COPD and Alcohol Alcohol’s Effects on the Lungs
Although the majority of data focuses on the effects of chronic alcohol ingestion, experimental evidence further suggests that even acute exposure has similar detrimental effects on alveolar macrophage immune function, although these defects readily resolve (Libon et al. 1993). Taken together, these alcohol-mediated defects in alveolar macrophage function contribute to increased vulnerability to pulmonary infections. The pathophysiological mechanisms discussed thus far undoubtedly are just components of a highly complex network of alcohol-induced cellular perturbations.
Mutations of ADH and ALDH can increase the speed by which alcohol is broken down while increasing the concentration of the “feel-good” hormone dopamine in the brain. Other genes—ADH1B, GCKR, SLC39A8, and KLB—are also linked to alcohol use disorder. “The evidence for alcohol causing lung cancer is inconsistent and is considered limited,” says Marji McCullough, a registered dietitian and senior scientific director of epidemiology research for the American Cancer Society. If a person begins to worry about their drinking and its effects on their physical health, they can contact a doctor. Pneumonia is the medical term for infection and inflammation of the tiny air sacs or “alveoli” within the lungs. If our condition is chronic or we’ve had repeated bouts of ARDS, the damage might be hard to reverse completely.
COPD and Alcohol: Is There a Connection?
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How Alcohol Addiction Is Like an Abusive Relationship
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.
Still, quitting or cutting back on alcohol and receiving proper medical care can help us manage our symptoms or slow their progression. That makes understanding the relationship between drinking, smoking, and COPD hard to pin down. Formalin fixed, paraffin-embedded liver and lung tissue was cut at 5 µm and mounted on glass slides, and stained with hematoxylin and eosin (H&E). Neutrophils were visualized by staining for chloroacetate esterase (CAE) by incubating tissue sections in a solution of napthol AS-D chloroacetate (1 mg/ml) in N,N-dimethylformamide, with 4% sodium nitrite and 4% new fuchsin.
Reduced Antioxidant Levels
If you’ll be driving or otherwise doing something that relies on skill, coordination, and/or alertness, don’t pick up an alcoholic drink. The earliest indication of alcohol as a treatment for asthma appears on Egyptian papyri ca. The term asthma likely encompassed any number of chest ailments in ancient Egypt where beer and wine were prescribed for chest tightness with apparent relief of asthma symptoms (Ayres, 1987).
- In this manner, the epithelium of the conducting airways is continually exposed to ethanol during alcohol ingestion.
- Although chronic alcohol consumption is not directly linked to the development of lung disease per se, it appears to sensitize the lung to damage from other causes (Massey et al., 2015a, 2015b).
- One well recognized risk factor for developing lung infections is heavy alcohol intake.
Some chemotherapy drugs that treat lung cancer are processed in the liver, where alcohol can cause swelling. People who are having chemo are usually advised to limit their drinking, McCullough says. In the 19th century, Hyde Salter reported self-administration of high amounts of oral alcohol by three of his patients with severe asthma exacerbations and noted improvement of their symptoms (Salter, 1863). Soon after this finding was published, intermittent reports on the use of oral administration of pure alcohol diluted in water for treatment of asthma appear (Leffman, 1885; Richardson, 1881). Indeed, the use of alcohol as a treatment was widespread by physicians in the United States well into the early 20th century until Prohibition when its use was officially renounced by the American Medical Association (AMA, 1922). Following the repeal of Prohibition in 1933, more rigorous studies using alcohol as a treatment for asthma began to appear.
For example, Jerrells and colleagues (2007) demonstrated that alcohol-fed mice are inefficient in clearing RSV from the lungs. In addition, the alcohol-consuming mice exhibited enhanced and prolonged RSV infection compared with nondrinking RSV-infected animals. RSV infection itself causes a significant loss of ciliated cells from the airway epithelium and the remaining cilia beat more slowly compared with control cells from uninfected epithelia (Slager et al. 2006). This ciliary slowing is regulated by the activation of another signaling protein called protein kinase Cε (PKCε); moreover, once PKCε becomes inactivated again, the ciliated cells detach from the epithelium (Slager et al. 2006). It is unknown how concurrent alcohol exposure impacts these consequences of RSV infection. In summary, these studies demonstrate that alcohol exposure compromises innate defenses against viral pathogens such as RSV in part by disrupting airway ciliary function.
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 similar U-shaped risk curve for reduced pulmonary function was observed among non-drinkers, mild drinkers and moderate-to-heavy drinkers.
