Essay Color Key

Free Essays
Unrated Essays
Better Essays
Stronger Essays
Powerful Essays
Term Papers
Research Papers




Caffeine

Rate This Paper:

Length: 2039 words (5.8 double-spaced pages)
Rating: Red (FREE)      
- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -

Caffeine


Caffeine is the most-widely consumed psychoactive
substance by human beings throughout the world (Reid, 2005).
This report will detail its natural origins, chemical
structure (as well as those of similar substances), and the
methods and dosages in which it is rendered into its usable
form. Additionally, this report will detail caffeine's various
biological pathways within the human body, including access to
the brain and various neurotransmitter pathways.

Caffeine is a chemical that occurs naturally in over 100
plant species throughout the world (Steffen, 2000). Perhaps
the most widely recognized of these plants is the coffee tree,
whose small seed (commonly referred to as a "bean") is roasted
and then crushed into a fine powder (Weinberg and Bealer,
2001). Caffeine also occurs naturally in cocoa beans, tea
leaves, kola nuts, and gurana seeds, and mate. Some of these
plants, such as tea, actually bear a distinct, but similar
chemical to caffeine (i.e. theophylline); these chemicals will
be discussed further in the chemistry section (Steffen, 2000).

Caffeine is chemically known by two names. The first is
1,3,7 -trimethylxanthine; the second is 3,7,-Dihydro-1,3,7-
trimethyl-1H-purine-2,6-dione. Historically, caffeine has also
gone by the name of methyltheobromine, as well as thein
(Weinberg and Bealer, 2001). The chemical formula of caffeine
is C8 H10 N4 O2. The molecular weight for this chemical is
194.19 atomic units. Its composition is as follows: 49.5
percent carbon, 5.2 percent hydrogen, 28.9 percent nitrogen,
and 16.5 percent oxygen. Caffeine melts from a solid hexagonal
crystal at 238 degrees Celsius (Karch, 1993).

Caffeine is a methylated purine derivative and is
classified as an alkaloid. An alkaloid is a class of organic
compounds composed of carbon, hydrogen, and nitrogen; oxygen
is usually found amongst these compounds. The term "alkaloid"
refers to compounds that can be extracted from plants, and
whose salts can be crystallized. Other alkaloids include
cocaine, serotonin, and the hallucinogenic compound, LSD. A
purine is a base compound, consisting of a six-membered and
five-membered nitrogen containing ring fused together; other
examples of purines include adenine and guanine, two bases
found in human DNA (Angstadt, 1997). The term "methylated"
refers to the fact that hydrogen atoms upon the compound have
been replaced with a methyl (CH3) compound (Methylation,
2005).[See figure 3]

Caffeine is often served within hot beverages, such
as coffee or tea. In the case of the latter, the coffee bean
is ground up into a coarse powder, which is used as a filtrate
for hot water (Weinberg and Bealer, 2001). Hot water can also
be passed through tea leaves. At hot temperatures, such as
those found within serving temperatures of coffee and tea,
provide for the complete solubility (Weinberg and Bealer,
2001). Caffeine can also be found in solid food substances
such as chocolate and gurana fudge (Steffen, 2000).Certain
soft drinks and so-called "energy" drinks also contain
caffeine additives (Reid, 2005). All of the above substances
are ingested orally. The percentage of caffeine in the above
substances varies. In coffee, for example, caffeine composes
1.34% of the drink by weight; in tea, this number is 3.24%
(Weinberg and Bealer, 2001). Chemical extraction of caffeine
from roasted coffee beans yields between 8 and 20 milligrams
(mg) of caffeine per gram (g) of coffee beans (Karch, 1993).

Human consumption varies across demographic
characteristics, especially nationality. In the Scandinavian
countries, such as Norway and Denmark, the average daily
consumption of caffeine for a 60-70 kilogram (kg) subject 7.0
milligrams (mg) per kilogram of body mass; in American and
United Kingdom subjects, this daily average is between 2.4
mg/kg and 4.0 mg/kg of body mass. In Denmark, the mean daily
intake for children under the age of 18 years is 2.5 mg/kg of
body mass, and in the United States, this number is 1.0 mg/kg.
(Nehlig, 2000)

There is considerable variation amongst persons in
terms of bodily concentrations of caffeine (Weinberger and
Bealer, 2001). In an experiment in which the participants each
consumed 568 milliliters (ml) of coffee, peak blood levels of
caffeine were reached between 15 and 45 minutes after
ingestion; the amount of caffeine present per liter of blood
was 5.3 micrograms (Marks and Kelly, 1973, as cited in Karch,
1993). The half-life of caffeine in the body varies as well:
in healthy adults, the half-life of caffeine is 3.5 hours on
average, in pregnant women, the half life of caffeine up to 18
hours, and in term infants, the half life of caffeine is 82
hours. Additionally, other substance use factors, such as the
ingestion of alcohol or tobacco products can significantly
impact the half-life of caffeine within human blood. (Weinberg
and Bealer, 2001). Eventually, the caffeine is metabolized
by the liver, where, according to Weinberg and Bealer (2001),
it is either "demethylated" into dimethylxanthine and
monoethylxanthine, or oxidized and converted into uric acid,
and eventually excreted in the urine.

NEUROLOGICAL PATHWAYS OF CAFFEINE:

Caffeine acts upon the human central nervous
system (Spiller, 1998). The central nervous system encompasses
the brain and the spinal cord (Kalat, 2001). Caffeine is
designated as a stimulant drug; according to Kalat, stimulants
produce "…excitement, alertness, elevated mood, decreased
fatigue, and sometimes increased motor activity (2001, p.
70)." Indeed, many people report using caffeine, often in the
form of coffee or other beverages, as a means of staying alert
during activities requiring intense concentration (Reid,
2005). Additionally, caffeine also works as a vasoconstrictor
within the brain, causing the blood vascular to constrict
whilst increasing the overall heart rate (Kalat, 2001). The
subsequent vasodilation occurring upon withdraw of caffeine
from the brain may be responsible for the severe headaches
endured by habitual users (Spiller, 1998)

The following sections will detail the effects of
caffeine upon the neurotransmitters adenosine, dopamine, and
serotonin, respectively:

CAFFEINE AND ADENOSINE:

Over the years, there have been competing reports
of the action of caffeine upon brain physiology (in example,
see Weinberg and Bealer, 2001). Theories included caffeine as
means of increasing calcium secretion of neurons, as calcium
is a necessary agent for nervous impulse transmission (Myers,
Johnson, and McVey, 1999). Another theory posited that
phosphodiesterase became inhibited by caffeine (Spiller,
1999). At the present time, both of these theories have been
more or less abandoned, mainly along the lines that the
dosages required of caffeine to activate these systems are so
large that ingestion would most likely yield lethal effects
(Weinberg and Bealer, 2001; see also Nehlig, 2000).
Researchers now look to the neuromodulator adenosine as the
molecule that plays a direct role in the neurological effects
associated with caffeine (Weinberg and Bealer, 2001).

Caffeine works directly upon the neuromodulator
adenosine as an antagonist (Daly et al, 1999). An antagonist
is a chemical that blocks the effect of a neurotransmitter
(Kalat, 2001). During metabolic activity, adenosine
monophosphate breaks down into adenosine. Adenosine inhibits
the brain's arousal system by binding to receptors in the
basal forebrain, an area responsible for wakefulness. As a
person goes about the day, adenosine accumulates; at high
enough levels, the adenosine inhibits the arousal centers and
induces sleepiness. (Kalat, 2001)

Caffeine binds with presynaptic adenosine receptors
(Daly et al, 1999). The primary molecular sites for the action
of caffeine are A1 and A2a receptors; these are high affinity
and low affinity receptor, respectively (Myers, Johnson, and
McVey, 1999). Adenosine mediates the release inhibition of
various neurotransmitters, including serotonin, dopamine,
glutamate, GABA, and acetylcholine. These neurotransmitters
are instrumental themselves in mediating alertness, sleep
cycles, attention, and memory, to name a few (Weinberg and
Bealer, 2001). The next two sections will briefly discuss the
inhibition of adenosine upon the neurotransmission of
serotonergic and dopaminergic pathways.

CAFFEINE AND THE DOPAMINERGIC PATHWAYS

Dopamine is a catecholamine neurotransmitter,
meaning that it is composed of a catechol and an amine group
compound (Kalat, 2001). Dopamine is often found in
reinforcement and reward pathways, hence its designation as a
"pleasure" molecule (Kalat, 2001). In a study involving rats,
caffeine was administered to two different dopaminergic
pathways (Nehlig, 2000). Regarding the first of these
pathways, the nigrostriatal dopaminergic system, caffeine was
found to activate a structure known as the caudate nucleus,
inducing dopamine release by modifying the spontaneous
electrical activity of the neurons within this structure.
Dopamine release in the nigrostriatal system accounts for the
stimulant effects of caffeine on locomotor activity (Nehlig,
2000).

The second dopaminergic pathway in the Nehlig
study, the mesolimbic dopaminergic system, has been studied as
a possible site for the formation of a physical dependency on
caffeine; it should be noted, though, that the issue of
caffeine and dependence is somewhat controversial (2001; see
also Weinberg and Bealer, 2001, and Spiller, 1999). This
system originates in the ventral tegmental area of the
midbrain, "…projects into the nucleus accumbens, and
terminates in the medial prefrontal cortex ( Nehlig, 2000,
p.50)." The nucleus accumbens is divided into a core and a
shell unit. The medioventral shell is thought to be a key
component of emotional, motivational, and reward functions;
the laterodorsal core regulates somatomotor functions. Other
stimulants, such as nicotine and cocaine, selectively
activate dopamine release within the shell; caffeine, however,
does not display any similar stimulation of dopamine release
at a normal dosing level of 0.5 to 5 mg/kg. In fact,
activation of the nucleus accumbens occurs only at high doses
(i.e 10 mg/kg), an amount 4 to 5 times greater than the
average adult American's daily consumption. (Nehlig, 2000)

CAFFEINE AND SEROTONERGIC PATHWAYS

Serotonin is a 5-HT indoleamine neurotransmitter;
amongst other attributes, serotonin is known for its influence
upon arousal and sleep activity (Kalat, 2001). Serotonergic
neuron cell groupings play a part in the regulation of sleep,
mood, and general well being (Nehlig, 2000). At low-to-medium
doses, caffeine stimulates electrical activity in reticular
formation neurons, as well as lowering electrical activity in
the thalamus, a site known to be connected with caffeine-
induced arousal (Nehlig, 2000). Serotonin availability is also
reduced by medium levels of caffeine, which in turns reduces
the sedative effects of the neurotransmitter at the
postsynaptic level (Myers, Johnson, and McVey, 1999). This can
lead to an interference of the sleep cycle, as well as changes
in motor function (Nehlig, 2000). Additionally, caffeine has
been shown to induce serotonin release in the cerebellum and
cerebral cortex (Spiller, 1998).

CONCLUSION:

Caffeine and its methylxanthine relatives compose
the most widely used psychoactive substances in the world.
This widely available drug can be found in beverages such as
coffee and tea, and in foods like chocolate. Much research
exists describing its chemical and molecular properties, as
well as its human dosing information. Caffeine works directly
upon the neuromodulator adenosine; this effect subsequently
influences the neurotransmission of hormones and
neurotransmitters, such as dopamine and serotonin. As more
research unfolds regarding neurological physiology and
chemistry, the scientific community will no doubt discover
many more facets of the workings of caffeine.

WORKS CITED

Angstadt, C. (1997). Purines and pyrimidine metabolism.
Retrieved March 6, 2005 from Net Biochem
website:http://wwwmedlib.med.utah.edu/NetBiochem/pupyr/pp.htm.

Daly, J., Shi, D., Nikodijevic, O., and Jacobson, K. (1999).
The role of adenosine receptors in the central action of
caffeine. In B. Gupta and U. Gupta (Eds.), Caffeine and
behavior: Current views and research trends (p.1-16). New
York: CRC Press.

Kalat, J. (2001). Biological psychology,7th ed.. Belmont:
Wadsworth-Thompson.

Karch, S. (1993). The pathology of drug abuse. Boca Raton: CRC
Press.

Methylation (2005). Retrieved March 6, 2005 from Wikipedia,
the Free Encyclopedia website:
http://en.wikipedia.org/wiki/Methylation.

Myers, P., Johnson, D., and McVey, D. (1999). Caffeine in the
modulation of brain function. In B. Gupta and U. Gupta (Eds.),
Caffeine and behavior: Current views and research trends
(p.17-30). New York: CRC Press.

Nehlig, A. (2000). Caffeine effects on the brain and behavior:
a metabolic approach. In H. Parliament, C.Ho, and P.Schieberle
(Eds.), Caffeinated beverages: Health benefits, physiological
effects, and chemistry (p.46-53). Washington, D.C: American
Chemical Society.

Spiller, G. (1998). Basic metabolism and physiological effects
of the methylxanthines. In G. Spiller (Ed.), Caffeine (p.225-
231). New York: CRC Press.

Steffen, D.(2000). Chemistry and health benefits of
caffeinated beverages: symposium overview. In H. Parliament,
C.Ho, and P.Schieberle (Eds.), Caffeinated beverages: Health
benefits, physiological effects, and chemistry (p.2-8).
Washington, D.C: American Chemical Society.

Reid, T. (2005). Caffeine: What's the buzz? Why we love
caffeine. National Geographic, 207, 1, p.2-33.

Weinberg, B., and Bealer, B. (2001). The world of caffeine:
The science and culture of the world's most popular drug. New
York: Routledge.

How to Cite this Page

MLA Citation:
"Caffeine." 123HelpMe.com. 01 Oct 2014
    <http://www.123HelpMe.com/view.asp?id=33320>.




Related Searches





Important Note: If you'd like to save a copy of the paper on your computer, you can COPY and PASTE it into your word processor. Please, follow these steps to do that in Windows:

1. Select the text of the paper with the mouse and press Ctrl+C.
2. Open your word processor and press Ctrl+V.

Company's Liability

123HelpMe.com (the "Web Site") is produced by the "Company". The contents of this Web Site, such as text, graphics, images, audio, video and all other material ("Material"), are protected by copyright under both United States and foreign laws. The Company makes no representations about the accuracy, reliability, completeness, or timeliness of the Material or about the results to be obtained from using the Material. You expressly agree that any use of the Material is entirely at your own risk. Most of the Material on the Web Site is provided and maintained by third parties. This third party Material may not be screened by the Company prior to its inclusion on the Web Site. You expressly agree that the Company is not liable or responsible for any defamatory, offensive, or illegal conduct of other subscribers or third parties.

The Materials are provided on an as-is basis without warranty express or implied. The Company and its suppliers and affiliates disclaim all warranties, including the warranty of non-infringement of proprietary or third party rights, and the warranty of fitness for a particular purpose. The Company and its suppliers make no warranties as to the accuracy, reliability, completeness, or timeliness of the material, services, text, graphics and links.

For a complete statement of the Terms of Service, please see our website. By obtaining these materials you agree to abide by the terms herein, by our Terms of Service as posted on the website and any and all alterations, revisions and amendments thereto.



Return to 123HelpMe.com

Copyright © 2000-2014 123HelpMe.com. All rights reserved. Terms of Service