Thiamine, a water-soluble vitamin, is found abundantly in meat and grain products. A deficiency of thiamine is commonly referred to as beriberi. Bariatric beriberi, a condition preceding the more severe Wernicke’s encephalopathy, Korsakoff’s syndrome, and Wernicke–Korsakoff syndrome, has its highest prevalence within the first three months following a bariatric operation. Preoperative and postoperative prevalence are reported to be as high as 29 and 49 % respectively [6]. Preoperative deficiency is most commonly seen in African Americans and Hispanics. Etiologic factors are multifaceted and include non-adherence to supplementation, food intolerance, rapid weight loss, and poor hydration. In small number of cases where thiamine substitution is ineffective in clinical resolution, this may be caused by intestinal bacterial overgrowth, which results in malabsorption of thiamine [7]. AGB and laparoscopic sleeve gastrectomy are risk factors for such a deficiency as recurrent vomiting may persistently occur after these procedures. Intravenous glucose infusion before vitamin B₁ administration also presents risk to beriberi.

The fact that the body’s store of thiamine is only 30 mg with a half-life of 9–18 days explains why severe depletion can occur in such a short period with a very rapid onset of symptoms. Because the clinical presentation of beriberi is highly variable, regular laboratory evaluation of whole blood thiamine levels may be helpful for its diagnosis. Early postoperative factors leading to thiamine deficiency include nausea, food intolerance, and decreased oral intake with vomiting and constipation. This condition is historically classified into wet beriberi and dry beriberi. Dry beriberi involves the central and peripheral nervous system whereas the wet form involves the cardiovascular system. Patients with dry beriberi exhibit symptoms of paraplegia, ataxia, and peripheral neuritis, typically with an onset 4 weeks or more after operation.

Thiamine levels are measured by erythrocyte transketolase activity assay or by urine and plasma thiamin levels. It should be noted that serum thiamine responds to dietary supplementation but poorly reflects total body stores. The best single test to assess whole body thiamine is whole blood (or RBC) thiamine. Due to practical constraints of availability, post-bariatric patients displaying signs and symptoms of beriberi may begin treatment without laboratory confirmation. In patients with symptoms suggestive of nervous system involvement, head CT or MRI should be performed.

While many surgeons suggest following patients after surgery with whole blood thiamine levels at 6–12 month intervals surveillance for 3 years, consensus in monitoring guidelines for thiamine deficiency is lacking. If patients present with symptoms of Wernicke encephalopathy or acute psychoses, inpatient intravenous thiamine under close monitoring is recommended with a dose of 500 mg three times per day up to 5 days. This should be followed by intravenous thiamine 250 mg daily until clinical improvement of oculomotoric symptoms [8, 9]. Water-soluble vitamins and magnesium deficiency must be treated simultaneously.

Anamnestic and gait disorders resulting from severe beriberi are seen to be irreversible in over 50 % of patients. Central nervous system damage may even lead to coma from delayed treatment. Subclinical cases in patients with high suspicions of thiamine deficiency or early symptoms of neuropathy can be treated with 100 mg of oral thiamine daily until symptoms resolve. Bariatric candidates with preoperative marginal thiamine level can be given 100 mg oral thiamine twice daily until levels are normalized (10–64 μg/L) [10]. For prevention after surgery, standard multivitamins are sufficient. When recurrent vomiting is experienced postoperatively, oral thiamine 100 mg twice daily for 1 month is needed. Although deficiency is rare, these key points of thiamine deficiency and treatment are essential for bariatric surgeons in both large and small volume centers.

Vitamin B₆ is found in a wide range of food sources from meats to vegetables. The active form of vitamin B₆ is pyridoxal 5′-phosphate (PLP), which is vital in amino acid, glucose, and lipid metabolism. Vitamin B₆ is mainly absorbed in the jejunum and ileum through passive diffusion. B₆ deficiency is characterized by dermatitis, glossitis, angular cheilitis, conjunctivitis, neuropathy from impaired sphingosin synthesis, and impaired heme synthesis resulting in sideroblastic anemia. Vitamin B₆ deficiency should be considered when there is unresolved anemia in pre- and post-bariatric patients. The preoperative and postoperative prevalence remain poorly understood, since this deficiency is considered rare and thus the vitamin is not routinely measured. Vitamin supplementation appears to be effective in maintaining B₆ levels before and after obesity surgery. However, serum PLP levels may not be representative of vitamin B₆ status in patients on standard recommended multivitamin with normal PLP levels [11]. RBC glutamic pyruvate transaminase as a marker for B₆ instead of serum PLP has demonstrated deficiency in post-bariatric patients, suggesting greater dosage of the recommended amount may be required. Oral vitamin B₆ up to 100 mg daily may be used to treat deficiency.

A water-soluble vitamin and member of the vitamin B group, folic acid (often referred to as folate, its anion form) is also known as vitamin B₉ and plays critical roles in prevention of congenital neural tube defects. Rich sources of folate can be found in vegetables, particularly spinach and fruits, as well as in grains and liver. Deficiency may occur due to low intake and poor adherence to supplementation rather than from malabsorption, as folate is well-absorbed through both the small intestine and colon. Thus, deficiency can simply be corrected by oral supplementation [12]. Patients should also be educated that certain medications such as anticonvulsants, oral contraceptives, and cancer agents can cause folate deficiency.

The prevalence of folate deficiency is relatively low, up to 10 % preoperatively and 38 % postoperatively. Folate deficiency is particularly common in female bariatric patients during pregnancy [12, 13]. Unlike thiamine and zinc where body stores may last for years, folate stores are minimal and deficiency can appear early in the postoperative phase.

Macrocytic anemia, palpitations, irritability, hostility, and fatigue are clinical abnormalities seen with folate deficiency. Deficiency is detected by measuring red blood cell (RBC) folate levels. Serum folate can vary and reflects dietary intake rather than providing a true representation of whole-body folate status. RBC folate has proven to be a more appropriate and sensitive marker since red blood cells store 95 % of circulating folate [14].

The recommended dosage to treat deficiency after obesity surgery is up to 5 mg per day orally for up to 3 months. Gastric bypass patients on this regimen have shown to maintain normal serum levels while clear deficiency is seen in non-adherent patients. Prevention in the postoperative period is achieved by a routine multivitamin preparation consisting of at least 800 μg of folic acid daily, particularly in women of child-bearing age. In contrast to iron and vitamin B₁₂, folate contained in multivitamin preparations is sufficient to alleviate deficiency. Persistent deficiency indicates poor adherence to prescribed supplementation. It should be mentioned that excessive folic acid supplementation is a risk for vitamin B₁₂ deficiency as clinical signs and symptoms can be masked with persistence of neurologic injury. Thus, supplementation greater than 1000 mg per day is not recommended. In cases of high suspicion, homocysteine is the most sensitive marker for folate deficiency. Additionally, folate deficiency can result from vitamin B₁₂ deficiency as B₁₂ is essential in the production of active tetrahydrofolic acid [15]. Abstinence from alcohol is encouraged during treatment for deficiency as alcohol interferes with folate absorption.

Vitamin B₁₂ (cobalamin), found in fish, meat, and dairy, is critical for DNA synthesis. Deficiency can lead to both hematologic and neuropsychiatric pathologies. After iron deficiency, Vitamin B₁₂ deficiency is the second most common cause of anemia in deficient post bariatric patients. Due to the gastric and intestinal mechanisms of gastric acid and intrinsic factor in vitamin B₁₂ absorption, deficiency after gastric band or sleeve gastrectomy is rare. However, the prevalence of B₁₂ deficiency may be higher in malabsorptive procedures; deficiency has been noted in up to 35 % of patients 5 years after RYGB and up to 62 % of patients 2 years after BPD-DS [16]. These procedures are characterized by incomplete digestion and decreased production of hydrochloric acid, which is necessary for B₁₂ separation from food sources. Preoperative deficiency has been reported in up to 18 % [17]. Although human body storage of B₁₂ is adequate to maintain levels for years, vegetarians or vegans, obese patients commonly on proton pump inhibitors (or H₂ blockers) and metformin, and individuals with intestinal bacterial overgrowth are particularly prone to becoming deficient. Obesity is associated with a 4.3 fold increased in risk of B₁₂ deficiency. Each unit increase in BMI was demonstrated to result in an increased risk of 1.24 [18].

Early symptoms of B₁₂ deficiency include paresthesias and numbness of the limbs. Concentration disturbances and depression may also manifest early. Symptoms may ultimately irreversibly progress to unsteady gait and dementia. The American Society for Metabolic and Bariatric Surgery (ASMBS) recommends annual B₁₂ screening in post-bariatric patients who underwent procedures excluding the lower stomach. In healthy individuals with no history of obesity surgery, only 10 mcg of 500 mcg oral B₁₂ supplement is absorbed. Due to the fact that intrinsic factor and gastric acid are produced in the lower stomach, gastric bypass patients require oral crystalline B₁₂ supplementation.

Serum B₁₂ measurement is known to inaccurately detect deficiency in up to 30 %, and thus, high suspicion is required in the presence of symptoms and signs [19]. Serum homocysteine is the test of choice due to its high sensitivity. The methylmalonic acid serum test is also excellent, reported to be greater than 98 % specific and sensitive for B₁₂ deficiency, and can be used in combination with the serum homocysteine test. For therapy, the timing and dosage of vitamin B₁₂ are wide ranging. Treatment must account for the fact that symptoms manifest when body stores (5 mg) of B₁₂ decrease to 10 % of normal. Vitamin B₁₂ intramuscular injection of 1000 μg daily for 1 week followed by weekly injections of 1000 μg for 1 month is recommended for rapid repletion in post-bariatric patients. Monthly 1000 μg injection for life could be recommended, and neurologic disease may be irreversible [20]. Preoperative B₁₂ deficient patients may follow the abovementioned dosage for repletion preceding surgery. For maintenance postoperatively from RYGB and BPD/DS, the ASMBS recommends intramuscular 1000 μg per month or crystalline oral 350–500 μg per day for 3 months after surgery. In B₁₂ vitamin deficient patients on folate acid supplementation, there should be critical awareness that excessive folic acid supplements can mask B₁₂ deficiency. This can lead to exacerbation of neurological deterioration.

In general, iron deficiency is the most common nutritional deficiency with 9–16 % of adult women in the general population affected. This trace element is abundantly found in red meat, poultry, and leaf vegetables. Dissociation of the duodenum from chyme, food intolerance of red meat, decreased gastric acid, and anemia of chronic disease are contributing factors. Iron deficiency is found in up to 18 % of preoperative bariatric patients. Preoperative and postoperative deficiency was shown to be statistically significantly more common in men (35.5–40.7 %) than in women (14–19.1 %) [10]. As men have higher levels of cytokine and leptin than women, this contributes to hepcidin synthesis that results in decreased iron absorption. Iron deficiency is considered a long-term complication from obesity surgery that appears frequently in 20–49 % of patients. Two-year postoperative prevalence is demonstrated to be 17 % after LSG and 30 % after vertical banded gastroplasty (VBG), BPD, or RYGB . After 5 years, the prevalence rises to 45 % from RYGB and BPD [21]. In addition, many superobese patients and 51 % of menstruating women who underwent RYBG are also found to be iron deficient [22].

Signs and symptoms of iron deficiency are non-pathognomonic in nature. These include anemia, fatigue, irritability, pallor, brittle nails, Plummer–Vinson syndrome, and restless leg syndrome. Screening consists mainly of serum ferritin, serum iron, and total iron binding capacity (TIBC). It should be mentioned that ferritin, an acute phase reactant, is elevated with active disease or inflammation, including the common cold. Additional laboratory indexes can include hemoglobin and hematocrit levels. Therapy for iron deficiency involves iron supplements. The type of supplement depends upon the severity and the required speed of improvement. Parenteral iron administration (e.g., high molecular intravenous ferric carboxymaltose) is recommended for rapid responses in post-bariatric treatment. Infusion should begin with 1000 mg, then 500 mg up to the calculated dose weekly. This iron dose strategy is based on hemoglobin levels and body weight and has been shown by Evstatiev et al. to be safe and effective [23]. Due to dissociation of the duodenum from bypass surgery, oral iron is likely to be relatively ineffective, and may be associated with abdominal pain, nausea, and diarrhea. Of note, oral contraceptives can reduce blood loss in menstruating females and may be a helpful adjunct in treatment. In women with preexisting use of oral contraceptives, they may have lower requirements for iron supplementation. As preventative maintenance following obesity surgery, oral iron supplementation with oral ferrous sulfate 300 mg two times per day is used in many programs, although organic or chelated iron formulations may be better absorbed and tolerated. In low risk patients-men and postmenopausal women-, using complete multivitamins with 36 mg of ferrous sulfate may be sufficient [24]. Serum iron and TIBC should be screened at 6 months postoperatively and then annually.

While not abundant in food sources, sun exposure on human skin produces vitamin D3 and supplies 90 % of vitamin D. Vitamin D is paramount in calcium and bone metabolism, regulating parathyroid hormone functions. Preoperative and postoperative vitamin D deficiencies appear in 68 and 80 % of patients respectively as secondary hyperparathyroidism (PTH) is frequent after bariatric surgery. It is reported to be common in malabsorptive procedures, appearing in BPD-DS patients after 1 year, and to a lesser extent in SG and RYGB patients. Although SG is considered a pure restrictive procedure, vitamin D deficiency can still occur. Up to 53 % of patients are found to have increased serum PTH post-obesity surgery [25]. Despite receiving vitamin D supplementation after gastric bypass surgery, vitamin D deficiency with hyperparathyroidism is seen to continue to 50 % of patients [26]. The reasons remain unknown but may be attributed to various factors in dietary intake, season of the year, and socioeconomic status. Deficiency of vitamin D will in turn lead to decreased calcium absorption. This may result in low calcitriol, which favors fat accumulation.

Signs and symptoms of vitamin D deficiency include osteomalacia, osteoporosis, arthralgia, myalgia, fasciculation, and depression. Considering the high prevalence of preoperative deficiency, all candidates for obesity surgery should undergo 25-hydroxy vitamin D screening. Awareness should be noted that serum calcium may be low or normal with a decrease in serum phosphorus and increase in serum alkaline phosphatase. There is no agreement on recommendations for vitamin D therapy after bariatric surgery as few evidence-based regimens exist.

With severe deficiency, 50,000–150,000 IU of vitamin D3 per day can be sufficient with oral calcitriol if necessary. Some studies have recommended 5000 IU per day and 50,000 IU 2 times per day for prophylaxis and maintenance in RYGB and BPD patients correspondingly [27, 28]. Proper dosage may widely vary in each individual patient, and 25-hydroxy vitamin D levels should be monitored 2 weeks after initiation. These levels should be repeated up to every 3 months in the first year after surgery. Suggested supplementation for prevention after surgery is generally 400–800 U per day of oral vitamin D2 or D3. For patients who underwent malabsorptive procedures, vitamin D levels of ≥100 nmol/L have been demonstrated to be effective in prevention of secondary hyperparathyroidism [29]. Rigorous vitamin D supplementation is an important concern preceding and following bariatric surgery as incidences remain high.

The human body has more calcium than any other mineral as 99 % of reserves are stored in bones. Dietary sources include dairy products, leafy vegetables, and fish with edible soft bones. Out of 1000 mg of intake, only 400 mg is absorbed passively in the ileum and jejunum, and actively by 1,25 OH vitamin D in the duodenum in the presence of acid. The incidence of both preoperative and postoperative calcium deficiency is 10 % [30]. Postoperative anatomical changes, i.e., the bypass of the duodenum, the relatively short common channel in distal RYGB or BPD, and including decreased mixing of bile salts, can lead to malabsorption of calcium and vitamin D.

Acute hypocalcemia can manifests as paresthesia of the limbs and oral cavity, and progress to tetany. Cardiac arrhythmia is a serious complication and must be acutely recognized. Long-term deficiency presents with increased risk for bones fractures and osteoporosis from low bone density. Thus, clinical signs and symptoms may suddenly become apparent when skeletal calcium stores become depleted.

In determining calcium status, serum calcium levels have limited value due to serum calcium being regulated by PTH-vitamin D. Hypoalbuminemia, common after bariatric surgery, may simulate hypocalcemia because of the high affinity between albumin and calcium. Calcium excretion in 24-h urine along with alkaline phosphatase may be performed at 6 month intervals to assess calcium levels. Bone turnover and mineral density can be also measured by serum PTH and the DEXA test. Some authors recommend spine and hip DEXA scans for osteoporosis monitoring in post-RYGB and BPD patients at baseline then after 2 years [31]. In terms of prevention and treatment following obesity surgery, calcium supplementations (calcium citrate) can be up to 2000 mg daily, especially when serum PTH is increased [32]. Calcium carbonate has shown to absorb poorly in low acid environments (e.g., gastric bypass). An important consideration: oral calcium is known to hinder intestinal absorption of copper, iron, and zinc. A DEXA T-score of less than 2.5 may warrant intravenous bisphosphonates when calcium deficiency continues to persist after exhausting oral supplementations.

Vitamin A is a fat-soluble vitamin existing in numerous forms. The two different types of vitamin A are preformed vitamin A (retinols) in animal products and pro-vitamin A in plant-based products with beta-carotene being the most common. The difference is the high saturated fat and cholesterol content in animal preformed vitamin A. The active form for vitamin A is retinol. In dietary supplements, retinyl acetate or palmitate (preformed vitamin A) and beta-carotene (pro-vitamin A) are generally the usual forms. It plays an intricate role in healthy skin, bones, mucus membranes, the retina, and is important in the prevention of low-density lipoprotein oxidation (atherosclerosis prevention). Obese individuals are shown to have lower serum concentrations of vitamin A compared to the normal weight population [33]. This has been attributed to inadequate dietary intake along with tobacco smoking. Low carotenoid and alpha-tocopherol serum levels have been demonstrated to be associated with impaired glucose metabolism and insulin resistance.