Author: John Carter

Alcoholism And COPD Does Alcohol Affect COPD?

The applicability of the frog palate as a model of human airways is uncertain and the extremely high concentrations of alcohol used in these experiments are not relevant to human alcohol consumption. Another study in cultured human bronchial epithelial cells found that alcohol caused a concentration- and time-dependent increase in the expression of the tracheo-bronchial mucin (TBM) gene (Verma and Davidson, 1997). This finding suggests that alcohol regulates mucin expression in the airway epithelium at a biologically relevant concentration. A lung cancer case-control study conducted in Los Angeles County between 1991 and 1994 enrolled 261 incident cases of lung cancer and 615 population controls (22). Recent and past type-specific alcohol consumption, smoking history, dietary habits and other lung cancer risk factors were examined by the investigators. 1.02–3.42] was noted for recent hard liquor consumption [≥ 1.5 ounces hard liquor daily] vs. infrequent liquor drinking [0 to 3 drinks per month].

As a group there was no difference between particle clearance rates following alcohol or juice alone but the variance of clearance time was greater following alcohol ingestion and was related to each subject’s previous alcohol intake history. In subjects with a “moderate” history of drinking, defined as at least one drink per week but less than two drinks per day, clearance was notably faster following alcohol ingestion. In contrast, half of the subjects with a history of “mild” alcohol ingestion, defined as less than one drink per week and no more than two drinks on one occasion, clearance was significantly slowed by alcohol. This variance could not be explained by other obvious factors such as cigarette smoking. Another study examined ciliary beat frequency (CBF) from airway tissue obtained during bronchoscopy under general anesthesia from 50 subjects with respiratory problems in which alcohol intake ranged from “none” to “heavy” (Dulfano et al., 1981). They found no differences in CBF among the subjects related to alcohol intake.

Sulfite in Wines: Relation to Asthma

It’s important that you never quit alcohol cold-turkey without support, as doing so can cause serious health complications. It can also lead to withdrawal symptoms like sweating, restlessness, irritability, nausea, tremors, hallucinations, and convulsions. Patients with severe COPD symptoms who don’t respond to treatment may need surgery to improve their breathing. 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.

1. 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).
2. Airflow obstruction diseases continue to increase in prevalence and that chronic obstructive pulmonary disease (COPD) will become the third most common cause of death in the United States by the year 2020 (Mannino et al., 2003).
3. As a group there was no difference between particle clearance rates following alcohol or juice alone but the variance of clearance time was greater following alcohol ingestion and was related to each subject’s previous alcohol intake history.
4. Although one can hypothesize that brief exposure to modest amounts of alcohol improves airway clearance, there are no studies to directly support this hypothesis.

This is in contrast to our knowledge of alcohol intake and asthma from population studies. Airflow obstruction diseases continue to increase in prevalence and that chronic obstructive pulmonary disease (COPD) will become the third most common cause of death in the United States by the year 2020 (Mannino et al., 2003). Aside from smoking, which is a well-known risk factor for developing COPD, little is known about other factors that impact risk for developing airflow obstruction. The term “whiskey bronchitis” is an expression that was often used to describe the high prevalence of bronchitis in alcoholics (Lyons et al., 1986). Such common clinical observations likely prompted George Burch to write a provocative editorial in 1967 in the American Heart Journal entitled “Alcoholic lung disease-An hypothesis” (Burch and DePasquale, 1967).

The first careful in vitro experiments that examined the effects of modest concentrations of alcohol on CBF in tracheal tissues were done in airway tissue from unanaesthetized sheep during fiberoptic bronchoscopy (Maurer and Liebman, 1988). These investigators found that CBF was stimulated by low concentrations of alcohol (0.01–0.1% or ≈ 2–20 mM), not changed by modest concentrations of alcohol (0.5–1.0% or ≈ 100–200 mM) and slowed at higher concentrations of alcohol (2% or ≈ 400 mM). This transient alcohol stimulation effect on cilia was recapitulated in vivo in alcohol-fed rats (Wyatt et al., 2004). 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. These findings indicate that brief exposure to alcohol stimulated ciliary motility both in vitro and in vivo. Alcohol (pure ethanol), in the absence of any metabolites or congeners, relaxes airway smooth muscle tone resulting in bronchodilated airways.

Alcohol has various physical and mental effects on anyone who chooses to drink. For people with COPD, alcohol can increase the risk of lung problems, sleep disruptions, and allergies. Alcohol has an even stronger effect on heart disease than it does on lung disease. Heart disease impairs breathing and can compound the respiratory problems of lung diseases like COPD. Without COPD treatment from your doctor, the condition will continue to worsen and become more life-threatening.

Summary of Alcohol and COPD

In contrast to these few clinical studies, a larger body of literature indicates both short and long term effects of alcohol on the mucociliary apparatus. 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).

The authors were able to provoke bronchospasm in the laboratory in six of the eleven subjects challenged with the offending alcoholic beverage precipitating a ≥ 15% reduction in the forced expiratory flow in the first second (FEV1) on spirometry. Importantly, in three of these patients, drink-precipitated bronchospasm was not triggered by an oral ingestion of an equivalent amount of pure alcohol in water implicating the non-alcohol components of the beverage as the likely asthma trigger. Indeed, treatment with disodium cromoglycate, a drug that inhibits mast cell granule release and used in the treatment of asthma, prevented bronchospasm to the offending alcoholic beverage.

Although one can hypothesize that brief exposure to modest amounts of alcohol improves airway clearance, there are no studies to directly support this hypothesis. In contrast, prolonged exposure to high concentrations of alcohol desensitizes airway cilia to external stimuli and impairs airway clearance of bacterial pathogens. In heavy drinkers, alcohol-induced impairment of mucociliary clearance represents a major breach of lung host defenses and contributes to the high incidence of lung infections encountered in heavy drinkers. Boyd reported that inhaled alcohol, in a dose-dependent manner, augmented the volume and mucus content from the lungs of anesthetized rabbits at very high doses (5 ml/kg) of inhaled alcohol (Boyd and Sheppard, 1969). Using the frog palate model, Leitch found that high concentrations of alcohol (3–5% or 0.6–1.1 M) depressed both mucus clearance and secretion (Leitch et al., 1985).

Alcohol caused a rapid and reversible concentration-dependent slowing of airway particle clearance compared to control kittens. This important study established that alcohol clearly impairs mucociliary clearance. While the focus of these experiments was mucociliary clearance, the impact of alcohol on mucus production was not examined. This effect was blocked by a β-adrenergic blocker and was not reproduced in isolated first passage cultured airway epithelial cells. These findings suggested that autonomic innervation and functional β-adrenergic receptors participate in alcohol-induced relaxation of airway smooth muscles. The applicability of this study, however, is uncertain since most of the bronchoreactivity of asthma occurs in the small airways and not the trachea.

Can I Drink Alcohol If I Have COPD?

Acetaldehyde is produced by the metabolism of ethanol through the action of alcohol dehydrogenases. Acetaldehyde has long been recognized as a trigger for asthma in Asians and is referred to as “alcohol-induced bronchial asthma” (Shimoda et al., 1996). The most susceptible individuals are Asians who have greatly reduced function of the enzyme aldehyde dehydrogenase isoform 2 (ALDH 2) and can be identified through genetic testing and/or ethanol challenge testing (Matsuse et al., 2001). About half of Japanese have inadequate ALDH2 activity and cannot effectively metabolize acetaldehyde. This results in facial flushing, wheezing and other undesirable side effects following the ingestion of modest amounts of alcohol (Gong et al., 1981).

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). The first reported use of intravenous (IV) alcohol for the treatment of asthma appeared in 1947 when Brown infused 5% ethanol into children with severe asthma attacks who were unresponsive to conventional asthma therapy (Brown, 1947). Five of the six patients improved with the alcohol infusion and no adverse reactions were reported.

For most people who have breathing problems, small amounts of alcohol aren’t shown to significantly affect their COPD. However, even small amounts of alcohol can lead a person to experience side effects that could have an impact on their breathing. While many people can have an occasional social drink, others struggle to control their alcohol intake.

The conducting airways of the lung, including the trachea, bronchi and bronchioles, function to distribute air throughout the lung and represent the proximal and often rate-limiting component of the air distribution system. Normal lung airways branch and taper from the trachea down to terminal bronchi providing balanced and regulable airflow throughout the lung. By virtue of their proximal location in lung airflow distribution, the conducting airways are the first interface of the lung with the outside environment. Despite this front line position, the airways below the vocal cords are normally sterile because of highly effective defense mechanisms (Laurenzi et al., 1961).