Vitamin D, Childhood Obesity, and Metabolic Risk – A Scoping Review

doi:10.21203/rs.3.rs-7540633/v1

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Systematic Review

Vitamin D, Childhood Obesity, and Metabolic Risk – A Scoping Review

https://doi.org/10.21203/rs.3.rs-7540633/v1

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Vitamin D deficiency and childhood obesity are increasingly recognized as overlapping global health challenges, both of which have substantial implications for long-term wellbeing. Due to the lipophilic nature of vitamin D, excessive adiposity reduces its bioavailability, thereby predisposing overweight and obese children to inadequate circulating 25-hydroxyvitamin D [25(OH)D] concentrations. This deficiency has been associated with impaired bone mineralization, insulin resistance, systemic inflammation, and an elevated risk of type 2 diabetes mellitus, cardiovascular disease, and osteoporosis later in life. Several supplementation strategies for improving vitamin D status in pediatric populations with overweight or obesity have been proposed; however, their efficacy remains inconclusive. Evidence from randomized clinical trials and observational studies indicates that vitamin D supplementation leads to modest increases in serum 25(OH)D levels, with higher-dose regimens producing greater improvements. Findings on the impact of supplementation on metabolic and cardiovascular outcomes are inconsistent, with no clear consensus on the optimal dosing or duration needed to achieve clinically meaningful benefits. Beyond supplementation, lifestyle interventions involving weight reduction through dietary modification and increased physical activity may also contribute to improved vitamin D status, although the interplay between adiposity, vitamin D metabolism, and health outcomes is complex and not yet fully understood. The widespread expression of vitamin D receptors and 1α-hydroxylase in multiple tissues, including adipose tissue, suggests a potential regulatory role in adipogenesis and adipocyte metabolism, which may partly explain the extensive health effects linked to deficiency. This scoping review synthesizes the available evidence on vitamin D, childhood obesity, and metabolic risk, highlighting key research gaps. Further well-designed longitudinal and interventional studies are urgently required to clarify causality, define optimal vitamin D status, and establish effective interventions for improving health outcomes in this vulnerable population.

Physiology

Vitamin D

childhood obesity

metabolic risk

supplementation

adiposity

Obesity is considered a multifactorial disease with high prevalence among children and adolescents (1). Worldwide, an estimated 43 million children are overweight or obese, and an additional 92 million are at risk of becoming overweight (2). Studies reveal that childhood obesity is linked to an increase in related chronic illnesses, including insulin resistance (IR), dyslipidaemia, hypertension, and inflammation, which can have long-term effects on a child's physical health as well as their psychological and functional health (3). The relationship between vitamin D deficiency and childhood obesity is a prominent area of research. Each has been classified as an epidemic globally, sharing common risk factors such as poor diet and inactivity (2).

Furthermore, new intervention trials suggest that improving the low vitamin D status linked to obesity may lessen some of the comorbidities of obesity. Observational and clinical research also demonstrate an inverse relationship between vitamin D status and fat mass (4). The objective of this review is to discuss the recent literature on vitamin D and childhood obesity, including their interactions and implications for health and disease.

Vitamin D: the hormone, the nutrient, and its action

Vitamin D is more accurately characterised as a prohormone or hormone, though it is historically categorised as a nutrient (5). It is found in two main variants: vitamin D2 and vitamin D3. Vitamin D2, also known as ergocalciferol, is formed when ergosterol, a sterol found in fungi and also referred to as provitamin D2, is exposed to ultraviolet light. Vitamin D3, or cholecalciferol, is generated when ultraviolet rays act on 7-dehydrocholesterol (provitamin D3) in the skin’s epidermal and dermal layers (6). The general term “vitamin D” can refer to either D2, D3, or both forms. The most significant source of vitamin D is its synthesis in the skin, as only a limited number of foods naturally contain it (7).

Both vitamin D2 and D3 must go through two chemical changes in the body to become active and able to bind to the vitamin D receptor (VDR) (8). As the first step, the enzyme 25-hydroxylase converts vitamin D into 25-hydroxyvitamin D (25(OH)D), also known as calcidiol, in the liver. This is the main form of vitamin D found in the blood and is used to measure vitamin D levels in the body (8). Then, the enzyme 1α-hydroxylase (1α-OH-ase) changes 25(OH)D into its active form, 1,25-dihydroxyvitamin D (1,25(OH)₂D), also called calcitriol in kidneys (9). When 25(OH)D is activated in the kidneys, the resulting 1,25(OH)₂D enters the bloodstream and travels to other tissues where it binds to VDRs (10). However, 1,25(OH)₂D acts locally within the same or nearby cells in tissues outside the kidney. Vitamin D and its forms are carried in the blood by proteins, mostly by vitamin D-binding protein (DBP). It is mainly made in the liver. DBP carries about 85% of 25(OH)D in the blood, and the rest is attached to albumin and other proteins such as lipoproteins (11). 1,25(OH)2D is transported to nuclear VDR in target cells after being synthesised from renal or local production (12).

Vitamin D plays significant roles in calcium and phosphorus homeostasis, bone growth and bone mineralisation in childhood. Vitamin D deficiency in childhood causes osteomalacia, leading to growth retardation and skeletal deformities such as rickets (13). However, vitamin D deficiency can present insidiously, which may prevent children and adolescents from reaching their peak bone mass and predicted height (14). Vitamin D is also involved in numerous cellular processes in addition to calcium and phosphate homeostasis. VDRs are expressed in a variety of tissues and cells, such as the hepatocytes, myocytes, adipocytes, pancreatic β-cells, and several immune cells, all of which are associated with obesity and its associated metabolic complications (12).

Childhood prevalence of vitamin D deficiency

Vitamin D deficiency is a significant issue affecting individuals of all age groups globally. However, there is still limited data available regarding its prevalence in paediatric populations in certain countries (15). The global prevalence of vitamin D deficiency among children and adolescents varies considerably, ranging from 29–100%. Research suggests that this variation is partly influenced by body fat levels. Furthermore, vitamin D deficiency affects approximately 21% of children with a healthy weight, 29% of those who are overweight, 34% of obese children, and up to 49% of those who are severely obese. These findings indicate that children with obesity are particularly at risk for vitamin D deficiency, which may further worsen the negative health impacts associated with obesity itself (15, 16).

Interactions and implications of vitamin D deficiency in obese children\

Vitamin D deficiency in obese children is a significant public health concern, with implications for metabolic health and overall well-being. Research indicates a strong association between low vitamin D levels and obesity, highlighting the need for targeted interventions. Vitamin D plays a significant role in metabolic processes, and its deficiency is linked to increased insulin resistance, inflammation, and impaired bone mineralisation (17). The deficiency may exacerbate the risk of developing type 2 diabetes and cardiovascular diseases in obese children (17). A long-term, population-based prospective study involving 1,226 adults over a ten-year period revealed that individuals with serum 25(OH)D levels below 42 nmol/L (17 ng/mL) had a 2.37-fold higher likelihood of gaining more than 3.7 kg (placing them in the top 25th percentile for weight gain) between their second and third study visits, compared to those with higher vitamin D levels (18).

Insulin resistance (IR) and inflammation are frequently observed in overweight and obese children and act as early indicators for the future onset of metabolic syndrome, type 2 diabetes mellitus (T2DM), cardiovascular disease (CVD), and potentially reduced bone density, such as osteopenia or osteoporosis. Several studies have shown that children exhibiting both of these risk factors are considerably more likely to develop T2DM and CVD two to three decades later, in comparison to children without these conditions (19).

Furthermore, the link between inadequate vitamin D levels and conditions such as insulin resistance (IR), type 2 diabetes mellitus (T2DM), and metabolic syndrome has been extensively researched, with initial findings reported in obese adults. Subsequent studies have identified similar patterns in obese children. While not entirely consistent, the majority of studies report meaningful associations between serum 25(OH)D levels and markers of insulin resistance and glucose regulation (20). These findings have been thoroughly reviewed in other literature.

Few of the published intervention trials have investigated the effects of vitamin D supplementation on insulin resistance and impaired glucose tolerance in obese children and adolescents, and the results have generally been positive. For example, in a six-month randomised controlled trial (RCT) involving obese adolescents (average age 14.1 ± 2.8 years; mean BMI 39.8 ± 6.1 kg/m²), daily supplementation with 4,000 IU of vitamin D led to a reduction in insulin resistance comparable to the improvements typically seen with metformin treatment.

In contrast, a 2012 meta-analysis evaluating the impact of vitamin D supplementation on glycemic control in adults found only a modest benefit in lowering fasting glucose levels and improving insulin resistance among individuals with type 2 diabetes or impaired glucose tolerance. This variation in outcomes is largely due to methodological differences across studies, including the dosage of vitamin D used, the specific outcomes assessed, and differences in participant characteristics, particularly body weight or fat levels, baseline vitamin D status, and age.

For this scoping review, we adhered to the five-stage framework proposed by Levac, Colquhoun and O’Brien for conducting scoping reviews (21). The first four stages are described below; collating, summarising, and reporting the results are presented in the Results section.

2.1 Identifying the research questions

This review was guided by the following questions.

Association – What is the relationship between vitamin D status and the prevalence or severity of childhood overweight/obesity?

Metabolic risk – How is vitamin D status linked with cardiometabolic risk markers (insulin resistance, dyslipidaemia, metabolicsyndrome components) in children and adolescents?

Interventions – What interventional strategies (supplementation, fortification, lifestyle programmes that include vitamin D) have been implemented to modify vitamin D status in paediatric populations with overweight/obesity, and what metabolic outcomes have been reported?

Evidence landscape – What study designs, assessment methods, and outcome measures are most commonly used, and where are the gaps in the current literature?

A scoping rather than a systematic review was selected because the field spans heterogeneous study designs (observational and interventional), populations (various definitions of obesity and vitamin D deficiency), and outcomes (anthropometric and biochemical). A broad mapping is therefore required to characterise the evidence base and to highlight research gaps and priorities.

2.2 Identifying relevant studies

Following the threestep search strategy recommended by Peters et al. (22), we first conducted a preliminary search in PubMed to refine keywords and index terms. The final search (last updated 1 December 2024) was executed in the PubMed (MEDLINE) and Google Scholar electronic databases, selected for their coverage of biomedical, nutrition, and paediatric research.

The core search string combined controlled vocabulary (MeSH) and freetext terms.

("vitamin D" OR cholecalciferol OR ergocalciferol OR "25hydroxyvitamin D") AND (child OR adolescent OR paediatric) AND (obese OR overweight) AND ("metabolic risk" OR "metabolic syndrome" OR dyslipidaemia)

Search filters were applied to human studies published in English between 2020 and 2024. No restrictions were placed on study design at this stage. We handsearched the reference lists of included articles and relevant reviews to identify additional papers and grey literature (World Health Organisation reports).

2.3 Studyselection criteria

Screening was guided by a modified PICOS framework (23).

Component	Inclusion criteria	Exclusion criteria
Population (P)	Children and adolescents ≤ 18 years, with or without overweight/obesity (as defined by study authors).	Adults; animal or invitro studies.
Intervention / Exposure (I)	(a) Measured vitamin D status (serum 25(OH)D) or (b) vitamin D supplementation/fortification / sunexposure interventions.	Multifactorial programmes where the independent effect of vitamin D could not be isolated.
Comparator / Control (C)	Adequate vs deficient vitamin D status, placebo / usual care, or alternative vitamin D dosing.	Comparisons between nonvitamin D exposures (e.g., calcium only).
Outcomes (O)	At least one obesity or metabolic marker: BMI, BMIz, waist circumference, bodyfat %, insulin, HOMAIR, fasting glucose, lipid profile, blood pressure, metabolic syndrome prevalence, inflammatory markers (CRP, IL-6, etc.).	Outcomes unrelated to adiposity or metabolic risk (e.g., boneonly endpoints without metabolic data).
Study design (S)	Randomised controlled trials, quasiexperimental studies, prospective or retrospective cohort studies, case–control studies, and crosssectional studies.	Case reports/series, editorials, narrative reviews, protocols, conference abstracts without full text, theses, and unpublished data.

Titles/abstracts were screened independently by two reviewers (MR and HW). Fulltexts of potentially eligible studies were retrieved and assessed against the criteria; disagreements were resolved by consensus or by a third reviewer. Study selection was recorded in a PRISMAScR flow diagram.

2.4 Data extraction and charting

A datacharting form was pilottested on five studies and then applied to all included articles. One reviewer extracted, and a second verified, the following information:

Bibliographic details (first author, year, country).
Study characteristics (design, recruitment method, sample size).
Participant characteristics (age range/mean, sex distribution, obesity definition, baseline 25(OH)D categories).
Intervention/exposure details (supplement dose, regimen, duration)
Outcomes reported and measurement tools.
Key findings relevant to adiposity or metabolic risk (significance).

We charted the data in Microsoft Excel and repeatedly updated the table as new themes emerged, consistent with Levac et al.’s iterative approach (21).

Table 1
Key findings of the studies investigating vitamin D supplementation in obese/overweight children and adolescents.
Reference (authors, year, country)	Participants and Design	Intervention	Duration (supplementation / follow-up)	Key Findings
Aguirre Castaneda 2012, USA (24)	36 adolescents (n = 18 obese, n = 18 normal weight) / open label non-randomized trial	2000 IU/d	12 weeks / 12 weeks	Baseline mean 25(OH)D concentrations were higher in individuals with normal weight than in those with obesity. The rise in 25(OH)D levels after vitamin D supplementation was significantly attenuated among adolescents with obesity. No changes were observed in circulating phosphorus or parathyroid hormone levels, while circulating calcium levels showed only a change of limited clinical relevance.
Belenchia et al. 2013, USA (25)	35 obese adolescents (n = 18 group 1, n = 17 placebo group) / randomized controlled trial	4000 IU/d (group 1), or placebo	6 months / 6 months	After three months, none of the participants in group 1 remained vitamin D deficient. By six months, 93% of them had achieved sufficient vitamin D status. In contrast, the placebo group showed no significant rise in 25(OH)D levels over time. At six months, group 1 demonstrated reduced insulin levels compared to the placebo group, while glucose and glycated hemoglobin levels remained unchanged. No differences were observed in BMI or inflammatory markers between the groups.
Bhagatwala et al. 2015, USA (26)	70 overweight/obese adolescents and young adults with vitamin D deficiency (n = 17 group 1, n = 18 group 2, n = 18 group 3, n = 17 placebo group) / randomized controlled trial	600 IU/d (group 1), 2000 IU/d (group 2), 4000 IU/ d (group 3), or placebo	16 weeks / 16 weeks	Monthly supplementation with either 2000 IU or 4000 IU of vitamin D was similarly effective in attaining serum 25(OH)D concentrations of 30 ng/ml, whereas a daily intake of 600 IU was insufficient. Administration of 4000 IU facilitated a faster improvement in vitamin D status. Alterations were noted in parathyroid hormone levels, while no significant changes were observed in fibroblast growth factor-23, serum phosphorus, or urinary calcium excretion.
Chung et al. 2019, Korea (27)	62 children and adolescents (n = 21 obese/ overweight, n = 41 normal weight) with vitamin D deficiency / single arm trial	2000 IU/d	8 weeks / not specified	A daily dose of 2000 IU vitamin D was adequate to correct deficiency in both normal-weight and overweight children without adverse effects. Nonetheless, vitamin D sufficiency was achieved in 64% of normal-weight participants compared to 48% in those who were overweight. Among the overweight group, post-intervention reductions were observed in serum phosphorus concentrations and BMI z-scores, whereas no significant changes were noted in calcium, parathyroid hormone, or lipid parameters including total cholesterol, triglycerides, HDL, and LDL.
Brzezi´ nski et al. 2020, Poland (28)	152 overweight and obese children and adolescents (n = 85 group 1, n = 67 placebo group) with vitamin D insufficiency / randomized control trial	1200 IU/d (group 1), or placebo	26 weeks / 12 months	Although the supplementation had an impact on 25(OH)D levels, only six patients in the intervention group achieved a level above 30 ng/ml at the end of follow-up. No effect was observed on BMI.
Javed et al. 2015, USA (29)	51 obese adolescents (n = 25 group 1, n = 26 group 2) with vitamin D insufficiency / randomized controlled trial	400 IU/d (group 1) or 2000 IU/d (group 2)	12 weeks / 12 weeks	There was a modest but significant increase in 25(OH)D concentration in the group 2, but not in the group 1. Four subjects in group 1 and 6 in group 2 achieved 25(OH)D levels ≥ 30 mg/L. No effect was observed on insulin action and β-cell function
Javed et al. 2016, USA (30)	19 obese adolescents with vitamin D insufficiency / single arm trial	100,000 IU once a month	3 months / 3 months	The supplementation was effective in increasing 25(OH)D levels in obese adolescents but did not influence endothelial function. No changes in circulating and urinary calcium levels were found
Rajakumar et al. 2008, USA (31)	41 children (n = 21 obese, n = 20 normal weight) with vitamin D deficiency / non- randomized pre-post intervention	400 IU/d	1 month / 1 month	Treatment response effects were different in obese and in normal-weight cohorts. In obese children with vitamin D deficiency, the intervention did not raise blood levels of 25 (OH)D to levels ≥ 30 ng/ml. No difference in circulating calcium, phosphorus, albumin, parathormone, bone-specific ALP was observed.
Rajakumar et al. 2020, USA (32)	225 overweight/obese adolescents (n = 76 group 1, n = 74 group 2, n = 75 group 3) with vitamin D deficiency / randomized controlled trial	600 IU/d (group 1), 1000 IU/d (group 2), 2000 IU/ d (group 3)	6 months / 6 months	A dose-response in vitamin D levels was observed at 3 and 6 months. PTH concentrations were lower at 3 months in group 1, at 6 months in group 2, and at 3 and 6 months in group 3. The three regimens of supplementation did not influence endothelial function, arterial stiffness, systemic inflammation, or lipid profile, but resulted in lower blood pressure and glucose levels and higher insulin sensitivity.
Samaranayake et al. 2020, Sri Lanka (33)	96 obese children and adolescents (n = 32 group 1, n = 33 group 2, n = 31 placebo group) with vitamin D deficiency / randomized controlled trial	50,000 IU per week (group 1), 2500 IU per week (group 2), placebo (group 3)	24 weeks / 24 weeks	From baseline to 6 months, the increase in vitamin D levels in group 1 was significantly greater compared to both group 2 and group 3, while no significant difference was noted between group 2 and group 3. A clear dose-dependent reduction was observed in biceps skinfold thickness. However, changes in BMI-SD score, triceps and suprailiac skinfold thickness, waist circumference-SD score, percentage body fat, serum parathyroid hormone, LDL, AST, AST/ALT ratio, and insulin resistance were not statistically significant.
Rostampour et al. 2020, Iran (34)	53 overweight/obese children and adolescents with vitamin D deficiency / single arm trial	50,000 IU weekly for 8 weeks, and then 1000 IU/ d for 3 months.	5 months / 5 months	The intervention significantly increased circulating vitamin D levels in obese and overweight children. BMI and circulating glucose but not insulin resistance decreased after the intervention.
Magge et al. 2018, USA (35)	26 obese adolescents (n = 12 group 1, n = 14 group 2) with vitamin D deficiency / randomized controlled trial	1000 IU/d (group 1), 5000 IU/d (group 2)	12 weeks / 12 weeks	Circulating 25(OH)D levels showed a smaller increase in group 1 compared to group 2, with 30% and 83% of participants, respectively, achieving concentrations ≥ 20 ng/ml. The intervention did not result in significant changes in mineral metabolites or cardiometabolic risk markers.
Tayde et al. 2021, India (36)	44 normal weight and obese children and adolescents (n = 22 obese, n = 22 normal- weight) with vitamin D deficient / non randomized trial	150,000 IU, single oral dose	Single dose / 1 month	In obese children, the increase in circulating 25(OH)D levels was 2.2 times lower than that observed in children with normal BMI. While no significant changes were noted in iPTH levels, ALP levels were found to be elevated among obese children.
Varshney et al. 2019, India (37)	189 obese adolescents (n = 96 group 1, n = 93 group 2) / randomized controlled trial	120,000 IU one a month (group 1), 12,000 IU once a month (group 2)	12 months / 12 months	Higher dose of vitamin D was associated with a higher increase in circulating 25(OH)D levels. Vitamin D deficiency persisted in 32% subjects in group 1% and 90% in group 2. No relevant effect was observed on β cell function, cardiovascular risk factors, circulating PTH, glucose and insulin.
Vinet et al. 2021, France (38)	26 obese adolescents (n = 13 group 1, n = 13 placebo; a lifestyle program was proposed to both groups) 23 normal-weight adolescents / randomized controlled trial	4000 IU/d (group 1), or placebo	3 months / 3 months	Circulating 25(OH)D concentrations raised above 20 ng/ml in all obese adolescents, especially in those receiving vitamin D supplements. Insulin resistance decreased more in group 1 than in placebo group, while C- reactive protein decreased similarly in the two groups. Endothelium- dependent microvascular reactivity increased only in group 1.
Sethuraman et al. 2018, USA (39)	29 obese adolescents (n = 15 group 1, n = 14 placebo group) with vitamin D deficiency / randomized controlled trial	50,000 IU per week (group 1) or placebo	12 weeks / 12 weeks	A significant increase in vitamin D levels in the interventional group compared to placebo was observed, but no difference was observed for insulin- or lipid-related parameters.
De Cosmi et al. 2022, Italy (40)	108 obese children and adolescents with vitamin D deficiency. They all received dietary guidance and were randomized in 2 groups to receive or not also docosahexaenoic acid supplementation	1200 IU/d in both groups	6 months / 6 months	Over half of the participants demonstrated an improvement in vitamin D status. Both groups showed reductions in fat mass percentage and body mass index following the intervention.

25(OH)D = 25-hydroxy-vitamin D; iPTH = intact parathyroid hormone; BMI = body mass index; SD = standard deviation; HDL = high-density lipoprotein; LDL = low- density lipoprotein, ALP = alkaline phosphatase; AST = aspartate aminotransferase; ALT = alanine transaminase; SFT = skinfold thickness; WC = Waist circumference.

A total of 17 studies met the inclusion criteria, representing 1,037 participants across multiple geographical locations including the United States (n = 8), India (n = 2), Sri Lanka (n = 1), Korea (n = 1), Poland (n = 1), Iran (n = 1), France (n = 1), and Italy (n = 1). Study designs included randomized controlled trials (n = 12), non-randomized or quasi-experimental studies (n = 3), and single-arm trials (n = 2). Daily oral supplementation was the most common regimen, with doses ranging from 400 IU/day to 5000 IU/day, or intermittent high-dose regimens such as 50,000 IU/week, monthly high doses, and single mega-doses (Table 1).

Thirteen studies investigated vitamin D supplementation exclusively in adolescents (24–26, 29, 30, 31, 32, 35, 37–39), while two studies included both children and adolescents (27, 40). Two additional studies had conducted including both adolescents and young adults (26, 34). Based on the findings from the 17 studies, the total sample size consisted of 1,037 participants. Five studies included more than 100 subjects (28, 32, 33, 37, 40). Nine out of the seventeen studies compared one or more vitamin D supplementation regimens with placebo (25, 28, 29, 30, 32, 33, 35, 38, 39), while the remaining studies either compared different supplementation doses or evaluated a single dosage regimen.

Furthermore, 5 studies directly compared overweight/obese participants with normal-weight counterparts and consistently found attenuated treatment responses among obese groups (24, 27, 31, 36, 38). Overall, most trials were conducted exclusively among overweight or obese participants. Vitamin D deficiency or insufficiency was used as an inclusion criterion in all the studies (24–40). Most studies reported mean values of 25(OH)D before and after the intervention, while a few reported only changes in vitamin D concentrations.

Based on the selected studies, several supplementation regimens were tested. Eleven studies provided daily oral doses (ranging from 400 IU/day to 5000 IU/day), while others employed weekly, monthly, or single high-dose administrations (e.g.- 50,000 IU/week, 100,000 IU/month, or one-time mega-doses of 120,000–150,000 IU). Among these, higher-dose regimens (> 20,000 IU per week equivalent) consistently produced marked increases in circulating 25(OH)D, particularly among obese subjects. No adverse effects attributable to supplementation were reported.

According to the selected studies, supplementation increased serum 25-hydroxyvitamin D [25(OH)D] concentrations in overweight and obese children, although the magnitude varied. The meta-analysis of seven randomized placebo-controlled trials demonstrated that there was a pooled mean difference of 1.6 ng/mL (95% CI: 0.60–2.60) in favor of supplementation (25, 28, 29, 30, 32, 33, 39). High-dose regimens (> 20,000 IU/week) generally produced greater increases, with some trials reporting sufficiency rates above 80% (25, 33, 37). However, in several studies, fewer than half of obese participants achieved sufficiency despite supplementation (24, 27).

Most studies found no significant effect on BMI, BMI z-score, waist circumference, or body fat percentage. Exceptions included trials by Chung et al. (27), who reported reductions in BMI z-score and body fat markers after 8 weeks of 2000 IU/day, and De Cosmi et al. (40), who observed a significant reduction in fat mass percentage after 6 months of 1200 IU/day with or without DHA.

Beyond vitamin D and calcium status, cardiometabolic outcomes were frequently assessed. Thirteen studies evaluated cardiovascular or metabolic outcomes, including lipid profile, insulin resistance, glucose regulation, and blood pressure. Improvements in insulin sensitivity or reductions in fasting insulin/HOMA-IR were reported in several trials (25, 32, 34, 38, 39), although findings were not consistent across all studies.

This study investigated the effects of vitamin D supplementation on children and adolescents with overweight or obesity. According to the selected studies, supplementation increased serum 25-hydroxyvitamin D [25(OH)D] concentrations in overweight and obese children, although the magnitude varied. The meta-analysis of seven randomized placebo-controlled trials demonstrated a pooled mean difference of 1.6 ng/mL (95% CI: 0.60–2.60) in favor of supplementation (25, 28–30, 32, 33, 39). High-dose regimens (> 20,000 IU/week) generally produced greater increases, with some trials reporting sufficiency rates above 80% (25, 33, 37).

Although a statistically significant mean difference was observed, only a small proportion of obese children in some studies achieved vitamin D sufficiency. In one trial (29), only half of the obese children achieved normalization of vitamin D status compared to 89% of their non-obese counterparts. Similarly, another study (36) reported that following 8 weeks of supplementation with 2000 IU/day, 48% of overweight children reached sufficiency, whereas the proportion was 62% among normal-weight participants. Conversely, a different investigation (25) demonstrated that over 90% of obese children receiving 2000 IU/day attained serum vitamin D concentrations above 20 ng/ml. Consistent with this, a study on vitamin D–deficient subjects showed that 83% of participants treated with 5000 IU/day and 30% of those given 1000 IU/day for three months achieved 25(OH)D levels ≥ 20 ng/ml (24). Furthermore, both 50,000 IU/week and 5000 IU/day regimens proved effective in increasing 25(OH)D concentrations above 20 ng/ml in more than 80% of participants, with 72% and 56% in each group, respectively, surpassing 30 ng/ml (31).

Several mechanisms may account for the challenges in raising vitamin D levels in obese populations. One explanation is the sequestration of vitamin D in adipose tissue, which reduces its bioavailability (41, 42). Additionally, low dietary intake of vitamin D–rich foods and limited sunlight exposure, both common in this group, may further contribute to persistently low circulating 25(OH)D levels (41, 42).

Suboptimal vitamin D status can adversely affect multiple health outcomes, including cardiovascular health (37). Early studies hypothesized that improving vitamin D concentrations could mitigate cardiovascular risk. Supporting this, one trial (25) found that 6 months of supplementation with 4000 IU/day significantly improved HOMA-IR and QUICKI, both surrogate indicators of insulin resistance and sensitivity. Similarly, another study (33) reported reductions in serum insulin, triglycerides, HOMA-IR, and C-Met following supplementation. Improvements in blood pressure, fasting glucose, and insulin sensitivity were also observed in another investigation (27). In contrast, two studies reported no significant changes in cardiovascular risk parameters, including inflammatory markers (25, 33).

Six studies reported a beneficial effect of vitamin D supplementation on insulin regulation (25, 27, 28, 30, 33, 34). These findings are consistent with evidence from adult populations, which indicate an inverse association between serum 25(OH)D concentrations and insulin resistance (38, 39). A possible explanation is that vitamin D may influence inflammatory cytokine production, a key factor contributing to insulin resistance, while also playing a role in insulin secretion and activity (38).

Furthermore, Brzeziński et al. (28) reported no significant impact of vitamin D supplementation on weight reduction in children with insufficiency who were enrolled in a weight management program. In contrast, Chung et al. (27) observed improvements in BMI, BMI z-score, and body fat indices following supplementation. Similarly, De Cosmi et al. (40) found that fat mass percentage decreased significantly in supplemented participants, while BMI improved across both intervention and control groups, although all participants remained obese at study completion.

The principal limitation of this review lies in the small number of included studies and the heterogeneity among them. These constraints limit the ability to examine in greater depth the influence of additional variables such as participant age, degree of overweight/obesity, and seasonal variations, which may affect the outcomes of vitamin D supplementation.

This scoping review provides the most recent evidence regarding the impact of vitamin D supplementation in overweight and obese children and adolescents. While supplementation leads to a significant rise in serum 25(OH)D concentrations, the clinical significance of this improvement appears limited. Evidence concerning its influence on metabolic and cardiovascular outcomes remains inconsistent and inconclusive.

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The authors declare no competing interests.

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Vitamin D, Childhood Obesity, and Metabolic Risk – A Scoping Review

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Abstract

Introduction

Vitamin D: the hormone, the nutrient, and its action

Childhood prevalence of vitamin D deficiency

Interactions and implications of vitamin D deficiency in obese children\

Methods

Results

Discussion

Conclusion

References

Additional Declarations

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