I see these search terms a lot, in fact, too often. WHAT ARE YOU PEOPLE EATING?!
"side effects when a patient doesn't eat protein."
"Will I die if I don't eat protein?"
Protein and the Bariatric Patient
October 2008
by Laura Frank, PhD, MPH, RD, CD
Part 2 of 3
INTRODUCTION
All macronutrients (proteins, carbohydrates, and fat) have interrelationships in terms of bioenergetics.
Amino acids, primarily alanine and glutamine, interact with glucose metabolism both as carbon substrates and by recycling glucose carbon via transamination/deamination reactions. Therefore, protein metabolism provides the body with essential building blocks from amino acids to provide carbon substrates for energy metabolism and/or nitrogen compounds needed for nitrogen balance.1
When nutrition is scarce, or when humans experience anorexia, prolonged vomiting, diarrhea, food intolerance, depression, alcohol/drug abuse, or other reasons for food deprivation, protein-energy malnutrition (PEM) will most likely ensue.2 When inadequate protein intake occurs (especially inadequate intake of indispensable amino acids), coupled with adequate carbohydrate and energy intake, this condition is termed protein malnutrition (PM).
Hormonal state is an important covalent modulator for metabolic processes in the body.1 In PEM, the body is generally in a hypoinsulinemic and hyper-gluconemic state.2,3 Low levels of insulin allow for a shift in substrate utilization to stored body fuels, such as muscle and liver glycogen and stored fat. Initially, weight loss occurs as a result of water loss due to the metabolism of liver and muscle glycogen stores. Muscle protein breakdown also occurs in order to supply the amino acids needed to preserve the visceral protein pool. Carbon liberation from either fatty acid oxidation or from the deamination of amino acids, such as glutamate, glutamine, and alanine (process of gluconeogenesis), help to supply fuel for the body and to maintain vital organs (brain, heart, and kidney).1 The body eventually enters a “protein sparing” state as ketone-bodies (byproducts of fat breakdown in the absence of carbohydrate intakes) increase in abundance. This condition is called ketosis. Weight loss occurs with the breakdown of muscle mass and a reduction of adipose tissue as the body strives to maintain homeostasis.
Continued negative nitrogen balance will result in decreased hepatic proteins, including albumin, with concomitant muscle wasting, asthenia (weakness), and alopecia (hair loss). PEM is typically associated with anemia related to iron, B12, folate, and/or copper deficiency. Deficiencies in zinc, thiamin, and B6 are commonly found with a deficient protein status. In addition, catabolism of lean body mass (LBM) and diuresis cause electrolyte and mineral disturbances with sodium, potassium, magnesium, and phosphorus.2
During PM, the protein deficit occurs in conjunction with excessive intake of carbohydrate calories, resulting in a hormonal state of hyperinsulinemia, inhibiting fat and muscle breakdown.1 When the body is not able to hormonally adapt to spare protein, a decrease in visceral protein synthesis will result along with hypoalbuminemia, anemia, and impaired immunity. If left undiagnosed, this may result in an illness where fat stores are preserved, LBM is decreased, and appropriate weight loss is not seen due to accumulation of extra-cellular water. This edema is associated with PM.2
Preoperative Risk
No risk of preoperative PM among pre-gastric bypass and duodenal switch
patients has been reported;4, 5 however, a thorough history and
physical is needed in the preoperative patient. It is also prudent
medical or dietetic practice to complete a thorough screening of
nitrogen balance and body composition in the preoperative bariatric
patient. Note that increased body mass index (BMI) does not ensure that
a patient does not have PM. It is important to emphasize that an obese
patient can still have low muscle mass (sarcopenia) and/or PM.6
Routine preoperative screening, including laboratory measures of visceral proteins, can be used to assess the risk of PM. Serum albumin (normal range 3.5–5.0g/dL) can be used as an indicator of long-term protein status (half-life approximately 3 weeks). Serum transferrin and serum transthyretin (or thyroxine-binding prealbumin) are referred to as intermediate- (half-life 8–10 days) and short- (half-life 2 days) term indicators, respectively.7 Retinol binding protein (RBP) may also be useful in diagnosing acute changes in protein status.2
Body composition measures, such as fat free mass (FFM) or lean body mass (LBM) versus fat mass (FM) (or the ratio of FFM:FM or LBM:FM), are helpful to assess functional nitrogen balance among patients.3 Sophisticated models of body composition assessment, such as underwater (hydrostatic) weighing or air displacement plethysmography (e.g., Bod-Pod), are generally more practical in academic settings. Dual-energy absorptiometry (DEXA) and computed tomography (CT) can also be used to measure total body fat and intraabdominal or visceral adiposity, respectively.8 A less expensive option to measure body composition includes bioelectrical impedance (BIA) (e.g., Tanita body-fat analyzer, Arlington Heights, Illinois). Good agreement between BIA measures and DEXA has been reported by some9 but not all10 researchers. In addition, creatinine-height index is reflective of somatic or skeletal muscle protein and can be used as a surrogate biomarker for LBM.7 Clinical signs of PM may also include excess hair loss, edema, anemia, and impaired wound healing.2 Protein deficiency may be masked by the adipose tissue, edema, and general malaise potentially shown by the patient.11
It would not be appropriate to assume that the obese patient has good nutritional status and appropriate dietary intake. Therefore, a complete dietary assessment is also recommended for the preoperative bariatric patient in order to determine typical protein intakes and determination of patient’s protein food preferences. This information can then be used to recommend an appropriate food plan with adequate healthy proteins prior to the patient’s surgery.
Postoperative Risk
Bariatric patients can be at risk for PM due to inadequate protein
intakes possibly from food intolerances to good quality protein, such
as meat.12 This can occur after restrictive surgeries (e.g., adjustable
gastric band [AGB] or gastric sleeve [GS]) and
restrictive/malabsorptive surgeries (e.g., Roux-en Y gastric bypass
[RYGBP]). Other reasons why bariatric patients are at risk for PM
and/or PEM depend upon the type of surgery that they have undergone and
include small upper stomach pouch with an approximate 20–30mL capacity,
decreased intestinal limb length (and therefore decreased and
compromised absorption capacity), and increased protein needs due to
wound healing immediately post-surgery.7,13 For post-RYGB patients, the
degree of protein malabsorption will depend on the length of the
bypassed segment of the small intestine.14 Nutritional deficiencies in
patients after RYGB operations have been mainly attributed to dietary
restriction.15 Other variables include the patient’s food adversions or
food faddisms, failure to comply with or ignorance of post-surgical
nutrition guidelines, and/or the inability to recognize or afford high
quality protein.
Outcomes of studies investigating the incidence of protein malnutrition after surgery have been equivocal. Furthermore, several of these studies have been performed during the period of greatest caloric restriction.15 In a recent review of the literature, Shah et al16 stated that protein deficiency, assessed by serum albumin levels, is less common than most other nutrient deficiencies among post-surgical patients. To confirm these findings, other investigators have reported that PEM and PM are rarely found among patients after RYGBP.7,17 Two hundred patients who were morbidly obese were followed for 6 to 8 years (mean: 6.7 years) after RYGBP surgery. Meat intolerance was observed in 51 percent, 60.3 percent, 59.5 percent, and 55.1 percent of the patients during zero to 12 months, 13 to 24 months, 25 to 72 months, and 73 to 96 months after surgery, respectively. However, these patients had no caloric malnutrition or protein deficiency. Moize et al12 studied 93 patients retrospectively over 12 months post-RYGBP. Significant differences in total calorie intakes occurred comparing three-month (849±329 calories) to 12-month intakes (1,101±400 calories) (p=.009) and significant differences in protein intakes (g/day) were also observed over the 12-month period (45.6±14.2 g/day at three months versus 58.5±17.1 g/day at 12 months). Although protein intakes met the minimum recommendation of 0.8g/kg/day, these intakes were significantly different than the recommended 1.5g/kg/day (p=0.01). At 12 months, protein intakes were significantly lower among patients with protein intolerance (p=0.02). However, despite low energy and protein intakes, normal protein status (as measured by serum albumin) was reported throughout the 12-month follow-up.
As stated, the degree of protein malabsorption will depend to some extent on the length of the bypassed segment of the small intestine.14 In a prospective, randomized, clinical study, Brolin and LaMarca et al14 reported that 13 percent of patients status-post-two-years distal (long-limb) RYGB had hypoalbuminemia (albumin <3.5mg/dL) compared to normal albumin levels reported among patients with short Roux limbs (<150cm). In agreement with this study, Nelson et al18 followed 257 super-obese patients after receiving a long Roux limb of 400 to 500cm and a 100-cm common channel (for digestion and absorption). Eighty-two percent of patients returning the survey an average of 48 months postoperatively (range 12–148 months) lost greater than 50 percent of excess body weight. Nine patients (4%) who developed or were developing impending protein/calorie malnutrition required proximal relocation of the enteroenterostomy with symptom resolution. In contrast, protein deficiency was not found in long-limb super-obese (BMI>50kg/m2) patients who were a mean 43 months out from surgery.19
Among patients with malabsorptive surgeries (e.g., biliopancreatic diversion [BPD] and duodenal switch [DS]), the degree of malabsorption will determine the patient’s risk status for PM. Secondary PM caused by malabsorption of protein has been reported to be more common after BPD/DS procedures compared to RYGBP procedures, especially during the first or second year postoperative.7, 17 Overall, the incidence of PM after BPD has been reported to be approximately 15 percent.20 Scopinaro et al21 reported that intestinal albumin and nitrogen absorption was 73 percent and 57 percent, respectively, among BPD patients (N=15). It was concluded that loss of endogenous nitrogen (approximately 5-fold the normal value) plays a significant role in the development of PM after BPD, especially during the early postoperative period when restricted food intake may cause a negative balance of both calories and protein. In a prospective study of 65 RYGBP versus 65 BPD patients (BMI range 35–50kg/m2), Scroubis et al22 showed negligible risk of protein deficiency (as measured by albumin) after two-year follow-up; hypoalbuminemia occurred in one (1.5%) RYGBP patient and in 6six (9.2%) BPD patients. In a 15-year follow-up using questionnaires on BPD patients (N=858), there were 32 re-hospitalizations for severe protein deficiency.23 Revisions were performed in 54 (6.3%) patients mainly due to recurrent protein malnutrition. Totté et al24 followed 180 BPD patients (using Scopinaro’s method with a 50cm common channel) and found that protein deficiency, unrelated to the surgery, developed in only two patients at 16 and 24 months postoperative, requiring parenteral nutrition, conversion of the alimentary tract, and psychiatric counseling for correction. They concluded that metabolic complications after BPD were the result of patient non-compliance with dietary recommendations (70–80g protein per day) during preoperative counseling administered by a registered dietitian. Other researchers have reported sporadic cases of recurrent late PM requiring 2 to 3 weeks of parenteral feeding for correction20 and/or elongation of the common limb.24 Scopinaro et al21 has reported that by varying the length of the intestinal limb and the common channel, varying degrees of protein malabsorption can be increased or decreased.
In DS patients, the common channel is 75 to 100cm or 125cm in length for absorption of nutrients.25 Protein malnutrition occurs in 3 to 5 percent of this cohort. Rabkin et al5 followed a cohort of 589 sequential DS patients (with a gastric sleeve and common channel of 100cm) and found annual laboratory measures of serum markers for protein metabolism to slightly decrease at one year postoperative but then stabilize at two and three years postoperative well within normal limits.
The relationships between body composition and dietary protein intakes have been studied by few researchers. Several researchers have reported that the weight loss associated with bariatric surgery results in appropriate proportions of lean body mass (LBM) versus fat mass (FM).26-28 In contrast, in a prospective study, Carey et al29 measured body composition and metabolic changes for one year following bariatric surgery without concomitant dietary intake data in 19 bariatric patients (14 female, 5 male). Data collection occurred within one week preoperatively and one, three, six, and 12 months postoperatively. Two female subjects were lost to the study between six months and one year, resulting in 17 subjects (12 female, 5 male) completing the entire 12-month follow-up. Significant losses in LBM were observed in all time periods except 6 to 12 months, where no change in LBM (60.6 vs. 61.1kg) was observed. The equivocal results of these studies emphasize the need to establish an optimal evidence-based level of protein intakes among bariatric patients for maximal LBM preservation.
Based on the outcomes of most of these studies as indicated by serum protein markers, with and without dietary intake data, it does appear that bariatric surgery poses a relatively low risk of developing obvious signs of protein malnutrition. However, evidenced by substantial LBM loss and below-standard creatinine-height index values, clinicians should also use body composition and somatic protein assessments in order to detect early signs of low protein nutriture.7 It also appears that the BPD procedure has the greatest impact on protein nutrition. However, prospective, longitudinal, randomized, clinical studies are needed to determine the effects of all types of weight loss surgeries on the risk of protein deficiency, negative nitrogen balance, PM, and/or PEM. Frequent continued monitoring of signs of PM or PEM are necessary in this population.
Protein Prescription for the Bariatric Patient
Usual protein recommendations for the post-bariatric surgery patient
are anywhere from 1 to 2g protein per kg of adjusted body
weight—calculated as current body weight (CBW) minus ideal body weight
(IBW) multiplied by 25 percent plus IBW [CBW-IBW x 25% + IBW]).25 A
minimum of 60 to 70g of protein per day should be ingested.13 Many
programs recommend a range of 60 to 80 grams total protein intake per
day or 1.0 to 1.5g/kg IBW, although exact needs have yet to be defined.
The use of 1.5g/kg IBW/day beyond the early post-surgical phase is
probably above metabolic requirements for non-complicated patients and
may prevent the consumption of other macronutrients in the context of
volume restrictions. An analysis of the RYGB patient’s typical nutrient
intake at one year postoperative found no significant changes in
albumin with daily protein consumption at 1.1g/kg IBW.12 Following
BPD/DS procedures, the amount of protein should be increased by
approximately 30 percent to accommodate for malabsorption, making the
average protein requirement for these patients approximately 90g/day.30
Treatment for Protein Malnutrition in the Bariatric Patient
Unfortunately, loss of muscle mass is an inevitable part of the weight
loss process after obesity surgery or any very low calorie diet
(VLCD).31 Patients, especially those undergoing BPD/DS, should be
encouraged to focus on protein-rich foods of good quality protein
(providing a complete protein of all IAAs). Patients need to eat slowly
and to masticate their food well to compensate for the reduced grinding
capacity of the stomach.25 Foods that are moist, either by preparation
methods or by saliva, can also facilitate food to pass from the
esophagus to the pouch.
When a deficiency occurs and there is no mechanical explanation for vomiting or food intolerance, patients can often be successfully treated with a high-protein liquid diet and slow progression to a regular diet.11 As the protein deficiency is corrected and edema is decreased around the anastomosis, food tolerance and vomiting may resolve. If protein deficiency cannot be corrected with dietary protein intake, the patient may require hospitalization for enteral or parenteral treatment to sufficiently return the total body protein to normal levels. Patients may also require psychological evaluation and/or counseling to determine the degree to which a psychosocial etiology is involved. It is important to rule out or treat all possible underlying mechanical and behavioral causes before considering a surgical revision such as lengthening of the common channel or surgery reversal.
Conclusion
Due to the equivocal nature of current research, clinicians need to
continually assess the prevalence and incidence of PM pre- and
post-bariatric surgery. Clinicians need to screen and monitor pre- and
post-bariatric patients for protein malnutrition using tools, such as
dietary assessment, serum biomarkers of protein status, and body
composition measures. Recommendations of types and amounts of good
quality protein from food and supplemental sources can assist in the
prevention and treatment of protein malnutrition.
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