However, when alcohol combines with other pollutants, the results can be very damaging. Unfortunately, many studies don’t effectively separate drinking from smoking, which makes it difficult to decipher the exact effect of alcohol on COPD. Although the effects of alcohol on the heart, liver and brain are widely known, recent research suggests that the lungs deserve more attention – especially when a lung disorder is involved. While alcohol can complicate issues of COPD, alcohol use doesn’t cause this condition. Instead, there are certain risk factors and markers that make a person more likely to develop COPD.
Bacterial Pneumonia
As prevalence of chronic obstructive pulmonary disease (COPD) continues to rise, many people have to reevaluate their lifestyle to make modifications. Those who have concerns about their lung health or alcohol consumption can speak with their doctor for further advice and guidance. Excessive alcohol consumption can also worsen asthma and increase the risk of choking and aspiration pneumonia. According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), AUD is a medical condition in which a person has difficulty controlling their alcohol intake despite negative effects on their health, work life, and social life.
The expression and function of both the Na/K-ATPase complexes and epithelial sodium channels are increased in the alveolar epithelium of alcohol-fed animals (Guidot et al. 2000; Otis et al. 2008). In the presence of an acute inflammatory stress, such as sepsis or aspiration, however, the paracellular leak increases dramatically, and the alveoli flood with proteinaceous edema fluid that overwhelms the already upregulated transepithelial pumping mechanisms. This risk further is exacerbated by the negative effects of chronic alcohol ingestion on the lower airways. In particular, animal models have established that chronic excessive alcohol ingestion causes dysfunction of the mucociliary apparatus, an important host defense mechanism responsible for clearing harmful pathogens and mucus from the lower airways (Happel and Nelson 2005).
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. The recognition that excessive chronic alcohol ingestion has such a dramatic and independent effect on the risk of acute lung injury prompted a search for the underlying mechanisms. Because one of the cardinal features of ARDS is disruption of the alveolar epithelial barrier that regulates the fluid content of the airspace, this was a logical target for investigation.
If a patient has severe COPD, the body no longer adequately responds to a buildup of carbon dioxide by naturally increasing the breathing rate to get rid of this waste product. Another potential therapeutic target is Nrf2, which can be activated by plant-derived compounds (i.e., phytochemicals), such as sulforaphane (Hybertson et al. 2011; Jensen et al. 2013). One clinical study (Burnham et al. 2012) evaluating the effects of 7-day treatment with the Nrf2 activator Protandim® in patients with does alcohol affect copd AUD did not identify any significant improvement in glutathione levels or epithelial function. However, it is possible that combination therapy with an Nrf2 activator plus zinc and/or SAMe may be more effective than zinc and/or SAMe alone, and clinical trials in the near future hopefully will be able to answer that question.
Health Conditions
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).
Alcohol and the Lung
Among the many organ systems affected by harmful alcohol use, the lungs are particularly susceptible to infections and injury. The mechanisms responsible for rendering people with alcohol use disorder (AUD) vulnerable to lung damage include alterations in host defenses of the upper and lower airways, disruption of alveolar epithelial barrier integrity, and alveolar macrophage immune dysfunction. Collectively, these derangements encompass what has been termed the “alcoholic lung” phenotype.
Maintaining the fluid balance of the alveolar space is critical for normal gas exchange. Acute lung injury involves the rapid development of noncardiogenic pulmonary edema, and patients with impaired alveolar epithelial fluid clearance are three times more likely to die from ARDS than patients with a maximal ability to clear lung fluid (Ware and Matthay 2001). Although the fluid balance in the lungs is regulated by the concerted actions of both epithelial and endothelial barriers (Mehta et al. 2004), it is the alveolar epithelium which primarily prevents protein and fluid flow into airspaces (Mutlu and Sznajder 2005). A pathological hallmark of ARDS is heterogeneous damage of the alveolar epithelium, with complete loss of the epithelial surface in some areas, whereas other alveoli remain relatively intact. 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. To supplement the various anecdotal reports of using alcohol in the treatment of airway diseases, early mechanistic investigations demonstrated that alcohol itself seems to have bronchodilating properties in asthmatics.
- Researchers have not found clear evidence that drinking alcohol can directly cause chronic obstructive pulmonary disease (COPD).
- Since COPD is a lung condition, any negative impact of alcohol on the lungs may make a person more predisposed to develop a COPD disease.
- This damage may result from various lung conditions, such as viral infections, pneumonia, and acute lung injury.
T cells are an important part of the immune system and fulfill a variety of functions in defending the organism against various pathogens. To do this, T cells are divided into different subgroups that all have specific functions. T helper cells, as the name implies, assist other immune cells in various ways. These T cells are characterized by the presence of a molecule called CD4 on their surface and therefore also are called CD4+ cells.
When it comes to alcohol intake, some studies have shown that moderate drinking can actually decrease a person’s number of COPD “flare-ups.” That said, it’s important to note that moderate drinking means 1-2 standard drinks of alcohol. This could mean that for a short time, drinking will relieve symptoms of shortness of breath, but this is a dangerous form of self-medication. The respiratory depression can increase the buildup of carbon dioxide, which can sedate a COPD sufferer more than a non-sufferer would experience from the same alcohol intake.
TB signs and symptoms
One-third of adults with chronic health problems, including COPD, reported that they drink regularly. The relationship between drinking alcohol and smoking is well established. It’s a good question to ask since alcohol can cause problems with a number of medications. Han says alcohol doesn’t interact with many of the main COPD meds, which you inhale. But it might cause problems with antibiotics or oral steroids sometimes used to treat lung infections that can come with COPD.
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