to be more likely to predict weight bias than income. The review revealed a lack of research when it came to examining the impact of socioeconomic capital on weight bias.
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Examining Weight Bias among Practicing Canadian Family Physicians.
Alberga, AS, Nutter, S, MacInnis, C, Ellard, JH, Russell-Mayhew, S
Obesity facts. 2019;12(6):632-638
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Weight bias represents negative attitudes and beliefs about individuals because of their weight. The aim of this study was to examine: a. weight bias in a national sample of family physicians in Canada, b. the relationships between weight bias, attitudes about treating patients with obesity, and how people with obesity are perceived as a burden to the public healthcare system. A probability sample of 400 currently practicing family physicians completed the survey by phone or online. Results show that most respondents were white (63.3%) men (61.3%) aged 45 years or older. The average total score of explicit weight bias was 2.95 (1.17) evaluated on a 7-point Likert scale. Furthermore, although weight bias was not present in the majority of the sample, it was present among some physicians. Authors conclude that future work is needed to investigate weight bias reduction techniques targeted at physicians.
Abstract
OBJECTIVES The aim of this study was to examine the attitudes of practicing Canadian family physicians about individuals with obesity, their healthcare treatment, and perceptions of obesity treatment in the public healthcare system. METHOD A national sample of Canadian practicing family physicians (n = 400) completed the survey. Participants completed measures of explicit weight bias, attitudes towards treating patients with obesity, and perceptions that people with obesity increase demand on the public healthcare system. RESULTS Responses consistent with weight bias were not observed overall but were demonstrated in a sizeable minority of respondents. Many physicians also reported feeling frustrated with patients with obesity and agreed that people with obesity increase demand on the public healthcare system. Male physicians had more negative attitudes than females. More negative attitudes towards treating patients with obesity were associated with greater perceptions of them as a public health demand. CONCLUSION Results suggest that negative attitudes towards patients with obesity exist among some family physicians in Canada. It remains to be determined if physicians develop weight bias partly because they blame individuals for their obesity and its increased demand on the Canadian public healthcare system. More research is needed to better understand causes and consequences of weight bias among health professionals and make efforts towards its reduction in healthcare.
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The skin microbiome in psoriatic disease: A systematic review and critical appraisal.
Yerushalmi, M, Elalouf, O, Anderson, M, Chandran, V
Journal of translational autoimmunity. 2019;2:100009
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Psoriasis is a common inflammatory skin disease that results in patches of dry, scaly skin that can be itchy or sore. Psoriatic arthritis is an inflammatory arthritis that affects up to 30% of psoriasis patients. The role of skin bacteria (the skin microbiome) is not well understood. This systematic review summarised the literature on the microbiome in psoriatic disease. The researchers looked at nine studies: seven on psoriasis only, and two studies comparing the microbiome characteristics between psoriasis and psoriatic arthritis. Compared to healthy controls, the skin of psoriasis patients demonstrated a decreased species diversity, higher relative abundances of Firmicutes, and lower relative abundances of Actinobacteria. Less conclusive were genus-level results, which demonstrated trends towards increased Streptococcus, Staphylococcus, and Corynebacterium, and decreased Propionibacterium in the skin of psoriasis patients versus healthy controls. However, the studies’ designs and methodologies varied, and therefore the researchers concluded that further research into the role of the skin microbiome in psoriatic disease is needed.
Abstract
BACKGROUND Psoriasis affects 1-3% of the Canadian population. Psoriatic arthritis (PsA), the most common comorbidity of psoriasis, affects up to 30% of psoriasis patients. The skin microbiome is hypothesized to play a role in the pathogenesis of psoriatic disease (PsD-psoriasis and PsA). OBJECTIVE To summarize the current state of literature on the skin microbiome in PsD. METHODS A systematic review was performed using searches in Ovid, Medline, Embase, Medline Epub Ahead of Print and In-Process & Other Non-Indexed Citations, and Cochrane Central Register of Controlled Trials (CENTRAL). Search was limited to humans and English language, with no limits for date or publication type. RESULTS Of 4,032 citations identified, 9 studies met inclusion criteria (7 on psoriasis only and 2 studies compared the microbiome characteristics between psoriasis and PsA). Compared to healthy controls, lesions demonstrated a decreased alpha diversity, higher relative abundances of Firmicutes, and lower relative abundances of Actinobacteria. Less conclusive were genus-level results, which nonetheless demonstrated trends towards increased Streptococcus, Staphylococcus, and Corynebacterium and decreased Propionibacterium in lesions vs. control. LIMITATIONS Study designs were heterogeneous, including sampling technique and exclusion criteria. CONCLUSIONS Phyla- and selected genus-level characteristic of the psoriatic microbiome are presented; further research is warranted.
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Effects of resveratrol on VEGF & HIF1 genes expression in granulosa cells in the angiogenesis pathway and laboratory parameters of polycystic ovary syndrome: a triple-blind randomized clinical trial.
Bahramrezaie, M, Amidi, F, Aleyasin, A, Saremi, A, Aghahoseini, M, Brenjian, S, Khodarahmian, M, Pooladi, A
Journal of assisted reproduction and genetics. 2019;36(8):1701-1712
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Polycystic ovary syndrome (PCOS) is a condition in women characterised by disruptions in the ovulation cycle and hormonal imbalances causing infertility. There are several biological mechanisms involved in the development of PCOS, including hormonal imbalance. Recently, high levels of a protein known as VEGF, which stimulates the formation of new blood vessels, has been detected in the ovaries of women with PCOS and is thought to be involved in its development. Resveratrol is a herbal supplement, which has been shown in animal studies to reduce VEGF. This randomised control trial of 61 women with PCOS aimed to determine if there was a similar effect in humans. The results showed that VEGF was decreased following the supplementation of resveratrol, and that it also helped to achieve a more normal hormonal balance. As a result, this improved the quality of embryos, but did not increase the rate of fertility. It was concluded that resveratrol may be of benefit to women with PCOS by decreasing the production of VEGF and helping to achieve a better hormonal balance in women with PCOS.
Abstract
OBJECTIVES Management options for PCOS, as the most prevalent endocrine disorder in women of reproductive age, using natural supplements have a high priority for physicians, especially based on the etiological pathways. Therefore, this study was conducted to describe the effect of resveratrol on the angiogenesis pathway, for management of PCOS through assessing VEGF, HIF1 gene expression, and laboratory parameters. METHODS In this triple-blind RCT, PCOS was confirmed in ICSI candidates based on the Rotterdam criteria. Sixty-two patients that met the inclusion criteria were randomly assigned to two groups. All patients took resveratrol 800 mg/day or placebo for 40 days orally from the beginning of their previous menstruation cycle until the oocyte retrieval day. The serum levels of different hormones were measured, and the expression of HIF1 & VEGF genes was quantified by real-time PCR. RESULTS As for the laboratory hormone assay in 61 PCOS patients, a significant mean difference was seen in the FSH, LH, TSH, and testosterone between the two groups (P < 0.05). The results showed a reduction in the expression of VEGF & HIF1 genes under the effect of resveratrol in the granulosa cells (P = 0.0001). The number of mature oocytes, cleavage rate, fertilization rate, and fertility rate were not significantly different between the two groups (P > 0.05), but the high-quality oocyte rate and high-quality embryo rate were higher in the resveratrol group (P < 0.05). CONCLUSIONS Based on the results, resveratrol may improve some outcomes of PCOS patients, probably through changing the serum levels of some sex hormones and expression of VEGF & HIF1 genes in the angiogenesis pathway of granulosa cells.
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Oral glutamine supplements reduce concurrent chemoradiotherapy-induced esophagitis in patients with advanced non-small cell lung cancer.
Chang, SC, Lai, YC, Hung, JC, Chang, CY
Medicine. 2019;98(8):e14463
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Non-small cell lung cancer (NSCLC) is commonly treated with concurrent chemo- and radiation therapy (CCRT). This treatment often causes acute radiation-induced oesophagitis (ARIE) which can lead to significant weight loss and unplanned treatment delays. This prospective randomised study assessed whether glutamine supplementation may prevent ARIE in advanced NSCLC patients. Patients were randomised to receive either standard treatment (CCRT) with prophylactic oral glutamine, 30 grams/day, or standard treatment alone. The patients in the glutamine group received glutamine for 1 year. Compared with the control group, the oral glutamine supplement group had significantly less severe ARIE, and in those patients who developed ARIE, onset was significantly delayed in the glutamine group. The incidence of weight loss was also significantly reduced in the glutamine group. There was no statistically significant difference in cancer progression-free survival between the two groups (median follow-up period 26.4 months). Glutamine supplementation was well tolerated by all patients. The authors conclude that oral glutamine supplementation has a benefit in delaying onset of and decreasing the severity of ARIE in advanced lung cancer patients undergoing CCRT.
Abstract
BACKGROUND Complications related to concurrent chemoradiotherapy (CCRT) such as acute radiation-induced esophagitis (ARIE) may cause significant morbidity and unplanned treatment delays in patients with advanced non-small cell lung cancer (NSCLC). We designed a prospective randomized study to assess the impact of glutamine (GLN) supplementation in preventing CCRT-induced toxicities of advanced NSCLC patients. METHODS From September 2014 to September 2015, 60 patients diagnosed with NSCLC were included to the study. Thirty patients (50%) received prophylactic powdered GLN orally at a dose of 10 g/8 h. The prescribed radiation dose to the planning target volume was 30 Gy in 2-Gy fractions. The endpoints were radiation-induced esophagitis, mucositis, body weight loss, overall survival and progression-free survival. RESULTS The 60 patients with NSCLC included 42 men and 18 women with a mean age ± standard deviation of 60.3 years ± 18.2 (range, 44-78 years).At a median follow-up of 26.4 months (range 10.4-32.2), all patients tolerated GLN well. A administration of GLN was associated with a decrease in the incidence of grade 2 or 3 ARIE (6.7% vs 53.4% for Gln+ vs Gln-; P = .004). GLN supplementation appeared to significantly delay ARIE onset for 5.8 days (18.2 days vs 12.4 days; P = .027) and reduced incidence of weight loss (20% vs 73.3%; P = .01). DISCUSSION Our study suggests a beneficial effect of oral glutamine supplementation for the prevention from radiation-induced injury and body weight loss in advanced NSCLC patients who receiving CCRT.