Abstract
Since many common drugs such as caffeine and alcohol are psychoactive in
nature, there may be a tendency for habitual users of such substances to
experience more dramatic changes in mood than those who do not use them
frequently. For this study, the researcher investigated the possibility of a
correlation between drug use and mood symptoms typically associated with
clinical depression. The participants, a convenience sample of approximately 100
students from a small, midwestern university, completed a short survey relating
to drug use and depression-like feelings. The survey featured a self-report
scale indicating agreement with a particular statement or frequency of personal
events e.g. intense sadness. The results suggested that individuals who reported
regular use of common psychoactive drugs (caffeine in particular) were more
likely to indicate occurrence of depression-related effects. The study findings
may be useful in investigating the chemical factors in the brain that contribute
to clinical depression.
Keywords: Depression, drugs,
psychoactive
Every year, millions of citizens in the United States suffer from the
effects of clinical depression and/or its associated symptoms. The DSM IV
criteria for defining a major depressive episode include depressed mood and/or
loss of interest or pleasure accompanied by any five or more other descriptive
factors such as fatigue, thoughts of death, feelings of worthlessness, etc.
Major depressive disorder is described as separate, recurrent episode events
(American Psychiatric Association, 1994). Also, the modern lifestyle of many
Americans exposes them daily to a number of common, psychoactive drugs such as
caffeine, alcohol and marijuana. These substances are often used (or abused) for
their calm-inducing, stimulant or otherwise mind-altering qualities.
Psychoactive drugs act upon and change the brain’s neurochemistry, producing the
“high” or “buzz” effects that many users seek. However, clinical depression is
also associated with chemical changes in neurotransmitter levels within the
brain (sometimes in combination with personal conflict or other sources of
distress in a particular individual’s life). Since depression symptoms are
connected with imbalances in brain chemistry, the presence of psychoactive drugs
may be linked with an individual person’s likelihood of experiencing those
symptoms at some point in life.
According to a recent analysis of data on the presence of depression in
the United States, the disorder affects over 21 million American children and
adults each year. It is often concurrent with other serious, ongoing medical
illnesses such as cancer and heart disease (Ranking America’s Mental Health,
2011). The same study indicates that depression is responsible for approximately
$31 billion in lost productive time among American workers and is a primary
factor in over 30,000 cases of suicide annually, particularly in the age range
of 15-24 years (Ranking America’s Mental Health, 2011). These statistics suggest
that clinical depression is a serious detriment to the overall health and
wellbeing of United States citizens. Furthermore, habitual abuse of legal and
illegal drugs continues to be an issue associated with social problems such as
drunk driving, secondhand smoking and accidental death from drug overdose. Since
depression and drug use are both serious societal issues and share a common
dimension (effects on brain chemistry), it may be worthwhile to investigate the
potential correlation between the two.
Depression has been associated with neurochemical changes in the brain
for some time. Sigmund Freud once commented that he believed science would
eventually describe the physiochemical effects of psychological events in
detail, although the groundwork for such studies had not yet been laid when he
was doing his research (Gilbert, 1984). Since the late 1950s and 1960s,
researchers have been putting together information relating depression to
catecholamines and the neurotransmitters known as monoamines (includes dopamine,
norepinephrine and 5-HT). Major antidepressants, monoamine-oxidase inhibitors
(MAOIs) and tricyclic compounds, generally act on the synaptic mechanisms for
these neurotransmitters (Gilbert, 1984). Drugs that are subject to common abuse
also tend to target the same neurotransmitters (Rudnick, 1998). The observed
physiochemical effects for different drugs range widely; for instance, cocaine
is known to block certain neurotransmitter transporters while amphetamines cause
neurotransmitter release (Rudnick, 1998). Careful research is needed to
establish the potential interaction of drugs and depression since an imbalance
in a common neurotransmitter caused by one of the two factors could have an
impact on the other.
Fredholm, Bättig, Holmén, Nehlig and Zvartau (1999) stated that the primary
action of caffeine in the brain is that of an adenosine receptor antagonist.
However, they also noted that other behavioral experiments may indicate other
functional mechanisms. Caffeine is recognized as an increase factor for
dopaminergic transmission, an interesting point considering that amphetamines
and cocaine cause the release of dopamine. With regard to behavioral
observations, caffeine appears to have an initial stimulant effect in humans but
seems to lead to a delayed behavioral depression when applied in high doses to
experimental animals. For humans, high doses of caffeine are also associated
with increased anxiety symptoms, though individuals with anxiety due to
depression do not seem to exhibit unusual sensitivity to caffeine (Fredholm, et
al. 1999).
One early psychological study investigating a link between depression and
caffeine consumption indicated a positive correlation between caffeine and both
depression and anxiety symptoms (Veleber & Templer, 1984). The experimenters
administered a Multiple Affect Checklist (self-report) to volunteer participants
both before and one hour after a double-blind dosage of either 150 mg or 300 mg
of caffeine. They found that dose level appeared to be a significant predictor
for anxiety at the .001 level and for heightened hostility and depression at the
.01 level. In addition, the research included covariate analysis of gender, age
and occupation; the results indicated that gender (males having higher scores)
was a significant predictor for posttest depression and hostility at the .01
level but found no relation of the other two variables to experimental measures.
In the discussion of the project, the researchers noted that since caffeine is
associated with a more “delayed” effect with regard to depressive symptomology,
they may have observed more anxiety if the posttest had been administered sooner
following caffeine intake (Veleber & Templer, 1984).
Other studies place more of a principle focus upon the involvement of anxiety
disorders in any correlation between depression and caffeine. Luebbe and Bell
(2009) conducted an experiment with sets of 5th and 10th
grade children to investigate parameters of intake and subsequent negative
effects of caffeine in these age groups. The students self-reported their
caffeine intake, gave height/weight information and completed a Likert scale
inventory to assess any symptomology associated with the drug. The study was
undertaken in response to other reports of caffeine-related physical dependence
and withdrawal evidence in children. The researchers found a positive
correlation between depression and caffeine intake in both age groups. Both had
also exhibited a positive relation between weekly intake and other subjective
effects with the exception of stimulation. In teens, depression and reported
withdrawal effects were related as well as anxiety and stimulation. From their
data, the experimenters concluded that most children and teens experience little
restriction regarding caffeine consumption and that higher intake appears to put
youth at an increased risk for depressive symptomology (Lubbe & Bell, 2009).
A related 2008 study examined similar qualities but also included the parameter
of sleep (Whalen, Silk, Semel, Forbes, Ryan, Axelson, Birmaher & Dahl). Their
experiments assessed relationships among sleep quality, caffeine intake and
affect using two groups of youth: one that was comprised of individuals with
major depressive disorder (MDD) and one group of healthy controls (no history of
mental diagnosis). The participants self-reported caffeine use, quality of sleep
and feelings/behaviors (affect) over a period of eight weeks during which the
MDD group received depression treatment. The researchers hypothesized that the
experimental group would experience an increase in sleep quality and a decrease
in caffeine use over the treatment period. Youth with MDD reported more caffeine
use and sleep problems as well as more anxiety on days they consumed caffeine
relative to healthy youth. Caffeine/sleep analysis yielded only a connection
between caffeine use in a given day and number of nighttime awakenings the
following night. Caffeine/negative affect analysis yielded only a connection
between caffeine and feelings of nervousness (not anger, sadness or upset). The
experimenters noted that children with MDD and comorbid anxiety reported higher
caffeine intake than any other participants. Since the MDD group’s caffeine use
decreased but sleep quality did not improve significantly during the treatment,
the experiment suggests that youth with MDD may use caffeine to self-medicate
for depression symptoms (Whalen, et al. 2008).
Alcohol
With regard to alcohol and depression, some studies similarly include
several other factors that may interact with the drug and behavioral effects.
Dennhardt and Murphy (2011) performed research exploring racial differences
(European-American vs. African-American) in depression, distress tolerance,
delay discounting and alcohol-related problems. Hypotheses included the
projection that high levels of delay discounting and depression and low levels
of distress tolerance would be associated with more alcohol problems, and
specifically with more dependence-related symptoms (impaired control over
drinking and physical dependence). Depression and distress tolerance were
assessed with self-report scales, drinking with a questionnaire and delay
discounting using preference questions. The experimenters found that
European-American students showed a correlation between depression and physical
dependence, African-American students showed an association between depression
and impaired control/physical dependence and both races showed a significant
relationship between depression and alcohol problems. They suggested that
drinking may be associated with distress tolerance in African-American students
because they are likely to encounter more discrimination and hardship in college
than European-Americans (Dennhardt & Murphy, 2011).
Another study considered whether participants’ dispositions to rash
action moderate the effects of concurrent alcohol use or depressive symptoms on
alcohol problems (King, Karyadi, Luk & Patock-Peckham, 2011). The basis for the
research was the idea that impulsivity (a core personality trait) may increase
an individual’s vulnerability to both alcohol use disorders and use of alcohol
as a coping method for dealing with feelings of depression. 573 participants
self-reported on impulsivity, alcohol use and depression symptom measures. The
researchers found that lower levels of premeditation enhanced the association
between depressive symptoms and alcohol problems, while lower perseverance and
higher sensation seeking were related to more alcohol problems at higher levels
of alcohol use. Their findings suggested that feelings of negative urgency may
be directly related to alcohol problems while premeditation, perseverance and
sensation seeking qualities are indirectly related by modifying the relations
between depressive symptoms/alcohol use and alcohol problems (King, Karyadi, Luk
& Patock-Peckham, 2011).
Other work has taken a more biological view of the association between
alcohol and depression. Stevenson, Schroeder, Nixon, Besheer, Crews and Hodge
(2009) conducted an experiment wherein the researchers used mice to investigate
whether alcohol exposure and subsequent abstinence contributes to
depression-like behavior and decreased hippocampal neurogenesis. Groups of mice
were allowed to drink alcohol-water and tested for depression symptoms using a
forced swim test. One group was given the antidepressant desipramine. Brain
changes were assessed through immunohistochemistry. Alcohol group mice showed a
significant increase in depression behavior 14 days after abstinence and also
showed a significant but temporary increase in anxiety behavior after one day of
abstinence which was gone by 15 days. In addition, desipramine treatment reduced
immobility and depression behavior in mice when administered during the 14 days
of abstinence. The researchers also observed a decrease in the number of neural
progenitor cells (NPCs) in the dentate gyrus of the brains of alcohol group
mice. The results of the study supported the hypothesis that alcohol affects
molecular pathways in the brain that are also associated with the
pathophysiology of depression; they also indicated that antidepressant treatment
may alleviate some of pathological neurobehavioral adaptations of alcohol
abstinence (Stevenson, et. al. 2009).
However, another study on methods of measurement could influence how the
results of many others are viewed. Graham, Massak, Demers and Rehm (2007)
investigated how different ways of assessing alcohol use and depression symptoms
could produce varying research results. Alcohol use was judged in four ways
(frequency, volume, quantity per occasion and heavy episodic drinking) and two
types of depression assessment were used (clinical method of diagnosing major
depressive disorder and basic depressed affect). The sample size for this study
was very large; over 14,000 participants were evaluated via phone interview. The
researchers found that gender and method of measurement did indeed produce
significantly different results when searching for a link between alcohol and
depression. From the data gathered, they determined that studies using heavy
drinking per occasion as the standard of alcohol use found more significant
relationships to depression than those using frequency or volume of alcohol
consumed overall. In addition, the alcohol-depression connection appeared to be
stronger for women than for men only when depression was assessed based on
clinical criteria rather than affect. The researchers noted that future studies
may benefit from separate gender analyses and more focus on episodic binge
drinking when searching for significant associations (Graham, Massak, Demers &
Rehm, 2007).
Marijuana & Tobacco
It is not that unusual for a particular individual to use caffeine or
alcohol alone on a regular basis while exposing themselves to no other
psychoactive drugs. However, drugs such as marijuana are often used concurrently
with tobacco or other more illicit substances. Bonn-Miller, Zvolensky and
Johnson (2010) conducted a study to examine uni-morbid and co-occurring tobacco
and marijuana use in relation to the negative emotional symptoms of anxiety and
depression. 250 participants were divided into four groups: tobacco use only,
marijuana use only, concurrent use of both drugs and use of neither drug. The
researchers administered questionnaires regarding frequency of smoking,
frequency of marijuana use and mood/anxiety (an assessment of alcohol use was
also included). The results of the study indicated that people who use tobacco
alone experience higher levels of depression symptoms and more negative affect
than other groups while the combined drug group reported the highest levels of
anxiety. In addition, the two groups that included marijuana use were associated
with greater use of alcohol than the tobacco or drug-free groups. The
experimenters concluded that those who use tobacco alone may be more subject to
depression than users of other drugs or non-drug users (Bonn-Miller, Zvolensky &
Johnson, 2010).
Another study investigated the effects of marijuana and MDMA (ecstasy) on
major depression; it also searched for gender differences with stratification
studies (Durdle, 2008). The researchers assessed 226 participants using the DSM
Structured Clinical Interview for depression and a drug use questionnaire. They
also considered whether or not marijuana use met the criteria for a DSM-defined
lifetime disorder. The results yielded a significant correlation between
marijuana use disorder and major depressive disorder (MDD) but no similar
relationship between ecstasy and MDD. Use of ecstasy and marijuana were not
significantly associated with each other. Separate gender analysis produced a
significant correlation between combined marijuana use disorder and ecstasy use
with MDD in females, but found no similar correlation for males. The
experimenters theorized that the difference in females could be due to marijuana
effects in the female 5-HT system that manifest as depression or a dose-specific
relationship between ecstasy and MDD (females would be more susceptible due to
lower body weight). In addition, the findings suggested that marijuana use may
be a confounding variable in studies that indicate a definite relationship
between ecstasy and MDD (Durdle, 2008).
With regard to marijuana and depression, motive for use of the drug may
act as a confounding variable in any correlational study, a problem that
Bonn-Miller, Zvolensky, Bernstein and Stickle (2008) sought to address. 149
participants completed the Marijuana Motives Measure Test as well as
questionnaires regarding mood/anxiety and agoraphobia (an alcohol questionnaire
was also included). The researchers posited that frequent use of marijuana and
coping motive would be more predictive of anxiety and mood problems. They
covaried factors such as alcohol use and total years of marijuana use and
discovered that frequency of marijuana use (past 30 days) and presence of coping
motives reliably predicted anxious arousal symptoms, agoraphobic cognitions, and
worry. In addition, daily tobacco use was significantly correlated with anxiety,
worry, agoraphobic cognitions and anhedonia. The experimenters concluded that it
is important to consider motive for drug use when examining the relationship
between marijuana and anxiety/depression (Bonn-Miller, et al. 2008).
Another particularly thorough study attempted to find a causal
relationship between marijuana and depression (Harder, Morral & Arkes, 2006).
The researchers attempted to determine whether marijuana use predicts later
development of depression after accounting for differences between users and
non-users of marijuana and hypothesized that ongoing marijuana use is an
independent predictor of depression in adults. The longitudinal study began in
1984; respondents were asked about their frequency and duration of marijuana use
with follow-up assessments made in 1988, 1992, 1994 and 1998. During the 1992,
1994 and 2002 interviews, respondents were also asked about their mood within
the past week. Factors such as age, race and socioeconomic status were used as
baseline covariates. The researchers also employed two experimental models; one
consisted of individuals who had used marijuana during the past year and one
included a four-year time lag. After adjusting for differences in baseline risk
factors of marijuana use and depression, past-year marijuana use did not
significantly predict later development of depression. Odds of depression for
past marijuana users was reported to be only 1.1 times higher than odds for
non-marijuana users (Harder, Morral & Arkes 2006).
Other Drugs
“Harder” illicit drugs such as cocaine and ecstasy have also been
examined with relation to depressive symptomology. Rubin, Aharonovich, Bisaga,
Levin, Raby and Nunes (2007) investigated the interaction of comorbid major
depression with abstinence effects in cocaine users; the researcher posited that
cocaine users who also suffer from MDD will experience more severe withdrawal
effects than those with no history of MDD. Participants were divided into
cocaine-dependent and cocaine-dependent with MDD groups and assessed using the
Beck Depression Index (BDI) and Hamilton Depression Rating Scale. Results
indicated that individuals with cocaine dependence and MDD had significantly
higher BDI scores during abstinence than those with cocaine dependence alone.
There appeared to be no relationship between abstinence and anxiety over three
days, but researchers noted a correlation between anxiety and years of drug use.
The experimenters concluded that monitored abstinence for cocaine users may help
distinguish between withdrawal and actual depression and that the sustained
dysphoria experienced by MDD patients may be related to drug-induced changes in
the brain (Rubin, et al. 2007).
Another study examined the relationship between former chronic use of
ecstasy (chronic use defined as 100 lifetime exposures or more) and elevated
depression scores (MacInnes, Handley & Harding, 2001). 29 participants reported
former ecstasy use, depression using the BDI and daily life hassles/stress.
Levels of depression were significantly elevated compared to a matched non-drug
using control group; frequent but mild life stress and number of ecstasy tablets
consumed in a 12-hour period were the only significant predictors of depression
ratings in the experimental group. Levels of depression were not significantly
impacted by reports of alcohol, amphetamines or any other type of psychoactive
drug assessed in the study. The researchers concluded that binge consumption of
ecstasy appears to have a significant relationship to depression ratings, which
suggests a rationale for a biological basis for depression reported by ecstasy
users (MacInnes, Handley & Harding, 2001).
A related experiment investigated the ecstasy-depression correlation
while specifically controlling for concurrent use of other drugs (Roiser &
Sahakian, 2003). The basis for the study was observed damage to serotonin
neurons in the brains of laboratory animals that were treated with ecstasy.
Participants were 30 current ecstasy users, 30 poly-drug controls who had never
used ecstasy, 30 drug-naïve controls with no history of illicit drug use and 20
past ecstasy users. Current and past ecstasy users scored significantly higher
on the BDI than non-drug users but were not significantly different from the
poly-drug group. Participants were also given an affective test to determine
whether ecstasy users show the same kind of attention bias toward
negatively-toned material as depressed people; this section of the study found
no significant similarity. Overall, the research indicated that previously
observed correlations between ecstasy use and depression may be confounded by
use of other psychoactive drugs (Roiser & Sahakian, 2003).
In addition to illegal drugs, researchers have investigated the
relationships of depression to therapeutic drugs such as Ritalin. One study
examined the effects of Ritalin in depressed individuals to differentiate
between pharmacological effects and its effects on target symptoms (Kerenyi,
Koranyi & Sarwer-Foner, 1960). 159 participants were divided into two groups,
one of which was assessed in psychiatric treatment clinics and the other in
private practices. Lab tests and reported changes in weight, sleep, eating, etc.
were used to assess the physiological effects of the drug. 81% of cases showed
reported improvement in mood and 62% showed increased psychomotor activity such
as speech in psychotherapy sessions. Patients with depression responded better
than those with schizophrenia or other illnesses with depression symptoms. The
research indicated that Ritalin may be useful in treatment of depression due to
its effect of giving a little more energy to the patient with which he/she can
better communicate with a therapist or doctor. It appeared less effective with
administered without or with little therapeutic interaction. The researchers
concluded that Ritalin may be useful in treatment of depressive symptoms as long
as it is applied to the right patients with proper therapeutic support (Kerenyi,
Koranyi & Sarwer-Foner, 1960).
Another study employed a general drug-using population to determine how
combinations of psychoactive substance use, personality, psychosocial and
negative life events affect risk for developing depressive symptoms (Buckner &
Mandell, 1990). The research involved a short-term longitudinal study wherein
participants who reported depressed symptoms at time 2 but not time 1 were
defined as experimental “cases” and others used as “controls”. Researchers
assessed drug use, negative life events and social supports; the investigated
factors were found to be significantly related to depression symptoms in drug
users. Of the drugs investigated, methaqualone (a synthetic central nervous
system depressant compound that is similar to barbiturates) appeared to show the
most specific and significant relationship to depression independent of
self-esteem ratings or negative events. Heroin also showed significant
prediction value for depressive episodes, but lost it when adjusted for
social/life event factors. The researchers also cited another study that found
evidence supporting the theory that methaqualone could be an antecedent to
depression rather than a consequence (Buckner & Mandell, 1990).
Research Hypotheses
Many past studies investigating a connection between drug use and
depression have found statistically significant results of some kind. Several of
these research projects have included a biological basis for the correlation;
the chemical or physical changes in the brain brought about by one of the
factors may have an impact on the presence or intensity of the other. The
current study hypothesizes that individuals who report high levels of drug use
on a short, self-report survey will also be more likely to report frequent
occurrences of depressive symptomology. Also, since many of the reviewed studies
included some evidence that observed effects of these conditions vary based on
gender, this project will investigate differences in response for males and
females. All variables will be operationalized as survey responses given by
participants.
Participants
Study participants were a convenience sample of undergraduate students
from a small, rurally located, midwestern university. They were approached at
the beginning of classes and asked to fill out a voluntary, anonymous survey.
Classes surveyed included two introductory psychology classes, one introductory
biology class and one upper level adult psychology class. A total of 100
students participated, but only 96 returned usable surveys. The only demographic
requested other than gender was year in school. Out of 96 participants, 50 were
male, 42 were first year students, 22 sophomores, 17 juniors, 12 seniors and 3
fifth year students or above.
Materials
The survey distributed was designed by the researcher and included two
demographic questions, 11 drug analysis questions and 14 questions to assess
depressive symptomology (Appendix B). Responses for all non-demographic
questions were given on a six-point Likert type scale or a yes/no option. All
participants received the same survey (balanced research) and the direction of
several questions was reversed to eliminate potential effects of yea/naysaying.
Participants were given contact information for the researcher and school
counselors and asked to initial a consent slip. Consent slips were returned
separately from surveys (See Appendix A). Participants were informed before
taking the survey that it was optional and had no impact upon class grades. A
total of 100 surveys were distributed, but four were eliminated from the study
based on insufficient responses (each of the four was missing an entire page of
answers). However, the number of unusable surveys was relatively small and
unlikely to have a negative effect on study results.
Procedure
The researcher created an initial draft of the survey which was then
field tested and revised before submission to the McKendree University
Institutional Review Board (IRB) with a request for expedited review. The IRB
approved the revised survey and found no ethical problems with the proposed
study. The surveys were then distributed and data was analyzed using SPSS 14.0
software. The relationship between drugs (both individual types and overall) and
depression was examined using a Pearson’s Correlation test, gender differences
using a two-tailed independent samples t-test and variations in drug
use/depression by year in school using a one-way analysis of variance (ANOVA).
ANOVA tests included Scheffe, Tukey (Honestly Significant Difference) and Fisher
(Least Significant Difference) measures.
Results
To test the hypothesis that higher reported drug use will be related to
higher reported depression symptoms, the Pearson Correlation test of overall
drug use (M=19.86, SD=4.77) and depression symptoms (M=31.89, SD=10.15) showed a
significant positive relationship, r=.27, p=.008. Analysis of the correlation
between depression and individual drug types yielded no significant findings
with the exception of caffeine, r=.06, p=.045. Analysis of depression and the
“other drugs” category (other narcotics that were not caffeine, alcohol, tobacco
or marijuana) could not be assessed because all survey responses to the question
regarding them were equal to 1 (No use). Mean values for responses regarding use
of each individual drug type are shown in Table 1.
Mean Values of Responses to Drug Use Questions
Note.
Possible range for responses to tobacco, marijuana, other psychoactive drugs and
alcohol score = 1 to 7. Possible range for total caffeine score = 4 to 24.
To assess gender variation in reported depression symptoms, the
independent samples t-test comparing male and female depression scores found no
significant differences between male (M=31.40, SD=9.57) and female responses
(M=32.39, SD=10.78), t(94)=-.48, p=.64. To assess gender variation in reported
drug use, the independent samples t-test for comparing male and female drug
scores also did not find any significant differences between males (M=19.90,
SD=4.82) and females (M=19.83, SD=4.76), t(94)=.06, p=.95.
To investigate variation of drug use reports among years in school, the
one-way analysis of variance (ANOVA) of drug use of first years (M=19.19,
SD=3.95), second years (M=18.82, SD=4.43), third years (M-21.53, SD=5.87),
fourth years (M=20.67, SD=4.85), fifth years and up (M=24.33, SD=8.33) indicated
no significant differences, F (4, 91)=1.80, p=.14.
To investigate variation of depression symptoms among years in school, the ANOVA
test comparing depression score of first year (M=30.70, SD=9.24), second years
(M=29.95, SD=8.39), third years (M=37.41, SD=12.16), fourth years (M=30.83,
SD=11.18), fifth years and up (M=35.67, SD=13.78) produced no significant
results, F (4, 91)=1.79, p=.14. Mean total responses to depression questions are
plotted for each year in Table 2. The post hoc testing using Fisher’s LSD test
for variation of depression symptoms among years in school indicated significant
differences between first year students and third year students, p=.022 as well
as between second year students and third year students, p=.023. However, since
the ANOVA and more conservative post hoc tests (Scheffe, Tukey) did not produce
significant results, this finding is likely negligible.
Table 2
Mean Total Depression Scores by Year in School
Note.
Possible range for depression score total was 16 to 92.
Discussion
The data gathered and analyzed in this study appear to support the
hypothesis that there could be a positive correlation between reported
depression symptoms and drug use. However, the relationship observed does not
indicate directional correlation, so further investigation into causation
factors may be useful. The overall association between the two factors
corresponded to prior evidence reported by Buckner and Mandell (1990). The
earlier research included analysis of negative life events and social distress,
which may be a useful addition to an improved study. The present research also
found results consistent with the significant relationship between depression
and caffeine indicated in previous studies (Veleber & Templer, 1984; Lubbe &
Bell, 2009). The even numbers of male and female participants lend strength to
the finding that gender may not be significantly related to depression or drug
use. However, the high number of first-year students compared to upperclassmen
may have unbalanced the findings for the same relationships among years in
school.
Since the participants indicated no use of “harder” drugs such as ecstasy or
heroin, this study provides no evidence to support findings such as the
connection between binge consumption of ecstasy and depression reported by
MacInnes, Handley and Harding (2001). In addition, this study found no
significant relationship between marijuana and depression, which supports other
evidence that marijuana is either unrelated to depression or related primarily
by motive for use of the drug (Bonn-Miller, et al. 2008; Harder, Morral & Arkes
2006). In the case of alcohol, this research found no significant results, but
assessed use of the drug only by frequency of drinking alcoholic beverages.
Previous research by Graham, Massak, Demers and Rehm (2007) posits that the
depression/alcohol relationship appears more significant when measured by
occasions of binge drinking, so an improved study may include further inquiry
into the nature of participants’ alcohol use.
Since the present research was conducted
using only a small convenience sample of participants from a private, midwestern
university, larger samples of non-student populations or from other geographical
areas would be helpful for comparison. In addition, the treatment of the subject
was rather broad in that the survey distributed included questions regarding
several different types of drugs. More useful and significant results may be
obtained with more focused studies pertaining to each individual substance.
Also, it is difficult to gauge causation using only a survey study. If future
research can pinpoint particular chemical relationships, more controlled,
experimental-style studies would likely provide information that is more useful
for the purpose of developing treatments for depression.
In particular, the strong correlation observed between caffeine and depression
warrants further investigation. Since college students are often thought to be
vulnerable to stress and depression as well as be more likely to use large
amounts of caffeine, it may be helpful to report more data about the
relationship between those factors. The original premise of this research
included the idea that psychoactive drugs and depression may be related on the
basis of similar effects upon the brain. Since caffeine use ratings demonstrated
the strongest and most significant connection to depression symptoms, continued
research may be best directed toward investigation of caffeine’s action within
the brain. Future studies may also examine the possibility of caffeine use as a
self-treatment for feelings associated with depression.
This research was conducted by Sarah L. Adams, McKendree University.
Correspondence concerning this article should be addressed to Sarah Adams, 610
Lila Court, New Baden, IL 62265 or by email: sadams@mckendree.edu or phone:
618-514-4286.
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Appendices
Appendix A: Consent Form
Read this consent form. If you have any questions, ask the experimenter and
he/she will answer your questions
“I have read the above statement and have been fully advised of the procedures
to be used in this project. I have been given sufficient opportunity to ask
questions I had concerning the procedures and possible risks involved. I
understand the potential risks involved and I assume them voluntarily.”
Please sign your initials, detach below the dotted line and continue with the
survey.
Sign your initials here_________________
Date_________________
The McKendree University Psychology Department supports the practice of
protection for human participants participating in research and related
activities. The following information is provided so that you can decide whether
you wish to participate in the present study. Your participation in this study
is completely voluntary. You should be aware that even if you agree to
participate, you are free to withdraw at any time, and that if you do withdraw
from the study, your grade in this class will not be affected in any way.
This survey is being conducted to assist the researcher in fulfilling a partial
requirement for PSY 496W.
You must be over 18 years of age to participate in the survey. It should not
take more than 10 minutes for you to complete and will be completely
anonymous. If you should have any other questions, don’t hesitate to contact
me, Sarah Adams 618-514-4286 or at
sadams@mckendree.edu
or Dr. Murella Bosse, 618-537-6882 or at
mbosse@mckendree.edu.
Some of the questions in the survey may confront sensitive topics. If answering
any of these questions causes you problems or concerns, please contact one of
our campus psychologists, Bob Clipper or Amy Champion, at 537-6503.
Student Survey
1.
Please indicate your gender.
M
F
2.
Please indicate your year in school.
First
Second
Third
Fourth
Fifth+
For questions 3-13, please choose a response describing yourself from 1 (Never)
to 6 (Very frequently).
3.
I drink caffeinated soft drinks.
Never
1
2
3
4
5
6
Frequently
4.
I drink energy drinks.
Never
1
2
3
4
5
6
Frequently
5.
I smoke cigarettes.
Never
1
2
3
4
5
6
Frequently
6.
I drink caffeinated coffee.
Never
1
2
3
4
5
6
Frequently
7.
I use energy/caffeine pills.
Never
1
2
3
4
5
6
Frequently
8.
I feel worthless or hopeless
Never
1
2
3
4
5
6
Frequently
9.
I have trouble sleeping.
Never
1
2
3
4
5
6
Frequently
10.
I have trouble staying awake.
Never
1
2
3
4
5
6
Frequently
11.
I smoke marijuana.
Never
1
2
3
4
5
6
Frequently
12.
I use other psychoactive drugs (cocaine, heroin, ecstasy, etc.)
Never
1
2
3
4
5
6
Frequently
13.
I drink alcoholic beverages.
Never
1
2
3
4
5
6
Frequently
For questions 14-25, please choose a response describing yourself from 1
(Disagree) to 6 (Agree)
14.
I have strong feelings of sadness.
Disagree
1
2
3
4
5
6
Agree
15.
I often worry unnecessarily.
Disagree
1
2
3
4
5
6
Agree
16.
I am energetic during the day.
Disagree
1
2
3
4
5
6
Agree
17.
Facing difficult and/or unfamiliar tasks causes me to panic.
Disagree
1
2
3
4
5
6
Agree
18.
I get frustrated quickly.
Disagree
1
2
3
4
5
6
Agree
19.
I look forward to spending time with
friends.
Disagree
1
2
3
4
5
6
Agree
20.
I have high self-esteem.
Disagree
1
2
3
4
5
6
Agree
21.
I try to take care to eat healthy foods.
Disagree
1
2
3
4
5
6
Agree
22.
I cry or want to cry often.
Disagree
1
2
3
4
5
6
Agree
23.
I laugh a lot.
Disagree
1
2
3
4
5
6
Agree
24.
I enjoy my daily life.
Disagree
1
2
3
4
5
6
Agree
25.
I have experienced a loss of interest in things I used to enjoy.
Disagree
1
2
3
4
5
6
Agree
For questions 26 and 27, please answer Yes or No
26.
I take/have taken Ritalin, Adderall or similar medication.
Yes
No
27.
I take/have taken medication for symptoms of clinical depression.
Yes
No
Thank you for completing this survey!