Mechanisms of Metabolic Bone Disease in Bariatric Surgery Patients

| April 15, 2011 | 0 Comments

This ongoing column is dedicated to providing evidence-based bites of information for the clinician on nutritional considerations in the bariatric patient.

This Month’s Contributor:

Liz Goldenberg, MPH, RD, CDN
Ms. Goldenberg is a nutritionist at New York Presbyterian Hospital, Weill Cornell College of Medicine of Cornell University, Department of Surgery, New York, New York.

Bariatric Times. 2011;8(4):28–29

It is commonly understood that increased body weight defends against osteoporosis.[1] Unfortunately, the rapid, and often considerable, weight loss induced by bariatric surgery has been associated with a reversal of this protection. Numerous studies correlate weight loss operations with increased risk for developing metabolic bone disease, defined as a disease of the bone, which may be attributed to cellular changes or to nutritional deficiencies or excesses, which are brought on by dietary imbalances. Vitamin and mineral deficiencies; accelerated loss of bone mass; loss in height; falls; and fractures of the hip, vertebrae, wrist, and teeth are among the concerns for those undergoing bariatric operations.[2–6] Morbid obesity status alone (non/presurgical patients) may play a role in bone loss. This column discusses a number of mechanisms that have been blamed for having a negative impact on bone health.

Low vitamin D levels from decreased synthesis and sun exposure
Adequate vitamin D is mandatory for bone health due to its role in calcium absorption. Insufficiency of vitamin D leads to decreased calcium absorption, which in turn, stimulates an increase in parathyroid hormone (PTH). PTH acts to resorb calcium from bone in an effort to maintain appropriate blood levels. However, approximately 60 to 80 percent[7,8] of the patients with morbid obesity suffer from hypovitaminosis D, commonly defined as serum 25-hydroxyvitamin D level of ≤20ng/mL. The amount of sun exposure significantly impacts vitamin D synthesis since this hormone is produced in the skin of vertebrates by exposure to ultraviolet B (UVB) radiation from the sun or artificial sources. When skin is exposed to UVB, there is synthesis of the active form of the vitamin, known as vitamin D3. However, vitamin D3 has been found to be less bioavailable from the skin (as well as from food and supplements) of individuals with obesity. This is likely due to the deposition of this fat-soluble vitamin in the excess body fat compartments where it cannot be easily utilized.[9]

In addition to the decreased bioavailability associated with obesity, individuals with obesity may be less likely to expose enough of their skin to the sun for reasons of embarrassment. Stein et al[7] used the Sun Score tool, which gathers information on recent travel, season, clothing worn, and sunscreen use, to assess the amount of weekly sun exposure. Authors found a positive correlation between Sun Score and total vitamin D as well as with vitamin D3 levels in patients presenting for bariatric surgery.

Melanin blocks UVB radiation from allowing conversion to vitamin D3, therefore, individuals with dark skin who have larger amounts of melanin fare even moor poorly than those with light skin when it comes to vitamin D status. African Americans may be twice as likely to have vitamin D deficiency as other ethnicities (e.g., Caucasian, Hispanic, and Asian). In one study, 48 percent of Caucasian patients versus 91 percent of African American patients were found to be deficient in vitamin D.[7]

Lastly, it has been proposed that there may be lessened production of vitamin D in the fatty livers of those suffering from obesity.[8]

Low vitamin D and calcium levels from decreased intake
Dietary intake of vitamin D and calcium from food and supplements has been found to be below recommended levels in the population with obesity.[7,10,11] Inadequate calcium intake and decreased consumption of dairy products has also been observed after bariatric surgery. In one study, 33 percent of patients surveyed reported that they limited milk intake and seven percent limited cheese and dairy products. The avoidance of these may be due to lactose intolerance, wariness of dumping syndrome, or perhaps fear of weight regain.[4,12,13]

Malabsorption of fat-soluble vitamin D and calcium losses
Gastric bypass and biliopancreatic diversion with or without duodenal switch alters the gastrointestinal tract such that food and supplements bypass the duodenum and proximal jejunum. These are the main sites of calcium and vitamin D absorption, thus nutrient malabsorption is another mechanism linked to the development of metabolic bone disease. Furthermore, malabsorption of fat can increase loss of calcium by binding to fatty acids and forming insoluble soaps.[14]

Prescription of proton pump inhibitors
Recently, more attention has been given to the impact of proton pump inhibitors (PPIs) on bone health. Bariatric surgery patients, specifically those who have undergone sleeve gastrectomy and adjustable gastric banding operations, are commonly given these medications as treatment for postoperative gastroesophageal reflux (GERD) and/or dysmotility. PPIs work by inhibiting parietal cell acid secretion. Lower stomach acid levels can consequently inhibit the release of ionized (i.e., the more absorbable) calcium from food and supplements. Large doses and long-term use of these drugs may be additional mechanisms whereby bariatric surgery is linked with the development of bone disease.[13,15]

It is important to note that while there are many mechanisms whereby patients may be at risk for developing bone disease after bariatric surgery, further and more long-term studies are needed to clarify this association. Not all studies find bone mass to be significantly decreased after surgery; a recent review paper notes that a Mayo Clinic study presented at the 91st Annual Meeting of the Endocrine Society reported that the increased fracture risk in patients who had undergone bariatric surgery was comparable to what would be expected for the general population.[8] Even so, close observation for nutritional deficiencies and bone loss in patients, as well as timely intervention and treatment, both before and after bariatric surgery, would seem to be crucial steps to preventing or minimizing metabolic complications of these operations.

For further reading on metabolic bone disease associated with bariatric surgery, its identification, prevention and treatment, the author recommends references 6 and 8.

1.    Valtueña Martínez S. Obesity and osteoporosis: effect of weight variation on bone mass. Nutr Hosp. 2002;17 Suppl 1:49–54.
2.    Nogués X, Goday A, Peña MJ, et al. Bone mass loss after sleeve gastrectomy: a prospective comparative study with gastric bypass. Cir Esp. 2010;88(2):103109.
3.    Berarducci A, Haines K, Murr MM.  Incidence of bone loss, falls, and fractures after Roux-en-Y gastric bypass for morbid obesity. Appl Nurs Res. 2009;22(1):35–41.
4.    Duran de Campos C, Dalcanale L, Pajecki D, et al Calcium intake and metabolic bone disease after eight years of Roux-en-Y gastric bypass.  Obes Surg. 2008;18:386–390.
5.    Fleischer J, Stein EM, Bessler M, et al. The decline in hip bone density after gastric bypass surgery is associated with extent of weight loss. J Clin Endocrinol Metab. 2008;93(10):3735–3740.
6.    Aills L, Blankenship J, Buffington C, Furtado M, Parrott J. ASMBS allied health nutritional guidelines for the surgical weight loss patient. Surg Obes Relat Dis. 2008;4(5 Suppl):S73–108.
7.    Stein EM, Strain G, Sinha N, et al. Vitamin D insufficiency prior to bariatric surgery: risk factors and a pilot treatment study. Clin Endocrinol (Oxf). 2009;71(2):176–183.
8.    Viégas M, Vasconcelos RS, Neves AP, Diniz ET, Bandeira F. Bariatric surgery and bone metabolism: a systematic review. Arq Bras Endocrinol Metabol. 2010;54(2):158–163.
9.    Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF. Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr. 2000;72(3):690–693.
10.    Vasconcelos RS, Viégas M, Marques TF, et al. Factors associated with secondary hyperparathyroidism in premenopausal women undergoing Roux-en-Y gastric bypass for the treatment of obesity. Arq Bras Endocrinol Metabol. 2010;54(2):233–238.
11.    Goldberg TB, da Silva CC, Peres LN. Calcium intake and its relationship with risk of overweight and obesity in adolescents. Arch Latinoam Nutr. 2009;59(1):14–21.
12.    Silver HJ, Torquati A, Jensen GL, Richards WO. Weight, dietary and physical activity behaviors two years after gastric bypass. Obes Surg. 2006;16(7):859–864.
13.    Deitel M. Bariatric surgery, proton pump inhibitors, and possibility of osteoporosis. Surg Obes Relat Dis. 2010;6(4):461–462. Epub 2010 Apr 24.
14.    Kumar R, Lieske JC, Collazo-Clavell ML, et al. Fat malabsorption and increased intestinal oxalate absorption are common after Roux-en-Y gastric bypass surgery. Surgery. 2011 Feb 4. [Epub ahead of print].
15.    Keidar A, Appelbaum L, Schweiger C, et al. Dilated upper sleeve can be associated with severe postoperative gastroesophageal dysmotility and reflux. Obes Surg. 2010;20(2):140–147. Epub 2009 Dec 1.

Category: Nutritional Considerations in the Bariatric Patient, Past Articles

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