What organ deals with alcohol

In this case, the liver uses an enzyme called alcohol dehydrogenase to convert the alcohol into what is actually a pretty toxic substance called acetaldehyde sometimes the production of this substance is what can make you feel hungover. At least acetaldehyde doesn't make you feel intoxicated though, and it can be worked on more easily to shunt the rest of the alcohol from your system.

After this it's broken down into fatty acids, carbon dioxide or water, all of which the body likes. Currently, the drink-drive limit is 80mg of alcohol per ml of blood in England and 50mg of alcohol per ml of blood in Scotland. Forensic toxicologist Dr Hazel Torrance says that on average, it takes a person an hour to clear between 15mg and 18mg of alcohol per ml of blood.

In real terms, that 50mg limit would mean an average man can drink just under a pint of beer or a large glass of wine and women could drink a half a pint of beer or a small glass of wine.

Alcohol and the Digestive System

Having zero tolerance is not thought to be practical because alcohol can be found in things like mouthwash and desserts. However alcohol does not occur in the body naturally. Eating a large meal before you drink slows down the effects of alcohol. This is because when you eat the combined alcohol and food stays longer in the stomach.

Fizzy alcohol will make you feel the effects of alcohol more quickly as the bubbles increase the pressure in your stomach, forcing alcohol into your bloodstream faster. Muscle has more water than fat, so alcohol will be diluted more in a person with more muscle tissue. Women are also thought to have less of the enzyme alcohol dehydrogenase, which breaks down alcohol, so they will get drunk more easily. It can mean it is metabolised faster. Particular effects of alcohol on the body make drinking dangerous for drivers. Alcohol affects the brains 'neurotransmitters', the chemicals in the brain which carry messages to other parts of the body and tell it what to do.

These damaged liver cells no longer function as well as they should and allow too much of these toxic substances, ammonia and manganese in particular, to travel to the brain.

These substances proceed to damage brain cells, causing a serious and potentially fatal brain disorder known as hepatic encephalopathy. Hepatic encephalopathy causes a range of problems, from less severe to fatal. These problems can include:. Alcohol can affect the brain at any stage of developmentā€”even before birth. Fetal alcohol spectrum disorders encompass the full range of physical, learning, and behavioral problems, and other birth defects that result from prenatal alcohol exposure.

It only recently has been recognized that alcohol abuse also increases the risk of acute lung injury following major trauma, such as a serious motor vehicle accident, gunshot, or other event requiring hospitalization, or the spread of bacteria attributed to infection i.

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The well-known acute intoxicating effects of alcohol and the concomitant risk of aspiration of secretions or foreign material into the trachea and lungs are components in the development of alcohol-associated lung i. In the past decade, clinical and experimental evidence has emerged that implicates a chronic imbalance in the cell i. Based on these recent studies, the concept of the alcoholic lung is emerging, which is characterized by severe oxidative stress that alone may not cause detectable lung impairment but may predispose those who are dependent on or abuse alcohol to severe lung injury if they are unfortunate enough to suffer serious trauma or other acute illnesses, and makes them more prone to lung infections.

Long-term heavy drinking weakens the heart muscle, causing a condition called alcoholic cardiomyopathy. A weakened heart droops and stretches and cannot contract effectively. As a result, it cannot pump enough blood to sufficiently nourish the organs. In some cases, this blood flow shortage causes severe damage to organs and tissues. Symptoms ofcardiomyopathy include shortness of breath and other breathing difficulties, fatigue, swollen legs and feet, and irregular heartbeat.

It can even lead to heart failure. Both binge drinking and long-term drinking can affect how quickly a heart beats. The heart depends on an internal pacemaker system to keep it pumping consistently and at the right speed. Alcohol disturbs this pacemaker system and causes the heart to beat too rapidly, or irregularly. These heart rate abnormalities are called arrhythmias.

Both binge drinking and long-term heavy drinking can lead to strokes, even in people without coronary heart disease. Recent studies show that people who binge drink are about 56 percent more likely than people who never binge drink to suffer an ischemic stroke over 10 years. Binge drinkers also are about 39 percent more likely to suffer any type of stroke than people who never binge drink.

In addition, alcohol exacerbates the problems that often lead to strokes, including hypertension, arrhythmias, and cardiomyopathy. Chronic alcohol use, as well as binge drinking, can cause high blood pressure, or hypertension. Your blood pressure is a measurement of the pressure your heart creates as it beats, and the pressure inside your veins and arteries. Heavy alcohol consumption triggers the release of certain stress hormones that in turn constrict blood vessels.

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This elevates blood pressure. In addition, alcohol may affect the function of the muscles within the blood vessels, causing them to constrict and elevate blood pressure. And yet the alcohol-liver connection is critical, as more than 2 million Americans suffer from liver disease caused by alcohol.

By performing more than different functions, the liver is essential to our health. Its primary role is to filter all the blood in our bodies by breaking down and eliminating toxins and storing excess blood sugar. Abstinence from drinking in such patients may reduce further risk and improve survival Nicolas et al. Cardiac disease remains an essential burden that causes death in chronic alcoholic population Kannel, ; Banks, Excessive and prolonged alcohol drinking can lead to cardiovascular injuries known as alcoholic heart muscle disease leading to reduced ejection fraction and decreased contractility; a syndrome that is not usually caused by short-term consumption Danziger et al.

Correlating with the quantity and duration of drinking, the progressive disarrangement, functional loss, and fragmentation of the myocytes' sarcomeres seems to interfere with pumping machinery of the heart and reduces its performance Vary et al. However, causal relationship between heaving drinking and alcoholic heart disease remains equivocal and debatable Richardson et al.

Unlike with liver disease, no studies have determined the relation between the quantity of consumption and alcoholic cardiomyopathy, rather it is a clinical diagnosis in heavy drinkers who have no other obvious causes for their heart disease Richardson et al. Despite the lack of clear understanding of the exact mechanism by which chronic alcohol consumption causes heart failure, stroke volume reduction and low ejections fraction was found in alcoholic population Patel et al.

Hence, alcoholic cardiomyopathy occurs in chronic alcohol heavy drinkers, who do not manifest any other cause for their underlying pathology Wodak and Richardson, ; Richardson et al. Recent evidence shows that cardiomyocyte apoptosis appears to play a major role in many alcoholic cardiomyopathies leading to heart failure Fernandez-Sola et al. Specifically, alcohol seems to decrease the activation of a very important survival pathway, Akt Aroor et al.

Such effects have been shown to be agonistic and time dependent, showing an early activation with acute exposure, shifting into deactivation after chronic exposure Table 2 ; Li et al. This is consistent with the J-shaped inverse association between alcohol and cardiovascular disease morbidity and mortality Panagiotakos et al. Furthermore, acute exposure to high-doses of ethanol treatment induces cardiomycyte apoptosis in a concentration-dependent manner Altura et al. High alcohol consumption is associated with myocyte metabolic changes such as decrease in respiratory enzyme and lactate dehydrogenase activity, a decrease in beta oxidation of fatty acids, increase in alcohol dehydrogenase activity which may lead to acetaldehyde accumulation and impaired protein synthesis eventually leading to myocardial injury Guo et al.

Sparagna et al. However, there was a higher basal level of IGF-1 receptor activation in alcoholic cardiac protein preparations. This may imply that the alcohol-induced depression in I K reported earlier maybe mediated by IGFdependent signaling pathway. Even though long-term alcohol abuse has been associated with defect in cardiac contractility and eventual development of dilated cardiomyopathy and low-output heart failure Table 2 ; Preedy et al.

Although several hypotheses have been postulated for alcoholic cardiomyopathy and for the low-dose beneficial cardiovascular effects, the precise mechanisms and mediators remain largely undefined. There is a remarkable lack of data in the literature regarding the electrophysiological alterations associated with different levels and length of alcohol exposure in cardiomycytes. Interestingly, no data is available on the electrophysiological effects of low alcohol exposure or on the exposure frequency. It was shown that the density of dihydropyridine binding sites were greater in cardiomycytes isolated from ethanol-consuming rats as compared to control groups Brown et al.

How Does Alcohol Affect My Liver

Moreover, the beneficial effect of low-dose alcohol was also attributed in part to the fact that ethanol is metabolized differently at low and high concentrations. It was suggested that low ethanol intake has the ability to increase antioxidant capacity, however, at high concentrations ethanol is metabolized to acetaldehyde without producing reduced nicotinamide adenine dinucleotide NADH.

Instead, this pathway utilizes reduced nicotinamide adenine dinucleotide phosphate NADPH , another reducing equivalent, thus producing an oxidative environment Lieber, Interestingly, several studies reported beneficial effects with supplementation of antioxidants in people with essential hypertension and atherosclerotic endpoints Rimm et al. Although once thought of as part of inflammatory cells only, cytokines and chemokines are now recognized to play pivotal role in cardiac homeostasis and repair Tarzami et al.

Ever since, studies postulated the important role of cytokines in cardiovascular diseases Ferrari, It has been found that cytokines are continuously produced, however, they are upregulated in oxidative stress status of the heart. Furthermore, the level of circulating cytokines was inversely associated with left ventricular function Aukrust et al. For example, Interleukin-8 was one of the first chemokines to be related to myocardial injury Oz et al. Similarly, Chemokines c-c motif Ligand2 CCL2 and CCL5 are tremendously involved in heart failure and the death of injured myocardial cells, respectively Braunersreuther et al.

Nevertheless, the exact role different cytokines in cardiac pathology remains a largely disputable issue among scientists. The relationship between inflammation and inflammatory markers with alcoholic heart disease has gained much attention lately. In an in vivo study on pregnant Wistar Rats, the authors extrapolated that the inflammation and oxidative stress are the mechanisms of the destructive effect of ethanol on their hearts Shirpoor et al.

How much alcohol is too much?

Furthermore, association studies have undoubtedly affirmed the presence of fluctuating levels of inflammatory markers in alcoholic heart disease. Moiseev and colleagues found the same results in patients with congestive heart failure who had a previous history of alcohol-induced cardiac damage compared to patients who have ischemic cardiomyopathy Moiseev et al.

Alcoholism is a multifactorial disorder that requires a multidisciplinary approach to treat depending on the organs affected.

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Heavy drinkers suffer from many organ damages; among the most effected organs are liver and kidney. As we mentioned before, heart and brain can be affected either directly or indirectly by alcohol and or its breakdown metabolites. So far, conventional treatment strategies have used a combination of a reduction of ethanol-dependent inflicted damage by control drinking and increasing local and systemic protective mechanisms of the body by using antioxidant supplementation Mailloux, In the cases of alcohol induced cardiovascular damage the use of anti-inflammatory Doe et al.

Other non-conventional suggested approaches included the use of microRNAs since they are shown to play an important role in multi-organ alcohol-induced damages including brain and heart Natarajan et al.

Altered expression of circulation microRNAs in response to alcoholism has been reported, it was suggested that circulating microRNAs could serve as biomarker and prognostic marker for alcoholism and the degree of damages Chen Y. The importance of alcohol induced-microRNAs in regulating proinflammatory cytokine e. Mice deficient in miR did not show any increase in proinflammatory cytokine levels e. This suggests an association between certain microRNAs and proinflammatory cytokine e. Alcohol consumption effects cardiovascular system and predisposes to the development of cardiac abnormalities such as cardiac remodeling, cardiac arrhythmia, cardiomyopathy myocardia infarction, and even SCD Table 3 ; Djousse and Gaziano, b ; Lai et al.

Consequently, many of these cardiac abnormalities will predispose the patients to development of heart failure thus treatment of alcohol induced heart damages is in accordance with the current clinical treatment of their specific heart condition. Heavy drinking has been shown to increase the risk of heart failure, thus in addition to the conventional approach to control alcoholism, it is critical to focus on preventive measures that could reduce the risk to heart failure in these patients.

Such an increase was found to have a linear correlation with the prognosis of chronic heart failure patients Heberto Herrera Garza et al. Yet, variation in expression of these receptors and its regulation during cardiac disease status is not known.