Nutrition and the skin

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Definition

Nutritional dermatology covers cutaneous signs of nutrient deficiency, excess, or imbalance. The skin is a structural and metabolic interface whose appearance depends on vitamins, trace elements, essential fatty acids, and protein. Cutaneous findings may be the presenting clue — as in post-bariatric breastfeeding women whose first symptoms were skin lesions from combined deficiencies. ^[8]

Four bedside patterns organise teaching: follicular (phrynoderma; scurvy corkscrew hairs), periorificial and acral (acrodermatitis enteropathica; biotin-associated hair loss when deficiency is documented), photodistributed (pellagra Casal dermatitis), and mucocutaneous (riboflavin cheilosis, angular stomatitis, and glossitis; B12 hyperpigmentation; scurvy gingival bleeding). ^{[36][8][19][10][13]}

Severe acute malnutrition — what is sourced

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Pathophysiology — sourced nutrient-skin links

Normal skin contains high concentrations of vitamin C, which stimulates collagen synthesis and assists in antioxidant protection against UV-induced photodamage. The epidermal outer layer is highly cellular and provides the barrier; the inner dermal layer ensures strength and elasticity and gives nutritional support to the epidermis. ^[1]

The skin is the third most zinc-abundant tissue in the body. Acrodermatitis enteropathica is linked to ZIP4 in intestinal epithelium (and possibly epidermal basal keratinocytes). Zinc cannot be stored in significant amounts, so regular dietary intake is essential; ZIP4 and/or ZnT5B transport dietary zinc into the enterocyte and ZnT1 exports it to the circulation. About 70 percent of circulating zinc is bound to albumin. Excessive zinc intake can inhibit copper and iron absorption. ^[5][26]

Niacin (nicotinamide or nicotinic acid) is part of NAD and NADP coenzymes for macronutrient metabolism. Sixty milligrams of tryptophan is needed to produce 1 mg of niacin. Pellagra is niacin deficiency or disrupted niacin metabolism: dermatitis with pronounced photosensitivity, gastrointestinal symptoms, and neuropsychiatric ailments. ^[19][20]

B vitamins have overlapping mucocutaneous signs because their metabolic pathways interconnect; deficiencies often occur with alcohol abuse, chronic inflammatory disease, or antiepileptic drugs, so test for more than one micronutrient. ^[7]

Clinical features — sourced patterns

Scurvy (vitamin C). Corkscrew hairs, follicular hyperkeratosis, perifollicular haemorrhages, gingival bleeding, fatigue, and delayed wound healing. Risk includes diets devoid of fruit and vegetables, dialysis without vitamin replacement, restrictive eating, socioeconomic barriers, and food insecurity. ^[36][37][6]

Pellagra (niacin). Photosensitive dermatitis (Casal's description), diarrhoea, dementia, and death if untreated — the 4 Ds; diarrhoea and dementia may not always be present. Primary disease tracks maize/corn staple diets; secondary disease tracks chronic alcoholism, malabsorption, immunosuppressive and anti-tuberculosis drugs, and bariatric surgery. Diagnosis is primarily clinical. Therapy is causal niacinamide; a reported case used niacin 500 mg once daily until lesions resolved. Failure to treat early leads to death. ^[19][20][21]

Zinc / acrodermatitis enteropathica. Pink scaly plaques and erosions in periorificial and acral regions, with diarrhoea and alopecia in the classical triad; a bullous variant with painful acral bullae exists if diagnosis is delayed. Inherited disease is autosomal recessive zinc-transporter failure requiring oral supplementation. Acquired disease presents later with malabsorption, gastrointestinal tuberculosis, renal transplant, diuretics, angiotensin-receptor blockers, or long-term enteral nutrition; where serum zinc is unavailable, a trial of oral zinc may be given. Changela: zinc 36 mcg/dL and oral zinc sulfate 220 mg 3 times a day produced rapid resolution. Barbarot: premature TPN infants developed periorificial dermatitis despite 146 to 195 percent of 400 microg/kg/day; increased supplementation for 6 to 18 days resolved symptoms. ^{[27][28][29][30][26]}

Phrynoderma and combined post-bariatric deficiency. Monshi: two breastfeeding women after Roux-en-Y gastric bypass — follicular papules (phrynoderma with low vitamin A) versus genitoanal/acral plaques of acquired acrodermatitis enteropathica (low zinc); mixed signs, missed surgical follow-up, onset during lactation. ^[8]

Riboflavin. Severe deficiency: cheilosis, angular stomatitis, glossitis, seborrheic dermatitis, and severe anaemia with erythroid hypoplasia. Riboflavin is the precursor of FMN and FAD; humans cannot synthesise it. ^[10][9]

B12 hyperpigmentation. Mathur: symmetric pigmentation on the dorsum of hands and palms in a long-term vegetarian can be an early clue; timely treatment reverses pigmentation and systemic symptoms. ^[13]

Biotin. Congenital biotinidase lack or acquired failure of absorption (inflammatory bowel disease, avidin-rich diet, magnesium deficiency, smoking, broad-spectrum antibiotics, anticonvulsants, sulfonamides). Biotin may improve hair loss when deficiency is documented. ^[12]

Vitamin K. Ballal: nodular purpura is an uncommon infantile manifestation of late-onset vitamin K deficiency bleeding; four infants had bluish-gray nodules, hepatic dysfunction, deranged coagulation, and improvement with parenteral vitamin K. ^[16]

Iron / koilonychia. Concave nail dystrophy associated with iron-store abnormalities, Plummer-Vinson syndrome, nutritional deficiency, inflammatory dermatoses, onychomycosis, occupational trauma; transient idiopathic toenail koilonychia in young children. ^[17]

Kwashiorkor. Protein deficit despite appropriate caloric intake. Mann: xerosis with a flaking enamel-paint aspect, red to gray-white hair, the flag sign, oedema of lower limbs and face (full moon). Cohen: hair flag sign as alternating hypopigmented bands in kwashiorkor-type protein-calorie malnutrition. Maltos: flaky paint dermatosis, often bilateral, mostly in sun-unexposed areas, must be distinguished from chapped/xerotic skin and pellagra; patients showed low urinary N1-methylnicotinamide plus IDO activation with infection. Xavier: a 12-month-old with oedema, desquamation, and irritability misdiagnosed as atopic dermatitis after a potato-gelatin-juice diet. van den Brink: pigmentary changes were the most common finding in hospitalised Malawian children; severe flaky-paint dermatosis was rarely identified. ^{[22][23][24][34][35]}

Menkes disease. X-linked copper-metabolism disorder; predicted minimum birth prevalence 1 in 34,810 live male births. Therapeutic opportunity is the first 4 to 6 weeks of life. Kaler: dried-blood-spot WGS detected all studied ATP7A variants as a complement to Ohio newborn screening. This page does not teach an unsourced copper-histidinate milligram recipe. ^[15]

Keshan disease and selenium. Selenium deficiency is an established etiological risk factor for Keshan disease. Hao modelled selenium biomarkers in 6987 adults from 29 Chinese provinces (endemic vs non-endemic) plus a rat selenite experiment; biomarkers showed non-linear, threshold-saturation dynamics rather than simple linear deficiency. ^[14]

Essential fatty acids. Conventional teaching names linoleic and alpha-linolenic acids as essential; Le: patients on fish-oil lipid emulsion (AA and DHA, insignificant LA/ALA) did not develop EFAD (Mead acid/AA above 0.2, growth retardation, or dermatitis), and about 13 percent of calories from fish oil prevented EFAD in a murine model. AA and DHA alone may be the true EFAs. ^[31]

Investigations

Layer tests to the cutaneous pattern rather than a universal panel. Zinc, ferritin, and related proteins are acute-phase reactants — interpret with CRP. Where zinc assays are unavailable, Ghuge supports an empirical oral zinc trial in the right clinical setting. B-vitamin pathways overlap, so Ghosh recommends testing multiple micronutrients. Pellagra diagnosis is primarily clinical (Hołubiec). Scurvy may be confirmed by the cutaneous response to ascorbic acid (El Khoury). Menkes: ATP7A-inclusive genomic testing is entering newborn-screening workflows (Kaler). Hartnup teaching on this page is limited to Ajayi: SLC6A19 encodes the B0AT1 broad neutral amino-acid transporter among recognised aminoaciduria genes. ^{[28][7][20][36][15][33]}

Management — sourced replacement only

Replacement must match a cited regimen or stay qualitative. ^[21][29][36]

• Pellagra: niacinamide is causal therapy; Hassan used niacin 500 mg once daily until lesions resolved, with topical betamethasone plus salicylic acid. Untreated early disease leads to death. ^[20][21]
• Zinc deficiency / AE pattern: oral zinc; Changela used zinc sulfate 220 mg 3 times a day with rapid resolution. Premature TPN infants may need more than 400 microg/kg/day. Genetic AE needs ongoing supplementation. ^[29][30][27]
• Scurvy: El Khoury used ascorbic acid 500 mg twice daily for 2 weeks with complete rash resolution. Pullar favours optimising dietary vitamin C over assuming topical vitamin C is equivalent. ^[36][1]
• Severe acute malnutrition: WHO two-phase F-75 then F-100 is feasible even in small district hospitals with limited resources (Rashid RCT). ^[25]
• Vitamin K deficiency bleeding with nodular purpura: parenteral vitamin K improved coagulation and lesions in Ballal's infants. ^[16]
• Wound healing: Seth: vitamins A, B, and C and zinc positively influenced healing stages; malnutrition associated with more postoperative complications; preoperative nutritional support correlated with shorter stays. ^[3]
• Biotin hair loss: only when deficiency is documented (Piraccini). ^[12]

Unsourced milligram schedules that do not appear in these abstracts are omitted rather than guessed. ^[1][7]

Nutrition in common skin conditions

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• Psoriasis: Garbicz — metabolic syndrome is a frequent comorbidity; low-energy diet if excess weight; limit saturated fat and prefer omega-3 polyunsaturated fat; antioxidants (vitamins A, C, E, carotenoids, flavonoids, selenium) and vitamin D supplementation are discussed; gluten-free, vegetarian, or Mediterranean patterns are suggested by some authors; folic acid is introduced in persons taking methotrexate. ^[4]
• Acne nutraceuticals: Shields systematic review of 42 RCTs (3346 participants) — fair or good quality studies showed potential benefit of vitamins B5 and D, green tea extract, probiotics, and omega-3 fatty acids; adverse effects were rare except gastrointestinal effects with zinc. Elgharably: cyanocobalamin, pyridoxine, and riboflavin supplementation have been linked with exacerbating existing acne, and parenteral cobalamin can cause acne, rosacea, site reactions, or anaphylaxis. ^[32][11]
• Wound healing: as above (Seth). ^[3]

Exam pearls

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Exam application bank (NEET-PG / INICET)

One-line answer

Micronutrient deficiency produces a characteristic cutaneous signature. This page teaches sourced deficiency dermatoses (scurvy, pellagra, acrodermatitis enteropathica, phrynoderma, kwashiorkor flaky-paint, Menkes, Keshan-associated selenium) and omits unsourced refeeding milligram protocols.

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map corkscrew hairs to scurvy, Casal/4 Ds to pellagra, periorificial-acral triad to zinc, flaky paint plus oedema to kwashiorkor. Name the sourced first treatment when one exists (ascorbic acid 500 mg twice daily for 2 weeks in El Khoury; niacin 500 mg once daily in Hassan; zinc sulfate 220 mg three times daily in Changela). ^{[36][19][21][29]}

Stem 2 — Misdiagnosis trap. Kwashiorkor misdiagnosed as atopic dermatitis (Xavier); scurvy missed because the patient is not classically cachectic (El Khoury dialysis case). ^[34][36]

Stem 3 — Special group. Premature TPN zinc failure despite 400 microg/kg/day (Barbarot); post-bariatric lactation phrynoderma vs acquired AE (Monshi); vegetarian B12 pigmentation (Mathur); Menkes first 4 to 6 weeks (Kaler). ^{[30][8][13][15]}

Stem 4 — Differential. Flaky paint vs pellagra vs xerosis (Maltos); AE vs bullous AE (Iyengar); pellagra vs other photodermatoses — diagnosis is clinical (Hołubiec). ^[24][27][20]

Stem 5 — Disposition. SAM needs WHO F-75/F-100 capability; untreated pellagra can kill; genetic AE needs ongoing zinc. ^[25][20][27]

References37ShowHide

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