Alcoholism as a Risk Factor for COVID-19: The Alcoholic Storm

Received: 12-Oct-2021;Accepted Date: Nov 26, 2021; Published: 02-Nov-2021

Introduction

Lives of a huge number of people had changed intensely when pandemic of severe acute respiratory syndrome corona virus appeared in 2019. The outburst commenced in December 2019 from the Wuhan city of China and till March 2020, the World Health Organization (WHO) had announced it as a pandemic [1]. COVID-19 is an extremely contagious transferable disease; most frequently initiates muscular pain, fatigue, fever, dry cough and dyspnea. What differentiates this recent disease from others is its extremely quick spread and comparatively high death rate. This was endorsed in mid of the March 2020 when patients were documented in around 135 countries; approximately 12 weeks after the first case had appeared. On 1st March 2020, death rates extended >3.5% in China and 1.5% in countries other than China [2]. The whole situation is certainly a catastrophe sensed by great numbers of individuals, leading to challenging psychological reactions. It requires substantial strength to readapt to an unidentified and ambiguous condition and how to deal with numerous distressing emotions, regular frustrations, and the outlook of a susceptible material presence to family and oneself. Because of the famous and recognized effects of impeding the nervous system, psychoactive ingredients including alcohol are utilized by numerous people in search of relief from anxiety, irritating or displeasing emotions, stress, or depression [3-5]. This entreats the query of whether the substantial escalations in sales of alcohol, observed in numerous countries are because of the pandemic when associated with the similar period in the preceding year.

Impact of COVID 19 Pandemic on Mankind

Right now, the state of pandemic i.e., challenging mankind can be contemplated to be somewhat a multiple stage complicated calamity, distressing the numerous facets of health, counting psychological health; in both individual and societal aspects [6]. Nevertheless, the risk presented by the virus itself, numerous psychological issues may appear from the obligatory quarantine and lockdown together with the financial threats. Among other things the studies conducted upon animals have revealed the negative influence that loneliness has on enhancing stress levels in the body with both raised responsiveness to stress and neuroendocrine reactions [7]. All this can provoke a broad range of diseases of changing brutality, principally difficulties in concentrating, depression, anxiety, anger, insomnia, violence, and interpersonal clashes. The severity of these symptoms may at least in fragment be because of the degree and extent of the quarantine, a sensation of isolation, distress of infection, and approach to suitable or unsuitable facts and figures [8]. Existing evidence proposes the involvement of organ results from uninterrupted viral encouraged and cytokine arbitrated impairment [9]. In the attempt to generate a reaction to the entrance of SARSCoV- 2, there is a secretion of immune cells such as pro-inflammatory cytokines which frequently becomes amplified and originates fluctuating degrees of damage to the tissues. Raised pro-inflammatory cytokines for instance TNF-α, IL- 6, IL-1, and interferon-γ have been linked with advanced severity of disease in COVID-19 [10]. The pulmonary system is the principal system involved in COVID-19. Apart from general symptoms for instance sore throat, cough, and rhinitis; respiratory manifestation of Acute Respiratory Distress Syndrome (ARDS) Severe Acute Respiratory Syndrome Coronavirus (SARS) is the foremost reason of demise in corona virus disease-19 [11]. Additionally, there is a proof that people who have survived from this deadly COVID-19 could progress post-recovery fibrosis in lungs [12]. The liver is similarly influenced by COVID-19. Indicators of hepatic injury for instance raised aminotransferases, bilirubin, and GGT (gamma-glutamyl transferase) have been established to associate with severity of disease [13]. Though the particular mechanism of hepatic damage is not identified, there are assumptions that this is because of viral arbitrated damage to cell as a consequence of the existence of angiotensin converting enzyme 2 in cholangiocytes and cytokine persuaded hepatic injury [14]. Moreover, hepatic damage could mess up with the usage of antiviral drugs used in the management of Corona virus disease-19. Severe inflammation in muscles of pericardium, shock, arrhythmias, and cardiac failure has also been described as cardiac signs of COVID-19 [15]. Because of the existence of angiotensin converting enzyme-2 in the heart, it is considered that both viral arbitrated and cytokine prompted damage are accountable for damage to the cardiac muscles [16]. Involvement of heart with or deprived of pulmonary failure has been linked in as much as forty percent of corona virus disease deaths [17]. Escalated cardiac enzymes for instance creatinine kinase MB, troponin I, troponin T, and proBNP which are also indicators of cardiac damage have been establish to relate with the threat of admissions to the ICU and demises [18]. Proteinuria, hematuria, raised creatinine and BUN have been stated in patients of COVID-19; with approximately 5% of them coming with severe kidney damage [19,20] pressure, cardiac disease, violence, road accidents, and interpersonal clashes [21].

Alcoholism and Its Effects on Systems of the Body and Covid-19

It would be anticipated that the negative effects of alcohol on the human body become intensified when associated with COVID-19 which correspondingly has multisystem outcomes; and so far, is in itself linked with a health response of community that persuades a big deal of psychological suffering and an enhanced probability of alcohol abuse, activating a vicious cycle. The harmful effects of alcohol on the pulmonary system have been defined in various research projects Among them one is compromised mucociliary stairway mechanism because of less sensitive cilia which is a significant adjustment for the eradication of particulate material, mucus and infectious agents from the airways has been documented [22]. This is associated with an enhanced risk of pulmonary infections. A compromised function of pulmonary cilia has also been related to other pulmonary ailments for instance asthma, COPD, bronchiectasis, and pulmonary abscess [23]. In persistent alcoholics, defense mechanism of host against infectious diseases is undermining.

Tight epithelial junctions of broncho-alveoli, a significant constituent of the innate immunity against infectious agents, are interrupted [21]. Additionally, alcoholism has been made known to cause dysfunction in alveolar macrophages [22]. The threat of ARDS has been established to be three to four times greater in alcoholics in contrast with the common population [23]. A significant antioxidant, glutathione, has been revealed to be reduced in the alcoholic’s alveolar epithelial substance [24]. Reduction in alveolar glutathione is also a distinctive discovery in acute respiratory distress syndrome which is the principal reason of demise in COVID-19 [25]. Effects on heart in alcoholics depend on the extent of use, dosage, and distinct particularities of alcohol extensive dosage and prolonged use of alcohol have been associated with harmful consequences on the heart. Diseases of cardiac muscles in alcoholic is distinguished by cardiomegaly because of hypertrophy in heart wall, expanded chambers of heart, and interstitial fibrosis; all of which come up with decreased capacity of contraction, cardiac failure, and unexpected death of heart [26]. Other negative effects of prolonged alcoholism on the heart comprises of dyslipidemia, hypertension, and cardiac arrhythmias [27]. Hepatic disease is a significant cause of alcohol associated morbidity and fatality, because alcohol is principally processed by liver cells [28]. In contrast, the frequency of hepatic injury amid patients of COVID-19 varies from 14.8%-53%, described by disturbed LFTs [29].

The development process of SARS-CoV-2 contagion can be defined in 2 stages: in the first stage, an early inherent defense happens in an effort to give pulmonary defense. Subsequently by a resulting second stage of inflammation related tissue damage. In vulnerable people, SARS-CoV-2 infection can advance to acute viral pneumonia and can lead to Acute Respiratory Distress Syndrome (ARDS). Acute respiratory distress syndrome is a diffuse, critical, inflammatory pulmonary damage that frequently needs mechanical air circulation. In reaction to such a “storm of cytokine”, unrestrained hyper inflammation can cause a failure in multiple organs. It is identified about how substantial consumption of alcohol might affect in infection of COVID-19. Whereas <15% of drunk alcohol go into the lung, exhalation is nevertheless an important process for elimination of alcohol, as demonstrated by the common utilization of the Breathalyzer test to consistently evaluate levels of blood alcohol [30]. Excessive consumption of alcohol deeply alters inherent and adaptive immunity of lungs, leading to cause greatest degrees of viral pneumonia [31], RSV infection [32,33], influenza A infection [34], and microbial pneumonia [35-37]. In 1918 Spanish flu pandemic, substantial consumption of alcohol was identified as a risk factor for deprived consequences [38]. Numerous current publications reporting patients of COVID-19 failed to involve history of alcohol use [39,40]. More than half of the people scanned in China discuss intensifications in anxiety, depression, or stress in reaction to COVID-19 [41]. Throughout the period of social segregation, AUDs (alcohol usage disorders) amplified in province of Hubei in contrast with other provinces of China because of COVID-19 outburst. Hubei, the province in central China undergone a ten times escalation in harmful consumption contrasted with other provinces having smaller number of limitations [42]. In the US, sales of alcohol showed a 477 percent raise in April 2020 compared to the similar week in month of April 2019. Loneliness, Social isolation and quarantine have long been identified as an inclining factor for problem of alcohol consumption [43]. Depending upon confined situations of economy throughout the pandemic of COVID-19, in the initial phase people may drunk a smaller amount of alcohol because of monetary limitations, but ultimately surge in consumption of alcohol was a result of enhanced stress with passage of time [44]. Another way alcohol can stimulate infection is because of the myths that consuming alcohol can defend against infection of COVID-19. This misconception was spread in Iran that consuming alcoholic drinks or gargling or with it would sterilize the mouth or internal parts of the body and prevent contamination by destructing the virus. Since production of alcohol is illegal in Iran, it is characteristically acquired by means of the black market. As a minimum 180 individuals in Iran expired by consuming black market alcohol that was adulterated with methyl alcohol, with more than 2500 looking for medical care [45]. The misconception that alcohol averts infection of COVID-19 encouraged the WHO (World Health Organization, 2020) and the NIAAA (National Institute on Alcohol Abuse and Alcoholism, 2020) to announce that excessive consumption of alcohol does not prevent or cease COVID-19. However, it has a harmful effect on innate immunity of lungs [46]. It has extensively been identified that alcohol damages the capability of the pulmonary system to combat infection [47]. A distinctive feature of infection COVID-19 is shortness of breath. So far Alcohol is related in number of situations with shortness of breath [48], therefore implying the threat for enhanced dyspnea in the patients of COVID-19 along with alcohol use disorder. Alveolar phagocytes play an indispensable part in protecting the respiratory system from viral diseases. Rats that were deficient of alveolar phagocytes have more acute hypoxia and pulmonary failure in reaction to viral influenza [49]. Substantial use of alcohol considerably decreases production of pulmonary macrophage cytokine [50] and intensely disturbs the functions of alveolar macrophage [51]. Alcohol also weakens the function of macrophage ensuing engulfment, as antigen demonstration, along with numbers of lymphocyte, are decreased by alcohol [52]. After consumption Alcohol begins to absorb by means of the ciliated epithelium straight across the respiratory circulation. Evaporation in the course of exhalation is followed by the process of condensation because the air in the trachea makes the vapors cool ultimately leading to a greater alcohol concentration [52] which alters host defenses of respiratory epithelium by changing barrier function, cytokine discharge, and functions of cilia [53].

Discussion

This modification in defense mechanism of lungs could increase the threat of getting SARS-CoV-2 infections. Furthermore, acute respiratory distress syndrome is expect to be more severe in patients who have damage to the pulmonary system by infectious agents including viruses. Meta-analysis of thirteen longitudinal studies established a relationship between consumption of alcohol and the possibility of developing SARS among adults. This proposition has thoughtful consequences as consumption of alcohol is extensive all over the world. Furthermore, alcohol is barely identified as harmful substance for the health of lungs in contrasts with other organs for instance the liver generally by the public.

Conclusion

Alcohol negatively affects nearly each and every cell of the pulmonary system and a lot of these alterations strongly put those who consume alcohol in large quantity at greater risk of developing COVID-19, more severe acute respiratory distress syndrome and pneumonia. Further extensive research is required to assist in understanding how to better manage those who consume alcohol or are addicts of alcohol with COVID-19.

Conflict Of Interest Statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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