Alcohol Use and Health Risks: Survey Results

| March 25, 2007

by Cynthia K. Buffington, PhD

INTRODUCTION

As discussed in the recent October issue of Bariatric Times, gastric bypass surgery may enhance alcohol sensitivity by altering the rate that alcohol is absorbed or metabolized. Such changes in alcohol sensitivity and clearance significantly increase the risk for alcohol toxicity and its deleterious consequences (i.e., liver disease, cardiomyopathy, loss of muscle mass and strength, neuromuscular and cognitive defects, gastritis, pancreatitis, acid reflux, and specific vitamin deficiencies).1- 7 Alcohol use may also adversely affect the health of the bariatric patient by increasing the risk for hypoglycemia and its potentially negative influence on cognitive function and neuromuscular control. 8-12 Furthermore, as discussed by Drs. Moorehead and Alexander in the January/February 2007 issue of Bariatric Times, bariatric patients with pre-existing addictive behavior toward food could, with food restriction, transfer such addiction to alcohol. All of these observations point to the likelihood of alcohol use having a more negative influence on health status postoperatively than was previously recognized.

In an attempt to more clearly understand the effects that alterations in gastrointestinal anatomy and metabolic status with gastric bypass have on alcohol actions, readers of the Bariatric Times October article on alcohol were asked to direct their patients to a website questionnaire designed to identify postoperative changes in alcohol use and effects. The survey included questions pertaining to alcohol sensitivity, postoperative changes in alcohol use and clearance, changes in the patient’s perception of their control over alcohol use, and frequency of conditions suggestive of hypoglycemia. A total of 318 patients (20 males and 298 females) responded from nearly 100 practices located throughout the United States, northern Europe, and Israel. The majority (84%) of the respondents were one or more years postoperative and almost all (97.4%) had received a gastric bypass. Approximately half of the patients queried (49.4%) were between the ages of 36 and 50. Prior to surgery, 50 percent of the respondents had a BMI between 41 and 50 and 43 percent were either super obese (BMI>50) or supersuper obese (BMI>60). At the time of the survey, 56 percent of patients were no longer categorized as obese (i.e., BMI=19 to 29).

FINDINGS AND DISCUSSION

According to the survey results, 83 percent of the respondents said that since their surgery, they had consumed alcohol either upon occasion or regularly. Another 17 percent of patients reported drinking no alcohol at all since their surgery. Nearly all of the nondrinkers (80%) were six months or less postoperative, a time period when alcohol is generally discouraged. In contrast, nearly all (90%) of the people who said they had consumed alcohol since their surgeries were one or more years postoperative.

Most bariatric patients (84%) who were considered regular users of alcohol (i.e., those who reported drinking one or more alcoholic beverages weekly) claimed that they were far more sensitive to the effects of alcohol postoperative than before. Many patients (44%) could ‘feel’ (had a physical response to) the effects of alcohol after having only a few sips of one drink. Another 45 percent of the population reported ‘feeling’ the effects of alcohol after having only one alcoholic beverage. Such enhanced alcohol sensitivity following gastric bypass is likely due, in part, to a more rapid increase in the rate of alcohol absorption. When consumed by the gastric bypass patient, alcohol readily passes through the stomach pouch largely unimpeded and into the jejunum where, due to its large surface area, it is rapidly absorbed. Research has shown that gastric bypass patients—even those that are three or more years postoperative—have a more rapid absorption of alcohol and a peak in blood alcohol content that is considerably higher than that of someone with normal gastrointestinal anatomy.13

Sensitivity to alcohol and the length of time the effects of alcohol persist may also occur secondary to postoperative changes in alcohol clearance.1, 3-6 Among the patients queried, 29 percent claimed that, since their surgeries, the effects of alcohol persist for a longer period of time than before surgery. An individual who ‘feels’ the effects of alcohol for a longer period of time than they did prior to surgery may be metabolizing alcohol at a slower rate. The alcohol dehydrogenase (ADH) pathway is one of the primary pathways for alcohol clearance by the liver.1-2, 3-5 This pathway, however, is rate-limiting, meaning that only a given amount of alcohol at any one time can be metabolized. Although the metabolism of alcohol by the ADH pathway cannot be increased further with greater intake, the rates of alcohol metabolism can be reduced by a backup of products along the ADH pathway, increasing the length of time blood alcohol content is elevated and, consequently, its effects.3-6 Several conditions that the gastric bypass patient may experience, particularly in the early postoperative period, may cause a backup of ADH products, including high fatty acid turnover, ketosis, fatty liver, or fatty liver disease.1-6 Such conditions may explain why 50 percent of the early postoperative patients (6 months or less) surveyed, as compared to 26 percent of patients who were one or more years postoperative, reported experiencing the effects of alcohol for a longer period of time than they had prior to their gastric bypasses.

Many of the surveyed patients (52%) claim that the effects of alcohol now last for a shorter period of time than before surgery. A reduced alcohol clearance rate is possible with induction of the second major pathway for alcohol metabolism, the microsomal ethanol metabolizing (MEM) system and cytochrome (CY) 2E1, in particular.3–5 Consistent alcohol use as well as fatty acids from the breakdown of adipose depots induce (increase in volume) the MEM system for alcohol metabolism by as much as 3- to 10-fold.5, 14-15 Unlike the ADH pathway for alcohol clearance, the MEM system is not rate-limiting, meaning that the greater the amount of alcohol consumed, the greater its rate of metabolism. The individual with elevated MEM activities can generally consume higher amounts of alcohol with less risk for intoxication, a condition sometimes jokingly referred to as the ‘hollow leg syndrome.’ However, high MEM activities have serious health consequences, resulting in substantial liver damage with alcohol use and enhanced sensitivity to the toxic and cancerpromoting effects of pollutants in the air, industrial solvents, specific drugs, and various other agents.3-5

Alcohol can also cause hypoglycemia by reducing glucose availability via suppression of both gluconeogenesis and glycogenesis.8 Bariatric patients may be particularly sensitive to hypoglycemic episodes when using alcohol due to a possible blunted stress hormone response to low blood sugar,11 to gastric dumping,16 and inappropriate insulin secretion with17-18 or without16 an increase in islet mass. A hypoglycemic episode with alcohol could cause an individual to lose neuromuscular control and normal cognitive functions for prolonged periods of time. According to the results of the alcohol survey, nearly half (49%) of respondents claimed that they had symptoms of a hypoglycemic episode upon one occasion or more when drinking alcohol. Such symptoms had occurred for many patients after consuming only 1 to 2 drinks and had lasted for up to two hours. Although these findings may be indicative of conditions other than hypoglycemia, the results do emphasize the need for future research regarding the effects of alcohol on glucose homeostasis in the gastric bypass patient.

Another health risk of alcohol use postoperatively, according to the observations of various psychologists (please see Drs. Moorehead and Alexander’s recent Bariatric Times article from the January/February 2007 issue) is the possibility for a transfer of addiction from food to alcohol. Although there are known shared neurochemical pathways for addictive stimuli,19 there are no published reports of the addiction potentials of bariatric surgical patients before or after surgery and no studies of the numbers of bariatric patients who transfer their obsession for food to alcohol. Furthermore, until the completion of this survey, there was no information as to the percentage of the gastric bypass population with problems in alcohol management either before or after surgery. It was, therefore, of considerable interest that 28.4 percent of survey participants, or more than one quarter of the gastric bypass population queried, claimed that they have a problem with alcohol control. In contrast, only 4.5 percent of patients said they had a problem managing their use of alcohol preoperatively.

CONCLUSION

The results of the alcohol survey provide evidence that alcohol sensitivity and effects are influenced by gastric bypass in such a manner as to adversely affect health and behavior. Prior to surgery, gastric bypass patients should be warned of the increased risk for alcohol sensitivity and toxicity that can occur with alcohol use, particularly if they choose to drink during the weight loss period. Patients should further be advised that alcohol could become a substitute for food postoperatively, increasing the risk for alcohol abuse and addiction.

REFERENCES

1. West Virginia University School of Medicine. Alcohol Metabolism and Absorption. Available at: www.hsc.wvu.edu/som/cmed/alcohol/metabolis m.htm. Access date: February 27, 2007.

2. The Merck Manual of Diagnosis and Therapy. Chapter 40. Alcohol Liver Disease. Available at: www.merck.com/mrkshared/mmanual/section4 /chapter40/40a.jsp. Access date: February 27, 2007.

3. Lieber CS. Alcohol and the liver: Metabolism of alcohol and its role in hepatic and extrahepatic disease. Mt Sinai J Med 2000;67:84–94.

4. Lieber CS. Metabolism of alcohol. Clin Liver Dis 2005;9:1-35.

5. Lieber CS. From ASH to NASH. Hepatol Res 2004;28:1–11.

6. Zorzano A. Effect of liver disorders on ethanol elimination and alcohol and aldehyde dehydrogenase activities in liver and erythrocytes. Clin Sci 1989;76:51–7.

7. Eriksson CJ. The role of acetaldehyde in the actions of alcohol (update 2000). Alcohol Clin Exp Res 2001;25:15S–32S.

8. Mokuda O, Tanaka H, Hayashi T, et al. Ethanol stimulates glycogenolysis and inhibitis glycogenesis via gluconeogenesis and from exogenous glucose in perfused rat liver. Ann Nutr Metab 2004;448:276–80.

9. Mitrakou A, Ryan C, Veneman T, et al. Hierarchy of glycemic thresholds for counterregulatory hormone secretion, symptoms, and cerebral dysfunction. Am J Physiol 1991;260:E67–74.

10. Cryer PE. Glucose counterregulation: Prevention and correction in humans. Am J Physiol 1993;264:E149–55.

11. Guldstrand M, Ahren B, Wredling R, et al. Alteration of the counterregulatory response to insulin-induced hypoglycemia and of cognitive function after massive weight reduction in severely obese subjects. Metabolism 2003;52:900–7.

12. Heymsfield SB, Stevens V, Noel R, et al. Biochemical composition of muscle in normal and semistarved human subjects: Relevance to anthropometric measurements. Am J Clin Nutr 1982;36:131–42.

13. Klockhoff H, Naslund I, Jones AW. Faster absorption of ethanol and higher peak concentration in women after gastric bypass surgery. Br J Clin Pharmacol 2002;54:587–91.

14. O’Shea D, Davis SN, Kim RB, et al. Effect of fasting and obesity in humans on the 6- hydroxylation of chlorzoxazone: A putative probe of CYP2E1 activity. Clin Pharmacol Ther 1994;56:359–67.

15. Emery MG, Fisher JM, Chien JY, et al. CYP2E1 activity before and after weight loss in morbidly obese subjects with nonalcoholic fatty liver disease. Hepatology 2003;38:428–35.

16. Meier JJ, Gutler AE, Galasso R, Butler PC. Hyperinsulinemic hypoglycemia after gastric bypass is not accompanied by islet hyperplasia or increased beta-cell turnover. Diabetes Care 2006;29:1554–9.

17. Patti ME, McMahon G, Mun EC, et al. Severe hypoglycemia post-gastric bypass requiring pancreatectomy: Evidence of inappropriate insulin secretion and pancreatic islet hyperplasia. Diabetololgia 2005;48;2236–40.

18. Service GJ, Thompson GB, Service FJ, et al. Hyperinsulinemic hypoglycemia with nesidioblastosis after gastric-bypass surgery. N Engl J Med 2005;353:249–54.

19. Simansky KJ. NIH symposium series: Ingestive mechanisms in obesity, substance abuse, and mental disorders. Physiol Behav 2005;86:1–4.

Category: Past Articles, Research Perspective

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