Water-Soluble Vitamins: Deficiency and Excess

General and subspecialty pediatricians frequently encounter vitamin deficiencies and excesses in their practices. However, despite the importance of these issues, there are significant education gaps, underscoring the necessity for further and deeper training on the various etiologies and manifestations of vitamin derangements.1After completing this article, readers should be able to: Discuss the risk factors and describe the clinical manifestations associated with specific water-soluble vitamin deficiencies and excesses (B1, B9, B12, and C).List the contributions of natural foods, fortified foods, and supplements in achieving the dietary reference intakes for various water-soluble vitamins.Describe the biological roles of different water-soluble vitamins and their importance in disease prevention.Discuss the utility of laboratory tests in the diagnosis of water-soluble vitamin deficiencies and excesses.Outline strategies for the treatment and prevention of various water-soluble vitamin deficiencies.Water-soluble vitamins are a group of essential dietary micronutrients. Water-soluble vitamins are not stored in the body in significant quantities, thereby requiring regular ingestion. Although this review will not cover every water-soluble vitamin, this review will focus on vitamins B1, B9, B12, and C, as these vitamins are the most common water-soluble vitamin deficiencies seen in children in the United States.The most recent National Health and Nutrition Examination survey found that 34% of children and adolescents used some form of dietary supplement in the past 30 days, with nearly half using them daily. The prevalence is higher in athletic subpopulations, such as National Collegiate Athletic Association division I athletes, among whom 45.2% reported taking supplements regularly. Supplement use was higher among underweight patients and those from higher-income, non-Hispanic Asian or white households with secure health care access.2 Supplement use has remained stable over the past 15 years, although micronutrient-enriched foods increased among food-insecure children from 24% to 31%.3 Despite varied diets and widespread fortification, deficiencies in vitamins B1, B9, B12, and C still persist in the United States, often copresenting with malabsorptive pathologies, chronic illnesses, and voluntary or involuntary dietary restrictions.4Although supplementation helps address deficiencies, it raises concerns about toxicity from exceeding upper intake levels. A recent study found 17% of vitamin A and 49% of vitamin B9 supplements exceeded safe levels.5 These findings highlight the need for physicians to be cautious about the risks of supplement use.According to the Institute of Medicine, the nutrient-based reference values used to assess and plan the diet of healthy individuals include: Recommended dietary allowance (RDA): This is the average daily nutrient intake level sufficient to meet the nutrient requirements of nearly all (97%–98%) healthy individuals in a specific life stage and gender group.Adequate intake (AI): This is a recommended intake level based on observed or experimentally determined approximations of nutrient intake by a group of healthy people. It is used when there is insufficient evidence to establish an RDA.Tolerable upper intake level (UL): This is the highest average daily nutrient intake level that is unlikely to pose a risk of adverse health effects to almost all individuals in the general population.6Thiamine, also known as vitamin B1, is an essential vitamin crucial for energy metabolism. It is vital for the proper functioning of the nervous system, heart, and muscles.7 Thiamine is found in a variety of dietary sources. Major sources include fortified and enriched whole grains (such as breads and cereals), pork, legumes, nuts, seeds, fish, beans, and some vegetables like peas and spinach. Supplements that contain thiamine are commonly taken by children and therefore should be noted by pediatricians as a potential unseen source of toxicity. The dietary reference intakes (DRIs) for children vary by age.Thiamine is essential for energy metabolism and ATP production, particularly in the citric acid cycle and in the pentose phosphate pathway. Thiamine also plays a key role in neurotransmitter synthesis and nerve function, affecting both the central and peripheral nervous systems, including acetylcholine production and myelin sheath maintenance for proper nerve conduction.8 The DRIs for children vary by age: 0 to 6 months: 0.2 mg/d (AI)7 to 12 months: 0.3 mg/d (AI)1 to 3 years: 0.5 mg/d (RDA)4 to 8 years: 0.6 mg/d (RDA)9 to 13 years: 0.9 mg/d (RDA)14 to 18 years (male): 1.2 mg/d (RDA)14 to 18 years (female): 1.0 mg/d (RDA)9Pediatric thiamine deficiency is rare in the United States and Europe, typically occurring with comorbidities that affect dietary intake. It is most common in children with autism spectrum disorder (ASD), who often have food selectivity and restrictive eating behaviors leading to nutritional inadequacies.10 A similar mechanism is seen in children with avoidant/restrictive food intake disorder (ARFID). Feeding difficulties like oropharyngeal dysphagia, common in conditions such as cerebral palsy and spinal muscular atrophy, can also cause severe malnutrition and thiamine deficiency. Thiamine studies are often ordered in adolescents with eating disorders such as anorexia nervosa and bulimia nervosa, given their high risk for nutrient deficiency. Thiamine deficiency can worsen neuropsychiatric conditions and complicate psychiatric diagnoses.11,12Thiamine deficiency is known to have several syndromic manifestations. Wernicke encephalopathy is an acute neuropsychiatric syndrome caused by thiamine deficiency. It results from impaired glucose metabolism due to thiamine's role as a cofactor in the citric acid cycle and pentose phosphate pathway, leading to neuronal damage in high-demand brain areas like the mammillary bodies, thalamus, and periaqueductal gray matter. Signs and symptoms include the classic triad of mental confusion, ophthalmoplegia (eg, nystagmus, diplopia), and gait ataxia, although this triad is present in only a minority of cases. Additional signs and symptoms may include hypothermia, hypotension, and coma. Prompt thiamine administration, typically parenterally, is essential to prevent progression to Korsakoff syndrome and severe complications. Early recognition and intervention are key for favorable outcomes: this often includes preemptive treatment when awaiting confirmative laboratory testing.13Wernicke-Korsakoff syndrome is a chronic, irreversible condition that often follows untreated or inadequately treated Wernicke encephalopathy. It is characterized by severe memory impairment, confabulation, and persistent cognitive deficits. About 80% of untreated Wernicke encephalopathy patients progress to this syndrome. It is rare in children.14Dry beriberi primarily affects the nervous system, caused by thiamine deficiency disrupting neurotransmission and myelin maintenance. This leads to peripheral neuropathy and central nervous system dysfunction. Signs and symptoms include muscle weakness, paresthesia, and loss of reflexes. Severe cases may progress to Wernicke encephalopathy, marked by confusion, ataxia, and ophthalmoplegia. For acute cases, intravenous thiamine (100–200 mg daily for several days) is recommended, followed by oral supplementation (50–100 mg daily) until recovery, and then followed by thiamine maintenance.15○ Wet beriberi primarily affects the cardiovascular system. Thiamine deficiency impairs glucose metabolism, reducing ATP production in cardiac myocytes, leading to high-output heart failure, peripheral vasodilation, and fluid retention. Signs and symptoms include tachycardia, dyspnea, edema, and signs of congestive heart failure. Severe cases may result in cardiomegaly and lactic acidosis. Treatment for thiamine deficiency is similar to dry beriberi.16The most common method for examining thiamine levels is determining the erythrocyte transketolase activity coefficient (ETKAC), which measures transketolase activity in red blood cells requiring thiamine diphosphate (TDP) as a cofactor. ETKAC is a sensitive biomarker of thiamine status, providing an indirect functional measure.17 In younger pediatric populations, direct measurement of TDP in whole blood or dried blood spots via high-performance liquid chromatography or liquid chromatography-tandem mass spectrometry is commonly used.18 Plasma levels of thiamine and its metabolites can also be measured using ELISA, which have been used to assess thiamine status in children with ASD, showing decreased TDP levels compared with healthy controls.19Folate, or vitamin B9, is vital for DNA synthesis, repair, and methylation, and amino acid metabolism. Vitamin B9 is essential for cell division, especially during periods of rapid growth, like fetal development, to prevent neural tube defects (NTDs).20Dietary folate refers to the naturally occurring form found in foods such as leafy greens, fruits, legumes, and some animal products. Total folate includes both dietary folate and synthetic folic acid added to fortified foods and supplements. Natural sources include leafy greens, fruits, legumes, and animal products, whereas fortified grains like cereals and flours also provide folate.21 The DRIs for folate are: 0 to 6 months: 65 μg/d7 to 12 months: 80 μg/d1 to 3 years: 150 μg/d4 to 8 years: 200 μg/d9 to 13 years: 300 μg/d14 to 18 years: 400 μg/d22Pure folate deficiency in children is rare, often occurring with other comorbidities or disease processes. As folate is absorbed in the jejunum, conditions that affect absorption, such as celiac disease and Crohn disease, can lead to deficiencies.23 Premature infants with reduced stores and those consuming unfortified goat milk, which lacks folate, are at higher risk.24Antiseizure medications, such as phenytoin and phenobarbital, increase hepatic enzyme activity, leading to increased folate utilization and decreased serum levels. These medications also impair intestinal folate absorption through disruption of passive folate transport and by altering the functioning of intestinal ATPase. Methotrexate is a folate antagonist that inhibits dihydrofolate reductase, which leads to a direct reduction of folate available for DNA synthesis and repair. Supplementation is frequently advised for patients receiving these medications.25Folate deficiency in children and adolescents is most often linked to megaloblastic anemia due to folate's role in DNA synthesis and repair. When deficient, thymidylate and purine synthesis is disrupted, impairing DNA synthesis. This leads to the accumulation of immature, large erythroblasts (megaloblasts) in the bone marrow, characterized by nuclear-cytoplasmic asynchrony, in which the cytoplasm matures normally, but the nucleus remains immature.26 It typically takes several months of inadequate folate intake for megaloblastic anemia to develop, with how and when clinical signs appear based on initial folate stores and the severity of deficiency.26Folate deficiency is well-known for its role in NTDs during embryogenesis. Rapid cell proliferation and differentiation, particularly in early development, are essential for neural tube closure. Folate deficiency disrupts these processes through several mechanisms. First, adequate folate ensures proper DNA synthesis and repair.27 Second, folate is a precursor for S-adenosylmethionine, which is crucial for gene expression, chromatin structure and successful neural tube closure.28 Third, folate receptor 1 is necessary for neural tube formation by mediating cell adhesion and cytoskeletal dynamics.29 Lastly, folate deficiency reduces DNA and histone methylation, impacting key developmental genes, such as Sox2, which can lead to neural crest defects.30Although there is not a currently recommended treatment for folate deficiency aside from preventive dosing, The US Preventive Services Task Force recommends women of childbearing age take 400 to 800 μg of folic acid daily to reduce NTD risk. Further, deficiency can be treated with oral vitamin B9 (1 mg/d), increasing to 5 mg/d in malabsorptive states or high-risk pregnancies. Supplementation should start at least 1 month before conception and continue through the first trimester to ensure adequate folate levels during neural tube development.31According to the European Food Safety Authority, the tolerable upper intake levels for folic acid in children are as follows: 200 μg/d for children 1 to 3 years of age300 μg/d for children 4 to 6 years of age400 μg/d for children 7 to 10 years of age600 μg/d for children 11 to 14 years of age800 μg/d for children 15 to 17 years of ageFolate toxicity is not typically a major concern, but excessive intake can mask vitamin B12 deficiency. High folic acid levels can correct the hematologic signs and symptoms of B12 deficiency, such as megaloblastic anemia, without addressing the neurological damage, which can become irreversible.32Vitamin B12, or cobalamin, is essential for DNA synthesis, erythroblast formation, neuron myelination, and the synthesis of neurotransmitters. Vitamin B12 is mainly obtained from animal-based foods like meat, fish, poultry, eggs, and dairy. It is synthesized by bacteria and accumulates in animal tissues. Plant-based foods generally lack vitamin B12 unless fortified. Additional sources include fortified foods like breakfast cereals, plant-based milk, and nutritional yeast, which are key for people who are vegetarian and vegan. Some edible algae, like dried nori, and certain mushrooms also contain bioactive B12, although bioavailability varies.33Vitamin B12 absorption involves several steps. After ingestion, it binds to haptocorrin in saliva and gastric juices. In the stomach, gastric enzymes and acid release B12 from haptocorrin, allowing B12 to bind to intrinsic factor, which is secreted by parietal cells. This B12–intrinsic factor complex then travels to the terminal ileum. The complex is internalized, and intrinsic factor is degraded. Vitamin B12 is released into the bloodstream, binding to transcobalamin 2 for transport to tissues, including the liver for storage.34According to the Food and Nutrition Board, National Academy of Science–National Research Council, the DRIs for vitamin B12 for children are as follows: 0 to 6 months: 0.4 μg/d7 to 12 months: 0.5 μg/d1 to 3 years: 0.9 μg/d4 to 8 years: 1.2 μg/d9 to 13 years: 1.8 μg/d35Older children and adults can have low vitamin B12 intake for years before symptoms appear. Signs and symptoms of B12 deficiency include peripheral neuropathy such as numbness or tingling of the hands and feet, defects in proprioception, and symmetric dysesthesia. Commonly, patients can present with pallor and fatigue with exertional dyspnea. Conditions that impair absorption, such as pernicious anemia (intrinsic factor deficiency), gastrointestinal surgeries, or chronic diseases (eg, celiac and Crohn's), can also cause deficiency.36Infants rely on maternal stores and breast milk or formula for vitamin B12. If the mother is vitamin B12 deficient, the breast-fed infant is at high risk of deficiency, which can cause developmental delays, growth faltering (failure to thrive), and hematologic abnormalities. Treatment involves addressing both the infant's immediate needs and the underlying maternal deficiency. First-line treatment for the infant is intramuscular hydroxocobalamin injections, which rapidly correct the deficiency and normalize metabolic markers. A typical regimen includes an initial 1.0-mg dose, followed by additional doses as needed to maintain levels and prevent irreversible neurological damage.37Treatment for older children and adults involves either oral supplementation or intramuscular injections, based on deficiency severity and cause (eg, dietary insufficiency or malabsorption). Ongoing monitoring of vitamin B12 levels is essential, including regular biochemical tests and dietary assessments to prevent future deficiencies.38Vitamin B12 levels are assessed using several biomarkers to improve diagnostic accuracy and prevent deficiencies that can lead to hematologic and neurological issues, especially in at-risk populations such as pregnant women, individuals who are vegan, and infants. Serum vitamin B12 (Total B12): This is the most commonly used initial test. It measures the total amount of vitamin B12 in the blood, including both active and inactive forms. A level below approximately 148 pmol/L (200 ng/L) typically indicates deficiency.39Holotranscobalamin (HoloTC): This test measures the biologically active form of vitamin B12. HoloTC is considered a more sensitive marker than total B12, especially in the early stages of deficiency. Levels below 35 pmol/L are suggestive of deficiency.40Methylmalonic acid (MMA): Elevated levels of MMA in the blood or urine indicate vitamin B12 deficiency, as MMA accumulates when B12-dependent methylmalonyl–coenzyme A mutase activity is impaired. A serum concentration above 280 nmol/L suggests suboptimal B12 status in patients with normal renal function.40Total plasma homocysteine: Elevated homocysteine levels can also indicate B12 deficiency, as B12 is required for the conversion of homocysteine to methionine. Levels above 20 μmol/L may suggest B12 deficiency in folate-replete patients.40○ Diagnostic algorithms: Combining these tests can improve diagnostic accuracy. For example, starting with HoloTC and following up with MMA testing in cases in which HoloTC levels are in the indeterminate range (23–75 pmol/L) can help identify additional deficient cases.40Vitamin C, or ascorbic acid, is essential for processes like collagen synthesis and antioxidant functions.41 Although rare today, scurvy remains difficult to diagnose because of nonspecific symptoms that mimic other conditions, such as vasculitis or hematologic disorders. At-risk pediatric populations include those with restrictive diets or malabsorptive syndromes, whereas adults with alcohol use disorder may also develop scurvy.42Vitamin C is absorbed in the small intestine, primarily the duodenum and jejunum.43 In the body, vitamin C acts as a potent antioxidant and cofactor for enzymatic reactions. It is vital for collagen synthesis, essential for connective tissue formation, wound healing, and blood vessel integrity. Additionally, vitamin C helps in synthesizing neurotransmitters and L-carnitine, and certain peptide hormone dietary sources of vitamin C include citrus fruits (such as oranges and grapefruits), tomatoes, broccoli, strawberries, and bell peppers. For example, 1 orange provides approximately 70 mg of vitamin C. It is also commonly found in multivitamins and in supplement form.44Nicotine exposure affects vitamin C requirements because of increased oxidative stress and higher vitamin C turnover, thereby requiring a higher intake of vitamin C. As a result, the American Association of Clinical Endocrinologists recommends increasing intake by 35% to 40% to meet these needs. This is of critical concern as a growing number of adolescents are consuming vape and oral products with high levels of nicotine. Vitamin C absorption is dose-dependent, with kidneys regulating its levels. Excessive intake is usually well-tolerated but may cause gastrointestinal upset and osmotic diarrhea.45The RDA for vitamin C is supported by the guidelines published by the American Association of Clinical Endocrinologists, the American College of Endocrinology, and The Obesity Society: 15 to 45 mg/d: 1 to 13 years age65 to 75 mg/d: 14 to 18 years of ageVitamin C deficiency, or scurvy, results from inadequate intake or absorption, impairing collagen synthesis because of the lack of ascorbic acid. Vitamin C deficiency weakens connective tissues, causing signs such as perifollicular hemorrhages, corkscrew hairs, petechiae, gingival bleeding, and impaired wound healing.45 Severe deficiency can also lead to anemia, fatigue, and joint pain.46 Vitamin C enhances iron absorption by reducing ferric iron (Fe3+) to ferrous iron (Fe2+), which is more easily absorbed in the small intestine. Vitamin C also forms a chelate with iron, increasing bioavailability, especially for people who are vegan and consume nonheme iron from plant-based foods.47Immediate vitamin C repletion is the standard treatment for scurvy. Oral supplementation of 100 to 300 mg daily is first-line therapy, with rapid improvement often seen within days and full recovery in weeks. Children with scurvy may have underlying conditions that make oral supplementation difficult, in which case intravenous administration and hospitalization may be necessary. For children with restrictive eating patterns due to ASD, gastrostomy tube placement and formula feeding may be required for definitive treatment if oral dietary changes are not possible.48The gold standard for diagnosing vitamin C deficiency is measuring serum ascorbic acid levels. Levels below 23 μmol/L indicate deficiency. Because vitamin C deficiency can affect bones, vessels, and soft tissues, magnetic resonance imaging (MRI) findings may include increased T2-weighted signal in lower-extremity long bone metaphyzes, periosteal reaction, and soft-tissue edema. These findings are not diagnostic but may assist in diagnosing scurvy.49This review does not include a discussion of every water-soluble vitamin. Of note, vitamin B2 (riboflavin) plays a critical role in neurological and cognitive development and in protecting DNA damage from oxidative stress. It is frequently supplemented in processed foods in the United States.50 Vitamin B3 (niacin) is also critical for neurological development as it is necessary for the synthesis of nicotinamide adenine dinucleotide. Deficiency can classically cause pellagra, a life-threatening condition characterized by dermatitis, diarrhea, and mental status changes. Providers should be keen to identify this condition in children who might be consuming heavily maize-based diets, as that staple is low in vitamin B3.51,52 Vitamin B5 (pantothenic acid) is a precursor for coenzyme A, which is essential for the metabolism of carbohydrates, fats, and proteins.53 Vitamin B6 (pyridoxine) is critical for serotonin, dopamine, and gamma-aminobutyric acid synthesis, as well as immune function by serving as a cofactor in interleukin-2 production. Vitamin B6 supplementation is useful in vitamin B6-dependent epilepsies (pyridoxine-dependent epilepsy and pyridoxamine 5′-phosphate oxidase deficiency); inborn errors of metabolism, such as hyperprolinemia type 2 and hypophosphatasia; isoniazid use, which leads to vitamin B6 deficiency; renal dialysis; and at times to mitigate the neuropsychiatric adverse effects of the antiseizure medication, levetiracetam.54,55 Lastly, vitamin B7 (biotin) is a coenzyme for carboxylases used in fatty acid synthesis, amino acid catabolism, and gluconeogenesis. It is also critical for maintaining a healthy skin barrier. Classically, overconsumption of egg whites can lead to deficiency because of the high content of avidin, a protein that binds vitamin B7 and prevents its absorption.56Vitamin deficiencies are a significant concern in pediatrics, especially among children with restrictive diets, malabsorptive disorders, chronic illnesses, and socioeconomic barriers. Despite widespread supplementation, deficiencies in water-soluble vitamins such as thiamine (B1), folate (B9), and cobalamin (B12) persist with serious neurological, hematologic, and metabolic risks.Pediatricians are key in identifying at-risk populations, using appropriate laboratory assessments, and implementing timely interventions. Diagnosis should be based on clinical suspicion, dietary history, and biochemical markers such as ETKAC for thiamine, methylmalonic acid for B12, and serum ascorbic acid for vitamin C deficiency.Management includes dietary changes, oral supplementation, and parenteral therapy for severe cases, which are often best managed with diverse teams that include registered dietitians. Preventive measures, such as nutritional screening and caregiver education, particularly in high-risk populations, help reduce deficiency-related morbidity.Dietary restriction: Children with ASD, ARFID, and selective eating behaviors are at heightened risk for multiple micronutrient deficiencies. ○ Evidence level: B (observational studies, expert consensus).11–13Malabsorptive conditions: Celiac disease, Crohn disease, and cystic fibrosis impair vitamin absorption, necessitating routine monitoring. ○ Evidence level: A (strong evidence from clinical guidelines and cohort studies).24,35,37,39,43Chronic illnesses and medication use: Anticonvulsants (eg, phenytoin, phenobarbital) increase folate metabolism, whereas metformin and proton pump inhibitors impair B12 absorption. ○ Evidence level: A (multiple studies and pharmacologic data).26Socioeconomic barriers: Food insecurity contributes to inadequate intake of fresh fruits, vegetables, and fortified foods, increasing risk for vitamin C, iron, and folate deficiencies. ○ Evidence level: B (population health data, public health studies).4,22,36Vitamin B1 (thiamine): ETKAC is the most sensitive marker for vitamin B1, with whole-blood thiamine diphosphate preferred in young children. ○ Evidence level: A (biochemical validation studies).18Vitamin B9 (folate): Serum folate levels may not reflect intracellular status; methylmalonic acid and homocysteine levels can provide indirect insight. ○ Evidence level: B (clinical and laboratory correlation studies).27,28,40Vitamin B12 (cobalamin): Elevated methylmalonic acid (>280 nmol/L) and homocysteine (>20 μmol/L) confirm deficiency even when serum B12 appears normal. ○ Evidence level: A (clinical diagnostics literature).40,41Vitamin C: Serum ascorbic acid levels <23 μmol/L suggest vitamin C deficiency; MRI findings in severe cases show periosteal reaction and increased T2 signal in metaphyzes. ○ Evidence level: B (case series, diagnostic imaging correlation).52Vitamin B1(Thiamine):○ Neurologic: Wernicke encephalopathy (confusion, ophthalmoplegia, ataxia) and dry beriberi (peripheral neuropathy, muscle weakness).○ Cardiac: Wet beriberi (heart failure, tachycardia, edema). ▪ Evidence level: A (neurology and cardiology consensus).14–17Vitamin B9(Folate):○ Hematologic: Megaloblastic anemia with macrocytosis.○ Neurologic: NTDs in utero, impaired cognitive development. ▪ Evidence level: A (randomized clinical trials, maternal-fetal studies).21,28–31Vitamin B12(Cobalamin):○ Hematologic: Megaloblastic anemia with hypersegmented neutrophils.○ Neurologic: Developmental delay, paresthesia, and ataxia, often irreversible if untreated. ▪ Evidence level: A (pediatric neurology data).37,39,40Vitamin C:○ Classic scurvy: Perifollicular hemorrhages, corkscrew hairs, gingival bleeding, poor wound healing.○ Systemic: Fatigue, anemia, musculoskeletal pain, pseudoparalysis. ▪ Evidence level: B (clinical case reports and reviews).45,49,50Vitamin B1: Severe deficiency (Wernicke encephalopathy) requires intravenous thiamine (100–200 mg/d), followed by oral maintenance (10–50 mg/d). ○ Evidence level: B (American Academy of Pediatrics [AAP] recommendations, preventive health literature).16Vitamin B9: Treat deficiency with oral folic acid (1 mg/d), increasing to 5 mg/d in malabsorptive states or high-risk pregnancies. ○ Evidence level: A (World Health Organization and Centers for Disease Control and Prevention guidelines).32Vitamin B12: For symptomatic deficiency, initiate intramuscular hydroxocobalamin (1 mg every other day for 2 weeks), followed by maintenance therapy (1 mg monthly IM or high-dose oral therapy). ○ Evidence level: A (hematology consensus, absorption studies).38,39Vitamin C: Treat scurvy with oral ascorbic acid (100–300 mg/d), with symptomatic improvement typically seen within days. ○ Evidence level: B (historical and modern clinical studies).51Routine screening: Integrate dietary assessments by primary pediatricians into well-child visits, emphasizing early identification of high-risk groups. ○ Evidence level: B (AAP recommendations, preventive health literature).57,58Parental Education: Provide guidance on nutrient-rich food sources and risks of unregulated supplement use. ○ Evidence level: C (expert opinion, public health recommendations).59,60Targeted supplementation: Prescribe evidence-based vitamin supplementation for at-risk populations rather than indiscriminate multivitamin use. ○ Evidence level: B (clinical practice guidelines).62,63Monitoring and follow-up: Reevaluate at-risk children every 3 to 6 months to ensure nutritional adequacy and prevent recurrence. ○ Evidence level: C (clinical consensus).61By maintaining a proactive approach in screening, diagnosis, and treatment of pediatric vitamin deficiencies, clinicians can prevent severe complications and promote optimal child development and well-being.