564995

research-article2014
NCPXXX10.1177/0884533614564995Nutrition in Clinical PracticeHandzlik-Orlik et al

Review
Nutrition in Clinical Practice
Volume XX Number X
Nutrition Management of the Post–Bariatric Month 201X 1­–10
© 2014 American Society
Surgery Patient for Parenteral and Enteral Nutrition
DOI: 10.1177/0884533614564995
ncp.sagepub.com
hosted at
online.sagepub.com
Gabriela Handzlik-Orlik, MD1; Michał Holecki, MD, PhD1,2; Bartłomiej
Orlik, MD, PhD3; Mariusz Wyleżoł, MD, PhD4; and Jan Duława, MD, PhD1

Abstract
Bariatric surgery is considered one of the most effective methods of achieving long-term weight loss when all other medical treatments
have failed. The number of bariatric procedures increases each year. Nevertheless, bariatric procedures are associated with a number of
complications that require careful multidisciplinary management. Nutrition supervision is of substantial value, as malnutrition, vitamin,
and micro- and macronutrient deficiencies may lead to deleterious consequences. In this review, we provide essential information on
nutrition management, both before and after bariatric surgical procedures. (Nutr Clin Pract.XXXX;xx:xx-xx)

Keywords
bariatrics; gastric bypass; avitaminosis; bariatric surgery; obesity; malnutrition; vitamin deficiency

Obesity is one of the most prevalent healthcare problems
worldwide. According to the World Health Organization
(WHO) classification, around 1.6 billion adults are considered
overweight (body mass index [BMI] between 25 and 30 kg/m2)
and 400 million are obese (BMI ≥30 kg/m2).1 It is estimated
that in the United States, by 2030, 51% of population will be
obese. Furthermore, the prevalence of severe obesity (BMI
>40 kg/m2), which was 5% of adults in 2010, is growing much
faster than that of moderate obesity and will increase in preva-
lence to 11% by 2030.2 Being overweight or obese is a major
risk factor of chronic diseases, including cardiovascular dis-
ease, type 2 diabetes mellitus (T2DM), musculoskeletal disor-
ders, and some types of neoplastic disease. Obesity is not only
a medical condition but also an economic problem. It accounts
for 2%–10% of national healthcare expenditures in the United
States and Western Europe countries.3
Nonsurgical management of obesity includes lifestyle
changes aimed at increasing physical activity, diet and behav-
ior modifications, and pharmacologic intervention. Medical
management can induce mean weight loss of 5%–10%, but it is
not always sufficient over the long term, especially for the
severely obese. If nonsurgical treatment fails, patients with an
increased risk of obesity-related mortality and those who meet
the criteria for surgery are encouraged to consider bariatric sur-
gical procedures.
Bariatric surgical procedures can be grouped into 3 main
categories: restrictive, malabsorptive, and mixed procedures.
Restrictive procedures, such as adjustable gastric banding
(AGB) or sleeve gastrectomy (SG), act to reduce oral intake by
limiting gastric volume, produce early satiety, and leave the ali-
mentary canal intact, minimizing the risks of metabolic compli-
cations. Malabsorptive procedures, such as biliopancreatic
diversion (BPD), reduce stomach size and create physiologic
conditions for malabsorption. Mixed procedures, such as gas-
tric bypass or sleeve gastrectomy with duodenal switch, apply
both techniques simultaneously. It appears that when compared,
malabsorptive procedures tend to have a lower rate of failure
and subsequent weight gain than do restrictive surgeries. The
most commonly performed procedures are Roux-en-Y gastric
bypass (RYGB), BPD, AGB, and SG.4 Bariatric surgery induces
significant long-lasting weight loss, ameliorates obesity-associ-
ated comorbidities, and reduces mortality.5
Despite this, bariatric procedures are burdened by early and
late complications.6 Among the early complications, the most
alarming are anastomotic leakage, bleeding, and pulmonary or
venous thromboembolism. However, the incidence of early
postoperative complications is low and usually does not exceed
1%. Late complications of bariatric surgery, although usually
less urgent, provide a wide range of health risks, such as
From 1Department of Internal Medicine and Metabolic Diseases, Medical
University of Silesia, Katowice, Poland; 2EASO Collaborating Center for
Obesity Management, Obesity Management Clinic WAGA, Katowice,
Poland; 3Center for Cardiovascular Research and Development,
American Heart of Poland, Katowice, Poland; and 4Department of
Surgery, Military Institute of Aviation Medicine, Warsaw, Poland.
Financial disclosure: Gabriela Handzlik-Orlik was supported by the
European Community from the European Social Fund within the
DoktoRIS project.
Corresponding Author:
Gabriela Handzlik-Orlik, MD, Department of Internal Medicine and
Metabolic Diseases, Medical University of Silesia, ul. Ziołowa 45/47,
40-635 Katowice, Poland.
Email: gabriela.handzlik@hotmail.com

Downloaded from ncp.sagepub.com at GEORGIAN COURT UNIV on January 11, 2015

2 Nutrition in Clinical Practice XX(X)
gallstone formation, anastomotic strictures, regaining weight,
dumping syndrome, and mental disorders. A detailed discus-
sion of the main issues for the prevention and management of
late surgical complications and other coexisting disorders,
such as diabetes mellitus, lipid disorders, bone mineral metab-
olism, and psychological care, is beyond the scope of this
review. We focus on essential knowledge of nutrition-related
pre- and postbariatric conditions as well as nutrition manage-
ment of patients after bariatric surgeries.
Diagnosis and Management of Nutrition
Deficiencies
According to the guidelines of the American Association of
Clinical Endocrinologists, every patient should be evaluated
before and after surgery for the ability to comply with nutrition
and lifestyle modifications.7 Malabsorptive effects of bariatric
surgeries are most frequently seen after RYGB and BPD and
less commonly after SG. Nutrition deficiencies observed after
bariatric surgeries arise from 2 main factors: (1) poor compli-
ance of the patient to treatment and (2) malabsorption induced
by modification in the gastrointestinal (GI) tract. While the last
one is not modifiable, proper supplementation combined with
dietary education can be efficient in avoiding malnutrition.
Prebariatric Nutrition Deficiencies and
Management in Obese Patients
The data published so far demonstrate a high prevalence of
preexisting nutrition deficiencies prior to any bariatric surgery
among patients. One of the principal aspects of malnutrition in
morbidly obese patients is initially poor nutrition status. Excess
energy consumption is paradoxically very often associated
with altered micronutrient intake and higher intake of poor-
quality, processed foods. The diet of obese patients has been
shown to contain a significantly lower percentage of protein
and a higher percentage of fat compared with the nonobese,8
which may predispose them to malnutrition. Protein and iron
deficiencies tend to increase simultaneously with BMI, result-
ing in preexisting iron deficiency in up to 35% of adults prior
to bariatric surgery.9 Similarly, obese patients have been shown
to be at greater risk of vitamin D deficiency than nonobese
individuals. Several hypotheses may account for such a dis-
crepancy in the incidence rate. Obese people tend to have very
low exposure to sunlight, which may lead to reduced vitamin D
skin production. Furthermore, the enlarged fat mass accumu-
lates but slowly releases vitamin D. Bioavailability of
25-hydroxyvitamin D3 (25(OH)D3), a stored form of vitamin
D, is impaired due to sequestration in fat compartments, which
subsequently leads to low serum levels and deficiency.10 It may
be also partially explained by inhibition of 25(OH)D3 synthesis
in hepatocytes by 1,25(OH)2D3 (its levels are elevated in obe-
sity) and by increased catabolism.11 Finally, higher doses of
Downloaded from ncp.sagepub.com at GEORGIAN COURT UNIV on January 11, 2015
vitamin D are required to compensate for deficiency in these
patients.12 The very interesting theory explaining vitamin D
deficiency in obese patients was recently presented by Drincic
et al.13 The authors suggested that there is no evidence for
sequestration (a notion suggesting aggressive uptake and stor-
age) of supplemental or endogenous cholecalciferol. Drincic
et al13 claimed that dilution of ingested or cutaneously synthe-
sized vitamin D in the large fat mass of obese patients as a
result of greater volume of distribution fully explains their
typically low vitamin D status. An increase in serum 25(OH)D3
levels after weight loss and a stronger correlation of these lev-
els with fat content than with the BMI may confirm the previ-
ously mentioned hypothesis. In a prospective observational
study of patients prior to the bariatric surgery, 56% had vitamin
D levels <30 nmol/L (12 ng/mL), and 40% had vitamin D val-
ues between 30 nmol/L (12 ng/mL) and 50 nmol/L (20 ng/
mL).14 Other studies confirmed this observation.14,15 In line
with these findings is preexisting subclinical calcium defi-
ciency (defined as elevated parathyroid hormone [PTH], with
normal Ca2+ level) in 25% of morbidly obese patients prior to
bariatric surgery.16 This constellation of abnormalities predis-
poses extremely obese patients to low bone mass and osteoma-
lacia even before surgery.
Such an initial state of malnutrition requires careful preop-
erative assessment by an experienced dietitian to identify psy-
chosocial and economic factors contributing to abnormal
eating patterns and to modify dietary beliefs and behaviors
before surgery. Interestingly, proper nutrition education prior
to surgery improves postoperative outcomes and reduces the
risk of weight regain. Comprehensive presurgical screening for
malnutrition is recommended to correct deficiencies before
surgery.7,17 Nutrition therapy combined with a very-low energy
diet, 2–4 weeks before surgery, reduces intra- and postopera-
tive complications.18 However, the exact content of a pre–bar-
iatric surgery diet is a matter of debate. A recent observational
study of 7000 bariatric procedures carried out in the United
Kingdom highlighted variability (low-carbohydrate/low-
energy diet; milk/yoghurt; liquid meal replacement) and lack
of consensus in this field.19
Postbariatric Nutrition Deficiencies and
Management
Protein malnutrition.  Features of protein malnutrition include
anemia, edema, alopecia, and asthenia. The most severe com-
plication is protein malnutrition. Hypoalbuminemia <3.5 mg/
dL used to be the gold standard in nutrition state assessment,
but as a negative acute phase reactant, it has limited diagnostic
value as a protein malnutrition marker. As protein intake plays
a pivotal role in muscle health, it is postulated that muscle
mass measured by hand grip and back strength assessed by
dynamometry might be a useful method in nutrition status
assessment.20 Other diagnostic options include measurement
Handzlik-Orlik et al 3
of body composition by body bioimpedance (a simple, nonin-
vasive tool) and dual-energy X-ray absorptiometry (DEXA),
but the accuracy of both of these techniques is limited due to
the tendency to overestimate fat mass in obese individuals.20
The phenomenon of malnutrition develops as a result of
malabsorption from bypassing a segment of small bowel and
less frequently due to diet restriction. Another component of
the malnutrition pathomechanism is postoperative avoidance
of specific nutrient-rich foods due to intolerance. The inci-
dence of protein malnutrition is relatively low after restrictive
procedures, affecting no more than 2% of patients after AGB.21
By comparison, malabsorptive surgeries are high-risk tech-
niques leading to protein deficiencies in up to 18%–25% of
patients.22,23 The degree of malnutrition is dependent on the
length of bypass, with an incidence of 25% when the length of
remaining bowel equals 50 cm24; as high as 6% of patients
after BPD require a revision surgery due to severe protein
malnutrition.8
Approximately 1.1–1.5 g/kg ideal body weight/d of protein
supply is needed for morbidly obese patients postoperatively.7
Of total energy intake, 10%–35% should be delivered with
protein.25 Patients with severe protein malnutrition who do not
respond to oral protein supplementation may require parenteral
nutrition (PN).
Iron deficiency. Patients undergoing bariatric surgery are at
risk of developing iron deficiency and subsequent anemia. The
pathogenesis of this disease comprises 3 main factors: (1)
impaired ability of the GI tract to reduce Fe3+ into the more
absorbable Fe2+, (2) reduced iron absorption due to the bypass
of the duodenum and proximal jejunum, and (3) intolerance/
avoidance of red meat, which is a main source of heme iron,
after bariatric surgery.
Low tolerance to red meat seems to be frequent after bariat-
ric surgery. More than 50% of patients experience chronic
meat intolerance after RYGB in long-term observation.26
Paradoxically, patients after a banding procedure who experi-
ence greater meat intolerance than bypass patients tend to have
a reduced prevalence of iron deficiency.27 Thus, decreased
meat consumption may be only partially responsible for iron
deficiency in this group of patients.
In 1 study, 20%–26% of patients preparing to undergo
RYGB had preexisting iron deficiency,24 and the percentage of
iron-deficient patients increased over time, affecting 39% after
a 4-year follow-up. A number of studies demonstrated that up
to 50% of RYGB patients have iron deficiency at 4 years, and
it is twice as more common in women.22,28,29 Similarly, iron
deficiency anemia is estimated to occur in 6%–50% of post-
RYGB patients29; however, the data regarding iron deficiency
after malabsorptive procedures are inconsistent. One study
demonstrated iron deficiency at a rate of almost 23% after BPD
in a 28-month follow-up, while another large-scale study of
589 patients who underwent laparoscopic BPD with duodenal
Downloaded from ncp.sagepub.com at GEORGIAN COURT UNIV on January 11, 2015
switch (BPD-DS) revealed normal iron levels within 3 years
of observation.23,30 Nevertheless, inconsistencies in method
and limitations of these studies (such as undefined iron supple-
mentation) do not allow definite conclusions.
In a recent study by van Rutte et al,31 anemia was found in
6% of patients 1 year after SG. Although it is indicated that
fewer deficiencies develop after restrictive procedures, a meta-
analysis by Kwon et al32 established the risk of postoperative
anemia and iron deficiency as comparable after SG and RYGB.
Therefore, iron prophylaxis is recommended both after restric-
tive and malabsorptive procedures.
In a randomized controlled trial, 65 mg of elemental iron
twice daily prevented development of iron deficiency but did
not always prevent anemia.33 Some evidence suggests that
supplementation of iron together with vitamin C significantly
increases iron absorption and ferritin levels and is far more
efficient than administration of iron alone. For those who
develop iron deficiency anemia, 150–200 mg of elemental iron
daily in the form of ferrous sulfate, fumarate, or gluconate
(preferably with vitamin C) is recommended.7
Anemia occurring after bariatric procedures cannot be
explained simply by iron, vitamin B12, and/or folate defi-
ciency.33,34 In the study by von Drygalski et al,35 a significant
weight loss 12 months after surgery was accompanied by
decreases in hemoglobin and ferritin levels despite a signifi-
cant increase in serum iron, folate, and vitamin B12 concentra-
tion. Ferritin as an acute phase reactant cannot be a reliable
measure of iron stores in the presence of inflammation associ-
ated with obesity. Taken together, postbariatric reduction of
inflammation and iron store depletion might be responsible for
the ferritin decrease. Normal serum iron levels could be still a
precursor to iron deficiency and anemia. However, “anemia of
obesity” is a complex and still unclear problem, which cannot
be simply explained by nutrition deficiencies.35
Calcium deficiency. Calcium depletion is among the most
prevalent deficiencies encountered in bariatric surgical prac-
tice. The main sites of calcium absorption are the duodenum
and proximal jejunum. The impact of RYGB surgery on bone
metabolism is a result of decreased calcium absorption, sec-
ondary hyperparathyroidism, and enhanced bone loss. Postop-
erative calcium supplementation is used in conjunction with
vitamin D administration and should be adjusted to serum
markers, bone density, vitamin D concentration, and concomi-
tant disorders (eg, chronic kidney disease). Recommended
doses of calcium after bariatric procedures range from 1200–
2000 mg/d.7,25
Vitamin B1, vitamin B12, and folate deficiency.  Vitamin B12
deficiency is highly prevalent after bariatric surgery and
develops mainly due to malabsorption resulting from reduced
intrinsic factor (IF) secretion.16 The true incidence of vitamin
B12 deficiency is difficult to determine because of differences
4 Nutrition in Clinical Practice XX(X)
in laboratory methods and normal physiologic ranges between
26% and 70%.28,36,37 However, the only prospective study
conducted to date was in a group of 298 patients after RYGB,
and it estimated vitamin B12 deficiency at a rate of 33%–37%
after 3 years of follow-up.22 Potential complications from
vitamin B12 deficiency include anemia, neuropathy, and cog-
nitive dysfunction. To avoid vitamin B12 deficiency, routine
supplementation after bariatric surgeries is recommended.
Approximately 1%–5% of vitamin B12 is absorbed in the
small intestine independent of IF transport. Thus, high-dose
oral vitamin B12 therapy (1000 mcg/d) may be effective.
However, the research on enteral supplementation is conflict-
ing,38,39 and the effectiveness of this type of treatment, par-
ticularly after gastric bypass procedures, seems to be of a
limited value. Impaired vitamin absorption in the presence of
accelerated food transit time through the small bowel may be
one explanation for ineffective treatment. Therefore, intra-
muscular vitamin B12 supplementation (500–1000 mcg/mo)
is preferred, particularly after malabsorptive procedures.36
There is no evidence supporting the use of high-dose supple-
mentation after restrictive surgeries.40 It seems that 500
mcg/d oral intake of vitamin B12 is sufficient for this group of
patients,36 but further studies on this subject are necessary.
Vitamin B12 serum concentration should be assessed prior to
surgery, every 6 months after the procedure for 2 years, and
annually thereafter.25
While folic acid deficiency might be predicted to occur less
commonly as it is absorbed throughout the small intestine, in
practice, many patients have diets deficient in folic acid, and as
many as 25% of obese patients have been demonstrated to be
deficient in folic acid prior to bariatric procedures.41 In line
with these findings are the results of another study, which dem-
onstrated that 22% of postbariatric patients were deficient after
2 years of follow-up.16 Oral multivitamin supplements admin-
istered after RYGB providing 600 mcg of folate for pregnant
women and 400 mcg for other adults can effectively prevent
folate deficiency.
Vitamin B1 (thiamine) is absorbed in the acidic environ-
ment of the duodenum. The deficiency results from a combina-
tion of reduced intake, excessive vomiting (eg, due to stomal
stenosis), and malabsorption due to decreased acid production
(as a result of reduced mucosal area of the stomach, particu-
larly after malabsorptive procedures).16 Thiamine deficiency
may occur as specific subtypes: (1) neuropsychiatric (Wernicke
encephalopathy/Korsakoff syndrome), (2) high-output cardio-
vascular disease (wet beriberi), (3) neuropathy (dry beriberi—
altered tendon reflexes, polyneuritis), and (4) GI beriberi
(nausea, vomiting, constipation, megajejunum). Until recently,
thiamine deficiency after bariatric surgery was considered rela-
tively uncommon, with total incidence not exceeding 0.18% in
patients who underwent BPD.42 However, a recent prospective
study by Shah et al43 found that the prevalence of symptomatic
thiamine deficiency after RYGB was 18%. On the basis of
Downloaded from ncp.sagepub.com at GEORGIAN COURT UNIV on January 11, 2015
these findings, the prevalence of constipation, dyspepsia, or
vomiting after bariatric surgery should be considered symp-
toms of thiamine deficiency. According to the guidelines of the
Endocrine Society, it is still optional to follow up the thiamine
serum concentration after bariatric procedures, whereas the
European Federation of Neurological Societies recommends
observation of thiamine status for at least 6 months and paren-
teral vitamin B1 supplementation (in case of persisting vomit-
ing). However, there is no evidence of an effective dosage in
deficiency prophylaxis.44 For active neurologic symptoms, the
recommended parenteral thiamine dosage is 500 mg/d for 3–5
days, followed by 250 mg/d for 3–5 days, and then optionally
oral supplementation of 100 mg/d until the resolution of symp-
toms or indefinitely.7
Acute post–gastric reduction surgery neuropathy
(APGRSN), a new term that has been introduced recently,
refers to a polynutritional, multisystem disorder characterized
by a triad of findings: protracted postoperative vomiting, hypo-
reflexia, and muscular weakness secondary to multifocal axo-
nopathy.45 The incidence of APGRSN is approximately 5.9 per
10,000 operations. The etiology is uncertain, but it is specu-
lated that vitamin B12, folate, and thiamine deficiency might be
reversible causes of APGRSN. This hypothesis is supported by
the fact that the compilation of symptoms is improved when
treated with vitamins, nutrition intervention, and intravenous
(IV) gamma-globulin administration. The symptoms may be
entirely reversible provided that the onset of the treatment is
initiated at an early stage.45
Unknown is the role of vitamin B6 in APGRSN etiology.
Peripheral neuropathy with symptoms including paresthesia,
burning and painful dysthesias, and thermal sensations has been
reported in pyridoxine depletion due to demyelination of periph-
eral nerves.46 Around 17% of RYGB patients develop vitamin
B6 deficiency a year after surgery,47 but the role of this phenom-
enon in postbariatric neuropathy has not been established yet.
Fat-soluble vitamin deficiencies. Fat-soluble vitamin defi-
ciencies are most commonly observed following malabsorp-
tive procedures, such as BPD, which limits the exposure of
food to biliopancreatic secretions. Steatorrhea induced by mal-
absorptive procedures may also lead to fat-soluble vitamin
deficiencies. Comparatively, purely restrictive procedures
rarely produce fat-soluble vitamin deficiencies.48
Suboptimal vitamin D level is currently a common condi-
tion in the general population and particularly the obese. A
64% deficiency rate (defined as 25(OH)D3 level <30 ng/mL)
is reported among the adult population.49 These observations
are in line with post–bariatric surgery findings. Up to 63% of
patients develop vitamin D depletion and 69% have elevated
PTH 4 years after BPD48 and 10 years after RYGB.50 Not
surprisingly, bone turnover after RYGB has been demon-
strated to be increased after 6–9 months with increased PTH
and decreased vitamin D despite supplementation during
Handzlik-Orlik et al 5
follow-up. It was also demonstrated that bone mineral density
at the hip decreased by 4.9% and in the whole body by 2.1%.51
AGB was observed to be associated with smaller increases in
bone resorption markers, lower rates of femoral bone loss,
and a paradoxical sparing or even increase in spine BMD
compared with RYGB patients, and thus it seems to be rea-
sonable to use restrictive rather than malabsorptive surgeries
when bone mineral depletion is a significant risk.52
Recent prospective analysis presents a similar response to
supplementation after malabsorptive and restrictive surgeries,
as reflected by a comparable increase of 25(OH)D concentra-
tion in both RYGB and SG groups.53 Nevertheless, it is
undoubtedly essential to provide long-term vitamin D supple-
mentation. In the research by Moore and Sherman,53 daily
supplementation of 2000 IU and 1500 mg of calcium for 3
months was effective and reduced the percentage of vitamin
D–deficient women from 60.6% to 26.1%. However, vitamin
D serum concentration did not reach the recommended 30 ng/
mL in 63% of patients. Therefore, it is reasonable to provide at
least 3000 IU of vitamin D, but in fact, doses should be titrated
to a therapeutic level of >30 ng/mL.7
Vitamin A deficiency has been demonstrated in 61% of
patients after BPD during a 28-month follow-up23 and in 69%
of individuals after a 4-year follow-up post–BPD-DS.48 It
appears that after RYGB surgeries, vitamin A deficiency is less
common, with an incidence of around 10% at 4 years of fol-
low-up. Clinical manifestations of vitamin A deficiency are
rare, and it presents mainly as ophthalmologic complications
(night blindness or ocular xerosis). If symptoms develop, oral
supplementation of vitamin A at a dose of 5000–10,000 IU/d is
recommended, until the vitamin A level normalizes, which
should be rechecked quarterly for 6–12 months.7,25
Although vitamin K deficiency has been identified in 68%
of BPD and BPD-DS patients up to 4 years after surgery, there
were no clinical manifestations of increased bleeding or altered
clotting.48
Vitamin E deficiency is an uncommon finding, with an inci-
dence rate not exceeding 4% of patients for 4 years after BPD,48
and no significant clinical manifestation of its deficiency has
been presented so far.
Gastroenterological and Eating Behavior
Management
Vomiting
The limited capacity of the gastric pouch after restrictive sur-
geries (30–60 mL) results in significant limitation of the
amount of food consumption. Of bariatric patients, 30%–60%
report postoperative vomiting, mostly within the first months
after surgery, when patients are adapting to a smaller gastric
pouch.25 Nausea, regurgitation, and vomiting are particularly
likely when compliance with nutrition recommendations (such
Downloaded from ncp.sagepub.com at GEORGIAN COURT UNIV on January 11, 2015
as small volumes of food chewed slowly) is neglected.
Persistent vomiting, nausea, abdominal pain, diarrhea, and
constipation should lead to the further assessment of other pos-
sible causes such as bacterial overgrowth, ulcer disease, anas-
tomotic complications (fistula), bowel obstruction, and so on.
Dumping Syndrome
The pathogenesis of dumping syndrome (DS) consists of rapid
gastric emptying and delivery to the small intestine of a signifi-
cant proportion of energy-dense food, which exerts local
osmotic effects and delayed hypoglycemia.54 Other elements
contributing to the syndrome are the release of GI and pancre-
atic hormones. Early symptoms comprise GI and vasomotor
manifestations, while late DS develops as a result of postpran-
dial hypoglycemia. Key symptoms of DS develop 15–30 min-
utes after meals and include abdominal pain, nausea, epigastrial
fullness, dizziness, flushing, dyspnea, tachycardia, apathy,
weakness, and syncope.25 The prevalence of DS ranges between
40% and 76% of patients after RYGB, and it may develop in
around 30% of patients after SG.25,55,56 Reinforcement of nutri-
tion changes is the first step in the treatment of DS. Patients
should eat small, frequent (3+) meals, and they should avoid
refined carbohydrate–dense foods and drinking liquids within
30 minutes of a solid-food meal. Ingestion of protein, fiber, and
complex carbohydrates should be increased. If nonpharmaco-
logic intervention is unsuccessful, somatostatin analogues, such
as octreotide 50 mg subcutaneously given 30 minutes prior to
the meal, may improve symptoms in some patients.25
Symptoms of DS usually resolve spontaneously after 18–24
months postsurgery. Although perceived as a complication, it
may be in fact an expected and desired component of behavior
modification, because it discourages the intake of calorie-
dense food and beverages.25 However, nondumpers tend to
have greater decrease in BMI at 1 and 2 years of follow-up,
probably due to better adherence to dietary advice among this
group of patients from the very beginning.55
Postprandial Hypoglycemia
Hyperinsulinemic hypoglycemia observed in some patients
after RYGB is frequently identified with dumping syndrome,
although in distinction to DS, hyperinsulinemic hypoglycemia
presents with symptoms of neuroglycopenia.57 The risk for
hypoglycemia is increased 2- to 7-fold in patients after RYGB.
It tends to develop usually 2–9 years after gastric bypass.57
Patients presenting with postprandial hypoglycemia, espe-
cially neuroglycopenic symptoms, who do not respond to
nutrition modification, should be evaluated to differentiate
dumping syndrome, insulinoma, and noninsulinoma pancrea-
togenous hypoglycemia syndrome (NIPHS).58,59 NIPHS was
introduced by Service et al,58 and its diagnostic criteria include
the following:
6 Nutrition in Clinical Practice XX(X)
•• positive Whipple’s triad-episodic hypoglycemia, cen-
tral nervous system dysfunction temporally related to
hypoglycemia (confusion, anxiety, stupor, paralysis,
convulsions, coma), and dramatic reversal of these
abnormalities by glucose administration;
•• a negative 72-hour fast;
•• negative observation toward insulinoma;
•• positive calcium stimulation test;
•• islet hypertrophy or nesidioblastosis (β-cell hyperplasia
and diffuse proliferation and hypertrophy of islet cells
from pancreatic ducts).
Thus, the etiology of postprandial hypoglycemia is complex.
Suggested mechanisms have included expansion of β-cell
mass (eg nesidioblastosis), alterations in β-cell function (glu-
cagon-like peptide-1 contribute to β-cell proliferation), and
non–β-cell related factors (decreased levels of the appetite-
stimulating and insulin counterregulatory GI hormone) or pos-
sibly a combination of mechanisms.59
The somatostatin analogue, octreotide, has been shown to be
effective in NIPHS treatment as it inhibits gastric emptying, GI
hormones, and insulin secretion.7,25 Acarbose has been shown
to improve symptoms due to carbohydrate digestion and absorp-
tion. The calcium-induced insulin release inhibitor, diazoxide,
has also been presented to adequately control symptoms in a
group of patients.7,25 Some authors suggest partial pancreatec-
tomy as a treatment strategy in patients who do not improve
after pharmacologic treatment, but this should be reserved for
the rare severe cases resistant to medical treatment.59
Behavioral Support and Weight Regain
Prevention
Multidisciplinary surveillance after bariatric surgery is impor-
tant for maintaining optimal health of patients in the long term.
Dietary and psychological interventions are 2 main elements in
prevention of weight regain. A lot of patients continue to have
emotional disturbances, mainly due to unrealistic presurgical
expectations concerning weight loss and difficulties associated
with the necessity of postbariatric lifestyle changes.60 Thus,
dietary and psychological assessment is an essential part of
preoperative evaluation, identifying potential contraindica-
tions for bariatric surgery (such as severe depression and per-
sonality disorders) and postoperative risks. Preexisting eating
disorders such as binge eating, which occurs in 5%–10% of
patients who present for surgery, are risk factors of postsurgical
weight loss failure.61 Therefore, particular attention should be
focused during the follow-up period in this group of patients.
Postbariatric psychological and dietary treatment should be
provided for as long as the patient demonstrates psychological
distress and has difficulties in maintaining behavioral changes
and the diet regime.62
The type of surgery is an unmodifiable factor influencing
weight outcome. However, when well educated, patients can
Downloaded from ncp.sagepub.com at GEORGIAN COURT UNIV on January 11, 2015
control modifiable factors, such as errors in estimating total
energy intake. Patient must be aware of the risks associated
with incorrect food and beverage choices as they may result in
GI symptoms, such as reflux, regurgitation, vomiting, diarrhea,
abdominal pain, and so on. Patients must also be able to recog-
nize multiple negative behavioral drivers that trigger excessive
food intake, such as alcohol consumption, sleep deprivation,
and watching television.63 Furthermore, weight should be
monitored on a regular basis to identify early relapse.
General Nutrition Recommendations
To avoid postoperation nutrition complications, every patient
should be advised on the general importance of a nutritionally
adequate diet and necessary vitamin and microelement supple-
mentation. Prior to bariatric procedures, patients should be
educated by an experienced dietitian on the principles of grad-
ual meal progression depending on the bariatric technique
performed.
General rules of postoperative eating behavior include
some of the following:
1. To prevent lean body mass loss, an individualized pro-
tein supply should be provided, with a minimum of 60
g/d to 120 g/d7,51 (preferably 1.1–1.5 g/kg/d after
RYGB and up to 90 g/d after BPD).
2. Sucrose should be eliminated from the diet to avoid DS
and excessive calorie intake after both restrictive and
malabsorptive surgeries.64
3. Patients should also avoid fruit juices, fried foods,
high-saturated fat, carbonated beverages, alcohol, and
caffeine.65
4. Patients should eat 3–6 small meals daily and chew
small bites of food prior to swallowing.7 Every meal
should last at least 30 minutes. A regular eating pattern
must be established to prevent meal skipping.
5. For the first 3–6 months after surgery, patients should
be provided with preferably a chewable or liquid form
of vitamin and mineral supplementation.7
6. Routine long-term adult multivitamin and mineral supple-
mentation must be considered in all patients after bariatric
surgeries, with those who underwent malabsorptive proce-
dures requiring more intensive replacement therapy:
a. Elemental iron: 45–60 mg/d, preferably with vita-
min C64
b. Folic acid: 400 mcg/d7
c. Vitamin B1: 50–100 mg/d optionally (at the onset
of thiamine deficiency symptoms, administer
intramuscularly or intravenously 50–100 mg/d for
7–14 days, then 10 mg/d orally until neurologic
symptoms resolve)66
d. Vitamin B12: 500–1000 mcg orally, if deter-
mined to be adequately absorbed, or 1000 mcg
Handzlik-Orlik et al 7

Table 1.  Suggested Dietary Proceedings After Bariatric Surgery.

Time After Operation Dietary Recommendation After Bariatric Surgery

Days 1–2 •• Clear liquids (sugar free, no caffeine, noncarbonated, nonalcoholic) administered under registered
dietitian supervision7
•• Drink liquids in small portions as tolerated, volume of daily supply should not exceed 1500 mL,56 do not
drink too quickly—200 mL over a minimum of 1 hour
•• Avoid drinking liquids from a straw to reduce intake of air56
Days 3–7 •• Continue clear liquids and start full liquids in a 1:1 proportion (nonfat milk, soy milk, plain or blended
yogurt, blended soups)56
•• Total fluid intake should not exceed 1500–1900 mL/d56
•• Addition of soy protein powder to full liquids is acceptable (<20 g protein/serving)56
•• Start multivitamin and mineral supplementation (chewable form preferred)58
Week 2–3 •• Increase clear liquids to 1500–1900 mL/d56
•• Replace full liquids with solid foods: soft, moist, pureed, ground, low-fat, high-protein foods—eggs,
cottage cheese, fish, poultry, lean meat, cooked beans60
•• Consume 4–6 meals/d (limit portion size to ~¼ cup)56
•• Consume protein first (at least 60 g/d)56,58
Week 4–6 •• Advance diet as tolerated (well-cooked vegetables, soft and/or peeled or canned fruits—sugar free)56,58
•• Add one more soft, moist, solid meal/d as tolerated
•• Consume 4–6 meals/d (limit portion size to ~½ cup)56
•• Consume protein first (60–80 g/d)56,58
•• Total clear liquid volume per day ~1500–1900 mL56
•• No beverages 30 minutes before eating and 30–60 minutes after eating56
•• Chew small bites of food thoroughly before swallowing56,60
Week 7 and beyond •• Daily caloric intake adequately to height, weight, and age7
•• Balanced diet with lean protein, fruits, vegetables, and whole grains58
•• Avoid raw fruits and vegetables with high fibrous consistency (celery stalks, corn, artichokes, pineapple,
orange) unless they are pureed or well cooked58
•• Consume 3 meals and 2 snacks/d (limit portion size to ~1 cup)56
•• Total clear liquid volume per day ~1500–1900 mL58
•• No beverages 30 minutes before eating and 30–60 minutes after eating56
•• Chew small bites of food thoroughly before swallowing (aim for 30 chews for each bite)56

monthly as intramuscular preparation67; alterna- min B12, methylmalonic acid, and homocystine
tively, 1000–3000 mcg every 6–12 months intra- should be examined68
muscularly or 500 mcg every week intranasally7
e. Calcium citrate: 1200–2000 mg/d7,25— Detailed postbariatric dietary recommendations and monitor-
preferably 1500 mg after AGB and 2000 after ing are presented in Table 17,65,67,69 and Table 2.7,25,64
RYGB

Furthermore:
f. RYGB, BPD, and SG are indications for 2 adult
multivitamin doses daily, and AGB is an indica-
tion for 1 adult multivitamin dose daily7,25,64
g. Daily supplementation of vitamin D should pro-
vide at least 3000 IU, titrated to therapeutic
25-hydroxyvitamin D levels >30 ng/mL7; control
of vitamin D concentration should be provided 6
weeks after the initiation of supplementation
h. To improve iron and calcium absorption, calcium
and iron tablets should be administered about 4
hours apart
i. In patients who develop a neuropathy after a bar-
iatric procedure, levels of thiamine, copper, vita-
Conclusions
Nutrition deficiency in morbidly obese bariatric surgery
patients is a complex problem, both pre- and postoperatively,
and treatment of nutrition deficiencies should be initiated
preoperatively. One of the most important aspects of post-
bariatric follow-up is adequate and sufficient nutrition care
and eating behavior modification. Severe nutrition deficits
can be avoided, provided that patients are systematically
supplemented with multivitamins, macroelements, and
microelements, as well as systematically monitored.
Multidisciplinary surveillance requires efficient cooperation
of surgeons, internists, psychologists, and dietitians, but the
one who plays the pivotal role in this battle against malnutri-
tion, weight gain, and other complications of bariatric sur-
gery is the patient.

Downloaded from ncp.sagepub.com at GEORGIAN COURT UNIV on January 11, 2015

8 Nutrition in Clinical Practice XX(X)

Table 2.  Monitoring and Symptoms of Nutrition Deficiencies After Bariatric Surgery.7,21,43

Nutrient Schedule for Monitoring Symptoms of Deficiency

Vitamin B12 •• Preoperatively •• Anemia
•• After 6, 12, 18, and 24 months •• Neuropathy
•• Subsequently annually •• Cognitive disorders
•• Quarterly for 3–6 months if supplemented
Folic acid •• Preoperatively •• Megaloblastic anemia
•• After 6, 12, 18, and 24 months •• Neurologic symptoms
•• Subsequently annually •• Psychiatric problems
Vitamin D/calcium •• Preoperatively •• Osteoporosis
•• After 6, 12, 18, and 24 months •• Hypocalcemia
•• Subsequently annually •• Tetany
•• If therapeutic doses of vitamin D administered—reevaluation •• Cramping
after 1–3 months
•• If maintenance dose of vitamin D instituted—reevaluation
after 3–4 months, then semiannually
Vitamin A •• Preoperatively •• Night blindness
•• Optionally after 24 months and annually thereafter •• Ocular xerosis
•• Quarterly for 6–12 months if supplemented •• Altered immunity
Vitamin B1 •• Optionally after 3, 6, 12, 18, and 24 months and annually •• Confusion
thereafter •• Disorientation
•• Polyneuritis
•• Nausea, vomiting, constipation
Vitamin K •• Not recommended •• Increased bleeding
•• Altered clotting (not observed after
bariatric surgery)
Iron •• Preoperatively •• Iron deficiency anemia
•• 3, 6, 12, 18, and 24 months •• Fatigue
•• Subsequently annually •• Generalized weakness
•• Irritability
•• Pica
•• Koilonychia
•• Brittle hair

References
1. Pêgo-Fernandes PM, Bibas BJ, Deboni M. Obesity: the greatest epidemic
of the 21st century? Sao Paulo Med J. 2011;129:283-284.
2. Finkelstein EA, Khavjou OA, Thompson H, et al. Obesity and severe obe-
sity forecasts through 2030. Am J Prev Med. 2012;42:563-570.
3. Andreyeva T, Sturm R, Ringel JS. Moderate and severe obesity have large
differences in health care costs. Obes Res. 2004;12:1936-1943.
4. Neff KJ, le Roux CW. Bariatric surgery: a best practice article. J Clin
Pathol. 2013;66:90-98.
5. Sjöström L, Peltonen M, Jacobson P, et al. Bariatric surgery and long-term
cardiovascular events. JAMA. 2012;307:56-65.
6. Nguyen NT, Wilson SE. Complications of antiobesity surgery. Nat Clin
Pract Gastroenterol Hepatol. 2007;4:138-147.
7. Mechanick JI, Youdim A, Jones DB, et al. Clinical practice guidelines for
the perioperative nutritional, metabolic, and nonsurgical support of the bar-
iatric surgery patient—2013 update: cosponsored by American Association
of Clinical Endocrinologists, the Obesity Society, and American Society
for Metabolic & Bariatric Surgery. Surg Obes Relat Dis. 2013;9:159-191.
8. Davies DJ, Baxter JM, Baxter JN. Nutritional deficiencies after bariatric
surgery. Obes Surg. 2007;17:1150-1158.
9. Ammor N, Berthoud L, Gerber A, Giusti V. Nutritional deficiencies in
candidates for bariatric surgery. Rev Med Suisse. 2009;5:676-679.
10. Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF. Decreased bio-
availability of vitamin D in obesity. Am J Clin Nutr. 2000;72:690-693.
11. Bell NH, Epstein S, Greene A, Shary J, Oexmann MJ, Shaw S. Evidence
for alteration of the vitamin D–endocrine system in obese subjects. J Clin
Invest. 1985;76:370-373.
12. Ducloux R, Nobécourt E, Chevallier JM, Ducloux H, Elian N, Altman JJ.
Vitamin D deficiency before bariatric surgery: should supplement intake
be routinely prescribed? Obes Surg. 2011;21:556-560.
13. Drincic AT, Armas LA, Van Diest EE, Heaney RP. Volumetric dilution,
rather than sequestration best explains the low vitamin D status of obesity.
Obesity (Silver Spring). 2012;20:1444-1448.
14. Goldner WS, Stoner JA, Thompson J, et al. Prevalence of vitamin D insuf-
ficiency and deficiency in morbidly obese patients: a comparison with
non-obese controls. Obes Surg. 2008;18:145-150.
15. Carlin AM, Rao DS, Meslemani AM, et al. Prevalence of vitamin D deple-
tion among morbidly obese patients seeking gastric bypass surgery. Surg
Obes Relat Dis. 2006;2:98-103.
16. Bloomberg RD, Fleishman A, Nalle JE, Herron DM, Kini S. Nutritional
deficiencies following bariatric surgery: what have we learned? Obes
Surg. 2005;15:145-154.
17. Chapman CD, Benedict C, Brooks SJ, Schiöth HB. Lifestyle deter-
minants of the drive to eat: a meta-analysis. Am J Clin Nutr. 2012;96:
492-497.
18. Van Nieuwenhove Y, Dambrauskas Z, Campillo-Soto A, et al. Preoperative
very low-calorie diet and operative outcome after laparoscopic gas-
tric bypass: a randomized multicenter study. Arch Surg. 2011;146:
1300-1305.

Downloaded from ncp.sagepub.com at GEORGIAN COURT UNIV on January 11, 2015

Handzlik-Orlik et al 9
19. Baldry EL, Leeder PC, Idris IR. Pre-operative dietary restriction for
patients undergoing bariatric surgery in the UK: observational study of
current practice and dietary effects. Obes Surg. 2014;24:416-421.
20. Jones CH, Newstead CG, Will EJ, Smye SW, Davison AM. Assessment
of nutritional status in CAPD patients: serum albumin is not a useful mea-
sure. Nephrol Dial Transplant. 1997;12:1406-1413.
21. Steffen R, Horber F, Hauri P. Swedish adjustable gastric band (SAGB)–
distal gastric bypass: a new variant of an old technique in the treatment of
superobesity and failed band restriction. Obes Surg. 1999;9:171-176.
22. Brolin RE, LaMarca LB, Kenler HA, Cody RP. Malabsorptive gas-
tric bypass in patients with superobesity. J Gastrointest Surg. 2002;6:
195-203.
23. Dolan K, Hatzifotis M, Newbury L, Lowe N, Fielding G. A clinical and
nutritional comparison of biliopancreatic diversion with and without duo-
denal switch. Ann Surg. 2004;240:51-56.
24. Sugerman HJ, Kellum JM, DeMaria EJ. Conversion of proximal to distal
gastric bypass for failed gastric bypass for superobesity. J Gastrointest
Surg. 1997;1:517-524.
25. Heber D, Greenway FL, Kaplan LM, Livingston E, Salvador J, Still C;
Endocrine Society. Endocrine and nutritional management of the post-bar-
iatric surgery patient: an Endocrine Society Clinical Practice Guideline. J
Clin Endocrinol Metab. 2010;95:4823-4843.
26. Avinoah E, Ovnat A, Charuzi I. Nutritional status seven years after Roux-
en-Y gastric bypass surgery. Surgery. 1992;111:137-142.
27. Brolin RE, Robertson LB, Kenler HA, Cody RP. Weight loss and dietary
intake after vertical banded gastroplasty and Roux-en-Y gastric bypass.
Ann Surg. 1994;220:782-790.
28. Skroubis G, Sakellaropoulos G, Pouggouras K, Mead N, Nikiforidis G,
Kalfarentzos F. Comparison of nutritional deficiencies after Roux-en-Y
gastric bypass and after biliopancreatic diversion with Roux-en-Y gastric
bypass. Obes Surg. 2002;12:551-558.
29. 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;18:288-293.
30. Rabkin RA, Rabkin JM, Metcalf B, Lazo M, Rossi M, Lehman-Becker
LB. Nutritional markers following duodenal switch for morbid obesity.
Obes Surg. 2004;14:84-90.
31. van Rutte PW, Aarts EO, Smulders JF, Nienhuijs SW. Nutrient defi-
ciencies before and after sleeve gastrectomy. Obes Surg. 2014;24(10):
1639-1646.
32. Kwon Y, Kim HJ, Lo Menzo E, Park S, Szomstein S, Rosenthal RJ.
Anemia, iron and vitamin B12 deficiencies after sleeve gastrectomy com-
pared to Roux-en-Y gastric bypass: a meta-analysis. Surg Obes Relat Dis.
2014;10(4):589-597.
33. Brolin RE, Gorman JH, Gorman RC, et al. Prophylactic iron supplementa-
tion after Roux-en-Y gastric bypass: a prospective, double-blind, random-
ized study. Arch Surg. 1998;133:740-744.
34. von Drygalski A, Andris DA. Anemia after bariatric surgery: more than
just iron deficiency. Nutr Clin Pract. 2009;24:217-226.
35. von Drygalski A, Andris DA, Nuttleman PR, Jackson S, Klein J, Wallace
JR. Anemia after bariatric surgery cannot be explained by iron deficiency
alone: results of a large cohort study. Surg Obes Relat Dis. 2011;7:151-156.
36. Majumder S, Soriano J, Louie Cruz A, Dasanu CA. Vitamin B12 defi-
ciency in patients undergoing bariatric surgery: preventive strategies and
key recommendations. Surg Obes Relat Dis. 2013;9:1013-1019.
37. Marcuard SP, Sinar DR, Swanson MS, Silverman JF, Levine JS. Absence
of luminal intrinsic factor after gastric bypass surgery for morbid obesity.
Dig Dis Sci. 1989;34:1238-1242.
38. Adachi S, Kawamoto T, Otsuka M, Todoroki T, Fukao K. Enteral vita-
min B12 supplements reverse postgastrectomy B12 deficiency. Ann Surg.
2000;232:199-201.
39. Bolaman Z, Kadikoylu G, Yukselen V, Yavasoglu I, Barutca S, Senturk T.
Oral versus intramuscular cobalamin treatment in megaloblastic anemia:
Downloaded from ncp.sagepub.com at GEORGIAN COURT UNIV on January 11, 2015
a single-center, prospective, randomized, open-label study. Clin Ther.
2003;25:3124-3134.
40. Capoccia D, Coccia F, Paradiso F, et al. Laparoscopic gastric
sleeve and micronutrients supplementation: our experience. J Obes.
2012;2012:672162.
41. de Luis DA, Pacheco D, Izaola O, Terroba MC, Cuellar L, Cabezas G.
Micronutrient status in morbidly obese women before bariatric surgery.
Surg Obes Relat Dis. 2013;9:323-327.
42. Primavera A, Brusa G, Novello P, et al. Wernicke-Korsakoff encepha-
lopathy following biliopancreatic diversion. Obes Surg. 1993;3:
175-177.
43. Shah HN, Bal BS, Finelli FC, Koch TR. Constipation in patients with
thiamine deficiency after Roux-en-Y gastric bypass surgery. Digestion.
2013;88:119-124.
44. Galvin R, Bråthen G, Ivashynka A, Hillbom M, Tanasescu R, Leone
MA; EFNS. EFNS guidelines for diagnosis, therapy and prevention of
Wernicke encephalopathy. Eur J Neurol. 2010;17:1408-1418.
45. Chang CG, Adams-Huet B, Provost DA. Acute post–gastric reduction sur-
gery (APGARS) neuropathy. Obes Surg. 2004;14:182-189.
46. Spinneker A, Sola R, Lemmen V, Castillo MJ, Pietrzik K, González-Gross
M. Vitamin B6 status, deficiency and its consequences—an overview.
Nutr Hosp. 2007;22:7-24.
47. Clements RH, Katasani VG, Palepu R, et al. Incidence of vitamin defi-
ciency after laparoscopic Roux-en-Y gastric bypass in a university hospi-
tal setting. Am Surg. 2006;72:1196-1204.
48. Slater GH, Ren CJ, Siegel N, et al. Serum fat-soluble vitamin deficiency
and abnormal calcium metabolism after malabsorptive bariatric surgery. J
Gastrointest Surg. 2004;8:48-55.
49. Mitchell DM, Henao MP, Finkelstein JS, Burnett-Bowie SA. Prevalence
and predictors of vitamin D deficiency in healthy adults. Endocr Pract.
2012;18:914-923.
50. Karefylakis C, Näslund I, Edholm D, Sundbom M, Karlsson FA, Rask
E. Vitamin D status 10 years after primary gastric bypass: gravely high
prevalence of hypovitaminosis D and raised PTH levels. Obes Surg.
2014;24:343-348.
51. Coates PS, Fernstrom JD, Fernstrom MH, Schauer PR, Greenspan
SL. Gastric bypass surgery for morbid obesity leads to an increase in
bone turnover and a decrease in bone mass. J Clin Endocrinol Metab.
2004;89:1061-1065.
52. Yu EW. Bone metabolism after bariatric surgery. J Bone Miner Res.
2014;29:1507-1518.
53. Moore CE, Sherman V. Vitamin D supplementation efficacy: sleeve
gastrectomy versus gastric bypass surgery. Obes Surg. 2014;24(12):
2055-2060.
54. Tack J, Arts J, Caenepeel P, De Wulf D, Bisschops R. Pathophysiology,
diagnosis and management of postoperative dumping syndrome. Nat Rev
Gastroenterol Hepatol. 2009;6:583-590.
55. Banerjee A, Ding Y, Mikami DJ, Needleman BJ. The role of dump-
ing syndrome in weight loss after gastric bypass surgery. Surg Endosc.
2013;27:1573-1578.
56. Tzovaras G, Papamargaritis D, Sioka E, et al. Symptoms suggestive of
dumping syndrome after provocation in patients after laparoscopic sleeve
gastrectomy. Obes Surg. 2012;22:23-28.
57. Bernard B, Kline GA, Service FJ. Hypoglycaemia following upper
gastrointestinal surgery: case report and review of the literature. BMC
Gastroenterol. 2010;10:77.
58. Service FJ, Natt N, Thompson GB, et al. Noninsulinoma pancreatog-
enous hypoglycemia: a novel syndrome of hyperinsulinemic hypoglyce-
mia in adults independent of mutations in Kir6.2 and SUR1 genes. J Clin
Endocrinol Metab. 1999;84:1582-1589.
59. Foster-Schubert KE. Hypoglycemia complicating bariatric surgery:
incidence and mechanisms. Curr Opin Endocrinol Diabetes Obes.
2011;18:129-133.
10 Nutrition in Clinical Practice XX(X)

60. Johnson Stoklossa C, Atwal S. Nutrition care for patients with weight
regain after bariatric surgery. Gastroenterol Res Pract. 2013;2013:
256145.
61. Meany G, Conceição E, Mitchell JE. Binge eating, binge eating disorder
and loss of control eating: effects on weight outcomes after bariatric sur-
gery. Eur Eat Disord Rev. 2014;22:87-91.
62. Kubik JF, Gill RS, Laffin M, Karmali S. The impact of bariatric surgery
on psychological health. J Obes. 2013;2013:837989.
63. Chapman CD, Benedict C, Brooks SJ, Schiöth HB. Lifestyle determinants
of the drive to eat: a meta-analysis. Am J Clin Nutr. 2012;96:492-497.
64. Fried M, Yumuk V, Oppert JM, et al. Interdisciplinary European guide-
lines on metabolic and bariatric surgery. Obes Facts. 2013;6:449-468.
65. Kulick D, Hark L, Deen D. The bariatric surgery patient: a growing role
for registered dietitians. J Am Diet Assoc. 2010;110:593-599.
66. Becker DA, Balcer LJ, Galetta SL. The neurological complications
of nutritional deficiency following bariatric surgery. J Obes. 2012;
2012:608534.
67. Aills L, Blankenship J, Buffington C, et al. ASMBS Allied Health nutri-
tional guidelines for the surgical weight loss patient. Surg Obes Relat Dis.
2008;4:S73-S108.
68. Rudnicki SA. Prevention and treatment of peripheral neuropathy after bar-
iatric surgery. Curr Treat Options Neurol. 2010;12:29-36.
69. Moizé VL, Pi-Sunyer X, Mochari H, Vidal J. Nutritional pyramid for post-
gastric bypass patients. Obes Surg. 2010;20:1133-1141.

Downloaded from ncp.sagepub.com at GEORGIAN COURT UNIV on January 11, 2015