*3.3.2 Vitamin B12 (cobalamin)*

Vitamin B12 (cobalamin) binds to the intrinsic factor, a protein secreted by the stomach. The complex formed is then absorbed by the small intestine [16]. Vitamin B12 deficiency post BS can result from inadequate secretion of intrinsic factor, limited gastric acidity, and most importantly from the bypassing of the duodenum, which is the main site of vitamin B12 absorption [6, 24]. Cobalamin stores in the liver are usually high and therefore vitamin B12 deficiency is rare in the first year after BS; however the incidence tends to increase on the long term [25]. The prevalence vitamin B12 deficiency is 14.3% after LSG and 16% post RYGB [26]. In addition to anemia, vitamin B12 deficiency can cause neurological and psychiatric symptoms [6] (**Table 1**). Therefore, regular screening is required (e.g., every 3 months) in the first year after BS and at least annually after that or as clinically indicated. This is particularly important with chronic use of medications that worsen B12 deficiency such as metformin, proton-pump inhibitors, and seizure medications [10]. In some instances, serum B12 may not be adequate to identify B12 deficiency; in such cases measuring serum methylmalonic acid, with or without homocysteine, should be considered to identify metabolic deficiency of B12, especially in symptomatic or in patients with history of B12 deficiency [10]. Intramuscular or intranasal regimens is preferred over oral supplementation as only 1% of oral vitamin B12 is passively absorbed without intrinsic factor [14].

#### *3.3.3 Folic acid*

Complex dietary folates are absorbed throughout the small intestine but mainly at the brush border of the duodenum and upper jejunum [16]. Since folate is absorbed throughout the small intestine, the deficiency is primarily induced by the decrease in dietary intake and to a lesser extent due to malabsorption specially after procedures that bypass the first part small intestine (RYGB, BPD/DS) [6]. Furthermore, folate deficiency can be aggravated by vitamin B12 deficiency since the latter is necessary for the conversion of inactive methyltetrahydrofolic acid to the active tetrahydrofolic acid [6]. The reported prevalence of folate deficiency after LSG and RYGB is 3.6% and 4.2% respectively [26]. Folate deficiency has been associated with a variety of symptoms (**Table 1**) [6, 23]. Maternal folate deficiency in pregnancy can cause fetal neurological abnormalities such as growth retardation, and congenital defects (neural tube) [16, 27]. Therefore, adequate folate supplementation is particularly important after malabsorptive procedures and in women of the childbearing age [10].

#### **3.4 Fat soluble vitamin deficiency post bariatric surgery**

#### *3.4.1 Vitamin A*

The absorption of vitamin A is reduced after bariatric procedures. The incidence of vitamin A deficiency is 11.1% at one year post LSG [26]. A higher prevalence is

#### *Nutritional Deficiencies Post Bariatric Surgery: A Forgotten Area Impacting Long-Term Success... DOI: http://dx.doi.org/10.5772/intechopen.95123*

reported after malabsorptive procedures where deficiency was found in up to 70% of patients 4 years after RYGB and BPD/DS [28]. This is due to fat malabsorption and steatorrhoea. Therefore, routine fat-soluble vitamin supplementation is recommended in all patients post BPD/DS [10]. The clinical manifestations of vitamin A deficits are night blindness, xerophthalmia and dry hair [6].
