million in health care expenditures.4 Various options for surveillance and treatment of Barrett’s high-grade dysplasia are available; however, the risk/benefit of prophylactic esophagectomy versus less invasive mucosal ablative techniques is a contentious topic. Older patients have a greater risk of complications from esophagectomy, and patient preference in surveys of informed subjects shows a clear preference for surveillance (70% prefer) over esophagectomy or photodynamic therapy (15% prefer).47 The percentage of older patients diagnosed with GERD and its complications is expected to increase by at least 50% in the next 10 years. Current guidelines do not address the issue of when to stop screening in older patients; therefore, defining appropriate guidelines for initiation and termination of screening in geriatric patients with GERD and Barrett’s esophagus has major implications for public health costs and utilization of gastroenterology resources. Age-Associated Changes in Gastric Function Decreased clearance of liquids from the stomach has been documented in older patients and can be exacerbated by anticholinergic medications. Aging is also associated with decreased perception of gastric distention, as measured by subjective fullness during inflation of a gastric barostat balloon.48 Delayed emptying may prolong the gastric contact time of noxious agents such as nonsteroidal anti-inflammatory drugs (NSAIDs). This may have serious consequences, because significant age-related changes do occur in gastric mucosal defense mechanisms. These may predispose the aged to gastric mucosal injury and subsequent complications of ulceration.49 Increased risk of gastric injury does not seem to be due to excessive secretion of agents that promote mucosal injury, because most healthy older individuals have minimal decreases in acid and pepsin output.50 A small minority has severe acid hyposecretion (achlorhydria) associated with atrophic gastritis. This may be related to Helicobacter pylori colonization, because studies in cohorts of aged Japanese subjects segregated by birth year indicate a decreasing incidence of both H pylori colonization and achlorhydria in individuals born later in the 20th century, when presumably hygiene and socioeconomic conditions improved.51 Animal studies have shown a small reduction in gastric acid secretion.52 Human studies indicate that gastrin levels tend to increase with age, possibly as a compensatory response to an increased prevalence of gastric autoantibodies and H pylori colonization.53 The increased prevalence of H pylori carriage in the elderly does not seem to result in increased rates of duodenal ulceration but is associated with increased risk of pernicious anemia and gastric lymphoma. It is more likely that the increased susceptibility to gastric mucosal injury from NSAIDs in the elderly is a result of reduction in gastric mucosal cytoprotective factors such as mucosal prostaglandins.50, 54 Human and animal aging is associated with a significant decrease in gastric bicarbonate, sodium ion, and nonparietal fluid secretion,55, 56, 57 and thinning of the mucus gel layer, particularly in H pylori–positive individuals.58 Aging is also associated with a decrease in the basal and injury-induced rate of proliferation of stem cells in the neck of gastric glands in rats. In vivo expression and activity of several intestinal growth factors, such as transforming growth factor α and epithelial growth factor,59, 60 are decreased in animal models of aging. However, activation of