Alcohol and the Gastric Bypass Patient

| October 22, 2006 | 0 Comments

by Cynthia K. Buffington, PhD


A 32-year-old man, four months out from gastric bypass surgery, was issued a citation for driving under the influence (DUI) of alcohol shortly after leaving his brother’s wedding reception. According to the patient, he had only consumed one glass of champagne, although his blood alcohol content was above the legal limit to operate a motor vehicle (i.e., 0.08%).

A female patient, 50 years of age and one year post-gastric bypass, hit and killed a pedestrian with her automobile after having less than two glasses of wine. When police arrived, she was staggering and slurring her words and was taken into custody. Two hours later, she was still unable to maintain her balance or to speak clearly, causing officials to suspect that she had  drunk a bottle or two of wine instead of two glasses.

Were these patients telling the truth about the amount of alcohol they had consumed, or did bariatric surgery affect the way their bodies absorb or metabolize alcohol? In order to answer these questions, we queried our gastric bypass population to identify changes in their response to alcohol since surgery. Nearly all patients surveyed (90%) claimed that they were more sensitive to alcohol postoperatively versus preoperatively. Most patients reported that they could feel the effects of alcohol after taking only a few sips of their drink. More than 25 percent of patients said that they had, on occasion, lost muscular coordination after having only one to two drinks, and several of these patients claimed that they were unable to regain control of their balance and coordination for up to two hours. Nearly five percent of the patients who completed the survey said that they have received a DUI and that the incidence had occurred in the early postoperative months and after having only one alcoholic beverage.

These findings suggest that gastric bypass alters the absorption and/or metabolism of alcohol in such fashion as to increase alcohol sensitivity. In order to determine how gastric bypass may affect the body’s response to alcohol, we reviewed the process of alcohol absorption and metabolism in the non-surgical and gastric bypass patient. This article includes the findings and, based upon such, provides the healthcare professional suggested guidelines for patient use of alcohol post-surgery.


Why would alcohol absorption be more rapid and alcohol levels higher for someone who has had a gastric bypass? When alcohol enters the stomach of someone with normal gut anatomy, some of it is metabolized in the stomach by the enzyme alcohol dehydrogenase in a process known as first pass gastric alcohol metabolism.[1-4] Conditions that reduce gastric metabolism of alcohol increase blood alcohol levels and its effects. Such conditions include female gender, aging, and various medications (i.e., H2 blockers and aspirin).[3-4]

The length of time alcohol stays in the stomach also regulates blood alcohol levels by controlling the rate of absorption.[1-3] Although a small amount of alcohol is absorbed in the stomach, most is absorbed into the circulation via the small intestines. Alcohol absorption is primarily regulated by the rate that alcohol empties into the intestines from the stomach. The longer alcohol remains in the stomach, the less is absorbed and the lower the blood alcohol content is and risk for intoxication and toxicity. Food slows gastric emptying and, consequently, reduces the rate of alcohol absorption by the intestines. Conversely, alcohol consumed on an empty stomach substantially enhances absorption and increases blood alcohol content and risk for intoxication.[5,6]

With gastric bypass, more than 95 percent of the stomach is bypassed, including the pylorus. Under these conditions, first pass alcohol metabolism is negligible because alcohol passes directly from the stomach pouch, via gravity, into the intestines where, due to the large surface area of the intestines, it is rapidly absorbed. To make matters worse, when drinking alcohol, many patients obey the postoperative dietary rule of no eating while drinking, causing alcohol to be absorbed at an even faster rate.

A 2002 study published in the British Journal of Clinical Pharmacology[7] found that gastric bypass patients have significantly higher rates of alcohol absorption and blood alcohol content than do age- and weight-matched controls. According to the study protocol, gastric bypass patients three years out from surgery and their non-surgical controls were asked to consume an alcoholic drink after an overnight fast, and blood alcohol levels were followed over time. The data showed that blood alcohol levels of the gastric bypass patients were significantly higher (about 50%) than their non-surgical counterparts and required much less time to peak (10 vs. 30 minutes). These findings may, in part, explain why, when queried, the majority of our gastric bypass patients claimed they could “feel” the effects of alcohol after having only a few sips of their drink.

The more rapid absorption of alcohol and heightened blood alcohol levels with gastric bypass would cause the patient to “feel” the effects of alcohol after having consumed less alcohol than before their surgery. Such effects may have serious ramifications with regard to driving an automobile or performing other skilled tasks, such as operating heavy machinery, piloting a plane, or any other task that could jeopardize the safety of the individual or that of others.


In the non-surgical patient, 60 to 90 percent of alcohol that enters the body is metabolized in the liver by the alcohol dehydrogenase (ADH) pathway. ADH is maximally activated by small amounts of alcohol but activity along the pathway can be reduced by an accumulation of end-products (i.e., NADH, acetaldehyde). Fasting and low calorie intake—such as occurs in the early postoperative period—as well as defects in hepatic mitochondrial function with obesity, per se, may reduce the metabolism of products of the ADH pathway, decreasing hepatic clearance of alcohol.[8-10] Furthermore, activities along the ADH pathway may be impaired by steatosis or fatty liver disease,[11] conditions that are relatively common among individuals with morbid obesity. The gastric bypass patient, therefore, may not only have higher rates of alcohol absorption, but at least in the early postoperative period, possible defects in alcohol clearance as well.

Metabolic changes that occur with massive and rapid weight loss may also affect the amount of alcohol cleared by the liver via the microsomal ethanol metabolizing system (P4502E1).[9,10,12] Activities along this pathway are increased in association with obesity[12-14] and are induced both by alcohol intake, free fatty acids and, possibly, ketone bodies.[12] Alcohol metabolism by the microsomal ethanol metabolizing system substantially increases the risk for liver damage, while at the same time making an individual more sensitive to the toxic and cancer-promoting effects of pollutants in the air, industrial solvents (such as those in household cleaners), and certain drugs, including acetaminophen.[9,10,12]

Alcohol use may cause hypoglycemia and, through reduction in the supply of glucose to neural tissue, cause possible neuromuscular and cognitive dysfunction, loss of consciousness, or even death.[15,16] To maintain appropriate glucose levels, the body stores sugar in the form of glycogen. Glycogen stores, however, can be depleted in a short period of time with fasting or a diet low in carbohydrates. Furthermore, alcohol reduces the process, glycogenesis, that allows sugar to be stored as glycogen.[15]

The bariatric patient, particularly in the rapid weight loss period and if on a carbohydrate-restricted diet, may have low amounts of glycogen. Drinking alcohol could deplete glycogen stores and reduce glucose homeostasis. The body, however, has another mechanism to maintain appropriate glycemic status, gluconeogenesis, the chemical pathway that converts certain components of protein, lactic acid, and other substances into glucose. Unfortunately, alcohol also reduces the production of glucose by this process.[9,10,15]
A decline in blood glucose usually increases the production of glucagon and certain hormones of the autonomic nervous system and hypothalamic-pituitary-adrenal axis to restore blood glucose levels to normal by stimulating glycogenolysis or gluconeogenesis.[16,17] However, when someone drinks alcohol, the response of these hormones to a fall in blood sugar is blunted. To make matters worse, counterregulatory hormone responses to low blood sugar are also blunted or depressed in postoperative bariatric patients.[18] The bariatric patient when using alcohol may have a higher risk of becoming hypoglycemic than someone who has not had the surgery, particularly in the early postoperative period when calorie intake is substantially reduced and glycogen stores are likely to be low.[19]

Since neural tissue requires glucose for fuel, low blood levels could adversely affect neuromuscular and cognitive functions, causing a loss of coordination and balance, slurred speech, poor vision, and confusion.[16,17] These are all conditions that mimic those associated with intoxication. The patient described in the introduction who appeared extremely intoxicated even though she had not consumed a large amount of alcohol may have been hypoglycemic. Hypoglycemia could also have possibly accounted for the loss of coordination and balance that some of our surveyed patients claim they experienced hours after drinking alcohol.

The use of alcohol after surgery may cause irreversible brain and nerve damage, coma, and possible death by inhibiting the absorption of important vitamins, including B-complex vitamins, such as thiamin (B1) or Vitamin B12. Alcohol inhibits the absorption of thiamin and other B-complex vitamins, reduces activation of certain vitamins, and stimulates the breakdown of Vitamin A, pyridoxine, and folate.[9,10] These vitamins may already be deficient in bariatric patients because of nutrient restriction, malabsorption, or impartial digestion of foods produced by the respective surgery.20 Alcohol use, then, could compound the negative effects that bariatric surgery has on vitamin/mineral status and increase the risk for associated health problems, including neuropathy, an irreversible loss of various cognitive functions, defects in metabolism, a decrease in the body’s ability to heal, low immunity, and fatigue.[20,21]

Alcohol has numerous other toxic effects in the body. Not only does alcohol cause liver disease, but it also negatively affects other tissues.[1,8-12,22] Alcohol’s influence on the heart includes myocarditis, cardiomyopathy, arrythmias, and increased risk for sudden death. Skeletal muscle is particularly susceptible to alcohol toxicity with loss of muscle mass and strength. Alcohol causes inflammation of the intestinal tract, gastritis, pancreatitis, acid reflux disease, and increased risk for gastric and esophageal cancers. Alcohol also causes damage—often irreversible—to neural tissue.


In addition to the numerous health problems that drinking alcohol after surgery may cause, the bariatric patient should also be cautious of alcohol addiction. The prevalence of food addiction and associated eating abnormalities (i.e. binge eating, carbohydrate cravings) are high in association with obesity.[23,25] With bariatric surgery, aberrant eating behaviors are considerably improved.[18] However, individuals with addictions often transfer those addictions to yet another substance, such as alcohol.[23] Our data, presented as a poster at the 2006 meeting of the American Society for Bariatric Surgery, showed that approximately 14 percent of gastric bypass patients have increased alcohol consumption post-surgery.

Drinking alcohol after surgery may also reduce maximal weight loss success. Alcohol has no nutrient benefits and contains high numbers of calories that may cause weight gain or prevent weight loss. For instance, one 12-ounce can of beer contains 150 calories; 3.5 ounces of wine contain 70 calories; 1.5 ounces of gin, rum, vodka, or whiskey contain between 97 and 124 calories; and 1.5 ounces of liquor contain 160 calories.


Are there guidelines for using alcohol after surgery? Presently, there are no official guidelines that have been established pertaining to the use of alcohol after having bariatric surgery. However, based upon knowledge of changes in the absorption and metabolism of alcohol, coupled with the metabolic state of the bariatric patient at various stages postoperatively, the following suggestions are recommended:
1.    Do NOT drink alcohol during the rapid weight loss period.
2.    When drinking, remember that small amounts of alcohol can cause intoxication or can result in low blood glucose with serious consequences.
3.    Do not drive or operate heavy equipment after drinking alcohol—even small amounts.
4.    Eat if you plan to have a drink.
5.    Make certain to take your bariatric vitamin and mineral supplements.

1.    West Virginia University School of Medicine. Alcohol Metabolism and Absorption. Available at: Access date: September 7, 2006.
2.    Buffington CK A review of alcohol absorption and metabolism in non-surgical and bariatric surgical patients., 2005.
3.    Sharma R, Gentry RT, Lim RT, Jr., et al. First-pass metabolism of alcohol. Dig Dis Sci 1995;40:2091–7.
4.    Palmer RH, Frank WO, Nambi P, et al. Effects of various concomitant medications on gastric alcohol dehydrogenase and the first-pass metabolism of ethanol. Am J Gastroenterol 1991;86:1749–55.
5.    Jones AW, Jonsson KA, Neri A. Peak blood-ethanol concentration and the time of its occurrence after rapid drinking on an empty stomach. J Forens Sci 199136:376–85.
6.    Hahn RG, Norberg A, Jones AW. ‘Overshoot’ of ethanol in the blood after drinking on an empty stomach. Alc Alcohol 1997;32:501–5.
7.    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.
8.    Merck, Inc. The Merck Manual of Diagnosis and Therapy, Chapter 40. Alcohol Liver Disease. Available at: Access date: September 7, 2006.
9.    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.
10.    Lieber CS. Metabolism of alcohol. Clin Liver Dis 2005;9:1–35.
11.    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.
12.    Lieber CS. From ASH to NASH. Hepatol Res 2004;28:1–11.
13.    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.
14.    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.
15.    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.
16.    Mitrakou A, Ryan C, Veneman T, et al. Hierachy of glycemic thresholds for counterregulatory hormone secretion, symptoms, and cerebral dysfunction. Am J Physiol 1991;260:E67–74.
17.    Cryer PE. Glucose counterregulation: prevention and correction in humans. Am J Physiol 1993;264:E149–55.
18.    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.
19.    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.
20.    Malinowski SS. Nutritional and metabolic complications of bariatric surgery. Am J Med Sci 2006;331:219–25.
21.    Gollobin C, Marcus WY. Bariatric beriberi. Obes Surg 2002;12:309–11.
22.    Eriksson CJ. The role of acetaldehyde in the actions of alcohol (update 2000). Alcohol Clin Exp Res 2001;25:15S–32S.
23.    Simansky KJ. NIH symposium series: Ingestive mechanisms in obesity, substance abuse, and mental disorders. Physiol Behav 2005;86:1–4.
24.    Wurtman RJ and Wurtman JJ. Brain serotonin, carbohydrate craving, obesity, and depression. Obes Res 1995;4:477S–89.
25.    Herpertz S, Kielmann R, Wolf AM, et al. Does obesity surgery improve psychosocial functioning? A Systematic review. Int J Obes Relat Metab Disord 2003;27:1300–14.
26.    Buffington CK, Warthen RT, Daley DL, et al. Changes in alcohol sensitivity and effects with gastric bypass (abstract). SOARD 2006;2:317–8.

Tags: ,

Category: Past Articles, Review

Leave a Reply