Secondary Logo

Journal Logo

Clinical Nutrition

Bariatric Surgery

A Double-Edged Sword

Ranjit, Rajesh MD; Alexandrovna Lapik, Irina PhD; Minkailovna Gapparova, Kamilat PhD; Vladimirovich Galchenko, Alexey MD

Author Information
doi: 10.1097/NT.0000000000000540


Obesity is a condition of a body in which an excessive or abnormal amount of adipose tissue is accumulated such that it may impair health.1 The number of individuals with obesity has doubled from 1980 to 2014 and has nearly tripled since 1975. In 2016, more than 1.9 billion people in the world were overweight, and 650 million were suffering from obesity.2 A recent study (2015-2016) in the United States has pointed out that 39.8% of adults and 18.5% of youths (body mass index [BMI] ≥95th percentile of age- and sex-specific growth charts) were suffering from obesity, that is, BMI 30 kg/m2 or greater.2,3 Morbid obesity (BMI >40 kg/m2), which represents at least 50-kg overweight,4 shortens life expectancy by 5 to 20 years.5 The prevalence of obesity has risen to a global epidemic in recent decades. Some conservative measures have been tried to treat morbid obesity. However, bariatric surgery is still superior to any medical treatment in terms of results.6 That is why bariatric operations should be performed in such patients.7–11 It should also be noted that conservative treatment such as GLP-1 RA (glucagon like peptide-1 receptor agonists)–based therapy after surgery was found to be effective to prevent postbariatric weight regain.12 Similarly, genomics of obesity also suggest that gene therapies and gene editing may have a future role in the management of some patients,13,14 but more research must be done before it can be made widely available. There are several medical indications for the surgical treatment of obesity. According to the recommendations of the American Society of Metabolic and Bariatric Surgery, operations are indicated when BMI exceeds 40 kg/m2 or when an individual with a concomitant disease such as hypertension, obstructive sleep apnea, nonalcoholic fatty liver disease, or bronchial asthma has a BMI of more than 35 kg/m2.15 Each year, the number of bariatric procedures is increasing exponentially. By 2013, more than 468 000 bariatric surgeries had been performed.16

With the implementation of these surgeries, higher rates of diabetes remission and lower risk of cardiovascular and other health outcomes have been found out.17 Similarly the surgery can also result in substantial weight loss, resolution of comorbid conditions, and improved quality of life.18 Besides decreasing weight, these surgeries have been found to improve metabolic health and prolong life for patients suffering from obesity.19

Russian Experience in the Treatment of Obesity

According to the practice in Russia, if BMI is 30 kg/m2 or greater or if there are obesity-associated diseases in patients with a BMI of 27 to 29.9 kg/m2, the prescription of pharmacological agents is recommended.

Currently, there are 5 drugs that are widely used. Orlistat (intestinal lipase inhibitor) is a peripheral drug that has a therapeutic effect within the gastrointestinal tract and does not have systemic effects. As a long-acting inhibitor of gastrointestinal lipases, orlistat prevents the breakdown and subsequent absorption of fats from food, thereby creating an energy deficit, which leads to a decrease in body weight.20

Acarbose is the next drug that is commonly used for treating obesity. It is an α-glucosidase inhibitor that treats obesity by inhibiting the digestion of oligosaccharides and disaccharides at the brush border of the small intestine.21

Similarly, metformin is also one of the widely used drugs in reducing obesity. It reduces the absorption of carbohydrates,22 decreases plasma ghrelin,23 and induces lipolysis and anorexia by activating GLP-1.24 Moreover, it also reduces insulin and leptin resistance.25

Another drug used to treat obesity is liraglutide (an analog of human GLP-1, which is a physiological regulator of appetite and food intake). It is found to have an additional effect on weight loss in diabetic patients and patients with obesity26 by inhibiting appetite27,28 and by changing the gut microbiota.29,30 Liraglutide also stimulates insulin secretion, suppresses glucagon secretion, and improves the function of pancreatic beta cells, which leads to a decreased postprandial glucose concentration. Furthermore, delayed gastric emptying also lowers blood glucose concentration.31

And finally, the next drug in use for treating obesity is sibutramine (an inhibitor of the reuptake of serotonin and norepinephrine and, to a lesser extent, dopamine, in the synapses of the central nervous system). This drug has a dual mechanism of action: it accelerates the feeling of fullness and increases the body's energy consumption, which together leads to a negative energy balance.32

Diet therapy remains the main method in the treatment of obesity. However, for most patients with morbid obesity, changing the diet over a long period is a dauntingly difficult task. A decrease in caloric intake by 500 to 1000 kcal per day usually leads to a decrease in body weight by 0.5 to 1.0 kg per week. This rate of weight loss persists for 3 to 6 months. But, on the other hand, a decreased body mass inadvertently leads to a decreased basal metabolic rate by 16 kcal/kg per day in men and by 12 kcal/kg per day in women.33 So, eventually, the body acquires a steady state, and body weight decrease slows. After this, pharmacotherapy is added to diet therapy.

But, unfortunately, a long-term sustained positive effect cannot always be obtained, especially in patients with morbid obesity; therefore, bariatric surgery is recommended for this category of patients. In Russia, surgery is considered to be indicated as per guidelines of the World Association for Surgery of Obesity and Metabolic Disorders, European interdisciplinary guidelines for metabolic and bariatric surgery, and National Clinical Guidelines for the treatment of morbid obesity in adults.33

Currently, in Russia, bariatric surgery is widely carried out for morbid obesity (BMI ≥40 kg/m2) and obesity with BMI ≥35 kg/m2 or greater in combination with severe concomitant diseases that are poorly controlled by lifestyle changes and drug therapy. The number of bariatric surgeries in Russia is increasing every year. According to the data, 16 980 operations have been performed in Russia since 1999. Half of these interventions were longitudinal gastric resection (49%). Forty-eight percent of all operations were performed in Moscow.34


An electronic search was conducted in PubMed. A MeSH search was done with terms including “Micronutrients” AND “Bariatric Surgery.” The details of selection criteria are shown in the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) flow diagram in Figure 1. Eventually, 63 studies were selected as eligible for our review.

PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) flow diagram of study selection process.


Micronutrient Status in Individuals With Obesity Before Bariatric Intervention

Bariatric surgery implies an artificial disruption of the gastrointestinal tract. However, this intervention not only reduces the amount of ingested food but also disrupts its digestion and reduces the availability of micronutrients. Moreover, many authors agree that some individuals with obesity already have micronutrient deficiencies even before surgery35–38 due to consumption of a diet low in nutritional quality,38,39 which may adversely affect nutritional status. For example, hepcidin is a hormone secreted by the liver whose level is regulated by iron overload and by inflammation.40,41 These conditions trigger the mechanisms that inhibit iron entry into the circulation by the disintegration of iron exporter ferroportin-1, thereby blocking its absorption from the gastrointestinal tract, and by locking iron inside hepatocytes.42,43 As inflammation accompanies severe obesity,44 a higher amount of hepcidin is produced that inhibits iron absorption and release of iron from the hepatocytes. The effect is more profound in females, who are already at higher risk of being deficient in iron.

Many studies show that patients with morbid obesity, even before undergoing bariatric surgery, already have multiple micronutrient deficiencies. Several studies have found that in patients with morbid obesity, serum concentrations of 25(OH)D, folic acid, and vitamins B12 and A were reduced before bariatric intervention.45–48 A number of studies have found that vitamin D deficiency is a characteristic feature of the majority of the patients before bariatric surgery.49–51 In a systematic review, Chakhtoura et al52 have analyzed 51 different studies and have found the mean presurgery calcidiol level in 29 studies to be less than 30 ng/mL and in 17 studies to be less than 20 ng/mL. Before undergoing bariatric intervention, most patients with morbid obesity were simultaneously deficient in 3 or more micronutrients (folate; vitamins B12, B6, D, and A; sodium; chlorine; calcium; phosphorus; magnesium; and iron).39,53–61 At the same time, a decrease in serum iron was more frequently observed in women before the surgery than in men.62 The detailed information is presented in Table 1.

TABLE 1 - Deficiency of Vitamins and Chemical Elements in Patients With Morbid Obesity Before Bariatric Surgery
Micronutrient Percentage of Deficiency References
25(ОН)D 100% Bodunova et al63
97.9% Ben-Porat et al56
97.5% Krzizek et al45
93% Peterson et al49
83%–86% Verger et al64
83% Malek et al65
83% Damms-Machado et al; Wang et al53,66
81% Van Rutte et al54
76.9% Sun et al35
75.6% Al-Mutawa et al59
74.35% Arias et al67
68% Lefebvre et al55
60% Grace et al68; Al-Mulhim60
58%–65% Homan et al69
53.6% Asghari et al61
39.5% Schiavo et al (2019)70
35.2% Paredes et al51
35% Remedios et al71
33% Ybarra et al72
20.4% Gillon et al73
Folic acid 63.2% Krzizek et al45
32.2% Wang et al53
25% (1 y before LG) Bodunova et al63
24% Van Rutte et al54
20% (1 y before GBn) Bodunova et al63
15.8% Bloomberg et al74
13% Madan et al46
8.8% Gillon et al73
7.4% Paredes et al51
5.3% Peterson et al49
5.5% Damms-Machado et al66
3%–4% Patel et al75
0%–2% Homan et al69
0.9% Al-Mulhim60
0% Al-Mutawa et al59
0% Sun et al35
Vitamin В12 56.7% Remedios et al71
50% Malek et al65
34.4% Asghari et al61
16% Al-Mutawa et al59
13.9% Antoine et al76
13% Madan et al46
12.3% Arias et al67
11.7% Ben-Porat et al56
10.5% Schiavo et al (2019)70
10% (before LG) Ferraz et al77
9.3% Damms-Machado et al66
9% (before GBy) Ferraz et al77
8.4% Lefebvre et al55
7%–8% Homan et al69
6.4% Gillon et al73
5.1% Krzizek et al45
4.7% Wang et al53
4.6% Paredes et al51
3.6% Schweiger et al47
3.5% Peterson et al49
3%–8% Patel et al75
3%–5% Verger et al64
1.8% Al-Mulhim60
0% Sun et al35
Vitamin В6 24% Van Rutte et al54
11% Damms-Machado et al66
0% Sun et al35
Vitamin А 70% (1 y before GBy) Bodunova et al63
52.5% (1 y before LG) Bodunova et al63
23% Coupaye et al (2009)78
21% Pereira et al (2013) group 179
21% Pereira et al (2013) group 279
20% Pereira et al (2013) group 379
17% Lefebvre et al55
16% Coupaye et al (2014)80
14% Pereira et al (2009)81
14% Coupaye et al (2009)78
9% Donadelli et al82
7% Madan et al46
7% Aasheim et al (2009)83
7% Ledoux et al84
6.2% Krzizek et al45
1.7% Peterson et al49
1.61% Sun et al35
0% Aasheim et al (2012)85
0% Schollnberger et al86
0% Provenzale et al87
0% Damms-Machado et al66
0% Van Rutte et al54
Iron 57% Peterson et al49
51% Al-Mutawa et al59
43% Remedios et al71
40.4% Ben-Porat et al56
38% Van Rutte et al54
29% Damms-Machado et al66
26.3% Bloomberg et al74
29% (before GBy) Ferraz et al77
24% (before LG) Ferraz et al77
18.% Paredes et al51
17.3% Lefebvre et al55
11.6% Al-Mulhim60
10.2% Asghari et al61
9.6% Krzizek et al45
9% Wang et al53
7%–37% Patel et al75
7%–18% Verger et al64
4%–8% Homan et al69
3.16% Sun et al35
2.77% Gobato et al88
Calcium 13.7% Wang et al53
11% Remedios et al71
4.05% Sun et al35
4% Paredes et al51
1.3% Lefebvre et al55
0.5% Van Rutte et al54
Magnesium 35.4% Lefebvre et al55
13.1% Paredes et al51
0% Sun et al35
Phosphorous 21.6% Lefebvre et al55
10.4% Wang et al53
0% Sun et al35
Sodium 11.02% Sun et al35
7.6% Wang et al53
Chlorine 15.6% Wang et al53
10.48% Sun et al35
Zinc 55.5% Gobato et al88
40% (before LG) Ferraz et al77
34% (before GBy) Ferraz et al77
14–50 Patel et al75
10.16% Sun et al35
7.9% Schiavo et al (2019)70
Abbreviations: GBn, gastric banding; GBy, gastric bypass; LG, longitudinal gastrectomy.

Thus, it is clear that many patients today have serious micronutrient disorders even before surgery; especially deficiencies of folate, vitamins D and B12, iron, and magnesium are observed. In all cases, it is necessary to monitor the micronutrient status before performing bariatric surgery. If a deficit is identified, it is necessary to replenish it. Uncorrected deficiency of iron, folate or Vitamin B12, particularly in the combined form, can seriously disrupt hematopoiesis in the postoperative period, especially in the case of blood loss. Lack of zinc and vitamin D significantly increases the risk of infectious complications and deficiency of magnesium and potassium—disorders in the cardiovascular system. In addition, numerous delayed consequences are possible.

Bariatric Surgery: Types, Outcomes, and Complications

There are three types of bariatric surgeries: blocking (malabsorption), restrictive, and mixed (Figure 2 and Table 2)92–96 Blocking procedures restrict the absorption of nutrients by cutting off a part of the intestine from digestion. Restrictive surgery reduces the volume of the stomach and limits the amount of food intake. Mixed surgery includes a combination of restrictive and malabsorptive surgeries.97 Mixed surgeries (gastric bypass [GBy], biliopancreatic diversion [BPD]) provide a more significant reduction in body weight.97 However, after such operations, patients require micronutrient supplement therapy, as metabolic disorders are among its’ frequent adverse effects.98

Schemes of different types of bariatric surgeries.90
TABLE 2 - Different Types of Bariatric Surgeries and Their Brief Procedures63,91
Types of Bariatric Surgeries Procedure
Restrictive LG The main essence of these types of operations is to either shrink down the size of the stomach or occupy space inside the stomach, such that the patient would feel more full when they eat less. In LG, a large portion of the stomach, following the major curve is surgically removed. After the surgery, the stomach acquires a tube-like structure, which is like a banana in shape, and the size of the stomach is reduced to 60-150 mL. It is to be noted that the change is irreversible.
GBn In this procedure, an inflatable silicone device is installed around the top of the stomach such that a smaller stomach pouch is formed. The smaller pouch gets filled quickly and a false message is sent to the brain that the entire stomach is full, which gives the sensation of satiety. Thus, it down-regulates the intake of food by slowing down the amount of food consumed at each meal. As the patient loses weight, the size of the gastric band is changed by introducing saline solution through the port placed under the skin.
IGB IGB involves introducing a deflated balloon into the stomach. The balloon is then filled with saline or radioactive marker, which subsequently reduces the gastric space for the food consumed by the patient. This method treats obesity by increasing satiety, delaying gastric emptying, and reducing the amount of food eaten at one time.
Blocking (JIB) The essence of the different blocking surgeries is related to the shunting of the various parts of the small intestine, which reduces the absorption of food. This type of surgical intervention is no longer performed.
Mixed GBy In mixed surgeries, both restrictive and blocking methods are applied at the same time in the same patient. It includes 2 different components: restrictive and blocking surgeries. Initially, the stomach is surgically divided into 2 parts—the upper smaller pouch and the lower much larger pouch. Then, the intestine is rearranged such that it gets connected with both of these. There are different ways to connect the intestine, thus there exist different variations of this procedure. The Roux-en-Y gastric bypass is the most common variant of this type of surgery. In this operation, the small intestine is cut approximately 45 cm below the lower stomach, and the distal outlet is connected with the smaller upper stomach pouch. The other proximal end of the intestine is also connected with the intestine forming Y-intersection.
BPD In this procedure, longitudinal resection of the stomach is performed along its greater curve. The stomach is then disconnected from the duodenum and reconnected to the distal small intestine, nearly at approximately 75-100 cm from the colon.
Abbreviations: BPD, biliopancreatic diversion; GBn, gastric banding; GBy, gastric bypass; IGB, intragastric balloon; JIB, jejunoileal bypass; LG, longitudinal gastrectomy.

Blocking Surgery

Today, these procedures are usually not performed because of the numerous complications. For example, jejunoileal bypass (JIB) reduces the length and area of the inner surface of the small intestine, impairing food digestion and absorption of nutrients.99Although the surgery is effective in decreasing body weight, it is rife with complications: a decrease in the levels of sodium, potassium, magnesium, bicarbonate, chloride, calcium, B vitamins and vitamin D leads to osteoporosis, secondary hyperparathyroidism, phosphaturia, and oxaluria; iron deficiency, folic acid, and vitamin B12 deficiency may cause anemia; and hypoproteinemia with hypoalbuminemia may be seen due to insufficient protein absorption.100 Extensive resection of the small intestine causes malabsorption of carbohydrates and an increase in the osmolarity of the chyme. Because of the malabsorptions of the fats and bile acids, steatorrhea may develop.101 In addition, the ingress of free bile acids into the large intestine inhibits the absorption of sodium ions and stimulates the secretion of chloride, causing diarrhea. As a result of microbial contamination, disturbances of microcirculation on the wall of the small intestine, and irritation of the wall of the large intestine with bile acids, enteritis develops.102 These complications arise from the active multiplication of bacteria in the area of intestinal anastomoses. From 1960 to 1970, approximately 100 000 JIB operations were performed in the world.103 However, because of a large number of complications, these surgical interventions were almost redundant by the beginning of the 1980s. Currently, only some modifications of this operation are used with the formation of various lengths of the ileum, which is determined by the patient's body weight, gender, and age.

Restrictive Operations

Restrictive operations on the stomach (installation of an intragastric balloon, gastric banding [GBn], sleeve gastrectomy, or longitudinal gastrectomy [LG]) are physiologically more appropriate. After such surgical interventions, there is a decrease in body weight and a low rate of postoperative complications. Similarly, there is an absence of unwanted metabolic disorders with a minimum amount of replacement therapy. When carrying out restrictive operations, the volume of the stomach is decreased or its lumen has narrowed, leading to a decrease in the volume of food consumed.

Intragastric balloons are used as a temporary measure for weight loss in patients with a BMI of 35 to 38 kg/m2.104 The balloon is placed with the help of a gastroscope for 6 months. Common complications of intragastric balloons include gastric erosion and obstructive intestinal obstruction.

Gastric banding is used in patients with a BMI of 35 to 45 kg/m2. But, nowadays, it has been applied to people with a BMI of less than 35 kg/m2 as well. The purpose of the operation is to drastically reduce the amount of food consumed. This goal is achieved by placing a special ring (band) on the upper part of the stomach, below the gastroesophageal junction. After this surgery, complications such as gastric erosion around the band and band displacement may occur.105,106 As a result of the displacement of the ring, patients may need to repeat the surgical interventions. So, in Europe, the relative number of operations performed with this method has decreased from 63.7% in 2003 to 17.8% in 2011.107

In 2006 longitudinal gastrectomy was introduced as an independent method of bariatric surgery.108 Until that time, gastrectomy had been a part of a more complex operation, BPD, which significantly reduced not only the body fat mass but also normalized carbohydrate metabolism.109 With LG, 80% to 90% of the stomach is resected, which reduces its volume to 100-150 mL. In this case, the patient's intestines remain unaffected, which eliminates the risk of a number of metabolic complications. As a result of LG, patients lose nearly up to 80% of their excess body weight.110 However, the long-term consequences of the operation have not yet been sufficiently studied because this surgical method is relatively new. Currently, the results of the LG are being actively studied, and the procedure is constantly being improved. Unlike operations with a blocking component, such surgical techniques are associated with fewer long-term complications.105 Longitudinal gastrectomy is less complex than GBy, has a lower incidence of postoperative complications,111 and shows comparable results in terms of losing excess body fat.112 Initially, kidney transplantation was contraindicated in patients with obesity, but after the LG was performed in them, it was possible to perform kidney transplantation.113 Since the LG came into use, transplantation is no longer contraindicated in patients suffering from obesity. This type of bariatric intervention eliminates the contraindication for kidney transplantation due to obesity, in most patients within less than 1 year of postoperative follow-up.113

After bariatric surgery, the most severe complication is the appearance of a fistula,89 the frequency of which continues to decrease, which may be associated with the advancements of surgical procedures and postoperative care. Currently, fistula formation occurs in 0.6% to 5% of cases after shunting114,115 and in approximately 1% of patients after LG.116,117

Gehrer et al118 found that after the LG operation, fewer micronutrient deficiencies were observed in comparison with GBy. Before the surgery, it is recommended to assess the micronutrient status119–121 because many studies show that micronutrient deficiencies identified preoperatively highly correlate with the risk of deficiency of the same nutrients postoperatively (Table 3).

TABLE 3 - Deficiency of Vitamins and Chemical Elements in Patients With Morbid Obesity After Bariatric Surgery
Micronutrient Percentage of Deficiency Before the Operation Percentage of Deficiency After the Operation References
Vitamin А 70% 92.5% (1 y after GBy) Bodunova et al63
71.6% 55.2% (1 y after LG) van Rutte et al54
52.5% 52.5% (1 y after LG) Bodunova et al63
N/Da 52% (1 y after BPD) Patel et al75
14% 39% (6 mo after GBy) Pereira et al (2009)81
N/Da 36% (≤1 y after GBy) Ledoux et al84
N/Da 33.2% (≤1 y after LG) Ledoux et al84
9% 28% (1 y after GBy) Donadelli et al82
16% 23% (1 y after GBy) Coupaye et al (2014)80
21% 21% (6 mo after GBy) Pereira et al (2013) group 179
N/Da 21% (1 y after GBy) Gong et al122
16% 20% (1 y after LG) Coupaye et al (2014)80
20% 20% (6 mo after GBy) Pereira et al (2013) group 379
7% 17% (after 1 y of GBy) Madan et al46
7.9% 15.3% (1 y after LG) Caron et al123
7% 13% (after 1 y of GBy) Ledoux et al84
N/Da 11% (after 1 y of GBy) Lovette et al124
23% 10% (1 y after GBn) Coupaye et al (2009)78
14% 10% (1 y after GBy) Coupaye et al (2009)78
0% 9.4% (1 y after LG) Schollnberger et al86
21% 8.7% (6 mo after GBy) Pereira et al (2013) group 279
1.7% 7.7% 1 y after GBy) Johnson et al125
7% 7% (1 y after GBy) Aasheim et al (2009)83
N/Da 5.5% (1 y after GBy) Boyce et al126
2.7% 5.2% (1 y after LG) Johnson et al125
N/Da 4.9% (1 y after GBy) James et al127
0% 4% (1 y after GBy) Aasheim et al (2012)85
1.9% 3.7% (1 y after GBy) Voglino et al128
0% 2% (1 y after GBy) Provenzale et al87
0% 0% (1 y after LG) Van Rutte et al54
0% 0% (1 y after LG) Damms-Machado et al66
17% 0% (2 y after GBy) Billeter et al129
N/Da 0% (1 y after GBy) Arias et al67
Vitamin С 100% 100% (1 y after GBy) Bodunova et al63
87.5% 87.5% (1 y after LG) Bodunova et al63
43% 48% (1 y after GBn) Coupaye et al (2009)78
N/Da 34.6% (after 1 y of GBy) Lovette et al124
9% 29% (1 y after GBy) Donadelli et al82
63% 23% (1 y after GBy) Aasheim et al (2009)83
40% 20% (1 y after LG) Coupaye et al (2014)80
N/Da 11.1% (≤1 y after LG) Ledoux et al84
15% 11% (1 y after GBy) Aasheim et al (2012)85
43% 10%–50% (after GBy) Patel et al75
47% 10% (1 y after GBy) Coupaye et al (2009)78
47% 10% (1 y after GBy) Coupaye et al (2014)80
23% 9.7% (1 y after GBy) Ledoux et al84
N/Da 4.7% (≤1 y after GBy) Ledoux et al84
Vitamin D 100% 100% (1 y after GBy) Bodunova et al63
100% 100% (1 y after LG) Bodunova et al63
97.9% 93.6% (1 y after LG) Ben-Porat et al56
86% 71% (1 y after GBy) Verger et al64
83% 70.4% (1 y after LG) Damms-Machado et al66
83% 68% (1 y after LG) Verger et al64
N/Da 61.1% (≤1 y after GBy) Ledoux et al84
N/Da 57% (1 y after BPD) Patel et al75
N/Da 54.6% (≤1 y after LG) Ledoux et al84
74.35% 50% (1 y after GBy) Arias et al67
49% 49% (1 y after GBy) Henfridsson et al130
84.62% 48% (1 y after LG) Vix et al131
92% 43% (1 y after LG) Toh et al132
74.5% 42.6% (1 y after GBy) Voglino et al128
90% 37% (1 y after LG) Moize et al133
81% 36% (1 y after LG) Van Rutte et al54
N/Da 34.2% (1 y after GBy) Boyce et al126
60.6% 32.5% (1 y after GBy) Moize et al133
N/Da 30.8% (5 y after LG) Boyle et al134
46% 30% (1 y after GBy) Toh et al132
N/Da 27% (after bariatric surgery) Calderón et al135
N/Da 22.7% (1 y after GBy) Leeman et al136
N/Da 21% (1 y after LG) Lovette et al124
26.9% 20.3% (1 y after GBy) Johnson et al125
40% 19% (1 y after GBy) Madan et al46
N/Da 15.4% (1 y after GBy) James et al127
26.8% 13.4% (1 y after LG) Johnson et al125
N/Da 12% (1 y after GBy and LG) Antoine et al76
N/Da 7% (after 1 y of GBy) Lovette et al124
35% 7.5% (1 y after bariatric/metabolic surgery) Remedios et al71
35% 6.7% (6 mo after bariatric/metabolic surgery) Remedios et al71
37.2% 5.5% (1 y after LG) Caron et al123
20.4% 4.9% (after a year of LG) Gillon et al73
26.4% 4.8% (1 y after LG) Vage et al137
65% 4% (1 y after GBy) Schijns et al138
Vitamin E N/Da 20% (≤1 y after GBy) Ledoux et al84
20% 16% (1 y after GBy) Coupaye et al (2014)80
10% 16% (1 y after GBy) Ledoux et al84
0% 15% (1 y after GBy) Aasheim et al (2012)85
12% 3% (1 y after LG) Coupaye et al (2014)80
3% 3% (1 y after GBy) Aasheim et al (2009)83
0% 1.8% (1 y after GBy) Voglino et al128
N/Da 1.8% (≤1 y after LG) Ledoux et al84
N/Da 0% (1 y after GBy) James et al127
0% 0% (1 y after LG) Damms-Machado et al66
0% 0% (1 y after GBy) Coupaye et al (2009)78
0% 0% (1 y after GBn) Coupaye et al (2009)78
0% 0% (2 y after GBy) Billeter et al129
Folic acid 20% 50% (1 y after GBn) Bodunova et al63
25% 42,7% (1 y after LG) Bodunova et al63
3%–4% 22% (after LG) Patel et al75
40,5% 21.4% (1 y after LG) Ben-Porat et al56
5.5% 13.8% (1 y after LG) Damms-Machado et al66
0% 13.7% (1 y after LG) Antoniewicz et al139
N/Da 12.7% (1 y after GBy and LG) Antoine et al76
24% 12.5% (1 y after LG) Van Rutte et al54
8.8% 12.3% (1 y after LG) Gillon et al73
3%–4% 10% (after GBn) Patel et al75
7.5% 8% (1 y after LG) Vage et al137
2% 8% (1 y after GBy) Madan et al46
12.8% 6.4% (6 mo after GBy) Antoniewicz et al139
3%–4% 5% (after BPD) Patel et al75
N/Da 3.9% (≤1 y after LG) Ledoux et al84
7% 3.4% (1 y after GBy) Donadelli et al82
0% 2.77% (6 mo after GBy) Gobato et al88
6.5% 1.2% (1 y after GBy) Blume et al140
3%–4% 0-12 (after GBy) Patel et al75
0% 0.5% (1 y after LG) Caron et al123
N/Da 0.4% (≤1 y after GBy) Ledoux et al84
N/Da 0% (1 y after GBy) Arias et al67
0% 0% (1 y after GBy) Voglino et al128
0% 0% (1 y after GBy and LG) Toh et al132
0% 0% (1 y after GBy) Schijns et al138
0% 0% (1 y after GBy) Henfridsson et al130
0% 0% (2 y after GBy) Billeter et al129
N/Da 0% (1 y after GBy) Arias et al67
Vitamin В1 38% 57% (1 y after GBn) Coupaye et al (2009)78
N/Da 49% (1 y after GBy) Kaidar-Person and Rosenthal.141
37% 23% (1 y after LG) Coupaye et al (2014)80
35% 23% (1 y after GBy) Coupaye et al (2014)80
N/Da 18.3% (1 y after GBy) Lovette et al124
0% 17.7% (6 mo after LG) Belfiore et al142
N/Da 15% (≤1 y after LG) Ledoux et al84
0%–29% 12%–18% (after GBy) Patel et al75
25% 12% (1 y after GBy) Coupaye et al (2009)78
N/Da 11.3% (≤1 y after GBy) Ledoux et al84
15% 11% (1 y after GBy) Ledoux et al84
0% 10% (1 y after GBy) Aasheim et al (2009)83
0% 9.1% (1 y after LG) Moize et al133
0% 9% (1 y after LG) Moize et al133
5.5% 9% (1 y after LG) Van Rutte et al54
8.1% 7.2% (1 y after LG) Johnson et al125
5.5% 6.1% (1 y after GBy) Moize et al133
6% 6% (1 y after GBy) Moize et al133
1.7% 5.9% (1 y after GBy) Johnson et al125
N/Da 3.3% (1 y after GBy) Boyce et al126
N/Da 1% (1 y after GBy) Arias et al67
17% 0% (1 y after LG) Verger et al64
9% 0% (1 y after LG) Saif et al141
9% 0% (1 y after GBy) Verger et al64
0% 0% (2 y after GBy) Billeter et al129
Vitamin В2 N/Da 13.6% (after 1 y of GBy) Lovette et al124
Vitamin В3 70% 100% (1 y after LG) Bodunova et al63
32.5% 82.5% (1 y after GBy) Bodunova et al63
N/Da 13.1% (≤1 y after GBy) Ledoux et al84
N/Da 10.7% (≤1 y after LG) Ledoux et al84
Vitamin В5 87.5% 87.5% (1 y after LG) Bodunova et al63
67.5% 82.5% (1 y after GBy) Bodunova et al63
Vitamin В6 92.5% 92.5% (1 y after LG) Bodunova et al63
90% 90% (1 y after GBy) Bodunova et al63
20.9% 47.3% van Rutte et al54
N/Da 17.6% (1 y after GBy) Lovette et al124
75% 11.1% (1 y after LG) Moize et al133
N/Da 6.4% (≤1 y after LG) Ledoux et al84
N/Da 5.4% (≤1 y after GBy) Ledoux et al84
3% 4% (1 y after LG) Van Rutte et al54
11.3% 2.8% (1 y after GBy) Moize et al133
11% 0% (2 y after GBy) Billeter et al129
N/Da 0% (1 y after GBy) Arias et al67
Vitamin В12 56.7% 44.5% (after 1 y of bariatric/metabolic surgery) Remedios et al71
56.7% 37% (after 6 mo of bariatric/metabolic surgery) Remedios et al71
3%–8% 33%–58 (after GBy) Patel et al75
30.3% 25.8% (1 y after LG) Caron et al123
6.4% 25.5% (1 y after GBy) Antoniewicz et al139
19% 23% (1 y after GBy) Schijns et al138
3%–8% 22% (after BPD) Patel et al75
12.3% 19% (1 y after GBy) Arias et al67
6.4% 19% (1 y after LG) Gillon et al73
3%–4% 18% (after LG) Patel et al75
11.7% 16.7% (1 y after LG) Ben-Porat et al56
1% 13% (1 y after GBy) Henfridsson et al130
N/Da 12.7% (≤1 y after GBy) Ledoux et al84
11.5% 11.5% (1 y after LG) Van Rutte et al54
1% 11% (1 y after GBy) Toh et al132
0% 10% (1 y after GBy) Vargas-Ruiz et al144
10% 9% (1 y after LG) Ferraz et al77
N/Da 9% (1 y after GBy) Leeman et al136
9% 8% (1 y after GBy) Ferraz et al77
5.9% 7.8% (1 y after LG) Antoniewicz et al139
N/Da 7.7% (5 y after LG) Boyle et al134
N/Da 7.5% (≤1 y after LG) Ledoux et al84
13.9% 7% (1 y after GBy and LG) Antoine et al76
N/Da 7% (after bariatric surgery) Calderón et al135
5.2% 6.9% (1 y after GBy) Donadelli et al82
3.6% 6.5% (1 y after LG) Vage et al137
3%–8% 0%-19% (after GBn) Patel et al75
1.8% 6.2% (1 y after GBy) Moize et al133
6.8% 5.6% (1 y after GBy) Voglino et al128
0% 5% (1 y after GBy) Madan et al46
N/Da 4.8% (1 y after GBy) Boyce et al126
N/Da 3.6% (1 y after GBy) Lovette et al124
2.9% 3.5% (1 y after GBy) Blume et al140
2.7% 3.2% (1 y after LG) Moize et al133
1.6% 1.4% (1 y after GBy) Johnson et al125
5% 0% (1 y after GBy) Verger et al64
4% 0% (1 y after LG) Toh et al132
3% 0% (1 y after LG) Verger et al64
1.3% 0% (1 y after LG) Johnson et al125
N/Da 0% (1 y after GBy) James et al127
0% 0% (2 y after GBy) Billeter et al129
Iron 43% 31% (after 6 mo of bariatric/metabolic surgery) Remedios et al71
34.5% 29.6% (1 y after GBy) Voglino et al128
40,4% 27.7% (1 y after LG) Ben-Porat et al56
N/Da 23.4% (1 y after GBy) Leeman et al136
15% 21% (1 y after GBy) Toh et al132
43% 21.9% (after 1 y of bariatric/metabolic surgery) Remedios et al71
7%–37% 21%–100% (after BPD) Patel et al75
16.6% 20% (1 y after GBy) Vargas-Ruiz et al144
N/Da 16.9% (1 y after GBy) Boyce et al126
N/Da 20% (after bariatric surgery) Calderón et al135
26.5% 15.9% (1 y after GBy) Moize et al133
30.8% 10.3% (1 y after LG) Moize et al133
14% 6% (1 y after GBy) Madan et al46
5.3% 4.1% (1 y after GBy) Blume et al140
5.9% 2% (1 y after LG) Antoniewicz et al139
38% 18.5% (1 y after LG) Van Rutte et al54
29% 19% (1 y after GBy) Ferraz et al77
N/Da 15.8% (1 y after GBy and LG) Antoine et al76
7%-37% 14% (after LG) Patel et al75
18% 11% (1 y after LG) Toh et al132
N/Da 10.3% (5 y after LG) Boyle et al134
24% 10% (1 y after LG) Ferraz et al77
20% 8.9% (1 y after LG) Caron et al123
4.3% 8.5% (1 y after GBy) Antoniewicz et al139
7% 5% (1 y after LG) Verger et al64
7%-37% 5%-42% (after GBy) Patel et al75
7%-37% 0-32 (after GBn) Patel et al75
5% 3% (1 y after GBy) Arias et al67
2.77% 0% (6 mo after GBy) Gobato et al88
18% 0% (1 y after GBy) Verger et al64
Calcium 0% 13.3% (1 y after GBy) Johnson et al125
11% 9.1% (after 6 mo of bariatric/metabolic surgery) Remedios et al71
11% 6.9% (after 1 y of bariatric/metabolic surgery) Remedios et al71
6.4% 4.3% (1 y after GBy) Antoniewicz et al139
0% 4.3% (1 y after LG) Damms-Machado et al66
5% 4% (1 y after GBy) Henfridsson et al130
7.8% 3.9% (1 y after LG) Antoniewicz et al139
2.9% 3.6% (1 y after LG) Moize et al133
9.6% 3.5% (1 y after GBy) Moize et al133
N/Da 3% (1 y after GBy) Arias et al67
13.88% 2.77% (6 mo after Gby) Gobato et al88
1.9% 2.6% (1 y after LG) Caron et al123
0.5% 2% (1 y after LG) Van Rutte et al54
N/Da 1.8% (≤1 y after LG or Gby) Ledoux et alet al84
5.1% 0.9% (1 y after LG) Vage et al137
21% 0% (2 y after Gby) Billeter et al129
0.9% 0% (1 y after LG) Johnson et al125
0% 0% (1 y after GBn and GBy) Coupaye et al (2009)78
Potassium 6.5% 0% (1 y after LG) Damms-Machado et al66
Phosphate 24% 15% (2 y after GBy) Billeter et al129
21.8% 3.9% (1 y after LG) Caron et al123
N/Da 3.5% (1 y after LG) Van Rutte et al54
Magnesium N/Da 19% (1 y after GBy) Arias et al67
29.4% 14.1% (1 y after GBy) Moize et al133
N/Da 12.7% (≤1 y after GBy) Ledoux et al84
N/Da 11.1% (≤1 y after LG) Ledoux et al84
37.8% 10.3% (1 y after LG) Moize et al133
12% 8% (2 y after GBy) Billeter et al129
4.3% 4.3% (1 y after GBy) Antoniewicz et al139
N/Da 3% (1 y after LG) Van Rutte et al54
7.8% 2% (1 y after LG) Antoniewicz et al139
2.77% 0% (6 mo after GBy) Gobato et al88
Zinc N/Da 64% (≤1 y after GBy) Ledoux et al84
55.55% 61.11% (6 mo after GBy) Gobato et al88
8.1% 39.3% (1 y after LG) Moize et al133
28% 36% (1 y after GBy) Madan et al46
34% 34% (1 y after GBy) Ferraz et al77
N/Da 33% (after bariatric surgery) Calderón et al135
N/Da 32.2% (≤1 y after LG) Ledoux et al84
N/Da 29% (1 y after GBy) Gong et al122
11.5% 27.5% (1 y after GBy) Moize et al133
40% 20% (1 y after LG) Ferraz et al77
0% 15% (2 y after GBy) Billeter et al129
N/Da 12% (1 y after GBy) Arias et al67
N/Da 5% (1 y after LG) Van Rutte et al54
Copper N/Da 27% (after bariatric surgery) Calderón et al135
10% 15% (2 y after GBy) Billeter et al129
0% 8.33% (6 mo after GBy) Gobato et al88
Selenium 11% 46% (2 y after GBy) Billeter et al129
N/Da 41.8% (≤1 y after GBy) Ledoux et al84
N/Da 20.4% (≤1 y after LG) Ledoux et al84
N/Da 11% (1 y after GBy) Gong et al122
58% 3% (1 y after GBy) Madan et al46
Abbreviations: BPD, biliopancreatic diversion; GBn, gastric banding; GBy, gastric bypass; LG, longitudinal gastrectomy.
aThe concentrations of micronutrients were not assessed before the operation.

Mixed Restrictive and Malabsorptive Procedures

Currently, GBy is the criterion standard of bariatric surgery.5,70 As a result of GBy, patients can lose from 66% to 75% of their excess body weight in the first 24 months after surgery.145,146 After GBy, patients not only successfully lose weight, but also decrease activity of serum transaminases147 and improve glycemic control.148,149 There are several modifications of the GBy, but their essence boils down to the fact that by crossing the stomach in the upper part of it, a “small stomach” with a volume of 20 to 30 mL is formed, to which a loop of the small intestine is sutured. By reducing the amount of food consumed and the absorption of nutrients, a decrease in body weight is obtained.150 The frequent surgical complications after GBy are stenosis of the anastomosis between the stomach and duodenum, ulcers between the stomach and small intestine, hernia of the abdominal wall,151,152 insufficient protein absorption,153 and micronutrient deficiencies.71

Vitamin B12 deficiency is usually observed several years after bariatric surgery because it has a large reserve in the liver. The reserves of vitamin B12 in the liver are sufficient to fulfill the physiological needs of the body for 3 to 5 years after the disappearance of Castle's gastric intrinsic factor. But, in the absence of enterohepatic circulation, this period is reduced from 3-5 years to a few months (sometimes up to a year). Deficiency of vitamin B12 is observed in all types of mixed operations because of a decrease in or lack of production of hydrochloric acid, a decrease in the production of Castle's intrinsic factor by parietal cells, and a decrease in the number of cells with receptors for the complex “vitamin B12—intrinsic factor.” Moreover, vitamin B12 deficiency develops with pancreatic insufficiency because there is an insufficient amount of the enzyme that releases B12 from the carrier protein and a calcium deficiency, which is necessary for the combination of the vitamin B12 complex (intrinsic factor) with a receptor. After bariatric surgery, thiamine deficiency develops in the postoperative period from 6 to 15 weeks.154 Vitamin E deficiency may occur in 6 to 12 months after surgery (mixed and blocking), but it can develop even after several years.154 Vitamin E is absorbed in the upper parts of the small intestine; bile acids and fatty acids are needed for its absorption. Usually, vitamin E deficiency develops in patients with malabsorption.

In a Russian study, the change in the vitamin nutritional status in patients with obesity after GBy, GBn, and LG was studied.63 Gastric bypass was performed in patients with the most severe forms of obesity. After surgery, a significant decrease in body weight was observed in patients who underwent GBy and LG. When examining a group of patients who underwent GBn, it was found that even before the operation, more than 50% of patients had a deficiency of vitamins C (95%), B6 (95%), D (80%), and Folate (50%) in blood.63 In the postoperative period, the number of patients with a deficiency of folic acid and niacin also increased. In the group of patients who underwent LG, vitamins C, D, B6, and folate; retinol and niacin were significantly reduced before the operation (in 87.5%, 100%, 92.5%, 87.5%, 52.5%, and 70% of patients, respectively). A year after the operation, the number of patients with deficiencies of these vitamins remained the same or increased (the number of patients with niacin deficiency increased to 100%). The concentrations of other vitamins did not significantly decrease after 1 year of the operation. In the group of patients who underwent GBy, there was a significant decrease in vitamins C, D, B6, and folate and retinol both before and after surgery.63 The authors surmise the niacin deficiency revealed in most patients to be associated with the fact that when performing the above operations that the anatomy of the stomach and the proximal small intestine gets changed, where this vitamin is absorbed. The authors associate the folate deficiency in patients who have undergone GBn and LG with the “termination” of the stomach from the process of folic acid assimilation. In addition, gastric absorption is critical for the metabolism of copper, the bulk of which is absorbed in the stomach.155

With JIB, there is protein malabsorption in the shortened small intestine. Similarly, with GBy, the protein absorption in the shortened small intestine is disrupted, and its denaturation by gastric hydrochloric acid and initial breakdown by pepsin are impaired. In addition, many patients who have undergone GBy develop an aversion to protein foods. After GBy, there is a high risk of developing B12-deficiency anemia due to a decrease in the production of Castle's intrinsic factor by the stomach. The risk of folate-deficiency anemia also increases.153 In this regard, patients after GBy are prescribed to take high oral doses of cobalamin—at least 350 μg/day—as a result of its extremely low bioavailability. The daily dosage of folic acid in the postoperative period is usually at least 800 μg/day.

Also, after GBy, iron-deficiency anemia is observed (the incidence ranges from 15% to 60%).153 Usually, in the acidic environment of the stomach, iron complexes are formed with ascorbic acid, bile acids, amino acids, monosaccharides, and disaccharides, which are then absorbed in the duodenum and jejunum. When most of the stomach and especially the duodenum do not take part in the digestion of the food, the iron content of the food could not be utilized properly. Thus, patients constantly need to take iron supplements. Moreover, metabolism of iron, vitamin B12, and folic acid must be assessed after 3 to 6 months of surgery and then annually.153

After GBy, most patients also develop deficiencies of vitamin D, calcium, zinc, copper, magnesium, and selenium.156–163 For the prevention of calcium metabolism disorders in patients, on the 7th to 10th day after GBy, 1500 to 1800 mg of alimentary calcium and 800 to 1000 IU of vitamin D per day are prescribed. Calcium metabolism as well as 25(OH)D levels should be measured after 6 months of having surgery and appropriate therapy should be selected to correct the abnormality. Osteodensitometry is required 2 years after GBy. After performing GBy, the absorption of lipids and lipophilic substances, including fat-soluble vitamins, is sharply reduced.156

Among the mixed operations, the BPD was first carried out in 1976 by Scopinaro et al109 and was based on the achievement of restriction and malabsorption. In this operation, gastric resection is performed with the formation of a proximal gastric pocket with a volume of 500 mL (in patients with a BMI <50 kg/m2) or 200 mL (in patients with a BMI ≥50 kg/m2). A 250-cm portion of the intestine is cut off from the ileocecal flap, the distal end is connected to the gastric pocket, and the proximal end is finally connected to the ileum at a distance of 50 cm from the ileocecal flap. The formation of these anastomoses creates a “digestive tract” 200 to 300 cm long, a “biliary tract” 300 to 500 cm long, and a “common tract” 50 to 100 cm long, in which food is digested and nutrients are absorbed. This operation helps to reduce the body weight up to 75%.103 However, despite the good results, metabolic complications typical for GBy are possible after BPD; especially iron-deficiency anemia and osteoporosis are prevalent because of impaired absorption of lipophilic substances, including vitamin D.83,164 The detailed information about deficiencies of micronutrients after different bariatric surgeries is illustrated in Table 3.


Today, bariatric surgery is the most effective treatment for morbid obesity and metabolic complications associated with it. Often, obesity is not a sole indication for bariatric surgery. The operation is performed when other pathologies are associated, such as progressive diabetes mellitus, obstructive sleep apnea, severe hypertension, and other life-threatening conditions. After analyzing the results of the bariatric surgeries in patients with obesity, many researchers have shown that mixed surgeries (GBy, BPD) have higher efficacy in reducing the body weight as compared with restrictive surgeries (GBn, LG).165,166Gastric bypass and BPD, which combine restrictive and blocking components, are characterized by greater complexity and risk of complications. On the other hand, they also provide a more pronounced long-term result, positively affecting the course of metabolic disorders that occur with obesity. Longitudinal gastrectomy is less complex than GBy, has a lower incidence of postoperative complications,111 and shows similar results in terms of excess body fat loss.112 Currently, the results of the LG are being actively studied, and the method is being improved. Blocking surgery is practically not used because of the numerous serious complications associated with it.

It must be noted that any type of bariatric surgery ultimately leads to a direct and irreversible digestive disorder. This is, after all, surgical manipulation. Even restrictive surgeries significantly increase the risk of micronutrient deficiencies. Most postbariatric patients have to receive micronutrient replacement therapy for their whole life. In addition, a significant proportion of patients have a number of deficiencies even before surgery. Bariatrics is a radical and extreme treatment for obesity. It significantly reduces the quality of life despite effective weight loss. Therefore, obesity treatment should begin with dietary and, in extreme cases, with pharmacotherapy. Psychotherapists and psychotropic drugs may also be used.

Furthermore, morbid obesity is not a monolithic disease, but a large set of varied pathologies, not all of which by any stretch are targets for elective surgical intervention. For example, hypothyroidism can also lead to obesity, which, by no means, should be treated by bariatric surgery. The main point here is the patient's attitude on the treatment of his/her disease. Bariatric surgeries are not only the most effective but also the most dangerous method of treating obesity; so, it should only be resorted to as a final option to those patients who do not get persistent effective results from the complex of conservative therapy or to those who have urgent medical indications.



1. Ofei F. Obesity—a preventable disease. Ghana Med J. 2005;39(3):98–101.
2. WHO. Obesity and overweight. Accessed January 14, 2021.
3. Purnell JQ. Definitions, classification, and epidemiology of obesity. Endotext. 2018.
4. Malone J, Del Rosario Perez M, Friberg EG, et al. Justification of CT for individual health assessment of asymptomatic persons: a World Health Organization consultation. J Am Coll Radiol. 2016;13(12):1447–1457. doi:10.1016/j.jacr.2016.07.020.
5. Landin M, Sudan R. This is how we do it: laparoscopic Roux-en-Y gastric bypass. J Laparoendosc Adv Surg Tech A. 2020;30(6):619–622. doi:10.1089/lap.2020.0155.
6. Schneider R, Kraljević M, Peterli R, et al. GLP-1 analogues as a complementary therapy in patients after metabolic surgery: a systematic review and qualitative synthesis. Obes Surg. 2020;30(9):3561–3569. doi:10.1007/s11695-020-04750-7.
7. Sjöström L, Narbro K, Sjöström CD, et al. Effects of bariatric surgery on mortality in Swedish obese subjects. N Engl J Med. 2007;357(8):741–752. doi:10.1056/NEJMoa066254.
8. Colquitt JL, Picot J, Loveman E, Clegg AJ. Surgery for obesity. Cochrane Database Syst Rev. 2009;(2):CD003641. doi:10.1002/14651858.CD003641.pub3.
9. Buchwald H, Estok R, Fahrbach K, et al. Weight and type 2 diabetes after bariatric surgery: systematic review and meta-analysis. Am J Med. 2009;122(3):248–256. doi:10.1016/j.amjmed.2008.09.041.
10. Gapparova CM, Chekhonina YG, Lapik IA. Features of clinical and metabolic status after bariatric treatment of obesity. Exp Clin Gastroenterol. 2020;179(7):96–101. doi:10.31146/1682-8658-ecg-179-7-96-101.
11. Romero-Velez G, Pechman DM, Muñoz Flores F, Moran-Atkin E, Choi J, Camacho DR. Bariatric surgery in the super-super morbidly obese: outcome analysis of patients with BMI >70 using the ACS-NSQIP database. Surg Obes Relat Dis. 2020;16(7):894–899. doi:10.1016/j.soard.2020.03.025.
12. Gazda CL, Clark JD, Lingvay I, Almandoz JP. Pharmacotherapies for post-bariatric weight regain: real-world comparative outcomes. Obesity (Silver Spring). 2021;29(5):829–836. doi:10.1002/oby.23146.
13. Jimenez V, Jambrina C, Casana E, et al. FGF21 gene therapy as treatment for obesity and insulin resistance. EMBO Mol Med. 2018;10(8):e8791. doi:10.15252/emmm.201708791.
14. Gao M, Liu D. Gene therapy for obesity: progress and prospects. Discov Med. 2014;17(96):319–328.
15. Yumuk V, Tsigos C, Fried M, et al. European guidelines for obesity management in adults. Obes Facts. 2015;8(6):402–424. doi:10.1159/000442721.
16. Khorgami Z, Shoar S, Andalib A, Aminian A, Brethauer SA, Schauer PR. Trends in utilization of bariatric surgery, 2010–2014: sleeve gastrectomy dominates. Surg Obes Relat Dis. 2017;13(5):774–778. doi:10.1016/j.soard.2017.01.031.
17. Adams TD, Davidson LE, Litwin SE, et al. Health benefits of gastric bypass surgery after 6 years. JAMA. 2012;308(11):1122–1131. doi:10.1001/2012.jama.11164.
18. Karmali S, Johnson Stoklossa C, Sharma A, et al. Bariatric surgery: a primer. Can Fam Physician. 2010;56(9):873–879.
19. Björklund P, Fändriks L. The pros and cons of gastric bypass surgery—the role of the Roux-limb. Best Pract Res Clin Gastroenterol. 2019;40-41:101638. doi:10.1016/j.bpg.2019.101638.
20. Guerciolini R. Mode of action of orlistat. Int J Obes Relat Metab Disord. 1997;21(3):S12–S23.
21. William-Olsson T. Alpha-glucosidase inhibition in obesity. Acta Med Scand Suppl. 1985;706:1–39. doi:10.1111/j.0954-6820.1986.tb19118.x.
22. Glueck CJ, Fontaine RN, Wang P, et al. Metformin reduces weight, centripetal obesity, insulin, leptin, and low-density lipoprotein cholesterol in nondiabetic, morbidly obese subjects with body mass index greater than 30. Metabolism. 2001;50:856–861. doi:10.1053/meta.2001.24192.
23. Kusaka I, Nagasaka S, Horie H, Ishibashi S. Metformin, but not pioglitazone, decreases postchallenge plasma ghrelin levels in type 2 diabetic patients: a possible role in weight stability?Diabetes Obes Metab. 2008;10:1039–1046. doi:10.1111/j.1463-1326.2008.00857.x.
24. Mannucci E, Ognibene A, Cremasco F, et al. Effect of metformin on glucagon-like peptide 1 (GLP-1) and leptin levels in obese nondiabetic subjects. Diabetes Care. 2001;24:489–494. doi:10.2337/diacare.24.3.489.
25. Astrup A, Rössner S, Van Gaal L, et al. Effects of liraglutide in the treatment of obesity: a randomised, double-blind, placebo-controlled study. Lancet. 2009;374(9701):1606–1616. doi:10.1016/S0140-6736(09)61375-1.
26. Vilsbøll T, Christensen M, Junker AE, Knop FK, Gluud LL. Effects of glucagon-like peptide-1 receptor agonists on weight loss: systematic review and meta-analyses of randomised controlled trials. BMJ. 2012;344:d7771. doi:10.1136/bmj.d7771.
27. Drucker DJ, Nauck MA. The incretin system: glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors in type 2 diabetes. Lancet. 2006;368(9548):1696–1705. doi:10.1016/S0140-6736(06)69705-5.
28. Baggio LL, Drucker DJ. Glucagon-like peptide-1 receptors in the brain: controlling food intake and body weight. J Clin Invest. 2014;124(10):4223–4226. doi:10.1172/JCI78371.
29. Remely M, Aumueller E, Merold C, et al. Effects of short chain fatty acid producing bacteria on epigenetic regulation of FFAR3 in type 2 diabetes and obesity. Gene. 2014;537(1):85–92. doi:10.1016/j.gene.2013.11.081.
30. Basso N, Soricelli E, Castagneto-Gissey L, et al. Insulin resistance, microbiota, and fat distribution changes by a new model of vertical sleeve gastrectomy in obese rats. Diabetes. 2016;65(10):2990–3001. doi:10.2337/db16-0039.
31. Guidelines. Treatment of morbid obesity in adults. Approved by the Russian Association of Endocrinologists. 2016:33. Available from Accessed May 1, 2022.
32. Poston WS, Foreyt JP. Sibutramine and the management of obesity. Expert Opin Pharmacother. 2004;5(3):633–642. doi:10.1517/14656566.5.3.633.
33. Bondarenko IZ, Butrova SA, Goncharov NP, et al. Treatment of morbid obesity in adults. National Clinical Guidelines. Obes Metab. 2011;3:75–83.
34. NBP. National Bariatric Congress 2021. Accessed January 14, 2021.
35. Sun L, Wang C, Sun W, Wang C. A pilot study of nutritional status prior to bariatric surgery in South China. Front Nutr. 2021;8:697695. doi:10.3389/fnut.2021.697695.
36. Lapik IA. The features of micronutrient status in patients with type 2 diabetes mellitus. Alm Clin Med. 2016;(29):56–61.
37. Lapik IA, Sokol'nikov AA, Sharafetdinov KHKH, Sentsova TB, Plotnikova OA. Assessment of efficiency of dietotherapy with addition of a vitamin-mineral complex in patients with diabetes mellitus type 2. Vopr Pitan. 2014;83(3):74–81.
38. Moizé V, Deulofeu R, Torres F, de Osaba JM, Vidal J. Nutritional intake and prevalence of nutritional deficiencies prior to surgery in a Spanish morbidly obese population. Obes Surg. 2011;21(9):1382–1388. doi:10.1007/s11695-011-0360-y.
39. Aasheim ET, Hofso D, Hjelmesaeth J, Birkeland KI, Bøhmer T. Vitamin status in morbidly obese patients: a cross-sectional study. Am J Clin Nutr. 2008;87(2):362–369. doi:10.1093/ajcn/87.2.362.
40. Weinstein DA, Roy CN, Fleming MD, Loda MF, Wolfsdorf JI, Andrews NC. Inappropriate expression of hepcidin is associated with iron refractory anemia: implications for the anemia of chronic disease. Blood. 2002;100(10):3776–3781. doi:10.1182/blood-2002-04-1260.
41. Krause A, Neitz S, Mägert H, et al. LEAP-1, a novel highly disulfide-bonded human peptide, exhibits antimicrobial activity. FEBS Lett. 2000;480(2–3):147–150. doi:10.1016/s0014-5793(00)01920-7.
42. Ganz Т. Hepcidin. Rinsho Ketsueki. 2016;57(10):1913–1917.
43. Galchenko АV, Sherstneva AA. Association of microelementos with the risk of hypochromic anemia in vegetarians and vegans. Biogeochemical innovations under the conditions of the biosphere technogenesis correction. Tiraspol. 2020;352–359.
44. Wiebe N, Stenvinkel P, Tonelli M. Associations of chronic inflammation, insulin resistance, and severe obesity with mortality, myocardial infarction, cancer, and chronic pulmonary disease. JAMA Netw Open. 2019;2(8):–e1910456. doi:10.1001/jamanetworkopen.2019.10456.
45. Krzizek EC, Brix JM, Herz CT, et al. Prevalence of micronutrient deficiency in patients with morbid obesity before bariatric surgery. Obes Surg. 2018;28(3):643–648. doi:10.1007/s11695-017-2902-4.
46. Madan AK, Orth WS, Tichansky DS, Ternovits CA. Vitamin and trace mineral levels after laparoscopic gastric bypass. Obes Surg. 2006;16(5):603–606. doi:10.1381/096089206776945057.
47. Schweiger C, Weiss R, Berry E, Keidar A. Nutritional deficiencies in bariatric surgery candidates. Obes Surg. 2010;20(2):193–197. doi:10.1007/s11695-009-0008-3.
48. Sanchez A, Rojas P, Basfi-fer K, et al. Micronutrient deficiencies in morbidly obese women prior to bariatric surgery. Obes Surg. 2016;26(2):361–368. doi:10.1007/s11695-015-1773-9.
49. Peterson LA, Cheskin LJ, Furtado M, et al. Malnutrition in bariatric surgery candidates: multiple micronutrient deficiencies prior to surgery. Obes Surg. 2016;26(4):833–838. doi:10.1007/s11695-015-1844-y.
50. Cheng S, Massaro JM, Fox CS, et al. Adiposity, cardiometabolic risk, and vitamin D status: the Framingham Heart Study. Diabetes. 2010;59(1):242–248. doi:10.2337/db09-1011.
51. de Sousa Paredes SC, Mota-Garcia F. Prevalence of nutritional deficiencies in bariatric surgery candidates and its effect on metabolic status. Hormones (Athens). 2020;19(4):505–514. doi:10.1007/s42000-020-00234-6.
52. Chakhtoura MT, Nakhoul NN, Shawwa K, Mantzoros C, El Hajj Fuleihan GA. Hypovitaminosis D in bariatric surgery: a systematic review of observational studies. Metabolism. 2016;65(4):574–585. doi:10.1016/j.metabol.2015.12.004.
53. Wang C, Guan B, Yang W, Yang J, Cao G, Lee S. Prevalence of electrolyte and nutritional deficiencies in Chinese bariatric surgery candidates. Surg Obes Relat Dis. 2016;12(3):629–634. doi:10.1016/j.soard.2015.12.009.
54. van Rutte PW, Aarts EO, Smulders JF, Nienhuijs SW. Nutrient deficiencies before and after sleeve gastrectomy. Obes Surg. 2014;24(10):1639–1646. doi:10.1007/s11695-014-1225-y.
55. Lefebvre P, Letois F, Sultan A, Nocca D, Mura T, Galtier F. Nutrient deficiencies in patients with obesity considering bariatric surgery: a cross-sectional study. Surg Obes Relat Dis. 2014;10(3):540–546. doi:10.1016/j.soard.2013.10.003.
56. Ben-Porat T, Elazary R, Yuval JB, Wieder A, Khalaileh A, Weiss R. Nutritional deficiencies after sleeve gastrectomy: can they be predicted preoperatively?Surg Obes Relat Dis. 2015;11(5):1029–1036. doi:10.1016/j.soard.2015.02.018.
57. Pinhas-Hamiel O, Doron-Panush N, Reichman B, Nitzan-Kaluski D, Shalitin S, Geva-Lerner L. Obese children and adolescents: a risk group for low vitamin B12 concentration. Arch Pediatr Adolesc Med. 2006;160(9):933–936. doi:10.1001/archpedi.160.9.933.
58. Gunanti IR, Marks GC, Al-Mamun A, Long KZ. Low serum vitamin B-12 and folate concentrations and low thiamin and riboflavin intakes are inversely associated with greater adiposity in Mexican American children. J Nutr. 2014;144(12):2027–2033. doi:10.3945/jn.114.201202.
59. Al-Mutawa A, Anderson AK, Alsabah S, Al-Mutawa M. Nutritional status of bariatric surgery candidates. Nutrients. 2018;10(1):67. doi:10.3390/nu10010067.
60. Al-Mulhim AS. Laparoscopic sleeve gastrectomy and nutrient deficiencies: a prospective study. Surg Laparosc Endosc Percutaneous Tech. 2016;26(3):208. doi:10.1097/SLE.0000000000000270.
61. Asghari G, Khalaj A, Ghadimi M, et al. Prevalence of micronutrient deficiencies prior to bariatric surgery: Tehran Obesity Treatment Study (TOTS). Obes Surg. 2018;28(8):2465–2472. doi:10.1007/s11695-018-3187-y.
62. Flancbaum L, Belsley S, Drake V, Colarusso T, Tayler E. Preoperative nutritional status of patients undergoing Roux-en-Y gastric bypass for morbid obesity. J Gastrointest Surg. 2006;10(7):1033–1037. doi:10.1016/j.gassur.2006.03.004.
63. Bodunova NA, Sabelnikova EA, Parfenov AI, et al. The change in the concentration of vitamins after bariatric surgery. Klin Med (Mosk). 2015;93(12):28–31.
64. Verger EO, Aron-Wisnewsky J, Dao MC, et al. Micronutrient and protein deficiencies after gastric bypass and sleeve gastrectomy: a 1-year follow-up. Obes Surg. 2016;26(4):785–796. doi:10.1007/s11695-015-1803-7.
65. Malek M, Yousefi R, Safari S, Seyyedi SHS, Mottaghi A. Dietary intakes and biochemical parameters of morbidly obese patients prior to bariatric surgery. Obes Surg. 2019;29(6):1816–1822. doi:10.1007/s11695-019-03759-x.
66. Damms-Machado A, Friedrich A, Kramer KM, et al. Pre- and postoperative nutritional deficiencies in obese patients undergoing laparoscopic sleeve gastrectomy. Obes Surg. 2012;22(6):881–889. doi:10.1007/s11695-012-0609-0.
67. Arias PM, Domeniconi EA, García M, et al. Micronutrient deficiencies after Roux-en-Y gastric bypass: long-term results. Obes Surg. 2020;30(1):169–173. doi:10.1007/s11695-019-04167-x.
68. Grace C, Vincent R, Aylwin SJ. High prevalence of vitamin D insufficiency in a United Kingdom urban morbidly obese population: implications for testing and treatment. Surg Obes Relat Dis. 2014;10(2):355–360. doi:10.1016/j.soard.2013.07.017.
69. Homan J, Schijns W, Aarts EO, van Laarhoven CJHM, Janssen IMC, Berends FJ. An optimized multivitamin supplement lowers the number of vitamin and mineral deficiencies three years after Roux-en-Y gastric bypass: a cohort study. Surg Obes Relat Dis. 2016;12(3):659–667. doi:10.1016/j.soard.2015.12.010.
70. Schiavo L, Pilone V, Rossetti G, et al. Correcting micronutrient deficiencies before sleeve gastrectomy may be useful in preventing early postoperative micronutrient deficiencies. Int J Vitam Nutr Res. 2019;89(1–2):22–28. doi:10.1024/0300-9831/a000532.
71. Remedios C, Bhasker AG, Dhulla N, Dhar S, Lakdawala M. Bariatric nutrition guidelines for the Indian population. Obes Surg. 2016;26(5):1057–1068. doi:10.1007/s11695-015-1836-y.
72. Ybarra J, Sánchez-Hernández J, Gich I, et al. Unchanged hypovitaminosis D and secondary hyperparathyroidism in morbid obesity after bariatric surgery. Obes Surg. 2005;15(3):330–335. doi:10.1381/0960892053576758.
73. Gillon S, Jeanes YM, Andersen JR, Våge V. Micronutrient status in morbidly obese patients prior to laparoscopic sleeve gastrectomy and micronutrient changes 5 years post-surgery. Obes Surg. 2017;27(3):606–612. doi:10.1007/s11695-016-2313-y.
74. Bloomberg RD, Fleishman A, Nalle JE, Herron DM, Kini S. Nutritional deficiencies following bariatric surgery: what have we learned?Obes Surg. 2005;15(2):145–154. doi:10.1381/0960892053268264.
75. Patel JJ, Mundi MS, Hurt RT, Wolfe B, Martindale RG. Micronutrient deficiencies after bariatric surgery: an emphasis on vitamins and trace minerals. Nutr Clin Pract. 2017;32(4):471–480. doi:10.1177/0884533617712226.
76. Antoine D, Li Z, Quilliot D, et al. Medium term post–bariatric surgery deficit of vitamin B12 is predicted by deficit at time of surgery. Clin Nutr. 2021;40(1):87–93. doi:10.1016/j.clnu.2020.04.029.
77. Ferraz ÁAB, Carvalho MRC, Siqueira LT, Santa-Cruz F, Campos JM. Micronutrient deficiencies following bariatric surgery: a comparative analysis between sleeve gastrectomy and Roux-en-Y gastric bypass. Rev Col Bras Cir. 2018;45(6):e2016. doi:10.1590/0100-6991e-20182016.
78. Coupaye M, Puchaux K, Bogard C, et al. Nutritional consequences of adjustable gastric banding and gastric bypass: a 1-year prospective study. Obes Surg. 2009;19(1):56–65. doi:10.1007/s11695-008-9571-2.
79. Pereira S, Saboya C, Ramalho A. Impact of different protocols of nutritional supplements on the status of vitamin a in class III obese patients after Roux-en-Y gastric bypass. Obes Surg. 2013;23(8):1244–1251. doi:10.1007/s11695-013-0885-3.
80. Coupaye M, Rivière P, Breuil MC, et al. Comparison of nutritional status during the first year after sleeve gastrectomy and Roux-en-Y gastric bypass. Obes Surg. 2014;24(2):276–283. doi:10.1007/s11695-013-1089-6.
81. Pereira S, Saboya C, Chaves G, Ramalho A. Class III obesity and its relationship with the nutritional status of vitamin a in pre- and postoperative gastric bypass. Obes Surg. 2009;19(6):738–744. doi:10.1007/s11695-008-9478-y.
82. Donadelli SP, Junqueira-Franco MV, de Mattos Donadelli CA, et al. Daily vitamin supplementation and hypovitaminosis after obesity surgery. Nutrition. 2012;28(4):391–396. doi:10.1016/j.nut.2011.07.012.
83. Aasheim ET, Bjorkman S, Sovik TT, et al. Vitamin status after bariatric surgery: a randomized study of gastric bypass and duodenal switch. Am J Clin Nutr. 2009;90(1):15–22. doi:10.3945/ajcn.2009.27583.
84. Ledoux S, Calabrese D, Bogard C, et al. Long-term evolution of nutritional deficiencies after gastric bypass: an assessment according to compliance to medical care. Ann Surg. 2014;259(6):1104–1110. doi:10.1097/SLA.0000000000000249.
85. Aasheim ET, Johnson LK, Hofso D, Bøhmer T, Hjelmesæth J. Vitamin status after gastric bypass and lifestyle intervention: a comparative prospective study. Surg Obes Relat Dis. 2012;8(2):169–175. doi:10.1097/SLA.0000000000000249.
86. Schollnberger AE, Damms-Machado A, Kaiser D, et al. Influence of laparoscopic sleeve gastrectomy on the micronutrient status. Aktuelle Ernahrungsmedizin. 2016;41(1):15–20.
87. Provenzale D, Reinhold RB, Golner B, et al. Evidence for diminished B12 absorption after gastric bypass: oral supplementation does not prevent low plasma B12 levels in bypass patients. J Am Coll Nutr. 1992;11(1):29–35. doi:10.1080/07315724.1992.10718193.
88. Gobato RC, Seixas Chaves DF, Chaim EA. Micronutrient and physiologic parameters before and 6 months after RYGB. Surg Obes Relat Dis. 2014;10(5):944–951. doi:10.1016/j.soard.2014.05.011.
89. Marie L, Robert M, Montana L, et al. A French national study on gastropleural and gastrobronchial fistulas after bariatric surgery: the impact of therapeutic strategy on healing. Obes Surg. 2020;30(8):3111–3118. doi:10.1007/s11695-020-04655-5.
90. Ulker I, Yildiran H. The effects of bariatric surgery on gut microbiota in patients with obesity: a review of the literature. Biosci Microbiota Food Health. 2019;38(1):3–9. doi:10.12938/bmfh.18-018.
91. Kashenko VA, Strizheletsky VV, Neimark AE, et al. Bariatric surgery. St Petersburg: St Petersburg State University; 2020;47. Available from Accessed May 1, 2022.
    92. Fried M, Yumuk V, Oppert JM, et al. Interdisciplinary European guidelines on metabolic and bariatric surgery. Obes Surg. 2014;24(1):42–55. doi:10.1007/s11695-013-1079-8.
    93. Kissler HJ, Settmacher U. Bariatric surgery to treat obesity. Semin Nephrol. 2013;33(1):75–89. doi:10.1016/j.semnephrol.2012.12.004.
    94. Moxthe LC, Sauls R, Ruiz M, Stern M, Gonzalvo J, Gray HL. Effects of bariatric surgeries on male and female fertility: a systematic review. J Reprod Infertil. 2020;21(2):71–86.
    95. Troshina EA, Ershova EV, Mazurina NV. Endocrinological aspects of bariatric surgery. Cons Med. 2019;21(4):50–55.
    96. Babenko AY, Neymark AE, Anisimova KA, et al. Effects of bariatric surgery on the level of hormones that regulate body weight what is the basis of success?Obes Metab. 2014;11(4):3–11.
    97. Ershova EV, Yashkov YI. Status of carbohydrate and lipid metabolism in obese patients with type 2 diabetes mellitus after biliopancreatic diversion surgery. Obes Metab. 2013;3:28–36.
    98. Yashkov YI. Surgery of obesity: modern status and perspectives. Obes Metab. 2005;2(2):11–16.
    99. Fogel MR, Ravitch MM, Adibi SA. Absorptive and digestive function of the jejunum after jejunoileal bypass for treatment of human obesity. Gastroenterology. 1976;71(5):729–733.
    100. Singh D, Laya AS, Clarkston WK, Allen MJ. Jejunoileal bypass: a surgery of the past and a review of its complications. World J Gastroenterol. 2009;15(18):2277–2279. doi:10.3748/wjg.15.2277.
    101. Khan A, Syed A, Martin D. Jejunal-Ileal bypass and its complications: case report and review of the literature. Cureus. 2020;12(7):e9276. doi:10.7759/cureus.9276.
    102. Fromm H, Sarva RP, Ravitch MM, et al. Effects of jejunoileal bypass on the enterohepatic circulation of bile acids, bacterial flora in the upper small intestine, and absorption of vitamin B12. Metabolism. 1983;32(12):1133–1141. doi:10.1016/0026-0495(83)90060-4.
    103. Dewind LT, Payne JH. Intestinal bypass surgery for morbid obesity: long-term results. JAMA. 1976;236(20):2298–2301.
    104. Yashkov YI, Danyushin VM. Treatment of patients with overweight and obesity using intragastric balloons. Obes Metab. 2007;4(4):26–29.
    105. Sedov VM, Fishman MB. Use of gastric balloon in treatment of patients with obesity. Vestn Khir Im I I Grek. 2008;167(1):33–36.
    106. Schouten R, Wiryasaputra DC, Van Dielen FM, et al. Long-term results of bariatric restrictive procedures: a prospective study. Obes Surg. 2010;20(12):1617–1626.
    107. Buchwald H, Owen H, Wangensteen SD, et al. Consensus conference statement bariatric surgery for morbid obesity: health implications for patients, health professionals, and third-party payers. Surg Obes Relat Dis. 2005;1(3):371–381. doi:10.1016/j.soard.2005.04.002.
    108. Bamehriz F, Alali MN, Arishi H, et al. Characteristics of morbid obese patients with high-risk cardiac disease undergoing laparoscopic sleeve gastrectomy surgery. Saudi J Anaesth. 2020;14(2):182–185. doi:10.4103/sja.SJA_749_19.
    109. Scopinaro N, Papadia F, Camerini G, et al. A comparison of a personal series of biliopancreatic diversion and literature data on gastric bypass help to explain the mechanisms of resolution of type 2 diabetes by the two operations. Obes Surg. 2008;18(8):1035–1038. doi:10.1007/s11695-008-9531-x.
    110. Batar N, Pulat Demir H, Bayram H. Assessment of nutritional status, body composition and blood biochemical parameters of patients following sleeve gastrectomy: 6 months follow up. Clin Nutr ESPEN. 2021;43:184–190. doi:10.1016/j.clnesp.2021.04.016.
    111. Osland E, Yunus RM, Khan S, Alodat T, Memon B, Memon MA. Postoperative early major and minor complications in laparoscopic vertical sleeve gastrectomy (LVSG) versus laparoscopic Roux-en-Y gastric bypass (LRYGB) procedures: a meta-analysis and systematic review. Obes Surg. 2016;26(10):2273–2284. doi:10.1007/s11695-016-2101-8.
    112. Kang JH, Le QA. Effectiveness of bariatric surgical procedures: a systematic review and network meta-analysis of randomized controlled trials. Medicine (Baltimore). 2017;96(46):e8632.
    113. Gaillard M, Tranchart H, Beaudreuil S, et al. Laparoscopic sleeve gastrectomy for morbid obesity in renal transplantation candidates: a matched case-control study. Transpl Int. 2020;33(9):1061–1070. doi:10.1097/MD.0000000000008632.
    114. Vidarsson B, Sundbom M, Edholm D. Incidence and treatment of leak at the gastrojejunostomy in Roux-en-Y gastric bypass: a cohort study of 40,844 patients. Surg Obes Relat Dis. 2019;15(7):1075–1079. doi:10.1016/j.soard.2019.04.033.
    115. Rogalski P, Swidnicka-Siergiejko A, Wasielica-Berger J, et al. Endoscopic management of leaks and fistulas after bariatric surgery: a systematic review and meta-analysis. Surg Endosc. 2021;35(3):1067–1087. doi:10.1007/s00464-020-07471-1.
    116. Gagner M. Decreased incidence of leaks after sleeve gastrectomy and improved treatments. Surg Obes Relat Dis. 2014;10(4):611–612. doi:10.1016/j.soard.2014.04.002.
    117. Rosenthal RJ, Diaz AA, Arvidsson D, et al; International Sleeve Gastrectomy Expert Panel. International sleeve gastrectomy expert panel consensus statement: best practice guidelines based on experience of >12,000 cases. Surg Obes Relat Dis. 2012;8(1):8–19. doi:10.1016/j.soard.2011.10.019.
    118. Gehrer S, Kern B, Peters T, Christoffel-Courtin C, Peterli R. Fewer nutrient deficiencies after laparoscopic sleeve gastrectomy (LSG) than after laparoscopic Roux-Y-gastric bypass (LRYGB)—a prospective study. Obes Surg. 2010;20(4):447–453. doi:10.1007/s11695-009-0068-4.
    119. Mechanick JI, Youdim A, Jones DB, et al. Clinical practice guidelines for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric surgery patient-2013 update: cosponsored by American Association of Clinical Endocrinologists, the Obesity Society, and American Society for Metabolic & Bariatric Surgery. Obesity. 2013;21(1):S1–S27. doi:10.1002/oby.20461.
    120. Schiavo L, Scalera G, Pilone V, De Sena G, Capuozzo V, Barbarisi A. Micronutrient deficiencies in patients candidate for bariatric surgery: a prospective, preoperative trial of screening, Diagnosis, and Treatment. Int J Vitam Nutr Res. 2015;85(5–6):340–347. doi:10.1024/0300-9831/a000282.
    121. Ernst B, Thurnheer M, Schmid SM, Schultes B. Evidence for the necessity to systematically assess micronutrient status prior to bariatric surgery. Obes Surg. 2009;19(1):66–73. doi:10.1007/s11695-008-9545-4.
    122. Gong K, Gagner M, Pomp A, et al. Micronutrient deficiencies after laparoscopic gastric bypass: recommendations. Obes Surg. 2008;18(9):1062–1066. doi:10.1007/s11695-008-9577-9.
    123. Caron M, Hould FS, Lescelleur O, et al. Long-term nutritional impact of sleeve gastrectomy. Surg Obes Relat Dis. 2017;13(10):1664–1673. doi:10.1016/j.soard.2017.07.019.
    124. Lovette AS, Shope TR, Koch TR. Origins for micronutrient deficiencies. In: Huang C, ed. Advanced Bariatric and Metabolic Surg. London: IntechOpen; 2012:229–254.
      125. Johnson LM, Ikramuddin S, Leslie DB, Slusarek B, Killeen AA. Analysis of vitamin levels and deficiencies in bariatric surgery patients: a single-institutional analysis. Surg Obes Relat Dis. 2019;15(7):1146–1152. doi:10.1016/j.soard.2019.04.028.
      126. Boyce SG, Goriparthi R, Clark J, Cameron K, Roslin MS. Can composite nutritional supplement based on the current guidelines prevent vitamin and mineral deficiency after weight loss surgery?Obes Surg. 2016;26(5):966–971. doi:10.1007/s11695-015-1853-x.
      127. James H, Lorentz P, Collazo-Clavell ML. Patient-reported adherence to empiric vitamin/mineral supplementation and related nutrient deficiencies after Roux-en-Y gastric bypass. Obes Surg. 2016;26(11):2661–2666. doi:10.1007/s11695-016-2155-7.
      128. Voglino C, Tirone A, Ciuoli C, et al. Controlling Nutritional Status (CONUT) score and micronutrient deficiency in bariatric patients: midterm outcomes of Roux-en-Y gastric bypass versus one anastomosis gastric bypass/mini gastric bypass. Obes Surg. 2021;31(8):3715–3726. doi:10.1007/s11695-021-05486-8.
      129. Billeter AT, Probst P, Fischer L, et al. Risk of malnutrition, trace metal, and vitamin deficiency post Roux-en-Y gastric bypass—a prospective study of 20 patients with BMI < 35 kg/m2. Obes Surg. 2015;25(11):2125–2134. doi:10.1007/s11695-015-1676-9.
      130. Henfridsson P, Laurenius A, Wallengren O, et al. Micronutrient intake and biochemistry in adolescents adherent or nonadherent to supplements 5 years after Roux-en-Y gastric bypass surgery. Surg Obes Relat Dis. 2019;15(9):1494–1502. doi:10.1016/j.soard.2019.06.012.
      131. Vix M, Liu KH, Diana M, D'Urso A, Mutter D, Marescaux J. Impact of Roux-en-Y gastric bypass versus sleeve gastrectomy on vitamin D metabolism: short-term results from a prospective randomized clinical trial. Surg Endosc. 2014;28(3):821–826. doi:10.1007/s00464-013-3276-x.
      132. Toh SY, Zarshenas N, Jorgensen J. Prevalence of nutrient deficiencies in bariatric patients. Nutrition. 2009;25(11–12):1150–1156. doi:10.1016/j.nut.2009.03.012.
      133. Moize V, Andreu A, Flores L, et al. Long-term dietary intake and nutritional deficiencies following sleeve gastrectomy or Roux-En-Y gastric bypass in a Mediterranean population. J Acad Nutr Diet. 2013;113(3):400–410. doi:10.1016/j.jand.2012.11.013.
      134. Boyle M, Carruthers N, Mahawar KK. Five-year outcomes with stand-alone primary sleeve gastrectomy. Obes Surg. 2019;29(5):1607–1613. doi:10.1007/s11695-019-03756-0.
      135. Calderón B, Gómez-Martín JM, Cuadrado-Ayuso M, et al. Circulating zinc and copper levels are associated with sperm quality in obese men after metabolic surgery: a pilot study. Nutrients. 2020;12(11):3354. doi:10.3390/nu12113354.
      136. Leeman M, Gadiot RPM, Wijnand JMA, et al. Effects of standard v. Very long Roux limb Roux-en-Y gastric bypass on nutrient status: a 1-year follow-up report from the Dutch Common Channel Trial (DUCATI) study. Br J Nutr. 2020;123(12):1434–1440. doi:10.1017/S0007114520000616.
      137. Våge V, Sande VA, Mellgren G, Laukeland C, Behme J, Andersen JR. Changes in obesity-related diseases and biochemical variables after laparoscopic sleeve gastrectomy: a two-year follow-up study. BMC Surg. 2014;14:8. doi:10.1186/1471-2482-14-8.
      138. Schijns W, Schuurman LT, Melse-Boonstra A, van Laarhoven CJHM, Berends FJ, Aarts EO. Do specialized bariatric multivitamins lower deficiencies after RYGB?Surg Obes Relat Dis. 2018;14(7):1005–1012. doi:10.1016/j.soard.2018.03.029.
      139. Antoniewicz A, Kalinowski P, Kotulecka KJ, et al. Nutritional deficiencies in patients after Roux-en-Y gastric bypass and sleeve gastrectomy during 12-month follow-up. Obes Surg. 2019;29(10):3277–3284. doi:10.1007/s11695-019-03985-3.
      140. Blume CA, Boni CC, Casagrande DS, Rizzolli J, Padoin AV, Mottin CC. Nutritional profile of patients before and after Roux-en-Y gastric bypass: 3-year follow-up. Obes Surg. 2012;22(11):1676–1685. doi:10.1007/s11695-012-0696-y.
      141. Kaidar-Person O, Rosenthal RJ. Malnutrition in morbidly obese patients: fact or fiction?Minerva Chir. 2009;64(3):297–302.
      142. Belfiore A, Cataldi M, Minichini L, et al. Short-term changes in body composition and response to micronutrient supplementation after laparoscopic sleeve gastrectomy. Obes Surg. 2015;25(12):2344–2351. doi:10.1007/s11695-015-1700-0.
      143. Saif T, Strain GW, Dakin G, Gagner M, Costa R, Pomp A. Evaluation of nutrient status after laparoscopic sleeve gastrectomy 1, 3, and 5 years after surgery. Surg Obes Relat Dis. 2012;8(5):542–547. doi:10.1016/j.soard.2012.01.013.
      144. Vargas-Ruiz AG, Hernández-Rivera G, Herrera MF. Prevalence of iron, folate, and vitamin B12 deficiency anemia after laparoscopic Roux-en-Y gastric bypass. Obes Surg. 2008;18(3):288–293. doi:10.1007/s11695-007-9310-0.
      145. Marc-Hernández A, Ruiz-Tovar J, Jimenez JM, et al. Short-term changes on body composition and bone mass after one-anastomosis gastric bypass: a prospective observational study. Obes Surg. 2020;30(9):3514–3521. doi:10.1007/s11695-020-04603-3.
      146. Podnos YD, Jimenez JC, Wilson SE, Stevens CM, Nguyen NT. Complications after laparoscopic gastric bypass: a review of 3464 cases. Arch Surg. 2003;138(9):957–961. doi:10.1001/archsurg.138.9.957.
      147. Borges-Canha M, Neves JS, Mendonça F, et al. The impact of bariatric surgery on hepatic function and predictors of liver steatosis and fibrosis. Obes Surg. 2020;30(8):2935–2941. doi:10.1007/s11695-020-04622-0.
      148. Ozmen MM, Guldogan CE, Gundogdu E. Changes in HOMA-IR index levels after bariatric surgery: comparison of single anastomosis duodenal switch–proximal approach (SADS-p) and one anastomosis gastric bypass–mini gastric bypass (OAGB-MGB). Int J Surg. 2020;78:36–41. doi:10.1016/j.ijsu.2020.04.008.
      149. Rodieux F, Giusti V, D'Alessio DA, Suter M, Tappy L. Effects of gastric bypass and gastric banding on glucose kinetics and gut hormone release. Obesity (Silver Spring). 2008;16(2):298–305. doi:10.1038/oby.2007.83.
      150. Laferrere B, Heshka S, Wang K, et al. Incretin levels and effect are markedly enhanced 1 month after Roux-en-Y gastric bypass surgery in obese patients with type 2 diabetes. Diabetes Care. 2007;30(7):1709–1716. doi:10.2337/dc06-1549.
      151. Herron D, Roohipour R. Complications of roux-En-Y gastric bypass and sleeve gastrectomy. Abdom Imaging. 2012;37(5):712–718. doi:10.1007/s00261-012-9866-6.
      152. Steinemann DC, Schiesser M, Clavien PA, Nocito A. Laparoscopic gastric pouch and remnant resection: a novel approach to refractory anastomotic ulcers after Roux-en-Y gastric bypass: case report. BMC Surg. 2011;11(1):33. doi:10.1186/1471-2482-11-33.
      153. Ruz M, Carrasco F, Rojas P, et al. Iron absorption and iron status are reduced after Roux-en-Y gastric bypass. Am J Clin Nutr. 2009;90(3):527–532. doi:10.3945/ajcn.2009.27699.
      154. Becker DA, Balcer LJ, Galetta SL. The neurological complications of nutritional deficiency following bariatric surgery. J Obes. 2012;2012:608534. doi:10.1155/2012/608534.
      155. Wapnir RA. Copper absorption and bioavailability. Am J Clin Nutr. 1998;67(5):1054S–1060S. doi:10.1093/ajcn/67.5.1054S.
      156. Aills L, Blankenship J, Buffington C, Furtado M, Parrott J; Allied Health Sciences Section Ad Hoc Nutrition Committee. ASMBS allied health nutritional guidelines for the surgical weight loss patient. Surg Obes Relat Dis. 2008;4(5):S73–S108. doi:10.1016/j.soard.2008.03.002.
      157. Ammor N, Berthoud L, Gerber A, Giusti V. Nutritional deficiencies in candidates for bariatric surgery. Rev Med Suisse. 2009;5(196):676–679.
      158. Dedov II, Mazurina NV, Ogneva NA, et al. Vitamin D metabolic disorders in obesity. Obes Metab. 2011;8(2):3–10.
      159. Dolan K, Hatzifotis M, Newbury L, Lowe N, Fielding G. A clinical and nutritional comparison of biliopancreatic diversion with and without duodenal switch. Ann Surg. 2004;240(1):51–56. doi:10.1097/01.sla.0000129280.68540.76.
      160. Griffith DP, Liff DA, Ziegler TR, Esper GJ, Winton EF. Acquired copper deficiency: a potentially serious and preventable complication following gastric bypass surgery. Obesity (Silver Spring). 2009;17(4):827–831. doi:10.1038/oby.2008.614.
      161. Muschitz C, Kocijan R, Haschka J, et al. The impact of vitamin D, calcium, protein supplementation, and physical exercise on bone metabolism after bariatric surgery: the BABS study. J Bone Miner Res. 2016;31(3):672–682. doi:10.1002/jbmr.2707.
      162. Shanbhogue VV, Stoving RK, Frederiksen KH, et al. Bone structural changes after gastric bypass surgery evaluated by HR-pQCT: a two-year longitudinal study. Eur J Endocrinol. 2017;176(6):685–693. doi:10.1530/EJE-17-0014.
      163. Switzer NJ, Marcil G, Prasad S, et al. Long-term hypovitaminosis D and secondary hyperparathyroidism outcomes of the Roux-en-Y gastric bypass: a systematic review. Obes Rev. 2017;18(5):560–566. doi:10.1111/obr.12525.
      164. Scopinaro N, Adami GF, Marinari GM, et al. Biliopancreatic diversion. World J Surg. 1998;22(9):936–946. doi:10.1007/s002689900497.
      165. Le Roux CW, Welbourn R, Werling M, et al. Gut hormones as mediators of appetite and weight loss after Roux-en-Y gastric bypass. Ann Surg. 2007;246(5):780–785. doi:10.1097/SLA.0b013e3180caa3e3.
      166. Cummings DE, Overduin J, Foster-Schubert KE. Gastric bypass for obesity: mechanisms of weight loss and diabetes resolution. J Clin Endocrinol Metab. 2004;89(6):2608–2615. doi:10.1210/jc.2004-0433.
      Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.