Vitamin and mineral deficiencies in children and adolescents with obesity and consequences of bariatric surgery  

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Author(s):

 Marie-Laure Frelut Marie-Laure Frelut
Marie-Laure Frelut is a Pediatrician. She became involved in the field
of childhood obesity in the 1990s when she had to run an inpatient
unit for severely obese adolescents.
View Author’s Full Biography

 

Obesity (OB) is defined as an excess fat mass (FM). Its occurrence requires that energy, i.e. food intakes exceed energy expenditure. Examining the nutritional status of the OB child and adolescent may seem paradoxical, but lifestyle and environment, as well as adipose tissue metabolism, and metabolic complications of OB, all have consequences on nutritional status:  

Lifestyle and environment 

Ultra-processed  foods (UPFs) has dramatically increased all around the world during the last decades.  It is still steeply increasing in most countries except in those rising above 50 % of energy contribution where it tends to stabilize indicating an established dietary pattern. These categories of food include sweeten carbonated or not beverages, baked goods, sweet or savory snacks, ready meals, some dairy products, sauces and dressings, reconstituted meat products and other solid foods.  

Both drinks and foods are the most common sources of excess energy intakes of poor nutritional quality, lacking fiber, proteins, essential nutrients (potassium, zinc, magnesium) and several vitamins in association to high sugar and high fat content. Their consequence is a worldwide escalating double burden of malnutrition1.  

Decreased energy expenditure: Spending less time being active outdoors and wearing supersized clothing hiding the body has another set of consequences, especially in the least sunny countries: vitamin D deficiency and metabolic consequences of inactivity.  

 

 

Storage into fat mass 

FM acts as a reservoir of fat-soluble vitamins (A, D, E, K) and nutrients. Serum concentrations of these substrates may not reflect actual status while their roles and bioavailability must be better understood.  

Metabolic changes induced by obesity 

A low-grade inflammation is an early feature of OB, correlated to its severity, which impacts many aspects of the metabolism and generates higher risk of related complications. Its effects on the synthesis or bioavailability on some of the proteins that transport vitamins and nutrients into the blood may lead to over- or under-estimation of the nutritional status. Increased oxidation may enhance requirements for antioxidant nutrients. Newly discovered roles of vitamins, like the role of vitamin D in the anti-inflammatory cascade, lead to reevaluate the adequacy of the classical criteria for nutritional status. Assessing the individual nutritional status of children and adolescents with OB is a key step of any management or prevention program.  Food frequency and lifestyle questionnaire are part of the evaluation in addition to anthropometry and clinical examination. Micronutrient guideline was published by the ESPEN. It provides information about micronutrient status, monitoring and prescription for daily practice 2.   

In this chapter we shall review the evidence for nutritional deficiencies in OB children and adolescents and the impact of obesity on the criteria of diagnosis, supplementations and the consequences of bariatric surgery.  

 

1.THE FAT-SOLUBLE VITAMINS 

 

1.1 VITAMIN D  

 

Vitamin D, or calciferol, a fat-soluble vitamin has long been known for its role on intestinal calcium absorption and key role in the prevention of rickets. Nowadays it is acknowledged as a key factor in a wide range of biological processes which have implications in energy and adipose tissue metabolisms.  

 

 

Metabolism and storage  

Vitamin D is a group of fat-soluble prohormones with the two major forms being ergocalciferol (Vitamin D2) and cholecalciferol (Vitamin D3) which differ by their sidechains.  Ergocalciferol or vitamin D2 originates from plants. Cholecalciferol or vitamin D3 is the natural form produced in the skin by photosynthesis through exposure to UVB, maximized at levels of sunlight exposures that do not burn the skin, or originating from animal products, mainly fatty fish.  Melanin in the epidermis, by absorbing UV irradiation, can reduce the effectiveness of sunlight on the skin. The seasonal variation of 25 OH vitamin D (25OHD) level can be quite pronounced depending on the latitude and clothing.  

Vitamin D3 is preferentially removed from the skin bound to a circulating binding protein (DBP). Dietary vitamin D2 and D3 are absorbed in the duodenum and jejunum as lipids, incorporated into chylomicrons and transported through the lymphatic pathway, with subsequent transfer, at least in part, to DBP.   

The liver and other tissues metabolize vitamin D, whether from the skin or oral ingestion, to 25OHD, its principal circulating form. The vitamin D metabolites are transported in blood bound primarily to DBP (85 to 88%) and albumin (12-15%). The bioavailable vitamin D consists primarily of albumin bound 25OHD with less than 1% in its free form. 

DBP is produced primarily in the liver but also in other sites such as the kidney and fat tissues. Vitamin D3 seems to be approximately 87% more potent in raising and maintaining serum 25OHD concentrations and produces 2 to 3 fold greater storage of vitamin D than does equimolar D2 in healthy adults3. These metabolites are further hydroxylated primarily by the kidney by 1α hydroxylase (gene: CYP27B1) to produce the bioactive forms 1α,25(OH)2D3 and 1α,25(OH)2D2. Extra-renal production of 1,25(OH)2D as in macrophages is under different control, primarily by cytokines such as tumor necrosis factor α (TNFα) and interferon ɤ (IFNɤ).  Catabolism of vitamin D and its metabolites occurs in the liver through cytochrome P450 enzymes.  

Vitamin D is stored in the adipose tissue where it regulates adipogenic gene expression, adipocyte apoptosis, modulates adipose tissue inflammatory response, affects adipokines (leptin and adiponectin) secretion by adipocytes, and lipids and energy metabolism4. 

The vitamin D receptor (VDR), a member of the nuclear receptor superfamily, is widely distributed and not restricted to those tissues considered as classical targets of vitamin D. This distribution explains why more than 1000 genes are either directly or indirectly regulated by 1,25(OH)2D: VDR has been found in most human tissues including osteoblasts, muscle, pancreatic β cells, macrophages and adipocytes. Its polymorphism also provides a link between vitamin D deficiency and diseases4,5,6.  

The non-classic action of 1α,25(OH)2D includes regulation of cellular proliferation, and differentiation, regulation of hormone secretion and of immune function.  1α,25(OH)2D has been shown to display anti-inflammatory effects on adipocytes. It may modulate inflammation and expression of genes in other metabolic tissues by modulating the content in miRNAs in extracellular vesicles of adipose tissue7,8 . 

 

Vitamin D status: low plasma 25OHD concentrations do not necessarily reflect true deficiency 

Vitamin D status is especially difficult to analyze because of the storage in FM and because of the unknown proportion of bioavailable forms4. Plasma concentrations of 25OHD are used in routine clinical practice to evaluate vitamin D status.  International guidelines classify vitamin D status into 4 groups according to serum concentrations: vitamin D sufficiency/optimal level ≥75 nmol/, insufficiency 50-75 nmol/l, deficiency 27.5-49.99 nmol/l, severe deficiency <27.5 nmol/l9.  The status of vitamin D stores can neither be easily measured in clinical settings, nor differentiated from a genuine deficiency as long as plasma parathyroid hormone (PTH) concentrations have not started to rise, which would be evidence for the need for 25OHD supplementation. Low levels of 25OHD DBP may also explain low circulating vitamin D and protect against the manifestation of vitamin D deficiency since DBP acts as a reservoir and aids the reabsorption of filtered vitamin D through the kidney. However, evidence is lacking in children and adolescents.  Low circulating vitamin D in OB may rely to genuine vitamin D deficiency in children and adolescents but low plasma 25OHD may be due to an increased storage in adipose tissue, an impaired vitamin D release from adipose tissue, or a lower bioavailability of vitamin D synthesized in the skin despite adequate UVB exposure through yet unknown mechanisms, as reported in OB adults4,10.  Genuine deficiency may arise in OB children, as in any child, from insufficient exposure to sunshine either due to covering cloths, or for psychosocial reasons, from living at Northern latitude, from low dietary intake, or for a combination of  these factors11.  

 

Epidemiological data 

Results from epidemiological studies vary across continents and populations. In India, the Comprehensive National Nutrition Survey, in 2016-18 in children and adolescents from 6 months to 19 years, with respective prevalence of overweight (OW) and OB of 2.69%, 4.18% and 4.99%, found more vitamin D deficiencies in OW/OB school age children and adolescents but not in pre-schoolers 12. In the USA, the NHANES (National Health and Nutrition Examination Survey) 2011-2018 study, in adolescents of mean age 15.4 years reported a percentage of general and central OB of about 38%. After adjustment for confounding factors, the fully OR of deficient or insufficient vitamin D were respectively 1.602 (95% CI: 1.116 – 2.211) and 1.659 (95% CI: 1.385 – 1.986) with general OB and 2.025 (95% CI: 1.445 – 2.837) and 1.557 (95% CI: 1.287 – 1.884) with central OB. Interestingly, the proportion mediated by insulin resistance, as assessed by the Homeostasis Model Assessment (HOMA-IR) index, was as high as 31.7% for global OB and 50.3% for central OB (both p<0.01) 13.  In Chile, a study was conducted in three different geographic areas in children aged 4 to 14 years old.  The overall prevalence of vitamin D deficiency was 80.4% with 1.7% severe, 24.6% moderate and 54.1 % mild and correlated to the nutritional status (ANOVA, p = 0.038)14. In China (Beijing), in pre-schoolers aged 1-6 years old, with a prevalence of OW of 7.24 % and OB 2.4 % respectively, vitamin D deficiency or insufficiency was more common in children aged 36-56 months. Less time spent outdoor, winter season and BMI were negatively correlated to serum 25OHD. After adjustment, the risk of vitamin D deficiency and insufficiency in OW or OB were respectively 1.025 (95% CI: 1.0002-1.1174) and 1.218 (1.099-1.708) 15.  

In Europe, according to the Healthy lifestyle In Europe in Adolescence study (HELENA), 38% of the healthy adolescents had 25OHD plasma concentrations below the reference threshold of 49 nmol/l and 15% were severely deficient (<27.5 nmol/l)16. Lower concentrations have been reported in OW/OB children and adolescents. A first meta-analysis, based on 25OHD plasma concentrations, found that the prevalence of vitamin D deficiency is 35% higher (prevalence ratio PR 1.35, 95% CI: 1.21 – 1.50) in OB children and adolescents, and  24% higher in the OW group,  compared to the normal weight  children, irrespective of age, latitude  and cut-offs used to define deficiency17. In a meta-analysis 9 out of 41 articles included vitamin D. This deficiency was more frequent in children with OW/OB. The pooled odds ratio (OR) was 1.9 (95% CI: 1.4 – 2.5) but, when deficiency cut-offs were accounted for, it dropped to 1.7 (95% CI: 1.3 – 2.3)18.  

Vitamin D and bone health in children and adolescents with OW/OB 

Bone mineralization adequacy is still a matter of discussion in OB children and adolescents. Lower circulating levels of 25OHD are not associated with increased PTH concentrations. Some study hypothesize that a protection may be conferred by increased plasma leptin concentrations, hyperinsulinemia, increased circulating IGF1, androgen aromatization to oestrogens in the adipose tissue that may counteract the effect of low circulating 25(OH)2D4. However, markers of bone turnover, osteocalcin (OC), type 1 N-propeptides (PINP) and carboxy terminal cross-linking telopeptide of type 1 collagen (CTX- 1) as well as 25OHD and PTH show differences between OB and normal weight children. Children with OB had significantly lower SDS ls for OC (-0.44), CTX- (-0.33), PINP (-0.27), CTX-1(-0.33), 25OHD (-0.43) and higher SDS for PTH (+0.44) than the reference cohort 19.  

Slipped capital femoral epiphysis (SCFE) and Blount disease (severe tibia vara) are both disorders of growth plate dysfunction occurring in OB children. SCFE is expressed as either a slow slippage of the femoral-head plate or precipitated by an acute event during a trauma. Blount disease (OR = 7.33, p = 0.002) but neither SCFE nor bone fractures were associated with vitamin D deficiency (<40 nmol/L) in a retrospective study of 890 children and adolescents referred to an OB clinic20 but not in others. The relationship between vitamin D status and peak bone mass was investigated in 90 post pubertal females in California. 59% of the subjects were vitamin D deficient. In this group only 25OHD was negatively correlated to BMI.  No relationship was observed between circulating 25OHD and bone mineral density at any site21.   

Bone mineral content (BMC) was inversely correlated to systolic blood pressure in a cohort of OB Latino adolescent boys but not in girls. Hypertensive adolescent boys had lower BMC than their normotensive counterparts22. This observation raises the question of the early interaction between calcium status, bone mineralization and blood pressure regulation.  

Altogether, bone health requires further assessment and should still be carefully investigated.  

 

Impact of Vitamin D on muscle strength  

 

The link between muscle strength and vitamin D status has not yet been clearly established in children and adolescent, although several pathways may be implicated such as calcium metabolism or vitamin D cellular signaling. Handgrip strength was evaluated, as part of the larger IDEFICS/I. Family cohort study in children 7 to <16 years old. Vitamin D sufficient in children of low and normal BMI had higher OR for a high handgrip strength (OR = 1.92, 95% CI: 1.12 – 3.30). Children with OW (OR = 2.64, 95% CI: 2.00 – 3.49) and OB (OR = 4.53, 95% CI: 2.93 – 7.02) were more likely to have a higher handgrip strength than lean or normal weight but no correlation was significant with serum vitamin D concentrations23.  

 

Impact of vitamin D on obesity related breathing disorders  

 

Multiple studies report an inverse relationship between asthma severity and vitamin D level which may be related to the anti-inflammatory properties of vitamin D. Vitamin D replacement in children with OB-related asthma, in the VDORA1 open label Randomized Controlled Trial (RCT), aimed at identifying the vitamin D dose that safely achieves serum vitamin D ≥40 ng/mL. Four oral doses were administered as a single 50 000 IU dose plus 10 000 or 8000 IU or 6000 IU daily or a safety dose of 600 IU/day for 16 weeks. The 50 000 IU loading dose plus 8000 IU daily was safe and effective in increasing 25OHD levels at the goal set in 78.6% of the children on this dose. Asthma exacerbations were similar in all parts of the cohort across the study24.  

A cross-sectional study of 72 children aged 2 to 16 years with severe obstructive sleep apnoea (OSA) (apnoea hypopnea index AHI ≥20 on polysomnogram) was performed before adenotonsillectomy. Vitamin D deficiency (≤20 ng/mL) was present in 37.5% of the participants, and in multivariate analysis a 1.0 unit decrease in vitamin D was associated with an AHI increase of 0.7% (95% CI: 0.04 – 1.40) 25. 

   

Vitamin D, oxidative DNA damage, non-alcoholic fatty liver disease (NAFLD) and early metabolic complications of obesity 

Late complications of OB include increased cancer risk and early mortality. A cross-sectional study carried out with 132 patients aged 10-18 years aimed at determining the link between anti-inflammatory properties of vitamin D and its role in genomic stability. The interesting point of this study is that non-invasive techniques only could be used: vitamin D and markers of inflammation and oxidative DNA were assessed using saliva, exfoliated cells from the buccal cavity and urinary samples. Genomic instability was assessed by the buccal cytome assay and oxidative damage via quantification of 8-hydroxy-2’deoxyguanosine in urine. OB was assessed by anthropometric measurements, and bioelectrical impedance was used for body fat percentage. Markers of adiposity positively correlated with acquired oxidative DNA damage (p<0.01). Multiple regression analysis identified OB, oxidative DNA damage and vitamin D deficiency as the 3 significant predictors of genomic instability 26.  

Several studies have shown a link between fatness and cardiovascular risk factors, but early risk factors are less known. A longitudinal study in Chile could show that serum 25OHD at 1 year of age was related to metabolic health through adolescence. Infancy serum 25OHD was inversely correlated with BMI z-score for age in childhood, percentage body fat and a metabolic syndrome score at 16/17 years of age.  Every 25 nmol/L of 25OHD in infancy was associated with an adjusted 1.3% percentage of FM (95% CI: -2.2 to -0.4; p = 0.005) and a lower metabolic syndrome score at 16/17 years of age, through inverse association with waist circumference and the HOMA-IR27. 

In a Swedish cohort of 202 OB children and adolescents, 33.2% had a low 25OHD (<30 nmol/L) which correlated negatively with glycaemia (r = – 0.15, p <0.005), fasting serum insulin (r = -0.18, p<0.01), and insulin resistance estimated by HOMA-IR (r = – 0.19, p<0.01). Fasting blood glucose was above 5.6 mmol/L in 16.7% of 25OHD deficient patients vs. 5.3% (p<0.01) in the non-deficient group. Vitamin D deficiency seems to be an independent risk factor of increased blood glucose  (OR = 2.3; 95% CI: 1.0 – 7.9, p<0.005), independent of age and season28. Another study showed that circulating 25OHD is negatively associated to markers of overall and visceral adiposity and insulin resistance (HOMA-IR and Quantitative Check Index, QUICKI) in a group of 435 prepubertal Chilean children. A serum 25OHD below the conventional cut-off of vitamin D sufficiency of 75 nmol/L appeared to be the best predictor of total and central OB (OR = 4.8; 95% CI: 1.9 – 12.1 in girls and OR = 2.0; 95% CI: 1.0 – 3.9 in boys) and insulin resistance (OR = 2.9; 95% CI: 1.2 – 7.1 in girls and OR = 3.3; 95% CI: 1.6 – 7.0 in boys)29.  

Effects of vitamin D supplementation 

Previous results underpinned the need to examine the effects of vitamin D early in life and its impact on short- and long-term metabolic outcomes.  A meta-analysis which retained 15 RCTs research articles, up to 2022, in children and adolescents 2 to 19 years old with daily vitamin D doses ranging from less than 1000 IU/d to 2000 to over 4000 IU, concluded that, compared with placebo and low doses, very high doses also decreased HOMA-IR and C-reactive protein (CRP). Ranking probability suggested that the higher doses ranked best for increasing 25OHD and decreasing HOMA-IR and CRP with respective probability of 86.1%, 83.1% and 76.0% 30. 

An open-label RCT compared the efficacy and safety of daily administration of 4000 IU/d or 6000 IU/d of oral vitamin D3 over 12 weeks in vitamin D deficient children with OW or OB. Both doses were effective for treating vitamin D deficiency, with higher doses allowing a quicker attainment of optimal levels, but no effect was observed on metabolic parameters31.  

MASLD (Metabolic dysfunction associated liver disease, formerly NAFLD), a major cause of chronic liver disease in children and adolescents due to the high prevalence of OB, is diagnosed in up to 70-80% of the OB subjects.  About 25% of MASLD are complicated by various degrees of liver fibrosis and classified as Metabolic dysfunction associated Steatohepatitis (MASH, formerly NASH). The severity of fibrosis which may lead to cirrhosis is the most important prognosis marker of liver damage.  In a cross-sectional study, liver disease was assessed through liver biopsies in 73 OB children and adolescents referred for persistent elevation of plasma alanine-aminotransferases (ALT) levels and diffusely hyperechogenic liver on ultrasonography.  Low vitamin D (25OHD <50 nmol/) was found in 46% and NASH in 67% of them. 25OHD levels were found to be 22.5 nmol/L (95% CI: 30 – 15, p<0.0001) lower in children with NASH than in those without NASH, while HOMA-IR index and metabolic syndrome features were independently correlated to plasma 25OHD. PTH and bone mineral density on lumbar spine were within normal ranges in all subjects. A RCT of vitamin D supplementation was performed in 41 children and adolescents with biopsy proven NAFLD or NASH, ALT levels >10 times the upper limit of normal, and 25OHD <50 nmol/L. The treatment group was administered vitamin D (800 UI) with docosahexaenoic acid (DHA, 500 mg) orally once daily during 24 weeks, while the control group received a placebo. The same research group had previously shown that DHA improved plasma triglyceride concentration and insulin resistance in a similar population.  In this study, lower levels of 25OHD3 at baseline were associated with greater fibrosis and steatosis. At 1 year, DHA plus vitamin D treatment reduced the NAFLD activity score (p<0.01). There was no change in fibrosis score but a reduction of two of its markers, the activation of hepatic stellate cells and fibrillar collagen. BMI, lipid profile, and insulin resistance were also improved in the treatment group. Vitamin D supplementation in OB vitamin D deficient adolescents seems to enhance the beneficial effect of DHA by acting on NAFLD and markers fibrosis but not on NASH32. 

In conclusion, nutritional and environmental risk factors of vitamin D deficiency should be systematically looked for in children and adolescents with OW or OB, and vitamin D status assessed in those facing significant risk of deficiency or showing evidence of complications11. Prevention of vitamin D deficiency according to latitudes of the countries and lifestyles should at least follow the same guidelines as in the general paediatric population 33. 

 

1.2 VITAMIN A   

 

Vitamin A is a fat-soluble vitamin which originates from plants as provitamin A carotenoids or from animals as retinol. It is easily accumulated in liver and adipose tissue. Vitamin A status is partly dependent on the efficiency with which β-carotene is converted to retinol. Many children around the world are still exposed to vitamin A deficiency risk. Classical multiple functions of vitamin A in vision, embryogenesis, maintenance of epithelial barriers, and immunity are well described in humans. Its role in adipose tissue biology and energy homeostasis is now evidenced in humans 34. Most actions of retinol are mediated by its metabolite retinoic acid which is synthesized intracellularly in target tissues from retinol. In a first step retinol is reversibly oxidized to retinaldehyde which is then irreversibly oxidized to retinoic acid by distinct enzymes.  Several retinoic acid receptors (RARs, RXRs, RORs) exist and belong to the superfamily of nuclear receptors as does VDR, in addition to newly discovered ones. As a consequence, hundreds of genes have been shown to be inducible by the retinoic acid. 

The liver plays a central role in vitamin A physiology. Vitamin A is delivered to the liver as a constituent of chylomicron remnants. In typical situation, hepatocytes capture 75% of retinyl esters contained in chylomicrons and their residual particles, while the adipose tissue retains the remaining part. Retinol bound to retinol binding protein (RBP) is secreted from the liver to maintain serum vitamin A levels and to deliver retinol to extra hepatic targets. In plasma, RBP circulates as a 1:1 complex with transthyretin and retinol. After post-prandial hepatic uptake retinol is released in the bloodstream linked to RBP4 or stored in hepatic stellate cells (also called Ito cells: in them, 90% of hepatic retinol is found) which represent the major storage site for vitamin A in the body in physiological situations. RBP4 and its STRA6 membrane receptor coordinate the uptakes of retinol by the adipose tissue35,36.  

 

Retinol is a modulator of fat deposition 

 

In healthy subjects, the adipose tissue seems to store 10-20% of total retinoids of the body as retinyl esters. β-carotene can be transformed to retinaldehyde and then retinoic acid in the adipose tissue. Adipocyte-derived RBP4 is an adipokine which contributes to the development of insulin resistance. Experimental research suggests that dietary retinol may influence adiposity in a depot-specific manner and RBP4 may moderate this effect through impact on delivery and uptake by the adipose tissue. The RBP4 genotype (rs 10882272, C/T) variant seems to play a key role in this process37. 

All-trans-retinoic acid can inhibit adipocytes differentiation by binding to activating retinoic acid receptor (RAR). It also induces lipolysis when applied to mature adipocytes. β-carotene, retinaldehyde and retinoic acid decrease adipocytes’ early differentiation38.  

 

Diagnosis of vitamin A deficiency 

 

Several analytical methodologies have been developed to measure the different forms of retinoic acid compounds. In daily routine, the most widely used for assessing retinoids and carotenoids are enzyme-linked immunosorbent assays (ELISA). The gold standard is the dosage of the retinol reserves of the liver. Serum retinol concentrations do not begin to decline until liver reserves of vitamin A are very low. RBP is a negative acute phase protein. Serum retinol and RBP fall during times of infection and may be altered by iron deficiency. Serum and RBP and RBP4 dosage have been shown to poorly reflect serum retinol concentrations39. Insufficient vitamin A levels are diagnosed when retinol plasma decrease below 0.52 µM or liver concentrations are lower than 5-20 µg/g.  

 

Genuine vitamin A deficiencies are reported in obese children   

 

Epidemiological studies looking at vitamin A status in OB populations show different results between countries. A reason behind this is the source of vitamin A:  in the Western diet, about 20 to 30% of the habitual intakes of vitamin A originate from provitamin A carotenoids. In contrast, up to 70% of carotenoids in the diet are required in developing countries40.  

In India, the Comprehensive National Nutrition Survey reported a negative association between vitamin A and OW/OB, a smaller proportion of these groups being less deficient in vitamin A12.  A systematic review and meta-analysis of 83 studies in 44 countries in qualitative synthesis, and of 7 studies in meta-analysis, looked at the risk of vitamin A deficiency in children and young people. Vitamin A status was evaluated in relation to body weight, mostly using plasma or retinol concentrations or serum carotenoids or RBP, which do not reflect its status until body stores  are very low. Studies results were quite contradictory with positive (n =17) or negative (n = 5) association with OW/OB or lack of association (n = 2) between Vitamin A and body weight. Negative associations were reported in Brazil in 4 studies and 1 in China41. 

Serum β-carotene, measured during the NAHNES III cycle between 1988 and 1994 was lower in OB than in lean children. Nearly half of the OB children had β-carotene concentrations in the lower quartile compared with about a quarter in lean children (p<0.001)42. In a sample of Mexican-American children, the later NAHNES 2001-2004 study found that 12.4% of the children had α-carotene deficiency (concentrations <1µg/dl). OB children had lower mean concentrations of trans-β-carotene and cis-β-carotene than lean counterparts. Concentrations of serum retinol were positively associated with BMI, trunk FM and total body FM whereas the opposite was found for serum α-carotene, trans-β-carotene and cis-β-carotene. Higher retinol quartile was associated with a 2 to 3- fold greater probability of OW/OB and the highest quartile of α-carotene and trans-β-carotene was associated with reduced probability of OB. Lower intakes of fruit and vegetables and higher energy intakes are a first plausible cause of this difference. Other hypotheses are carotenoids storage in adipose tissue, and higher antioxidant catabolism due to low grade inflammation associated with OB43. Another study, carried out in a population of 197 Mexican school children, found that 44% had OW or OB. Vitamin A intakes below 400 µg/d at 8 years old or 580 µg/d at 13 years old were found in 53% of this population. Vitamin A <20 µg/dl was found in 7.1% of the sample. Vitamin A concentration was positively associated with BMI, waist circumference and abdominal fat (p<0.05).  Children with OW/OB and low vitamin A concentrations had significantly higher CRP concentrations (p<0.05)44. Later, in the NAHNES 1999-2006, a positive correlation was reported between serum vitamin A levels and BMI (p<0.001) in a population of 8218 adolescents. Using the lowest quartile of BMI as a reference, serum vitamin A was 1.236 times higher (95% CI: 0.888 – 1585) in the highest quartile45.  

A study performed in Hungary did not find significant differences either in retinol or in carotenoids between lean and OB children. Only ratios of β-carotene to plasma triglycerides and cholesterol differed between the two groups46.  

 

Epidemiological data are in favor of a role of RBP4 genotype and its variant on obesity phenotype 

 

In Switzerland, 3% of the children had a retinol deficiency (<1.05 µmol/l) suggesting low vitamin A status in the general population. In the OB group serum RBP4, retinol, RBP4 to retinol and transthyretin were significantly increased. BMI, body fat percent and waist to hip ratio, i.e., central distribution of body fat, remained significant positive predictors of RBP4 after adjustment for age and sex47. Another study confirmed that RBP4 levels in children are associated with adipose tissue mass and BMI, independently of age (r = 0.33, p<0.0001). In a longitudinal study, OB children had higher RBP4 concentrations, and a higher serum RBP4 to retinol ratio compared with lean children. RBP4 levels were significantly associated with BMI and insulin. Substantial weight loss led to a significant decrease in RBP4 and RBP4 to retinol ratio. Changes correlated to changes in insulin resistance evaluated by HOMA-IR and QUICKI indexes and weight reduction48. A recent study performed in 947 Canadian adolescents from French founder population showed that dietary intake of vitamin A was negatively associated with visceral fat but not with subcutaneous fat, independently of age, sex, height and energy intake. The relationship was modulated by the rs10882272C/T variant of the RBP4 gene. In groups with low vitamin A intake, The C allele seems to facilitate adiposity reducing effects of vitamin A whereas the T allele would facilitate adiposity reducing effects in visceral fat and adiposity enhancing effects in subcutaneous fat. Moreover, the relationships appeared to be stronger in females37.  

A doubled blind placebo-controlled trial compared the effects at of the daily administration of a mixed carotenoids supplementation (MCS) in 17 OB children (8 cases, 9 placebo) following a weight reduction program. The MCS contained β-carotene, α-carotene, lutein, zeaxanthin lycopene, astaxanthin and γ-tocopherol. MCS led to a greater reduction in BMI z-score, waist to height ratio and subcutaneous adipose tissue compared with placebo. MCS also increased β-carotene and total and high molecular weight adiponectin. This study suggests a beneficial role of MCS in OB children. These results have to be confirmed49.  

So far, requirements in vitamin A seem to be covered by ad hoc food intakes in children and adolescents with OB/OW. Vitamin A intake should be evaluated through food frequency questionnaires in these populations and dosages performed when a deficiency is suspected. Marked genuine deficiency only would require cautious supplementation beyond RDAs. Genetic studies are still in the field of research and supplementation RCTs need to be replicated.  

 

1.3 VITAMIN E 

 

Vitamin E is the third fat soluble vitamin which requires evaluation in OB. Alpha-tocopherol, the most abundant lipid-soluble vitamin is a vital anti-oxidant in mammals, including humans. It prevents damage to lipids containing polyunsaturated fatty acids (PUFA). It is absorbed in the small intestine, transported to the liver in chylomicrons and then released in the plasma as a component of the VLDL. It is bound in the liver cells to a transporter, the α-tocopherol transporter protein (α-TTP) which moves vitamin E through the cell surface by exchanging it for a phosphoinositide in the plasma membrane. Other tocopherol species are moved with a lower affinity50. An early study has shown that tocopherol content in the adipocyte is 8 times greater in the bulk lipid than in membrane51.  

Bioavailability of vitamin E from foods for absorption seems to be highly variable according to food sources. Most dietary vitamin E comes from vegetable oils. Human studies do not yet allow ranking of foods as a function of vitamin E efficiency. Requirements may increase in parallel with the amount of  PUFA in the diet52.   

Plasma antioxidant vitamins were measured in a group of OB adolescents, as part of the EVASYON study, at the beginning, after 2 months, and at the end of a multidisciplinary weight loss program. Alpha-tocopherol, together with lipid-corrected retinol and β-carotene increased significantly whereas lipid corrected lycopene (a carotenoid) was unchanged53.  

Vitamin E status has been studied during the NHANES III cycle between 1988 and 1994. Serum α-tocopherol concentrations after adjustment for serum triglyceride and cholesterol levels were lower in OB than in lean children (p<0.001). Nearly one half of the OB children had adjusted α-tocopherol in the lowest quartile compared with about one quarter in the lean group (p<0.001)42. During the 2001-2004 NHANES cycle, α-tocopherol concentrations were measured in Mexican-American children. The proportion of vitamin E deficiency defined as an α-tocopherol:cholesterol ratio <2.2 (µmol of α-tocopherol: mmol of total cholesterol) was close to 1%. BMI was inversely correlated with α-tocopherol adjusted for total cholesterol ratio (β= -3.66, p<0.01). Similar correlations were found for trunk FM and total body FM. Higher α-tocopherol concentrations were associated with reduced probability of OW43. Another study carried out in a population of Mexican school children found that 44% were OW/OB and a mean serum vitamin E of 5.8 ± 1.42 µg/ml. Ninety-eight percent of vitamin E intakes were below recommended intakes of 7 and 11 mg/d in 8- and 13-years old children respectively. A third of the children had vitamin E concentrations <5 µg/ml, while 2% had vitamin E levels <3 µg/ml. When adjusted for lipids, vitamin E concentrations were negatively associated with all the measures of OB. Contrary to vitamin A, vitamin E and CRP were unrelated44. In Europe, concentrations of α-tocopherol were about 50% lower (p<0.05) in a sample of OB children than in lean counterparts46 and inversely correlated to fasting insulinemia54. Plasma tocopherol concentrations and insulin resistance markers were lower in a group of Spanish OB children with acanthosis nigricans than without it, and also lower than in the control group55.  A 4-month RCT intervention with daily antioxidants (vitamin E 400 UI, Vitamin C 500 mg, selenium 50 µg) vs placebo was performed in OW/OB adolescents participating in a lifestyle modification program. Plasma concentrations of all antioxidants were lower at baseline than in treatment group. Selenium and oxidative stress 8-iso-PGF2α, which are markers of oxidative stress, were significantly reduced. No effect was found on the inflammatory markers (CRP, IL-6, leptin, PGE2 and α-1 acid glycoprotein)56.  

Vitamin E use as an oxidant has been reported in 6 RCTs, among which only 2 were quoted as high quality studies, aiming at improving NAFLD and NASH in OB children and adolescents. The authors of the review conclude that vitamin E shows no significant benefit over placebo on ALT or ultrasonography though it may improve features of NASH. Data are insufficient to conclude about the benefit of the association of vitamin E with PUFA, and further high quality studies are still necessary57.  

The therapeutic use of vitamin E in OB children suffering of metabolic or cardiovascular complications should be performed in controlled conditions following careful medical evaluation.  

 

2. WATER SOLUBLE VITAMINS: FOLATES AND VITAMIN B12 

 

Folate and vitamin B12 together are important contributors to energy metabolism. Folate intake also provides dietary methyl groups required for DNA methylation and subsequent gene expression, i.e. they are key contributors to epigenetic determinants of cardiovascular risk and OB (see corresponding chapter). Five-methyl-tetra-hydrofolate is the active form of folate. Methyl radicals allow the conversion of homocysteine (Hcy), an independent cardiovascular risk factor, into methionine. Methylenetetrahydrofolate reductase (MTHFR) is a key enzyme of this process. Common mutations of the gene of this enzyme lower conversion rates and increase Hcy concentrations. Vitamin B12 is a main cofactor of this cycle58. Folate are found mostly in green leafy vegetables, nuts, and liver meat. Intakes vary widely according to food choices59.  Folate plasma concentration reflects recent folate consumption. Folate biological status is best evaluated by folate red blood cell content (EF).  

A systematic review and meta-analysis about vitamin B 12, folate and homocysteine in children and adolescents with OB, published in 2025, included 20 studies with a combined population of 7791 patients. No significant differences were evidenced in vitamin B12 and folate but OW/OB subjects had higher levels of Hcy60.  

In India, the Comprehensive National Nutrition survey reported significantly lower vitamin B12 in the OW/OB pre-school and school children but not adolescents than in the subjects underweight or normal. Results for erythrocyte folates were not consistent across age categories12. An epidemiological study performed in Greece has found similar mean folate intakes in OW and lean adolescents. The authors state that “a significant proportion did not reach recommended intakes”61. Data from the Mexican-American population studied in the NHANES 2001-2004 round found a low prevalence (0.3%) of RBC folate deficiencies whereas 89.3% had normal serum concentrations of vitamin B12. Normal weight children had higher mean concentrations of serum vitamin B12 than OW/OB children (p<0.01)62. Children aged 2 to 11 years old that consumed more than 7 g/days of nuts had higher BMIs but also higher folate, Mg, Cu, monounsaturated fatty acids (MUFA), PUFA, and fibers than small eaters59. Beyond 12 years of age, consumption of nuts was associated with a slightly lower body weight, and slightly lower triceps skinfolds (p<0.05). In a group of 57 severely OB French adolescent girls, folate intakes ranged from 104 to 412 µg/d and were below national recommended allowances of 300 µg/d in 80% of the subjects. The impact of a common mutation of the MTHFR (MTHFR, 677 CàT), which reduces by 28% the transfer of a methyl group from folate to substrates, was examined. Serum concentrations of liver ALT were negatively correlated to folate intakes (r = -0.32, p = 0.024) and higher in subjects carrying the homozygous mutation (p = 0.016)63. In another group of 130 severely OB adolescents, insulin concentration and resistance, evaluated by HOMA-IR index were increased in homozygote subjects despite similar folate intakes and EF concentrations (p = 0.017 and p = 0.04 respectively)64. Vascular function by flow mediated dilatation (FMD) was measured in 58 OB adolescents and 47 controls. The effect of a daily supplementation of 5 mg folate on FMD was evaluated according to the genotype of the endothelial nitric oxide synthase gene (NOS3). NOS is a key endothelial enzyme in maintaining vascular tone. NOS3 polymorphisms led to opposite significant changes in FMD induced by folates. Genetic background must be taken into account in analyses and intervention studies in OB children65. 

 

Folate, vitamin B12 and metformin 

 

Metformin, considered as the first line drug to treat type 2 diabetes (T2D) has been shown in adults to influence the status of several micronutrients including vitamin B12 and folate. Metformin has been suspected to impair one carbon metabolism in which Folate and B12 are key elements. Administration of metformin reduces the intestinal absorption of vitamin B12.  

In Australia, in a group of 103 OB adolescents with insulin resistance or prediabetes, 32.1% had a borderline status vitamin B 12 status compared to the general pediatric OB population66.  

In a case control study, vitamin B12 status (dietary intake and serum concentration) was evaluated in adolescent on metformin treatment (n = 23) compared to their peers (n = 46) not receiving the drug. While median values of insulin resistance and 25OHD did not differ, more patients on metformin had biochemical vitamin B12 deficiency while they consumed less energy, less vitamin B12, with median coverage reaching 54% of the RDA, more carbohydrates as a percentage of energy intake67.  

Information about other vitamin deficiencies is seldom reported in OB children. Evaluations of vitamin C as an antioxidant are in normal ranges in all studies quoted in this paper.  

 

3. MINERALS AND SERUM TRACE ELEMENTS

3.1 IRON 

Iron interplay with obesity 

A bidirectional relationship has been evidenced between adipose tissue metabolism and OB, a mild inflammatory disease. A current view is that energy substrate metabolism and iron sensing are co-regulated to ensure iron availability for efficient energy use and in times of energy excess, its adequate storage68.  

Biological iron status is assessed on serum concentrations of ferritin, a cage-like heteropolymer which can hold up to 4500 iron atoms. Most ferritin is used to store within cells, but a very small amount enters a distinct secretory pathway, destined for release in the serum. Another protein, transferrin, is secreted mostly by hepatocytes, and serves the general purpose of binding iron, keeping it soluble in an aqueous environment and delivering it to tissues. Hepcidin is a protein which regulates iron homeostasis. It is produced primarily by hepatocytes, reduces iron efflux from cells and duodenal iron absorption. In response to infection or inflammation, hepcidin rises, causing iron to be sequestered, a defense against siderophilic bacteria.  FM distribution associates with iron parameters in central OB but not in the gynoid one. In people with OB, the handling of iron by the adipose tissue is impaired by a shift in macrophages subpopulations, leading to its accumulation in adipose tissue but deficiency of hepatic iron along with elevated ferritin and transferrin. Mitochondrial damage and dysfunction in white adipose tissue, due to iron depletion or overload has been implicated in the biogenesis of metabolic disease. The sensibility of liver and adipose tissue to iron deposition explains why serum iron deficiency do not necessarily reflect tissue iron status68.  

Iron intakes vary widely around the world where anemia is still the most common nutrient deficiency and affects 25% of the world’s population. Iron deficiency originates from low intakes or low absorption. Iron sources are from both animal (meat, fortified dairy products, egg yolk) and vegetable origin (mainly legumes). Iron of vegetable origin (non-heme iron) is less absorbed than heme iron from animal tissue. Bioavailability varies greatly with diet composition and iron stores. Average absorption seems to be 5-8% across studies in a systematic review69.  

Iron status in obese children and adolescents 

Several studies have consistently reported an increase in the prevalence of iron deficiency in OW/OB children and adolescents70-74. A meta-analysis found that, out of 41 studies included, 9 appropriate ones pinpointed that OB doubled the risk of iron deficiency (OR = 2.1, 95% CI: 1.4 – 3.2) 18.  The Greek cross-sectional “Healthy Growth Study”, was carried out in nearly 2500 children aged 9 to 13 years, 42% of whom were OW/OB. The prevalence of iron deficiency, defined by a decrease in transferrin saturation, reached almost 29% in OB children vs. 15% in normal weight children. The prevalence of iron deficiency anemia (IDA) reached 5 to 8% in OB and 1.5 to 2% in normal weight children. The probability of iron deficiency, adjusted for several confounding factors (diet, education, puberty) was significantly higher in OB compared to normal weight children (OR = 2.5 in boys and 2.1 in girls) whereas the probability of IDA was tripled (OR = 3.1 and 3.3, respectively)74.  

The NHANES III study of 9698 American children aged 2-16 years, among whom 24% were OW/OB, also showed that the prevalence of iron deficiency increased with BMI: the prevalence of iron deficiency, defined by a decrease in plasma ferritin concentration or in transferrin saturation, or increased erythrocyte protoporphyrin, was also twice as high in OW/OB children as in normal weight children. However,  prevalence was lower than in the Greek study, reaching only 9.1% in OW/OB children aged 12 to 16 years vs 4.7% in normal weight children, with a statistical significant difference72. A recent pediatric review confirmed that studies based on several iron-status biomarkers showed concordant increases in the prevalence, risk and severity of iron deficiency in OW/OB children and adolescents in industrialized and in some emerging countries, especially in girls after menarche70. 

Iron deficiency rate ranged from 2.0% (ferritin cut off: 12 mg/l) to 4.8% (ferritin cut off: 15 mg/l) in a group of 502 OB children and adolescents in France. Multivariate regression analysis after correction for age, sex, BMI z-scores and fibrinogen showed independent correlations between ferritin and triglycerides, HDL cholesterol, transaminase, and hemoglobin concentrations75. Iron storage assessed by ferritin is associated with cardiovascular and fatty liver disease risk factors. In Switzerland, iron status was compared in OW and lean children and adolescents, aged 6-14 years old. Iron intakes and bioavailability estimated from food database was similar in OB and lean subjects. Iron deficient erythropoiesis estimated on serum transferrin concentrations (4.4 ± 0.77 vs. 3.94 ± 0. 88 mg/dl, p = 0.010) was 20% in OB children vs. 6% in their lean counterpart (p = 0.022). Serum hepcidin levels were higher in the OB group and in a multi-regression model correlated with BMI SDS (p = 0.02) and body iron (p = 0.029) but not with the inflammatory markers (CRP, IL6, leptin)73. Another study performed in Italy compared iron status in OB children and lean counterparts. Iron absorption studied 2 hours after absorption of 1 mg/kg of ferrous sulfate was similar in both groups. OB children showed lower iron and transferrin saturation (p <0.05) and higher hepcidin levels (p = 0.004) compared with controls. Hepcidin and OB degree were correlated (p = 0.0015). Iron status was also evaluated in Egyptian children. Serum iron and transferrin saturation were lower in OB than in lean children, whereas ferritin, soluble transferrin receptors and hepcidin were higher in OB subjects. BMI SDS correlated with ferritin and iron76. In prepubertal Egyptian children lower serum iron were found (p <0.01) while serum ferritin concentrations did not differ significantly. Serum iron was negatively correlated to BMI (p <0.05) but not to leptin concentrations77. Eighteen per cent of a group of OB Mexican-American children had low serum iron concentrations. Plasma CRP and iron concentrations were negatively correlated (p <0.05)44. 

Although the reasons behind the high prevalence of iron deficiency in the OB are not clearly established, it is a prevalent disorder in the most precarious population groups. The small number of available dietary surveys show little or no difference in nutritional intake between OB and non-OB children, whether for iron or either nutrients or antinutrients (such as phytates) likely to affect iron absorption70,73,74.  

Which biomarkers should be used to assess iron status in obesity? 

Most experts recommend for the evaluation of iron status in children or adolescents with OW/OB to avoid using serum iron or ferritin alone because of the positive correlation with inflammation but rather to combine several biomarkers such as transferrin saturation, erythrocyte protoporphyrin or soluble transferrin receptor. The use of several markers allows exploring different additional aspects of iron metabolism: transportation, storage, as well as  the  bioavailable iron pool70,72-74. Iron supplementation should be started with caution in children with OW/OB and rely on the evidence of insufficient dietary intakes or of its risk factors when ferritin level is low78. 

  

 

3.2 Zinc 

Zinc (Zn) is the second most abundant, unevenly distributed divalent cation in the body after calcium. Higher concentrations are found in bone and muscles. Main food sources are meat, fish, shellfish and nuts and whole grains. Availability is decreased by phytic acid. Zn metabolism is tightly regulated. Despite the lack of a storage form, unlike iron, steep increase in absorption and decrease in urinary losses maintain homeostasis. In healthy children a meta-analysis found that a doubling in Zn intakes is necessary to increase plasma or serum Zn levels by 9%. Excess Zn is toxic. This characteristic underlies its bactericidal action. It plays critical roles as a cofactor both to stabilize proteins structurally, as well as to facilitate enzymatic catalysis.  It allows insulin storage, action and release from pancreatic β-cells. Major Zn deficiencies are still common in association with protein deficiencies in developing countries and in rare digestive diseases. Zn insufficiency can manifest in diminished immune response, reduced tissue regeneration and healing after traumatic insults, as well as in the occurrence of selected neurological disorders79. Zn status is assessed by measuring its plasma concentrations. Urinary and hair Zn concentrations are also valuable markers of Zn status80. 

A meta-analysis in 2024, investigated Zn status in relation to body weight. Out of 28 studies, only 2 used international consensus-based thresholds. Four studies found a direct association between Zn levels and BMI, 2 found inverse relationship and 6 no association with OW.   The author concludes that there is no evidence for a higher risk for Zn deficiencies in OW/OB. A review published in 2023 reported contrasted results among the studies in link with childhood obesity, seven of them finding low serum or salivary levels in association with OW/OB while three did not find any relationship81. In India, the Comprehensive national nutrition survey, in 2016-2018 did not report significant differences according to weight status across age ranges12.  

A study performed in Mexican school-aged children found that a fourth of them had Zn deficiencies (Zn <65 µg/dl). OW/OB children with low Zn concentrations had higher insulin concentration and insulin resistance compared with children with adequate weight with low concentrations of these micronutrients (p <0.05). No correlation was found with CRP44. Serum Zn concentrations were markedly lower (p <0.01) in a group of OB prepubertal Egyptian children than in lean controls, and negatively correlated to BMI (r = -0.65, p <0.01) and leptin serum concentrations77. A group of OB prepubertal children was supplemented with 20 mg/d of elemental Zn for 8 weeks. A mild significant decrease in fasting insulin and HOMA-IR index was observed in supplemented children whereas a mild increase occurred in control group82. In Australia, 87 OB insulin-resistant adolescents followed a 12-week low-energy diet (6.0 – 8.0 MJ) either with moderate carbohydrate or low carbohydrate with increased protein in a RCT. At baseline, 11 subjects reported inadequate Zn intakes. Plasma Zn concentration was positively correlated with systolic blood pressure (r = 0.22, p = 0.043) and inversely correlated with percentage of body fat (r = -0.28, p = 0.008). At 12 weeks, a positive correlation was found with meat intake (r = 0.32, p = 0.005) and inversely with percentage of energy from carbohydrates (r = -0/31, p = 0.006). Plasma Zn concentrations remained within reference range at 12 weeks83. 

Although Zn plays an essential role in insulin metabolism, the benefit of Zn supplementation has not been established in the treatment of insulin-resistant OB children and adolescents. However, diets should provide adequate amount of Zn.  

 

3.3 Selenium 

 

Selenium is an antioxidant trace element which has seldom been measured in OB children.  A study performed in OB Egyptian children reports lower serum concentrations in OB than in lean controls (p<0.001) and a strong correlation with HOMA-IR index in OB (r=0.64, p< 0.01) but not in lean counterparts77. Another study reports lower selenium intakes in Spanish schoolchildren and lower serum concentrations in those who had OB. Selenium intakes and serum concentrations were positively correlated (p <0.05). A negative relationship was found between all anthropometric parameters and serum selenium. Logistic regression showed that the risk of selenium deficiency increases with BMI (OR =1.50, 95% IC: 1.38 – 1.63) and to decrease with age (OR = 0.68, 95% IC: 0.54 – 0.85). Blood glutathione peroxidase (GPx) was moderately correlated to selenium serum concentrations (r = 0.17, p <0.05) but not to anthropometry84. 

  

4. NUTRITIONAL DEFICIENCIES AND BARIATRIC SURGERY 

Bariatric surgery is intended to treat the most severe forms of OB. Therefore, it deals with adolescents, very rarely children, with complications, including nutrient deficiencies, as previously described. In this section, the key points of the nutritional consequences of bariatric surgery in adolescents will be briefly reported.  

Two surgical techniques are mainly used: the Roux-en-Y gastric bypass (RYGB) and the vertical sleeve gastrectomy (SG), and – to a lesser extent – the adjustable gastric binding procedure (AGB).  Of note is that drug treatment by glucagon like analogues type 1 (GLP1) and a whole set of new potent drugs tends now to be used instead (see the eBook chapter on Medication).  

RYBG, a complex rearrangement of the gastrointestinal anatomy (see dedicated chapter), is a form of gastric bypass in which the proximal end of the jejunum is reattached to a smaller gastric pouch and the distal portion of the duodenum is reattached to a more distal end of the jejunum. As such, it decreases energy intakes but may also alter the patient’s nutritional status because of malabsorption, bacterial overgrowth and changes in biliary acids distribution. SG removes approximately 75% of the stomach, leaving a narrow gastric tube which restricts food intake. Both gastric emptying and intestinal transit are markedly increased after SG because the intra-gastric pressure increases upon ingestion of foods, which in turn increases the tension of the gastric wall. Both techniques lead to major significant decreases in BMI and improvement in complications, but progressive weight regain tends to occur within a few years.  

Scientific evidence for the Updated Guidelines on Indications for Metabolic Surgery and Bariatric Surgery (MBS) was issued by the International Federation for the Surgery of Obesity (IFSO) and the American Society for Metabolic and Bariatric Surgery (ASMBS) in 2024. The analysis is based on 42 papers among which 10 used the teen-LABS database comparing different laparoscopic procedures. The overall conclusion is that the AGB seems to be a safer procedure, although it achieves less consistent and durable weight loss than RYGB or SG. They also conclude that MBS does not negatively impact pubertal development or linear growth85.  

When looking into detail of the data reported in high quality papers, Xanthakos et al. report a decrease in vitamin concentrations, in ferritin and an increase in transferrin and parathyroid hormone after RYGB. Ferritin levels also decreased significantly after SG, but not vit B12. In this study, no changes in serum levels of folate, vitamin A, B1, D were found at the baseline and 5 years later. However, 5 years after surgery, 59% of RYBG and 27% of SG recipients had 2 or more nutritional deficiencies86. In a systematic review and single arm meta-analysis published in 2025, Baara Saad and coworkers evaluate long term outcomes of RYBG in the adolescent population. Twelve studies including 522 adolescents were included. Eighteen percent of the patients were lost at follow-up. The most common postoperative nutritional deficiencies were vitamin D in 52.9% of the patients (95% CI: 28.2 – 76.2), iron deficiencies in 37% (95% CI: 17.2 – 62.5), and vitamin B12 deficiencies in 11.8% (95% CI: 8.1 – 17.1) of the patients. The postoperative group was more likely to develop iron and vitamin B12 deficiencies while risk levels remained stable for vitamin D 87.  Another systematic review and meta-analysis looking at 15 studies published between 2020 and 2023 found that in adolescents, the postoperative prevalence of low albumin, ferritin, vitamin D and vitamin B12 was 10%, 49%, 4 % and 20% respectively. Calcium deficiency was found in 10% and iron deficiency in 23% of the patients after bariatric surgery88. 

All studies evidence the high risk of nutrient deficiency prior and after bariatric surgery, RYGB carrying the higher risk which includes hypoalbuminemia. Adherence to vitamin supplementation was tested in teenagers, as part of the Swedish Adolescent Morbid Obesity Surgery (AMOS) study. Patients were prescribed daily multivitamin and mineral supplements. Blood samples were analyzed every year during their regular follow-up visits.  A significant association was found between self-reported adherence and vitamin D levels in blood, with rates of 15% of false positive and 10% of false negative. Two categories merged in the analysis: awareness and personal capability, and external factors. This study underlines the need to evaluate facilitators and barriers in these patients89.  

Supplementations covering vitamin and mineral deficiencies before and after MBS on a long-term basis are mandatory and must be individually adapted by a dietician. Key elements must be used in combination including iron, vitamin B12, folates and calcium and vitamin D combination tablets and proteins according to International Guidelines90.  

 

CONCLUSION  

The vitamin and mineral status in OB children are dependent upon the quality of the diet which is worsened by increased intakes of unbalanced diets and consumption of low quality, ultra-processed foods. Several factors including storage in adipose tissue, interplay between vitamins and minerals, consequences of mild inflammation, may play a role. Analysis of the nutritional status has therefore to rely on the confrontation of serum concentrations and dietary recall. The double burden of malnutrition, a common situation linked to social conditions all around the world, means that OB is associated to nutrients deficiencies. Management of OB requires to have an overall comprehension of each individual situation. Bariatric surgery requires lifelong term nutritional follow-up.  

 

 

REFERENCES 

  1. Monteiro CA, Louzada ML, Steele-Martinez E, et al.Ultra-processed foods and human health: the main thesis and the evidence.Lancet 2025;406(10520):2667-2684. DOI: 10.1016/S0140-6736(25)01565-X. 
  2. Berger MM, Shenkin A, Schweinlin A, et al. ESPEN micronutrient guideline. Clin Nutr 2022;41(6):1357-1424. DOI: 10.1016/j.clnu.2022.02.015.
  3. Heaney RP, Recker RR, Grote J, Horst RL, Armas LA. Vitamin D(3) is more potent than vitamin D(2) in humans. J Clin Endocrinol Metab 2010;96(3):E447-52. (In eng).DOI: jc.2010-2230 10.1210/jc.2010-2230.
  4. Vidailhet M, Mallet E, Bocquet A, et al.Vitamin D: still a topical matter in children and adolescents. A position paper by the Committee on Nutrition of the French Society of Paediatrics. Arch Pediatr 2013;19(3):316-28. (In eng). DOI: S0929-693X(11)00577-X 10.1016/j.arcped.2011.12.015.
  5. Ding C, Gao D, Wilding J, Trayhurn P, Bing C. Vitamin D signalling in adipose tissue. Br J Nutr;108(11):1915-23. (In eng). DOI: S0007114512003285 10.1017/S0007114512003285.
  6. Bennour I, Haroun N, Sicard F, Mounien L, Landrier JF. Recent insights into vitamin D, adipocyte, and adipose tissue biology.Obes Rev 2022;23(8):e13453. DOI: 10.1111/obr.13453.
  7. Payet T, Astier J, Bournot L, et al.Vitamin D modulates the content of inflammatory microRNAs in extracellular vesicles from human adipocyte cells in inflammatory context. Biofactors 2025;51(1):e70003. DOI: 10.1002/biof.70003.
  8. Bike D. Vitamin D, production, metabolism and mechanisms of action.In: al. FKe, ed. MDText.com. South Darmouth (MA)2025.
  9. Braegger C, Campoy C, Colomb V, et al.Vitamin D in the healthy European paediatric population.J Pediatr Gastroenterol Nutr 2013;56(6):692-701. (In eng). DOI: 10.1097/MPG.0b013e31828f3c0500005176-201306000-00022 . 
  10. Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF. Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr 2000;72(3):690-3. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10966885).
  11. Bennour I, Haroun N, Sicard F, Mounien L, Landrier JF. Vitamin D and Obesity/Adiposity-A Brief Overview of Recent Studies.Nutrients 2022;14(10). DOI: 10.3390/nu14102049.
  12. Verma M, Aditi A, Kapoor N, et al.Childhood Obesity and Essential Micronutrients: Insights from India’s Comprehensive National Nutrition Survey (2016-18). Diabetes Ther 2023;14(8):1267-1283. DOI: 10.1007/s13300-023-01424-2.
  13. Chen Z, Qiu X, Wang Q, Wu J, Li M, Niu W. Serum vitamin D and obesity among US adolescents, NHANES 2011-2018. Front Pediatr 2024;12:1334139. DOI: 10.3389/fped.2024.1334139.
  14. Perez-Bravo F, Duarte L, Arredondo-Olguin M, Iniguez G, Castillo-Valenzuela O. Vitamin D status and obesity in children from Chile. Eur J Clin Nutr 2022;76(6):899-901. DOI: 10.1038/s41430-021-01043-9.
  15. Yuan L, Wang H, Luo Y, Wang L. Association between overweight or obesity and vitamin D status in preschool children: an epidemiological survey in Beijing, China, 2021-2023. J Pediatr Endocrinol Metab 2025;38(7):679-689. DOI: 10.1515/jpem-2024-0330.
  16. Gonzalez-Gross M, Valtuena J, Breidenassel C, et al. Vitamin D status among adolescents in Europe: the Healthy Lifestyle in Europe by Nutrition in Adolescence study.Br J Nutr 2011;107(5):755-64. (In eng). DOI: S0007114511003527 10.1017/S0007114511003527.
  17. Pereira-Santos M, Costa PR, Assis AM, Santos CA, Santos DB.Obesity and vitamin D deficiency: a systematic review and meta-analysis. Obes Rev 2015;16(4):341-9. (In eng). DOI: 10.1111/obr.12239.
  18. Malden S, Gillespie J, Hughes A, et al. Obesity in young children and its relationship with diagnosis of asthma, vitamin D deficiency, iron deficiency, specific allergies and flat-footedness: A systematic review and meta-analysis.Obes Rev 2021;22(3):e13129. DOI: 10.1111/obr.13129.
  19. Geserick M, Vogel M, Eckelt F, et al.Children and adolescents with obesity have reduced serum bone turnover markers and 25-hydroxyvitamin D but increased parathyroid hormone concentrations – Results derived from new pediatric reference ranges. Bone 2020;132:115124. DOI: 10.1016/j.bone.2019.115124.
  20. Montgomery CO, Young KL, Austen M, Jo CH, Blasier RD, Ilyas M. Increased risk of Blount disease in obese children and adolescents with vitamin D deficiency. J Pediatr Orthop 2010;30(8):879-82. (In eng). DOI: 10.1097/BPO.0b013e3181f5a0b301241398-201012000-00020 .
  21. Kremer R, Campbell PP, Reinhardt T, Gilsanz V. Vitamin D status and its relationship to body fat, final height, and peak bone mass in young women. J Clin Endocrinol Metab 2009;94(1):67-73. (In eng). DOI: jc.2008-1575 10.1210/jc.2008-1575.
  22. Afghani A, Goran MI. Lower bone mineral content in hypertensive compared with normotensive overweight Latino children and adolescents.Am J Hypertens 2007;20(2):190-6. (In eng). DOI: S0895-7061(06)00505-X 10.1016/j.amjhyper.2006.07.014.
  23. Zeeb H, Brand T, Lissner L, et al.Vitamin D status and muscle strength in a pan-European cohort of children and adolescents with normal weight and overweight/obesity. Eur J Pediatr 2025;184(2):190. DOI: 10.1007/s00431-025-06024-9.
  24. O’Sullivan B, Ounpraseuth S, James L, et al. Vitamin D Oral Replacement in Children With Obesity Related Asthma: VDORA1 Randomized Clinical Trial. Clin Pharmacol Ther 2024;115(2):231-238. DOI: 10.1002/cpt.3086.
  25. Bluher AE, Kearney T, Vazifedan T, Baldassari CM. Vitamin D Deficiency and Pediatric Obstructive Sleep Apnea Severity. JAMA Otolaryngol Head Neck Surg 2025;151(1):72-77. DOI: 10.1001/jamaoto.2024.3737.
  26. Usman M, Woloshynowych M, Britto JC, et al. Obesity, oxidative DNA damage and vitamin D as predictors of genomic instability in children and adolescents. Int J Obes (Lond) 2021;45(9):2095-2107. DOI: 10.1038/s41366-021-00879-2.
  27. Garfein J, Flannagan KS, Gahagan S, Burrows R, Lozoff B, Villamor E. Vitamin D status in infancy and cardiometabolic health in adolescence. Am J Clin Nutr 2021;113(1):104-112. DOI: 10.1093/ajcn/nqaa273.
  28. Ekbom K, Marcus C. Vitamin D deficiency is associated with prediabetes in obese Swedish children. Acta Paediatr 2016;105(10):1192-7. (In eng). DOI: 10.1111/apa.13363.
  29. Cediel G, Corvalan C, Aguirre C, de Romana DL, Uauy R. Serum 25-Hydroxyvitamin D associated with indicators of body fat and insulin resistance in prepubertal chilean children. Int J Obes (Lond) 2015;40(1):147-52. (In eng). DOI: ijo2015148 10.1038/ijo.2015.148.
  30. Zhu L, Li S, Zhong L, Xu S, Zhu H. Optimal vitamin D supplement dosage for improving insulin resistance in children and adolescents with overweight/obesity: a systematic review and network meta-analysis. Eur J Nutr 2024;63(3):763-775. DOI: 10.1007/s00394-023-03301-x.
  31. Setia P, Seth A, Singh R, Malhotra RK, Singh P. Efficacy of daily 4,000 International Units (IU) versus 6,000 IU of oral vitamin D(3) in vitamin D deficient children with overweight and obesity: An open-label randomized controlled trial.Clin Nutr ESPEN 2025;68:806-813. DOI: 10.1016/j.clnesp.2025.06.007.
  32. Frelut ML, Girardet JP, Bocquet A, et al.Impact of obesity on biomarkers of iron and vitamin D status in children and adolescents: The risk of misinterpretation. Arch Pediatr 2018;25(1):3-5. DOI: 10.1016/j.arcped.2017.11.011.
  33. Ball GDC, Merdad R, Birken CS, et al. Managing obesity in children: a clinical practice guideline. CMAJ 2025;197(14):E372-E389. DOI: 10.1503/cmaj.241456.
  34. Sommer A, Vyas KS. A global clinical view on vitamin A and carotenoids. Am J Clin Nutr 2012;96(5):1204S-6S. (In eng). DOI: ajcn.112.034868 10.3945/ajcn.112.034868.
  35. Vidailhet M, Rieu D, Feillet F, et al.Vitamin A in pediatrics: An update from the Nutrition Committee of the French Society of Pediatrics. Arch Pediatr 2017;24(3):288-297. (In eng). DOI: S0929-693X(16)30604-2 10.1016/j.arcped.2016.11.021.
  36. Carazo A, Macakova K, Matousova K, Krcmova LK, Protti M, Mladenka P. Vitamin A Update: Forms, Sources, Kinetics, Detection, Function, Deficiency, Therapeutic Use and Toxicity. Nutrients 2021;13(5). DOI: 10.3390/nu13051703.
  37. Goodwin K, Abrahamowicz M, Leonard G, et al. Dietary Vitamin A and Visceral Adiposity: A Modulating Role of the Retinol-Binding Protein 4 Gene. J Nutrigenet Nutrigenomics 2015;8(4-6):164-73. DOI: 000442090 10.1159/000442090.
  38. Frey SK, Vogel S. Vitamin A metabolism and adipose tissue biology. Nutrients 2012;3(1):27-39. (In eng). DOI: 10.3390/nu3010027nutrients-03-00027 .
  39. Tanumihardjo SA. Assessing vitamin A status: past, present and future. J Nutr 2004;134(1):290S-293S. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14704336).
  40. Van Loo-Bouwman CA, Naber TH, Schaafsma G. A review of vitamin A equivalency of beta-carotene in various food matrices for human consumption. Br J Nutr 2014;111(12):2153-66. (In eng). DOI: S0007114514000166 10.1017/S0007114514000166.
  41. Tan X, Tan PY, Gong YY, Moore JB. Overnutrition is a risk factor for iron, but not for zinc or vitamin A deficiency in children and young people: a systematic review and meta-analysis. BMJ Glob Health 2024;9(4). DOI: 10.1136/bmjgh-2024-015135.
  42. Strauss RS. Comparison of serum concentrations of alpha-tocopherol and beta-carotene in a cross-sectional sample of obese and nonobese children (NHANES III). National Health and Nutrition Examination Survey. J Pediatr 1999;134(2):160-5. (In eng). DOI: S0022347699000517 .
  43. Gunanti IR, Marks GC, Al-Mamun A, Long KZ.Low serum concentrations of carotenoids and vitamin E are associated with high adiposity in Mexican-American children.J Nutr 2014;144(4):489-95. (In eng). DOI: jn.113.183137 10.3945/jn.113.183137. 
  44. Garcia OP, Ronquillo D, del Carmen Caamano M, et al.Zinc, iron and vitamins A, C and E are associated with obesity, inflammation, lipid profile and insulin resistance in Mexican school-aged children.Nutrients 2013;5(12):5012-30. (In eng). DOI: nu5125012 10.3390/nu5125012. 
  45. Su X, Patel N, Zhu S, et al.Association between serum vitamin A and body mass index in adolescents from NHANES 1999 to 2006. Sci Rep 2024;14(1):10859. DOI: 10.1038/s41598-024-61437-0.
  46. Decsi T, Molnar D, Koletzko B. Reduced plasma concentrations of alpha-tocopherol and beta-carotene in obese boys. J Pediatr 1997;130(4):653-5. (In eng). DOI: S0022-3476(97)70253-1 .
  47. Aeberli I, Biebinger R, Lehmann R, L’Allemand D, Spinas GA, Zimmermann MB.Serum retinol-binding protein 4 concentration and its ratio to serum retinol are associated with obesity and metabolic syndrome components in children. J Clin Endocrinol Metab 2007;92(11):4359-65. (In eng). DOI: jc.2007-0468 10.1210/jc.2007-0468.
  48. Reinehr T, Stoffel-Wagner B, Roth CL. Retinol-binding protein 4 and its relation to insulin resistance in obese children before and after weight loss. J Clin Endocrinol Metab 2008;93(6):2287-93. (In eng). DOI: jc.2007-2745 10.1210/jc.2007-2745.
  49. Canas JA, Lochrie A, McGowan AG, Hossain J, Schettino C, Balagopal PB. Effects of Mixed Carotenoids on Adipokines and Abdominal Adiposity in Children: A Pilot Study. J Clin Endocrinol Metab 2017;102(6):1983-1990. (In eng). DOI: 3067657 10.1210/jc.2017-00185.
  50. Mesmin B, Antonny B. Cell biology. Vitamin currency in a lipid exchange market. Science 2013;340(6136):1051-2. (In eng). DOI: 340/6136/1051 10.1126/science.1239800.
  51. Traber MG, Kayden HJ. Tocopherol distribution and intracellular localization in human adipose tissue. Am J Clin Nutr 1987;46(3):488-95. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3630967).
  52. Borel P, Preveraud D, Desmarchelier C. Bioavailability of vitamin E in humans: an update.Nutr Rev 2013;71(6):319-31. (In eng). DOI: 10.1111/nure.12026.
  53. Guerendiain M, Mayneris-Perxachs J, Montes R, et al.Relation between plasma antioxidant vitamin levels, adiposity and cardio-metabolic profile in adolescents: Effects of a multidisciplinary obesity programme. Clin Nutr 2017;36(1):209-217. DOI: 10.1016/j.clnu.2015.11.001.
  54. Decsi T, Molnar D, Koletzko B. Lipid corrected plasma alpha-tocopherol values are inversely related to fasting insulinaemia in obese children. Int J Obes Relat Metab Disord 1996;20(10):970-2. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8910105).
  55. Bonet B, Viana M, Sanchez-Vera I, Quintanar A, Martinez J, Espino M. Adipose tissue and liver lipid metabolism in obese children: role of the body mass index and the presence of acanthosis nigricans.Diabet Med 2007;24(11):1192-8. (In eng). DOI: DME2230 10.1111/j.1464-5491.2007.02230.x.
  56. Murer SB, Aeberli I, Braegger CP, et al.Antioxidant supplements reduced oxidative stress and stabilized liver function tests but did not reduce inflammation in a randomized controlled trial in obese children and adolescents. J Nutr 2013;144(2):193-201. (In eng). DOI: jn.113.185561 10.3945/jn.113.185561.
  57. Mann JP, Tang GY, Nobili V, Armstrong MJ. Evaluations of Lifestyle, Dietary, and Pharmacologic Treatments for Pediatric Nonalcoholic Fatty Liver Disease: A Systematic Review. Clin Gastroenterol Hepatol 2018 (In eng). DOI: S1542-3565(18)30555-X 10.1016/j.cgh.2018.05.023.
  58. Liew S, Gupta ED. Methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism: Epidemiology, metabolism and the associated diseases. Eur J Med Genet 2014;58(1):1-10. (In Eng). DOI: S1769-7212(14)00193-1 10.1016/j.ejmg.2014.10.004.
  59. O’Neil CE, Keast DR, Nicklas TA, Fulgoni VL, 3rd. Out-of-hand nut consumption is associated with improved nutrient intake and health risk markers in US children and adults: National Health and Nutrition Examination Survey 1999-2004. Nutr Res 2012;32(3):185-94. (In eng). DOI: S0271-5317(12)00027-9 10.1016/j.nutres.2012.01.005.
  60. Ulloque-Badaracco JR, Alarcon-Braga EA, Hernandez-Bustamante EA, et al. Vitamin B12, folate, and homocysteine levels in children and adolescents with obesity: a systematic review and meta-analysis. Front Public Health 2025;13:1481002. DOI: 10.3389/fpubh.2025.1481002.
  61. Hassapidou M, Fotiadou E, Maglara E, Papadopoulou SK. Energy intake, diet composition, energy expenditure, and body fatness of adolescents in northern Greece. Obesity (Silver Spring) 2006;14(5):855-62. (In eng). DOI: 14/5/855 10.1038/oby.2006.99.
  62. Gunanti IR, Marks GC, Al-Mamun A, Long KZ. Low serum vitamin B-12 and folate concentrations and low thiamin and riboflavin intakes are inversely associated with greater adiposity in mexican american children. J Nutr 2014;144(12):2027-33. (In eng). DOI: jn.114.201202 10.3945/jn.114.201202.
  63. Frelut ML, Emery-Fillon N, Guilland JC, Dao HH, de Courcy GP. Alanine amino transferase concentrations are linked to folate intakes and methylenetetrahydrofolate reductase polymorphism in obese adolescent girls. J Pediatr Gastroenterol Nutr 2006;43(2):234-9. (In eng). DOI: 10.1097/01.mpg.0000228110.83616.9200005176-200608000-00017 .
  64. Frelut ML, Nicolas JP, Guilland JC, de Courcy GP. Methylenetetrahydrofolate reductase 677 C->T polymorphism: a link between birth weight and insulin resistance in obese adolescents. Int J Pediatr Obes 2010;6(2-2):e312-7. (In eng). DOI: 10.3109/17477166.2010.486835.
  65. Wiltshire EJ, Pena AS, MacKenzie K, Bose-Sundernathan T, Gent R, Couper JJ. A NOS3 Polymorphism Determines Endothelial Response to Folate in Children with Type 1 Diabetes or Obesity. J Pediatr (In Eng). DOI: S0022-3476(14)01017-8 10.1016/j.jpeds.2014.10.050.
  66. Ho ML, Cowling BJ, Seto WH, Wong LC, Wong TY. Determinants of an effective antibiotic campaign: Lessons from Hong Kong. J Glob Antimicrob Resist 2014;2(4):334-337. DOI: 10.1016/j.jgar.2014.08.001.
  67. Tsiroukidou K, Paschalidou EG, Grammatikopoulou MG, et al. Serum Concentrations and Dietary Intake of Vitamin B(12) in Children and Adolescents on Metformin: A Case-Control Study. Int J Mol Sci 2023;24(4). DOI: 10.3390/ijms24044205.
  68. Hilton C, Sabaratnam R, Drakesmith H, Karpe F. Iron, glucose and fat metabolism and obesity: an intertwined relationship. Int J Obes (Lond) 2023;47(7):554-563. DOI: 10.1038/s41366-023-01299-0.
  69. Collings R, Harvey LJ, Hooper L, et al. The absorption of iron from whole diets: a systematic review.Am J Clin Nutr 2013;98(1):65-81. (In eng). DOI: ajcn.112.050609 10.3945/ajcn.112.050609.
  70. Hutchinson C. A review of iron studies in overweight and obese children and adolescents: a double burden in the young? Eur J Nutr 2016;55(7):2179-97. (In eng). DOI: 10.1007/s00394-016-1155-710.1007/s00394-016-1155-7 .
  71. Pinhas-Hamiel O, Newfield RS, Koren I, Agmon A, Lilos P, Phillip M. Greater prevalence of iron deficiency in overweight and obese children and adolescents.Int J Obes Relat Metab Disord 2003;27(3):416-8. (In eng). DOI: 10.1038/sj.ijo.08022240802224 .
  72. Nead KG, Halterman JS, Kaczorowski JM, Auinger P, Weitzman M. Overweight children and adolescents: a risk group for iron deficiency. Pediatrics 2004;114(1):104-8. (In eng) (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15231915).
  73. Aeberli I, Hurrell RF, Zimmermann MB. Overweight children have higher circulating hepcidin concentrations and lower iron status but have dietary iron intakes and bioavailability comparable with normal weight children. Int J Obes (Lond) 2009;33(10):1111-7. (In eng). DOI: ijo2009146 10.1038/ijo.2009.146.
  74. Manios Y, Moschonis G, Chrousos GP, et al. The double burden of obesity and iron deficiency on children and adolescents in Greece: the Healthy Growth Study. J Hum Nutr Diet 2013;26(5):470-8. (In eng). DOI: 10.1111/jhn.12025.
  75. Bougle D, Brouard J. Iron in child obesity. Relationships with inflammation and metabolic risk factors. Nutrients;5(6):2222-30. (In eng). DOI: nu5062222 10.3390/nu5062222.
  76. Hamza RT, Hamed AI, Kharshoum RR. Iron homeostasis and serum hepcidin-25 levels in obese children and adolescents: relation to body mass index. Horm Res Paediatr 2013;80(1):11-7. (In eng). DOI: 000351941 10.1159/000351941.
  77. Azab SF, Saleh SH, Elsaeed WF, Elshafie MA, Sherief LM, Esh AM. Serum trace elements in obese Egyptian children: a case-control study. Ital J Pediatr 2014;40:20. (In eng).DOI: 1824-7288-40-20 10.1186/1824-7288-40-20.
  78. Frelut ML, Girardet JP, Bocquet A, et al.Impact of obesity on biomarkers of iron and vitamin D status in children and adolescents: The risk of misinterpretation. Arch Pediatr 2018;25(1):3-5. (In eng). DOI: S0929-693X(17)30469-4 10.1016/j.arcped.2017.11.011.
  79. Marger L, Schubert CR, Bertrand D. Zinc: an underappreciated modulatory factor of brain function. Biochem Pharmacol 2014;91(4):426-35. (In eng). DOI: S0006-2952(14)00457-2 10.1016/j.bcp.2014.08.002.
  80. Lowe NM, Fekete K, Decsi T. Methods of assessment of zinc status in humans: a systematic review.Am J Clin Nutr 2009;89(6):2040S-2051S. (In eng). DOI: ajcn.2009.27230G 10.3945/ajcn.2009.27230G.
  81. Calcaterra V, Verduci E, Milanta C, et al.Micronutrient Deficiency in Children and Adolescents with Obesity-A Narrative Review. Children (Basel) 2023;10(4). DOI: 10.3390/children10040695.
  82. Hashemipour M, Kelishadi R, Shapouri J, et al. Effect of zinc supplementation on insulin resistance and components of the metabolic syndrome in prepubertal obese children. Hormones (Athens) 2009;8(4):279-85. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=20045801).
  83. Ho M, Heath AM, Gow M, et al. Zinc Intake, Zinc Bioavailability and Plasma Zinc in Obese Adolescents with Clinical Insulin Resistance Following Low Energy Diets.Ann Nutr Metab 2016;69(2):135-141. (In eng). DOI: 000450728 10.1159/000450728.
  84. Ortega RM, Rodriguez-Rodriguez E, Aparicio A, et al.Young children with excess of weight show an impaired selenium status. Int J Vitam Nutr Res 2012;82(2):121-9. (In eng). DOI: 10.1024/0300-9831/a000101.
  85. De Luca M, Shikora S, Eisenberg D, et al. Scientific Evidence for the Updated Guidelines on Indications for Metabolic and Bariatric Surgery (IFSO/ASMBS). Obes Surg 2024;34(11):3963-4096. DOI: 10.1007/s11695-024-07370-7.
  86. Xanthakos SA, Khoury JC, Inge TH, et al. Nutritional Risks in Adolescents After Bariatric Surgery. Clin Gastroenterol Hepatol 2020;18(5):1070-1081 e5. DOI: 10.1016/j.cgh.2019.10.048.
  87. Saad B, Rahima K, Mourad MM, et al. Long-term outcomes of Roux-en-Y gastric bypass in the adolescent population: a systematic review and single-arm meta-analysis. Surg Obes Relat Dis 2025. DOI: 10.1016/j.soard.2025.09.003.
  88. Zolfaghari F, Khorshidi Y, Moslehi N, Golzarand M, Asghari G. Nutrient Deficiency After Bariatric Surgery in Adolescents: A Systematic Review and Meta-Analysis. Obes Surg 2024;34(1):206-217. DOI: 10.1007/s11695-023-06955-y.
  89. Brorsson AL, Nordin K, Ekbom K. Adherence to Vitamin Supplementation Recommendations in Youth Who Have Undergone Bariatric Surgery as Teenagers: a Mixed Methods Study. Obes Surg 2020;30(12):4911-4918. DOI: 10.1007/s11695-020-04880-y.
  90. Parrott J, Frank L, Rabena R, Craggs-Dino L, Isom KA, Greiman L. American Society for Metabolic and Bariatric Surgery Integrated Health Nutritional Guidelines for the Surgical Weight Loss Patient 2016 Update: Micronutrients. Surg Obes Relat Dis 2017;13(5):727-741. DOI: 10.1016/j.soard.2016.12.018.

 

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