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ASMBS Nutrition Guidelines Micronutrient Evidence And Recommendations
ASMBS INTEGRATED HEALTH NUTRITIONAL GUIDELINES FOR THE
SURGICAL WEIGHT LOSS PATIENT — 2016 UPDATE: MICRONUTRIENTS
MICRONUTRIENTS: EVIDENCE AND RECOMMENDATIONS
The report below is organized into sections for each of the studied micronutrients, and
evidence pertaining to each of the four domains is further organized into subsections
within micronutrients. Each subsection begins with a brief literature review and concludes
with recommendations.
“Routine preoperative and postoperative screening” refers to acquiring a baseline
before WLS and a nutrient assessment after WLS every 3-6 months in the first year and
annually thereafter; unless otherwise specified in the recommendations.
If a nutrient deficiency is identified pre-WLS, nutrient repletion should be implemented
following the Recommended Dietary Allowance (RDA), plus an additional, individualized
amount to facilitate optimal absorption for repletion.
Definitions[2]
Dietary Reference Intake (DRI) is the general term for a set of reference values
used to plan and assess nutrient intakes of healthy people. These values, which
vary by age and gender, include:
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o Recommended Dietary Allowance (RDA): average daily level of intake
sufficient to meet the nutrient requirements of nearly all (97%-98%)
healthy people.
o Adequate Intake (AI): established when evidence is insufficient to
develop an RDA and is set at a level assumed to ensure nutritional
adequacy. Tolerable Upper Intake Level (UL): maximum daily intake
unlikely to cause adverse health effects.
Vitamin B1 (Thiamin)
Thiamin is a water-soluble vitamin absorbed primarily in the duodenum and upper
jejunum.[3-7] Thiamin plays both coenzyme and non-coenzyme roles within the body and
is found in several food sources, including whole grains, pork, and fish.[3-8] Absorption of
thiamin from food is thought to be high; however, thiamin is rapidly destroyed in an
alkaline environment with a pH >8 or with high temperatures.[4] Therefore, medications
such as antacids, H2 antagonists and proton pump inhibitors (PPIs) may inhibit thiamin
digestion; however, no studies have examined this relationship directly. Several foods and
beverages contain anti-thiamin factors, which also impair digestion and/or absorption;
these include alcohol, tea, coffee, raw fish, and shellfish.[4, 8]
Thiamin absorption is dependent upon the amount of thiamin present in the proximal
intestine.[3, 4, 7, 8] The average total thiamin storage in a healthy adult is approximately
0.11mmol (30 mg), with 40% stored in muscle.[9] The half-life of thiamin in humans has
been estimated to be 9.5 to 18.5 days.[4] Free thiamin in excess of tissue needs is excreted
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intact or catabolized for urinary excretion.[4, 8] Long-term diuretic therapy is associated
with increased urinary loss of thiamin.[10-12] Moreover, several studies have reported
thiamin deficiency (TD) among patients with cardiac failure who have been treated with
furosemide.[11-13] The limited total pool of thiamin, coupled with its short half -life and
constant requirement for use in metabolic processes, results in the need for consistent
thiamin intake.[14]
Thiamin deficiency (TD) results in impaired oxidative and energy metabolism, often
affecting various organ systems, including the heart, gastrointestinal (GI) tract, and
peripheral and central nervous systems.[4-6, 8] Patients with TD can develop high-output
cardiovascular disease (wet beriberi) and have been reported to exhibit tachycardia,
respiratory distress, or lower extremity edema, with right-to-left ventricular dilation and
lactic acidosis.[15, 16] Patients with neurologic (dry beriberi) may have numbness or
muscle weakness (neuropathy), pain of lower to upper extremities, convulsions, or
exaggerated tendon reflexes.[6, 15-18] GI symptoms associated with beriberi can include
delayed gastric emptying, nausea and emesis in patients with mega-jejunum, and
constipation in patients with megacolon.[19] In addition, patients with small bowel
bacterial overgrowth (SBBO) after WLS are at risk for TD.[19, 20] Patients with severe TD
often present with Wernicke encephalopathy (WE), with associated symptoms such as
confusion, nystagmus, ataxia and ophthalmoplegia.[6, 20-25] Patients with
neuropsychiatric beriberi may have auditory and visual hallucinations, aggressive
behavior, and selective memory disorders, which is often referred to as Wernicke’s
Korsakoff syndrome (WKS). [6, 24-28] Signs and symptoms of TD are summarized in Table
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5.
Assessment of thiamin status should be made by a whole blood (erythrocyte)
concentration of the active form of thiamin, TDP, or TDP activity/stimulation or
concentrations of the thiamin-dependent enzyme transketolase (Table 5).[4, 7, 29] This is
because 80-90% of body's thiamin is found in cells and only about 10% is found in plasma
or serum.[46] In the serum, thiamin is mostly carried by albumin; thus albumin status
would influence laboratory results, and plasma levels of thiamin more accurately reflect
recent intake.[22] An alternative approach to support a diagnosis of TD is measurement of
erythrocyte transketolase activity (Table 5). However, low concentrations of the vitamin do
not always result in clinical manifestations and there is not a specific threshold of serum or
red blood cell thiamin below which an individual will develop symptoms of TD. Therefore,
clinicians should be skilled at detecting physical signs and symptoms of TD.[6]
Identification of TD should include a thorough nutrition assessment, nutrition-focused
physical assessment, and if available, biochemical evaluation.[6, 30] In the acute-care
setting, reliable laboratory tests may not be available, may be too costly, or may be
impractical due to a long turnaround time. Since serious and potentially irreversible
neurological damage can occur with untreated TD, when the diagnosis of TD is suspected,
the patient should be treated before, or in the absence of, laboratory confirmation of
deficiency, and then monitored and evaluated for resolution of signs and symptoms.[6, 31]
According to the 1998 IOM report, there is no determined tolerable upper intake level
(UL) for thiamin.[5] In one study, oral doses of large amounts (500 mg daily) for >1 month
failed to elicit any adverse effects.[32] Large doses of thiamin given intravenously (IV) or
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intramuscularly (IM), however, have resulted in headaches, convulsions, cardiac
arrhythmias, anaphylactic shock, and other signs and symptoms.[26]
Preoperative Thiamin Screening
Prevalence of low preoperative levels of thiamin have been reported to range from
16% to 29%, and may be higher in African Americans and Hispanics.[33] Previously
published CPGs have not recommended routine preoperative screening of thiamin.[1, 31,
34, 35] However, patients with obesity have been shown to have lower plasma thiamin
concentrations, possibly due to increased intracellular thiamin storage.[36] In addition,
the risk of developing symptomatic TD after WLS is greater for those patients with low
thiamin status prior to surgery, [34] highlighting the importance of screening for and
repletion of low thiamin prior to surgery.
Postoperative Thiamin Screening
Prevalence of post-WLS TD has been reported to range from <1 to 49% [18, 20],
with variation based on the type of procedure, postoperative time frame, and risk factors.
Very few of the studies published since the 2008 nutrition guidelines, regarding
postoperative TD in RYGB, BPD/DS or SG[19, 33, 37-41] have been prospective studies;
most are retrospective or case studies. Some [37, 40, 41] but not all [19, 34, 36, 38, 40]of
these studies show decline in thiamin status despite patients receiving thiamin as part of a
multivitamin supplement. Reports of thiamin status post-WLS have been mixed. In a
cohort of 60 patients at 12 months post- SG; both hypervitaminosis B1 and
hypovitaminosis B1 were reported.[40] In a long-term examination of 5-year surveillance
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data of SG patients, 31% had low thiamin.[41] A randomized clinical trial comparing the
nutrition outcomes among RYGB and BPD patients over one year also showed thiamin
concentrations changed at different rates in the 2 groups; B1 concentrations declined
steeply and transiently after duodenal switch, but declined gradually after RYGB.[37] These
differences in outcomes underscore the methodological limitations of existing studies, such
as small sample sizes and heterogeneity of study design and outcomes, with most of these
studies relying upon self-report to assess multivitamin intake. Furthermore, different
studies assess thiamin status at different time points after surgery and by different
methodology. In accordance with the EFNS guidelines, monitoring of thiamin status for at
least 6 months post-WLS is recommended, however, more studies are needed to evaluate
the long-term impact of thiamin status after various surgical procedures.[42]
Risk factors associated with neurological complications following surgery include
the absolute amount of weight loss, malnutrition, prolonged GI symptoms, poor
postoperative nutritional follow up and reduced serum albumin and transferrin.[43] A
recent systematic review suggests that bariatric beriberi generally occurs 1-3 months after
surgery. [43] However, TD can occur at any time if risk factors are present.[6, 21, 23, 39]
Symptomatic TD occurs in up to 49% of patients post-surgery, varying by procedure.[6, 21,
23, 39] Several systematic reviews on the risk of WE after all types of WLS have been
published.[6, 21, 23, 39] All of these reports suggest, that a primary determinant and
predictor of this major neurological complication is persistent vomiting.
Routine screening is recommended after surgery for patients who present with the
following risk factors: rapid weight loss, protracted vomiting, parenteral nutrition,
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excessive alcohol use, neuropathy or encephalopathy and/or heart failure.[1, 31, 44] Based
on additional evidence, routine screening is also recommended in the following at-risk
groups: patients with alcoholism,[24-26, 31] malnourished patients,[6, 31, 45] female
patients[43, 46], African American or Hispanic patients[34, 35] and patients with GI
symptoms such as slow gastric emptying, nausea, vomiting, jejunal dilation, megacolon,
constipation and/or SBBO. [19, 20] [19, 20]
Preventative Supplementation of Thiamin
A multivitamin supplement containing 100% of the RDA of thiamin has been previously
recommended in order to prevent TD.[1] More recent guidelines suggest a minimal daily
nutritional supplementation of 1 adult multivitamin plus minerals for LAGB patients and 2
adult multivitamins plus minerals (each containing iron, folic acid, and thiamin) and a B-
complex preparation (amount not specified) for RYGB and SG patients.[31]
Practitioners should understand, however, that multivitamins, which generally provide
the RDA of thiamin (1.1 -1.2 mg/day), may not be adequate to prevent TD.[19, 37, 40, 41,
46] On the other hand, overuse should be avoided. For instance, data from Aarts et al.,[40]
also reported some hypervitaminosis B1 in 31% of their sample, despite, multivitamin use
up to three times daily. Supplementation of a bariatric B-vitamin preparation containing 12
mg of thiamin, along with 350 µg vitamin B12 and 800 µg folic acid, for three months did
not change mean blood thiamin levels.[47] Although these investigations had several
limitations, including a small, female-only sample, short duration and low blood thiamin
levels with no symptomatic TD, few dose-response studies exist on which to base
recommendations, and thus based on the studies cited above, it is recommended that 7
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patients receive a 50 mg oral dose of thiamin from a B-complex supplement once or twice
daily.[48]
Repletion of Postoperative Thiamin Deficiency
The AACE/TOS/ASMBS 2013 CPG[31] recommends that empiric thiamin
supplementation be considered in WLS patients with specific risk factors (rapid weight
loss, protracted vomiting, need for parenteral nutrition, excessive alcohol use, neuropathy
or encephalopathy, or heart failure). Patients with suspected or confirmed TD who are
seen on an outpatient basis or who do not have IV access may be treated with oral thiamin
supplementation. Previous CPGs suggested that early symptoms of neuropathy can often be
resolved by providing the patient with oral thiamin doses of 20–30 mg/day until symptoms
disappear.[1] Others recommend 100 mg oral thiamin two[16] to three[26] times daily
until symptoms resolve. However, oral therapy may be inadequate to treat symptomatic
patients, and data is lacking in WLS patients, in whom thiamin absorption may be impaired
due to altered GI structure and function. For patients with SBBO, 100 mg oral thiamin twice
daily for 2 months and antibiotic therapy with metronidazole, amoxicillin, or rifaximin for
7-10 days each month for 2 months on average has been suggested.[20]
For patients presenting with mild deficiency symptoms and who have access to IV
therapy, the AACE/TOS/ASMBS 2013 CPG recommends patients receive 100 mg IV thiamin
for 7-14 days.[31] These guidelines are similar to previous nutrition practice guidelines
recommending parenteral treatment for patients with hyperemesis with 100 mg/day for
the first 7 days followed by daily oral doses of 50 mg/day until complete recovery.[1]
Thiamin deficiency syndromes are typically initially treated with IV thiamin between 8
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100 mg once a day and 500 mg three times a day.[7, 26, 32] For WLS patients with
suspected or established severe TD (e.g. WE or WKS), there is a discrepancy between
existing CPGs. Aills et al., suggested that patients with WKS generally require ≥ 100 mg
thiamin administered IV for several days or longer, followed by IM thiamin or high oral
doses until symptoms have resolved or significantly improved.[1] In contrast, the
AACE/TOS/ASMBS 2013 CPG recommends 500 mg/day of parenteral thiamin for 3-5 days
followed by 250 mg/day for 3-5 days or until resolutions of symptoms, then to consider
treatment with 100 mg/day orally, usually indefinitely or until risk factors have been
resolved.[31] The European Federation of Neurological Societies (EFNS) recommends
monitoring thiamin status after WLS for up to 6 months , to provide parenteral thiamin
supplementation if indicated, and to provide 200 mg IV thiamin, three times daily for the
postoperative patient with WE.[42]
Other investigators recommend IM repletion of thiamin; however, recommendations
for IM protocols have been inconsistent. Some investigators have recommended 100-200
mg IM monthly or every other month with or without 200 mg oral thiamin,[19], while
others recommend a minimum of 250 IM mg daily for at least 3-5 days.[16, 24] Results of a
randomized, double-blind, multi-dose study showed a greater clinical benefit from giving ≥
200 mg IM thiamin compared to
≤ 100 mg IM thiamin, in alcoholic patients with WE or WKS.[27] However, according to the
European Federation of Neurological Societies (EFNS), use of the IM route for thiamin
repletion should be limited to patients without IV access in emergent situations.[42]
Furthermore, it may be impractical to treat patients IM, as many hospitals do not use the
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IM route for repletion but replete only through oral or parenteral routes. In summary,
although recommendations for the treatment of mild-to-severe TD for the WLS patient
appear to be discordant, there is agreement across studies that high, frequent doses of
thiamin via the IV or IM routes are more effective than oral supplementation.
The recommendations published by AACE/TOS/ASMBS 2013 CPG[31] are similar to the
practice guidelines for non-WLS patients with alcoholism published by the Royal College of
Physicians.[24-26, 49] The recommended dose of thiamin required to prevent or treat WE
in these patients has been >500 mg once or twice daily, provided parenterally for 3-5 days.
[49, 50] This estimate is based on data from uncontrolled trials and empirical clinical
practice. These authors conclude that oral thiamin is poorly absorbed and ineffective for
both prophylaxis and treatment of WE in patients with alcoholism.[26, 49] However,
further studies are needed to understand the applicability of these guidelines to the WLS
patient.
Administration of IV thiamin therapy should be provided slowly over 30 minutes to
minimize risk of anaphylaxis.[26, 32] Thomson[26] and Wrenn[32] prospectively
evaluated the safety of thiamine hydrochloride given as a 100 mg IV bolus in 989
consecutive patients (1,070 doses) and reported a total of 12 adverse reactions (1.1%), all
but one of which were minor, such as transient local irritation. The one major reaction
consisted of generalized pruritus.[26, 32] Treatment should be individualized, based on
severity of TD and availability of repletion options.
Caution needs to be taken when treating patients for dehydration with an IV dextrose
or an oral carbohydrate solution, because the oxidation of glucose is a thiamin-dependent
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process.[4, 8] To avoid prolonged or severe TD, thiamin should be given before any
carbohydrate [42] or at least simultaneously along with magnesium, potassium, and
phosphorus, among patients at risk for refeeding syndrome;[51] include the chronically
under-nourished, patients with dysphagia and/ or those with little intake for greater than
10 days.[52] Thiamin, vitamin B complex and multi-vitamin supplements should be started
with refeeding. Simultaneous therapeutic doses of other B vitamins including vitamin B6
and vitamin B12 at doses of 100 mg and 1000 mcg, respectively, may also be of benefit to
the WLS patient with TD.[28] The Royal College of Physicians’ guideline for the
management of WE, non-WLS patients, recommends that per 250 mg thiamin dose (e.g. 1
ampule), there should be the addition of 4 mg riboflavin (vitamin B2), 50 mg pyridoxine
(vitamin B6), 160 mg nicotinamide (vitamin B3), 500 mg vitamin C, 10-30 mEq magnesium,
60-180 mEq potassium, and 10-40 mmol/l phosphate daily.[26, 49] Although more high-
quality research is needed to develop standardized clinical practice guidelines for the WLS
patient with TD, it is agreed that therapy should be initiated urgently, as late interventions
may put the patient at risk for irreversible sequelae.[53]
Thiamin – Summary
Recommendations for preoperative screening of thiamin
Routine preoperative screening of thiamin is recommended for all patients.
(Grade C, BEL 3)
Recommendations for postoperative screening of thiamin
Routine postoperative screening of thiamin is recommended for high-risk groups:
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o Patients with risk factors for TD (Grade B, BEL 2)
o Patients with concomitant medical conditions such as cardiac failure
(especially those receiving furosemide) (Grade B, BEL 2)
o Females (Grade B, BEL 2)
o African Americans (Grade B, BEL 2)
o Patients not attending a nutritional clinic after surgery (Grade B, BEL 2)
o Patients with GI symptoms (intractable nausea and vomiting, jejunal dilation,
mega-colon, or constipation) (Grade B, BEL 2)
o Patients with SBBO (Grade C, BEL 3)
If signs and symptoms or risk factors are present in post WLS patients, thiamin
status should be assessed at least during the first 6 months, then every 3-6
months until symptoms resolve. (Grade B, BEL 2)
Recommendations for supplementation of thiamin for preventing deficiency
Thiamin Supplementation above the RDA is suggested to prevent TD:
o Post-WLS patients should take at least 12 mg thiamin daily (Grade C, BEL
3) and
o preferably a 50 mg dose of thiamin from a B-complex supplement or
multivitamin once or twice daily (Grade D, BEL 4) to maintain blood levels of
thiamin and prevent TD.
Recommendations for postoperative thiamin repletion12
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Practitioners should treat post-WLS patients with a suspected thiamin deficiency
before or in the absence of laboratory confirmation of deficiency AND monitor and
evaluate resolution of signs and symptoms. (Grade C, BEL 3)
Repletion dose for TD varies based on route of administration:
o Oral therapy: 100 mg orally two -to -three times daily until symptoms
resolve. (Grade D, BEL 4).
o IV therapy: 200 mg three times daily to 500 mg once or twice daily for 3-5
days followed by 250 mg/day for 3-5 days or until resolutions of symptoms,
then consider treatment with 100 mg/day orally, usually indefinitely or until
risk factors have been resolved. (Grade D, BEL 4)
o IM thiamin repletion: 250 mg once daily for 3-5 days or 100-250 mg monthly.
(Grade C, BEL 3)
Simultaneous administration of magnesium, potassium and phosphorus should
occur in patients at risk for refeeding syndrome. (Grade C, BEL 3)
Vitamin B12 (Cobalamin)
Cobalamin (B12) is a water-soluble vitamin that plays key roles in the normal
functioning of the brain and nervous system, in the maturation of red blood cells, in neural
functioning, and in DNA synthesis.[54] B12 is also believed to be a factor in the prevention
of osteoporosis and age-related macular degeneration.[54] Both vitamin B12, cobalamin,
and folate are often mentioned together in the literature because of the synergistic effect
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the two vitamins have on the synthesis and maturation of red blood cells. In addition, B12
and folate function in DNA synthesis, cellular metabolism, and the conversion of
homocysteine to methionine.[54] B12 and folate play a role in the prevention of
cardiovascular disease and cognitive decline.[18, 54, 55] B12 deficiency may also cause
folate deficiency. Deficiencies in either or both B12 and folate can manifest as
megaloblastic macrocytic anemia.
B12 metabolism involves a complex pathway.[56] B12 in food is bound to, protein, and
released from proteins by the action of a high concentration of hydrochloric acid (HCl)
present in the stomach. This process results in the free form of the vitamin, which is
immediately bound to a mixture of glycoproteins secreted by the stomach and salivary
glands. These glycoproteins, called R-binders, protect B12 from chemical denaturation in
the stomach. The stomach’s parietal cells, which secrete HCl, also secrete a glycoprotein
called intrinsic factor (IF). IF binds B12 and enables its active absorption. When the
contents of the stomach enter the duodenum, the R-binders become partly digested by
pancreatic proteases, which causes them to release their bound B12. The pH in the
duodenum is more neutral than that in the stomach, increasing the binding affinity of IF for
B12. Therefore, IF quickly binds B12 as it is released from R-binders in the duodenum, the
B12-IF complex then proceeds to the distal small intestine, where it is absorbed through
phagocytosis by specific ileal receptors.
Since B12 absorption and transport is dependent upon this complex mechanism, any
pre-existing medical or surgical condition that disrupts the normal mechanism of B12
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metabolism may be considered a preoperative risk for deficiency in patients seeking WLS.
[1]
Preoperative Vitamin B12 Screening
Obesity is a risk factor for B12 deficiency, [56] reported in 2%-18% of patients
seeking WLS.[34, 38, 57-64] Commonly used medications have also been noted to affect
preoperative B12 absorption and stores, most notably metformin and omeprazole.[65-70]
Approximately 6% to 30% of patients taking metformin present with B12 deficiency.[65-
69] The mechanism for this has not been fully elucidated but metformin is suspected to
either compete for absorption sites, alter IF, or change gut flora or motility.[71] In patients
with obesity and concomitant gastroesophageal reflux disease (GERD) requiring proton-
pump inhibitors (PPIs), long-term omeprazole use has been shown to decrease B12 levels
by up to 30%.[70, 72]
While long-term evidence is lacking, there is suspicion that Helicobacter pylori (H.
pylori) may have a causal role in B12 malabsorption and subsequent deficiency. Kaptan et
al., [73] reported that 56% of patients in their cohort who tested positive for H. pylori had a
concomitant B12 deficiency and megaloblastic anemia. Preliminary results support the
importance of screening WLS patients for both H. pylori infection, and B12 deficiency in the
preoperative period.
As noted above, the functions of B12 and folate are intertwined biochemically; thus, the
final common pathway that impairs DNA synthesis in hematopoietic cells is the same when
either vitamin is deficient. Neuropathy can occur in the setting of B12 deficiency, but not
with folate deficiency.. Due to the synergistic effect of both B12 and folate in 15
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hematopoiesis, the absence of anemia with adequate folate can mask a B12 deficiency.[1,
18] This can lead to irreversible neurologic damage.
A methylmalonic acid (MMA) assay is the preferred test for B12 status because
metabolic changes often precede low B12 levels in the progression to deficiency. An
elevated MMA result may be an early indicator of a B12 deficiency even when serum B12
levels are still within normal lab limits. Conversely, serum B12 assays may miss as many as
25-30% of cases of B12 deficiency.[59] Thus, MMA is the preferred assay when screening
for B12 deficiency.
Postoperative Vitamin B12 Screening
Risk for B12 deficiency after WLS is dependent upon a number of factors, including
type of surgical procedure (procedures that involve bypass or removal of all or part of the
stomach, such as the SG, RYGB and BPD/DS, put patients at higher risk for deficiency);
preoperative B12 deficiency; post-surgical timeframe and frequency of follow-up;
adequacy of dietary intake; concomitant use of medications that interfere with B12
bioavailability; and adherence to B12 supplementation.[1, 37, 39, 40, 66, 71, 74-76]
Disruption of B12 absorption may occur when a WLS procedure leads to a significantly
decreased intake of dietary protein and/or impairs hydrolysis of free cobalamin by
reducing pepsin and HCl production.[1] In purely restrictive procedures such as the LAGB,
B12 deficiency is less likely as there is no effect on gastric acid or IF production. However,
due to food intolerances, restriction of dietary protein intake, and chronic use of PPIs seen
in some LAGB patients, B12 deficiency can be seen in this population as well.
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Early research from the late 1990s to early 2000s indicated that the prevalence of B12
deficiency in RYGB typically ranged from 8% to >30%, but could be as high as 70% with a
length of follow-up between one and seven years.[77-81] It appears that the risk for
deficiency increases with duration of follow-up. One explanation for delayed manifestation
of B12 deficiency is that long-term hepatic storage of B12 is approximately 2000 mcg and
low values typically emerge two to three years after surgery. [68] Even though
recommendations for B12 supplementation have been widely published and accepted, B12
deficiency is still being seen in post RYGB patients.[1, 31, 82] Current research is
encouraging, however, with observed prevalence of B12 now under 20%, and
postoperative levels returning back to preoperative levels with routinely recommended
B12 supplementation.[39, 46, 64, 83, 84]
Current research suggests that patients taking B12 supplementation may initially show
elevated levels, but this stabilizes over time in RYGB patients;[84] whereas B12 levels were
reported stable in DS patients.[39] This may be due to better tolerance of animal proteins
in a larger sleeve rather than a pouch, greater pepsin and gastric acid production to release
protein-bound B12, and increased availability and interaction of IF with the sleeve
contents.[1, 85, 86] [87] SG has been shown to pose a risk for, B12 deficiency, with
reported prevalence ranging from 4%-20% at 2 to 5 years after surgery.[88-91] In this
procedure, the removal of 70%-85% of the stomach physically eliminates a majority of
parietal cells needed to secrete pepsinogen, HCl, and IF, potentially leading to B12
deficiency via the reduced formation of both free cobalamin and cobalamin-IF complex. It
is not clear whether there is a higher risk for B12 deficiency in SG compared to other
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bariatric surgical procedures, or if the risk for deficiency increases with post-surgical
duration. Some studies show B12 deficiency occurs in SG in the early post-operative period
and at one-year, but not in patients who had undergone SG three to five years earlier.[40,
41, 88] In some studies comparing the risk for B12 deficiency between SG and RYGB, no
significant difference was observed in the risk for B12 deficiency over the duration of five
years[74] while other studies have found that risk for B12 deficiency is higher in RYGB.[92]
Mechanisms underlying risk for B12 deficiency may differ between the two procedures: the
malabsorptive component of RYGB may have a greater deleterious effect on B12
absorption; whereas SG disrupts the cobalamin-IF complex.[92]Because research
regarding risk and frequency of vitamin B12 deficiency in SG patients is sparse and findings
are variable, it is recommended to screen all patients for B12 deficiency after SG.
Some authors have questioned the need to screen and treat asymptomatic patients for
B12 deficiency. However, given the possibility of irreversible neurological damage in the
setting of prolonged untreated B12 deficiency, routine screening is recommended. B12
status is typically assessed via serum or plasma levels. Values below approximately 170–
250 pg/mL (120–180 picomol/L) for adults indicate a B12 deficiency.[93] However,
evidence suggests that serum B12 concentrations may not accurately reflect intracellular
concentrations.[57] An elevated serum homocysteine level (values >13 micromol/L)might
also suggest a vitamin B12 deficiency.[94] However, this indicator has poor specificity
because it is influenced by other factors, such as low vitamin B6 or folate levels. [94]
Elevated MMA levels (values >0.4 micromol/L) might be a more reliable indicator of B12
status because they indicate a metabolic change that is highly specific to B12 deficiency.[38,
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57, 93] In addition, some literature on RYGB patients shows that symptoms of deficiency
may be present even in the setting of normal serum B12 levels. Thus, serum MMA and
homocysteine assays are the preferred method to assess B12 status,[69, 95-97] although
MMA has more specificity in detecting B12 deficiency than Hcy.
Preventative Supplementation of Vitamin B12
Cobalamin stores are known to persist for long periods of time (3 to 5 years) but levels
are dependent upon dietary repletion and daily depletion. Post-WLS patients have
decreased intake of dietary protein, decreased contact of stomach acid with food, and
decreased availability of IF and concomitant malabsorption; therefore, without appropriate
supplementation, B12 deficiency may develop. Since the typical absorption pathway cannot
be relied upon in SG, RYGB and BPD/DS, patients who have undergone these procedures
should consider supplementation that allows for passive absorption of B12, independent of
the cobalamin-IF complex pathway,[54, 79] Research supports additional supplementation
of B12 recommended beyond standard MVI that provide 100% DRI ([1, 57, 85, 98-100]
For SG patients, evidence supporting supplementation with B12 in order to maintain
normal levels up to three years post surgery is mixed. Meta-analyses show great variability
in findings, leading to recommendations for vitamin B12 in SG, that range from no
supplementation, supplementation contributed solely from a multivitamin (about 20 mcg),
to varying dosages (350 mcg, 500 mcg and 1000mcg per day) and varying frequencies of
B12 supplementation (daily to monthly).[41, 64, 91, 99, 101-103] It is difficult to gauge,
from the current body of research, what the optimal level of B12 supplementation should
be for SG patients. For instance, one study found elevated serum B12 at 3 months in 19
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patients who have SG when taking one of the lowest doses 350 mcg daily.[47] Taken
together, the body of literature on this topic suggests that SG patients do need B12
supplementation, though specifics regarding dosage and frequency cannot yet be derived
from existing data.
The most recent guidelines by AACE/TOS/ASMBS 2013 CPG are not specific and
detailed in regard to the supplement regimen for vitamin B12 for LAGB, RYGB, SG, and
BPD/DS , recommending only that supplementation is provided as needed to maintain
levels in the normal range.[31] Based on early research [37, 104, 105] the 2008 ASMBS
Nutrition CPG recommended 350-500 mcg oral crystalline B12 daily.[1] Until more
rigorous and long-term studies can be identified, the historical and current studies support
maintaining the current recommendation for B12 outlined by Aills et al.,[1]
B12 may be given in various forms including oral liquid or disintegrating tablet,
sublingual, parenteral (subcutaneous (SQ) or IM), or nasal spray. The choice of form and
frequency of supplementation should be guided by considerations of factors related to
postoperative anatomy and patient adherence. Poor adherence with vitamin regimens has
resulted in B12 deficiencies with serious consequences of B12 deficiency, including
pernicious anemia and neurological dysfunction. [75, 95, 106] Practitioners should assess
the patient’s preferences and potential barriers to adherence when considering a daily,
weekly, or monthly regimen of B12 supplementation.
Repletion of Postoperative Vitamin B12 Deficiency
Deficiency of B12 is typically defined at levels less than 200 pg/ml, although this
reference range has been questioned, as clinical manifestation does not always accompany 20
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abnormally low laboratory values;[1] conversely, about 50% of patients with obvious signs
and symptoms of deficiency (Table 5) also have normal B12 levels.[1, 107, 108]
The recommended treatment for B12 deficiency in the non-bariatric population in the
United States is 1000 mcg daily for 8 weeks and then once a month.[108] A monthly
dosage of 650 to 1000 mcg was found to adequately reduce MMA in an estimated 80%-
90% of an non-bariatric, elderly sample.[97] In early WLS research, B12 deficiency was
usually found to resolve after several weeks of treatment with 700 to 2000 mcg per week
(daily, twice daily, or weekly),[109] or with B12 1000 mcg IM once a month until the
deficiency is corrected.[110] Current research, however, indicates a dosage of 1000 mcg
daily to treat B12 deficiency in SG and 1000-3000 mcg B12 every 6-12 months if sufficiency
not maintained.[76] Because recent research on repletion of B12 in WLS patients is
limited, recommendations published in Aills et al., and the more recent AACE/TOS/ASMBS
2013 CPG have not been revised.[1, 31]
B12 – Summary
Recommendations for preoperative screening of vitamin B12
Routine pre-WLS screening of B12 is recommended for all patients.
(Grade B, BEL 2)
Serum B12 may not be adequate to identify B12 deficiency. It is recommended to
include serum MMA to identify metabolic deficiency of B12 in symptomatic or
asymptomatic patients, and in those with history of B12 deficiency or pre-
existing neuropathy (Grade B, BEL 2)
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Recommendations for postoperative screening of vitamin B12
Routine postoperative screening of vitamin B12 is recommended in patients
who have undergone RYGB, SG, or BPD/DS. (Grade B, BEL 2)
More frequent screening in the first post-operative year, every 3 months and
then at least annually or as clinically indicated is recommended for post-WLS
patients who are chronically using medications that exacerbate risk of B12
deficiency: nitrous oxide, neomycin, metformin, colchicine, PPIs, or seizure
medications (Grade B, BEL 2)
Serum B12 may not be adequate to identify B12 deficiency. It is recommended to
include serum MMA with or without homocysteine to identify metabolic
deficiency of B12 in symptomatic or asymptomatic patients, and in those
patients with history of B12 deficiency or pre-existing neuropathy(Grade B, BEL
2)
Recommendations for supplementation of vitamin B12 for preventing deficiency
All post-WLS patients should take vitamin B12 supplementation. (Grade B, BEL
2)
The recommended supplement dose for vitamin B12 varies based on route of
administration. (Grade B, BEL 2):
o Orally by disintegrating tablet, sublingual, or liquid: 350-500 mcg daily
o Nasal spray: as directed by manufacturer
o Parenteral (IM or SQ): 1000 mcg monthly
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Recommendations for postoperative vitamin B12 repletion
Post-WLS patients with a B12 deficiency should take 1000 mcg per day to
achieve normal levels and then resume dosages recommended in Table 5 to
maintain normal levels. (Grade B, BEL 2)
Folate (Folic Acid)
Folate (naturally food-derived) and folic acid (synthetic) are forms of the water-soluble
vitamin B9. Folate is essential for cell division, hematopoiesis, nucleic acid synthesis,
amino acid metabolism, and methionine regeneration from homocysteine.[111] Folate is
needed for single-carbon transfers for the production of the methylating agent, S-
adenosylmethionine, and the transfer of a methyl group that can yield products of energy
metabolism such as creatine, convert homocysteine to methionine, and produce certain
neurotransmitters and phospholipids.[112] The biochemically active form of folate, called
5-methyltetrahydrofolate, is believed to reduce cardiovascular disease by improving
endothelial function.[113] Folate is also essential for prevention of fetal neural tube
defects, megaloblastic pernicious anemia, stroke, osteoporosis, depression, elevated
homocysteine, some forms of cancer, Alzheimer’s disease and other forms of cognitive
decline.[55, 112]
Folate absorption from dietary sources occurs mainly in the jejunum, but passive
diffusion is seen at higher doses. Only a small amount of folate is stored. The total amount
of body folate is estimated to be approximately 10 to 30 mg, with the liver containing
approximately half of the total folate pool.[55] An estimated 0.3% to 0.8% of the total
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folate pool is excreted daily, which does not vary with levels of dietary or supplemental
folate intake.[55]
While the primary symptom of folate deficiency is megaloblastic anemia, this rarely
occurs independent of B12 deficiency since the two vitamins work synergistically in
hematopoiesis.[24] Folate deficiency can manifest in clinical signs such as oral mucosal
ulcerations, changes in skin and nail pigmentation, and elevated homocysteine serum levels
(See Table 5).[114]
Preoperative Folate Screening
Because folate works synergistically with B12, pre-WLS patients may be at risk for
concomitant folate deficiency as well.[112] The prevalence of folate deficiency has been
reported to be as low as 0% and as high as 54% in patients seeking WLS. More recent
research reports preoperative SG patients with 24% folate deficiency.[115] Risk of
deficiency is exacerbated by insufficient intake of folate-containing foods, alcoholism, and
aging.[38, 57, 58, 61, 64, 85, 116] It is recommended that all patients seeking WLS be
screened preoperatively for suboptimal or deficient folate. A folate deficiency can be
identified by decreased RBC folate, elevated serum homocysteine and normal MMA levels.
[112]
Patients who take medications that either decrease folate absorption or act as folate
antagonists are at particular risk for folate deficiency. In addition, surgical patients seeking
WLS who have pre-existing medical or surgical conditions that decrease gastric acid
secretion or interrupt absorption of folate in the jejunum are at increased risk for
deficiency. Particular attention should be paid to prospective WLS patients who plan future 24
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pregnancy, due to the profound effect of folate on prevention of neural tube disorders.
[117]
Postoperative Folate Screening
Post-WLS patients with rapid weight loss and/or malnutrition may be at an especially
high risk for micronutrient deficiencies. Risk for folate deficiency is reported in all
currently performed WLS procedures and may be secondary to low intake of folate-rich
foods, poor adherence to supplement regimens, taking vitamin regimens that contain less
than 400 mcg of folate, chronic use of medications that interfere with the bioavailability of
folate, alcoholism, pre-existing medical or surgical conditions that interfere with folate
absorption, and/or an existing preoperative folate deficiency.[54, 55, 76, 114, 118-121] In
earlier research studies, low serum folate levels have been observed in up to 65 % of post-
RYGB patients and more recent studies of post-SG report a prevalence of 18%.[58, 85, 116,
122] An increased risk of deficiency has also been noted even among LAGB patients,
possibly due to decreased folate intake. [121]
Similar to the case with B12, most post-WLS patients who are folate deficient are
asymptomatic or suffer from sub-clinical symptoms, so these deficient states may not be
easily identified.[54, 55]
Preventative Supplementation of Folate
While it is important to note that postoperative folate deficiencies may occur less
frequently than deficiencies of other vitamins after surgery, folate deficiency can occur
even in the context of routine supplementation, especially if multivitamins do not contain
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the proper dosage of folic acid and the dietary intake of folate is inadequate.
AACE/TOS/ASMBS 2013 CPG recommend taking two multivitamins that contain folic acid
for patients who have had WLS.[1] A multivitamin containing 100% or less of the RDA for
folic acid may be insufficient to maintain normal levels in a post- WLS patient. Two earlier
studies found that 47% and 41% of RYGB patients had low folate levels at 6 months and 1
year, respectively, despite patient adherence to a multivitamin supplement; however this
supplement contained less than the RDA for folate.[118] Folate deficiencies in RYGB and
SG has been linked to, and most likely exacerbated by, a sharp decrease in dietary intake
coupled with insufficient supplementation.[38, 40, 74, 88, 101] Despite recommendation
of a multivitamin containing 150% of the RDA for folate, 22% of patients in one study had
confirmed folate deficiency.[40]However, current research contradicts this finding. A
gradual increase in folate levels has been noted in RYGB patients over the course of 5 years
after surgery, even though during the same time period, folate intake was gradually
decreased.[84]
Recommended intake of folate for non-bariatric adult men and women is 400 mcg per
day.[123] However, the United States Preventative Services Task Force recommends that
women capable of or planning pregnancy take a daily supplement of 400 to 800 mcg per
day.[124] Research conducted in the WLS population has shown that taking up to 1000
mcg may be appropriate. Studies of RYGB and SG have produced evidence that folate
deficiency can be avoided and/or treated with supplemental dosages that range from 200
mcg to 1000 mcg per day.[41, 47, 74, 85, 86, 91, 99, 101, 125] Folate supplementation
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above 1 mg per day is not recommended due to the potential masking of vitamin B12
deficiency.[54]
Folic acid supplementation may be given as part of a multivitamin, B-complex, or as a
singular nutrient if necessary. The form of folic acid supplementation (i.e., liquid, chewable,
oral tablet) should be chosen with regard to enhancing patient adherence.
Repletion of Postoperative Folate Deficiency
As previously noted, WLS patients who have folate deficiency may be asymptomatic, so
these deficient states may not be easily identified, underscoring the need for routine
screening. Since rigorous research for repletion of folic acid is sparse, the current
recommendation concurs with Aills et al., and is not to exceed 1000 mcg per day due to the
potential masking of vitamin B12 deficiency.[1, 54]
Folate – Summary
Recommendations for preoperative screening of folate
Routine pre-WLS screening of folate status is recommended for all patients.
(Grade B, BEL 2)
Recommendations for postoperative screening of folate
Routine post-WLS screening of folate status is recommended in all patients. (Grade B,
BEL 2)
Particular attention should be paid to female patients of childbearing age. (Grade B, BEL
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Recommendations for supplementation of folate for preventing deficiency
Post-WLS patients who are not female and childbearing age should take 400-800 mcg
oral folate daily from their multivitamin. (Grade B, BEL 2)
Women of childbearing age should take 800-1000 mcg oral folate daily. (Grade B, BEL
2)
Recommendations for postoperative folate repletion
All post-WLS patients who have folate deficiency should take an oral dose of 1000 mcg
daily of folate to achieve normal levels and then resume the dosage recommended to
maintain normal levels. (Grade B, BEL 2).
Folate supplementation above 1 mg per day is not recommended in post-WLS patients,
due to the potential masking of vitamin B12 deficiency. (Grade B, BEL 2)
Iron
Iron is a component of hemoglobin and myoglobin and is critical for growth,
development, normal cellular functioning, and synthesis of some hormones and connective
tissue. Dietary iron has two main forms, heme (found in meat, seafood and poultry) and
non-heme (found in plants and iron-fortified foods). Most iron in the body is found in
hemoglobin, with the rest stored as ferritin or hemosiderin in the liver, spleen, and bone
marrow, or as, myoglobin in the muscle. Iron losses are greater in menstruating women
due to blood loss.[126, 127]
Absorption of iron occurs mainly in the duodenum and proximal jejunum.[126, 128]
Storage levels of iron have the greatest influence on iron absorption; however, the type of
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dietary iron consumed also affects absorption, with heme being more bioavailable.[127]
Non-heme iron absorption is affected by other foods consumed; foods high in vitamin C
improve absorption, while those high in tannins can decrease absorption. Ferrous and
ferric iron salts are the most commonly used forms of iron supplement. Ferrous iron is
more bioavailable than ferric iron, due to its higher solubility. Decreased exposure of
consumed foods or supplements to gastric acid can impair the conversion of ferric iron to
absorbable ferrous iron. However, high doses of ferrous and ferric iron supplements may
cause GI side effects, whereas other forms such as heme iron polypeptides, carbonyl iron,
iron amino-acid chelates, and polysaccharide-iron complexes may have fewer side effects.
[126-129]
Preoperative Iron Screening
The reported prevalence of iron deficiency in preoperative bariatric patients ranges
from 0-58%.[38, 41, 60, 88, 99, 116, 127, 130-134] In adults with obesity, multiple factors
may contribute to preoperative iron deficiency. These include poor diet; obesity-related
inflammation causing alterations in iron homeostasis; menstruation; menorrhagia (often
present in with polycystic ovarian syndrome); GERD with esophagitis; and/or other
factors.[130, 135, 136]
The highest rate of iron deficiency is typically seen in menstruating females. In the
presence of inflammation, diagnosing iron deficiency can be challenging. Although
screening for iron status may include the use of serum ferritin levels, these should not be
used to diagnose deficiency as ferritin is an acute phase reactant (APR) and may fluctuate
with age, inflammation, and infection.[1] It is useful to evaluate soluble transferrin 29
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receptor levels in addition to routine iron studies, as soluble transferrin is not an APR.[135]
Soluble transferrin receptor levels reflect the cellular need for iron, and are less impacted
by inflammation than are ferritin levels.[126] Hemoglobin and hematocrit changes reflect
late iron-deficient anemia, and are less valuable in identifying early anemia.[1] Iron
deficiency has been defined in different ways in the literature, which must be taken into
account when interpreting research results.[38, 41, 60, 88, 99, 116] Some researchers have
used a single laboratory value (serum iron, serum transferrin saturation, or serum ferritin);
[38, 60, 99, 116, 131, 133, 134] while others have used a combination of indices, including
serum iron and serum transferrin saturation; serum ferritin or soluble transferrin
receptor; serum iron with serum transferrin saturation; or serum iron, serum transferrin
saturation and total iron-binding capacity.[41, 88, 132] A combination of laboratory values
(serum iron with serum transferrin saturation and total iron-binding capacity) is
recommended for diagnosing iron deficiency.
Postoperative Iron Screening
The reported prevalence of iron deficiency in post-WLS patients is variable, differing by
procedure type and duration of time since surgery; ranging from 20-58% (RYGB), 0-18%
(SG), 13-62% (BPD), 8-50% (DS) and 14% (LAGB) from 3 months to 20 years follow-up.
[38, 41, 60, 88, 99, 116, 125, 129, 131-134, 137, 138] Post-WLS iron deficiency may occur
due to the bypassing of absorption sites in the GI tract; decreased intake of iron rich foods
due to intolerance or preference; age; gender; inadequate supplement adherence; and/or
altered absorption due to interaction of iron with calcium supplements or certain food
components.[80, 131-133, 135, 139]30
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Recent research indicates that patients who undergo SG or LAGB are at risk for iron
deficiency, but to a lesser extent than seen in RYGB or BPD/DS.[38, 41, 88, 116, 128, 132]
Clinicians should assess iron status in all patients post-WLS, using both physiological signs
and symptoms (Table 5) and laboratory results.[126] Laboratory values, including serum
iron, serum ferritin, transferrin saturation, and elevated total iron-binding capacity may be
affected by extraneous factors, such as inflammation and infection, and the clinician should
consider testing soluble transferrin receptor as well.[124]
Preventative Supplementation of Iron
Patients considered to be at high risk for iron deficiency include: menstruating females
and patients with history of anemia who have had RYGB, SG, or BPD/DS. These at-risk
patients should take a total of 45-60 mg of elemental iron daily, from all supplements
combined. Additional iron supplementation above the DRI (18 mg) may not be indicated in
LAGB patients.[31] However, if an LAGB patient is a female of childbearing age, the
multivitamin should contain at least the DRI. Iron supplements may be taken in the form of
a ferrous iron salt, heme iron polypeptide, carbonyl iron, iron amino-acid chelate, or
polysaccharide-iron complex, with the latter four having potentially fewer GI side effects. A
history of anemia or change in laboratory values may indicate the need for additional
supplementation, taking into account, age, gender, and reproductive considerations.[31]
Studies have shown a dose dependent effect of calcium on iron absorption, more so in
single meal studies than multiple meal studies.[140] Calcium doses > 300-1000 mg exhibit
an inhibitory effect on absorption of 5mg non-heme iron; calcium doses >300-800 mg also
inhibit the absorption of 5mg heme-iron; when taken together, either at a meal or on an 31
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empty stomach.[141, 142] More than one mechanism may be involved: 1) through
inhibition of the iron transfer process from the enterocyte to the plasma; and/or 2) high
calcium levels may affect the function of divalent metal ion transporter-1 (DMT-1), the
brush border transporter for elemental iron in duodenal enterocytes. [140, 143, 144] It
may also be possible that high levels of calcium alter the rheological properties of the
upper small intestine mucous layer. [140] However, the absorption of iron from a
multivitamin also containing calcium may not be inhibited due to the lower dosages
ingested.[140, 142-144]
Repletion of Postoperative Iron Deficiency
The development of iron deficiency develops over time, in the following stages:
Stage 1: Serum ferritin decreases to 20 ng/mLStage 2: Serum iron decreases to < 50 ug/dL; transferrin saturation <15% Stage 3: Anemia with normal-appearing RBCs and indexes is observed Stage 4: Microcytosis and then hypochromia developsStage 5: Iron deficiency affects tissues, resulting in clinical signs and symptoms
Similarly, repletion of iron stores takes time. Duration of treatment should be at least
three months, if not longer, since red blood cell turnover takes 120 days.[126] Oral
supplementation should be tried first and, if unsuccessful in correcting iron deficiency, IV
iron should be considered.[38, 102, 131, 138, 145] The recommended amount of iron
should be based on the needs of the patient, bearing in mind that different products contain
varying amounts of elemental iron. Ferrous calcium citrate and ferrous gluconate contain
9.5% and 12%, respectively, of elemental iron; carbonyl iron, heme iron polysaccharide
complex, and heme iron polypeptide contain 98-100% elemental iron.[126] Side effects of
iron therapy may include GI upset, nausea, vomiting, and constipation. Such side effects 32
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may hinder adherence. Dividing iron into smaller doses taken more frequently, and/or
taking iron supplements with food may decrease these side effects.[126] However,
consuming iron supplements simultaneously with foods rich in phytates (beans, peas,
lentils, nuts, seeds, grains) or polyphenols (herbal teas) can reduce ferrous iron absorption
by up to 50%.[126] Acid-reducing medications, calcium, and zinc may also affect
absorption rates Chan.[126, 145]
For correction of iron deficiency, the AACE/TOS/ASMBS 2013 CPG recommend taking
up to 150-200 mg of elemental iron daily, along with Vitamin C to increase absorption.[31]
However, taking ascorbic acid with iron better enhances absorption of iron from foods than
from iron supplements.[126] For severe intolerance to oral iron or refractory deficiency,
IV iron infusion (preferably with ferric gluconate or sucrose) may be used.[31, 102, 131,
145] The 2010 Endocrine Society published guidelines[82] recommended two phases of
treatment; of iron deficiency; the first phase consists of administration of ferrous sulfate
300 mg 2-3 times daily, taken with vitamin C, followed if needed by a second phase of
parenteral iron administration using iron dextran, ferric gluconate or ferric sucrose.
Iron – Summary
Recommendations for preoperative screening of iron deficiency
Routine pre-WLS screening of iron status is recommended for all patients. (Grade B,
BEL 2)
Screening patients for iron status, but not for the purpose of diagnosing iron
deficiency, may include the use of ferritin levels. (Grade B, BEL 2)
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A combination of tests (serum iron with serum transferrin saturation and total iron-
binding capacity) is recommended for diagnosing iron deficiency. (Grade B, BEL 2)
Pre-WLS screening for iron status should include assessment of clinical signs and
symptoms common to this condition (see Table 5). (Grade B, BEL 2)
Recommendations for postoperative screening of iron deficiency
Routine post-WLS screening of iron status is recommended for all patients within
three months after surgery, and then every 3- 6 months until the 12-month visit,
and annually thereafter. (Grade B, BEL 2)
Iron status in post-WLS patients should be monitored at regular intervals using an
iron panel, complete blood count, total iron-binding capacity, ferritin and soluble
transferrin receptor if available, along with clinical signs or symptoms. (Grade C,
BEL 3)
Additional iron screening in post-WLS patients who should be conducted as
warranted by clinical signs or symptoms and or laboratory findings, or in other
instances in which a deficiency is suspected. (Grade B, BEL 2)
Recommendations for supplementation of iron for preventing deficiency
Patients at low risk of postoperative iron deficiency should receive at least 18 mg of
iron from their multivitamin. (Grade C, BEL 3)
Menstruating females who have had RYGB, SG or BPD/DS should take 45-60mg of
elemental iron daily (cumulative from all vitamin and mineral supplements). (Grade
C, BEL 3)
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Oral supplementation should be taken in divided doses separately from calcium
supplements, acid-reducing medications, and foods high in phytates or polyphenols.
(Grade D, BEL 3)
Recommendations for postoperative iron repletion
In post-WLS patients with iron deficiency, oral supplementation should be increased
to provide from 150-200mg of elemental iron daily to amounts as high as 300 mg 2-
3 times daily. (Grade C, BEL 3)
Oral supplementation should be taken in divided doses separately from calcium
supplements, acid-reducing medications, and foods high in phytates or polyphenols.
(Grade D, BEL 3)Recommendation is downgraded to D, since majority of evidence
is from non-WLS patients.
If post-WLS iron deficiency does not respond to oral therapy, intravenous iron
infusion should be administered. (Grade C, BEL 3)
Vitamin D and Calcium
Vitamin D is important in calcium and phosphorus absorption and resorption, as well as
mineralization, and maturation of bone. It also modulates cell growth, neuromuscular and
immune function, and reduction of inflammation. Vitamin D exists in two forms: vitamin D2
(which is minimally obtained from the diet) and vitamin D3 (almost 80% obtained from
sun exposure).[8] As commonly used, the term "vitamin D” typically denotes D2, or D3, or
both. In the general population, daily intakes of vitamin D from foods average less than
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400 IU/d, but mean 25-hydroxy vitamin D [25(OH)D] levels are typically above 20 ng/ml
(50 nmol/liter).[146]
Once vitamin D is ingested, it is incorporated into chylomicrons, which are absorbed by
the lymphatic system and enter the venous blood. Without vitamin D, only 10–15% of
dietary calcium and about 60% of phosphorus are absorbed. Sufficient 25(OH)D levels
(greater than 30 ng/ml) enhance absorption of calcium by 30-40% and phosphorus
absorption by 80%.[147] Behavioral factors and genetics can have a profound effect on
vitamin D bioavailability.[148] Wearing a sunscreen with a sun protection factor of 30
reduces vitamin D synthesis in the skin by more than 95%. Additionally, people with a
naturally darker skin have extra sun protection and require at least three to five times
more sun exposure to convert the same amount of vitamin D as would people with lighter
skin.[149]
Calcium is integral to bone and tooth formation, as well as blood coagulation, muscle
contraction, myocardial conduction, nerve transmission, intracellular signaling and
hormonal secretion. There are several factors that impact the absorption of calcium
regardless of preoperative or postoperative status. These include dietary fat consumption
to facilitate vitamin D absorption, physiological levels of vitamin D, needed to facilitate
calcium absorption, and nutrient-nutrient interactions such as the creation of insoluble
salts from green leafy vegetables and foods containing high amounts of oxalates (spinach
and other greens, rhubarb, dry cocoa), and phytates (beans, peas, lentils, nuts, seeds,
grains), which inhibit the absorption of calcium and other minerals. [150, 151]
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25(OH)D is the primary circulating form of vitamin D, with a half-life of about 15 days;
it is the preferred biochemical assay for assessing vitamin D status. Serum 1,25(OH)2D has
a half-life of about 15 hours and is typically normal or even elevated in vitamin D
deficiency, due to secondary hyperparathyroidism. Thus, serum 1,25(OH)2D is neither
useful nor recommended as an indicator of vitamin D reserves or status.
Mildly reduced calcium and phosphate levels are commonly seen in vitamin D
deficiency (VDD), but levels may also be normal (Table 5). Often, alkaline phosphatase is
elevated due to increased bone turnover. VDD causes a decrease in the absorption of
dietary calcium and phosphorus, resulting in an increase in parathyroid hormone (PTH)
levels. The PTH-mediated increase in osteoclastic activity creates bone weakness and a
generalized decrease in bone mineral density, resulting in osteopenia and osteoporosis, as
well as skeletal deformities and muscle weakness.[147]
Preoperative Vitamin D and Calcium Screening
Studies have found that up to 90% of patients seeking WLS are deficient in 25(OH)D
levels.[35, 74, 76, 152-156] Obesity may promote VDD through several mechanisms,
including increased uptake of the circulating vitamin into adipose tissue, resulting in
sequestration and poor bioavailability, inadequate sun exposure, or 1,25(OH)2D
enhancement and concomitant negative feedback control on hepatic synthesis of 25(OH)D.
[1, 147, 149, 157] Numerous studies have reported an inverse relationship between
vitamin D levels and body mass index.[157-159] In fact, Stein et al.,[159] reported that
each body mass index increase of 1 kg/m2 was associated with a mean decrease of 1.3
nmol/l 25(OH)D.37
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There is strong evidence to recommend preoperative screening for vitamin D
insufficiency (VDI) or deficiency in all patients, which, if found, should be repleted with
appropriate supplementation before surgery.[31, 35, 101, 115, 158] Index levels for VDD,
insufficiency, and sufficiency have been defined as <20 ng/mL, 21-29 ng/mL, and 30-
100ng/mL, respectively.[147] With these newer, more conservative indices have come
increased reports of vitamin D deficiency in the general population and in patients with
obesity, [146, 160] and the reported prevalence of VDD in patients seeking WLS has
increased 20-30% since the 2008 Aills et al. guidelines were published.[1, 152, 153]
Most Americans, including pre-WLS patients do not consume adequate dietary calcium,
according to current recommendations.[146] Poor calcium intake in early childhood tends
to continue into the adult years.[161] Vitamin D is critical for calcium absorption and is
known to be a compounding factor, which makes it important to evaluate along with an
individual’s dietary calcium intake. Currently, there is no single commonly-recommended
labaratory assay used to determine calcium deficiency. There is, however, emerging
research on parathyroid hormone levels and bone density as they relate to calcium status.
[162-165] Due to the difficulty of screening for physiological adequacy of calcium intake, it
is critical to screen for vitamin D and to recommend preoperative supplementation of both
calcium and vitamin D.[158, 165]
Calcium requirements are known to increase with menopause due to decreasing
estrogen levels, which lead to an increase in bone resorption and a decrease in the
efficiency of both intestinal absorption and renal conservation of calcium.[166, 167]
Though screening for calcium sufficiency is difficult, WLS patients are at risk for calcium
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deficiency and can be screened with a combination of laboratory tests (vitamin D, 25-OH,
serum alkaline phosphatase, PTH, and 24 hour urinary calcium in relationship to dietary
intake).[168] Both pre-and post-menopausal women may be screened for increased bone
resorption by using urinary and/or serum type I collagen N-telopeptide (NTX) levels,
which are higher in patients with decreasing estrogen production.[167] In patients under
50 years of age, elevated values of carboxy- terminal telopeptide (CTX) have also been
reported in 67% of patients.[169]
Postoperative Vitamin D and Calcium Screening
Postoperative prevalence of VDD is high, approaching 100% in some samples.[35, 74, 76,
153, 169-172] Vitamin D insufficiency and deficiency rates are more pronounced in RYGB
and BPD/DS than in LAGB and SG due to procedure-specific factors, such as shortening or
bypassing portions of the small intestine, length of the common limb channel, bile
production and availability to mix with nutrients.[164, 173] A review of 30 clinical studies
identified VDD in 90% of both pre- and post- RYGB patients and VDI in up to 98% of post-
RYGB patients. A transient postoperative increase in vitamin D levels occurred by 6
months and a subsequent decrease in vitamin D levels with VDD persisted up to 18 months.
Prevalence of VDD in patients who had undergone SG was less than in RYGB patients and
decreased significantly from 84% to less than 50% at 12 months.[35] However, high rates
of VDI and VDD may persist for years after surgery.[74] In a Mediterranean population,
VDI and or VDD was the most common nutrient deficiency reported throughout 5 years for
both SG and RYGB (60% at all study time points). Correspondingly, a high proportion of
patients had elevated PTH throughout the study after both types of surgery. Dietary intake 39
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of calcium, phosphorus and magnesium were lower than current recommendations.[74]
More recent data, (5 year follow up data comparing BPD/DS and RYGB) demonstrated
10-20% greater weight loss with BPD/DS, but also more long-term deficiency of vitamin D
and other fat-soluble vitamins.[174] Other data for BPD/DS demonstrated that 45% of
patients continued to have VDD at 10-year follow-up, even though 65% patients were
taking both calcium and vitamin D supplements.[175]
Some methods of assessing insufficiency or deficiency of vitamin D and calcium may not
be completely accurate. There is a physiological compensatory mechanism between
calcium availability and actual absorption, as well as within bone mineral density (BMD)
preservation.[146, 176, 177] Due to the significant impact of WLS on bone health, it is
crucial to ensure robust screening, utilizing a variety of available screening tools in
addition to laboratory assays, in order to detect later-developing deficiencies. Particular
attention should be paid to BMD;[31, 163] as time elapses after WLS, dual-energy x-ray
absorptiometry (DXA) and PTH become more important in the interpretation of calcium
and vitamin D levels, and may be conducted at two years postoperatively or as indicated
after WLS.[31] It should be noted that recent research suggests that typically-used
methods for assessing VDI or VDD may not be accurate in some genetic subpopulations of
African Americans; [166, 167] and that PTH alone may not be sensitive enough to identify
BMD loss in post-WLS patients.
Pre- and post-menopausal patients, and patients who have had RYGB (with greater lean
mass loss), are at particular risk for BMD loss at the femoral neck and lumbar spine.[178]
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These patients should be followed closely, with periodic densitometries, as it is difficult to
determine BMD from biochemical markers alone.
Preventative Supplementation of Vitamin D and Calcium
Since post-WLS care begins preoperatively, it is important to begin a supplement
regimen pre-WLS. In patients preparing for WLS who are not vitamin D deficient, the RDAs
for vitamin D have been set at 600 IU/d for ages 1–70 years and increases to 800 IU/d for
71 years and older, corresponding to a serum 25(OH)D level of at least 20 ng/ml (50
nmol/liter). These RDAs were derived based on conditions of minimal sun exposure, due to
wide variability in vitamin D synthesis from ultraviolet light and the risks of skin cancer. In
vitamin D-sufficient patients, higher supplementation values have not consistently been
found to be associated with greater benefit.[146]
The RDA for calcium in the generally healthy population should be used for making
recommendations in patients who are pre-WLS and in patients without any identified
nutrient deficiencies.[147] The Institute of Medicine Committee concluded in 2011 that
available scientific evidence supported a key role of calcium and vitamin D in skeletal
health, consistent with a cause-and-effect relationship, and provided a sound basis for
determination of daily intake recommendations.[146] For optimal bone health, the RDAs
for calcium, which apply to >97.5% of the population aged > 1 year old, range from 700 to
1300 mg/d. For extraskeletal health, including cancer, cardiovascular disease, diabetes, and
autoimmune disorders, the evidence was inconsistent, and insufficient to inform
recommendations.[82][147]
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There are a number of recommendations currently in the lay media, suggesting how to
increase calcium and vitamin D absorption while inhibiting the formation of calcium
oxalate kidney stones. One particular suggestion, sauteéing green leafy vegetables to
increase calcium bioavailability seems intuitive, yet the research reports no beneficial
effects for either of the desirable outcomes.[150] There is emerging and promising
research in post-WLS patients, with regard to using calcium or potassium citrate
preferentially over other forms of calcium, and using probiotics to help inhibit formation of
oxalic salts via increased enteric oxalate absorption. Thus, educational strategies for
achieving adequate calcium and Vitamin D should take into account the individual patient’s
knowledge base and whether erroneous beliefs are contributing to a patient’s personal
dietary regimen.
In perimenopausal and postmenopausal women, the recommendations for optimal
bone health are higher. The North American Menopause Society[179] recommends
adequate calcium (<1000 mg calcium/day and UL <2500 mg/day for women < 50 yrs, and
< 1200 mg calcium/day and UL < 2000 mg/day for women >50 yrs) in the presence of
adequate vitamin D (serum 25(OH)D > 30 ng/mL).
Recommendations for vitamin D and calcium in post-WLS patients exceed the IOM
supplement recommendations for the general population.[146] Recommended levels of
supplementation are different for different types of surgery. For instance, distal RYGB and
BPD/DS alter digestion and nutrient absorption, thus creating a need for greater intake of
calcium and vitamin D.[31, 174] In one study of Mediterranean SG and RYGB patients, even
though participants were prescribed a multivitamin and mineral regimen which provided a
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total of 1,120 mg of calcium citrate plus 1040 IU of vitamin D, VDI or VDD was the most
common (>60% at all timepoints) nutrient deficiency reported for both procedures
throughout the 5 year follow up.[74] It is not clear if these patients were assessed
preoperatively, thus VDI or VDD may be exacerbated by lack of appropriate preoperative
diagnosis and repletion.[31, 101, 158]
Bone mineral loss is strongly associated with weight loss.[163] Research indicates that
even with vitamin D and calcium repletion, bone loss among WLS patients is still a concern.
[163, 164, 180] For instance, in one study, even though calcium, vitamin D and PTH levels
were reported to be within the norm, BMD continued to decrease an additional 9% by 2
years after RYGB as compared with a control group.[181] In WLS patients, who are at high
risk for pre- and postoperative calcium and VDD, it is imperative to supplement these
micronutrients to prevent acute problems. Bone loss may occur due to impaired calcium
absorption caused by decreased activation of vitamin D-dependent calcium absorption
mechanisms.[182] However, the clinician should be aware that, with calcium
supplementation, “more is not always better”. In fact, long-term intake of higher than
recommended calcium doses may be associated with health risks, though findings have
been inconsistent and it is difficult to infer causality in hypovitaminosis D or hypocalcemia
and non-skeletal diseases.[183] Thus, the current recommendations are for slightly lower
levels of calcium supplementation than detailed in the previous ASMBS guidelines, [1]
consistent with the AACE/TOS/ASMBS 2013 CPG.[31] Additionally, ranges that include
dietary sources and supplements rather than exact supplementation amounts are provided
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to allow for supplementation (or repletion, see below) to vary based on patient dietary
intake of vitamin D and calcium.
Although ergocalciferol (vitamin D2) may be used for supplementation, research
indicates that cholecalciferol (vitamin D3) is a more effective form,[184, 185] especially
when given in bolus dose, due to a potentially increased affinity of cholecalciferol to
vitamin D binding protein and receptors.[186] A dose of 2000 g (50 000 IU) vitamin D2 μ
should be considered equivalent to ≤375 g (15000 IU) vitamin D3, and likely closer to μ
125 g (5000 IU) vitamin D3.μ [184] When the varying modes of dosage administration was
compared in one study [184] there was a significant response for vitamin D3 when given as
a bolus dose (P = 0.0002) compared with administration of vitamin D2, but the difference
was not statistically significant when comparing daily doses of D2 and D3. More research is
needed to establish efficacious doses of each of the forms of vitamin D.
The most commonly available forms of calcium supplementation in the United States
are calcium carbonate and calcium citrate. Calcium lactate, gluconate, bone meal and
hydroxyapatite are also available, but the elemental calcium content in these supplements
varies. The type of nutrient delivery (capsules tablets, chews, wafers, powders, liquids)
impacts the bioavailability of the calcium in the supplement. Calcium carbonate provides
approximately 40% absorption of elemental calcium when taken in doses no greater than
500 mg and ingested with meals, which increases the acid production needed for
absorption. [187] Possible adverse reactions to calcium carbonate supplementation are
constipation, nausea and bloating. Calcium citrate provides approximately 21% elemental
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calcium, which can be absorbed in either an acidic or non-acidic environment. Other forms
of calcium salts provide less than 20% absorption.[187, 188]
Repletion of Postoperative Vitamin D and Calcium Deficiency
Vitamin D and calcium deficiency are very common in both pre- and post-WLS patients.
[153, 170, 171] Recommendations by Mechanick for treatment of vitamin D and calcium
deficiency or insufficiency after WLS concur with other research findings.[31, 147, 185,
188], Even with prescribed treatment for VDD, deficiencies may persist and multiple
treatment courses may be necessary. Lack of treatment effectiveness may be due, in part, to
inadequate patient adherence to the repletion regimen.[188, 189] However, more frequent
monitoring with adjustment of calcium and VDD may be needed in more malabsorptive
procedures; ie., a 200 cm BP limb may require more frequent monitoring than a 60 cm BP
limb or a 150cm RYGB limb.[132] As with supplementation, vitamin D3 is more potent
than vitamin D2 for repletion of vitamin D deficiencies.[186]
Vitamin D and Calcium – Summary
Recommendations for preoperative screening of Vitamin D insufficiency or deficiency
Routine pre-WLS screening of Vitamin D status is recommended for all patients.
(Grade A, BEL 1)
Routine pre-WLS screening of calcium status and vitamin D deficiency and
insufficiency is particularly important for peri-menopausal women. (Grade D, BEL
4)
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Recommendations for postoperative screening of Vitamin D and calcium
Routine post-WLS screening of vitamin D status is recommended for all patients.
(Grade B, BEL 2)
More research is needed before a recommendation can be made regarding the use
of vitamin D binding protein assays as an additional tool for determining vitamin D
status in post-WLS patients. (Grade C, BEL 3)
Recommendations for supplementation of vitamin D and calcium for preventing deficiency
All post-WLS patients should take calcium supplementation. (Grade C, BEL 3)
The appropriate dose of calcium varies by surgical procedure:
o BPD/DS: 1800-2400 mg/day
o LAGB, SG, RYGB: 1200-1500 mg/day
The recommended preventative dose of vitamin D in post-WLS patients should be
based on serum vitamin D levels:
o Recommended vitamin D3 dose is 3000 IU daily, until blood levels of 25(OH)D
are greater than sufficient (30 ng/mL) (Grade D, BEL 4)
o As compared to recommended vitamin D2 doses, a 70-90% smaller vitamin D3
bolus dose, is needed to achieve the same effects in healthy non-bariatric
surgical patients (Grade A, BEL 1)
In order to enhance calcium absorption in post-WLS patients, the following dosing
considerations apply (Grade C, BEL 3):
o Calcium should be given in divided doses
o Calcium carbonate should be taken with meals46
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o Calcium citrate may be taken with or without meals
Recommendations for repletion of postoperative vitamin D and calcium deficiency
Vitamin D levels must be repleted if deficient or insufficient, in order to normalize
calcium. (Grade C, BEL 3)
All post-WLS patients with vitamin D deficiency or insufficiency should be repleted with
the following doses:
Vitamin D3 dosages of at least 3000 IU/day and as high as 6000 IU/day or 50,000 IU
vitamin D2 once to three times weekly. (Grade A, BEL 1)
Vitamin D3 is recommended as a more potent treatment than vitamin D2 for
repletion of vitamin D. However, both forms can be efficacious, depending on the
dosing regimen. (Grade A, BEL 1)
The recommendations for repletion of calcium deficiency varies by surgical
procedure. (Grade C, BEL 3):
o BPD/DS: 1800-2400 mg/day calcium
o LAGB, SG, RYGB: 1200-1500 mg/day calcium
Vitamins A, E, K
Vitamin A is critical for normal vision; it supports cell growth and differentiation, and
plays a major role in the normal formation and maintenance of the heart, lungs, kidneys,
and other organs. It is important in maintaining healthy skin, teeth, skeletal and soft tissue,
and mucus membranes.[190, 191]
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Vitamin A exists in two forms: preformed vitamin A (found in animal products e.g., eggs,
meat, fortified milk, etc.) and pro-vitamin A, (found in plant-based foods (e.g., bright yellow
and orange fruits and vegetables)). The most common form of pro-vitamin A is beta-
carotene, a carotenoid. Alternative names for vitamin A include retinol, retinal, retinoic
acid, and carotenoid.
Vitamin E (alpha-tocopherol and gamma-tocopherol) is an antioxidant that protects the
body from the damages of free radicals, helps to strengthen the immune system; plays a
role in the formation of red blood cells; and helps the body use vitamin K by dilating blood
vessels and preventing thrombosis. Adequate vitamin E levels are best maintained by
obtaining this vitamin through food; sources of vitamin E include vegetable oils, nuts and
seeds. Though vitamin E levels may be increased through supplementation, high doses of
vitamin E in supplement form may increase the risk for bleeding.[191-194]
Vitamin K is integral to blood clotting, thus patients with a vitamin K deficiency may
present with bruising or bleeding; considered rare in the general population; but may
occur if the GI tract is not absorbing nutrients properly, such as after WLS or as a result of
long-term antibiotic treatment.[191, 193, 194]Patients taking blood-thinning drugs should
be cautioned about risks of excessive intake of vitamin K both from food and supplemental
sources.[191, 193, 194]
Lipid digestion is delayed in post-WLS patients, especially in patients who undergo
RYGB, and BPD/DS. In these procedures, the fats do not pass through the duodenum
impairing the release of bile and pancreatic lipase. Limited production of these enzymes
lead to the malabsorption of fat; thus, fat soluble vitamin deficiency may result. Water
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soluble vitamin deficiencies tend to occur early in the postoperative period, but fat soluble
deficiencies develop more slowly, based on the rate of the progression of fat
malabsorption.[195]
Preoperative Vitamin A, E and K Screening
Reported prevalences of vitamin A and E deficiencies in pre-WLS patients is low
(vitamin A (14%), vitamin E (2.2%); there are no data regarding the prevalence of vitamin
K deficiencies in this population.[35, 115, 156, 196, 197] However, AACE/TOS/ASMBS
2013 CPG recommended that all WLS patients undergo micronutrient assessment,
including screening for deficiencies of fat-soluble vitamins (A, E, D, K), before any WLS
procedure.[31]
The Aills guidelines do not include specific recommendations for preoperative
screening of fat-soluble vitamin deficiencies, as most research on these deficiencies has
focused on the postoperative period.[1] However, it is known that obesity increases the
need for vitamin A and contributes to the depletion of liver stores, enhancing the risk for
developing metabolic disorders.[192, 197, 198] High BMI, poor quality food choices and
inflammation are factors that may predispose some pre-WLS patients to be at risk for
vitamin A deficiency.[193, 197, 199]
Postoperative Vitamin A, E and K Screening
Vitamin A deficiency has been found to be relatively common (up to 70%) in LAGB,
RYGB, and BPD/DS patients within 4 years after surgery.[1, 199, 200] Additionally, vitamin
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A deficiency has been found to be associated with low serum concentration of pre-albumin.
[197]
In RYGB and to a more pronounced extent after BPD, there is a consistent and
continuous decline in all carotenoids to almost undetectable levels after surgery. In fact,
patients who had BPD/DS have been found to have serum vitamin A levels that were about
one-half to one-third the amount of vitamin A levels found in patients who had RYGB.[201]
Based on current data, vitamin A should be measured in patients who have undergone
BPD/DS or RYGB, and deficiency should be suspected in those with evidence of protein-
calorie malnutrition.[201]
As noted in the AACE/TOS/ASMBS 2013 CPG,[31] there is insufficient evidence to
support routine postoperative screening for vitamin E or vitamin K deficiencies, given that
the prevalence of these conditions is typically observed to be fairly low[31], and vitamin E
levels may actually increase after both RYGB and BPD/DS.[37] On the other hand, serum
concentrations of the vitamin E derivative alpha-tocopherol has been found to be
decreased after one year in both RYGB and BPD/DS.[201]The significance of alpha-
tocopherol levels is unclear, however, since normal vitamin E levels have been observed in
RYGB patients with subthreshold levels of alpha tocopherol.[202]
Data published both before and since the Aills guidelines suggest that it is unusual and
rare to observe complications related to vitamin K deficiency post-WLS; however, any
malabsorptive procedure (BPD/DS or RYGB) does confer an elevated risk for vitamin K
deficiency (Table 5).[1, 203] Low prothrombin time has been used as an indicator of
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vitamin K deficiency, and mean prothrombin time was found to be lower in the RYGB group
than either LAGB or conventional weight loss treatment groups.[203]
Preventative Supplementation of Vitamin A, E and K
Current research continues to suggest that the risk of fat-soluble vitamin deficiency is
greater in patients who have RYGB and BPD/DS.[37] Compared with RYGB, DS may be
associated with a greater risk of vitamin A deficiency in the first year after surgery,
indicating that long term vigilant monitoring of postoperative BPD/DS patients may be
warranted.[37]
There have been recent data showing that post-WLS patients who are inadequately
supplemented during pregnancy may expose the fetus or newborn to problems such as
cerebral hemorrhage or other bleeding disorders related to vitamin K deficiency, and
microcephaly, hypotonia, microphthamia, and permanent retinal damage due to vitamin A
deficiency.[204] Special attention should be given to prenatal supplementation of vitamin K
in early pregnancy in women who have undergone BPD/DS.
Repletion of Postoperative Vitamin A, E, and K Deficiency
Although recent literature does not suggest that any changes to the Aills guidelines[1]
are needed; there have been a number of case studies describing the sequelae of vitamin A,
E, or K deficiencies, underscoring the importance of addressing such deficiencies when
they are identified.[194, 205]
Vitamins A,E,K – Summary
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Recommendations for preoperative screening of vitamins A, E, K deficiency
Routine pre-WLS screening of vitamins A, E, K status is recommended for all
patients. (Grade C, BEL 3)
Recommendations for postoperative screening of vitamins A, E, K deficiency
Post-WLS patients should be screened for vitamin A deficiency within the first year
after surgery, particularly those who have had BPD/DS, whether symptoms are
present or not. (Grade B, BEL 2)
Vitamin A should be measured in patients who have had RYGB or BPD/DS,
particularly in those patients with evidence of protein-calorie malnutrition. (Grade
B, BEL 2)
While Vitamin E and K deficiencies are uncommon after WLS, patients who are
symptomatic should be screened. (Grade B, BEL 2)
Recommendations for supplementation of Vitamins A, E, K for preventing deficiency
Post-WLS patients should take vitamins A, E, and K, with the dosage based upon type of
procedure:
o LAGB: Vitamin A (5000 IU/d) and Vitamin K (90-120 ug/day)(Grade C, BEL 3)
o RYGB, and SG: Vitamin A (5000-10,000 IU/d) and Vitamin K (90-120 ug/day)(Grade
D, BEL 4)
o LAGB, SG, RYGB, BPD/DS: Vitamin E (15 mg/d) (Grade D, BEL 4)
o DS: Vitamin A (10,000 IU/d) and Vitamin K (300 µg/d) (Grade B, BEL 2)
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Higher maintenance doses of fat-soluble vitamins may be required for post-WLS
patients who have a previous history of vitamin A, E, or K deficiency. (Grade D, BEL 4)
Water-miscible forms of fat soluble vitamins are also available to improve absorption
(Grade D, BEL 4)
Special attention should be given to prenatal supplementation of vitamin A and K in
pregnant women who have had WLS. (Grade D, BEL 4)
Recommendations for postoperative Vitamin A, E, and K repletion
Vitamin A
In post-WLS patients with vitamin A deficiency and without corneal changes:
10,000-25,000 IU/d vitamin A should be administered orally until clinical
improvement is evident (1-2 weeks). (Grade D, BEL 4)
In post-WLS patients with vitamin A deficiency and with corneal changes: 50,000 –
100,000 IU vitamin A should be administered IM for 3 days followed by 50,000 IU/d
IM for 2 weeks. (Grade D, BEL 4)
Post-WLS patients with vitamin A deficiency should also be evaluated for
concurrent iron and/or copper deficiencies as these can impair resolution of
vitamin A deficiency. (Grade D, BEL 4)
Vitamin E
The optimal therapeutic dose of vitamin E in post-WLS patients has not been clearly
defined. There is potential for antioxidant benefits of vitamin E to be achieved with
supplements of 100-400 IU/d. This is higher than the amount typically found in a
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multivitamin; thus additional vitamin E supplementation may be required for
repletion. (Grade D, BEL 4)
Vitamin K
For post-WLS patients with acute malabsorption, a parenteral dose of 10 mg vitamin
K is recommended. (Grade D, BEL 4)
For post-WLS patients with chronic malabsorption, the recommended dosage of
vitamin K is either 1-2 mg/d orally or 1-2 mg/week parenterally. (Grade D, BEL 4)
Zinc
Zinc is a trace mineral that plays important roles in nucleic acid metabolism, gene
regulation, immune function, hormone activity, lipid and protein metabolism, cell growth,
cell replication, and cell death (apoptosis), as well as taste acuity, vision, wound healing,
growth and reproduction, and over 300 enzymatic reactions.[206, 207] Unlike other
nutrients, there are no body reserves of zinc beyond levels present in body tissues,
between 1.5 to 3.0 grams of zinc.[206, 207]
Zinc is absorbed in the proximal jejunum. Absorption efficiency is inversely
correlated with zinc intake.[208] Once zinc is absorbed in the intestinal mucosal cells, the
metal-binding protein metallothionein binds zinc and impedes its movement into the
bloodstream. More metallothionein is produced when zinc intake is high. When zinc intake
is low, zinc is absorbed into intestinal mucosal cells and circulates in the bloodstream to
tissues bound to albumin and alpha2- macroglobulin. Zinc contained in intestinal cells and
unabsorbed dietary zinc is excreted in the feces when not needed in the body.[206]
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Preoperative Zinc Screening
Research reports of estimated prevalence of zinc deficiency vary widely, ranging from
9% to 74% of patients seeking BPD/DS.[208-210] Copper, zinc, and iron compete for the
same trans-membrane transport molecule, which can lead to an imbalance of these
minerals. Zinc also causes up-regulation of the production of metallothionein, which can
bind and trap copper in small intestinal cells, leading to copper depletion with sloughing of
these cells.[211] High intake of dietary zinc increases the synthesis of metallothionein, and
because metallothionein has a higher affinity for copper than zinc, a decrease in copper
absorption can occur with high intake of dietary zinc or oral zinc supplementation, as
copper will displace zinc and remain in the enterocyte. On the other hand, it has been
questioned whether zinc competes with iron absorption.[212-215] However, use of a
modest zinc supplement (22 mg/day zinc gluconate) has been shown to induce a cellular
iron deficiency and, possibly, further reduce iron status.[216]
More recent studies in pre-WLS patients have found that patients with obesity have
lower serum zinc levels (and lower concentrations of zinc in plasma and erythrocytes than
leaner patients).[58, 208-210, 217] It is suggested that the accumulation of adipose tissue,
increases the production of adipocytokines, resulting in a chronic inflammatory state.[38]
The inflammation then induces the expression of metallothionein and zinc-copper
transporters in hepatocytes, proteins that promote metal accumulation in the liver and in
adipocytes, thus contributing to low zinc concentrations.[38]
Although Aills et al.,[1] suggest that there is no reliable way to determine zinc status,
plasma, urinary, and hair zinc have been established as reliable biomarkers of zinc status in
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healthy patients, and these are commonly used to assess zinc in WLS patients (Table 5).
[218] Zinc stable isotope techniques can be used to determine zinc absorption;[218]
however, serum zinc levels may be decreased in the pro-inflammatory state of obesity,
[209, 219, 220] rendering plasma zinc an unreliable marker in the presence of systemic
inflammation.[31, 93, 221] Plasma zinc corresponds to 0.1% of total body zinc, and small
alterations in the tissues will affect this value, which is why some authors advocate
evaluating zinc erythrocyte concentration.[153, 220, 222] On the other hand, plasma zinc
concentration is still the preferred biomarker, because the erythrocyte may contaminate
the zinc. In addition, plasma concentrations are maintained even in the setting of decreased
or increased intake of zinc unless such changes are prolonged.[198]
Despite evidence suggesting that patients with obesity are at higher risk for zinc
deficiency, routine screening of zinc has not been recommended by recent CPGs.[31, 93,
209] Because of the unreliability of measures of zinc status in patients with obesity, and
limited data regarding zinc status pre-WLS, there is limited evidence to recommend routine
screening for zinc deficiency prior to WLS. However, patients undergoing certain WLS
procedures are at higher risk for developing zinc deficiency after surgery, indicating the
need for a baseline assessment of zinc status prior to surgery.
Postoperative Zinc Screening
The risk for postoperative zinc deficiency varies by the type of surgical procedure.
Postoperative zinc deficiency has been reported in 34% of patients post LAGB, 19% post-
SG, 40% post RYGB, and 70% post-BPD/DS.[223-226] Factors that increase risk of zinc
deficiency include the bypassing of the duodenum and proximal jejunum, which is the 56
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primary site of zinc absorption; reduction in the digestive enzymes containing zinc that are
secreted by the pancreas into the small intestine; reduction in gastric production of
hydrochloric acid, which is needed to improve bioavailability of zinc and absorption;
intolerance to food rich in zinc; and decreased dietary intake of zinc.[225, 227, 228]
As is the case with most micronutrients, zinc deficiency is more common after BPD/DS
than after other WLS procedures.[37] The AACE/TOS/ASMBS CPG advised monitoring of
zinc status in patients who have undergone malabsorptive (RYGB or BPD/DS) procedures
and who have not had routine supplementation, due to the risk of iatrogenic copper
deficiency.[31] Reported rates of zinc deficiency in BPD/DS patients are variable. Studies
have found prevalence rates ranging from 33% to 74% anywhere from one to ten years
postoperatively.[175, 229, 230] Because zinc is excreted in the feces, patients who
experience chronic diarrhea (which occurs in a subset of BPD or BPD/DS patients) are at
increased risk for zinc deficiency.[31, 93, 221] Therefore, the updated AACE/TOS/ASMBS
guidelines recommend routine zinc screening and supplementation for BPD/DS patients.
[31]
Reported rates of zinc deficiency in RYGB patients range from 40% to 60% at 6 months
postoperatively, despite standard supplementation.[38, 98, 223, 225] In one study, for
instance, 40% of patients taking 15 mg daily zinc as part of their daily multivitamin/
mineral regimen and a separate group taking 25 mg daily as additional zinc experienced
zinc deficiency.[98, 208, 231] Despite patients taking a multivitamin and mineral
supplement containing 8 mg zinc daily, 3% and 12% of patients had zinc deficiency at 6
and 24 months postoperatively, respectively.[98] Overall, reports of increased frequency
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of zinc deficiency post-RYGB, despite standard zinc supplementation, justifying a
recommendation of postoperative monitoring of zinc status. It is recommended that
screening be conducted using the same biomarkers as employed in preoperative screening,
as described above.[31]
Recent studies have examining zinc deficiency in SG patients, have yielded mixed
results.[232] In post-SG patients, 19% prevalence of zinc deficiency has been reported at
one year.[208] In another study, 14% of patients who had SG and were not initially
supplemented with zinc had to be supplemented with 15 mg/day zinc when they presented
with zinc deficiency post-surgery.[90] On the other hand, several studies did not detect
postoperative zinc deficiencies in patients who had SG and who were provided with
standard multivitamin and mineral supplementation containing zinc.[41, 233] However, in
another study, 34% of SG patients provided with a multivitamin containing 10 mg zinc
presented with zinc deficiency within the first year after surgery.[38] Low serum zinc
levels and hair loss related to zinc deficiency was detected at 24 months postoperatively in
a different sample of SG patients.[234] These studies all suggest that the zinc content of
standard multivitamin and mineral supplementation may not be sufficient to prevent zinc
deficiency in SG patients.
Decreased intake of foods containing zinc after surgery is associated with lower zinc
concentrations.[235] One preliminary report found a larger change in erythrocyte and
urinary zinc concentrations versus plasma zinc in unsupplemented patients 2 months post-
RYGB.[235] The authors concluded that zinc supplementation was not necessary for the
first 2 months after RYGB surgery if nutritional status was adequate before surgery.
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However, food logs indicate that patients may have had a lower dietary zinc intake in the
postoperative period, putting them at risk for long-term deficiency and supporting the
need for supplementation. For example, low serum levels of zinc were found in a small
study (n=30) at 3 months post-LAGB, and this was attributed to decreased dietary intake of
zinc.[236] Further studies are needed to correlate dietary intake of zinc to the response of
different zinc biomarkers for zinc at various time periods following WLS. It was suggested
by the authors of one study that preoperative and early postoperative deficiency could be
related to protein status, as evidenced by differences in serum pre-albumin concentration.
[208] This was not correlated with reported protein intake, however, but rather only with
indirect markers of protein nutritional status[208].
Since zinc absorption efficiency is inversely correlated with zinc intake, adaptation to
zinc absorption is not possible after malabsorptive procedures, such as the BPD/DS and
RYGB, as greater intestinal absorption and reduced excretion are unlikely when the
duodenum and part of the proximal jejunum are bypassed.[208] Overall, zinc deficiency is
less common after purely restrictive procedures, such as the LAGB, but decreased intake of
zinc-containing foods after the LAGB, as well as other WLS procedures, increases the
likelihood of postoperative deficiency.[38]
The AACE/TOS/ASMBS 2013 CPG recommend regular zinc screening in RYGB and
BPD/DS patients, without specifying a frequency.[31] Review of new evidence, however,
suggests that it is appropriate to screen at least annually in RYGB and BPD/DS patients.
Screening for zinc status in post-LAGB and SG patients is not recommended in the
AACE/TOS/ASMBS 2013 CPG[31]; however, the current evidence suggests it is important
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to conduct zinc screening in patients presenting with clinical symptoms of deficiency,
particularly in patients who have undergone surgeries that affect nutrient absorption,
particularly after BPD/DS, RYGB, and (to a lesser extent) SG, using the same biomarkers
used preoperatively.
Preventative Supplementation of Zinc
The risk for zinc deficiency remains even in patients taking a standard multivitamin
and mineral supplement.[38, 206, 210, 220, 222, 224, 226, 230, 237] In the studies
reviewed, the researchers used various supplemental zinc dosages, ranging from 8-30
mg/day of elemental zinc. [38, 41, 98, 206, 208, 210, 222, 224, 226, 230] In these studies,
higher doses of zinc (15 mg/day to 30 mg/day) were reserved for BPD patients and lower
doses (8 to 10 mg/day) were provided to RYGB and SG patients.[90, 98, 223] Some of the
vitamin and mineral supplements used in these studies contained 100% of the RDA for
zinc, but even when 200% of the RDA was provided, deficiencies were observed. [38, 90,
98, 223]
Zinc deficiency appears to be more pronounced among BPD patients who do not
receive, or who do not adhere to, standard multivitamin and mineral supplementation after
surgery.[90] However, relatively small doses of zinc (0.8 mg zinc) used daily in a
multivitamin have been found insufficient to maintain zinc status within normal levels two
years after BPD, with 34% of one sample developing a zinc deficiency. In order to achieve
zinc levels within normal limits, elemental zinc was increased in 81% of these patients, to a
much larger dose, (60 mg/day).[238] This led the researchers to recommend a dose of 30
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mg/day elemental zinc, in addition to the zinc found in a multivitamin, following BPD in
order to prevent post-operative zinc deficiency following BPD.[238]
There are only two recent RCT’s that have assessed zinc status in RYGB patients given
various dosages of zinc. One study (n=67) found impaired zinc absorption among
participants 6 months and 18 months post-surgery, despite supplementation of 7.5 or 15
mg/day.[220] Based on these findings, the authors recommended daily supplementation
of 40-50 mg of zinc per day. This study was expanded by the same group of authors, who
gave a third group 24 mg/day zinc and examined inflammatory parameters.[237]
Increased plasma and hair zinc levels were found in all three treatment groups. The
authors attributed this to a decreased inflammatory state post-surgery.
Even though patients who had SG were provided daily standard multivitamin and
mineral supplementation containing zinc, patients still developed zinc deficiencies[41, 233]
In fact, in one study, 34% of patients supplemented with 10 mg zinc in a daily multivitamin
also presented with zinc deficiency within the first year after surgery.[38] Additionally,
zinc deficiency was detected at 24 months postoperatively in SG patients.[234] Thus, the
zinc content of standard multivitamin and mineral supplementation may not be sufficient
to prevent zinc deficiency in SG patients.
The AACE/ASMBS/TOS 2013[31] guidelines recommend routine zinc supplementation
post-WLS, and note that the dose must be carefully considered. Review of the recent
literature suggests that 100-200% of the RDA may not be adequate; yet seems to be most
appropriate to prevent zinc deficiency, especially in BPD/DS and RYGB patients.
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Supplementation with a standard multivitamin containing at least 100% of the RDA for
zinc (8-11 mg/day) is recommended for patients who have SG.
Multivitamin formulations vary in concentrations of elemental zinc and the salt form
of zinc. Zinc gluconate contains 14.3% elemental zinc, zinc oxide contains 80% elemental
zinc, zinc acetate contains 30% elemental zinc, and zinc sulfate contains 23% elemental
zinc.[1, 239]
Care must be taken to ensure that the appropriate ratio of zinc to copper
supplementation is achieved. Copper depletion can occur when large doses of zinc (e.g.,
>60 – 600 mg/day) are given for long periods of time. Nausea, vomiting, and cramping
have been reported with zinc intakes of 50-150 mg/day.[198] When daily doses of >60
mg/day of zinc are consumed for longer than 10 weeks, reduced copper biomarkers have
been observed.[198] At doses of 150 mg/day of elemental zinc, copper deficiencies can
arise.[207] At doses of 600 mg/day of elemental zinc, there have been case reports of
myeloneuropathies, thought to be a consequence of copper deficiency [240, 241] Typically,
multivitamin and mineral supplements contain a ratio of 15 mg of zinc for each 1-2 mg of
copper. Griffith et al. report that a zinc to copper ratio of 15 mg of zinc for each 1-2 mg of
copper [240] may be too high for patients post-RYGB, as over-supplementation with zinc
can lead to a copper deficiency-related anemia. Accordingly, AACE/TOS/ASMBS 2013
CPG[31] recommend that appropriate supplements contain 8-15 mg of elemental zinc for
every 1 mg of copper. Any supplementation with high doses of zinc greater than 50 mg/day
should be implemented with caution and closely monitored. In addition, despite the
uncertainty regarding whether zinc inhibits iron absorption, high dosages of supplemental
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iron (i.e., beyond the DRI of 18 mg), should be taken at different times than zinc
administration, in order to avoid competition for intestinal absorption.
Repletion of Postoperative Zinc Deficiency
There are very few studies examining repletion doses for zinc deficiency in WLS
patients. The Merck Manual of Diagnosis and Therapy recommends treatment with 15 to
120 mg/day elemental zinc in the non-bariatric patient.[242] Although no optimal dose for
zinc deficiency in WLS patients has been firmly established, the 2008 ASMBS Nutritional
Guidelines [1] recommend repletion with 60 mg elemental zinc orally twice a day.
However, as new research on this topic has emerged, this recommendation requires
further elaboration. Although studies with a high level of evidence are still needed, case
studies can provide a basis for recommendations regarding repletion of zinc. In one study
in which 90% of patients who had RYGB and SG were zinc deficient, 30 mg/day of oral zinc
gluconate (4.29 elemental) was needed for repletion.[38] However, repletion of zinc
deficient patients who were not given multivitamin and mineral supplementation, was
effectively achieved with 15 mg/day of oral elemental zinc.[90] The discussion by
Jeejeehboy et al.[232] of a pivotal paper by Kay et al., [243] describes repletion of zinc
deficiency in the non-bariatric patient with 220 mg oral or 80 mg IV zinc sulfate over 10
days to a few weeks in a series of three nonbariatric cases. A single case report described a
patient with acquired zinc deficiency 3 years post-RYGB who was effectively treated with
220 mg zinc sulfate (50 mg of elemental zinc), though the route of administration was not
specified. Based on this case report, the authors suggested that treatment for zinc
deficiency should be initiated at 3 mg/kg/day of elemental zinc.[244] In general, while 63
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some patients may require more than 30 mg of zinc for repletion therapy, it may be
beneficial to split doses to < 30 mg per dose period to reduce the risk of GI distress and side
effects. [198]
As noted above, while zinc toxicity is rare, high oral intake of zinc can lead to copper
deficiency. The risks of copper deficiency caused by zinc intake is decreased with IV
repletion, as the gut, which is the site of competition between zinc and copper absorption,
is bypassed. Although standard dosing for zinc repletion has not yet been established for
WLS patients, it is important to provide a repletion level that will not disrupt the
homeostasis of other micronutrients.
Zinc – Summary
Recommendations for preoperative zinc screening
Routine screening of zinc status is recommended for patients prior to RYGB or
BPD/DS. (Grade D, BEL 3)
Zinc assays in pre-WLS patients should be interpreted in light of the fact that
patients with obesity have lower serum zinc levels and lower concentrations of zinc
in plasma and erythrocytes than leaner patients. (Grade C, BEL 3)
Recommendations for postoperative screening
While evidence does not suggest that all post-WLS patients should be screened for
zinc deficiency, patients who have RYGB or BPD/DS should be screened at least
annually for zinc deficiency. (Grade C, BEL 3)
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Serum or plasma zinc are the most appropriate biomarkers for zinc screening in
post-WLS patients. The same biomarkers should be used in preoperative and post-
operative patients. (Grade C, BEL 3)
Zinc should be evaluated in all post-WLS patients when the screening results for
iron deficiency anemia are negative. (Grade C, BEL 3)
Post-WLS patients who have chronic diarrhea should be evaluated for zinc
deficiency. (Grade D, BEL 4)
Recommendations for supplementation of zinc for preventing deficiency
All post-WLS patients should take zinc, with the dosage based upon type of
procedure (Grade C, BEL 3):
o BPD/DS: Supplement with16-22 mg/day of zinc.
o RYGB: Supplement with 8-22 mg/day of zinc.
o SG/LAGB: Supplement with 8-11 mg/day of zinc.
To minimize the risk of copper deficiency in post-WLS patients, it is recommended
that the supplementation protocol contain a zinc-to-copper ratio of 8-15 mg of
supplemental zinc per 1 mg of copper. (Grade C, BEL 3)
Formulation and composition of zinc supplements must be taken into account for
accurate calculation of elemental zinc levels. (Grade D, BEL 4)
Recommendations for postoperative zinc repletion
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There is insufficient evidence to make a dose-related recommendation for repletion. The
previous recommendation of 60 mg elemental zinc, orally twice a day, needs to be re-evaluated
in light of emerging research that this dose may be inappropriate.
Repletion doses of zinc in post-WLS patients should be chosen carefully to avoid inducing a
copper deficiency. (Grade D, BEL 3)
Zinc status should be routinely monitored using consistent parameters throughout the course
of treatment. (Grade C, BEL 3)
Copper
Copper is an essential trace mineral that acts as an antioxidant and is involved in the
synthesis of the pigment melanin and the connective tissue proteins collagen and elastin.
[207] Copper is a component of ceruloplasmin, the enzyme that oxidizes ferrous iron to
ferric iron for incorporation into transferrin before it is transported in the plasma.
Ceruloplasmin is also involved in the erythrocyte-forming cells of bone marrow.[207]
Copper plays a role in myelinization of nerves, immune function, and cardiovascular
function.[206] Copper concentrations are highest in the liver, brain, heart, and kidney.
Copper is secreted from the liver as a component of bile.[207] The adult body stores about
100 mg of copper at any time, and excess copper is excreted in feces from unabsorbed
dietary copper; released in bile; and sloughed within cells from the intestinal wall.[206]
Copper is absorbed in the stomach and duodenum. Copper absorbed in the small
intestine is bound to metallothionein, a metal binding protein that has greater affinity for
copper than for zinc or other metal ions. Because of this affinity, copper may be trapped in
the enterocyte and sloughed off into the intestinal tract and eliminated, thus decreasing
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copper absorption.[245] Copper is bound to albumin and transported via the blood to the
liver. In the liver, copper binds to metallothionein, and is incorporated into ceruloplasmin,
enzymes, and bile. It is eventually secreted into the plasma and transported to the cells of
other tissues, while excess copper is excreted in bile.[206, 207]
Preoperative Copper Screening
There is a relative dearth of data regarding the prevalence of preoperative copper
deficiencies in WLS patients, as assessment of copper levels is not typically part of the
preoperative micronutrient evaluation. Recent data regarding copper status and/or
copper deficiencies in patients with obesity and/or seeking WLS are somewhat mixed, with
some studies finding rather high rates of copper deficiency or low copper levels (e.g., in
68% of women undergoing BPD)[85] or no differences in copper levels between patients
with and without obesity.[239, 240, 246] In two studies conducted in 2009 by Ernst et al.,
no copper deficiencies (as assessed with serum copper levels) were seen in two different
samples of pre-WLS patients.[58] More research is needed to determine the prevalence of
copper deficiency pre-WLS.
As has been the case with zinc, the inflammatory processes common in obesity have led
researchers to question the reliability of copper measures and status in pre-WLS patients.
Copper deficiency has historically been diagnosed by the observation of a decrease in
serum copper and ceruloplasmin levels, with superoxide dismutase levels also providing
supporting evidence of copper deficiency.[198, 207, 247] While ceruloplasmin is a marker
of copper status, its rate of synthesis is not affected by dietary copper intake, while serum
copper is low when copper is deficient.[198, 248, 249] Serum copper does not correlate 67
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with dietary intake of copper except in instances when serum copper is below a certain
level.[198] Another drawback of serum ceruloplasmin as a marker for copper deficiency is
that it is an acute phase reactant protein and increases with pregnancy, age, anemia, and
medications such as oral contraceptives, thus complicating the interpretation of this assay.
[198, 250] Erythrocyte superoxide dismutase may be a more valid biomarker of copper
status, as it does not vary with the conditions that increase serum copper and
ceruloplasmin, such as pregnancy and oral contraceptive use.[198, 250] It may also be
more sensitive to long-term copper status. However, this assay is not typically readily
available and is also costly.[198, 251]
Postoperative Copper Screening
Copper deficiency is more common following RYGB (10-20%) and BPD/DS (up to 90%),
as the stomach and duodenum, the primary sites of absorption, are bypassed.[37, 58, 219,
222, 223, 252, 253]
Patients with BPD/DS may also experience loss of copper due to chronic diarrhea. Gastric
pH, which is altered by certain WLS procedures, such as the BPD/DS and RYGB, plays a role
in freeing copper from food. The extent to which decreased dietary copper intake
increases the risk for copper deficiency post-WLS is unknown, but impaired ability to
absorb copper is likely a factor.[254]
Few large-scale studies have measured copper status after WLS using serum copper or
ceruloplasmin levels.[58, 219, 222, 223, 255, 256] In some studies, decreased biomarkers
for copper status have been observed as early as one year post-WLS, and in many of the
studies reviewed, copper deficiency was observed many years after surgery. These findings 68
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were mostly in BPD/DS and RYGB patients. In general, the prevalence of copper deficiency
post-RYGB has been found to be lower than that seen in BPD/DS, but case study data[223,
254] and larger studies suggest that RYGB patients are still at risk for this deficiency.[219,
223, 240, 255, 257-269]
Even though we would not expect to see copper deficiency in patients with LAGB, one
study found a decrease in serum copper and ceruloplasmin levels 3 months after LAGB
surgery compared to preoperative levels, though these levels were not in the deficiency
range.[236] Data are lacking regarding copper deficiency in SG patients, with only one case
report, which described peripheral and central neurological complications related to
copper deficiency after SG.[261] However, there is a somewhat larger body of literature
documenting copper deficiencies in patients who have undergone gastrectomy or partial
gastrectomy for non-bariatric indications, suggesting that the stomach, and not solely the
proximal jejunum, may play a role in copper absorption after RYGB and SG.[267]
AACE/TOS/ASMBS 2013 CPG’s recommend copper screening be undertaken only in
RYGB and BPD/DS patients, and only in those presenting with signs and symptoms of
deficiency of neuropathy, myeloneuropathy, impaired wound healing, or anemias not
related to iron deficiency anemia [31](see Table 5). While previous guidelines did not
recommend routine postoperative laboratory screening of copper in the absence of
symptoms [1, 31] recent case reports and surveillance studies suggest the appropriateness
of a recommendation for annual copper screening in BPD/DS and RYGB patients, even in
the absence of clinical signs/symptoms of copper deficiency.
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Serum ceruloplasmin is a better indicator of copper status than serum copper, and
serum biomarkers coincide with the physical presentation of copper deficiency.
Deficiencies in copper may not only cause anemia but also myelopathy and gait disturbance
similar to that found with deficiencies in vitamin B12.[219, 240, 247, 257, 258, 267, 269]
Preventative Supplementation of Copper
Existing reports regarding copper levels and deficiencies among post-WLS patients are
not always clear as to whether the participants were taking supplemental copper after
surgery. Of those studies that did describe the supplement regimen of their participants,
three observed copper deficiencies in patients whose multivitamin supplement did contain
copper.[222, 223, 253, 255]
These studies, along with reports of RYGB and BPD/DS patients presenting with long-term
copper-related complications, warrant recommending copper supplementation after WLS.
While AACE/TOS/ASMBS 2013 CPG recommends routine supplementation of copper to
prevent deficiencies, it is important to avoid over-supplementation, as this may result in
decreased oral bioavailability of copper from supplements or food, or even liver damage
when intake exceeds the recommended upper limits.[31, 38, 198, 263, 268] Care should be
taken in choosing the form of copper supplementation; for instance, copper oxide is poorly
absorbed, while copper gluconate may be a safer alternative, as it has not been reported to
cause liver failure or GI effects.[198, 263] At least 2 mg/day of copper supplementation is
recommended, in the form of copper gluconate or sulfate, as part of routine multivitamin
and mineral supplementation. As noted above regarding zinc, a ratio of 1 mg copper
supplementation has been recommended for every 8-15 mg of elemental zinc, to prevent 70
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copper deficiency.[31] Based on the literature reviewed above, RYGB and BPD/DS patients
are at a greater risk for copper deficiency than LAGB and SG patients; BPD/DS and RYGB
patients require 200% of the RDA for copper (2mg); SG and LAGB patients require only
100% of the RDA (1 mg).
Repletion of Postoperative Copper Deficiency
Treatment of copper deficiency typically involves intravenous repletion, followed by
oral supplementation to normalize serum levels. Although there is currently no standard
dosage recommended for repletion of copper deficiency, examination of the existing
surveillance studies and case reports provides the best available evidence on which to base
recommendations for clinical practice.[223, 247, 258, 260] One series described patients
who had been treated successfully with 2 mg copper sulfate intravenously for 5 days over
an 8 week period.[247] Two additional individual case studies describe patients with
copper deficiency and ataxia who were repleted with 2.4 mg elemental copper sulfate
infused (IV) daily for 5 to 6 days, in addition to an oral elemental copper (as copper
gluconate) at a dose of 2mg every 6 hours.[240, 258, 269] The 8 mg/day of oral elemental
copper was continued for months after the patients’ symptoms improved.[269]
Serum copper levels have also been restored to normal levels with an oral regimen of
copper. Studies describe the treatment of patients with hematological abnormalities were
treated with oral copper doses ranging from 2 to 8 mg/day, and while other patients with
pancytopenia, treated with 4 mg oral copper gluconate three times a day.[258, 260] Other
types of copper regimens have also been used for repletion; such as oral copper gluconate
provided with a multivitamin and a tube feeding (4.42 mg/day total copper).[260] In 71
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another study, a cohort of RYGB patients were treated with 1.6-7.5 mg/day of oral
elemental copper in the form of copper sulfate.[223] Though most reports in the literature
describe symptom improvement or resolution upon successful copper repletion, there may
be cases in which repletion does not lead to improvement of symptoms.[259, 262]
Treatment of copper deficiency will vary based on the severity of the deficiency.[1, 31]
Mild to moderate deficiency, as in patients with low hematological indices, may be treated
with 3 to 8 mg/day oral copper gluconate or sulfate until markers return to normal. In
severe deficiency, as in patients exhibiting hematological and neurological symptoms, 2 to
4 mg/day of intravenous copper can be administered for five to six days or until serum
levels return to normal and neurological symptoms resolve. Once copper deficiency is
treated, copper status should be monitored every 3 months.[31] The duration of repletion
required to bring serum levels to normal and resolve neurological symptoms has varied
across published studies, depending on the doses provided (1mg to 8mg, daily); frequency
(multiple times daily, daily and weekly,) and route of administration (oral and IV).[256,
260, 262]
Copper – Summary
Recommendations for preoperative screening of copper deficiency
Routine screening of copper status by using serum copper and ceruloplasmin is
recommended for patients prior to RYGB or BPD/DS, but results must be
interpreted with caution. (Grade D, BEL 4)
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Erythrocyte superoxide dismutase is the preferred assay for determining copper
status in patients who have WLS. It is a more precise biomarker for screening of
copper deficiency; when it is available and affordable. (Grade D, BEL 4)
Recommendations for postoperative screening of copper deficiency
Routine screening of copper status in post-WLS patients is recommended at least
annually after BPD/DS and RYGB, even in the absence of clinical signs or symptoms
of deficiency. (Grade C, BEL 4)
In post-WLS patients, serum copper and ceruloplasmin are the recommended
biomarkers for determining copper status, as they are closely correlated with
physical symptoms of copper deficiency. (Grade C, BEL 4)
Recommendations for supplementation of copper for preventing deficiency
All post-WLS patients should take copper as part of routine multivitamin and
mineral supplementation, with dosage based upon type of procedure (Grade C, BEL
3):
o BPD/DS or RYGB patients should supplement with 200% of the RDA for
copper (2 mg/day)
o SG or LAGB patients should supplement with 100% of the RDA for copper (1
mg/day)
In post-WLS patients, supplementation with 1 mg copper is recommended for every
8-15 mg of elemental zinc to prevent copper deficiency. (Grade C, BEL 3)
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In post-WLS patients, copper gluconate or sulfate is the recommended source of
copper for supplementation. (Grade C, BEL 3)
Recommendations for postoperative copper repletion
In post-WLS patients with a copper deficiency, the recommended regimen for repletion
of copper will vary with the severity of the deficiency (Grade C, BEL 3):
o Mild to moderate deficiency (e.g., in cases with low hematological indices): 3 to 8
mg/day oral copper gluconate or sulfate until indices return to normal
o Severe deficiency: 2 to 4 mg/day of intravenous copper, should be initiated for
six days or until serum levels return to normal and neurological symptoms
resolve.
o Once copper levels are normal: monitor copper levels every 3 months. (Grade C,
BEL 3)
SUMMARY
This paper is an update for the American Society for Metabolic and Bariatric Surgery
(ASMBS) Nutrition Committee’s Allied Health Nutritional Guidelines for the Surgical
Weight Loss Patient (2008)[1] and serves as an educational tool for not only dietitians,
but other providers working with pre-WLS patients. The focus of this paper has been to
up-date the guideline with findings from current literature regarding key micronutrient
deficiencies and WLS. As evidence-based guidelines continue to be updated and
recommendations become more established into the daily practice of perioperative
nutrition care, it will be important to investigate differences in responders to treatment
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and new potential mechanisms explaining changes in nutrient status. Additionally,
controlling for confounding factors (such as dietary intake of nutrients from both food
and supplements, food-medication interactions, food-nutrient interactions, and if, how,
and by whom nutrition assessment and counseling is conducted) in nutrient-related
studies will increase the rigor of data collection and consistency in the quality of
research reported.
The Nutrition Committee of the Integrated Health Clinical Issues and Guidelines
Committee of the ASMBS sincerely hopes that this document will serve to enhance the
general nutrition knowledge necessary for the care of the pre- and postoperative
patient, with consideration for the individual patient’s unique medical needs, as well as
the variable protocols established among surgical centers and individual practices.
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AUTHORS’ DISCLOSURES — POTENTIAL CONFLICTS OF INTEREST
Speaker’s bureaus, consultant fees, or research grants:
Anonymous
Acknowledgments:
We would like to thank Dr. Stephanie Sogg, Chair of the ASMBS Integrated Health Clinical Issues and Guidelines committee for her oversight and editing, advice and support. We thank our peer reviewers: Sue Cummings and Dr. Ann Rogers, and the encouraging guidance provided by Research Methodologist, Dr. James S. Parrott. We also thank the American Society for Metabolic and Bariatric Surgery Executive Council and the Integrated Health Executive Council.
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Appendices A-D
Appendix A. Literature Search and Review Process by Nutrient
77
Search History Articles identified Articles
Reviewed
Articles
Included
Vitamin B1 or
thiamin or thiamine
45 + hand searches 65 61
Vitamin B12
Folate or
folic acid
57
45
107 total 66
31
Iron 92 63 58
Calcium
Vitamin D
127
84
45
71
14
56
Vitamins A,E, K 50 40 36
Zinc
Copper
30 + hand searches
24 + hand searches
48
32
48
32
Total 554 471 402
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Appendix B. Grading Scheme for Sources Reviewed, per the 2010 AACE Protocol for
Production of Clinical Practice Guidelines–Step I: Evidence Ratinga
The evidence level and strength of evidence scheme follows that of Mechanick et al.10 A
brief summary of the evidence level and strength of evidence scheme is below.
Numerical descriptor (evidence level)
Semantic descriptor (reference methodology)
Strong1 Meta-analysis of randomized controlled trials (MRCT)1 Randomized controlled trial (RCT)
Intermediate2 Meta-analysis of nonrandomized prospective or case-
controlled trials (MNRCT)2 Nonrandomized controlled trial (NRCT)2 Prospective cohort study (PCS)2 Retrospective case-control study (RCCS)
Weak333
Nonrandomized noncontrolled trial (NRNCT)Retrospective Observational (RO)Cross-sectional study (CSS)
3 Surveillance study (registries, surveys, epidemiologic study) (SS)
3 Consecutive case series (CCS)3 Single case reports (SCR)
No Evidence4 No evidence (theory, opinion, consensus, or review)
(NE)a 1 = strong evidence; 2 = intermediate evidence; 3 = weak evidence; 4 = no evidence.
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Appendix C. 2010 American Association of Clinical Endocrinologists Protocol for
Production of Clinical Practice Guidelines—Step II: Evidence Analysis and Subjective Factors
Study Design Data AnalysisInterpretation of
ResultsPremise correctness Intent-to-treat GeneralizabilityAllocation concealment
(randomization) Selection bias Appropriate statistics LogicalAppropriate blinding IncompletenessUsing surrogate end points
(especially in “first-in-its-class” intervention) Validity
Sample size (beta error)Null hypothesis versus
Bayesian statistics
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Appendix D. Grading Scheme for Recommendations, per the AACE Protocol for Production
of Clinical Practice Guidelines–Step III: Grading of Recommendations; How Different Evidence
Levels can be Mapped to the Same Recommendation Grade10
Best Evidence Level
Subjective Factor Impact
Consensus
Mapping Recommendation Grade
Strong
1 None Yes Direct A
2 Positive Yes Adjust up A
Intermediate
2 None Yes Direct B
1 Negative Yes Adjust down B
3 Positive Yes Adjust up B
Weak
3 None Yes Direct C
2 Negative Yes Adjust down C
4 Positive Yes Adjust up C
No Evidence
4 None Yes Direct D
3 Negative Yes Adjust down D
1,2,3,4 N/A No Adjust down D
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ASMBS Nutrition CPG List of Abbreviations
Academy Of Nutrition And Dietetics (AND)Acute Phase Reactant (APR)Acute Post-Gastric Reduction Surgery (APGARS)Adequate Intake (AI)Adjustable Gastric Band (Agb)American Association Of Clinical Endocrinologists (AACE)American Society For Metabolic And Bariatric Surgery (ASMBS)American Society For Parenteral And Enteral Nutrition (ASPEN)Biliopancreatic Diversion With Duodenal Switch BPD/DSCarboxy-Terminal Telopeptide (CTX)Case Reports (CS)Clinical Practice Guideline (CPG)Consecutive Case Series (CCS)Cross-Sectional Studies (CSS)Deciliter (DL)Daily Value (DV)Dual-energy x-ray absorptiometry (DXA)Des-Gamma-Carboxy Prothrombin (DCP)Dietary Reference Intake (DRI)Duodenal Switch (Ds)European Federation Of Neurological Societies (EFNS)Gastrointestinal (GI)Gram (Gm)Homocysteine (Hcy)Institute Of Medicine (IOM)Intact Parathyroid Hormone (Ipth)International Unit (IU)Intramuscular (IM)Intravenous (IV)Iron (Fe)Liter (L)Medical Nutrition Therapy (Mnt)Meta-Analysis Non-Randomized Controlled Trial (MNRCT)Meta-Analysis Randomized Controlled Trials (MRCT)Methyl Malonic Acid (MMA)
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Microgram (Mcg)Milligram (Mg)Milliliter (Ml)No Evidence (Theory, Opinion, Consensus, Or Review) (NE)Nutrition Care Process (NCP)Nutrition-Focused Physical Assessment (NFPA)Office Of Dietary Supplements (ODS)Parathyroid Hormone (PTH)Picogram (Pg)Prospective Cohort Studies (PCS)Proton Pump Inhibitors (Ppis)Randomized Controlled Trials (RCT)Recommended Dietary Allowance (RDA)Red Blood Cell (RBC)Registered Dietitian (RD)Retrospective Cohort Studies (RCS/RCCS)Roux-En-Y Gastric Bypass (RYGB),Sleeve Gastrectomy (SG)Small Bowel Bacterial Overgrowth (SBBO)Surveillance Study (Registries, Surveys, Epidemiologic Study) (SS)The Obesity Society (TOS)Thiamin Deficiency (TD)Thiamin, whole blood (TDP)Thiamin Pyrophosphate (TPP)Tolerable Upper Intake Level (UL)Total Iron Binding Capacity (TIBC)Transferrin Saturation (Tsat)Type 1 Collagen N-Telopeptide (NTX)Upper Intake Level (UL)Vitamin D Deficiency (VDD)Vitamin D Insufficiency (VDI)Weight Loss Surgery (WLS)Wernicke-Korsakoff Syndrome (Wks)Wernicke's Encephalopathy (WE)
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[86] Shikora SA, Kim JJ, Tarnoff ME. Nutrition and gastrointestinal complications of bariatric surgery. Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition. 2007;22:29-40. EL 4, NE; Review[87] Ocon Breton J, Perez Naranjo S, Gimeno Laborda S, Benito Ruesca P, Garcia Hernandez R. [Effectiveness and complications of bariatric surgery in the treatment of morbid obesity]. Nutricion hospitalaria. 2005;20:409-14. EL 2, Retrospective and Descriptive[88] Hakeam HA, O'Regan PJ, Salem AM, Bamehriz FY, Eldali AM. Impact of laparoscopic sleeve gastrectomy on iron indices: 1 year follow-up. Obesity surgery. 2009;19:1491-6. EL 2, PCS[89] Kehagias I, Karamanakos SN, Argentou M, Kalfarentzos F. Randomized clinical trial of laparoscopic Roux-en-Y gastric bypass versus laparoscopic sleeve gastrectomy for the management of patients with BMI < 50 kg/m2. Obesity surgery. 2011;21:1650-6. EL 1, RCT[90] Pech N, Meyer F, Lippert H, Manger T, Stroh C. Complications and nutrient deficiencies two years after sleeve gastrectomy. BMC surgery. 2012;12:13. EL 2, PCS[91] Eltweri AM, Bowrey DJ, Sutton CD, Graham L, Williams RN. An audit to determine if vitamin b12 supplementation is necessary after sleeve gastrectomy. SpringerPlus. 2013;2:218. EL 2, Retrospective and Descriptive[92] Alexandrou A, Armeni E, Kouskouni E, Tsoka E, Diamantis T, Lambrinoudaki I. Cross-sectional long-term micronutrient deficiencies after sleeve gastrectomy versus Roux-en-Y gastric bypass: a pilot study. Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery. 2014;10:262-8. EL 3, CSS[93] Mechanick JI, Kushner RF, Sugerman HJ, Gonzalez-Campoy JM, Collazo-Clavell ML, Guven S, et al. American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery Medical Guidelines for Clinical Practice for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric surgery patient. Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery. 2008;4:S109-84. EL4, NE CPG[94] National Institute of Health OoDS.2015.Vitamin B12 Dietary Supplement Fact Sheet. June 25, 2015.2015.https://ods.od.nih.gov/factsheets/list-all/VitaminB12. EL 4, NE[95] Vieira C, Cosmo C, Lucena R. The importance of methylmalonic acid dosage on the assessment of patients with neurological manifestations following bariatric surgery. Obesity surgery. 2011;21:1971-4. EL 3, SCR[96] Vidal-Alaball J, Butler CC, Cannings-John R, Goringe A, Hood K, McCaddon A, et al. Oral vitamin B12 versus intramuscular vitamin B12 for vitamin B12 deficiency. Cochrane database of systematic reviews. 2005:CD004655. EL 4, NE; Review[97] Eussen SJ, de Groot LC, Clarke R, Schneede J, Ueland PM, Hoefnagels WH, et al. Oral cyanocobalamin supplementation in older people with vitamin B12 deficiency: a dose-finding trial. Archives of internal medicine. 2005;165:1167-72. EL 1, RCT[98] Gasteyger C, Suter M, Gaillard RC, Giusti V. Nutritional deficiencies after Roux-en-Y gastric bypass for morbid obesity often cannot be prevented by standard multivitamin supplementation. The American journal of clinical nutrition. 2008;87:1128-33. EL 3, Retrospective Observational
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[99] Vargas-Ruiz AG, Hernandez-Rivera G, Herrera MF. Prevalence of iron, folate, and vitamin B12 deficiency anemia after laparoscopic Roux-en-Y gastric bypass. Obesity surgery. 2008;18:288-93. EL 2, PCS[100] Carvalho IR, Loscalzo IT, Freitas MF, Jordao RE, Friano Tde C. Incidence of vitamin B12 deficiency in patients submitted to Fobi-Capella Roux-en-Y bariatric surgery. Arquivos brasileiros de cirurgia digestiva : ABCD = Brazilian archives of digestive surgery. 2012;25:36-40. EL 2, Retrospective and Descriptive[101] Pech N, Meyer F, Lippert H, Manger T, Stroh C. Complications, reoperations, and nutrient deficiencies two years after sleeve gastrectomy. Journal of obesity. 2012;2012:828737. EL 2, PCS[102] Malone M. Recommended nutritional supplements for bariatric surgery patients. The Annals of pharmacotherapy. 2008;42:1851-8. EL 4, NE; Review[103] Kwon Y, Kim HJ, Lo Menzo E, Park S, Szomstein S, Rosenthal RJ. Anemia, iron and vitamin B12 deficiencies after sleeve gastrectomy compared to Roux-en-Y gastric bypass: a meta-analysis. Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery. 2014;10:589-97. EL 2, MNRCT[104] Rhode BM, Tamin H, Gilfix BM, Sampalis JS, Nohr C, MacLean LD. Treatment of Vitamin B12 Deficiency after Gastric Surgery for Severe Obesity. Obesity surgery. 1995;5:154-8. EL 2, PCS[105] Brolin RE, Gorman JH, Gorman RC, Petschenik AJ, Bradley LJ, Kenler HA, et al. Are vitamin B12 and folate deficiency clinically important after roux-en-Y gastric bypass? Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract. 1998;2:436-42. EL 2, PCS[106] Warde-Kamar J, Rogers M, Flancbaum L, Laferrere B. Calorie intake and meal patterns up to 4 years after Roux-en-Y gastric bypass surgery. Obesity surgery. 2004;14:1070-9. EL 3, SS[107] Malinowski SS. Nutritional and metabolic complications of bariatric surgery. The American journal of the medical sciences. 2006;331:219-25. EL 4, NE; Review[108] Stabler SP, RH A. 2004.Megolastic anemias. In: L G, D A.Philadelphia, PA: W.B. Saunders Company. EL 4, NE; Review[109] Kaplan LM. Pharmacological therapies for obesity. Gastroenterol Clin North Am. 2005;34:91-104. EL 4, NE; Review[110] Poitou Bernert C, Ciangura C, Coupaye M, Czernichow S, Bouillot JL, Basdevant A. Nutritional deficiency after gastric bypass: diagnosis, prevention and treatment. Diabetes & metabolism. 2007;33:13-24. EL 4, NE Review[111] Bailey LB, Gregory JF, 3rd. Folate metabolism and requirements. The Journal of nutrition. 1999;129:779-82. EL 3, SS[112] Caudill MA. Folate bioavailability: implications for establishing dietary recommendations and optimizing status. The American journal of clinical nutrition. 2010;91:1455S-60S. EL 4, NE; Review[113] Verhaar MC, Wever RM, Kastelein JJ, van Dam T, Koomans HA, Rabelink TJ. 5-methyltetrahydrofolate, the active form of folic acid, restores endothelial function in familial hypercholesterolemia. Circulation. 1998;97:237-41. EL 2, NRCT
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[114] Carmel R. 2005.Folic Acid In: M. Shils MS, A. Ross, B. Caballero and R. Cousins.Baltimore, MD,: Lippincott Williams & Wilkins. EL 4, NE; Review[115] van Rutte PW, Aarts EO, Smulders JF, Nienhuijs SW. Nutrient deficiencies before and after sleeve gastrectomy. Obesity surgery. 2014;24:1639-46. EL 2, PCS[116] Damms-Machado A, Friedrich A, Kramer KM, Stingel K, Meile T, Kuper MA, et al. Pre- and postoperative nutritional deficiencies in obese patients undergoing laparoscopic sleeve gastrectomy. Obesity surgery. 2012;22:881-9. EL 2, PCS[117] Centers for Disease Control and Prevention.2015.Folic Acid Data and Statistics. June 25, 2015.2015.http://www.cdc.gv/ncbddd/data.html EL4, NE Review[118] Boylan LM, Sugerman HJ, Driskell JA. Vitamin E, vitamin B-6, vitamin B-12, and folate status of gastric bypass surgery patients. Journal of the American Dietetic Association. 1988;88:579-85. EL 3, SS[119] Dixon JB, Dixon ME, O'Brien PE. Elevated homocysteine levels with weight loss after Lap-Band surgery: higher folate and vitamin B12 levels required to maintain homocysteine level. International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity. 2001;25:219-27. EL 2, NRCT[120] Mallory GN, Macgregor AM. Folate Status Following Gastric Bypass Surgery (The Great Folate Mystery). Obesity surgery. 1991;1:69-72. EL 2, PCS[121] Gasteyger C, Suter M, Calmes JM, Gaillard RC, Giusti V. Changes in body composition, metabolic profile and nutritional status 24 months after gastric banding. Obesity surgery. 2006;16:243-50. EL 2, Retrospective Observational[122] Brolin RE, Gorman RC, Milgrim LM, Kenler HA. Multivitamin prophylaxis in prevention of post-gastric bypass vitamin and mineral deficiencies. Int J Obes. 1991;15:661-7. EL 2, PCS[123] National Institute of Health OoDS.2015.Folate Dietary Supplement Fact Sheet. June 25,2015.https://ods.od.nih.gov/factsheets/list-all/Folate/. EL 4, NE, Review[124] Force USPST.2015.Folic Acid for the Preventin of Neural Tube Defects: Preventive MedicationFinal Update Summary: Folic Acid to Prevent Neural Tube Defects: Preventive Medication. . June 25, 2015.2015.http://www.uspreventiveservicestaskforce.org/Page/Document/UpdateSummaryFinal/folic-acid-to-prevent-neural-tube-defects-preventive-medication. EL 4, NE; Review[125] Capoccia D, Coccia F, Paradiso F, Abbatini F, Casella G, Basso N, et al. Laparoscopic gastric sleeve and micronutrients supplementation: our experience. Journal of obesity. 2012;2012:672162. EL 2, PCS[126] Chan LN, Mike LA. The science and practice of micronutrient supplementations in nutritional anemia: an evidence-based review. JPEN Journal of parenteral and enteral nutrition. 2014;38:656-72. EL 4, Review[127] National Institute of Health OoDS.2016.Iron Dietary Supplement Fact Sheet. June 25, 2015.2015.https://ods.od.nih.gov/factsheets/Iron-HealthProfessional/. EL 4, NE[128] Ruz M, Carrasco F, Rojas P, Codoceo J, Inostroza J, Basfi-Fer K, et al. Heme- and nonheme-iron absorption and iron status 12 mo after sleeve gastrectomy and Roux-en-Y
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gastric bypass in morbidly obese women. The American journal of clinical nutrition. 2012;96:810-7. EL 2, PCS[129] Avgerinos DV, Llaguna OH, Seigerman M, Lefkowitz AJ, Leitman IM. Incidence and risk factors for the development of anemia following gastric bypass surgery. World journal of gastroenterology : WJG. 2010;16:1867-70. EL 3, SS[130] Munoz M, Botella-Romero F, Gomez-Ramirez S, Campos A, Garcia-Erce JA. Iron deficiency and anaemia in bariatric surgical patients: causes, diagnosis and proper management. Nutricion hospitalaria. 2009;24:640-54. EL 4, Review[131] Kotkiewicz A, Donaldson K, Dye C, Rogers AM, Mauger D, Kong L, et al. Anemia and the Need for Intravenous Iron Infusion after Roux-en-Y Gastric Bypass. Clin Med Insights Blood Disord. 2015;8:9-17. EL 2, PCS[132] Nergaard BJ, Leifsson BG, Hedenbro J, Gislason H. Gastric bypass with long alimentary limb or long pancreato-biliary limb--long-term results on weight loss, resolution of co-morbidities and metabolic parameters. Obesity surgery. 2014;24:1595-602. EL 1, RCT[133] Dogan K, Aarts EO, Koehestanie P, Betzel B, Ploeger N, de Boer H, et al. Optimization of vitamin supplementation after Roux-en-Y gastric bypass surgery can lower postoperative deficiencies: a randomized controlled trial. Medicine (Baltimore). 2014;93:e169. EL 1, RCT[134] Marceau P, Biron S, Marceau S, Hould FS, Lebel S, Lescelleur O, et al. Long-Term Metabolic Outcomes 5 to 20 Years After Biliopancreatic Diversion. Obesity surgery. 2015;25:1584-93. EL3, Retrospective Observational[135] Cheng HL, Bryant C, Cook R, O'Connor H, Rooney K, Steinbeck K. The relationship between obesity and hypoferraemia in adults: a systematic review. Obesity reviews : an official journal of the International Association for the Study of Obesity. 2012;13:150-61. EL 4, Review[136] Jauregui-Lobera I. Iron deficiency and bariatric surgery. Nutrients. 2013;5:1595-608. EL 4, Review[137] Gracia JA, Martinez M, Aguilella V, Elia M, Royo P. Postoperative morbidity of biliopancreatic diversion depending on common limb length. Obesity surgery. 2007;17:1306-11. EL 3, SS[138] Pata G, Crea N, Di Betta E, Bruni O, Vassallo C, Mittempergher F. Biliopancreatic diversion with transient gastroplasty and duodenal switch: long-term results of a multicentric study. Surgery. 2013;153:413-22. EL 3, SS[139] Obinwanne KM, Fredrickson KA, Mathiason MA, Kallies KJ, Farnen JP, Kothari SN. Incidence, treatment, and outcomes of iron deficiency after laparoscopic Roux-en-Y gastric bypass: a 10-year analysis. J Am Coll Surg. 2014;218:246-52. EL 3, RCS; no supplement or dietary intake considered[140] Lynch SR. The effect of calcium on iron absorption. Nutr Res Rev. 2000;13:141-58. EL 4, NE, review[141] Hallberg L, Brune M, Erlandsson M, Sandberg AS, Rossander-Hulten L. Calcium: effect of different amounts on nonheme- and heme-iron absorption in humans. The American journal of clinical nutrition. 1991;53:112-9. EL 2, NRCT
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[142] Gaitan D, Flores S, Saavedra P, Miranda C, Olivares M, Arredondo M, et al. Calcium does not inhibit the absorption of 5 milligrams of nonheme or heme iron at doses less than 800 milligrams in nonpregnant women. The Journal of nutrition. 2011;141:1652-6. EL 2, PCS[143] Hallberg L, Rossander-Hulten L. Iron requirements in menstruating women. The American journal of clinical nutrition. 1991;54:1047-58. EL 4, NE Review[144] Hurrell R, Egli I. Iron bioavailability and dietary reference values. The American journal of clinical nutrition. 2010;91:1461S-7S. EL 4, NE[145] DeFilipp Z, Lister J, Gagne D, Shadduck RK, Prendergast L, Kennedy M. Intravenous iron replacement for persistent iron deficiency anemia after Roux-en-Y gastric bypass. Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery. 2013;9:129-32. EL 3[146] Institute of Medicine, Standing Committee on the Scientific Evaluation of Dietary Reference intakes and Its Panel on Calcium and Vitamin D. Dietary Reference Intakes for Calcium and Vitamin D. Journal. 1998. EL 4, NE[147] Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. The Journal of clinical endocrinology and metabolism. 2011;96:1911-30. EL 4, NE[148] Candido FG, Bressan J. Vitamin D: link between osteoporosis, obesity, and diabetes? Int J Mol Sci. 2014;15:6569-91. EL 4, NE; Review[149] Nair R, Maseeh A. Vitamin D: The "sunshine" vitamin. Journal of pharmacology & pharmacotherapeutics. 2012;3:118-26. EL 4, NE[150] Amalraj A, Pius A. Bioavailability of calcium and its absorption inhibitors in raw and cooked green leafy vegetables commonly consumed in India--an in vitro study. Food Chem. 2015;170:430-6. EL4, NE, experiment[151] Frossard E, Bucher, M., Mächler, F., Mozafar, A. and Hurrell, R. . Potential for increasing the content and bioavailability of Fe, Zn and Ca in plants for human nutrition. . J Sci Food Agric. 2000;80: 861–79. EL 4, NE Review[152] Fish E, Beverstein G, Olson D, Reinhardt S, Garren M, Gould J. Vitamin D status of morbidly obese bariatric surgery patients. J Surg Res. 2010;164:198-202. EL 3, Retrospective observational[153] de Luis DA, Pacheco D, Izaola O, Terroba MC, Cuellar L, Cabezas G. Micronutrient status in morbidly obese women before bariatric surgery. Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery. 2013;9:323-7. EL 3, SS[154] Dagan SS, Zelber-Sagi S, Webb M, Keidar A, Raziel A, Sakran N, et al. Nutritional Status Prior to Laparoscopic Sleeve Gastrectomy Surgery. Obesity surgery. 2016EL 3, CSS[155] van der Beek ES, Monpellier VM, Eland I, Tromp E, van Ramshorst B. Nutritional deficiencies in gastric bypass patients; incidence, time of occurrence and implications for post-operative surveillance. Obesity surgery. 2015;25:818-23. EL 2, PCS[156] Wolf E, Utech M, Stehle P, Busing M, Stoffel-Wagner B, Ellinger S. Preoperative micronutrient status in morbidly obese patients before undergoing bariatric surgery:
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results of a cross-sectional study. Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery. 2015;11:1157-63. EL 3, CSS[157] Signori C, Zalesin KC, Franklin B, Miller WL, McCullough PA. Effect of gastric bypass on vitamin D and secondary hyperparathyroidism. Obesity surgery. 2010;20:949-52. EL 4, RNCS[158] Goldner WS, Stoner JA, Lyden E, Thompson J, Taylor K, Larson L, et al. Finding the optimal dose of vitamin D following Roux-en-Y gastric bypass: a prospective, randomized pilot clinical trial. Obesity surgery. 2009;19:173-9. EL 1, RCT[159] Stein EM, Strain G, Sinha N, Ortiz D, Pomp A, Dakin G, et al. Vitamin D insufficiency prior to bariatric surgery: risk factors and a pilot treatment study. Clinical endocrinology. 2009;71:176-83. EL 3, CSS[160] Rosen CJ. Clinical practice. Vitamin D insufficiency. The New England journal of medicine. 2011;364:248-54. EL NE, Review[161] Anderson CAM, and Wayne W. Campbell. . 2015 Dietary Guidelines Advisory Committee Report Nutrition Today 2015;50:172-73. Web. EL 4, NE[162] Abbasi AA, Amin M, Smiertka JK, Grunberger G, MacPherson B, Hares M, et al. Abnormalities of vitamin D and calcium metabolism after surgical treatment of morbid obesity: a study of 136 patients. Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2007;13:131-6. EL 3, Retrospective observational[163] Fleischer J, Stein EM, Bessler M, Della Badia M, Restuccia N, Olivero-Rivera L, et al. The decline in hip bone density after gastric bypass surgery is associated with extent of weight loss. The Journal of clinical endocrinology and metabolism. 2008;93:3735-40. EL, PCS, sml sample size (n=23)[164] Sinha N, Shieh A, Stein EM, Strain G, Schulman A, Pomp A, et al. Increased PTH and 1.25(OH)(2)D levels associated with increased markers of bone turnover following bariatric surgery. Obesity. 2011;19:2388-93. EL 2, PCS[165] Wang M, Yang X, Wang F, Li R, Ning H, Na L, et al. Calcium-deficiency assessment and biomarker identification by an integrated urinary metabonomics analysis. BMC Med. 2013;11:86. Not classified for treatment grade[166] Powe CE, Evans MK, Wenger J, Zonderman AB, Berg AH, Nalls M, et al. Vitamin D-binding protein and vitamin D status of black Americans and white Americans. The New England journal of medicine. 2013;369:1991-2000. EL 3, CSS[167] Toelle P, Peterli R, Zobel I, Noppen C, Christoffel-Courtin C, Peters T. Risk factors for secondary hyperparathyroidism after bariatric surgery: a comparison of 4 different operations and of vitamin D-receptor-polymorphism. Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association. 2012;120:629-34. EL 3, CSS[168] Weaver CM. Assessing calcium status and metabolism. The Journal of nutrition. 1990;120 Suppl 11:1470-3. EL 4, NE[169] Costa TL, Paganotto M, Radominski RB, Kulak CM, Borba VC. Calcium metabolism, vitamin D and bone mineral density after bariatric surgery. Osteoporosis international : a journal established as result of cooperation between the European Foundation for
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Osteoporosis and the National Osteoporosis Foundation of the USA. 2015;26:757-64. EL 3, NRNCT[170] Johnson JM, Maher JW, DeMaria EJ, Downs RW, Wolfe LG, Kellum JM. The long-term effects of gastric bypass on vitamin D metabolism. Annals of surgery. 2006;243:701-4; discussion 4-5. EL 2, PCS[171] 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. Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery. 2014;10:540-6. EL 3, CSS[172] Aridi HD, Alami RS, Fouani T, Shamseddine G, Tamim H, Safadi B. Prevalence of vitamin D deficiency in adults presenting for bariatric surgery in Lebanon. Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery. 2016;12:405-11. EL 2, RCCS[173] Abellan I, Lujan J, Frutos MD, Abrisqueta J, Hernandez Q, Lopez V, et al. The influence of the percentage of the common limb in weight loss and nutritional alterations after laparoscopic gastric bypass. Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery. 2014;10:829-33. EL 2, PCS[174] Risstad H, Sovik TT, Engstrom M, Aasheim ET, Fagerland MW, Olsen MF, et al. Five-year outcomes after laparoscopic gastric bypass and laparoscopic duodenal switch in patients with body mass index of 50 to 60: a randomized clinical trial. JAMA surgery. 2015;150:352-61. EL 2, PCS[175] Bolckmans R, Himpens J. Long-term (>10 Yrs) Outcome of the Laparoscopic Biliopancreatic Diversion With Duodenal Switch. Annals of surgery. 2016EL 3, SS[176] Shapses SA, Lee EJ, Sukumar D, Durazo-Arvizu R, Schneider SH. The effect of obesity on the relationship between serum parathyroid hormone and 25-hydroxyvitamin D in women. The Journal of clinical endocrinology and metabolism. 2013;98:E886-90. EL 3, Retrospective Observational[177] Shapses SA, Sukumar D, Schneider SH, Schlussel Y, Sherrell RM, Field MP, et al. Vitamin D supplementation and calcium absorption during caloric restriction: a randomized double-blind trial. The American journal of clinical nutrition. 2013;97:637-45. EL 1, RCT; Double blind[178] Vilarrasa N, Gomez JM, Elio I, Gomez-Vaquero C, Masdevall C, Pujol J, et al. Evaluation of bone disease in morbidly obese women after gastric bypass and risk factors implicated in bone loss. Obesity surgery. 2009;19:860-6. EL 2, PCS[179] Straub DA. Calcium supplementation in clinical practice: a review of forms, doses, and indications. Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition. 2007;22:286-96. EL 4, Review[180] Stein EM, Carrelli A, Young P, Bucovsky M, Zhang C, Schrope B, et al. Bariatric surgery results in cortical bone loss. The Journal of clinical endocrinology and metabolism. 2013;98:541-9. EL 2, PCS[181] Yu EW, Bouxsein ML, Putman MS, Monis EL, Roy AE, Pratt JS, et al. Two-year changes in bone density after Roux-en-Y gastric bypass surgery. The Journal of clinical endocrinology and metabolism. 2015;100:1452-9. EL 2, PCS
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[182] Elias E, Casselbrant A, Werling M, Abegg K, Vincent RP, Alaghband-Zadeh J, et al. Bone mineral density and expression of vitamin D receptor-dependent calcium uptake mechanisms in the proximal small intestine after bariatric surgery. The British journal of surgery. 2014;101:1566-75. EL 2, mixed design: RCT and 2 NRNCT[183] Ross AC, Manson JE, Abrams SA, Aloia JF, Brannon PM, Clinton SK, et al. The 2011 Dietary Reference Intakes for Calcium and Vitamin D: what dietetics practitioners need to know. Journal of the American Dietetic Association. 2011;111:524-7. EL 4, NE; Review of CPG[184] Armas LA, Hollis BW, Heaney RP. Vitamin D2 is much less effective than vitamin D3 in humans. The Journal of clinical endocrinology and metabolism. 2004;89:5387-91. EL 2, NRCT[185] Tripkovic L, Lambert H, Hart K, Smith CP, Bucca G, Penson S, et al. Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: a systematic review and meta-analysis. The American journal of clinical nutrition. 2012;95:1357-64. EL 1, MRCT[186] Galassi A, Bellasi A, Auricchio S, Papagni S, Cozzolino M. Which vitamin D in CKD-MBD? The time of burning questions. BioMed research international. 2013;2013:864012. EL 4, NE; Review[187] Bauer DC. Clinical practice. Calcium supplements and fracture prevention. The New England journal of medicine. 2013;369:1537-43. EL4, NE review[188] Mahlay NF, Verka LG, Thomsen K, Merugu S, Salomone M. Vitamin D status before Roux-en-Y and efficacy of prophylactic and therapeutic doses of vitamin D in patients after Roux-en-Y gastric bypass surgery. Obesity surgery. 2009;19:590-4. EL 3, CSS[189] Boyce JA, Gleaves DH, Kuijer RG. Measuring Dietary Restraint Status: Comparisons between the Dietary Intent Scale and the Restraint Scale. Front Nutr. 2015;2:8. EL 4, NE Review[190] Mason J. 2011.VITAMINS, TRACE MINERALS, AND OTHER MICRONUTRIENTS. In: Goldman I, Ausiello D.Philadelphia, PA: W. B. Suanders Company. [191] Escott-Stump S. 2008.In: Troy DB.Baltimore, MD: Lippincott Williams and Wilkins. EL 4, NE, Book[192] Panel on Dietary Antioxidants and Related Compounds, Subcommittee on Upper Reference Levels of Nutrients, Subcommittee on Interpretation and Uses of DRIs, Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. Aug 27, 2000 Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. National Academies Press. EL 4, NE[193] Isom KA, Andromalos L, Ariagno M, Hartman K, Mogensen KM, Stephanides K, et al. Nutrition and metabolic support recommendations for the bariatric patient. Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition. 2014;29:718-39. EL 4, NE, Review[194] Mason ME, Jalagani H, Vinik AI. Metabolic complications of bariatric surgery: diagnosis and management issues. Gastroenterol Clin North Am. 2005;34:25-33. EL 4, NE[195] Shankar P, Boylan M, Sriram K. Micronutrient deficiencies after bariatric surgery. Nutrition. 2010;26:1031-7. EL 4, NE
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[196] Kaidar-Person O, Person B, Szomstein S, Rosenthal RJ. Nutritional deficiencies in morbidly obese patients: a new form of malnutrition? Part B: minerals. Obesity surgery. 2008;18:1028-34. EL 4, NE Review[197] 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. Obesity surgery. 2009;19:738-44. EL 2, PCS[198] Institute of Medicine, Standing Committee on the Scientific Evaluation of Dietary Reference intakes Food and Nutrition Board. . 2001.Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Coper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press. EL 4, NE[199] Pereira SE, Saboya CJ, Saunders C, Ramalho A. Serum levels and liver store of retinol and their association with night blindness in individuals with class III obesity. Obesity surgery. 2012;22:602-8. EL 3, CSS[200] Zalesin KC, Miller WM, Franklin B, Mudugal D, Rao Buragadda A, Boura J, et al. Vitamin a deficiency after gastric bypass surgery: an underreported postoperative complication. Journal of obesity. 2011;2011EL 2, RCCS[201] Granado-Lorencio F, Simal-Anton A, Salazar-Mosteiro J, Herrero-Barbudo C, Donoso-Navarro E, Blanco-Navarro I, et al. Time-course changes in bone turnover markers and fat-soluble vitamins after obesity surgery. Obesity surgery. 2010;20:1524-9. EL 2, PCS[202] Dadalt C, Fagundes RL, Moreira EA, Wilhelm-Filho D, de Freitas MB, Jordao Junior AA, et al. Oxidative stress markers in adults 2 years after Roux-en-Y gastric bypass. European journal of gastroenterology & hepatology. 2013;25:580-6. EL 2, PCS[203] Ledoux S, Msika S, Moussa F, Larger E, Boudou P, Salomon L, et al. Comparison of nutritional consequences of conventional therapy of obesity, adjustable gastric banding, and gastric bypass. Obesity surgery. 2006;16:1041-9. EL 3, CSS[204] Magdaleno R, Jr., Pereira BG, Chaim EA, Turato ER. Pregnancy after bariatric surgery: a current view of maternal, obstetrical and perinatal challenges. Arch Gynecol Obstet. 2012;285:559-66. EL 4, NE Review[205] Stroh C, Weiher C, Hohmann U, Meyer F, Lippert H, Manger T. Vitamin A deficiency (VAD) after a duodenal switch procedure: a case report. Obesity surgery. 2010;20:397-400. EL 3, SCR[206] Insel P, Ross D, McMahon KBM, Bernstein M. Nutrition. My Plate Update. Burlington, MA: Jones and Bartlett Learning; 2013. EL 4, NE[207] Mahan L, Escott-Stump S. 2003.Medical Nutrition Therapy for Anemia. Philadelphia, PA: W.B. Saunders Company. EL 4, NE[208] Salle A, Demarsy D, Poirier AL, Lelievre B, Topart P, Guilloteau G, et al. Zinc deficiency: a frequent and underestimated complication after bariatric surgery. Obesity surgery. 2010;20:1660-70. EL 3, Retrospective Observational[209] Di Martino G, Matera MG, De Martino B, Vacca C, Di Martino S, Rossi F. Relationship between zinc and obesity. J Med. 1993;24:177-83. EL 2, RCCS[210] Madan AK, Orth WS, Tichansky DS, Ternovits CA. Vitamin and trace mineral levels after laparoscopic gastric bypass. Obesity surgery. 2006;16:603-6. EL 2, Retrospective Chart Review
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[211] von Drygalski A, Andris DA. Anemia after bariatric surgery: more than just iron deficiency. Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition. 2009;24:217-26. EL 4, NE[212] Crofton RW, Gvozdanovic D, Gvozdanovic S, Khin CC, Brunt PW, Mowat NA, et al. Inorganic zinc and the intestinal absorption of ferrous iron. The American journal of clinical nutrition. 1989;50:141-4. El 1, RCT[213] Kordas K, Stoltzfus RJ. New evidence of iron and zinc interplay at the enterocyte and neural tissues. The Journal of nutrition. 2004;134:1295-8. EL 4, NE[214] Olivares M, Pizarro F, Ruz M. Zinc inhibits nonheme iron bioavailability in humans. Biological trace element research. 2007;117:7-14. EL 1, RCT[215] Olivares M, Pizarro F, Ruz M. New insights about iron bioavailability inhibition by zinc. Nutrition. 2007;23:292-5. EL 2, NRCT[216] Donangelo CM, Woodhouse LR, King SM, Viteri FE, King JC. Supplemental zinc lowers measures of iron status in young women with low iron reserves. The Journal of nutrition. 2002;132:1860-4. EL 2, PCS; Small sample size (zinc=11, iron=12) non WLS samples[217] Gerig R, Ernst B, Wilms B, Thurnheer M, Schultes B. Preoperative nutritional deficiencies in severely obese bariatric candidates are not linked to gastric Helicobacter pylori infection. Obesity surgery. 2013;23:698-702. EL 3, SS[218] Lowe NM, Fekete K, Decsi T. Methods of assessment of zinc status in humans: a systematic review. The American journal of clinical nutrition. 2009;89:2040S-51S. EL 2, MNRCT[219] Gletsu-Miller N, Wright BN. Mineral malnutrition following bariatric surgery. Advances in nutrition. 2013;4:506-17. EL 3 SS; EL 3 CSS[220] Ruz M, Cavan KR, Bettger WJ, Thompson L, Berry M, Gibson RS. Development of a dietary model for the study of mild zinc deficiency in humans and evaluation of some biochemical and functional indices of zinc status. The American journal of clinical nutrition. 1991;53:1295-303. EL 3, SS[221] Mechanick JI, Apovian CM. Stressing over obesity. Current opinion in endocrinology, diabetes, and obesity. 2009;16:339. EL 4, NE[222] de Luis DA, Pacheco D, Izaola O, Terroba MC, Cuellar L, Martin T. Zinc and copper serum levels of morbidly obese patients before and after biliopancreatic diversion: 4 years of follow-up. Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract. 2011;15:2178-81. EL 3, SS[223] Balsa JA, Botella-Carretero JI, Gomez-Martin JM, Peromingo R, Arrieta F, Santiuste C, et al. Copper and zinc serum levels after derivative bariatric surgery: differences between Roux-en-Y Gastric bypass and biliopancreatic diversion. Obesity surgery. 2011;21:744-50. EL 3, SS[224] Gong K, Gagner M, Pomp A, Almahmeed T, Bardaro SJ. Micronutrient deficiencies after laparoscopic gastric bypass: recommendations. Obesity surgery. 2008;18:1062-6. EL 3, SS[225] Rosa FT, de Oliveira-Penaforte FR, de Arruda Leme I, Padovan GJ, Ceneviva R, Marchini JS. Altered plasma response to zinc and iron tolerance test after Roux-en-Y gastric
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bypass. Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery. 2011;7:309-14. EL 2, PCS[226] Pires LV, Martins LM, Geloneze B, Tambascia MA, Hadad do Monte SJ, do Nascimento Nogueira N, et al. The effect of Roux-en-Y gastric bypass on zinc nutritional status. Obesity surgery. 2007;17:617-21. EL 3, SS[227] de Torres Rossi RG, Dos Santos MT, de Souza FI, de Cassia de Aquino R, Sarni RO. Nutrient intake of women 3 years after Roux-en-Y Gastric bypass surgery. Obesity surgery. 2012;22:1548-53. EL 3, CSS; Controlled [228] Sturniolo GC, Montino MC, Rossetto L, Martin A, D'Inca R, D'Odorico A, et al. Inhibition of gastric acid secretion reduces zinc absorption in man. Journal of the American College of Nutrition. 1991;10:372-5. EL 3, SS; small sample sz (n=11)[229] Slater GH, Ren CJ, Siegel N, Williams T, Barr D, Wolfe B, et al. Serum fat-soluble vitamin deficiency and abnormal calcium metabolism after malabsorptive bariatric surgery. Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract. 2004;8:48-55; discussion 4-5. EL 3, SS[230] Larrad-Jimenez A, Diaz-Guerra CS, de Cuadros Borrajo P, Lesmes IB, Esteban BM. Short-, mid- and long-term results of Larrad biliopancreatic diversion. Obesity surgery. 2007;17:202-10. EL 2, PCS[231] Dalcanale L, Oliveira CP, Faintuch J, Nogueira MA, Rondo P, Lima VM, et al. Long-term nutritional outcome after gastric bypass. Obesity surgery. 2010;20:181-7. [232] Jeejeebhoy KN. Human zinc deficiency. Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition. 2007;22:65-7. EL 4, NE[233] Ruiz-Tovar J, Oller I, Llavero C, Zubiaga L, Diez M, Arroyo A, et al. Hair loss in females after sleeve gastrectomy: predictive value of serum zinc and iron levels. The American surgeon. 2014;80:466-71. EL 2, PCS[234] Pirolla EH, Jureidini R, Barbosa ML, Ishikawa LC, Camargo PR. A modified laparoscopic sleeve gastrectomy for the treatment of diabetes mellitus type 2 and metabolic syndrome in obesity. American journal of surgery. 2012;203:785-92. EL 1, RCT[235] Cominetti C, Garrido AB, Jr., Cozzolino SM. Zinc nutritional status of morbidly obese patients before and after Roux-en-Y gastric bypass: a preliminary report. Obesity surgery. 2006;16:448-53. EL 3, NRNCT[236] Boyuk A, Banli O, Gumus M, Evliyaoglu O, Demirelli S. Plasma levels of zinc, copper, and ceruloplasmin in patients after undergoing laparoscopic adjustable gastric banding. Biological trace element research. 2011;143:1282-8. EL 3, SS[237] Rojas P, Carrasco F, Codoceo J, Inostroza J, Basfi-fer K, Papapietro K, et al. Trace element status and inflammation parameters after 6 months of Roux-en-Y gastric bypass. Obesity surgery. 2011;21:561-8. EL 2, PCS[238] Topart P, Becouarn G, Salle A, Ritz P. Biliopancreatic diversion requires multiple vitamin and micronutrient adjustments within 2 years of surgery. Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery. 2014;10:936-41. EL 3, Retrospective Observational weaker than EL 2, NRCT
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[239] Saper RB, Rash R. Zinc: an essential micronutrient. Am Fam Physician. 2009;79:768-72. EL 4, NE[240] Griffith DP, Liff DA, Ziegler TR, Esper GJ, Winton EF. Acquired copper deficiency: a potentially serious and preventable complication following gastric bypass surgery. Obesity. 2009;17:827-31. EL 3, CSS[241] Willis MS, Monaghan SA, Miller ML, McKenna RW, Perkins WD, Levinson BS, et al. Zinc-induced copper deficiency: a report of three cases initially recognized on bone marrow examination. Am J Clin Pathol. 2005;123:125-31. EL 3, CCS[242] Beers M. Ther Merck Manual of Diagnosis and Therapy. White Station, NJ: Merck Research Laboratories; 2006. EL 4, NE[243] Kay RG, Tasman-Jones C, Pybus J, Whiting R, Black H. A syndrome of acute zinc deficiency during total parenteral alimentation in man. Annals of surgery. 1976;183:331-40. EL 2, PCS[244] Bae-Harboe YS, Solky A, Masterpol KS. A case of acquired Zinc deficiency. Dermatology online journal. 2012;18:1. EL 3, SCR[245] Fiske DN, McCoy HE, 3rd, Kitchens CS. Zinc-induced sideroblastic anemia: report of a case, review of the literature, and description of the hematologic syndrome. American journal of hematology. 1994;46:147-50. EL 3, SCR[246] Alasfar F, Ben-Nakhi M, Khoursheed M, Kehinde EO, Alsaleh M. Selenium is significantly depleted among morbidly obese female patients seeking bariatric surgery. Obesity surgery. 2011;21:1710-3. EL 3, SS[247] Kumar N, McEvoy KM, Ahlskog JE. Myelopathy due to copper deficiency following gastrointestinal surgery. Archives of neurology. 2003;60:1782-5. EL 3, CCS[248] Hellman NE, Gitlin JD. Ceruloplasmin metabolism and function. Annual review of nutrition. 2002;22:439-58. EL 4, NE[249] Jaiser SR, Winston GP. Copper deficiency myelopathy. Journal of neurology. 2010;257:869-81. EL 3, CCS[250] Goldberg ME, Laczek J, Napierkowski JJ. Copper deficiency: a rare cause of ataxia following gastric bypass surgery. The American journal of gastroenterology. 2008;103:1318-9. EL 3, SCR[251] Iskandar M, Swist E, Trick KD, Wang B, L'Abbe MR, Bertinato J. Copper chaperone for Cu/Zn superoxide dismutase is a sensitive biomarker of mild copper deficiency induced by moderately high intakes of zinc. Nutrition journal. 2005;4:35. EL 2, NRCT[252] Gobato RC, Seixas Chaves DF, Chaim EA. Micronutrient and physiologic parameters before and 6 months after RYGB. Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery. 2014;10:944-51. EL2, PCS[253] Papamargaritis D, Aasheim ET, Sampson B, le Roux CW. Copper, selenium and zinc levels after bariatric surgery in patients recommended to take multivitamin-mineral supplementation. J Trace Elem Med Biol. 2015;31:167-72. EL 2, PCS[254] Btaiche IF, Yeh AY, Wu IJ, Khalidi N. Neurologic dysfunction and pancytopenia secondary to acquired copper deficiency following duodenal switch: case report and review of the literature. Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition. 2011;26:583-92. EL 3, SCR
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[255] Ernst B, Thurnheer M, Schultes B. Copper deficiency after gastric bypass surgery. Obesity. 2009;17:1980-1. EL 3, SS[256] Shahidzadeh R, Sridhar S. Profound copper deficiency in a patient with gastric bypass. The American journal of gastroenterology. 2008;103:2660-2. EL 3, SCR[257] Juhasz-Pocsine K, Rudnicki SA, Archer RL, Harik SI. Neurologic complications of gastric bypass surgery for morbid obesity. Neurology. 2007;68:1843-50. EL 3, CCS[258] Kumar N, Ahlskog JE, Gross JB, Jr. Acquired hypocupremia after gastric surgery. Clin Gastroenterol Hepatol. 2004;2:1074-9. EL 3, CCS[259] Naismith RT, Shepherd JB, Weihl CC, Tutlam NT, Cross AH. Acute and bilateral blindness due to optic neuropathy associated with copper deficiency. Archives of neurology. 2009;66:1025-7. EL 3, SCR[260] O'Donnell KB, Simmons M. Early-onset copper deficiency following Roux-en-Y gastric bypass. Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition. 2011;26:66-9. EL 3, SCR[261] Oliveira YS, Iba Ba J, Mba Angoue JM, Emery Itoudi Bignoumba P, Nzenze JR. [Copper deficiency and peripheral neuropathy as an outcome of gastrectomy]. Rev Med Interne. 2013;34:234-6. EL 3, SCR[262] Pineles SL, Wilson CA, Balcer LJ, Slater R, Galetta SL. Combined optic neuropathy and myelopathy secondary to copper deficiency. Survey of ophthalmology. 2010;55:386-92. EL 3, CCS[263] Pratt WB, Omdahl JL, Sorenson JR. Lack of effects of copper gluconate supplementation. The American journal of clinical nutrition. 1985;42:681-2. EL 1, RCT 2; small sample size (n=14)[264] Prodan CI, Bottomley SS, Vincent AS, Cowan LD, Greenwood-Van Meerveld B, Holland NR, et al. Copper deficiency after gastric surgery: a reason for caution. The American journal of the medical sciences. 2009;337:256-8. EL 2, RCCS; Small sample size[265] Rapoport Y, Lavin PJ. Nutritional Optic Neuropathy Caused by Copper Deficiency After Bariatric Surgery. J Neuroophthalmol. 2016;36:178-81. EL 3, SCR[266] Robinson SD, Cooper B, Leday TV. Copper deficiency (hypocupremia) and pancytopenia late after gastric bypass surgery. Proc (Bayl Univ Med Cent). 2013;26:382-6. EL 3, CCS[267] Tan JC, Burns DL, Jones HR. Severe ataxia, myelopathy, and peripheral neuropathy due to acquired copper deficiency in a patient with history of gastrectomy. JPEN Journal of parenteral and enteral nutrition. 2006;30:446-50. EL 3, SCR[268] Wapnir RA. Copper absorption and bioavailability. The American journal of clinical nutrition. 1998;67:1054S-60S. EL 4, NE[269] Yarandi SS, Griffith DP, Sharma R, Mohan A, Zhao VM, Ziegler TR. Optic neuropathy, myelopathy, anemia, and neutropenia caused by acquired copper deficiency after gastric bypass surgery. J Clin Gastroenterol. 2014;48:862-5. EL 3, SCR
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