Drinking by the pool or at a barbecue can be tempting, but it’s important to stay safe amid summer fun. Every day in the U.S., about 37 people die from drunk driving crashes, according to the National Highway Traffic Safety Administration. And 31% of drowning deaths involve a blood alcohol concentration (BAC) over the legal limit. Even drinking a little too much (binge drinking) on occasion can set off a chain reaction that affects your well-being.
Alcohol – Beer, Wine, & Liquor in Glasses
Using the same model of intoxication and burn in which mice are deficient in TLR4 but not TLR2, IL-6 production and organ damage are attenuated after alcohol intoxication and burn injury compared to wild-type mice (Bird, Zahs, et al., 2010). Soon after the association between alcohol abuse https://rehabliving.net/ and ARDS was reported, researchers began to design studies of the mechanisms by which chronic alcohol ingestion increases susceptibility to acute lung injury. Such studies were designed and built on the foundations laid by comparable studies in experimental models of liver injury.
Can drinking alcohol be bad for your lungs? Learn more about how alcohol affects your lungs on this page.
But drinking any amount of alcohol can potentially lead to unwanted health consequences. Using the first approach, brief alcohol exposure (1 h with 100-mM ethanol) significantly stimulated serine/threonine phosphorylation of only 6 out of over 600 (1%) ciliary proteins. Most of the 6 were structural proteins, but conspicuous among that group was the striking phosphorylation of HSP90. Functional experiments were performed to confirm that HSP90 is required for alcohol to stimulate cilia via a chaperone and translocation mechanism, likely involving intraflagellar transport (Simet, Pavlik, & Sisson, 2013b).
Alcohol-induced mental health conditions
People have been drinking alcoholic beverages for millennia, and alcohol consumption has played an important role throughout human history, being linked to ancient and modern religions, early medicine, and social occasions and celebrations. Although alcohol consumption is socially accepted across many cultures, heavy and prolonged alcohol intake can lead not only to physical dependence but also to devastating long-term health problems. An estimated 18 million Americans have alcohol use disorder (AUD), including alcoholism and harmful drinking (National Institute on Alcohol Abuse and Alcoholism [NIAAA] 2014). NIAAA (2014) has established guidelines for low-risk drinking that are age and gender specific. Thus, for men ages 21–64, low-risk drinking is defined as consumption of no more than 4 drinks per day or 14 drinks per week.
- Clinically, elevated IL-6 correlates with increased mortality risk in burn patients (Drost et al., 1993; F. L. Yeh, Lin, Shen, & Fang, 1999).
- Alcohol has unique effects on the ciliated airways because it is rapidly and transiently absorbed from the bronchial circulation directly across the ciliated epithelium of the conducting airways.
- Since those effects don’t last long, you might not worry much about them, especially if you don’t drink often.
- One of the largest analyses, published in 2016 in the American Journal of Epidemiology, reported that heavy alcohol use (defined as over seven drinks per day) modestly increased the risk of lung cancer, but that moderate consumption (one drink or less per day) actually decreased the risk.
- A similar pattern of NADPH upregulation existed in human alveolar macrophages isolated from people with AUD.
Can Alcohol Cause a Heart Attack?
That is, low alcohol consumption appears to have a protective benefit while high consumption increases the cancer risk. The link between lung cancer and alcohol consumption has long been considered controversial. There has been debate about the nature of this relationship, with some studies arguing that there is no association and others contending that alcohol may have a protective benefit in certain cases. Until recently, there was no clear evidence that alcohol had the same association with lung cancer as other cancers, in part because many drinkers are smokers (making it hard to draw a clear cause-and-effect relationship). Moreover, of the studies that did exist, most were relatively small and often came to contradictory conclusions.
Alcohol and Your Overall Health
Neutrophils traverse the cells lining the blood vessels (i.e., vasculature endothelial cells) into the space between the lung cells (i.e., the interstitial space of the lung). From there, they migrate into the airspace within the alveoli to the sites of microbial invasion. Once in the alveolar space, neutrophils ingest, degrade, and remove invading pathogens (Nathan 2006). This neutrophil-recruitment process is impaired by alcohol; even brief alcohol exposure decreases neutrophil recruitment to infected sites (Astry et al. 1983). For example, alcohol studies in rodents infected with aerosolized Staphylococcus aureus or Proteus mirabilis have demonstrated that alcohol intoxication decreases bacterial clearance in conjunction with decreased pulmonary neutrophil recruitment (Astry et al. 1983).
Similarly, Boe and colleagues (2001) found that alcohol-exposed rats had decreased pulmonary neutrophil recruitment for up to 18 hours following S. Pneumoniae challenge; after that, however, neutrophil recruitment remained elevated even 40 hours post-challenge compared with nondrinking rats. This observation suggests that in individuals with heavy alcohol exposure, the host neutrophils arrive late at the infected lung but stay longer (Sisson et al. 2005). These findings highlight that alcohol intoxication impairs neutrophil recruitment into infected tissues and the lung and also hinders neutrophil clearance from the lung.
Although they haven’t found any clear answers, there’s broad evidence that drinking too much raises inflammation throughout the body as well as in separate tissues. Tolerance and dependence can both happen as symptoms of alcohol use disorder, a mental health condition previously referred to as alcoholism, that happens when your body becomes dependent on alcohol. This condition can be mild, moderate, or severe, depending on the number of symptoms you have. Over time, drinking can also damage your frontal lobe, the part of the brain responsible for executive functions, like abstract reasoning, decision making, social behavior, and performance. If your pancreas and liver don’t function properly due to pancreatitis or liver disease, you could experience low blood sugar, or hypoglycemia.
Two epidemiologic studies from Europe lend credence to the hypothesis that alcohol intake may reduce the risk for COPD. Because alcohol consumption shows a U-shaped curve with cardiovascular mortality (Murray et al., 2002; Rimm et al., 1991), these investigators hypothesized a similar relation between alcohol consumption and COPD mortality. The first study compared twenty-year COPD mortality and pulmonary function to alcohol consumption in three European countries (Tabak et al., 2001b). Analysis of data from 2,953 middle aged men from Finland, Italy and the Netherlands showed reduced COPD mortality in mild drinkers compared to non-drinkers (relative risk of 0.60). In contrast to mild drinkers, COPD mortality was increased in heavy-to-moderate drinkers (relative risk of 1.25).
A growing body of evidence points to alcohol as an important modifier of mucociliary clearance, which is the first line of defense for the lungs. Despite ongoing debate and gaps in research, it seems clear that heavy drinking is something that needs to be addressed if you are at risk of lung cancer. While there is nothing to suggest that alcohol causes lung cancer outright, the statistics strongly suggest that heavy drinkers are more likely to develop the disease—even if they don’t smoke. One potential explanation for the disparate findings in the literature regarding alcohol’s role in airway disease is that some forms (i.e., phenotypes) of asthma may be more sensitive to the effects of alcohol than others. Interestingly, alcohol-induced respiratory symptoms are more common in patients with aspirin-exacerbated respiratory disease than in aspirin-tolerant asthmatics (Cardet et al. 2014). These findings suggest that the potential irritant versus bronchodilator effects of alcohol may vary by disease subtype; however, further investigation is necessary to validate these observations.
Therefore, at a cellular level the extent of the alveolar epithelial damage may not be as widespread or as uniform as chest X-rays may suggest, and preservation and repair of the alveolar epithelium are key to survival. Schematic illustration of the mechanisms by which alcohol abuse increases the risk of pneumonia. For example, alcohol abuse impairs pathogen ingestion (i.e., phagocytosis) by white blood cells in the air sacs of the lungs (i.e., alveolar macrophages) and other infection-fighting white blood cells (i.e., neutrophils). The alcohol-induced inhibition of Nrf2–ARE signaling is mediated at least in part by zinc. Specifically, Nrf2 function depends on adequate zinc levels, and alcohol interferes with the transporter molecules that mediate zinc absorption from the diet as well as its transport into the alveolar space (Joshi et al. 2009).
If you’ve been diagnosed with COPD, quitting smoking and stopping chronic alcohol use can go a long way to reducing symptoms and helping you live a healthier life. But all of these studies are what scientists call “associational,” which means there was an overlap between people who did a certain thing (in this case, drinking alcohol) and https://rehabliving.net/how-long-does-alcohol-stay-in-your-blood/ then whether they developed a certain disease (in this case, COPD). While cirrhosis scars from excessive drinking are irreversible, quitting alcohol and leading a healthier lifestyle can help your liver heal from alcohol-related liver disease. People who struggle with alcohol use are at risk for lung issues and other airway problems.
Portal blood then carries the bacterial products to the body’s largest tissue-fixed macrophage population, the Kupffer cells of the liver. Kupffer cells continuously sample portal blood for foreign antigens and orchestrate the hepatic response to injury (Wisse, 1974). Kupffer cells can become activated when LPS binds to toll-like receptor 4 (TLR4), an interaction dependent on its co-receptor, CD14 (Su et al., 2002). At low levels, cytokines, such as IL-6, are beneficial to hepatocyte survival, but exposure to levels above an acceptable threshold can be detrimental (Jin et al., 2006). When alcohol precedes a burn, there is both increased stimulus for and sensitivity to TLR4 signaling, leading to harmful levels of IL-6 relative to either insult alone. Accordingly, the combined insult has been shown to result in greater hepatic damage as evidenced by elevated serum transaminase levels, hepatic triglycerides, and liver-weight to bodyweight ratio (M. M. Chen et al., 2014, 2015; M. M. Chen, Palmer, et al., 2013).
These combined studies suggest that alcohol-induced gut leakiness and liver macrophage activation may drive cytokine expression, resulting in systemic oxidative stress and lung injury. This lung injury starts with the desensitization of the ciliated airway epithelium, causing impaired clearance of inhaled pathogens from the upper airway. Altered activation of alcoholic alveolar macrophages in the lower airway not only impairs bacterial phagocytosis and clearance, but may also induce the release of more cytokines into the circulation. Kupffer cells, resident liver macrophages, demonstrate up-regulation of pro-inflammatory transcription factors and pathways, including hypoxia inducible factor-1 alpha and activator protein-1 (Yeligar, Machida, & Kalra, 2010).
The extensive research in this area suggests that although glutathione deficiency is a useful marker of severe structural and functional abnormalities in the alcoholic lung, treatment strategies necessary to modify the risk of lung injury will require more than glutathione replacement alone. Whereas oxidative stress is more directly involved in causing the pathophysiology of the alcoholic lung, the susceptibility to injury reflects cellular damage that cannot be quickly reversed with glutathione replacement alone. This is complicated by the fact that there are no feasible strategies to specifically block the actions of TGFβ1 in the clinical setting.