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. Of those 15 million, 39 percent still smoke, despite the obvious relationship between smoking and lung diseases. People with COPD typically have blocked airways and experience breathing-related problems. These problems result from reduced functional lung capacity along with lung inflammation and damage. If you or a loved one struggle with co-occurring alcohol abuse and COPD, treatment of the alcohol use disorder is necessary to improve health and prevent complications.
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- These studies offer the groundwork for understanding the importance of GM-CSF within the lung for the maturation and host immune function of the alveolar macrophage as well as the deleterious impact of chronic alcohol use on these processes.
- B cells are responsible for the second arm of the immune response (i.e., the humoral immunity) that is mediated not by specific cells but by immune molecules (i.e., antibodies) produced and secreted by B cells in response to exposure to a pathogen.
- In this model, 1 week of feeding 36% alcohol increased baseline CBF 40% over control animals and was comparable to stimulation with an exogenous beta agonist.
- Excessive alcohol consumption can impact the health of someone diagnosed with COPD.
- For example, type 1 CD4+ cells are characterized by the secretion of interferon γ (IFN-γ); they act primarily against pathogens that are found within cells.
Lastly, there are animal data suggesting that alcohol can promote neurogenic-driven airway inflammation. Trevisani and colleagues demonstrated in guinea pigs that alcohol intake triggers airway inflammation via a transient receptor potential vanilloid-1 (TRPV1) resulting in a calcium-dependent cannabis marijuana drugfacts national institute on drug abuse nida release of neuropeptides that contracted airway smooth muscle (Trevisani et al., 2004). The authors suggested that neurogenic airway inflammation may be an important mechanism by which alcohol causes asthma, which might be treatable with inhaled steroids (Antonicelli et al., 2006b).
Effects of alcohol on the lungs
This cilia-desensitization effect is known as alcohol-induced cilia dysfunction (AICD). In AICD, prolonged alcohol exposure results in failure to stimulate CBF, thereby desensitizing cilia to activating agents such as beta agonists (Wyatt and Sisson 2001). AICD likely results from decreased HSP90/eNOS association, which in turn attenuates the NO-stimulated cGMP/cAMP-dependent kinase activation pathway (Simet et al. 2013a; Wyatt and Sisson 2001). Alternatively, AICD may be related to oxidant-driven eNOS uncoupling, because AICD can be prevented in alcohol-drinking mice by concurrently feeding the animals dietary antioxidants, such as Procysteine™ or N-acetylcysteine (Simet et al. 2013a). Alcohol-related lung disease (ARLD) is the medical term for lung damage that develops in response to excessive alcohol consumption. This damage may result from various lung conditions, such as viral infections, pneumonia, and acute lung injury.
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Importantly, bacterial clearance was impaired by alcohol feeding in this same model and the degree of impaired clearance correlated with the degree of cilia desensitization (Vander Top et al., 2005). This same finding was reproduced in mice ingesting alcohol in their drinking water (Elliott et al., rewarding recovery 2007). Taken together, these studies fully recapitulated the in vitro findings of alcohol-desensitization of ciliary kinases. At this juncture, alcohol downregulation of airway ciliary PKA represents the most likely mechanism that causes alcohol-induced impairment of mucociliary clearance.
Treatment for Co-Occurring Alcohol Abuse and COPD
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.
For example, Davis and colleagues (1991) found that alcohol-fed rats failed to clear bacteria from the lungs and had increased mortality. Some of this discrepancy likely is related to differences in the bacterial pathogens barbiturates: usage effects and signs of barbiturate overdose studied. Thus, Jareo and colleagues (1995) noted impaired neutrophil killing of selected strains of S. Pneumoniae in vitro and a complete absence of killing of other bacterial strains in alcohol-exposed animals.
Five of the six patients improved with the alcohol infusion and no adverse reactions were reported. This report suggested that pure alcohol, when administered intravenously and, in the absence of any other ingredients, acted as a bronchodilator and could be used as a treatment of asthma. A later report noted that asthmatics cleared intravenous alcohol from the bloodstream significantly faster than controls (Sotaniemi et al., 1972) and was confirmed by a subsequent report (Korri and Salaspuro, 1988). They speculated that the difference in alcohol clearance was likely related to concomitant medication use or hypoxia and hypercapnea which can cause micosomal enzyme induction in the liver of the asthmatic patients that increased alcohol metabolism. While no change in any pulmonary function was noted in the normal subjects at any concentration of IV alcohol, concentration-dependent bronchodilation occurred in all of the asthmatics. At the highest concentration (8%) IV alcohol caused a 33% increase in airway conductance in the asthmatics, which was roughly one third of the response that inhaled salmeterol, a beta-agonist, could induce in the same patients.
Remember that drinks containing caffeine and alcoholic beverages can dehydrate you. The best drinks for staying hydrated include water, decaffeinated coffee or tea, and natural fruit juices. If you have chronic obstructive pulmonary disease (COPD), you already know that smoking and eating an unhealthy diet can worsen your condition. Because COPD disrupts a person’s ability to breathe normally, alcohol can exacerbate these symptoms for some people.
Your mucociliary transport system works continually to clear mucus and contaminants out of your airways. According to some researchers, heavy drinking reduces your levels of glutathione. Drinking high quantities of alcohol can harm healthy lung functioning and thereby worsen COPD. Over time, drinking too much alcohol can weaken the lungs’ ability to clear themselves of mucus. This issue can lead to breathing problems and symptom exacerbation in people with COPD. 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 then whether they developed a certain disease (in this case, COPD).
Similar findings were obtained in another study that implicated the sulfur dioxide content in red wine as a likely trigger for bronchospasm in asthmatics rather than the alcohol itself (Dahl et al., 1986). These studies indicate that both the purity (pure ethanol vs. an alcoholic beverage) and the route (oral vs. intravenous) are factors that may determine how alcohol might modify airway function. An excellent review of alcoholic drinks as triggers for asthma has been previously published (Vally et al., 2000). Diseases of the conducting airways are extremely common with prominent examples including bronchitis, asthma and chronic obstructive pulmonary disease (COPD). Although it is not widely recognized by many clinicians, alcohol has long been considered both a treatment and a cause for a variety of airway diseases. This review focuses on our current understanding of alcohol’s impact on airway functions based on clinical and experimental research.