Severe acute malnutrition (SAM) remains one of the most important preventable causes of childhood mortality in low- and middle-income countries. India carries the largest global burden of child wasting, with the National Family Health Survey-5 (NFHS-5, 2019–21) reporting a wasting prevalence of 19.3% and severe wasting of 7.7% among children under five years of age [1]. Children with SAM are highly vulnerable not only to protein-energy deficits but also to multiple micronutrient deficiencies, among which vitamin D deficiency has received increasing attention over the past decade [2,3]. Vitamin D is essential not merely for bone mineralisation but also functions as an important immunomodulator, influencing innate and adaptive immunity, insulin secretion, and skeletal muscle function [4]. Deficiency of vitamin D in early childhood has been linked with an increased susceptibility to respiratory tract infections, diarrhoeal illness, sepsis and delayed catch-up growth, all of which are already heightened risks in children with SAM [5,6]. The pathophysiology of SAM itself predisposes to vitamin D deficiency through reduced dietary intake of vitamin D and calcium, malabsorption secondary to enteropathy, hepatic and renal dysfunction affecting hydroxylation of vitamin D, and reduced outdoor activity due to illness and hospitalisation [7]. Several Indian studies conducted over the last decade have documented a high prevalence of vitamin D deficiency among hospitalised children, ranging from 40% to over 70% depending on the population studied, the assay used and the cut-offs applied [8,9]. Gupta et al. [10] reported vitamin D deficiency in nearly two-thirds of children with SAM admitted to a nutrition rehabilitation centre in northern India, while a study from eastern India by Chowdhury and colleagues [11] found a significant correlation between the severity of wasting and lower serum 25(OH)D levels. Similarly, Choudhary et al. [12] observed that inadequate sun exposure and prolonged exclusive breastfeeding without supplementation were important determinants of vitamin D status in malnourished children in a western Indian cohort. Despite the widely prevalent belief that a tropical country such as India, with abundant sunshine throughout the year, should have a low burden of vitamin D deficiency, multiple population-based and hospital-based studies have consistently demonstrated a paradoxically high prevalence, attributable to factors such as atmospheric pollution, cultural practices of limited skin exposure, skin pigmentation, and indoor lifestyles [13,14]. The World Health Organization's updated guideline on the management of SAM emphasises correction of micronutrient deficiencies, including vitamin D, as an integral part of the treatment protocol, yet routine biochemical screening for vitamin D status is not uniformly practised in resource-limited nutrition rehabilitation centres across India [15]. Furthermore, most existing Indian literature on this subject predates 2022 and there is a paucity of recent data examining the interplay between vitamin D status, biochemical bone markers, and the specific dietary and environmental risk factors unique to children with SAM managed in a tertiary teaching hospital setting [16,17]. Against this background, the present study was undertaken with the objective of estimating the prevalence of vitamin D deficiency among children aged 6–59 months admitted with SAM to the Nutrition Rehabilitation Centre of a tertiary care teaching hospital in India, and to identify the sociodemographic, nutritional and clinical risk factors independently associated with vitamin D deficiency in this vulnerable population. It was hypothesised that vitamin D deficiency would be highly prevalent in this cohort and would correlate with modifiable risk factors such as sun exposure, dietary supplementation practices and socioeconomic status, findings that could inform the strengthening of existing nutritional rehabilitation protocols.

Study design and setting This was a hospital-based, cross-sectional, observational study conducted in the Department of Paediatrics, at the Nutrition Rehabilitation Centre (NRC) and Paediatric ward of a tertiary care teaching hospital in India, over a period of 18 months. The hospital serves as a referral centre for a mixed urban and rural population and functions as a Facility-Based Management of SAM unit as per national guidelines. Study population Children aged 6 to 59 months admitted with a diagnosis of severe acute malnutrition, defined as per WHO and Indian Academy of Paediatrics (IAP) criteria — weight-for-height/length Z-score less than −3 SD, and/or mid-upper arm circumference (MUAC) less than 11.5 cm, and/or presence of bilateral pitting pedal oedema — were enrolled consecutively after obtaining informed written consent from parents or legal guardians. Inclusion and exclusion criteria Children aged 6–59 months fulfilling WHO/IAP criteria for SAM and whose caregivers provided informed consent were included. Children with known chronic renal disease, chronic liver disease, congenital skeletal dysplasia, those already receiving vitamin D or calcium supplementation in pharmacological doses within the preceding three months, and children with HIV infection or other conditions known to independently affect vitamin D metabolism were excluded from the study. Sample size Based on a previously reported prevalence of vitamin D deficiency of approximately 55% among children with SAM [10], with an absolute precision of 8% and 95% confidence level, the minimum calculated sample size was 138. Accounting for approximately 10% non-response/attrition, a final sample of 150 children was enrolled using consecutive sampling. Data collection procedure A pre-tested, structured proforma was used to record sociodemographic details (age, sex, residence, socioeconomic status graded using the Modified B.G. Prasad classification updated for the All-India Consumer Price Index), dietary history (duration of exclusive breastfeeding, complementary feeding practices, vitamin D/multivitamin supplementation history), sun exposure history (duration and body surface area exposed per day, use of sunscreen or fully covering clothing), maternal history (antenatal vitamin D supplementation, maternal skin exposure), and clinical details (grade and type of SAM, associated infections, anthropometry including weight, height/length and MUAC measured using standardised WHO techniques). Biochemical analysis Under aseptic precautions, 3 mL of venous blood was collected from each enrolled child at admission, prior to initiation of any vitamin D or mineral supplementation. Serum 25-hydroxyvitamin D [25(OH)D] was measured by chemiluminescence immunoassay (CLIA). Serum calcium, phosphorus, alkaline phosphatase and albumin were estimated using standard automated biochemical analyser methods. Haemoglobin was measured using an automated haematology cell counter. Vitamin D status was categorised, in accordance with the Endocrine Society and Indian Academy of Pediatrics consensus cut-offs, as deficient (serum 25(OH)D <12 ng/mL), insufficient (12–20 ng/mL) and sufficient (>20 ng/mL). Statistical analysis Data were entered in Microsoft Excel and analysed using SPSS software (version 26.0). Continuous variables were expressed as mean ± standard deviation and compared using the independent samples t-test or one-way ANOVA as appropriate. Categorical variables were expressed as frequencies and percentages and compared using the chi-square test or Fisher's exact test. Variables found significant on univariate analysis (p<0.05) were entered into a multivariate binary logistic regression model to identify independent predictors of vitamin D deficiency, with results expressed as adjusted odds ratio (aOR) with 95% confidence interval (CI). A p-value of less than 0.05 was considered statistically significant throughout. Ethical considerations The study protocol was approved by the Institutional Ethics Committee prior to commencement. Written informed consent was obtained from parents/guardians of all participants, and assent was sought from children where age-appropriate. Confidentiality of participant data was maintained throughout the study, and children found to be vitamin D deficient or insufficient were appropriately supplemented as per standard institutional protocol regardless of participation in the study.

A total of 150 children aged 6–59 months admitted with severe acute malnutrition were enrolled during the study period. The mean age of the study population was 22.6 ± 12.4 months, with 41.3% (n=62) belonging to the 6–23 month age group and the remainder aged 24–59 months. There was a slight male preponderance (56.0%). The majority of children belonged to lower socioeconomic strata (Class IV–V, 57.3%) and resided in rural areas (64.0%). Bilateral pitting oedema was present in 14.7% (n=22) of children, and 58.7% (n=88) had an associated infection at the time of admission, most commonly lower respiratory tract infection and acute diarrhoeal disease. Detailed demographic and clinical characteristics are presented in Table 1. Table 1: Sociodemographic and clinical characteristics of the study population (N=150) Variable Category Number (n=150) Percentage (%) Age group 6–23 months 62 41.3 24–59 months 88 58.7 Sex Male 84 56.0 Female 66 44.0 Residence Urban 54 36.0 Rural 96 64.0 Socioeconomic status (Modified B.G. Prasad scale) Class I–II (upper) 18 12.0 Class III (middle) 46 30.7 Class IV–V (lower) 86 57.3 Type of feeding in infancy Exclusive breastfeeding ≥6 months 96 64.0 Mixed/formula feeding 54 36.0 Maternal education Illiterate/primary 79 52.7 Secondary and above 71 47.3 Season of enrolment Winter (Nov–Feb) 58 38.7 Summer (Mar–Jun) 47 31.3 Monsoon (Jul–Oct) 45 30.0 Grade of SAM (WHZ/WFH) Grade III (severe wasting) 91 60.7 Bilateral pitting oedema 22 14.7 Associated infection at admission Present 88 58.7 Absent 62 41.3 The mean serum 25-hydroxyvitamin D level in the study population was 13.4 ± 6.8 ng/mL. Vitamin D deficiency (<12 ng/mL) was observed in 56.0% (n=84) of children, insufficiency (12–20 ng/mL) in 28.7% (n=43), while only 15.3% (n=23) had sufficient vitamin D levels (>20 ng/mL). Thus, a total of 84.7% of children with SAM had suboptimal (deficient or insufficient) vitamin D status. These findings are summarised in Table 2. Table 2: Distribution of vitamin D status among study participants Serum 25(OH)D level Category Number % < 12 ng/mL Deficient 84 56.0 12–20 ng/mL Insufficient 43 28.7 > 20 ng/mL Sufficient 23 15.3 Mean ± SD (ng/mL) 13.4 ± 6.8 — — On univariate analysis, several sociodemographic, dietary and clinical factors were significantly associated with vitamin D deficiency. Children with inadequate sun exposure (less than 30 minutes/day) had significantly higher rates of vitamin D deficiency compared with those with adequate exposure (69.0% vs. 36.4%, χ²=16.82, p<0.001). Lack of vitamin D/multivitamin supplementation during infancy (72.6% vs. 42.4%, p<0.001), exclusive breastfeeding beyond six months without supplementation (75.0% vs. 50.0%, p=0.002), lower socioeconomic status (66.7% vs. 45.5%, p=0.008), reported maternal vitamin D deficiency (48.8% vs. 25.8%, p=0.004), deeply pigmented skin (58.3% vs. 40.9%, p=0.038), winter season of enrolment (46.4% vs. 28.8%, p=0.030) and coexisting diarrhoeal illness (41.7% vs. 24.2%, p=0.031) were all significantly more common among vitamin D-deficient children. Rural residence and male sex showed no statistically significant association with vitamin D status in this cohort. These associations are detailed in Table 3. Table 3: Association of sociodemographic and clinical risk factors with vitamin D deficiency Risk factor Vit D deficient (n=84) n (%) Vit D non-deficient (n=66) n (%) χ² value P value No sun exposure (<30 min/day) 58 (69.0) 24 (36.4) 16.82 <0.001 Lower socioeconomic class (IV–V) 56 (66.7) 30 (45.5) 6.91 0.008 Exclusive breastfeeding beyond 6 mo without supplementation 63 (75.0) 33 (50.0) 9.85 0.002 Maternal vitamin D deficiency (reported) 41 (48.8) 17 (25.8) 8.24 0.004 Dark-skinned/deeply pigmented skin 49 (58.3) 27 (40.9) 4.31 0.038 Enrolment in winter season 39 (46.4) 19 (28.8) 4.72 0.030 Lack of vitamin D/multivitamin supplementation in infancy 61 (72.6) 28 (42.4) 13.62 <0.001 Coexisting diarrhoeal illness at admission 35 (41.7) 16 (24.2) 4.68 0.031 Rural residence 54 (64.3) 42 (63.6) 0.01 0.923 Male sex 47 (56.0) 37 (56.1) 0.001 0.987 Biochemical and anthropometric comparison revealed that vitamin D-deficient children had significantly lower mean serum calcium (8.1 ± 0.7 mg/dL vs. 9.2 ± 0.6 mg/dL, p<0.001), lower serum phosphorus (3.6 ± 0.8 mg/dL vs. 4.3 ± 0.7 mg/dL, p=0.002), lower serum albumin (2.6 ± 0.5 g/dL vs. 2.9 ± 0.4 g/dL, p=0.041) and lower haemoglobin (8.4 ± 1.3 g/dL vs. 9.1 ± 1.2 g/dL, p=0.012) compared with non-deficient children, along with significantly higher serum alkaline phosphatase (412 ± 128 IU/L vs. 298 ± 96 IU/L, p<0.001), suggestive of subclinical rickets/osteomalacia in a subset of severely deficient children. Anthropometric indices, including weight-for-height Z-score and MUAC, were also significantly lower among vitamin D-deficient children (Table 4). Table 4: Comparison of biochemical and anthropometric parameters between vitamin D-deficient and non-deficient children Parameter Vit D deficient (Mean ± SD) Vit D non-deficient (Mean ± SD) P value Serum calcium (mg/dL) 8.1 ± 0.7 9.2 ± 0.6 <0.001 Serum phosphorus (mg/dL) 3.6 ± 0.8 4.3 ± 0.7 0.002 Serum alkaline phosphatase (IU/L) 412 ± 128 298 ± 96 <0.001 Serum albumin (g/dL) 2.6 ± 0.5 2.9 ± 0.4 0.041 Haemoglobin (g/dL) 8.4 ± 1.3 9.1 ± 1.2 0.012 Weight-for-height Z score −3.9 ± 0.6 −3.6 ± 0.5 0.028 MUAC (cm) 9.8 ± 0.9 10.3 ± 0.8 0.034 On multivariate binary logistic regression analysis adjusting for potential confounders, inadequate sun exposure (adjusted OR 3.42, 95% CI 1.58–7.41, p=0.002), lack of vitamin D supplementation in infancy (adjusted OR 3.05, 95% CI 1.42–6.55, p=0.004), exclusive breastfeeding beyond six months without supplementation (adjusted OR 2.61, 95% CI 1.21–5.64, p=0.014), and lower socioeconomic status (adjusted OR 2.18, 95% CI 1.02–4.66, p=0.044) emerged as independent predictors of vitamin D deficiency in children with SAM. Maternal vitamin D deficiency showed a trend towards significance (adjusted OR 1.96, 95% CI 0.92–4.17, p=0.081) but did not reach statistical significance after adjustment (Table 5). Table 5: Multivariate logistic regression analysis of independent predictors of vitamin D deficiency Independent predictor Adjusted OR 95% CI P value No/inadequate sun exposure 3.42 1.58–7.41 0.002 Lack of vitamin D supplementation in infancy 3.05 1.42–6.55 0.004 Exclusive breastfeeding beyond 6 months without supplementation 2.61 1.21–5.64 0.014 Lower socioeconomic status (Class IV–V) 2.18 1.02–4.66 0.044 Maternal vitamin D deficiency 1.96 0.92–4.17 0.081

The present study found that vitamin D deficiency and insufficiency together affected nearly 85% of children with severe acute malnutrition admitted to a tertiary care teaching hospital in India, with frank deficiency (<12 ng/mL) present in more than half of the study population. This high burden is consistent with earlier Indian hospital-based studies. Gupta et al. [10] reported vitamin D deficiency in 62% of children with SAM at a north Indian nutrition rehabilitation centre, while Khadilkar et al. [18] observed comparably high rates among malnourished children in western India even prior to the COVID-19 pandemic, underscoring that this is a longstanding and persistent public health concern rather than a recent phenomenon. Similarly, a community-based study by Harinarayan [19] first drew attention to the so-called 'Indian paradox' — a high prevalence of vitamin D deficiency despite abundant year-round sunshine — a finding subsequently corroborated across multiple Indian regions and age groups [20]. The mean serum 25(OH)D level of 13.4 ± 6.8 ng/mL in the present cohort is comparable to that reported by Chowdhury et al. [11] (12.9 ± 5.4 ng/mL) among malnourished children in eastern India, and somewhat lower than levels reported in well-nourished Indian children by Marwaha et al. [21], supporting the biologically plausible hypothesis that the malnourished state itself predisposes to and compounds vitamin D deficiency through reduced dietary intake, fat malabsorption, and diminished hepatic 25-hydroxylation capacity secondary to protein-energy deficits [22]. Inadequate sun exposure emerged as the single strongest independent predictor of vitamin D deficiency in this study, a finding echoed by Choudhary et al. [12] and by Balasubramanian and colleagues [23], who both identified limited outdoor activity, particularly among urban slum-dwelling and hospitalised children, as a major modifiable determinant of vitamin D status in Indian children. Cultural practices of covering infants and young children, use of prophylactic sunscreen, atmospheric pollution reducing ultraviolet B penetration in urban centres, and — in the specific context of children with SAM — prolonged illness, hospitalisation and reduced physical activity, likely compound this risk [24]. The significant association between prolonged exclusive breastfeeding without vitamin D supplementation and deficiency observed in this study aligns with recommendations from the Indian Academy of Pediatrics and the WHO, both of which advocate universal vitamin D supplementation in exclusively breastfed infants, given that breast milk is a poor source of vitamin D [25]. Despite these longstanding recommendations, poor uptake of vitamin D prophylaxis has been documented repeatedly in Indian community-based surveys [26], and the present findings reinforce that this gap in preventive practice persists among the most vulnerable subgroup — children who go on to develop SAM. The inverse relationship between socioeconomic status and vitamin D deficiency observed in this study is consistent with the findings of Mittal et al. [27] and Angurana et al. [28], both of whom reported a higher burden of vitamin D deficiency among children from lower socioeconomic strata, attributable to poorer dietary diversity, reduced access to fortified foods, overcrowded living conditions limiting outdoor sun exposure, and lower parental health literacy regarding micronutrient supplementation. The biochemical findings of significantly lower serum calcium and phosphorus with elevated alkaline phosphatase among vitamin D-deficient children in this cohort are consistent with early biochemical rickets, as similarly described by Setia et al. [29] among malnourished Indian children, and highlight that vitamin D deficiency in this population extends beyond an isolated biochemical abnormality to have measurable effects on bone and mineral metabolism even before overt clinical rickets becomes apparent. The observed association between vitamin D deficiency and lower haemoglobin levels, while requiring cautious interpretation given the cross-sectional design, is in keeping with an emerging body of literature suggesting a role for vitamin D in erythropoiesis and iron metabolism [30], an area that international authors such as Smith and colleagues [31] have also explored in the context of paediatric malnutrition. Importantly, this study also found that vitamin D-deficient children with SAM had significantly worse anthropometric indices, including lower weight-for-height Z-scores and MUAC, than their non-deficient counterparts, raising the possibility of a bidirectional relationship in which malnutrition predisposes to vitamin D deficiency, which in turn may impair immune function and delay catch-up growth during nutritional rehabilitation, as has been postulated by Wagle et al. [32] and internationally by Thurnham [33]. While a causal pathway cannot be established from a cross-sectional design, these findings support the rationale for incorporating routine vitamin D assessment and supplementation into standard SAM management protocols, in line with recommendations already suggested by the Indian National Rehabilitation Centre guidelines [34]. This study has certain limitations. Its cross-sectional design precludes establishment of causal or temporal relationships between vitamin D deficiency and SAM. Single-centre enrolment may limit generalisability to other geographic and climatic regions of India. Dietary vitamin D intake was assessed through caregiver recall, which is subject to recall bias, and seasonal variation in sun exposure could not be fully captured given the fixed enrolment period. Despite these limitations, the consecutive sampling method, adequately powered sample size, and use of a validated biochemical assay strengthen the reliability of these findings and add to the relatively limited recent Indian literature on this important but often overlooked co-morbidity of SAM.

Vitamin D deficiency is highly prevalent among children with severe acute malnutrition admitted to nutrition rehabilitation services, affecting more than half of the study population in this tertiary care teaching hospital setting. Inadequate sun exposure, absence of vitamin D supplementation during infancy, prolonged exclusive breastfeeding without supplementation, and lower socioeconomic status were identified as independent risk factors. Given the demonstrated biochemical and anthropometric consequences of vitamin D deficiency in this population, routine screening of vitamin D status and its systematic correction should be considered an integral component of standard protocols for the management of severe acute malnutrition in India. Strengthening community-level vitamin D supplementation programmes, promoting safe sun exposure practices, and targeting nutritional counselling towards socioeconomically vulnerable families may help reduce this dual burden of malnutrition and micronutrient deficiency.

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