Alcohol Assignment Complete

Grace Farren
Nutritional Biochemistry
Alcohol Consumption & Metabolism Assignment
1) What many individuals of Asian decent experience is known as the Asian Flush.
This is due to a differentiation in genetic composition of enzymes. In their favor, this
population is seen as being protected from alcoholism due to the enzymatic structure in
their bodies. The specific enzyme that is common amongst people of Korean, Chinese
and Japanese descent is called ADH1B*2, which is a version of alcohol dehydrogenase
(ADH). This enzyme causes acetaldehyde levels to be high and can be considered toxic.
Since this group of people carry ADH1B*2, the acetaldehyde which is converted from
ethanol accumulates during alcohol consumption, and is present in extremely high levels
for this population. The effects of this enzyme caused by increased acetaldehyde levels
can create unpleasant drinking experiences for Asians. Such inconveniences from
drinking can include nausea and a rapid heartbeat. The high levels of acetaldehyde in the
blood can cause impaired contraction to the heart muscle, leading to hyperventilation. In
addition, this enzymatic makeup can also contribute to facial flushing. Acetaldehyde also
attaches to proteins, forming adducts which can potentially alter the protein function and
can induce harmful immune responses. This situation can occur even when moderate
amounts of alcohol are consumed. These symptoms worsen if larger quantities of alcohol
are consumed. Since it is so common for people of Asian decent to experience negative
effects while drinking alcohol, it is less likely for them to become alcoholics. However,
due to environmental factors that influence patterns of drinking, there has been an
increase in Japanese (alcoholic) individuals who carry ADH1B*2 from 2.5% to 13%.
2) Eicoasnoids are a group of lipids made from arachidonic acid. There are three main
types of eicosanoids are: prostaglandins, thromboxanes and leukotrienes (prostaglandins
and thromboxanes are grouped together). Though these lipids are similar to hormones,
they do not travel through the bloodstream. Prostaglandins and thromboxanes regulate the
tightening of smooth muscles, blood platelet agglomeration and gastric secretions.
Prostaglandins and thromboxanes are also known to raise bodily temperatures and lead to
inflammation. Leukotrienes constrict the bronchi and attract immune cells to the site of
injury, allowing for enzyme release. However, the overproduction of leukotrienes can
lead to asthma as well as anaphylactic shock. The over-consumption of alcohol can cause
inflammation and destruction of the mucosa. However, how alcohol corrupts gastric
mucosa has yet to be discovered. Studies show that prostaglandins and leukotrienes may
play a role in mucosal injury occurring from alcohol consumption. Prostaglandins shield
gastric mucosa from destruction by using inhibitors such as Aspirin, which allow the
gastric mucosal barrier to collapse without stopping acid secretion altogether. Extensive
alcohol abuse disrupts the microcirculation of cells in the body and leads to ongoing
damage in the mucosa. Decreased production of prostaglandins also disrupts the mucosa,
leading to alcohol-induced damage. However, studies also show that injured mucosa due
to excessive alcohol consumption may be caused by the overproduction of leukotrienes
because of alcohol dependency, causing allergic as well inflammatory bodily responses.
Because these eicosanoids are being over produced due to excessive alcohol
consumption, toxins are also being increased in circulation. Due to the injured mucosa,
endotoxins, bacterial toxins and other sizable molecules can more easily pass into the
blood or lymph. Toxic substances such as these can have serious detrimental effects on
the liver as well as other organs.
3) Alcoholics and excessive drinkers can take in up to 50% of their calories from alcohol.
Due to excessive alcohol consumption, they have built up a seemingly high tolerance, as
well as possible vitamin and mineral deficiencies (especially Vitamin A) due to the
damage of their mucosal lining. If an individual who was a heavy drinker or former
alcoholic takes time to be sober from drinking, it is most likely that they are going to
have a change in body composition. If an individual consumes large amounts of alcohol,
the ADH reaction is running at a very fast rate, which leads to high levels of NADH. This
means that there is a high ratio of NADH compared to NAD and that affects lipid and
glucose metabolism. The increased NADH levels signal that there is enough energy in the
body. This means that the body can stop oxidizing and that anabolism can take place,
where fat will be created in tissues due to the build up of molecules. When an alcoholic
doesnt drink, the fat can breakdown in response to their lifestyle change. The fat
originally allowed for a high alcohol tolerance since it absorbed most of what was being
consumed. Since there will be less fat, there is going to be a greater reaction to alcohol
when it is consumed again. This can make a person feel like they cant handle their liquor
like they used to.
4) Interior problems related to alcohol are due to alcohol use and are impacted by
differences in alcohol metabolism. Over-consumption of ethanol can cause alcoholism,
which is capable of bringing about pathological transformations. The breakdown of
alcohol occurs through several different processes, the most common of which involving
enzymes alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). These
enzymes metabolize alcohol and enable it to then be eliminated. Alcohol is first
metabolized into acetaldehyde, which is broken down to acetate, which is later
metabolized into H2O and CO2 for successful elimination. Ctyochrom P450 2E1
(CYP2E1) and catalase also work to break alcohol down to acetaldehyde, which is a toxic
carcinogen. CYP2E1, however, is only functional after the excessive consumption of
alcohol. Fatty acids then interact with alcohol to form fatty acid ethyl esters (FAFEEs),
which help to remove trace amounts of alcohol from the body. These compounds have
been known to damage the liver as well as the pancreas. Acetalaldehyde toxicity is
another metabolic effect that shows the detrimental effects of excessive alcohol intake. A
high NADH:NAD+ ratio does as well. The ratio of NADH:NAD+ is elevated by an
increase in the oxidation of ethanol. The rise in NADH concentration signals a metabolic
adjustment toward reduction, which occurs through hydrogenation. This change allows
for a fatty liver to develop in response to the fatty acids produced through anabolic
stimulation. Liver disease, such as fatty liver, occurs in over 90% of people that overconsume alcohol.
5) Over-consumption of ethanol can cause alcoholism, which is capable of bringing about

pathological transformations. The structure of ethanol, CH3-CH2-OH, is similar to that of
a carbohydrate, so after an alcohol binge, hypoglycemia can ensue. Hypoglycemia occurs
when blood glucose levels are below normal, usually 80-90mg/day, as opposed to 120140mg/day, which is the norm in hyperglycemic states. When the body enters
hypoglycemia, glucose is released into the bloodstream by the liver. As a result, muscle
and adipose tissue begin employing fatty acids as energy sources. Since alcohol provides
only empty calories, a term used to refer to foods or beverages with next to no nutritional
value, heavy drinkers can easily become malnourished. Alcohol allows for 7kcal/g, and
increased consumption only further lowers glucose levels. For moderate alcohol
consumers, 10% or less of total energy is taken in. But for alcoholics, up to 50% of total
energy is taken in. Because of this differentiation, the physiological and behavioral
effects of ethanol can be intensified by mass alcohol consumption. Although ethanol is
mainly oxidized in the liver, the rate of metabolism is influenced by many different
factors. Body mass, race, eating habits, gender, and genetic make up greatly influence the
rate of metabolism. The type of alcohol dehydrogenase (ADH) and aldehyde
dehydrogenase (ALDH) in each individual also plays a role in the risk for developing
alcoholism by partly determining how much a person drinks. High amounts of ALDH,
for example, can bring about flushing, heart palpitations and nauseousness, as seen in
people of Asian descent (as detailed in question #1). Because of the decrease in glucose
uptake by the muscles and adipose tissue, the tissues deplete less glucose than usual and
start fatty acid oxidation for energy production. Because fatty acids are used as for
energy, and blood glucose levels are extremely low in hypoglycemic states, behavioral
effects of alcohol consumption are intensified after an alcohol binge.

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Grace Farren

5) Over-consumption of ethanol can cause alcoholism, which is capable of bringing about

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