Food habits during treatment of childhood cancer: a critical review.

Several factors can affect the nutritional status of children undergoing cancer therapy. The present review aims to describe children's food intake during cancer treatments and to explore the contributing determinants. It also assesses the nutritional educational interventions developed for this clientele. Scientific literature from January 1995 to January 2018 was searched through PubMed and MEDLINE using keywords related to childhood cancer and nutritional intake. Quantitative and qualitative studies were reviewed: forty-seven articles were selected: thirty-eight related to food intake and parental practices and nine related to nutritional interventions. Patients' intakes in energy, macronutrients and micronutrients were compared with those of healthy controls or with requirement standards. Generally, patients ate less energy and proteins than healthy children, but adhered similarly to national guidelines. There is a lack of consensus for standard nutrient requirement in this population and a need for more prospective evaluations. Qualitative studies provide an insight into the perceptions of children, parents and nurses on several determinants influencing eating behaviours, including the type of treatment and their side effects. Parental practices were found to be diverse. In general, savoury and salty foods were preferred to sweet foods. Finally, most interventional studies in childhood cancer have presented their protocol or assessed the feasibility of an intervention. Therefore, because of the variability of study designs and since only a few studies have presented results, their impact on the development of healthful eating habits remains unclear. A better understanding of children's nutritional intakes and eating behaviours during cancer treatment could guide future nutritional interventions.

Is there a relationship between vitamin D nutritional status and metabolic syndrome in childhood acute lymphoblastic leukemia survivors? A PETALE study.

BACKGROUND: Treatment of childhood acute lymphoblastic leukemia (cALL) has reached unprecedented success leading to survival rates reaching 90%. This is regrettably linked to increased risk of developing long-term health-related sequels into early adulthood. OBJECTIVE: This study aims at assessing the relationship between the vitamin D status and metabolic biomarkers in PETALE, a well-characterized cohort of cALL survivors. RESULTS: We demonstrate that 15.9% of the study participants exhibited 3 or more metabolic syndrome (MetS) risk factors. We also show a direct relationship between s25OHD3 and plasma HDL-Cholesterol concentrations in female but not male participants. CONCLUSION: Our data, from a metabolically well-described cohort, support a modest role for vitamin D in lipid metabolism in childhood leukemia survivors. The major outcome of this study is the strong association between HDL-Cholesterol concentration and s25OHD3 only in female subjects, thereby conveying vitamin D a gender-specific cardio-protective effect. cALL survivors represent a population at higher risk for secondary diseases. For this reason thorough nutritional evaluation, including vitamin D should be part of the regular follow-up.

Vitamin D nutritional status and bone turnover markers in childhood acute lymphoblastic leukemia survivors: A PETALE study.

BACKGROUND: The remarkable progress in the treatment of childhood acute lymphoblastic leukemia (cALL) has led to a survival rate reaching 90%. This success story is unfortunately linked to increased risk of impaired skeletal mass accumulation during childhood and adolescence, predisposing the patients to osteoporosis and pathological fractures at adulthood. OBJECTIVE: This study aims at characterizing the vitamin D status and bone health biomarkers in a well-characterized cohort of cALL survivors. RESULTS: Food frequency questionnaires reveal that (i) the total vitamin D intake varies greatly (44-2132 IU/d), (ii) only 16.8% of the participants consume vitamin D supplements, and (iii) 74% of survivors' intakes are below the Recommended Daily Intakes (400 IU/d). For the 42 participants taking vitamin D supplements, the median (2.5-97.5%iles) intake is 600 IU/d (21.2-1972 IU/d). Sixteen participants are vitamin D deficient (<30 nM) and 66 insufficient (≥30 - <50 nM). Serum 24,25(OH)2D3 concentrations are directly related to those of 25OHD3, and those of 3-epi-25OHD3 below the Lower Limit of Quantification in most samples. The participants' serum concentrations of cross-linked C-telopeptide of type-I collagen and intact amino-terminal pro-peptide of type-I collagen decrease steadily with age, leveling at adulthood, and are at all times higher in males. CONCLUSION: The present study shows that the prevalence of vitamin D insufficiency or deficiency is not greater in cALL survivors compared to the general Canadian population despite low vitamin D food and supplement intakes. Furthermore, there seem to be no overt imbalance in the gender- and age-adjusted serum bone turnover marker concentrations.

Nutrition education and cooking workshops for families of children with cancer: a feasibility study.

BACKGROUND: Changes in food intake are common in children with cancer and are often caused by nausea and perturbations in sense of taste. The VIE (Valorization, Implication, Education) study proposes family-based nutrition and cooking education workshops during childhood cancer treatments. Process evaluation during implementation allows to assess if the intervention was delivered as planned and to determine its barriers and facilitators. The study objective was to describe the implementation process of a nutrition education and cooking workshop program for families of children actively treated for cancer in a non-randomized non-controlled feasibility study. METHODS: Six open-to-all in-hospital workshops were offered on a weekly basis during a one-year implementation phase. We collected qualitative and quantitative data using field notes and activity reports completed by the registered dietician facilitator; surveys and questionnaires fulfilled by the workshop participants and by the families enrolled in the VIE study. Field notes were used to collect only qualitative data. Survey respondents (n = 26) were mostly mothers (n = 19, 73%). Children's mean age was 7.80 (± 4.99) years and the mean time since diagnosis was 7.98 (± 0.81) months. Qualitative data were codified using hybrid content analysis. The first deductive analysis was based on the Steckler & Linnan concepts. Subthemes were then identified inductively. Quantitative data were presented with descriptive statistics. RESULTS: Workshop attendance was low (17 participants over 1 year) and 71% of the planned workshops were cancelled due to lack of participants. The principal barriers to participation referred the child's medical condition, parental presence required at the child's bedside and challenges related to logistics and time management. The level of interest in the topics addressed was found high or very high for 92% of the participants. The themes that were perceived as the most useful by parents were related to the child's specific medical condition. CONCLUSIONS: Despite high interest, workshops delivered in a face-to-face format were poorly feasible in our sample population. This supports the need to develop educational programs in pediatric oncology using strategies and delivery formats that address the major barriers for participation encountered by families.

Association between genetic variants in the HNF4A gene and childhood-onset Crohn's disease.

Hepatocyte nuclear 4 alpha (HNF4α), involved in glucose and lipid metabolism, has been linked to intestinal inflammation and abnormal mucosal permeability. Moreover, in a genome-wide association study, the HNF4A locus has been associated with ulcerative colitis. The objective of our study was to evaluate the association between HNF4α genetic variants and Crohn's disease (CD) in two distinct Canadian pediatric cohorts. The sequencing of the HNF4A gene in 40 French Canadian patients led to the identification of 27 single nucleotide polymorphism (SNP)s with a minor allele frequency >5%. To assess the impact of these SNPs on disease susceptibility, we first conducted a case-control discovery study on 358 subjects with CD and 542 controls. We then carried out a replication study in a separate cohort of 416 cases and 1208 controls. In the discovery cohort, the genotyping of the identified SNPs revealed that six were significantly associated with CD. Among them, rs1884613 was replicated in the second CD cohort (odds ratio (OR): 1.33; P<0.012) and this association remained significant when both cohorts were combined and after correction for multiple testing (OR: 1.39; P<0.004). An 8-marker P2 promoter haplotype containing rs1884613 was also found associated with CD (P<2.09 × 10(-4) for combined cohorts). This is the first report showing that the HNF4A locus may be a common genetic determinant of childhood-onset CD. These findings highlight the importance of the intestinal epithelium and oxidative protection in the pathogenesis of CD.

Analysis of the effects of iron and vitamin C co-supplementation on oxidative damage, antioxidant response and inflammation in THP-1 macrophages.

OBJECTIVES: The aims of the study were to test the susceptibility of THP-1 macrophages to develop oxidative stress and to deploy antioxidant defense mechanisms that insure the balance between the pro- and antioxidant molecules. DESIGN AND METHODS: Differentiated THP-1 were incubated in the presence or absence of iron-ascorbate (Fe/As) (100/1000µM) and the antioxidants Trolox, BHT, α-Tocopherol and NAC. RESULTS: Fe/As promoted the production of lipid peroxidation as reflected by the formation of malondialdehyde and H(2)O(2) along with reduced PUFA levels and elevated glutathione disulfide/total glutathione ratio, a reliable index of cellular redox status. THP-1 macrophages developed an increase in cytoplasmic SOD activity due in part to high cytoplasmic SOD1. On the other hand, a decline was noted in mRNA and protein of extra-cellular SOD3, as well as the activity of GSH-peroxidase, GSH-transferase and ATOX-1 expression. CONCLUSIONS: Macrophages activated under conditions of oxidative stress do not adequately deploy a powerful endogenous antioxidant response, a situation that can lead to an enhanced inflammatory response.

Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco-2 cells.

Cholesterol uptake and the mechanisms that regulate cholesterol translocation from the intestinal lumen into enterocytes remain for the most part unclear. Since scavenger receptor class B type I (SR-BI) has been suggested to play a role in cholesterol absorption, we investigated cellular SR-BI modulation by various potential effectors administered in both apical and basolateral sides of Caco-2 cells. With differentiation, Caco-2 cells increased SR-BI protein expression. Western blot analysis showed the ability of cholesterol and oxysterols in both cell compartments to reduce SR-BI protein expression. Among the n-3, n-6, and n-9 fatty acid families, only eicosapentaenoic acid was able to lower SR-BI protein expression on both sides, whereas apical alpha-linolenic acid decreased SR-BI abundance and basolateral arachidonic acid (AA) raised it. Epidermal growth factor and growth hormone, either in the apical or basolateral medium, diminished SR-BI cellular content, while insulin displayed the same effect only on the basolateral side. In the presence of proinflammatory agents (LPS, TNF-alpha, IFN-gamma), Caco-2 cells exhibited differential behavior. SR-BI was downregulated by lipopolysaccharide on both sides. Finally, WY-14643 fibrate diminished SR-BI protein expression when it was added to the apical medium. Biotinylation studies in response to selected stimuli revealed that regulatory modifications in SR-BI protein expression occurred for the most part at the apical cell surface irrespective of the effector location. Our data indicate that various effectors supplied to the apical and basolateral compartments may impact on SR-BI at the apical membrane, thus suggesting potential regulation of intestinal cholesterol absorption and distribution in various intracellular pools.

Mechanisms of lipid malabsorption in Cystic Fibrosis: the impact of essential fatty acids deficiency.

Transport mechanisms, whereby alimentary lipids are digested and packaged into small emulsion particles that enter intestinal cells to be translocated to the plasma in the form of chylomicrons, are impaired in cystic fibrosis. The purpose of this paper is to focus on defects that are related to intraluminal and intracellular events in this life-limiting genetic disorder. Specific evidence is presented to highlight the relationship between fat malabsorption and essential fatty acid deficiency commonly found in patients with cystic fibrosis that are often related to the genotype. Given the interdependency of pulmonary disease, pancreatic insufficiency and nutritional status, greater attention should be paid to the optimal correction of fat malabsorption and essential fatty acid deficiency in order to improve the quality of life and extend the life span of patients with cystic fibrosis.