Most people drink alcoholic beverages without actually knowing what happens to it as it enters into their body. "A hangover" is a common thing alcohol drinkers know, or maybe they have heard that it is the culprit of many car accidents, some liver problems, and a bulging stomach. What really happens to the alcohol in your alcoholic beverages as you suck and empty its bottle?
Yes! A Hangover
A hangover is not what alcohol drinkers want when they drink alcohol. What most people want is to enjoy, to socialize, or to be satisfied. How about a hangover? Is it the satisfaction we get from drinking alcohol? Let us see.
What is really a hangover?
A hangover is a state of being ill where the person experiences a set of symptoms after drinking heavily. This set of symptoms may include a combination of the following: sweating, increased pulse rate, elevated blood pressure, vomiting, nausea, stomach ache, muscle ache,fatigue, sensitivity to light, decrease attention and concentration,depression, anxiety, and irritability. ( Insel et al., 2004).
Alcohol Disappearing from the Mouth: Absorption in the G.I Tract
Your body loves it, for about 80 to 95% of alcohol is absorbed unchanged by the gastrointestinal (G.I.) tract. Absorption of alcohol starts in the mouth and esophagus, and it continuous to the stomach, and to the small intestine where major absorption happens. Alcohol goes to the liver via the hepatic portal vein, where it is acted upon in order to get rid of it. Oh no! Your body does not actually love it. It is a poison and can damage cells and organs.
Get Rid of That Poison: “My call” Says the Liver
What the liver does to the alcohol depends on how much alcohol you load on it.
Small to moderate amount of alcohol. Generally, alcohol in the liver is converted to a more toxic substance called acetaldehyde. This conversion is hastened by the presence of a biological catalyst (enzyme) called alcohol dehydrogenase (ADH).
FUNNY isn’t it? To detoxify your body from alcohol it has to convert it to a more toxic substance. Is it detoxification or suicide? Wait, the story does not end here.
The liver detoxifies the body further by converting the acetaldehyde into acetate and into acetyl-CoA. This detoxification is hastened by the enzyme acetaldehyde dehydrogenase (ALDH). Another enzyme, acetylCoA synthase, is responsible for converting acetate to acetylCoA.
Acetaldehyde + NAD+ + CoA ↔ Acetyl-CoA + NADH + H+
The conversion of alcohol to acetaldehyde requires the reduction of nicotinamide adenine dinucleotide (NAD+)into its reduced form NADH.
Large Excessive Amount of Alcohol. “It is too much,” says ADH enzyme. ADH cannot anymore cope with catalyzing the large amount of alcohol so the excess alcohol goes in another direction (metabolic pathway) called microsomal ethanol-oxidizing system (MEOS). In this system, the alcohol is still converted into acetaldehyde but instead of the required reduction of NAD+ to NADH, oxidation of nicotinamide adenine dinucleotide phosphate(NADPH) to NADP+ occurs. This process is catalyzed by the CYP2E1 enzyme (a part of cytochrome P450 enzyme family) instead of the aldehyde dehydrogenase (ALDH). The increase in MEOS activity stimulates the production of CYP2E1 (Lieber, 2004 in Wikipedia). The MEOS pathway is flexible, as it can increase its processing speed when needed so as its capacity in order to accommodate a larger amount of alcohol leading to an increase in alcohol tolerance. Indeed, a less experienced one gets drunk easily than the more experienced drinker.
Watch Out with Those Drugs
MEOS is also the pathway where drugs are metabolized, and unwanted chemicals are detoxified. The danger is that chronic alcohol drinkers seem to activate the enzymes involved in this system converting the pain reliever, acetaminophen, into a toxic chemical that can damage the liver. PAIN RELIEVER AND ALCOHOL- A BAD COMBINATION.
Actually, pain relievers are just one of the many drugs that interact with alcohol. Alcohol can interact with medication in many ways: alcohol affects the extent in which drug reaches its site of action; it inhibits drug metabolism by competing with drug for the same enzyme; and it activates drug metabolizing enzymes that alters the effect of drugs, activates enzymes that can convert the drugs into toxic chemicals, and magnifies the inhibitory effects of sedatives or narcotics in the brain (NIAA, 1995).
These drugs that interact with alcohols are anesthetics, antibiotics, anticoagulants, antidepressants, antidiabetic medication, antihistamine, antipsychotic medication, antiseizure medication,antiulcer medication, narcotic and non-narcotic pain reliever, sedative and hypnotic medications. For details, I will direct you to the site by NIAAA.
http://pubs.niaaa.nih.gov/publications/aa27.htm or google: "Alcohol-Medication Interactions Alcohol Alert No. 27-1995")
What About that Bulging Belly?
Synthesis of fatty acids (lipogenesis) happens in the cytosol. This process is enhanced by chronic alcohol intake. Fatty acids and glycerols in the body are assembled into FAT. Men are more likely to have a bulging belly than women. Women store fat more on their hips and thighs than in their belly.
As commonly known, when there are excess available ATP’s and building materials in the body, lipogenesis is favored so as FAT storage. Calorimetric analysis proved that alcohol produces energy of about 7 kcal/g. If we limit the definition of nutrient as to production of energy, alcohol qualifies as a nutrient, but as to the factor that regulates needed chemical reactions in the body to maintain health, alcohol is not a nutrient since alcohol does not provide the essential functions in the body (unless its functions that promote euphoria in small doses, as depressant, etc; its being addictive and withdrawal symptoms are considered essential functions)
As mentioned, alcohol in the liver is converted to acetaldehyde; then to acetate, to acetyl-CoA. Acetyl-CoA can either go into two pathways: production of fatty acids (lipogenesis) or production of energy (ATPs) via citric acid cycle (Kreb’s cycle). Both the citric acid cycle and the conversion of acetaldehyde to acetyl-CoA require the reduction of NAD+ to NADH. So that there is competition in the use of NAD+ in these two processes. If there is a shortage of NAD+ there is now the question as to which process will prevail. Well, the body chooses wisely in favor of detoxification/conversion of acetaldehyde to acetyl-CoA over the production of ATP’s. In this manner, the pathway going to the citric acid cycle is slowed down favoring lipogenesis Then, the fatty acids and glycerols are assembled into fats in the endoplasmic reticulum. Fat, Fat. Fat.
Another finding by Min You, et al (2009) suggests that ethanol induces fatty acid synthesis pathway by activation of the Sterol RegulatoryElement-Binding Protein (SREBP). SREBP is a transcription factor that binds with DNA and can trigger the synthesis of enzymes that indirectly favor lipogenesis.
What is Worse than a Bulging Belly?
WARNING: "A person with liver cirrhosis has 50% chance of death within 4 years"(Wardlaw, 2000, p. 501)
Increased synthesis of fatty acids can lead to the condition called hyperlipidemia (Jone, PJ et al., 1992). With this condition, fats may accumulate in the liver leading to a condition called fatty liver (Assy N, et al., 2000). When the fats in the liver block/interfere with the blood supply of oxygen and nutrients, cells in the liver can die and be replaced with scars (connective tissues) preventing the liver to do its normal functions in this condition called liver cirrhosis.
YES! ALCOHOL WILL JUST DISAPPEAR IN YOUR SYSTEM BUT NOT WITHOUT A PRICE. SO WATCH OUT!!!! ARE YOU THE CULPRIT OR THE VICTIM?
Assy N., et al.(2000). Fatty infiltration of liver in hyperlipidemic patients. US National Library of Medicine, National Institute of Health. Retrieved on March 14, 2013 from PubMed.gov http://www.ncbi.nlm.nih.gov/pubmed/11117562
Insel,P., et al. (2004). Nutrition2(nd ed.)40 Tall Pine Drive Sudbury: Jones and Bartlett
Jones, PJ., et al. (1992).Cholesterol and triglyceride fatty acid synthesis in a polipoprotein E2-associated hyperlipidemia. US National Library of Medicine, National Institute of HeaLTH. Abstract retrieved March 24,2013 from PubMed.gov http://www.ncbi.nlm.nih.gov/pubmed/1731853
Lieber,C. (2004). TheDiscovery of the microsomal ethanol oxidizing system and its
physiologicand pathogenic role. Drug Metabolism Reviews 36:511-529 .Retrieved March 23,2013 from www.wikepedia.com.Retrieved .
MinYou, et al (2009) Ethanol induces fatty acid synthesis pathway by activation of
sterol regulatory element-binding Protein (SREBP).
MolCell Biol. 2009 November; 29(21): 5974. Abstract retrieved March 23, 2013
National Institute on Alcohol Abuse and Alcoholism ( 1995, January) Alcohol Alert
No.27 PH 355- 1995. Retrieved March 23, 2013 from NIAAA website http://pubs.niaaa.nih.gov/publications/aa27.htm
NIAAA(updated Oct. 2000). Understanding the impact of alcohol on human health
and well being. US Department of Health and Human Services. Retrieved on March 23,2013 from pubs.niaaa.nih.gov/publications/aa27.htm.
StylerL. (1988). Biochemistry,3rd ed.New York: W.H. Freeman and Company
Wardlaw,G. (2000). Contemporary nutrition issues and insights, 4thed.USA:
MY STUDENT CONTRIBUTION
In my chemistry class when the topic is alcohol, I use this article as reading material for my student to understand the fate of alcohol in the human body. To ensure their understanding of the topic I let my students diagram the fate of alcohol in the body based on the article above. Refer to my article "Assessing Student's Understanding of a Science Article Through Diagramming."