[Iannys]

Most people consider cannabis to be an experience enhancer rather than an escape device. If you feel good, it may make everything seem even better. When some people feel down or depressed , smoking may be "inappropriate" and they might get more into their problems. But, many report that it may lead to a new understanding or perspective on a problem, helping to resolve it and lift one's mood . It has been extremely helpful to people with terminal illness, helping them shake off depression and live out their remaining time with dignity and relatively good cheer.
For some people it is definitely an escape, but whether that is good or bad depends on the way that it is used. If it allows perspective and insight, that is good; if it is an avoidance mechanism, that is not a good use of cannabis. This is where the concepts of wise and responsible adult use apply.

[getafix]

i think you've asked and answered your own question (very well!)

cannabis can be a getaway, or a way of getting deeper into your own thoughts. if that may be positive or negative

[chillyhilly]

Seems like that to me.

It is what it is,a habit forming funass erb.

[NoNameNoshame]

Ha, I've learned that fasting is the only way to truly escape or change shape.

Cannabis helps bring that earned rest, when I don't earn it, I don't get the rest.

[jcsmooth]

Some interesting questions you've asked! I ask these of myself all the time, and being a psychology student I'm constantly over-analyzing EVERYTHING that I cross paths with.

If you can somehow gain access to Psycinfo, you'll have the ability to review a vast amount of scholarly articles that would help to shed light on virtually any issue that deals with the mind and body.

For what it's worth, I did a paper for a research methods course, and the topic I chose to study was whether cannabis has a place among modern medicine as an anti-depressant. Let's see if I can copy and paste this bad boy....apologies for the incompatible ms word to vbulletin (coding?).

Abstract
The active compound in cannabis, 9-tetrahydrocannabinol (THC), exerts its effects through two main receptors found in both the brain and peripheral tissue, and are respectively known as CB1 receptor and CB2 receptors. Users of cannabis report its ability to induce euphoric feelings, but research has typically been plagued with the use of CB1 and CB2 receptor knock-out mice to study its effects. In the following study, the hypothesis that the activation of CB1 and CB2 receptors has alleviating effects on melancholic depression. 160 human participants were identified with melancholic depression through the Beck Depression Inventory (BDI), and a second set of scores were collected at the end of the study using the same test to develop correlation values. Through the use of marinol, a CB1 and CB2 receptor activating compound, as well as desipramine, a tricyclic (TCA) antidepressant, scores were gathered and compared to test whether cannabis is an effective antidepressant. The findings confirmed this hypothesis as scores in both drug groups paralleled each other. These findings suggest that cannabis can be used as an effective antidepressant, however more research is needed to develop safer (fewer health risks) methods of THC-administration.


Does Cannabis Have A Place In Modern Medicine As An Anti-depressant?

Cannabis sativa (Cannabis) is a plant with a long past but a short history. Although we have records from 8000-7000 B.C. explaining its use as a fabric on ships for its strength and durability, as well as records of its use in Chinese culture in 2700 B.C., its western pharmacological use only began to be understood in the 1990’s A.D. (Green, 2002). Since the 1990’s, much research has been devoted to finding merit and explanation to the therapeutic use of cannabis as antiemetics, antispasmodics, analgesics and appetite stimulants, as well as the potential use in epilepsy, glaucoma and asthma. Its function as an anti-depressant has been noted but never researched, specifically its effects on the neurotransmitters dopamine, serotonin, and norepinephrine. Research that is interested in controlling and examining these neurotransmitters must be through the identification of the pharmacological effects that are receptor-mediated, and with the proper use of agonists and antagonists, we can begin to understand the effects of cannabis on these three neurotransmitters. Existing research has been plagued by small sample sizes, lack of statistical power, the use of different cannabis or cannabinoid preparations, and heterogeneous patient groups. The proposal for this study is to examine if cannabis could play a role in modern medicine in the treatment of melancholic depression, and that the activation of the cannabinoid system elicits anti-depressant and anti-stress behaviour.

Any medicinal properties of Cannabis are due to its content of cannabinoids, which are entirely unique to this plant species. Over 60 cannabinoids have been identified and the pharmacological properties of most of these are unknown, however, the most potent known psychoactive agent is 9-tetrahydrocannabinol (THC). Cannabinoids interact with specific cannabinoid receptors in the body, and two receptors have been identified: CB1, which exists in the brain and central nervous system (CNS), and was cloned in 1990, and CB2 in macrophages in the spleen and immune cells in other tissues (n11), which was cloned in 1993 (Howlett, Barth, Bonner, Cabral, Casellas, Devane, Felder, Herkenhan, Mackie, Martin, Mechoulam, & Pertwee, 2002). A complete understanding of any receptor requires the development and testing of selective antagonists in addition to agonists at that receptor. One of these CB1 receptor antagonists, rimonabant (SR141716), acts to selectively block CB1 receptors (Rinaldi-Carmona, Barth, Heaulme, Shire, Calandra, Congy, Martinez, Maruani, Neliat, Caput, Ferrara, Soubrie', Breliere, & Le Fur, 1994; Compton, Aceto, Lowe, & Martin, 1996), and has been widely used to understand the effects of cannabinoids in the CNS. The principle agonist used in studies of CB1 receptors is WIN 55,212-2, which acts by exciting glutamate transmission (Levenes, Daniel, Soubrie, & Crepel, 1998). Utilizing these agonists and antagonists in conjunction with the selective breeding process of knockout mice (mice lacking the cannabinoid receptors), experimenters can begin to understand how THC affects dopamine, serotonin, norepinephrine, and ultimately depression in the human body.

The initial interest in understanding how the cannabinoid system plays a functional role in the expression of emotional behaviour came from the documentation of the medicinal and recreational consumption of cannabis. Reports of elevated moods and feelings of euphoria, with reductions in anxiety, stress and depressive symptoms (Green, Kavanagh, & Young, 2003), has opened doors for research into examining if cannabis could have a role in the treatment of melancholic depression. Melancholic depression is attributed to 25-30% of depressed persons, and is a subtype of depression that is marked with hyperarousal, heightened anxiety, insomnia, reduced appetite, anhedonia, impaired behavioural flexibility and a predominance of aversive memories (Gold & Chrousos, 2002; Rush & Weissenburger, 1994). The pharmacotherapy of melancholic depression has been directed by the mounting evidence that the CB1 receptor is almost exclusively located on presynaptic axon terminals, and is capable of regulating calcium influx and thus neurotransmitter release (Nakazi, Bauer, Nickel, Kathmann, Schlickler, 2000). In related research, moderate to high CB1 receptor densities are found in the pre-frontal cortex, hypothalamus, amygdala, and hippocampus; structures that regulate such neurotransmitters as serotonin and norepinephrine release, among many others (Nakazi et al., 2000). Herein lays one of the many significant holes in the research of this specific topic.

There are several lines of evidence that suggest that the CB1 and CB2 receptors may be involved in depression. The first is that the CB1 receptors are located in the prefrontal cortex, hippocampus, hypothalamus, and amygdala, which are brain regions crucial for stress and emotional regulation (Malone & Taylor, 2006). The second is that a phenotypic state reminiscent of depression has been observed upon the genetic and pharmacological blockade of CB1 receptors (Hill & Gorzalka, 2005b). The third is that enhancements of receptor activity has been found to elicit antidepressant and anti-stress responses in both human and rat research (Hill &Gorzalka, 2005b). The fourth piece of evidence comes from the observed up-regulation of cannabinoid receptors upon exercise, environmental enrichment, and pharmacological anti-depressant treatment, eliciting antidepressant responses (Witkin, Tzavara, & Nomikos, 2005). The fifth piece of evidence comes from the observations of a dramatic down-regulation of cannabinoid receptors upon exposure to chronic unpredictable stress, a well-known precursor to depression (Hill & Gorzalka, 2005a).

Examining The Evidence - 1

The presynaptic localization of CB1 receptors suggests a role for the cannabinoid system in moderating the release of neurotransmitters from axon terminals, and this has been confirmed by several studies (Roth, 1978; Iverson, 2003). CB1 receptors are primarily found in the prefrontal cortex, hippocampus, hypothalamus, and amygdala, and this knowledge has been put to use by Malone and Taylor (2006) in a study they conducted with socially isolated rats. Malone and Taylor (2006) utilized rats reared in an isolated environment, and found that a production of behavioural and neurochemical alterations was elicited through altered dopaminergic and serotonergic neurotransmitter systems, much resembling what we refer to as schizophrenia. After administering THC (stimulation of CB1 and CB2 receptors) to socially isolated rats, Malone and Taylor found the rats demonstrated deficits in sensorimotor gating, which is the process by which an individual screens or filters the large flow of information from its surroundings (Malone, et al., 2006). They also found a significant reduction in prepulse inhibition (PPI), which refers to the ability of a weak stimulus to transiently inhibit a response to a closely following strong sensory stimulus (Malone, et al., 2006). Deficits in sensorimotor gating as well as impairments in PPI are primary characteristics of schizophrenia (Quednow, Wagner, Westheide, Beckmann, Bliesener, Maier, Kuhn, 2006). In summary, THC produces these effects through the activation of the cannabinoid receptors, and through this activation decreases in PPI are observed in rats with already dysfunctional sensorimotor gating processes. In other words, mice exhibiting schizophrenic behaviour before THC ingestion are found to elicit less schizophrenic behaviour following THC ingestion.
Unfortunately it is hard to generalize these findings since schizophrenia was somewhat “artificially” created by isolating rats, and such human experimentation would be grossly unethical. Irrespective of these confounding results, the experiment raises some interesting questions into the possible use of cannabis in reducing schizophrenic behaviour. This statement is made without warrant, however, and further investigation is needed to draw more conclusive evidence.


Examining The Evidence – 2

Another reason why the cannabinoid system may be involved in melancholic depression stems from the apparent similarities in the symptoms of melancholic depression and those observed in knockout mice. As Figure 1 illustrates, CB1 -/- mice (a.k.a. CB1 receptor knock-out mice) have elevated levels of “depressive”-like behaviours. Specifically, mice have been found to exhibit decreased mobility in the forced-swim test and are more susceptible to developing “depressive”-like effects in response to chronic stress (Hill & Gorzalka, 2005b). One of the core symptoms of melancholic depression is the decreased responsiveness to rewarding stimuli, or pronounced anhedonia (Parker, 2000). A body of research has gathered suggesting that the presence of the cannabinoid system is necessary for the ability to process rewarding stimuli, as CB1 receptor deletion or blockade (via the antagonist SR 141716) can reduce the reinforcing effects of a diverse set of artificial and naturally rewarding stimuli such as ethanol, nicotine, heroin, and sucrose (Economidou, Daina, Mattioli, Laura, Cifani, Carol, et al. 2006; De Vries, Homberg, Binnekade, Raaso, Schoffelmeer, 2003). In other words, subjects who lacked the CB1 receptor showed lower levels of ethanol, nicotine, heroin, and sucrose when given free-access (i.e. self-administration) compared to subjects who were CB1 receptor-positive.


Marijuana users have known for years the appetite-stimulating effects of smoking a joint (or any THC-ingesting method), and in fact, people suffering from such debilitating diseases as AIDS use marijuana as an appetite aid. It therefore wasn’t a surprise to researchers that mice given THC had increased levels of food consumption. They also found that mice given THC along with the antagonist SR 141716 ate less and subsequently lost weight (Marx, 2006). From these findings we begin to understand the effects of the blockade or genetic deletion of the CB1 receptor, and the deficits they create in the ability to experience rewarding stimuli.

Examining The Evidence – 3

To examine if the activation of CB1 receptors elicits antidepressant-like effects, Hill and Gorzalka (2005b) created four sets of groups in a study performed with rats. Four groups were created and were as follows:
1 – Rats were given the cannabinoid uptake inhibitor AM404
2 – Rats were given the CB1 receptor agonist HU-210
3 – Rats were given the CB1 receptor antagonist AM251 along with desipramine, an antidepressant control.
4 – Rats were given oleamide, a cannabinoid receptor activating compound.
After inducing the subjects to the pharmacological state mentioned above (respective to their grouping), the rats were placed in a controlled environment swim-test for a duration of five minutes, and observed. Reductions in immobility (i.e. increased mobility) were observed in the groups with enhancements of CB1 receptors, which is said to be the signal of antidepressant effects much similar to those seen in conventional antidepressant studies (Hill & Gorzalka, 2005b). In related research, CB1 receptor knock-out mice revealed altered emotional behaviour, specifically, they were found to have elevated anxiety levels when observed to behavioural tests such as the light-dark box and the resident-intruder test (Martin, Ledent, Parmentier, Maldonado, Valdverde, 2002). Furthermore, the knock-out mice had increased sensitivities to such emotional-related behavioural responses, and exhibited greater depressive-like responses (Martin, et al., 2002).

Alternations in vegetative functioning (eating habits), is one of the hallmark symptoms in melancholic depression, and the cannabinoid system has a critical role in the regulation of this functioning. In regards to feeding behaviour, the activation of the cannabinoid system increases the consumption of palatable foods (Abel, 1975). This finding is so robust that the CB1 receptor antagonist SR141716, is being researched and marketed as an anti-obesity compound (Van Gaal, Rissanen, Scheen, Ziegler, Rossner, 2005).
Taken together, these findings demonstrate a correlation between the activation of the CB1 receptors and the regulation of emotional behaviours such as anxiety and depression.

Examining The Evidence – 4

Athletes have long been aware of a “euphoric-high” that is brought on by endurance exercise, and this has plagued researchers who have attempted to explore the phenomenon due to its subjective nature. The phenomenon is commonly referred to as the “runners-high”, and is describes as a momentary lapse of pure happiness, elation, inner harmony, and a reduction in pain sensation (Frayne, 2002). Research interested in this phenomenon have typically focused on the opioid receptor network, which was discovered in 1975, and one of the more popular explanations is to the runner’s high is the “endorphin hypothesis” (Heitkamp, Schmid, Scheib, 1993). The endorphin hypothesis states that when a subject undergoes rigorous (lengthy) exercise, elevated blood-levels of β-endorphin and adrenocorticotropic hormone can be found (Heitkamp, Schmid, Scheib, 1993).

Since the discovery of the cannabinoid receptors, the phenomenon has become better elucidated, as Dietrich and McDaniel (2004) have found a link between the subjective reports of a “runner’s high” with the activation of the cannabinoid system. Dietrich and McDaniel (2004), found increased levels of blood-serum concentrations of cannabinoids both during and following high-exercise activity, and which has reported decreases in pain-perception likely through the sequential activation of dopamine receptors (Dietrich, McDaniel, 2004). Since the cannabinoid system is found both in the brain and peripheral tissue, it is said that this hypothesis has greater validity than the endorphin hypothesis which does not give support to this decrease in pain-perception through the peripheral tissue (Dietrich, McDaniel, 2004). The interaction of the cannabinoid system with dopamine demonstrates an explanation to the brain’s reward system, and thus the addiction that is reported alongside the “runner’s high”. Further research is necessary to explain the precise nature of the activation of cannabinoid systems in response to exercise to help solidify the hypothesis that cannabis is an effective anti-depressant.

Examining The Evidence – 5

Another symptom that has been said to occur in melancholic depression is neurodegeneration (Gold & Chrousos, 2002). This is based on the findings of hippocampal and cortical atrophy in in vivo imaging scans of depressed persons (Sheline, Wang, Gado, Csernansky, Vannier, 1996). The hippocampus plays a key role in the regulation of food and cognition, and is often subject to evaluation in individuals with mood disorders. In several studies, subjects with major depression as well as with melancholic depression were found to have reduced hippocampal volumes (Sapolsky, 2001; Sheline et al., 1996). In related research, chronic exposure to unpredictable stress in rats has shown dramatic reductions in the down-regulation (the process by which a cell decreases the number of receptors to a given hormone or neurotransmitter, thus reducing its sensitivity to the molecule) of the cannabinoid system in the hippocampus (Hill & Gorzalka, 2005a). Under the same stress-inducing situation, enhanced basal levels of corticosterone (Hill & Gorzalka, 2005a) as well as the production of adrenal hypertrophy (Hill & Gorzalka, 2004), both comparable to the changes seen in patients with depression. Research with animals has also found evidence that environmental enrichment elicits antidepressant-like effects, and decreases the levels of neurodegeneration seen in subjects without such environmental enrichment (Young, Lawlor, Leone, Dragunow, & During, 1999; Brown, Cooper-Kuhn, Kempermann, Van Praag, Winkler, Gage, et al. 2003). In summary, the downregulation of cannabinoid receptors occurs when subjects are exposed to chronic unpredictable stress, and the enrichment of one’s environment has mediating effects on downregulated receptors.

Method

Participants
The participants were 160 individuals (M age = 30.20) who were recruited through ads placed in the local newspaper (83 female, 77 male), and were identified with melancholic depression by the administration of the Beck Depression Inventory (BDI). Administration of the BDI is done under a controlled environment (i.e. supervised) and took participants on average 10 minutes to complete.

Design and Materials

The participants were randomized into eight groups, proportionately. In three groups, the synthetic form of THC, marinol, was used in ranging dosages of 2.5mg, 5mg, and 10mg. In three groups, the tricyclic (TCA) antidepressant desipramine was given in dosages ranging from 2.5mg, 5mg, and 10mg. A control group was created for both independent variables (respectively, groups 1 and 5) with participants receiving placebo pills (0mg).

A 2 (marinol and desipramine) x 4 (0mg, 2.5mg, 5mg, 10mg) between-subjects design was used to explore the effects of the independent variables on scores of depression. To minimize confounding variables, all eight groups were randomly assigned and were “blind” in that they were unaware of not only what they received but also of the existence of multiple groups. Following the study, the BDI was administered again to attain the second set of scores (test-retest reliability, which lent data that was calculated into correlation coefficients). Since the administration of the independent variable was through the digestive tract, instantaneous testing would have been impossible or at least decrease the validity of scores. The study therefore was conducted over a period of thirty-days, and subjects were instructed to take their assigned pill once a day for the thirty-day duration.

Since the scoring of each item on the BDI ranged from zero to three (zero meaning neutral and three meaning severe), with a total of ten items, the higher the scoring values the greater the participants depression is said to be (Wikipedia, 2006). It was predicted that increasing negative correlation values would be found among the increasing dosages of marinol, with no correlation found among the control group. The same predictions were made for the second independent variable, desipramine, in that subjects were expected to score higher on the BDI the lower the dosage of the drug they received, and score lower on the BDI the higher the dosage they received.

Results

Figure 2 2 x 4 factorial design: Results of the BDI test 1 (before)

Drug Administration Type Level of Drug
0mg 2.5mg 5mg 10mg
Marinol 6.25 5.89 6.02 5.95
Desipramine 6.13 5.76 5.97 6.03


Figure 3 2 x 4 factorial design: Results of the BDI test 2 (after)

Drug Administration Type Level of Drug
0mg 2.5mg 5mg 10mg
Marinol 6.31 5.42 4.76 3.96
Desipramine 6.08 5.25 4.55 3.91


The data was analyzed using a 2 (marinol and desipramine) x 4 (0mg, 2.5mg, 5mg, 10mg) between-subjects design to determine the effects of variance on the BDI testing. Since the higher the dosage of drug administered correlated with lower scores on the second BDI (the re-test), we see a downward slope of the results between Figures 2 and 3. It is hard to visualize the variances between the two scores of each independent variable, but when we plot the values on graphs (graph 1 and 2) we can clearly see this negative correlation. This trend occurred in both groups using marinol and desipramine, confirming the hypothesis that the activation of the cannabinoid receptors elicits antidepressant effects similar to those found in conventional antidepressant drug treatment (i.e. desipramine). Mean values of the difference in scores in levels one to four in the marinol groups were (M = -0.06, 0.47, 1.26, 1.99), and the mean values of the differences in scores in levels one to four in the desipramine groups were (M = 0.05, 0.51, 1.42, 2.21). As expected, the results from the control group found no significance between scores on the first and second BDI testing.

Discussion

The results of the present study confirm the hypothesis that the activation of the cannabinoid system alleviates melancholic depression similar to those experienced by the more conventional anti-depressant medication desipramine. Although the hypothesis was validated through the study, it was not without limitation. Since the participants were attained through local newspaper ads, a true random sampling of the general population can not be reported. Similarly, scores on the BDI ranged significantly, in other words, the severity of melancholic depression ranged before the independent variables were introduced. Therefore, large differences in first and second scores on the BDI can be attributed to both the independent variable as well as the severity of each participant’s depression. In other words, it is easier to find significant differences in scores when participants began the study with severe cases of melancholic depression then it would be to find differences in scores when participants began the study with mild cases of melancholic depression.
Another potential limitation revolves around the self-reported fluctuations of depressive feelings, and since the study was conducted over a period of 30 days, participants could have been tested at times when they were feeling more or less melancholic then how they felt on average. This limitation could have been minimized had the study been performed in shorter duration with the use of a faster-acting form of THC-induction (i.e. smoking, intravenous, etc.) but this would have raised greater ethical limitations.


Aside from these limitations, the cannabinoid system was proven to play a role in alleviating melancholic depression, which is consistent with similar studies performed with rats. Further investigation into the effects of cannabis should be directed with the use of faster-acting forms of medication, as well as greater control of admitted participants in regards to pre-test melancholic depression levels.

Through the following study, we have helped to elucidate and correlate the effects of dopamine, serotonin, and norepinephrine in subjects with melancholic depression. However, there is still a large amount of unknown information in regards to the long term consumption of THC and its effects on the CB1 and CB2 receptors, and whatever health implications it may cause.







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[jcsmooth]

Alright, it worked!
I've been reading icmag for about two years now, and the old overgrow for one or two more....never really felt the urge to post.
Glad to know I can though

Hope that little paper didn't bore you to death.

JC

[I2KanGrow]

Yo JC, you forgot to include "And besides, it's fun!" in your dissertation.

You're welcome, and - there's absolutely no need to cite me!

Getaway from me, cannabis, you're always blowing smoke up my ass!!

Is Cannabis a getaway?

If done correctly...

ws