Gastric bypass surgeries have been demonstrated to offer an effective weight control option for severely obese people. The procedure works via a combination of gastric restriction and malabsorption. However, the malabsorption syndrome associated with the procedure may leave patients vulnerable to later neurological problems related to nutritional deficiencies. The current hypothesis is that over the long term there will be a greater prevalence of these disorders in bypass patents than normal controls.
Gastric bypass surgeries or gastric bypass procedures divide the stomach into two compartments or pouches: a small upper portion and a much larger lower portion that is not used in digestion. These procedures then rearrange the small intestine to connect to both stomachs (Adams et al., 2007). Gastric bypass procedures lead to significant reduced stomach volumes and change the physiological process of digestion. Gastric bypass procedures are typically used to treat morbid obesity and other related conditions. Gastric bypass procedures lead to weight loss mainly the restriction of food intake (gastric restriction) but also as a result of malabsorption. This small amount of food that can be taken and following the surgery significantly reduces food intake and ingested food bypasses most of the stomach, the duodenum (this is the first part of the small intestine), and a small portion of the jenunum (second part of the small intestine). The bypass results in mild protein and fat malabsorption because there is a slight delay in the mixing of ingested food with pancreatic enzymes and bile (Tice, Karliner, & Walsh, 2008). These procedures have been demonstrated to reduce mortality rates due to obesity significantly (Adams et al., 2007). However, there can be several significant complications from gastric bypass surgery. For example Tice et al. (2008) indicated that up to 15% of patients experienced some complications as a result of gastric bypass surgeries.
A malabsorption syndrome is one of a number of conditions whereby the nutrients from food eaten are not absorbed adequately into the small intestine (DeMaria, 2007). Normally food is eaten and digested and nutrients are absorbed into the bloodstream in the small intestine; however, a malabsorption disorder or the effects of surgery such as a gastric bypass procedure can disrupt the absorption of food in the bloodstream. There are three categories of malabsorption: (1) selective malabsorption, where certain nutrients are not absorbed; (2) partial malabsorption, where the absorption of certain vitamins and other nutrients is not complete; and (3) total malabsorption. The malabsorption in gastric bypass surgeries consists of a combination of both selective and partial malabsorption.
The deficiencies associated with malabsorption syndrome and gastric bypass surgery typically clued deficiencies in iron, calcium, B vitamins such as vitamin B12, folate, some deficiencies of the fat-soluble vitamins (A, D, E, and K), and protein (DeMaria, 2007). Anemia and vitamin B12 deficiencies can be quite common following gastric bypass procedures if these vitamins are not supplemented. Despite potential applications from malabsorption syndrome the majority of studies have indicated that many of the health issues related to severe obesity such as diabetes and cardiovascular problems are alleviated following gastric bypass procedures in most patients (e.g., Marsk, Jonas, Rasmussen, & Naslund, 2010). Nonetheless, there have not been a good number of long-term follow-up studies that have suggested that problems with malabsorption may affect gastric bypass patients over the long run.
Becker, Balcer, and Galetta (2012) discuss a number of potential neurological complications that can occur following bariatric surgery. These neurological complications can potentially occur as a result of nutritional deficiencies due to malabsorption syndromes produced by gastric bypass surgeries. Polyradiculoneuropathy (a syndrome that resembles Guillain-Barre syndrome) and encephalopathy (brain related syndromes) can be acute manifestations of vitamin B1 deficiencies and thiamin deficiencies. A particularly troubling syndrome known as Wernicke's encephalopathy may occur as a result of malabsorption syndromes associated with bariatric surgery. Long-term effects of thiamine deficiencies and untreated Wernicke's encephalopathy can lead to irreversible dementia. More late appearing symptoms such as myelopathy, myopathy, and peripheral neuropathies can be associated with certain B, E, and mineral deficiencies. Optic neuropathy can be associated with mineral and vitamin B12 deficiencies and have been reported to be present one to three years following bariatric surgery (Becker et al., 2012).
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