Alcohol Consumption Is the Most

Alcohol consumption is the most widely acknowledged harmful factor of the human body, and a primary cause for illness, disability and mortality. Indeed, its negative impact on a global level was found by World Health Organization in 2009 to be surpassed only by unsafe sex and childhood underweight status, yet it exceeded in prevalence the incidence of common risk factors such as tobacco use, unsanitary water, high cholesterol or hypertension (Rehm, 2011).

This paper's purpose it to outline the known scope of physical effects of alcohol on human body parts, with special focus on research directions from the last five years' span. In this recent light, the present work describes the relationship between alcohol, organs, immunity, and infectious diseases, together with the issue of alcohol consumption during pregnancy, its connection to breast cancer, intentional and unintentional injuries, and diabetes.

According to Rehm (2011), individual disease and injury conditions, for which alcohol consumption is the predominant cause, present a more significant contribution to the global burden of disease than alcohol-specific conditions. Overall, the main scope of disease and injury impacted by alcohol consumption includes infectious disease, cancer, diabetes, neuropsychiatric disease, cardiovascular disease, liver and pancreas disease, and unintentional and intentional injury.

The impact of alcohol abuse on risk and severity of infection has been demonstrated particularly well for infections of the respiratory tract, especially bacterial pneumonia and tuberculosis (Zhang et al. 2008). In fact, recent studies discovered that the overall impact of alcohol consumption on these infectious diseases is considerable. Although risk for infectious diseases does not differ greatly between moderate drinkers and abstainers, this risk seems to be greater for those who are used to drinking larger amounts of alcohol. Alcohol also enhances the symptoms of these diseases, accelerates their progress, helps develop multiple forms of drug resistance, and increases the prevalence of premature mortality from unsuccessful treatment.

One of the ways in which alcohol increases risk for infectious diseases is by attacking the immune system, which is thereby negatively influenced by alcohol consumption in general, and heavy drinking in particular. Alcohol has been proven to inflict a broad range of alterations on all components of the immune system. This alcohol-induced depression of immunity makes the individual vulnerable to a vast spectrum of infectious pathogen agents, which may result in dire biomedical consequences. For instance, a person may develop increased risk of infections after surgical interventions, bodily traumas or burns, increased risk of liver diseases such as hepatitis C infection, fibrosis or cancer, or increased risk of acute respiratory distress syndrome and other opportunistic infections pertaining to the lungs (Molina et al., 2010).

Most recent evidence seems to indicate that alcohol consumption has a major impact on capital infectious diseases, binge drinking being particularly connected with two chronic infections, such as hepatitis C and the human immunodeficiency virus (Baliunas et al., 2010). Chronic alcohol abuse has been identified to be particularly present in patients with AIDS, and its ability to interfere with the antiviral treatment by accelerating the disease course is now widely acknowledged (Shuper et al., 2010). Another consequence in cases with a compromised immune system as a result of HIV infection who chronically abuse alcohol is an increased risk to develop pneumonia. A similar array of effects has been recorded between adult alcohol abuse and hepatitis C infection (Molina et al., 2010).

It would be relevant to note that the relationship between alcohol consumption and acquired immunodeficiency syndrome is different from that with other infectious diseases. In order to become infected with a HIV virus, individuals must exchange bodily fluids, and this occurs in most cases either by injecting drugs with a contaminated needle or, more commonly, engaging in unprotected sexual intercourse. Therefore, notwithstanding the significant associations that exist between heavy alcohol consumption and HIV infection through alcohol-generated effects on the immune system (Baliunas et al., 2010; Shuper et al., 2010), it ought to be emphasized that other factors, such as situational coordinates, personality characteristics, or mental status, may be directly responsible for both risky drinking, and unsafe sex (Shuper et al. 2010).

To further impress the uncertain percentage of alcohol involvement in the process of being infected with HIV, researchers often contend that personality traits such as the inclination to take risks or seek thrills, and sexual impulsivity, may have a stronger influence in the risk of HIV infection. In fact, a 2009 consensus gathering concurred that there is not yet sufficient proof to conclude that alcohol has a causal connection to the incidence of HIV infection (Parry et al.). Nevertheless, it can be argued, through the existence of experimental studies in which alcohol use entailed a greater tendency to engage in unprotected sexual relations, that a causal relationship between alcohol and HIV infection is, to some extent, very real (George et al., 2009).

Alcohol consumption during the post-infection period has an uncontestable adverse impact on the course of the disease, especially through its interference with the antiretroviral treatment. In this light, a recent study concluded that hazardous drinking is associated with being less than 40% likely to comply with the antiretroviral treatment guidelines (Hendershot et al. 2009). Consequently, alcohol consumption is admittedly associated with negative outcomes for people afflicted with AIDS, due to the fact that the ensued lack of fidelity to the ART regimen threatens to annihilate the treatment's chances of success, as well as the individuals' outright survival.

Interestingly, habitual alcohol-ingesting carriers of the HIV virus have been found to present a greater transmissibility potential. Alcohol accelerates viral replication in HIV-infected persons, and may increase viral concentrated presence in male sperm and female vagina, thereby facilitating HIV transmission. Indeed, even for people who adjusted to the ART medication standards, both moderate and heavy drinking is now positively correlated with vaginal shedding of HIV (Pandrea et al., 2010).

Several of the more recent observational studies which concentrated on HIV-positive individuals have concluded that, in their case, alcohol consumption is significantly associated with the development of liver disease (Barve et al., 2010). Even more relevantly, alcohol drinking HIV-infected and hepatitis C-afflicted patients appear to be extremely predisposed to further harmful consequences for the liver. A group of researchers analyzed, in 2009, the proportion of deaths caused by end-stage liver disease among HIV-positive adults in France. The investigation revealed that in 2005, 17% of HIV-infected patients' deaths were directly related to end-stage liver disease, out of which 75% presented hepatitis C Moreover, heavy use of alcohol was observed in 48% of the patients who died from ESLD, and four deaths were even attributed to alcohol consumption devoid of the presence of hepatitis C (Barve et al., 2010).

Heavy alcohol use is also associated with cardiovascular diseases among HIV-positive individuals. Whereas moderate alcohol consumption in uninfected people may reduce the risk of CVD, the same is not true for HIV-positive persons, and the mechanisms by which alcohol enhances cardiovascular risk among those infected with HIV are not clear. However, it is likely that both traditional risk factors like increased blood pressure or high cholesterol, and microbial translocation, contribute (Freiberg, 2010).

The effects of alcohol consumption on heart-related diseases as a whole have been recently reconfirmed to be detrimental, in more than one way. For example, Taylor in 2009 asserted that the effect of alcohol consumption on hypertension is almost entirely detrimental, with a directly proportional dose-response rapport between cardiovascular risk and increased consumption (Rehm, 2011). A similar dose-response relationship exists between use of alcohol and the incidence of atrial fibrillation. On the other hand, in the case of heart disease originated in hypotension or ischemia, regular light drinking shows some protective effects. Nevertheless, irregular heavy drinking annihilates the cardio-protective effect when light or moderate drinking is mixed with irregular heavy drinking.

The relationship between alcohol consumption and diabetes is complex. Baliunas discovered in 2009 that moderate alcohol consumption levels have a protective effect, whereas higher consumption is associated with an increased risk. The greatest protective effect has been appreciated at a daily rate of about two average drinks containing 28 grams of pure alcohol, and the detrimental limit has been set at 50 to 60 grams of pure alcohol per day (Rehm, 2011).

Regarding the effects of alcohol consumption during pregnancy, its dangerous interference in the normal embryonic and fetal development is recognized as the predominant cause of birth defects and developmental disorders from the United States. The severity of birth defects resulting from exposure of the developing embryo or fetus to alcohol is determined by multiple factors, namely genetic background, level of exposure to alcohol, and nutritional status. In most cases, exposure to large amounts of alcohol in the womb may provoke alcohol-related brain and behavioral abnormalities upon birth, yet most children cannot be diagnosed with just fetal alcohol syndrome because they lack the characteristic facial abnormality, and thus the whole range of deficits is referred to as fetal alcohol spectrum disorders (Warren et al., 2011).

Concerning the liver and pancreas, alcohol is known to cause alcoholic liver disease, alcoholic liver cirrhosis, and alcohol-induced acute or chronic pancreatitis, the common incidence of disease being primarily connected to heavy drinking (Rehm, 2011). It is important to observe that the increase in risk for mortality pertaining to these diseases is greater than the increase in risk for morbidity, especially at lower levels of consumption. This finding suggests that continuous alcohol consumption, be it even in low doses, increases the gravity of liver or pancreas disease by risking yet more severe consequences.

A connection between the concentration of alcohol quota in the blood and almost any sort of unintentional injuries has long been established, as psychomotor fallacies emerge after consuming two to three drinks in one hour. However, Taylor in 2010 indicated that, even at lower BAC values, risk of injury is increased when compared with total lack of alcohol consumption (Rehm, 2011).

The acute effects of alcohol consumption on injury risk are also conditioned by the regularity of the individual's alcohol intake sessions. Gmel et al. consigned in 2010 that people who drink less frequently are more likely to be injured or to injure others at a certain alcohol concentration present in the blood, unlike regular drinkers, presumably because of the formers' diminished tolerance (Rehm, 2011). In addition, Tayor noted in 2008 that it is important to realize that, even if the absolute risk for injury may be relatively small for each occasion of moderate drinking -- moderation being appreciated at 36 grams of pure alcohol in one session, the lifetime risks from such drinking occasions adds up to considerable risk for those who drink at such a high level on a regular basis (Rehm, 2011).

Alcohol consumption is not only correlated with unintentional injury, it has a significant influence on intentional injury, as well. There is a clear connection between alcohol drinking and ensuing aggression, and in 2010 Borges and Loera shared that the average volume of alcohol consumption and the level of drinking before the event have been shown to affect suicide risk. A series of causal pathways that form this link have been identified, most notably biological pathways acting through alcohol's effects on the brain's neurotransmitter substances serotonin and amino butyric acid, or through alcohol's effects on an individual's cognitive capacities (Rehm, 2011).