Excessive alcohol use is the third leading cause of preventable death in the United States 2. Although normative alcohol use is ubiquitous, alcohol dependence is a serious medical illness 3, experienced by ≈14% of alcohol users 4. Alcohol abuse may also trigger a cascade of acute health problems such as traffic accident-related injuries, social problem including domestic violence, loss of work-place productivity, economic burden on society, crime and public disorder 13. Alcohol exposure affects the mitochondrial structure which became swollen and disaggregated, and the cristae were dissolved and disappeared 101, giving rise to megamitochondria 105, which have oxygen consumption, ATP synthesis, and ROS-formation rates lower than those of controls. Therefore, it was proposed that enlargement of the mitochondria is an adaptive process by which cells attempt to decrease the intracellular amount of ROS when they are drug addiction treatment subjected to oxidative stress 106.
- Pancreatitis can be a short-term (acute) condition that clears up in a few days.
- Approximately twenty-percent of heavy drinkers, those who binge drink (have 4 drinks for women and 5 drinks for men in about two hours) on 5 or more days a month, develop a fatty liver than non-drinkers.
- Numerous studies shows that mitochondrial levels of ROS may be increased by chronic alcohol consumption as a consequence of increased mitochondrial CYP2E1 levels 44,45 as well as a by-product of the matrix enzyme α-ketoglutarate dehydrogenase 42.
- Alcoholic liver disease is damage to the liver due to alcohol abuse and usually occurs after years of excessive drinking.
- NO and its metabolite peroxynitrite (ONOO−) have been implicated as key mediators of mitochondrial dysfunction 57.
Alcohol Effects on the Heart
Besides, mitochondria have an important role in the alcohol metabolism, and their function is affected by alcohol consumption. It has been hypothesized that upon chronic alcohol intake the brain starts using acetate rather than glucose as a source of energy 35, and the accumulated acetaldehyde exerts its toxic effects by inhibiting mitochondrial reactions and functions. In addition, there is considerable evidence that chronic alcohol exposure enhances the susceptibility of cells to undergo apoptosis, therefore is important to understand the role of mitochondria during alcohol consumption and metabolism in chronic alcohol consumption. Mitochondrial and cellular oxidative stress in chronic alcoholism appears to be the major cause of augmented mitochondrial production of superoxide anion (O2 •−) at complexes I and III, and consequently the production of H2O2 and other ROS, triggered by NADH overproduction. Mitochondrial oxidative stress renders hepatocytes susceptible to ethanol- or acetaldehyde-induced mitochondrial membrane permeability transition (MMPT), apoptosis in chronic alcoholism and biliary cirrhosis 118. Through phosphorylation/dephosphorylation of Bcl-2 proteins, chronic ethanol may control the sensitivity of mitochondria toward a variety of membrane permeabilization-inducing factors 119.
Alcohol Effects on the Liver
It has a high rate of NADPH oxidase activity, which leads to the production of large quantities of O2 •− and H2O2 48. Also, chronic alcohol exposure decrease the activities of all the oxidative phosphorylation complexes, except complex II 50 contributing to decreased functioning of the oxidative phosphorylation system and depressed rates of ATP synthesis 51. As well, ethanol has been demonstrated to increase the production of ROS and reactive nitrogen species (RNS) and decrease several antioxidant mechanisms in liver 38. This in turn might result in oxidative modification and inactivation of mitochondrial macromolecules, thereby contributing to mitochondrial dysfunction and a loss in energy conservation 38. On the other hand, lipid peroxidation has been linked to the impairment of mitochondrial oxidative phosphorylation and the appearance of megamitochondria 60. In patients with alcoholic liver disease (ALD) the serum markers of lipid peroxidation, such as conjugated dienes, malondialdehyde (MDA), 4-hydroxynonenal and F2-isoprostanes are increased 61.
Metabolism
Alcoholic beverages contain more than 200 compounds with different antioxidant activities to polyphenols, including quercetin, catechin, tannic acids 80, and resveratrol, among others 81. Resveratrol is a polyphenolic phytoalexin (trans-3,4′,5-trihydroxystilbene) present in purple grape juice, peanuts, and red wine 35,82 and has ability to prevent or slow the progression of a variety of pathologies 83. Alcohol consumption has both long-term and short-term effects, resulting in abnormal mental health and lifestyle of a person. Alcohol is carried to the liver through the blood stream; the liver metabolizes a certain level of alcohol, while the rest is circulated all over the body.
This is why it’s important to see your healthcare provider regularly and be open and honest about how much alcohol you drink so you any health-related damage can be found early. Regular health check-ups and blood tests can help detect early signs of disease in the brain, kidneys and liver. If you’re in Connecticut and would like to find a doctor near you, you can locate a board-certified PACT primary care physician using our searchable list here. Your liver is an essential organ to your body and produces hundreds of vital functions every day, including bile production, excretion of cholesterol and hormones and enzyme activation. In 2018, NIH states that of the 83,517 liver disease deaths among individuals 12 and older, 47.8% involved the use of alcohol. Alcohol can have serious, life-threatening health consequences for the liver, where alcohol is filtered and broken down in the body.
What Does Alcohol Do to Your Body? 9 Ways Alcohol Affects Your Health
Early symptoms of acute intoxication are euphoria and disinhibition, which progress to stupor and respiratory depression 122. Abrupt abstinence after prolonged or binge drinking can result in tremors, hallucinations (visual, auditory, or tactile), seizures, or delirium tremens, with severely constricted attentiveness, fluctuating levels of alertness, agitation, and autonomic instability 123. It is possible, moreover, that repeated binges and withdrawals cause permanent neuronal damage contributing to more lasting neurological disorders, including dementia 124. The noxious effects of alcohol are influenced by the amount of consumption, drinking pattern, and quality of the alcoholic beverage. Other factors such as gender, age, body size and composition, genetics, metabolism, nutritional status, and other social factors also play a vital role in causing dangerous effects of alcohol.
- Neuropathologic abnormalities in FAS include neuronal-glial heterotopias, cerebellar dysplasia, and agenesis of the corpus callosum, hydrocephalus, and microcephaly 140.
- It has been hypothesized that upon chronic alcohol intake the brain starts using acetate rather than glucose as a source of energy 35, and the accumulated acetaldehyde exerts its toxic effects by inhibiting mitochondrial reactions and functions.
- Then, proteomic analysis revealed that 40 additional mitochondrial proteins had altered levels in response to chronic alcohol consumption.
Piceatannol (3,3′,4′,5-tetrahydroxystilbene, astinginin) is a resveratrol derivative with higher antioxidant capacity, found in the seeds of Euphorbia lagascae 157. Piceatannol possesses an additional hydroxyl group than resveratrol (3,5,4′-trihydroxystilbene) and exerts higher radical scavenging activity which was considered to contribute to the cardioprotective and antiarrhythmic effects in ischaemic-reperfused rat heart 158,159. Another potential compound in mitochondrial therapeutics is the structural GABA analogue citrocard (phenibut citrate) that prevents the damaging effect of alcohol, which was observed from increased indexes of oxidative phosphorylation in treated animals 78. For a long time the effect of alcohol was thought to be a generalized depression of neural activity causing global impairment of cognitive, psychological, and behavioral domains 120. Recently, it has been shown that ethanol can alter mentation in a variety of ways affecting many neurotransmitter systems 121.
- The blood alcohol level (BAL) increases when a person consumes a higher amount of alcohol than the body can metabolize.
- Other factors such as gender, age, body size and composition, genetics, metabolism, nutritional status, and other social factors also play a vital role in causing dangerous effects of alcohol.
- Alcoholic beverages contain more than 200 compounds with different antioxidant activities to polyphenols, including quercetin, catechin, tannic acids 80, and resveratrol, among others 81.
- Chronic alcohol administration favors the formation of megamitochondria, due to increasing mitochondrial membrane permeability and decreasing mitochondrial membrane potential 116 and diminished activity of mitochondrial respiratory chain complexes 117.
Acetate increases blood flow into the liver and depresses the central nervous system, as well as affects various metabolic processes 35. The metabolism of ethanol is closely linked with stimulation of reactive oxygen species generation and oxidative stress. This knowledge will clearly advance the design kidney pain from drinking and testing of novel mitochondria-specific therapeutics on the treatment of diseases in alcoholic patients. Alcohol dependence is correlated with a wide spectrum of medical, psychological, behavioral, and social problems.