Compared to fat-soluble vitamins, water-soluble vitamins are not as easily stored and have fewer concerns for toxicity with over-supplementation [39, 40].

The water-soluble B vitamins are closely linked to aging processes such as oxidative stress, inflammation, and immune pathways that contribute to the onset of frailty [6]. Among the elderly, Vitamin B6, B9, and B12 deficiencies are known to affect cognitive functioning and depressive symptoms. Vitamin B deficiencies have shared cutaneous findings such as glossitis, angular cheilitis, and mucosal erosions [41].

Vitamin B1, also known as thiamine, is solely obtained via dietary intake and is not physiologically produced. Common food sources of thiamine include bread, whole grains, nuts, and meat [42].

Low thiamine concentration has been found in many older age populations in different countries [43]. Risk factors for thiamine deficiency include a vitamin B-deficient diet, malabsorption, impaired metabolism, and a diet high in thiaminases or thiamine antagonists [42]. Thiamine levels can be evaluated by assessing the degree of thiamine diphosphate (ThDP) saturation of a thiamine-dependent enzyme (erythrocyte transketolase assay) or by measuring thiamine metabolites in accessible tissues. Though there is no universally accepted cutoff value for thiamine deficiency, the expected concentration of ThDP in whole blood is approximately 70–180 nmol/L for healthy individuals [44].

Thiamine plays a significant role in oxidative metabolism that results in ATP production; a lack of ATP causes lactic acidosis and a decrease in important neurotransmitters [42]. Initial symptoms of thiamine deficiency include short-term memory impairment, anorexia, and irritability. Prolonged deficiency can lead to more serious neurologic and cardiovascular symptoms [45, 46]. Severe thiamine deficiency can lead to Korsakoff’s syndrome, beriberi, and Wernicke’s encephalopathy, which is characterized by the triad of loss in muscle coordination, irregular eye movement, and cognitive impairments [42].

In addition to cutaneous findings shared with B-complex vitamin deficiency, dermatologic changes such as skin atrophy, hair loss, and skin glossiness can occur due to a decrease in autonomic nerve fiber production [45]. Patients with vitamin B1 deficiency have also been found to present with facial seborrheic dermatitis [38].

The RDA of vitamin B1 for adults 51 years old and greater is 1.1 mg/day and 1.2 mg/day for women and men, respectively [47]. Supplementing the diet with foods higher in Vitamin B1 is often sufficient for physiological needs. Treatment for thiamine deficiency due to alcohol abuse must be administered intravenously because alcohol abuse depletes gastrointestinal absorption [42].

Vitamin B2, also known as riboflavin, is an important enzymatic cofactor in oxidation–reduction reactions that are critical in biosynthetic processes [42]. Vitamin B2 uptake comes solely from the diet due to inability of endogenous synthesis [42]. Food sources that supplement riboflavin are mainly milk and dairy products but also include eggs, meats, nuts, legumes, and some vegetables and grains. Risk factors for deficiency include elderly age, alcohol abuse, and vegetarian diet due to insufficient dietary intake [1]. Riboflavin levels can be measured in the urine and blood, however, the erythrocyte glutathione reductase assay is a more effective biomarker of riboflavin insufficiency, with an activity coefficient > 1.4 indicating riboflavin insufficiency.

Chronic vitamin B2 deficiency can present with cheilitis, conjunctivitis, and glossitis [1]. Oculo-orogenital syndrome from vitamin B2 deficiency is characterized by these ocular and mucosal findings as well as dermatitis involving the genital region [48, 49]. Other cutaneous findings of deficiency include hair loss, edema of mucous membranes, and facial seborrheic dermatitis [1, 42].

The RDA of riboflavin for adults is 1.1 mg/day and 1.3 mg/day for women and men, respectively. In some countries, foods fortified with riboflavin assist in supplying sufficient dietary levels [42].

Vitamin B3, also known as niacin, is sourced exogenously through diet. Common food sources of niacin include meat, dairy, wheat, peanuts, yeast, mushrooms, and fish [42]. Risk factors include alcohol abuse, malabsorption, and lack of access to fortified foods (e.g. certain developing countries) [42]. Laboratory testing includes testing for tryptophan, NAD, NADP, and niacin levels [50]. Urinary excretion rate of N1-methylnicotinamide < 5.8 umol/day is suggestive of niacin deficiency [51].

Pellagra, meaning “rough skin”, can result from niacin deficiency. The “3-D’s” of pellagra refer to dermatitis, diarrhea, and dementia, and more chronic cases could result in a fourth “D”, death [42]. Classic findings include a photosensitive eruption in sun-exposed areas that progress to leathery, hyperpigmented plaques. When this hyperpigmentation occurs around the neck and on the anterior chest in a collar-shaped band, this is known as Casal’s necklace [52]. With further progression of disease, “wet pellagra” may develop with bullae or vesicles [1]. Some non-cutaneous symptoms include muscle weakness, tremors, hallucinations, and mood changes [52].

The RDA for adults is measured in niacin equivalents (NE) and is 14 mg NE/day and 16 mg NE/day for women and men, respectively [50]. Treatment for this deficiency includes average daily supplementation of 10–300 mg of vitamin B3, and up to 1000 mg for more severe cases [42].

Vitamin B6, also known as pyridoxine, is an important cofactor in many metabolic processes and a strong antioxidant that plays a critical role in neutralizing reactive oxygen species that contribute to aging [6]. Food sources of vitamin B6 include meat, fish, and many fruits and vegetables [53].

Serum levels < 20 nmol/l indicate B6 deficiency [54]. Risk factors of vitamin B6 deficiency include the elderly, irritable bowel syndrome, alcoholism, pregnancy, obesity, celiac disease, HIV, renal and hepatic disease, and certain vitamin B6-inactivating medications such as isoniazid [6]. B6 deficiency is associated with lower immune function and makes geriatric patients more susceptible to infection [6, 54].

The most common cutaneous manifestation of vitamin B6 deficiency is seborrheic dermatitis, which may be found on the scalp, face, neck, shoulders, and buttocks [1]. Early onset symptoms include dermatitis, impaired mental status, and sensory neuropathy [55]. With progression of disease, oral ulcers, glossitis, and cheilitis may develop [13]. In severe cases, pellagra (due to vitamin B6 requirement for niacin production) and neurologic symptoms such as confusion, drowsiness, and peripheral neuropathy can develop [13].

The RDA of vitamin B6 for adults older than 50 years are 1.5 mg/day and 1.7 mg/day in women and men, respectively [56]. To treat vitamin B6 deficiency, 100 mg of vitamin B6 daily is recommended [13], and in severe cases, a higher dose or intravenous administration may be required [55].

Vitamin B7, commonly known as biotin, is an essential coenzyme for five carboxylases that catalyze pathways involved in fatty acid biosynthesis, gluconeogenesis, the tricarboxylic acid cycle and other metabolic processes [57]. Dietary intake is the main source of vitamin B7, however, some enteric bacteria can synthesize biotin. Food sources with high B7 levels include egg yolk, nuts, grains, and milk [53].

Risk factors include elderly age, pregnancy, alcohol abuse, smoking, medications such as phenobarbital and carbamazepine, and prolonged use of antibiotics [58, 59]. Low urinary excretion of biotin of < 18 nmol/day is an indicator of biotin deficiency [57, 60].

Biotin deficiency initially presents as gradual hair loss and dry skin. Cutaneous manifestations of biotin deficiency are mainly due to decreased fatty acid metabolism and present as alopecia, periorificial dermatitis, and skin infections [58]. Periorificial dermatitis, also common in zinc deficiency, is characterized by red, scaly plaques around the nose, mouth, and eyes [58]. Biotin deficiency may also cause neurological and gastrointestinal symptoms such as seizures, tingling of extremities, depression, lethargy, nausea, vomiting, and anorexia [58].

The RDA of biotin for adults 19 years and older is 30 ug biotin daily [60]. Biotin deficiency can be supplemented through dietary intake of foods rich in vitamin B7 [58].

Vitamin B9, also known as folate, functions as a coenzyme in nucleic acid synthesis and amino acid metabolism. Common dietary sources of folate include leafy greens, yeast, internal organs of animals, mushrooms, and grasses [53]. Some vitamin B9 comes from the human intestinal flora [53].

Folate absorption occurs in the proximal small intestine [61]. Intestinal diseases, alcoholism, and insufficient dietary intake increase the risk of vitamin B9 deficiency in the elderly [6]. Certain drugs such as methotrexate and trimethoprim act as folate antagonists and can cause folate deficiency by inhibiting the enzyme dihydrofolate reductase, which converts unreduced dietary folates to the biologically active tetrahydrofolates [62]. Diets poor in folate can lead to deficiency in just a few weeks or months [63]. Generally, a serum folate level < 2 ng/mL is considered deficient.

Vitamin B9 deficiency can cause several disorders such as megaloblastic anemia and neuropathy [6]. Low folate levels are associated with mild cognitive impairment, Alzheimer’s disease, and depression [64, 65]. Additionally, folic acid supplementation has been shown to lower risk of stroke and overall cardiovascular diseases [66]. Cutaneous findings include glossitis, cheilitis, and mucocutaneous hyper/hypo-pigmentation [13]. Studies have shown that patients with psoriasis have lower levels of folate compared to normal controls [67].

The RDA of folate for adults 19 years and older is 400 ug daily [68]. A diet rich in fruits and vegetables will help reverse folic acid deficiency [63]. Oral supplementation with 1 to 5 mg daily of folic acid is used to treat folate deficiency [69]. Patients who cannot handle oral intake can be supplemented intravenously [63].

Vitamin B12, also called cobalamin, is derived from animal products; dietary sources include red meats, cheeses, milk, eggs, and animal livers [53].

The prevalence of vitamin B12 deficiency among geriatric populations worldwide is 10–19% [7]. Risk factors for developing vitamin B12 deficiency include malabsorption, pernicious anemia, and a history of ileocecal resection [53]. Gastric atrophy found commonly in the elderly contributes to malabsorption of vitamin B12. Additionally, certain medications like metformin can lead to gastric atrophy in geriatric patients [6].

Serum B12 levels less than 200 pg/mL are suggestive of B12 deficiency [69]. Early signs of vitamin B12 deficiency include atrophic linear lesions on the tongue and hard palate. Chronic complications can lead to neurologic disorders such as neuropathy and dementia.

Cutaneous manifestations of vitamin B12 deficiency include hyperpigmentation, typically on the face, palmar creases, and flexural areas, pigmentation of the nails, as well as vitiligo and depigmentation of the hair. Oral changes such as glossitis, stomatitis, and oral ulcers may be present [1]. Vitamin B12 has been found to be helpful for re-pigmentation in vitiligo patients, but optimal dosage for this response still needs to be identified [70].

The RDA for adults 19 years and older is 2.4 ug daily [71]. Vitamin B12 supplementation has been shown to reverse symptoms and pathologic consequences [7]. Treatment includes intramuscular injection of hydroxocobalamin daily for five days [7].

Vitamin C is a water-soluble vitamin and an important antioxidant that supports the growth of skin, cartilage, bone, and teeth [72]. Dietary intake is the only source of vitamin C. Common dietary sources include fresh fruits and vegetables such as spinach, broccoli, and red peppers [73].

Insufficient dietary intake, which is common in the elderly, is the most common risk factor for vitamin C deficiency [72]. Alcohol abuse, restrictive diet, psychiatric disease, malabsorptive disorders, bariatric surgeries, food allergies, smoking, and Type 1 diabetes are all additional risk factors [72]. Increased inflammation and oxidative stress seen in individuals with diabetes and obesity have been linked to vitamin C depletion despite dietary uptake [74].

Scurvy can develop within 4 to 12 weeks of insufficient dietary intake of vitamin C [72]. Plasma vitamin C levels < 11 umol/L indicate vitamin C deficiency [75]. Symptoms of scurvy initially include lethargy, fatigue, anorexia, and malaise, and later progress to bone and joint aches, diminished wound healing, bleeding gums, and skin rash. Further progression can manifest as ocular diseases, seizures, and organ failure [76].

Vitamin C plays an important role in collagen production. Cutaneous findings include fragile skin, impaired wound healing, petechiae, gingivitis with bleeding, corkscrew hairs, alopecia, and bruising [76]. Evidence of dermal disruption resulting from vitamin C deficiency includes perifollicular hemorrhage, dilated hair follicles, and follicular hyperkeratosis (Fig. 2) [72].

The RDA of vitamin C for adults 19 years and older is 75 mg/day and 90 mg/day in women and men, respectively [77]. Treatment of scurvy includes 500 to 1000 mg/d of vitamin C until symptoms or signs resolve, and then adequate dietary intake of Vitamin C [72].