scholarly journals Obesity, oxidative DNA damage and vitamin D as predictors of genomic instability in children and adolescents

2021 ◽  
Author(s):  
Moonisah Usman ◽  
Maria Woloshynowych ◽  
Jessica Carrilho Britto ◽  
Ivona Bilkevic ◽  
Bethany Glassar ◽  
...  
Keyword(s):  
Vitamin D ◽  
Dna Damage ◽  
Genomic Instability ◽  
Oxidative Dna Damage ◽  
Nutritional Deficiencies ◽  
Aetiological Factor ◽  
Enzyme Linked Immunosorbent Assay ◽  
Childhood And Adolescence ◽  
Paediatric Obesity ◽  
Vitamin D Levels

Abstract Background/objectives Epidemiological evidence indicates obesity in childhood and adolescence to be an independent risk factor for cancer and premature mortality in adulthood. Pathological implications from excess adiposity may begin early in life. Obesity is concurrent with a state of chronic inflammation, a well-known aetiological factor for DNA damage. In addition, obesity has been associated with micro-nutritional deficiencies. Vitamin D has attracted attention for its anti-inflammatory properties and role in genomic integrity and stability. The aim of this study was to determine a novel approach for predicting genomic instability via the combined assessment of adiposity, DNA damage, systemic inflammation, and vitamin D status. Subjects/methods We carried out a cross-sectional study with 132 participants, aged 10–18, recruited from schools and paediatric obesity clinics in London. Anthropometric assessments included BMI Z-score, waist and hip circumference, and body fat percentage via bioelectrical impedance. Inflammation and vitamin D levels in saliva were assessed by enzyme-linked immunosorbent assay. Oxidative DNA damage was determined via quantification of 8-hydroxy-2′-deoxyguanosine in urine. Exfoliated cells from the oral cavity were scored for genomic instability via the buccal cytome assay. Results As expected, comparisons between participants with obesity and normal range BMI showed significant differences in anthropometric measures (p < 0.001). Significant differences were also observed in some measures of genomic instability (p < 0.001). When examining relationships between variables for all participants, markers of adiposity positively correlated with acquired oxidative DNA damage (p < 0.01) and genomic instability (p < 0.001), and negatively correlated with vitamin D (p < 0.01). Multiple regression analyses identified obesity (p < 0.001), vitamin D (p < 0.001), and oxidative DNA damage (p < 0.05) as the three significant predictors of genomic instability. Conclusions Obesity, oxidative DNA damage, and vitamin D deficiency are significant predictors of genomic instability. Non-invasive biomonitoring and predictive modelling of genomic instability in young patients with obesity may contribute to the prioritisation and severity of clinical intervention measures.

scholarly journals Vitamin D as a Key Player in Modulating Rheumatoid Arthritis-derived Immune Response

2020 ◽  
Vol 14 (4) ◽  
pp. 2453-2465
Author(s):  
Ramadan Yahia ◽  
Shereen M. Mohammed ◽  
Manal M. Hassanien ◽  
Shabaan H. Ahmed ◽  
Helal F. Hetta
Keyword(s):  
Rheumatoid Arthritis ◽  
Vitamin D ◽  
Serum Level ◽  
Growth Function ◽  
Enzyme Linked Immunosorbent Assay ◽  
Reactive Protein ◽  
Vitamin D Levels ◽  
Systemic Inflammatory Disease ◽  
Anti Inflammatory ◽  
Factor Α

Rheumatoid arthritis (RA) is a systemic inflammatory disease with chronic nature of joints related to autoimmunity. Vitamin D was found to modulate cell growth, function of immune cells and anti-inflammatory action. The aims of that study were to investigate serum level of vitamin D and some cytokines and to identify the correlation between vitamin D and these cytokines in RA. Totally 40 RA patients without vitamin D supplement were involved in this study. Serum level of vitamin D, interleukin-6 (IL-6), IL-10, IL-35, C-reactive protein (CRP) and tumor necrosis factor α (TNF-α), all of them were measure in all patients by enzyme-linked immunosorbent assay (ELISA). Patients were classified according to Vitamin D levels into two groups; RA patients with Vit. D deficiency (n=25) and RA patients with Vit. D sufficiency (n=15). IL-6 was lower significantly (P = 0.03) in RA patients with Vit. D sufficiency than RA patients with Vit. D deficiency. IL-10 and IL-35 were higher significantly (P = 0.0234, P = 0.0356 respectively) in RA patients with Vit. D sufficiency than RA patients with Vit. D deficiency. Vit. D was significantly positively correlated with both IL-10 (r = 0.4516, P = 0.0034) and IL-35 (r = 0.3424, P = 0.0329) and negatively correlated with IL-6 (r = -0.3188, P = 0.0479). Sufficient serum level of Vit. D is correlated with higher level of anti-inflammatory cytokines (IL-10 and IL-35) and lower level of IL-6. This support the immunomodulatory effect of Vit. D in RA.

scholarly journals HUBUNGAN KADAR VITAMIN D SERUM DENGAN KUALITAS HIDUP PADA PASIEN EPILEPSI

2018 ◽  
Vol 35 (4) ◽  
Author(s):  
Edith Fitriyana Girsang ◽  
Aris Catur Bintoro ◽  
Dwi Pudjonarko
Keyword(s):  
Quality Of Life ◽  
Vitamin D ◽  
Immunosorbent Assay ◽  
Serum Vitamin ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Epilepsy Patient ◽  
Vitamin D Levels ◽  
Spearman Test

  THE CORRELATION BETWEEN VITAMIN D SERUM LEVELS WITH QUALITY OF LIFE IN EPILEPSY PATIENTABSTRACTIntroduction: Epilepsy affects overall health status and decreases the life quality of epilepsy patient. Seizure frequency, seizure type, daily activity disorder, depression and anxiety also affect the quality of life epilepsy patient. Vitamin D is considered as a neurosteroid modulator of nerve excitability and seizure susceptibility. Studies of vitamin D direct role in epilepsy are limited. Nevertheless, some studies show the role of vitamin D as an anticonvulsant that reduces the incidence of seizures.Aim: To determine the correlation between vitamin D serum levels with quality of life in epilepsy patient.Method: A cross sectional observational study on people with epilepsy in neurology clinic at Dr. Soeselo Hospital, Slawi, Dr Kariadi Hospital, and Tugurejo Hospital, Semarang in July 2017-January 2018. The quality of life was assessed with Quality of Life in Epilepsy 31 (QOLIE-31). Vitamin D serum levels measured using enzyme-linked immunosorbent assay (ELISA) method. Data were analyzed using Spearman test. Results were considered significant if p<0.05.Results: There was no correlation between vitamin D serum levels with quality of life in epilepsy. There was significant correlation between anxiety with quality of life and there were difference between age group with quality of life. Discussion: There was no correlation between serum vitamin D levels and  quality of life in epilepsy patient.Keywords: Epilepsy,quality of life epilepsy, vitamin DABSTRAKPendahuluan: Epilepsi mempengaruhi status kesehatan secara keseluruhan dan menurunkan kualitas hidup pasien epilepsi. Frekuensi bangkitan, tipe bangkitan, gangguan aktivitas harian, depresi dan ansietas, juga memengaruhi kualitas hidup pasien epilepsi. Vitamin D dianggap neurosteroid, sebagai modulator eksitabilitas saraf dan kerentanan bangkitan. Bukti langsung untuk peran vitamin D dalam epilepsi terbatas. Namun beberapa penelitian menunjukkan peran vitamin D sebagai antikonvulsan yang mengurangi kejadian bangkitan.Tujuan: Mengetahui hubungan kadar vitamin D serum dengan kualitas hidup pada pasien epilepsi.Metode: Penelitian potong lintang terhadap pasien epilepsi yang berobat ke Poliklinik Saraf RSUD Dr. Soeselo, Slawi, RSUP Dr. Kariadi, Semarang, dan RS Tugurejo, Semarang pada bulan Juli 2017-Januari 2018. Kualitas hidup dinilai menggunakan kuesioner Quality of Life in Epilepsy 31 (QOLIE-31), pengukuran kadar vitamin D serum menggunakan metode enzyme-linked immunosorbent assay (ELISA). Data dianalisis dengan uji Spearman, hasil dianggap bermakna jika p<0,05.Hasil: Tidak didapatkan hubungan antara kadar vitamin D serum dengan kualitas hidup serta domainnya pada pasien epilepsi. Didapatkan hubungan yang bermakna antara ansietas dengan kualitas hidup dan antara kelompok usia dengan kualitas hidup.Diskusi: Tidak terdapat hubungan bermakna antara kadar vitamin D serum dengan kualitas hidup pada pasien epilepsi.Kata kunci: Epilepsi, kualitas hidup, vitamin D

scholarly journals Impact of increased serum 8-hydroxy-2′-deoxyguanosine levels on extent of coronary artery lesions in elderly patients with type 2 diabetes

2020 ◽  
Vol 48 (7) ◽  
pp. 030006052093465
Author(s):  
Yajie Zhao ◽  
Wei Liang ◽  
Shuya Tian ◽  
Linhui Shen ◽  
Hui Yang
Keyword(s):  
Type 2 Diabetes ◽  
Dna Damage ◽  
Coronary Artery ◽  
Elderly Patients ◽  
Oxidative Dna Damage ◽  
Enzyme Linked Immunosorbent Assay ◽  
Gensini Score ◽  
Coronary Artery Lesions ◽  
The Impact

Objective Patients with type 2 diabetes (T2DM) are prone to cardiovascular disease, and both conditions are linked to oxidative DNA damage, which produces 8-hydroxy-2′-deoxyguanosine (8-OHdG). We investigated the impact of 8-OHdG on coronary heart disease (CHD) in elderly patients with T2DM. Methods We assessed the demographic, clinical, and biochemical characteristics of 147 patients with T2DM (mean age 73.29 ± 8.19 years) with or without CHD. Serum 8-OHdG was detected by enzyme-linked immunosorbent assay. CHD was diagnosed as ≥50% stenosis in at least one main branch of the coronary arteries determined by coronarography, evaluated by Gensini score. Results Serum 8-OHdG, number of stenotic branches, and Gensini score were all significantly increased in the CHD group. After adjustment for various factors, the number of stenotic branches and Gensini score remained positively correlated with 8-OHdG levels in the CHD group. Coronary artery lesions were significantly more severe in the CHD compared with the non-CHD group when 8-OHdG levels were >0.523 ng/mL. The number of stenotic branches and Gensini score were significantly independently associated with 8-OHdG levels in patients with T2DM. Conclusions 8-OHdG is a marker of oxidative DNA damage, and is highly associated with the extent of coronary artery lesions in ageing patients with T2DM. Trial registration: Registration number: 1.0/20170720; date of registration 26/07/2016 (retrospectively registered).

CML-CP Mouse Model of Genomic Instability.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1210-1210
Author(s):  
Elisabeth Bolton ◽  
Linda Kamp ◽  
Hardik Modi ◽  
Ravi Bhatia ◽  
Steffen Koschmieder ◽  
...  
Keyword(s):  
Stem Cells ◽  
Dna Damage ◽  
Stem Cell ◽  
Mouse Model ◽  
Board Of Directors ◽  
Genomic Instability ◽  
Oxidative Dna Damage ◽  
Advisory Committees ◽  
Hematopoietic Stem ◽  
Dependent Effect

Abstract Abstract 1210 Background: BCR-ABL1 transforms hematopoietic stem cells to induce chronic myeloid leukemia in chronic phase (CML-CP). Although CML is stem cell-derived, it is a progenitor cell-driven disease. In CML-CP, leukemia stem cells (LSCs) are characterized by elevated BCR-ABL1 expression in comparison to leukemia progenitor cells (LPCs). Increased expression of BCR-ABL1 kinase is also associated with progression from CML-CP to CML-blast phase. Previously we showed that BCR-ABL1 kinase stimulates reactive oxygen species (ROS)-dependent DNA damage resulting in genomic instability in vitro, which was responsible for acquired imatinib-resistance and accumulation of chromosomal aberrations (Nowicki et al., Blood, 2005; Koptyra et al., Blood, 2006; Koptyra et al., Leukemia, 2008). Result: To examine the effects of BCR-ABL1 expression on genomic instability during in vivo leukemogenesis we employed an inducible transgenic mouse model of CML-CP with targeted expression of p210BCR-ABL1 in hematopoietic stem and progenitor cells (Koschmieder et al., Blood, 2005). Mice exhibiting CML-CP-like disease resulting from BCR-ABL1 induction demonstrated splenomegaly, leukocytosis, and Gr1+/CD11b+ myeloid expansion in bone marrow, spleen and peripheral blood, as detected by FACS analysis. BCR-ABL1 mRNA expression was higher in Lin-c-Kit+Sca1+ stem-enriched cells than in Lin-c-Kit+Sca1- progenitor-enriched cells, thus reminiscent of CML-CP (LSCs>LPCs). BCR-ABL1 increased levels of ROS (hydrogen peroxide, hydroxyl radical) and oxidative DNA lesions (8-oxoG) in LSC-enriched Lin-c-Kit+Sca1+ cells. Preliminary data also suggested that quiescent (CFSEmax) Lin-c-Kit+Sca1+ cells from BCR-ABL1-induced mice exhibited greater ROS (superoxide) production than non-induced counter parts. Moreover, higher levels of ROS were detected in BCR-ABL1-positive Lin-c-Kit+Sca1+ stem-enriched population in comparison to BCR-ABL1-positive Lin-c-Kit+Sca1- progenitor population, suggesting a dosage-dependent effect of BCR-ABL1. To confirm that BCR-ABL1 exerts a dosage-dependent effect on ROS-induced oxidative DNA damage, we showed that the levels of ROS, 8-oxoG and DNA double-strand breaks were proportional to BCR-ABL1 kinase expression in murine 32Dc13 and human CD34+ cells. Conclusion: In summary, this mouse model recapitulates the BCR-ABL1 expression profile attributed to stem and progenitor populations in human CML-CP. It also shows that the BCR-ABL1-positive, stem cell-enriched Lin-c-Kit+Sca1+ population displays elevated levels of ROS and oxidative DNA damage in comparison to normal counterparts, which makes it suitable to study the mechanisms of genomic instability in LSCs. Single nucleotide polymorphism (SNP) arrays will shed more light on the genomic instability of this BCR-ABL1-induced transgenic model of CML-CP. Disclosures: Koschmieder: Novartis: Membership on an entity's Board of Directors or advisory committees, Research Funding; BMS: Membership on an entity's Board of Directors or advisory committees.

scholarly journals BCR-ABL1 kinase inhibits uracil DNA glycosylase UNG2 to enhance oxidative DNA damage and stimulate genomic instability

Leukemia ◽  
2012 ◽  
Vol 27 (3) ◽  
pp. 629-634 ◽  
Author(s):  
A Slupianek ◽  
R Falinski ◽  
P Znojek ◽  
T Stoklosa ◽  
S Flis ◽  
...  
Keyword(s):  
Dna Damage ◽  
Genomic Instability ◽  
Oxidative Dna Damage ◽  
Dna Glycosylase ◽  
Uracil Dna Glycosylase

scholarly journals Changes in Fitness of Rural Primary School Students from Southwest China after Two-Year’s Nutrition Intervention

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3544
Author(s):  
Ran Zhao ◽  
Qian Gan ◽  
Zhuolun Hu ◽  
Peipei Xu ◽  
Li Li ◽  
...  
Keyword(s):  
Vitamin D ◽  
Primary School ◽  
Repeated Measures ◽  
Southwest China ◽  
Serum Vitamin ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Primary School Students ◽  
School Students ◽  
Vitamin D Levels

Children in China’s poor rural areas often have insufficient protein and micronutrient intake. There is little research about the effect of milk and egg supplementation published on these children. A prospective randomized controlled trial was applied to evaluate the effect of milk and egg supplementation on the growth and fitness of poor rural primary school students in southwest China whose physical development was below national averages. A total of 955 healthy students aged 6–13 years old were recruited. The intervention group (538) received 200 g milk and 50 g braised egg at each school day, while the control group (417) kept their normal diet and received no extra supplementation. Serum vitamin D levels were measured by an enzyme-linked immunosorbent assay. A mixed linear model with repeated measures was performed to analyze the efficacy of the supplementation. Statistically significant interactions between groups and time were seen in weight in boys, but not in girls. Significant improvement in vitamin D levels, the broad jump, and the 8 × 50 m shuttle run were observed in both genders. Therefore, the supplementation of egg and milk for two years might have a positive effect on growth and physical fitness and decreasing vitamin D deficiency in poor rural Chinese children.

scholarly journals Genomic Instability Originates From Leukemia Stem Cells in a Mouse Model of CML-CP

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 445-445 ◽  
Author(s):  
Elisabeth Bolton ◽  
Mirle Schemionek ◽  
Hans-Ulrich Klein ◽  
Linda Kerstiens ◽  
Steffen Koschmieder ◽  
...  
Keyword(s):  
Stem Cells ◽  
Dna Damage ◽  
Mouse Model ◽  
Progenitor Cells ◽  
Genomic Instability ◽  
Oxidative Dna Damage ◽  
Transgenic Mouse Model ◽  
Hematopoietic Stem ◽  
Genetic Aberrations ◽  
Stem And Progenitor Cells

Abstract Abstract 445 For decades, chronic myeloid leukemia (CML) has served not only as a paradigm for understanding the evolution and multi-step process of carcinogenesis but also for studying cancer stem and progenitor cells responsible for the initiation and/or maintenance of the disease. CML is initiated by BCR-ABL1 tyrosine kinase transformation of hematopoietic stem cells into leukemia stem cells (LSCs) to induce CML-chronic phase (CML-CP). The deregulated growth of LSC-derived leukemia progenitor cells (LPCs) leads to manifestation of the disease. It is unclear if LSCs and/or LPCs are able to acquire additional genetic changes that confer resistance to tyrosine kinase inhibitors (TKIs) and induce more aggressive CML blast phase (CML-BP). In addition, the mechanisms and consequences of genomic instability may differ substantially among these cells. For example, the effects of genetic aberrations acquired in quiescent LSCs may be dormant, but if the aberrations induce proliferation or appear in LSCs that are already cycling, they may generate TKI-resistant and/or more malignant clones. Alternatively, genomic instability in LPCs must be accompanied by the acquisition of LSC-like properties to prevent mutations from disappearing before they undergo terminal maturation. Previously, we reported that BCR-ABL1–transformed cell lines accumulate reactive oxygen species (ROS)-induced oxidative DNA damage [8-oxoguanine (8oxoG), double strand breaks (DSBs)] resulting in genomic instability in vitro, which was responsible for acquired imatinib-resistance and accumulation of chromosomal aberrations (Nowicki et al., Blood, 2005; Koptyra et al., Blood, 2006; Koptyra et al., Leukemia, 2008). To determine which populations of CML-CP cells, LSCs and/or LPCs, accumulate genomic instability we employed the SCLtTA/BCR-ABL1 tetracycline-inducible (tet-off) transgenic mouse model of CML-CP with targeted expression of p210BCR-ABL1 in hematopoietic stem and progenitor cells (Koschmieder et al., Blood, 2005). Mice exhibiting CML-CP-like disease resulting from BCR-ABL1 induction demonstrated splenomegaly and Gr1+/CD11b+ myeloid expansion in bone marrow, spleen and peripheral blood. BCR-ABL1 mRNA expression was higher in the Lin−c-Kit+Sca1+ murine leukemia stem cell–enriched population (muLSCs) than in the Lin−c-Kit+Sca1− murine leukemia progenitor cell–enriched population (muLPCs), thus reminiscent of human CML-CP (Lin−CD34+CD38− LSCs > Lin−CD34+CD38+ LPCs). BCR-ABL1 induction increased levels of ROS (hydrogen peroxide, hydroxyl radical) and oxidative DNA damage (8-oxoG, DSBs) in muLSCs, but not in muLPCs. In addition, CFSEmax/eFluor670max quiescent muLSCs displayed more ROS (superoxide, hydrogen peroxide) and oxidative DNA damage (8oxoG, DSBs) than non-induced counterparts. Currently, we are examining genomic instability in the most primitive long-term muLSCs (Lin−c-Kit+Sca1+CD34−Flt3−). Lastly, single nucleotide polymorphism (SNP) arrays detected a variety of genetic aberrations (addition, deletions) in BCR-ABL1–induced Lin− BM cells. Individual mice displayed a great degree of diversity in the intensity of genetic instability accumulating between 31 to 826 aberrations, which recapitulate heterogeneity of sporadic aberrations detected in CML-CP patients. These aberrations include deletions in Trp53 and Ikzf1, and additions in Zfp423 and Idh1 genes, which have been linked to progression from CML-CP to CML-BP. In summary, by using the SCLtTA/BCR-ABL1 inducible transgenic mouse model of CML-CP we showed that muLSCs, but not muLPCs, displayed elevated levels of ROS-induced oxidative DNA damage likely resulting in the accumulation of extensive genetic aberrations. This observation supports the hypothesis that genomic instability in CML-CP originates in LSCs. Current analysis of microarrays may shed some light on the mechanisms leading to enhanced ROS production and accumulation of oxidative DNA damage in muLSCs. Disclosures: Koschmieder: Novartis, Bristol-Myers Squibb: Consultancy.

scholarly journals Preventing calcium and vitamin D deficiencies following weight loss and metabolic surgery

BMC Surgery ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Reshi Suthakaran ◽  
Imeshi Indigahawela ◽  
Krinal Mori ◽  
Kiat Lim ◽  
Ahmad Aly
Keyword(s):  
Vitamin D ◽  
Serum Calcium ◽  
Metabolic Surgery ◽  
Surgical Techniques ◽  
Serum Vitamin ◽  
Nutritional Deficiencies ◽  
Serum Vitamin D ◽  
Metabolic Bone ◽  
Vitamin D Levels ◽  
Serum Pth

Abstract Introduction Uncertain nutritional outcomes following common metabolic surgical techniques are concerning given the long-term potential for postoperative metabolic bone disease. This study aims to investigate the variations in serum calcium, vitamin D, and parathyroid hormone (PTH) levels following Roux-en-Y Gastric bypass (RYBP) and Sleeve Gastrectomy (SG). Methods A retrospective analysis of 370 patients who underwent metabolic surgery at a single-centre group practice in Melbourne, Australia, over 2 years. Results Patients underwent SG (n = 281) or RYGP (n = 89), with 75% and 87% of the cohort being female, respectively. Postoperative mean serum calcium levels and median serum vitamin D levels improved significantly by 24 months within both cohorts. Serum PTH levels within the RYBP group were significantly higher than the SG group across all time points. PTH levels significantly fell from 5.7 (IQR 4.2–7.4) to 5.00 (4.1–6.5) pmol/L by 24 months following SG. However, PTH levels following RYBP remained stable at 24 months, from 6.1 (IQR 4.7–8.7) to 6.4 (4.9–8.1) pmol/L. Furthermore, we failed to notice a significant improvement in PTH levels following RYBP among those with higher PTH levels preoperatively. Conclusion Higher PTH levels following RYBP, compared to SG, may imply we are undertreating patients who are inherently subjected to a greater degree of malabsorption and underlying nutritional deficiencies. This finding calls for a tailored supplementation protocol, particularly for those with high preoperative PTH levels undergoing RYBP, to prevent deficiencies.

scholarly journals Adherence to Vitamin Supplementation Recommendations in Youth Who Have Undergone Bariatric Surgery as Teenagers: a Mixed Methods Study

2020 ◽  
Vol 30 (12) ◽  
pp. 4911-4918
Author(s):  
Anna Lena Brorsson ◽  
Karin Nordin ◽  
Kerstin Ekbom
Keyword(s):  
Bariatric Surgery ◽  
Vitamin D ◽  
Mixed Methods ◽  
Mixed Methods Study ◽  
Nutritional Deficiencies ◽  
Vitamin Supplementation ◽  
Structured Interviews ◽  
Vitamin D Levels ◽  
A Prospective Study ◽  
Qualitative Part

Abstract Purpose Adherence to vitamin supplementation recommendations after bariatric surgery is generally poor, which is associated with nutritional deficiencies. Patients’ own perspectives and reasons for poor adherence to vitamin supplementation recommendations have not yet been studied in depth. The purpose of this study was first to measure the accuracy of self-reported adherence to supplementation recommendations by using objective measures of vitamin D levels in blood and thereafter to explore perceptions of barriers and facilitators to participants’ adherence to supplementation recommendations. Material and Method Participants were recruited from a prospective study investigating the outcome of bariatric surgery in adolescents with severe obesity. Mixed methods were used, including a quantitative part where vitamin D levels were analysed through 25(OH)D levels in blood and/or a questionnaire on adherence to supplementation programmes 5 years after surgery (n = 40) plus a qualitative part with semi-structured interviews (n = 20). Results We found a convergence between self-reported adherence to vitamin supplementation and vitamin D 25(OH)D levels in blood indicating honestly in self-reported responses. The qualitative evaluations resulted in the categories awareness and personal capability and external factors. In the analysis, an overall theme emerged; capacity is crucial for adherence in youth who have undergone bariatric surgery. Conclusion Bariatric surgery is a comprehensive procedure that requires lifelong treatment afterwards. There is coherence between what adolescents actually do and what they say they do. Capacity is crucial for adherence and social support has been shown to be important.

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