Alcohol: A pharmacological approach 


History
By Jenna Devoid
 
"Virtually all cultures-whether hunter-gatherers or 
farmers; whether technologically advanced or primitive-share two 
universals: the development of a noodle and the discovery and 
use of the natural fermentation process (1)."
	Alcohol and humans share a long and sordid story.  The tale 
reveals a great deal about people and how we have developed and 
evolved as a culture.  Filled with the drama and twists of a 
soap opera, the story includes politics, religion, philosophy, 
psychology, medicine and social evolution.  
 The story begins 10,000 to 15,000 years ago, when alcohol 
use by humans is thought to have begun (1).  Alcohol is a 
naturally occurring process; airborne yeasts ferment sugars into 
alcohol in rotting fruit (3).  Primates are known to eat rotting 
fruit for its intoxicating effects and it is thought that humans 
got the idea from them and decided to try it out for themselves 
(1).
There is a strain of belief among anthropologists that 
mead, as "beer" was formerly known, is responsible for the 
development of civilization.  The idea is that in order to 
process alcohol, one necessitates a stable location (1).  Other 
accounts assert that agriculture would have needed to predate 
brewing due to a lack of naturally occurring sugars that are 
needed to produce alcohol on a larger scale (3). The ancient 
Greeks, Celts, Norse, Summerians, Egyptians and Babylonians have 
all documented the production and use of alcohol (4).  
The pervasive use of alcohol in ancient times had a 
utilitarian source, the lack of clean drinking water made 
alcohol use a matter of health.  In fact, the first beer used as 
a matter of practice (approximately around 8,000 B.C.), was very 
thick and nutritious with many needed vitamins and amino acids 
(1).  Alcohol has also had an important place in human cultures.  
The Greeks and Romans had Dionysus and Bacchus (respectfully), 
the god of wine, who they worshiped in an "orgy of intoxication" 
(4).  Alcohol has been involved throughout human history with 
burials, settling disputes, offering courage in war, 
celebration, consummating settlements and "seducing lovers" (4).
What seems evident is that as long as alcohol has been 
enjoyed by humans, it has also been the source of social 
problems.  In the world's very first legal text, developed by 
the Babylonians, regulations and laws for imbibing houses are 
present and their texts reveal societal problems caused by 
drunkenness (3).  Ancient Egyptian (4), Roman and Greek texts 
also includes warnings and concerns surrounding alcohol (3).  
Before and into the Middle Ages brewing was traditionally 
done primarily by women, as beer was considered a food.  In the 
middle ages superstitions were rampant and failures with the 
process of brewing would be blamed on "brew witches" and the 
devil.  Brew witches were burned for their infractions, with the 
last known burning occurring in 1591.  Monks were also avid 
brewers.  It was brewed to sell and also for personal 
consumption.  Beer added some flavor to an otherwise bland diet.  
It was allowed during the monks' fasts, offering nutrition; 
historical accounts find that each monk was allotted 5 liters of 
beer a day (4).  
Prohibition first reared its head in the 17th century.  The 
Plymouth Colony regulated the "sale of spirits" to no "more than 
2 pence worth to anyone but strangers just arrived" in 1633.  
Many early colonial writings reveal attempts at regulation of 
excessive alcohol use in members of the community.  This was in 
response to the unattractive behavior it inspired in community 
members such as ministers and the dangerous behaviors it evoked 
in Natives (2).  It was also around this time and into the next 
century that alcoholism gained understanding as a disease rather 
than a moral failing by the health community (5).
By the 18th century a new incentive to regulate alcohol 
became apparent: money.  For the first time in history alcohol 
manufacturing, importation, selling and consumption met 
prohibitions.  Regulation focused on fines, taxes and fees for 
licensing.  There were fines for selling alcohol to Natives, 
drunken behavior, and production without a license (2).
The New England Federalists fountainheaded the early 
temperance movement.  The first to assert the health benefits of 
temperance was Nathanial Ames in 1752 in an almanac wherein he 
wrote: "Strong Waters were formerly used only by the Direction 
of Physicians; but now Mechanicks and low-li'd Labourers drink 
Rum like Fountain-Water, and they can infinitely better endure 
it than the idle.  Unactive and sendentary Part of Mankind, but 
DEATH is at the bottom of the cup of every one (2)."  Also 
emerging as a strong voice in this movement was Benjamin Rush 
who was one of the first voices disputing the common belief in 
the medicinal benefits of alcohol (4).  He defined the symptoms 
of alcohol use as "unusual garrulity, unusual silence, 
captiousness…an insipid simpering…profane swearing…certain 
immodest actions [and] certain extravagant acts which indicate a 
temporary fit of madness" in 1785 (2). Despite the voices of 
temperance emerging, little if any effect has been found to have 
occurred at that time.
In 1791 the Revenue Act was passed by Alexander Hamilton 
which included a tax on distilled liquors.  This incited the 
Whisky Rebellion which was composed mostly of angry farmers in 
the Western part of Pennsylvania.  They mobbed collectors of the 
taxes and it eventually took 15,000 militia to control the armed 
farmers(2).  Around this time religious organizations began to 
come out against the sale and use of alcohol, including the 
Methodists, Presbyterian Synod of Pennsylvania and the Yearly 
Meeting of Friends of New England (2).  
In 1826 The American Temperance Society (later the American 
Temperance Union) was born and by 1835 there were 8,000 local 
groups.  In 1842 The Sons of Temperance came to be.  Both called 
for total abstinence from alcohol (2).  The first prohibition 
law was passed shortly after in 1851 in Maine, followed by 
twelve other states (3).  Between 1863 and 1868 the liquor and 
beer tax rose from 20 cents to two dollars per gallon.  However, 
the revenue taken in did not increase, as fraud and loophole 
enactment was rampant.  In 1869 the tax was reduced to fifty 
cents per gallon and revenue increased from 13.5 million dollars 
in 1868 to 45 million dollars in 1869 (2).
In 1869 the National Prohibition Party was formed, which 
won a seat in the House of Representatives in 1890 (3).  Three 
years later the Anti-Saloon League was formed (3).  This group 
would later be called "the most dangerous political movement 
that this country has ever known".  It asserted that "liquor is 
responsible for 19% of the divorces, 25% of the poverty, 25% of 
the insanity, 37% of the pauperism, 45% of child desertion, and 
50% of the crime in this country…and this is a conservative 
estimate (2)."
As the 19th century turned into the 20th century a great deal 
of social change was taking place in the United States.  In the 
1870's the feminist movement which had begun in the early part 
of the century began to add their voices to the temperance 
movement.  This was marked by the development of the Women's 
Crusade (b. 1873) and the Women's Christian Temperance Union (b. 
1874).  The latter saw the issue as crucial to creating equality 
between the sexes.  The leader Frances E. Willard asserted, 
"Drink and tobacco are the great separatists between men and 
women.  Once they used these things together, but woman's 
evolution has carried her beyond them; man will climb to the 
same level…but meanwhile…the fact that he permits himself fleshy 
indulgence that he would deprecate in her, makes their planes 
different, giving her an instinct of revulsion (2)."
By 1902 the temperance movement was beginning to have an 
impact.  In public schools "temperance education" was 
implemented, texts as rich with misinformation as facts were 
used (2). But it was the labor unions, motivated by impairment 
of workers that are cited as contributing the most to the 
temperance movement (2).
It became clear that an individual was either for or 
against prohibition, with little to no room between these 
polarities.  Workers viewed the fight for prohibition as 
paternalistic and resented the judgment towards themselves and 
their behaviors (2). 
National prohibition, known as the Volstead Act or the 18th 
Amendment, was instated from 1913 to 1933, a result of an 
amalgamation of strength gained in the temperance movements, the 
war and the pairing of alcohol with immigrants in a time of 
rigid patriotism (2).  However, the prohibition has been 
considered a failure due to bootlegging.  Speakeasies were 
numbered at 200,000 to 500,000 throughout the United States.  In 
1928 doctors earned $40 million dollars writing prescriptions 
for whiskey (2).  Indeed, there was a great deal of money to be 
made bootlegging, Al Capone's annual gains from bootlegging were 
estimated to be at $60 million (3)! Sacramental wine was exempt 
from the Volstead Act and suspicious amounts of wine were 
consumed via the churches.  Also, the age at which folks started 
to drink dropped during prohibition (see figure below)(2).
Period            Males             Females 
1914              21.4              27.9
1920-23           20.6              25.8
1936-37           23.9              31.7

Essentially, "prohibition destroyed the manufacturing and 
distributive agencies through which the demand for liquor had 
been legally supplied.  But the demand remained (2)."
When Roosevelt and a "wet" Congress were voted into office 
in 1933 the repeal amendment hit the floor February 14, 1933 and 
passed two days later 63 to 23.
Altho alcohol's popularity in American society peaked 
around 1830, and per capita estimates of use have dropped from 
2.76 gal. of pure alcohol in 1980 to 2.35 gal. in 1996, it 
remains a popular part of the culture and part of a societal 
problem.  Ten percent of users of alcohol account for 50% of 
alcohol consumed (1).  

References

1.Doweiko, H.E. (2002).  Concepts of Chemical Dependency, 
5th ed. Brooks/Coles.
2. History of Alcohol Prohibition (n.d.).  Retrieved April 2, 
2005 from http://www.druglibrary.org/schaffer/Library/studi
	es/nc/nc2a.htm.
3. Alcohol in History (n.d.). Retrieved April 2, 2005 from
	http://www.ephidrina.org/alcohol/history.html.
4. The History of Alcohol (n.d.). Retrieved April 2, 2005
	From http://www.drug-rehab.org/alcoholhistory.php.
5. Waguespack, R.S.  A History of Drug Use, Abuse and 
Addiction: History of Alcohol (n.d.).  Retrieved April 2, 
2005 from http://www.adjunctcollege.com/Unit_2_Summary.
html.

Route access, neurotransmitters and ion channels
By Joanna Rocco

The chemical formula for alcohol or ethanol is C2 H5 OH.  
Alcohol is the most popular and widely used drug in today's 
society.  It is usually consumed as a beverage and so enters the 
body orally.  From the mouth it travels to the stomach where 20% 
of the alcohol is absorbed.  It then moves on to the small 
intestine where 80% is absorbed.  The alcohol will circulate in 
the blood stream until it is metabolized by the liver.  The 
alcohol molecule is extremely small.  It is very water soluble 
and somewhat soluble in fats or lipids.  Due to its small size 
and solubility the alcohol molecule moves freely throughout the 
body and easily crosses the blood brain barrier (Palfai & 
Jankiewicz, 2001).	
Alcohol is a powerful substance that affects the brain in 
many ways.  Alcohol does not have a specific neurotransmitter 
binding site in the brain, but rather involves complex 
interactions in various parts of the brain. In order to see how 
alcohol may affect the human brain, researchers have mapped 
alcohol induced changes in rat brains.  Low doses of alcohol 
created changes in the neocortex, hippocampus and hypothalamus.  
This would account for some of the reinforcing properties of 
alcohol as well as some of the negative effects.  It is 
theorized that continued exposure to alcohol may change neuron 
functioning and receptors in the hippocampus and the 
hypothalamus (Ryabinin, Criado, Heniksen, Bloom, & Wilson, 1997.
It is still being researched whether or not alcohol alone 
can cause brain damage.  The brains of alcoholics do show a 
reduction in brain size and some permanent loss of white matter.  
There also appears to be the loss of neurons in the frontal 
cortex, hypothalamus and cerebellum.  Loss of a certain amount 
of functioning and cognitive ability in long term drinkers may 
be related to brain damage, dendritic and synaptic changes, and 
significant receptor and transmitter alterations (Harper, 1998).
As a drug, alcohol is classified as a depressant.  Alcohol 
slows down brain activity by reducing excitatory actions of the 
neurotransmitter glutamate and raising the inhibitory actions of 
gamma aminobutyric acid or GABA. Alcohol can also activate or 
stimulate serotonin receptor subtypes which stimulate production 
of dopamine and subsequent release of DA by the nucleus 
accumbens region of the brain.  Dopamine is involved in complex 
motor activities (think of someone who's had too much to drink 
stumbling around). Dopamine and the nucleus accumbens both play 
important roles in reward and motivation, two key components of 
addiction (Charness, 1990).
Alcohol also affects serotonin (5 HT) levels in the blood.  
Serotonin plays an important role in emotion, attention and 
motivation.  It is not known specifically if alcohol increases 
serotonin release or inhibits its uptake, only that there are 
higher levels of serotonin in the blood after drinking even a 
small amount of alcohol.  Alcohol also disturbs the serotonin 
receptor's ability to work properly.  There are certain 
serotonin receptor subtypes that seem to be influenced by 
alcohol.  5 HT1A may direct behaviors related to the consumption 
of alcohol.  5 HT1B seems to be a factor in intoxication and 
tolerance.  5 HT2 may play a part in reward and withdrawal. 5 
HT3 seems to have a role in the rewarding effects of alcohol.  
Rats selectively bred to prefer alcohol have lower levels of 
serotonin than normal rats, suggesting that alcoholics may be 
trying to raise or normalize their own serotonin levels by 
drinking (Lovinger, 1999).
	Alcohol affects NMDA and GABA receptors, which in turn 
activate ion channels.  This is one of the primary ways in which 
alcohol impacts the nervous system.  Ion channels play a role in 
stimulating activity at the neuronal synapse and by creating 
action potentials.  When one ingests alcohol, GABA and NMDA open 
a pore or ion channel in the cell membrane which allows 
electrically charged atoms to enter and affect the cell's 
balance. Alcohol causes intoxication and incoordination by 
inhibiting these NMDA glutamate ion channels.  Euphoria and 
sedation are contributed to by alcohol's effect on gycine, 
nicotinic, cholinergic and sertotonergic ion channels (Crews, 
Morrow, Criswell, & Breese, 1996).
	At the site of the ion channels alcohol alters neuronal 
calcium transport.  Once the calcium is elevated within the 
neuron, transport of calcium is inhibited.  GABA activated 
chloride channels are also sensitive to alcohol.  If one takes 
drugs that stop the action of alcohol on chloride channels, 
intoxication is reduced. Alcohol, as well as other drugs that 
cause intoxication, hinder the flow if sodium through synaptic 
membrane channels. Lastly, alcohol augments calcium activated 
potassium channels which have an inhibitory impact (Harris & 
Allan, 1989).  
	Alcohols effect on the body's systems is incredibly 
complex.  Alcohol affects brain processes such as attention, 
memory and mood.  Excessive use of alcohol can also create 
dependence and withdrawal.  Alcohol interacts with many 
neurotransmitter systems and upsets the brain's subtle balance 
between inhibitory and excitatory neurotransmitters.  Inhibitory 
neurotransmitters reduce sensitivity of other neurons to 
additional stimulation and excitatory neurotransmitters produce 
a converse effect.  This delicate balance is necessary for 
normal functioning.  Long term ingestion of alcohol can also 
change neurotransmitter systems, eventually leading to craving 
and alcohol seeking behavior (Valenzuela, 1997).

References

Charness, M.E. (1990). Alcohol and the brain. Alcohol Health and 
Research World, 14, 85-89.

Crews, F.T., Morrow, A.L., Criswell, H., & Breese, G. (1996). 
Effects of ethanol on ion channels. International Review of 
Neurobiology, 39, 283-367.

Harper, C. (1998). The neuropathology of alcohol specific brain 
damage, or does alcohol damage the brain? Journal of 
Neuropathology and Experimental Neurology, 57, 101-110.

Harris, R.A., & Allan, A.M. (1989). Alcohol intoxication: ion 
channels and genetics. Alcohol Neurochemistry, 3, 1689-1695.

Lovinger, D.M. (1999). The role of serotonin in alcohol's effect 
on the brain. Current Separations, 18, 23-28.

Palfai, T., & Jankiewicz, H. (2001). Drugs and human behavior 
(2nd ed.). New York: McGraw Hill.

Ryabinin, A.E., Criado, J.R., Henriksen, S.J., Bloom, F.E., & 
Wilson, M.C. (1997). Differential sensitivity of c Fos 
expression in hippocampus and other brain regions to moderate 
and low doses of alcohol. Molecular Psychiatry, 2, 32-43.

Valenzuela, C.F. (1997). Alcohol and neurotransmitter 
interactions. Alcohol Health and Research World, 21, 144-148.

Primary behavior changes and side effects
By Heather French

EFFECTS ON THE BRAIN AND CENTRAL NERVOUS SYSTEM

The primary behavior effects of alcohol are its 
psychoactive and disinhibition effects.  This is caused when the 
alcohol interferes with the normal working ability of inhibitory 
neurons in the cortex (Doweiko, 2002).  The cells are not 
destroyed, but rather they are impaired in their normal 
functioning due to the depressant action of the alcohol.  
Restoration of cellular functioning occurs when the alcohol is 
oxidized.  (Carroll, 1975).  
Alcohol, a neurotoxin, can affect memory formation after a 
single drink.  In some cases, the individual may experience the 
inability to remember events that occurred during intoxication.  
This is known as a blackout Doweiko, 2002).  Prolonged, heavy 
alcohol use reduces the sensitivity of the Central Nervous 
System to alcohol's effects.  It is this tolerance to alcohol 
that leads the user to increasing the dosage consumed in order 
to achieve the same effect (Carroll, 1975).  
Due to thiamine deficiency, approximately 15 to 20 percent 
of chronic alcohol users develop a condition known as Wernicke 
Korsakoff syndrome.  Wernicke Korsakoff syndrome is exhibited by 
a pattern of brain damage that results in confusion to the point 
of deliriousness or disorientation (Doweiko, 2002).  Various 
studies that compared men and women on their vulnerability to 
alcohol induced brain damage have yielded interesting results.  
Although there has been some conflicting evidence, it has been 
recently suggested that alcoholic women are more susceptible to 
alcohol induced brain damage than are alcoholic men (Hommer, 
2003).  

EFFECTS ON SEXUALITY

The consumption of alcohol decreases testicular synthesis 
and increases metabolic disposition of testosterone.  This 
results in an increased leutinizing hormone that is thought to 
be responsible for increasing sex drive (Cohen, 1983).  While 
short term effects of alcohol consumption may actually lead to 
increased sexual desire, long term alcohol abuse can lead to 
impotence.  It appears that alcohol may impair or destroy the 
neurological function that causes an erection (Carroll, 1975).  
Additionally, studies of alcoholics have shown that their sex 
life was deficient and ineffectual, and that even with sobriety, 
impotency may be irreversible (NIAAA, 1980).  

EFFECTS ON THE CARDIOVASCULAR AND SKELETAL SYSTEM

The initial effect of alcohol is a slight increase in heart 
rate and blood pressure.  Alcohol also dilates the peripheral 
blood vessels, contributing to loss of body heat, thereby 
decreasing body temperature (Carroll, 1975).  It has been 
suggested that as many as 50 percent of individuals with chronic 
alcoholism are prone to myopathy of skeletal muscles.  Myopathy 
is characterized by selective atrophy of Type II fibres and up 
to a 30 percent reduction in entire muscle mass (Preedy, Adachi, 
Ueno, Ahmed, Mantle, & Mullatti, 2001).  It has also been 
suggested that alcoholism leads to cardiomyopathy, and that 
alcohol is toxic to striated muscle (Urbano Marquez, Estruch, 
Navarro Lopez, Grau, Mont, & Rubin, 1989).  

EFFECTS ON THE LIVER

Due to the liver being primarily responsible for alcohol 
metabolism, the liver is very vulnerable to alcohol-related 
injury.  Alcohol liver disease (ALD) is a potentially fatal 
condition due to prolonged, heavy alcohol use.  ALD consists of 
three conditions: fatty liver, alcoholic hepatitis, and 
cirrhosis (Carroll, 1975; Marsano, et al., 2003). 
The existence of a fatty liver, or steatosis, occurs in 
about 20 percent of alcoholics.  There are no symptoms besides 
an enlarged liver and symptoms can often be reversed if alcohol 
consumption in stopped (Mann, Smart, & Govoni, 2004).  Fatty 
liver is often a precursor to an inflammatory liver disorder 
called alcoholic hepatitis (Mann, Smart, & Govoni, 2004). 
Alcohol hepatitis is characterized by fever, nausea, 
elevated white blood count, jaundice, and abdominal pain.  There 
is approximately a 50 percent mortality rate for severe cases, 
and about 40 percent of cases will develop into the most serious 
of all of the liver diseases, cirrhosis (Mann, Smart, & Govoni, 
2004).  
Cirrhosis typically develops after years of excessive 
alcohol use.  This is characterized by widespread scarring of 
the liver, which results in a shriveling and hardening of the 
fibrous tissue (Carroll, 1975; Marsano, et al., 2003).  
Furthermore, it has been found that patients with both alcoholic 
hepatitis and cirrhosis have a death rate greater than 60% over 
a 4 year period (Marsano, et al., 2003).  

EFFECTS ON PERSONAL AND FAMILIAL LIFE, AND EMPLOYMENT

It is known that alcohol abuse can be responsible for 
personal and familial disruptions.  Indeed, alcoholism is often 
characterized as "the family disease" because of its effects on 
emotional, physical, spiritual, and economic aspects of the 
entire family (Carroll, 1975).  
The individual with alcohol addiction may experience such 
psychological complications as frustration due to decreased 
efficiency, and having a preoccupation with drinking.  
Alcoholics may also experience feeling a loss of control, as 
exhibited through confabulation, passing out, memory lapses, and 
drinking binges (Palfai & Jankiewicz, 2001).  
Difficulties with employment, and possible death or injury 
by alcohol related accident are also major areas of concern for 
the individual addicted to alcohol.  It is estimated that more 
than 75 percent of the alcoholics in the United States are 
employed (NIAAA, 1980).  Although the individual who abuses 
alcohol frequently continues to work full-time, as alcohol use 
increases there is often an increase in decreased productivity, 
unauthorized absenteeism, and poor coworker relations (Carroll, 
1975).  

Lastly, Drinking and driving is a prevalent cause of 
automobile accidents, as well as Driving Under the Influence 
(DUI) citations each year (Carroll, 1975).  It has been 
estimated that alcohol is involved in roughly one-third to one-
half of all highway fatalities.  In addition, alcohol has been 
implicated in injury and death resulting from home, industrial, 
and recreational accidents (NIAAA, 1980). 

References

Carroll, C. (1975).  Alcohol: Use, nonuse, and abuse (2nd ed.)  
WM. C. BROWN COMPANY PUBLISHERS: Dubuque, IO.  
Cohen, S. (1983).  The alcoholism problems.  The Haworth Press: 
New York.  

Doweiko, H. (Ed.) (2002).  Concepts of chemical dependency (5th 
ed).  Pacific Grove, CA:  BROOKS/COLE.

Facts about alcohol and alcoholism.  (1980). Rockville, MD: 
National Institute on Alcohol Abuse and Alcoholism.  

Hommer, D. (2003).  Male and female sensitivity to alcohol-
induced brain damage.  Alcohol Research and Health, 27, 181-185.

Palfai, T., & Jankiewicz, H. (2001).  Drugs and human behavior 
(2nd ed.).  New York: McGraw Hill.

Preedy, V., Adachi, J., Ueno, Y., Ahmed, S., Mantle, D., & 
Mullatti, N. (2001).  Alcoholic skeletal muscle myopathy: 
definitions, features, contribution of neuropathy, impact and 
diagnosis.  European Journal of Neurology, 8, 677-687.

Urbano Marquez, D., Estruch, R., Navarro Lopez, F., Grau, J., 
Mont, L., & Rubin, E. (1989).  The effects of alcoholism on 
skeletal and cardiac muscle.  The New England Journal of 
Medicine, 320, 409-415.  



Treatment and effects of alcoholism
By Kiersten Kotaka


"Alcoholism must no longer be thought of as a single 
disease with a cause that is either genetic or environmental but 
as a group of illnesses in which the influences of genes and the 
environment ebb and flow over the course of the at-risk 
lifetime." (Devor 1994)
The research questions have evolved from whether there is a 
hereditary risk to the search for specific genes that contribute 
to the risk of alcoholism (Devor 1994). Devor explains that the 
developmental alcoholism model is composed of five parts. In the 
first part alcoholism specific genes confer the primary risk to 
developing the disease. In the second part of the model, if two 
or more primary risk genes are present in any one individual the 
possibility of primary gene-gene interactions exist. The third 
part recognizes the primary risk genotype that exists in a 
developmental milieu composed of the rest of the genome. Devor 
goes on to explain the fourth part of this model which 
recognizes the role of nongenetic factors in modifying the 
entire relevant genotype. The fifth part of the model suggests 
that the levels of interaction, the numbers of primary risk 
genes and secondary modifying loci are relatively small and 
manageable. "The overall effect of this interactive 
developmental is to produce precisely the types of clinical 
variations observed (age of onset, sex differences, response to 
treatment, severity, and familiality." (Devor 1994)
In 2003, 74% of adults age 21 or older reported that they 
had started drinking alcohol before the legal drinking age of 
21. (SAMHSA's National Survey on Drug Use and Health). The 
trajectories of alcohol and drug use and dependence from 
adolescence to adulthood was studied by Chasin, Flora, and King 
(2004).  Participants recruited for their study included 
participants from an ongoing study of parental alcoholism 
sampled from court records for driving under the influence of 
alcohol. At time 1 there were 454 adolescents ranging in age 
from 10.5 to 15.5 years. 246 of them had at least one alcoholic 
biological parent who was also a custodial parent and 208 
demographically matched adolescents with no alcoholic biological 
or custodial parents (control group). There were three annual 
assessments of the adolescents and their parents and two long 
term follow-ups (Times 4 and 5). The follow ups were done when 
the original adolescents were age 18-23, and 22-30. 
The researchers looked at parent alcoholism and 
psychopathology, alcohol consumption, drug consumption, alcohol 
and drug dependence diagnoses, adolescent negative emotionality 
and impulsivity, and young adult personality. The researchers 
modeled the trajectories as a function of age rather than of 
measurement occasion. They found that only 11.3% of the 
participants were lifelong abstainers from alcohol and drugs. 
"The most common trajectory involved moderate alcohol use 
coupled with low levels of drug use and it was also relatively 
common for individuals to drink lightly and infrequently with 
only very rare drug use" (Chassin, Flora, & King 2004). Most 
participants (61%) did not develop drug or alcohol dependence 
over the course of the study. Members of the heavy drinking 
group (20% of participants) were likely to be children of 
alcoholics and had the densest family histories of alcoholism. 
The researchers found that those people with dense family 
histories (averaging more than one first degree alcoholic 
relative) were overrepresented in both the comorbid and alcohol 
dependence only groups. The major limitation of this study is 
that it followed participants only to the age of thirty.
Binge drinking is defined as the 5 consecutive drinks for a 
man, and 4 consecutive drinks for a woman. In a study of student 
reports about drinking behaviors and harms collected through the 
Harvard School of Public Health College Alcohol Study, Weitzman 
and Nelson (2004) gave four measures of alcohol consumption and 
five measures of alcohol related consequences to 49,163 college 
students. They found that as the level of alcohol consumption 
increased so did the self report of drinking related harms. The 
analyses of the data revealed that the bulk of drinking related 
harms reported by college students are from drinkers who drink 
at nonextreme levels. They also found that most drinkers did not 
consume large quantities of alcohol. The researchers suggest 
that " from a public health perspective, targeting the entire 
population, including nonextreme drinkers, using environmental 
prevention strategies is both logical and likely to yield 
substantial community wide reductions in harm" (Weitzman & 
Nelson 2004).




References

Chassin, L., Flora,D. & King, K. (2004) Trajectories of alcohol 
and drug use and dependence from adolescence to adulthood: the 
effects of familial alcoholism and personality. Journal of 
Abnormal Psychology, 483-498.

Devor,E. (1994). A developmental genetic model of alcoholism: 
Implications for genetic research. Journal of Consulting and 
Clinical Psychology, 62, 1108-1115.

Gender Differences in Substance Dependence and Abuse. 
Http://www.drugabusestatistics.samhsa.gov/2k4/genderDependence/g
enderDependence.cfm. 4/2/05. 

Weitzman, E., & Nelson,T. (2004) College student binge drinking 
and the "prevention paradox" Implications for prevention and 
harm reduction. Journal of Drug Education, 34, 247-266.


The End

Copyright © 2005, Dr. John M. Morgan, All rights reserved - This page last edited 04-23, 2004
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