August 2, 2022
Alcohol and Obesity
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While little research exists on the effects of alcohol on weight gain, the statistics of concurrent alcohol use with the disease of obesity, and the incidence of alcohol use disorder after bariatric surgery, a body of research is growing. This article is intended to provide an overview of the topic of alcohol as it relates to obesity.
Many are familiar with the harmful effects of chronic alcohol use on the body but are unclear on the mechanism of how this happens. Regular ethanol intake creates dangerous protein-aldehyde compounds, pro-inflammatory chemical attractants, harmful immune cells, and dangerous free radicals. Even though alcohol itself is toxic to the liver, it also degrades intestinal mucosal barriers, altering the microbiome of the gut and triggering the growth of harmful bacteria. Ethanol is metabolized by both a CYP enzyme pathway and an alcohol dehydrogenase pathway. These pathways require the enzymes NADPH and NAD, respectively. As a result of these enzymes being used to degrade alcohol, the body creates free radical reactive oxygen species, which cause more damage. It has been established that the amount of damage to the liver is directly related to the amount and duration of exposure to ethanol and less related to the type of alcoholic beverage. Drinking just 4-5 standard drinks per day is associated with fatty liver (hepatic steatosis). The usual progression is from steatosis to steatohepatitis (inflamed fatty liver) to hepatic fibrosis (scarred liver). The fibrosis occurs due to the activation of "stellate cells" and a subsequent increase in liver collagen production (Subramaniyan et al., 2021).
In addition to the isolated effects of alcohol on the liver and overall health, more information is emerging regarding diet and body weight in conjunction with alcohol use. One group of authors demonstrated in mice that the murine equivalent of binge drinking combined with a high-fat diet (HFD) resulted in an increase of overactive immune fighting cells, called neutrophils, that were able to penetrate the liver. As a result, the liver can become more inflamed, contributing to liver injury (Hwang, Ren, & Gao, 2020).
Metabolic syndrome is defined as meeting 3 of 5 set criteria associated with insulin resistance; thus, metabolic syndrome is a syndrome of insulin resistance. Park et al. found an increased risk of metabolic syndrome and obesity in Korean men, women, and the elderly who drink more than 14 grams per day as compared to nondrinkers. In people with obesity or abdominal obesity, or those who need to manage their blood pressure, glucose, or triglyceride, drinking just 7 grams of alcohol per day may increase the risk of metabolic syndrome. For reference, 14 grams of alcohol equals one shot of liquor, 5-6 ounces of wine, or 12 ounces of beer (Park EJ, 2022).
Another topic worth mentioning is the increased use of alcohol after bariatric surgery. It is well-established that Alcohol Use Disorder (AUD) may increase after bariatric surgery. For example, one study showed that in their cohort. In contrast, most individuals reported needing to drink four or more alcoholic beverages before feeling the effects of alcohol before surgery; most participants reported feeling the effects of alcohol after one drink of ethanol after surgery. This began as early as five months after surgery, and a large portion of participants reported concurrent food and alcohol intake, ignoring guidelines recommending delaying beverage consumption at least 30 minutes after eating. In Smith et al.'s study, the first alcoholic drinks were approximately 21 weeks after surgery on average, with mean heaviest drink consumption being 71 weeks after surgery, averaging ~26 drinks a week.
Interestingly, the amounts of alcohol consumption before six months before surgery compared to consumption after surgery were very similar. In other words, "Participants generally returned to preoperative drinking frequencies." Yet despite drinking the same amount, "more individuals sought treatment for alcohol problems after surgery than before, which may reflect that the impact of alcohol use on functioning was more significant following surgery." In addition, nearly 1/3 of the participants met the criteria for newly diagnosed alcohol abuse or dependence (Mellinger et al., 2022).
Despite having no control for comparison, Smith's study also found that in a population of alcohol use disorder post-surgery, half the participants had a lifetime mood disorder such as depression, and 1/5th reported a lifetime eating disorder (Smith et al., 2018). Another study referenced, "Lifetime prevalence of Axis I psychiatric and substance use disorders in bariatric surgery patients may be as high as 73% and 32%, respectively" (Mellinger et al., 2022). Another stated, "Less Improvement/ worsening mental health, getting divorced (vs. remaining married), starting smoking (vs. remaining a non-smoker), and starting regular drinking (vs. remaining a non-regular drinker) post-surgery were independently associated with a higher risk of post-surgery [alcohol use disorder], illicit drug use, and [substance use disorder] treatment" (King et al., 2018). Rates of alcohol misuse, abuse, or dependence after bariatric surgery range from 1.3% to 28.4%, depending on multiple factors. The top factors known to predict alcohol use disorder were: "being male, younger age, smoking, regular alcohol consumption, pre-surgical [alcohol use disorder] AUD, and a lower sense of belonging." However, other factors could affect predictors, such as the type of surgical procedure (Ivezaj et al., 2020).
The surgery associated with the most significant alcohol misuse was a roux-en-y gastric bypass, followed by gastric sleeve (Mellinger et al., 2022). King et al. stated that "Among adults with severe obesity, undergoing RYGB was associated with increased risk of incident AUD symptoms, illicit drug use, and SUD treatment" (King et al., 2018). The gastric band did not have an increased association with alcohol misuse. The rate of abuse increased in both men and women after surgery, but especially in women. "In sum, the weight loss associated with bariatric surgery may explain the short-term decreased cirrhosis risk, but the longer-term increased risk of alcohol misuse may predispose to increased risk of [alcoholic cirrhosis]" (Mellinger et al., 2022).
Alcohol use disorder is more prevalent in men, but women are more likely to have bariatric surgery. "As such, a greater number of women than men may be struggling with post-bariatric [alcohol use disorder]. For example, among bariatric patients seeking substance abuse treatment in an inpatient treatment facility, 70.4% (n=38) were women" (Ivezaj et al., 2020). Alcohol dehydrogenase that comes from the liver metabolizes most ethanol, but some alcohol metabolism occurs in the digestive mucosa; therefore, bypassing the stomach may result in increased hepatic delivery of alcohol. Women have less gastric alcohol dehydrogenase and a smaller volume of distribution of alcohol than men. In addition, "Women in the general population, as well as those undergoing bariatric procedures, are more affected by anxiety and depressive disorders than men, which may predispose them to alcohol misuse. Alcohol problems more commonly go undetected in women, and women are less likely to access alcohol treatment." All these factors could contribute to the reason that women develop "[alcoholic cirrhosis] and alcoholic hepatitis with less total alcohol consumption as well as a shorter duration of alcohol consumption compared to men" (Mellinger et al., 2022).
Some studies have evaluated potential measures that can be taken to try to reduce public consumption of alcohol and obesity prevalence. A group in Australia found that introducing a volumetric tax reduced mean alcohol intake by 20.7%, and introducing a minimum floor price reduced alcohol consumption by 9.2%. The volumetric tax led to a −0.90 kg weighted average change in weight and a 0.34 kg/m2 decrease in BMI (Robinson et al., 2020).
Another group of researchers aimed to identify unique higher-risk groups based on reported alcohol, food addiction, and BMI and to see if these special groups differed in their risks of alcohol use disorder based on "behavioral reinforcer pathology." They found that those with higher weight and alcohol use severity also had higher environmental reward deprivation. In other words, their environments were "devoid of other sources of reward such as healthy recreational or leisure activities." The authors concluded that "environmental reward deprivation is a risk factor for both alcohol use disorder and obesity" (Buscemi, Acuff, Minhas, MacKillop, & Murphy, 2022). Another intervention by another group aimed to see if a community-based intervention could decrease alcohol consumption and obesity in men. In the intervention group, men received 95 text messages with questions asking for a response. Higher responses to texts related to those that dealt with "awareness that drinking encourages unhealthy eating perceive benefits of drinking less, and awareness of the harmful effects of obesity" with example responses such as "I eat a lot of junk food while having a can of beer in the house," "To stave off periods of gout, lose weight, generally feel healthier," and "I struggle on the golf course after 1st 9 when I drink more." Unfortunately, participants' average body weight did not change between baseline and follow-up. Over this period, some men lost weight, some remained unchanged, and some gained weight (Irvine et al., 2017).
In the look-ahead study, those in the intensive lifestyle intervention group lost the most weight regardless of alcohol consumption as compared to those without intensive lifestyle intervention. However, when evaluating alcohol consumption at year 4, those that met "a categorical weight loss of ≥10% differed by alcohol trajectory group (p=0.002;)." The percent of participants who achieved ≥10% weight loss was 27.5% in the alcohol-abstaining group vs. 4.8% in the consistent heavy drinker group. The alcohol abstainer group had 52.4% of participants who met a 5% weight loss, compared to 33.3% of consistent-heavy drinkers. Also interesting was the study found that "Contrary to previous reports of declines in alcohol consumption during behavioral obesity treatment, we found that individuals in the [intensive lifestyle intervention group] did not decrease their alcohol intake more than those in the [diabetes support and education control]" (Chao, Wadden, Tronieri, & Berkowitz, 2019).
Chao and colleagues stated in their study, "Alcohol is energy dense, containing 7.1 kcals/gram and may be an important factor related to weight. Alcohol is inefficient in facilitating satiety, and calories from alcohol usually add, rather than substitute, energy ingested through other dietary sources. Consumption of alcohol is linked to disinhibited eating and increased food intake, possibly through neural mechanisms related to energy regulation" (Chao, Wadden, Tronieri, & Berkowitz, 2019). Thus, the authors bring up a good point. Alcohol contributes to a high number of kcal/gram but also disinhibits individuals from dietary restraint, leading to excess intake of calories.
The evidence overall regarding alcohol contributing to weight gain is mixed. It is established men consume approximately three times more alcohol than women and report drinking more beer. Beer is higher in energy density per standard drink than wine, which women are more likely to drink. If studies do not consider the energy density of alcoholic beverages, this could explain some discrepancies. In addition, many studies also fail to assess physical activity when evaluating alcohol consumption and weight gain (Traversy & Chaput, 2015). These, as well as the factors above by Traversy & Chaput, could explain why there is a discrepancy between alcohol use and weight.
First, ethanol is toxic to the liver and the cells that line the gut and may affect gut and brain hormones. Secondly, men are more likely than women to have alcohol use disorder. Still, women are more likely to have a higher relative risk of alcohol use disorder after bariatric surgery than men. Thirdly, more research needs to be conducted on how alcohol can affect body weight. Alcohol also has hormonal influences on the body. Specifically, alcohol will lower Leptin, GLP1, and Serotonin—hormones associated with improved satiety signals and improved mood. Alcohol also inhibits fat oxidation (breakdown of fat), suggesting that frequent alcohol consumption could lead to fat-sparing and, thus, higher body fat in the long term. Despite these known physiological changes, "The mixed evidence concerning alcohol's role in promoting obesity is a product of many factors [e.g., gender, type, frequency, and amount of alcohol consumed, drinking pattern (e.g., binge drinking), physical activity level, sleeping habits, depression symptoms, psychosocial problems, chronic illness, medication use, disinhibition eating behavior trait, history of alcohol use, predisposition to gain weight, etc.]" (Traversy & Chaput, 2015).
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Buscemi, J., Acuff, S. F., Minhas, M., MacKillop, J., & Murphy, J. (2022). Identifying patterns of alcohol use and obesity-related factors among emerging adults: A behavioral economic analysis. Alcohol Clin Exp Res, 45(4), 828-840. Chao, A. M., Wadden, T. A., Tronieri, J. S., & Berkowitz, R. I. (2019). Alcohol intake and weight loss during an intensive lifestyle intervention for adults with overweight/obesity and diabetes. Obesity, 27(1), 30-40. Hwang, S., Ren, T., & Gao, B. (2020). Obesity and binge alcohol intake are deadly combination to induce steatohepatitis: A model of high-fat diet and binge ethanol intake. Clin Mol Hepatol, 26(4), 586-594. Irvine, L., Crombie, I., Cunningham, K. B., Williams, B., Sniehotta, F. F., Norrie, J., . . . Allan, S. (2017). Modifying alcohol consumption to reduce obesity: A randomized controlled feasibility study of a complex community-based intervention for men. Alcohol alcohol, 52(6), 677-684. Ivezaj, V. I., Benoit, S., Davis, J., Engel, S., Lloret-Linares, C., Mitchell, J. E., . . . Sogg, S. (2020). Changes in alcohol use after metabolic and bariatric surgery: Predictors and mechanisms. Curr Psychiatry Rep, 21(9), 85. King, W. C., Chen, J. Y., Courcoulas, A. P., Dakin, G. F., Engel, S. G., Flum, D. R., . . . Wol. (2018). Alcohol and other substance use after bariatric surgery: Prospective evidence from a US multicenter cohort study. Surg Obes Relat Dis, 13(8), 1392-1402. Mellinger, J. L., Shedden, K., Winder, G. S., Fernandez, A. C., Lee, B. P., Waljee, J., . . . Lok, A. S. (2022). Bariatric surgery and the risk of alcohol-related cirrhosis and alcohol misuse. Live Int, 41(5), 1012-1019. Park EJ, e. a. (2022). The effect of alcohol drinking on metabolic syndrome and obesity in koreans: Big data analysis. Int J Environ Res Public Health, 19(9), 4949. Robinson, E., Nguyen, P., Jiang, H., Livingston, M., Ananthapavan, J., Lal, A., & Sacks, G. (2020). Increasing the price of alcohol as an obesity prevention measure: The potential cost-effectiveness of introducing a uniform volumetric tax and a minimum floor price on alcohol in australia. Nutrients, 12(3), 603. Smith, K. E., Engel, S. G., Steffen, K. J., Garcia, L., Grothe, K., Koball, A., & Mitchell, J. E. (2018). Problematic alcohol use and associated characteristics following bariatric surgery. Obes Surg, 28(5), 1248-1254. Subramaniyan, V., Chakravarthi, S., Jegasothy, R., Seng, W. Y., Fuloria, N. K., Fuloria, S., . . . Das, A. (2021). Alcohol-associated liver disease: A review on its pathophysiology, diagnosis and drug therapy. Toxicol Rep(8), 376-385. Traversy, G., & Chaput, J.-P. (2015). Alcohol consumption and obesity: An update. Curr Obes Rep, 4(1), 122-130.