COPD: Is It Safe to Drink Alcohol?

Because of the key role of G-CSF in neutrophil regulation, investigators have hypothesized that alcohol-induced neutrophil dysfunction can be prevented by pretreatment with G-CSF (Nelson et al. 1991). Indeed, pre-treatment of alcohol-consuming mice with G-CSF for 2 days before K. Pneumoniae infection increased neutrophil recruitment compared with that of control animals not receiving G-CSF. In addition to increased neutrophil recruitment, the pre-treated animals also exhibited improved bacterial killing and decreased mortality (Nelson et al. 1991). The findings indicate that G-CSF can prevent alcohol-induced deficits in neutrophil-dependent pulmonary defenses by increasing neutrophil production and bacterial killing function.

Can Smoking and Drinking Affect COPD?

The potential influence of alcohol consumption on airway health and disease has been documented for a long time. Chronic alcohol ingestion constantly subjects the drinker’s airways to high concentrations of alcohol vapor, as best evidenced by the use of alcohol breath tests (i.e., Breathalyzer). The volatile nature of alcohol is exploited in this common field sobriety test, which is reliably used as a surrogate to quantify blood alcohol concentrations. Interestingly, the alcohol vapor found in the airways is not caused by inhalation but is a result of the ready diffusion of alcohol from the airway blood supply across the airway epithelium and into the airways themselves (George et al. 1996). This process explains why alcohol vapor in the breath may be used to determine blood alcohol concentration. This process leads to the formation of reactive aldehydes (e.g., acetaldehyde), which in turn can interact and form harmful adducts with proteins and DNA (Sapkota and Wyatt 2015).

Two centuries later, the correlation between alcohol abuse and lung infections still remains strong. According to the Centers for Disease Control and Prevention (CDC), people who abuse alcohol are 10 times more likely to develop pneumococcal pneumonia and 4 times more likely to die from pneumonia than nondrinkers (Lujan et al. 2010). 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).

Types of T Cells.

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). The identification of alcohol-driven oxidative stress as a contributor to alveolar macrophage dysfunction has led to promising antioxidant treatment approaches aiming to prevent alcohol-induced lung conditions in rodent models of prolonged alcohol consumption. For example, oral GSH treatment in alcohol-drinking mice was able to restore GSH pools, reverse alcohol-induced Nox increases, and restore alveolar macrophage function (Yeligar et al. 2012, 2014).

In this particular study, pulmonary inflammation in alcohol-exposed mice persisted for more than 7 days after infection, compared with 3 to 5 days in the control animals. Moreover, some alcohol-exposed mice showed severe inflammation with hemorrhage and edema. These results corroborate findings that infection in the setting of alcohol exposure increases the risk of complications such as ARDS. As discussed previously, alcohol not only alters the environment of the alveolar space but also directly affects GM-CSF signaling, which regulates the maturation, terminal differentiation, and function of alveolar macrophages.

Getting Help With Alcoholism And COPD

1. For example, oral GSH treatment in alcohol-drinking mice was able to restore GSH pools, reverse alcohol-induced Nox increases, and restore alveolar macrophage function (Yeligar et al. 2012, 2014).
2. Replacement IgG therapy only partially restored Ig levels in these people, although it decreased the rates of pulmonary infections (Spinozzi et al. 1992).
3. One clinical study (Burnham et al. 2012) evaluating the effects of 7-day treatment with the Nrf2 activator Protandim® in patients with AUD did not identify any significant improvement in glutathione levels or epithelial function.
4. Chronic alcohol intake also decreased alveolar binding of PU.1, a transcription factor responsible for GM-CSF activation.
5. While many people can have an occasional social drink, others struggle to control their alcohol intake.

In human studies, BACs as low as 0.2 percent (i.e., approximately 2.5 times the legal intoxication level) impaired neutrophil degranulation and bactericidal activity (Tamura et al. 1998). Another key function of the alveolar epithelium, namely the does alcohol affect copd synthesis and secretion of surfactant—which is required to maintain alveolar integrity and gas exchange—also is impaired by chronic alcohol ingestion (Holguin et al. 1998). This impairment also is mediated by glutathione deficiency in the cells, and particularly in the mitochondria, and is reversible with dietary procysteine supplementation (Guidot and Brown 2000).

Those kinds of studies aren’t the ones doctors use to make medical decisions. Chronic obstructive pulmonary disease – otherwise known as COPD – is a chronic lung disease. When you have COPD, you might have a cough, shortness of breath, wheezing, or have trouble breathing. Christine Kingsley, APRN is the Health and Wellness Director at the Lung Institute where she focuses on providing helpful online resources for people looking for information on various lung diseases, breathing exercises, and healthy lifestyle choices. She advocates for holistic care that involves working with your doctor to explore all options including traditional and alternative care while focusing on diet and exercise as proactive measures.

The symptoms of ARLD depend on the type of lung disease a person develops. Alcohol can interfere with many medications, especially glucocorticoids and antibiotics. If you are taking medication to manage your COPD, even a moderate amount of alcohol can reduce its effectiveness. But alcohol can also increase the power of certain medications, which may endanger your lungs. Additionally, although alcohol is initially relaxing for many, this substance has been shown to reduce a person’s quality of sleep.

Both clinical and experimental studies have detected increased oxidative stress in the alveolar space after alcohol exposure (Moss et al. 2000; Velasquez et al. 2002). The exact mechanisms responsible for inducing this redox imbalance remain uncertain, but several explanations have been put forth. An experimental rat model of chronic alcohol ingestion identified perturbations in lipid metabolism analogous to what is seen in alcohol-induced fatty liver (Romero et al. 2014).

Although these animal models provide convincing evidence implicating glutathione depletion as a mediator of alveolar epithelial barrier dysfunction, additional studies in humans are necessary to confirm these findings. ARDS develops in response to inflammatory stresses, including sepsis, trauma, gastric aspiration, pneumonia, and massive blood transfusions (Ware and Matthay 2000). Originally described by Ashbaugh and colleagues (1967), ARDS is characterized by alveolar epithelial and endothelial barrier disruption, dysfunction of the lipoprotein complex (i.e., surfactant) coating the lung surfaces, and intense inflammation.

Is There a Link Between Drinking and Getting COPD?

These analyses found that whereas pure alcohol did not appear to induce bronchial reactivity, some alcoholic beverages worsened asthma symptoms. These findings were the first to suggest that the nonalcohol components and additives of alcoholic beverages may be responsible for inducing asthma, rather than alcohol itself. Similar findings were seen in later studies that examined the effects of red wine in asthma (Dahl et al. 1986; Vally et al. 2000).