New Insights on Metabolic Syndrome: A “Silent” But Visible Epidemic

Abstract

As surgeons, we evaluate varied problems, depending on our background and experience, but rarely make formal recommendations regarding the abnormalities observed in the metabolic syndrome (MS). The article by Ryan et al, from St. James Hospital/ Trinity College Dublin which appears in this issue of Annals of Surgery, linking proinflammatory changes with the extent of squamous intestinal metaplasia in a cohort of patients with Barrett epithelium focuses attention on a common problem that should be more widely addressed by the medical community. As a surgeon, I readily admit a focus on the “presenting problem” and not on broader questions of health maintenance; this article forced me to recognize that I should be more involved in finding ways to deal with MS, which affects 25% to 45% of the population, depending on ethnicity and sex, and has such a variety of consequences, associated risks, including cardiovascular disease, and an ever widening list of cancers. Metabolic syndrome qualifies as a public health epidemic, but its cluster of abnormalities does not command the kind of attention directed towards more visible problems such as the preventable diseases of childhood or chronic lead poisoning, with more easily defined and recognizable consequences; this is probably not the correct approach. Because many of the component physiologic abnormalities of MS are improvable (if not preventable) and directly affected by personal choices regarding lifestyle, diet, and exercise, greater emphasis should be placed on this condition. Obesity and hyperinsulinemia have been correlated with disease conditions for more than 20 years and defined more specifically of late as the metabolic syndrome. Specific details are defined by the World Health Organization, National Cholesterol Education Program, and the National Diabetes Federation (Table 1) who periodically update their definitions of these abnormalities. The weight parameter, readily apparent when viewing an American population, and lipid levels are more amenable to modification in some populations compared with others. In the rodent, a low fat, low starch diet is effective in reversing abnormalities of MS resulting from a high fat and high refined sugar diet. Eating habits in human subjects are more difficult to control, but a low fat/starch diet combined with daily exercise program can be effective, as shown most effectively in patients after bariatric surgery. As epidemiologic studies reveal additional risks of MS (increased incidence rate for cardiovascular disease, cancers, and other conditions), it becomes apparent modifiable risks deserve more attention. The present study on Barrett esophagus from Dublin shows an independent association between MS and the severity of Barrett esophagus (as defined by the extent of abnormal epithelium); the association of MS and immunoinflammatory changes with the extent of SIM is intriguing in light of our understanding of esophageal inflammation. That obesity and esophageal diseases are related is known, with published studies including an epidemiologic report from the Trinity group showing greatly increased numbers of esophageal adenocarcinoma in obese compared with nonobese individuals. Furthermore, gastroesophageal reflux disease (GERD) and erosive esophagitis are more common in the obese, and the most likely explanation for these findings is the likely effect of obesity in promoting GER, followed initially by inflammation and esophagitis, and later