CANNABIS AND THE BRAIN

CANNABIS AND THE BRAIN: Iversen, L, Brain. 2003; 126: pp. 1252-1270. A large literature exists on the effects of cannabis,this review focuses mainly on the more recent literature in this field.

In 1990 Israeli scientists discovered 'receptors' in the human brain which are uniquely suited for cannabis. In 1992 a special protein binder was identified.

Cannabis acts on specific cannabinoid receptors in the brain. Such receptors have been found in humans, in rats, chickens, turtles, trout and possibly even in fruit flies.

This distribution may suggest that the gene responsible must have been present early in evolution, and its conservation implies that the receptor serves an important biological function.

Since THC is not a naturally occurring substance within the brain, the existence of a cannabinoid receptor implied the existence of a naturally occurring or 'endogenous' cannabinoid-like substance. A brain molecule which binds to the receptor was identified (by Devan in 1992). The molecule is called arachidnylethanolamide and is fat soluble like THC. It has been called anandamide from the Sanskrit word meaning bliss' This substance has no effect on cells which do not have the receptor. The biological role of the anandamide molecules remain unknown. (Above extracted from Australian Government Report)

The action of cannabis in the brain is completely different to the actions of hard drugs. The latter effect levels of a chemical called dopamine which occurs naturally in the brain. This is the chemical which enables us to feel pleasure. Heroin and cocaine and derivatives repress the production of dopamine. The pleasure or high of the drug is caused by artificially boosting the pleasure centres. When the drug wears off the natural dopamine production is lowered and the user wants more drug. This is particularly true of cocaine where the high is short lived. A snort of cocaine usually makes one want another line soon. Long term use of hard drugs has a more disastrous effect and abstinence produces withdrawal symptoms, the user often unable to feel any pleasure at all.

Many people who use cannabis think they simply do so for the buzz. In fact cannabis is not only a medicine which makes people well, it is also a preventative medicine. Some people seem miserable or even angry when their supply of cannabis runs out; this is because that is how they used to be before taking cannabis.

A very few people have allergic reactions to cannabis. Some of these are to grass and not to hash. Even fewer people have negative metal effects - sometimes wrongly called 'cannabis psychosis'. These reports are complicated because the person has sometimes consumed other substances such as cocaine or LSD at the same time as cannabis or in the past and have not reported it to their doctor, so cannabis gets the blame. Other complications are the impurities in the cannabis and a possibly unbalanced mind to start with.

THE RECEPTOR

TAMPA, Fla., June 9 /PRNewswire/ --
In Dr. Thomas Klein's crowded laboratory office, beneath the shelves of scientific journals hangs a preserved puffer fish with an imitation joint dangling from its mouth.

Even the ancient blowfish has been found to harbor chemical receptors that react to delta-9 tetrahydrocannabinol, or THC, the compound in marijuana that produces a high said Dr. Klein, professor of medical microbiology and immunology at the University of South Florida.

"It's fascinating," he said. "Why would both humans and this fish evolve with the genes for a receptor that would only be activated if you smoked marijuana? Conservation through evolution suggests that the gene is important.

"We now know there's a substance circulating in the body called anandamide that binds to cannabinoid receptors. So there's definitely a physiological role for endogenous cannabinoid receptors, possibly in behavior modification or defining moods as well as regulating immunity and other functions."

Dr. Klein is a pioneer in the new field of psychoneuroimmununology. He studies physical links between drugs of abuse and the brain, emotions and immunity.

Supported by a $674,000 National Institutes of Health grant, he heads one of few scientific groups in the world investigating the function of cannabinoid (marijuana) receptors in the immune system. Cannabinoid receptors have also been found in the brain, the gut and the reproductive system.

Cells imbedded with these receptors are inhibited from functioning when exposed to the THC molecule.

Pot's influence on the immune system continues to be hotly debated within the medical community. Animal and human studies have demonstrated that virtually every immune function, from antibody production to the destruction of invading microorganisms, is suppressed by relatively high concentrations of marijuana. In those whose immune responses are already poor, marijuana may aggravate deteriorating health.

"It's believed to be a rather benign drug, effective in reducing pain and nausea," Dr. Klein said, "but scientific evidence is accumulating, through the study of the cannabinoid receptor system, that THC might affect almost every cell in the body.

"People need to know that if they smoke marijuana, they are not just altering their moods. They're altering their immune systems."

Scientists may know more about marijuana's hazards or benefits to health once they understand how the cannabinoid system fits into the body's complex network of immune regulation.

Dr. Klein suspects the natural purpose of cannabinoid receptors may be to control more powerful immune systems serving as the body's first line of defense against infection or tumors.

"The horse gets the buggy started, but the cannabinoid system is like the driver with the whip who keeps things going," he said.

A BRAIN SHIELD FROM--WELL, MARIJUANA

From : Business Week, November 4, 1996, Pg. 199

The first drug to curtail the spread of brain damage resulting from strokes and head or spinal cord injuries has entered clinical tests at six hospitals in Israel. Its key ingredient is dexanabinol, a synthetic molecule based on the active agent in marijuana. Dexanabinol was discovered six years ago by Raphael Mechoullam, a researcher at Hebrew University in Jerusalem, and developed by the Rehovot (Israel) research arm of Pharmos Corp. in Alachua, Fla.

Dexanabinol has two novel properties: It can cross the so-called blood-brain barrier that prevents foreign molecules from entering the brain. And once in, the drug appears to halt the brain-cell deterioration that follows a blow to the head or a stroke. In four years of animal testing, the drug produced "outstanding" results, says Michael Schickler, vice-president of Pharmos' Israel operations. Pharmos expects clinical tests to be completed by the end of 1997. If it works, dexanabinol could hit the market by 2000.

CANNABIS AND I.Q.

The Coptic Study of 1981 stated: 
...I.Q.'s of Zion Coptics increased after they began to use ganga

Messengers of the Brain

by Marcia Purse

You're taking Prozac, and you've heard it described as an SSRI. Maybe you know that SSRI stands for selective serotonin reuptake inhibitor. But that's quite a mouthful -- what does it mean?

In other pages on this site, we look at medications that are commonly prescribed for mood disorders, such as manic depression. Included in these reviews is a brief description of how each functions -- or is thought to function, since many are still being studied.

In order to make sense of any of this, it is necessary to understand something about how impulses are transferred from one nerve to the next, since medications such as mood stabilizers, antidepressants and antipsychotics all affect this process to bring about changes. In this article, I will give a brief, simplified description of how the brain's message carriers (neurotransmitters) operate, and then try to clarify the process by telling the illustrated story, "GABAs in the 'Hood." *

Neurotransmitters

There are several of these, but the ones that are most related to mood disorders are:

• The monoamines - serotonin, norepinephrine and dopamine
• GABA (gamma amino butyric acid)
• Glutamate

Others that come into play, with some side effects, are acetylcholine, which transmits orders to the muscles, and histamine, which has a lot to do with allergies, appetite regulation, weight gain (for those on certain medications), and sleep quality.

When a message comes in at one end of a nerve cell, an electrical impulse travels down the "tail" of the cell, called the axon, and causes the release of the appropriate neurotransmitter. Molecules of the neurotransmitter are sent into the tiny space between nerve cells, called the synaptic cleft. There, one or more of the following can occur for each molecule:

1. It may bind (attach) to the receptors in the adjacent nerve cell, send the message on, leave the receptor, then repeat this process or go on to one of the other steps.
2. It may hang around in the synapse until a receptor becomes available, bind to it, release, and continue with steps 1 to 3 until its activity is ended by steps 4, 5 or 6.
3. It may bind to the first cell's autoreceptors, which tell that cell not to release any more of the neurotransmitter molecules, then leave the autoreceptor and continue trying to bind again somewhere until its activity is ended by step 4, 5 or 6.
4. It may be rendered inactive by an enzyme.
5. It may be reabsorbed by the first cell in the "reuptake" process, and recycled for later use or deactivated.
6. It may diffuse out of the synapse and be deactivated elsewhere.

Now, so many things can go wrong with this process that it's not surprising mood disorders are fairly common. For example:

• The nerve cells (neurons) might not be manufacturing enough of a neurotransmitter.
• Too many molecules of the neurotransmitter may be dissolved or deactivated by enzymes.
• Too much of a neurotransmitter may be released.
• The molecules may be reabsorbed too quickly by the reuptake transporters.
• The autoreceptors may be activated too soon, shutting down the release of neurotransmitter molecules prematurely.

Or there could be some other circumstance involving electrically charged particles of potassium, sodium, chloride or calcium. It's enough to make your head hurt, isn't it?

Here, let's look at it another way.

Communication at Brain Complex, or "GABAs in the 'Hood"

To start with, look at Figure 1, which is a very simplified drawing of a synapse.

Figure 1


Figure 2
For our story, let's change the components shown above into something more familiar -- parts of a neighborhood. The two neurons are Building A and Building B of Brain Complex. They are separated by a narrow street (the synaptic cleft). The GABA terminal button is now a motor pool. Each vesicle containing neurotransmitter molecules becomes a minibus filled with GABA Team messengers. The receptors and autoreceptor become phone booths. The reuptake transporter, where neurotransmitters are sucked back in to be recycled, changes to an inviting coffee shop. And the enzymes are assassins on motorcycles. (No offense meant to motorcycle lovers!)

So over in Building A, the driver of each minivan gets a call from the front office (that's the neuron's cell body, not shown) on his cell phone: "Send this Message over to Building B!" And right away things start to happen.

Figure 3

Immediately the drivers take their vehicles (that is, vesicles) to the garage exit and release the GABA Team messengers (neurotransmitters) into the street (synaptic cleft) between Building A (the sending neuron) and Building B (the receiving neuron). Like sprinters, the GABAs take off quickly, each looking for a phone booth that matches his or her uniform (they could not get into any other color booth). Gertrude, Gerald and Gloria get there first. Quickly each slips into a booth (Figure 4) and makes a call into the office (cell body) of Building B, relaying the Message. Then each backs out and looks for another booth. All the GABA messengers are elbowing each other out of the way (and dodging motorcycles) to get into the available booths and make the same call if they get in.

Figure 4
But there are some traps and hazards for the GABA team. George GABA never makes it to Building B at all -- he has been knocked unconscious by a motorcycle-riding assassin (enzyme). His color change denotes that he has forgotten the message now -- in essence, he has been "deactivated."

Meanwhile, Glenn GABA has gone to the phone booth attached to Building A. "There's too many of us out here," he tells the front office. "Don't send any more." Then he, too, goes back out into the street. When the front office gets enough similar calls, the minivan drivers will be told to return to the motor pool and not send any more messengers out.

And then there is that seductive coffee shop (reuptake transporter) on the other corner of Building A. If a messenger gets close enough to smell the heavenly aroma of fresh coffee and doughnuts, he or she will surely be sucked in, and once inside, will be refreshed and then return to the motor pool to await the next assignment. Eventually all the surviving GABAs will return home via the coffee shop.

The whole event has taken no more than a millisecond.

---

Now as you have probably realized, it isn't really this simple. But this illustration will give you a basic idea of how neurotransmitters operate and why it is so important that they operate correctly. It's crucial that neither too many nor too few of them are released into the cleft, the autoreceptors and enzymes are working properly, and that a myriad of other factors fall into place to contribute to a healthy process. When they don't, you can get illnesses like Parkinson's, which is caused by a dopamine deficiency; or you may have tetanus, which prevents the release of GABA and can be fatal if breathing muscle control is lost. Or you might have schizophrenia, which is thought to be caused by an imbalance of dopamine, or epilepsy, apparently caused in part by an overabundance of GABA.

My goal with "GABAs in the 'Hood" has been to provide an easy-to-understand description of basic neurotransmitter functions. Remember the team messengers and their adventures in the 'hood as you read other articles!


_{Thanks to Richard Schuergar, Former About Guide to Neuroscience, for his contributions to this article.}

Lithium: The First Mood Stabilizer

Part 1: History and a Mystery Solved

By Kimberly Read & Marcia Purse, About.com

Lithium, discovered in 1817, was noticed to have mood stabilizing properties in the late 1800s when doctors were using it to treat gout. (At least one doctor, in fact, concluded from this that gout was the cause of mood disorders.) It was Australian psychiatrist John Cade who, in 1949, published the first paper on the use of lithium in the treatment of acute mania. The U.S. Food and Drug Administration did not approve lithium for use until 1970.

It's important to know that bipolar disorder is not caused by a lithium deficiency. Rather, it happens that this naturally occurring substance has the fortunate effect of acting as a mood stabilizer.

For almost 50 years, manic-depressive people were treated with lithium even though medical science did not know why or how it worked. Then in 1998, University of Wisconsin researchers unlocked the mystery. It has to do with nerve cells in the brain, and the receptors for the neurotransmitter glutamate.

As I described in the article "Messengers of the Brain," neurotransmitters are released from one neuron (nerve cell) and may bond to the receptors of a neighboring cell or be picked up by autoreceptors from the releasing cell (among other things). The result varies depending on what the type of receiving cell and the type of neurotransmitter.

The University of Wisconsin researchers found that lithium exerts a dual effect on receptors for the neurotransmitter glutamate - acting to keep the amount of glutamate active between cells at a stable, healthy level, neither too much nor too little.

UW Medical School professor of pharmacology Dr. Lowell Hokin, who directed the research, said that from their research it could be postulated that too much glutamate in the space between neurons causes mania, and too little, depression. There has to be more to it than that, since antidepressant medications, for example, work on the receptors of other neurotransmitters such as serotonin and dopamine. However, this is certainly a giant step forward in understanding the biological basis of bipolar disorder.

Note: a large amount of extra glutamate can lead to epileptic seizures or even kill the second cell from overstimulation. Because of Lithium's stabilizing effect on glutamate receptors, scientists are also studying whether this medication can protect from the cell death that occurs in conditions such as Parkinson's, Huntington's and Alzheimer's.

Part 2: Tests and Toxicity
Part 3: Precautions and Warnings
Part 4: Whoa, Fat!

Cannabinoids in Bipolar disorder

Cannabinoids in Bipolar disorder

The role of cannabis (marijuana) in psychiatric disorders remains controversial. In bipolar disorder, it is known that many people use cannabis for various reasons. There are some reports that people use cannabis for help in alleviating mania and others report its use for relieving depression. However, these reports are anecdotal and no systematic research has ever been done to see if these effects apply to the population in general. Additionally, there are reports that indicate that cannabis can have a detrimental and potentially causative role in the development of psychosis and paradoxically, can induce mania. The authors of this paper conducted a literature search to identify what has been published regarding the relationship between cannabis and bipolar disorder. Additionally, they looked at other ways of ingesting cannabinoids (the type of molecule that is the active ingredient in marijuana). The active ingredient in marijuana is called delta-9 tetrahydracannabinol but there are other similar cannabinoid molecules that can be utilized to harbor similar effects.

When marijuana is ingested, the active ingredient triggers a receptor in the brain called the CB-1 receptor. CB-1 receptors are part of what is called the "endocannabinoid" system which broken down means "endo" or endogenous (naturally present in the body) cannabinoid system. The evolution of this system indicates that our bodies naturally produce cannabinoid-type molecules, which in fact is the case. CB-1 receptors are plentiful in the areas of the brain considered to be involved with bipolar disorder with the highest levels in the basal ganglia, cerebellum and hippocampus. There are similar receptors in the peripheral body, called CB-2 receptors. They are seen primarily in immune cells. It is not known precisely what effect the CB-2 receptors have with the effects of cannabis.

Unfortunately, no controlled trials of THC have been done in bipolar disorder. Anecdotal evidence is fraught with peril in terms of making major judgments because it is not controlled and there is no objective comparison to understand the benefit due to the drug itself versus other effects associated with taking the drug or placebo effect. Additionally, it is seen that the effects of THC are often "bidirectional" which means that it is possible that in some people THC will relax, often in similar effectiveness as benzodiazepine (valium for example) medications, but in other people will cause anxiety and change physiologic parameters that leads to furthering of anxiety. It may make people tired or in others increase alertness and in some it may lead to depressed feelings while others feel a high and levels of euphoria.

Because there is evidence, particularly in certain genetically susceptible individuals, of psychosis being related to usage of cannabis, it should be with extreme caution that one uses such a drug if they have a diagnosis of bipolar disorder. Additionally, as it can provoke mania in some people, extreme caution should be used before one takes this drug if they have a diagnosis of bipolar disorder. THC also can interfere with the action of psychiatric medications, primarily the atypical antipsychotics which are frequently used as anti-manic agents. Lastly, it has been shown that the effects of marijuana are often more severe in people already diagnosed with psychiatric disorders.

However, given the anecdotal evidence, it does appear that for some people marijuana is beneficial. Any decision to use it should be well considered and best discussed with physician and should be done under very careful supervision. Before an evidence-based recommendation can be made regarding marijuana, a double-blind, randomized controlled trial will need to be conducted both for safety and effectiveness. The authors are advocating for such research to be conducted and one can only feel that to know the results of this kind of research would be beneficial. Additionally, if such research were to show a positive benefit, more standardized methods of taking the THC, such as a sublingual spray, could be created such that it could be given in a therapeutic dose. Inhalational THC, smoked marijuana for example, varies in potency and in the depth of inhalation by the consumer and can lead to different effects even with the same product. Standardized dosing would also allow for a lower dose to be taken which may be equally effective but with fewer risks, (psychosis, mania, or hypomania in particular) than conventional inhalational means allow for. Additionally, a commercially prepared medication could include a similar cannabinoid called cannabidiol to further help temper the drug to lower side effects.

Ashton CH, Moore PB, Gallagher P, Young AH. 
Cannabinoids in bipolar affective disorder: a review and discussion of their therapeutic potential.
J Psychopharmacol. 2005 Sep;19(3):293-300.

Lithium, Circadian Clocks and Bipolar Disorder

Lithium, Circadian Clocks and Bipolar Disorder
I have previously only touched on the immensely interesting topic of the possible connection between circadian clocks and the Bipolar Disorder. A recent paper prompted me to look into this in a little more detail.

Lithium Affects the Circadian Clock

First, let's go a little bit into the past, the early history of chronobiology. During the 1940s and 1950s, while the field was still in its pioneering spirit and little was known about the circadian clocks, many researchers were using survey (or shot-gun) approaches to the studies of biological rhythms: studying as many organisms as they could get their hands on in order to come up with generalities and evolutionary answers, surgically removing every possible organ or brain region in order to find locations of clocks in various organisms, exposing the organisms to every possible light regimen imaginable in order to study the oscillatory properties of biological clocks, etc.

One of the approaches was to administer to animals every chemical one could find on the lab-shelf to see how it affects the circadian rhythms. This line of work yielded a big surprise - biological clocks are amazingly resistant to pharmacological agents. The few substances that had an effect were hormone melatonin (naturally, as it is the main signaling molecule of the circadian system), heavy water (deuterium oxide) and lithium (a few others were found much later, including sex steroid hormones). Lithium had the same effect - slowing down the clock, i.e., increasing the period - in a number of philogenetically very distant organisms.

Lithium affects the Bipolar Disorder

At the same time, lithium was one of the most prescribed drugs for treating bipolar disorder (at that time usually called "manic-depressive disorder"). Soon enough, people started making the links between effects of lithium on bipolar dissorder and the effects of lithium on the circadian clock. Is the bipolar disorder essentialy a circadian clock disorder?

During periods of depression, the circadian rhythms are phase-advanced.
Lithium is supposed to phase-delay the phase-advanced rhythms, i.e., bring them back to the normal phase. Here is an actograph of the sleep-wake cycle of a bipolar patient treated with various drugs, including lithium, as well as phase-shifts of the light-dark cycle, over a long period of time.
Lithium Affects Circadian Pacemaker Cells in a dish

Much more recently, it was discovered that each individual pacemaker cell (in the suprachiasmatic nucleus of the hypothalamus) in the mammalian circadian system responds to lithium. In other words, the effects of lithium are not at the system level (e.g., interfering with cell-cell communication), but on the level of the cell. This suggests that lithium may act on a particular clock gene and the search for the gene in question commenced.

To make things easier, the candidate clock-gene target of lithium is likely not to be limited to mammals, or vertebrates, as lithium has the same effects on rhtyhms in other organisms, including the fruitfly Drosophila melanogaster. Thus, it is likely that the target clock gene is one that is shared by the circadian clocks in Invertebrates and Vertebrates, thus somewhat narrowing down the list of candidates.

Molecular Mechanism of Circadian Rhythm Generation in Mammals

Let me now try to explain how the mammalian circadian clock works on the molecular level in as simple way as possible, so the non-scientists reading this can - hopefully - understand. Biologists can follow the links for more detailed information if so inclined. In order to do this, I will first give a super-simple primer on molecular biology (I hope I don't make any stupid mistakes on this part as I type it very fast in order to get to the cool new stuff). This is an oversimplification, so I hope molecular biologists do not chastise me for omitting all the extraneous details, as much as they may be important. This is BIO 101.

We are all composed of billions of cells. All of the genetic material - DNA - is found in the nucleus of each cell. DNA is a very long linear molecule, built like a chain out of many, many links. The links in the chain are the nucleotides, each made of a sugar molecule, a phosphate and a nucleic acid. There are four types of nucleic acids in the DNA: adenine, thymine, cytosine and guanine (A, T, C and G). The order of links with different types of nucleic acids on the DNA chain is the "code".

Genes involved in the generation of circadian rhythms can be loosely classified into core clock genes and associated clock genes. The core clock genes are almost all transcription factors. Their proteins act by inhibiting or stimulating transcription of other core clock genes (as well as regulating expression of other - downstream - genes that serve as functional outputs of the cell, i.e., telling the body when to relase a hormone and when not, when to sleep, when to wake up, etc.).

If core clock genes were all there is, the circadian cycle would last only a couple of hours, at best. That is how long it takes for all the players to switch on and off each other once. In order to prolong the cycle to be closer to 24 hours, oter genes are associated with the clock. Their protein products act as modifiers - they may add or remove phosphate groups on core clock genes, inhibit or stimulate expression of some of the core clock genes, degrade the core clock proteins either spontaneusly or upon receiving a signal that the retinae have perceived light, etc.

How lithium affects the molecular clock?

A couple of years ago, it was proposed that the protein involved in the clock mechanism that is sensitive to lithium is not one of the core clock genes, but one of the accessory genes - namely Glycogen Synthase Kinase 3ß (GSK3), which, in turn, acts on Rev-Erb, which in turn acts on Bmal.

Now, a new paper came out with more evidence that this is so:
Nuclear Receptor Rev-erb{alpha} Is a Critical Lithium-Sensitive Component of the Circadian Clock by Lei Yin, Jing Wang, Peter S. Klein and Mitchell A. Lazar. You can find the press-release and excellent media commentary here, here, here, here, and here.

According to this paper, lithium inhibits GSK3. GSK3 normally protects Rev-Erb from destruction. Rev-Erb normally inhibits expression of the core-clock gene Bmal (and perhaps also Period). Thus, when lithium is present, there is no GSK3 to protect Rev-Erb from being broken down. Without Rev-Erb, Bmal and Period get expressed again.

Perhaps this all means that in the Bipolar Disorder the clock gets "stuck" in some way. Perhaps Rev-Erb accumulates and stops the clock from running. Lithium indirectly aids the distruction of Rev-Erb, thus allowing the circadian cycle to proceed.

As they say:
"These results point to Rev-erb as a lithium-sensitive component of the human clock and therefore a possible target for developing new circadian-disorder drugs. Some patients taking lithium have developed kidney toxicity and other problems. Lazar surmises that new treatments that lead to the destruction of Rev-erb would have the potential of providing another point of entry into the circadian pathway."

from http://circadiana.blogspot.com/2006/...d-bipolar.html

City Attorney Silent on San Diego Cannabis Regulations

Hope Unlimited has asked the City Attorney's office to clarify the guidelines for cultivating and possessing medical cannabis in the City of San Diego. Patients are forced deal with San Diego law enforcement officials on a daily basis who have a variety of opinions on the current law regarding medical marijuana.
The City Attorney's office has the power to take a public stand for State Law.

Hope Unlimited members have contacted the City Attorney's office over 100 times requesting clarification on what the
current guidelines are for growing medical cannabis in the city of San Diego.  We have had no response from Mike Aguirre or his staff. 
His office has been informed that there are over 80 Hope members who are legitimate medical cannabis patients who deserve an answer.
They know that many of our members have families need to know they are within the established limits for possession and cultivation of medical cannabis.

If more Hope Unlimited members contact the City Attorney we can make it harder to ignore us!


You can either write an email or give her a phone call. --below find a script to send by email or read to his office.

REMEMBER EVEN A FEW PHONE CALLS or emails  MAKES A DIFFERENCE!

Office of the City Attorney
Civic Center Plaza
1200 Third Ave., #1620
San Diego, CA 92101
Phone: (619) 236-6220
TDD/TTY: (619) 702-7198
Fax: (619) 236-7215
E-mail: cityattorney@sandiego.gov


SAMPLE SCRIPT

Mr Aguirre,

Hope Unlimited is a group of patients and caregivers using cannabis for relief of chronic medical
conditions. Our group is concerned with following established guidelines for medical marijuana use. We are seeking
clarification from the City’s Attorney’s office on current policy towards medical marijuana in the City.
Patients and law enforcement officials need clear guidelines for this program to be successful.
We are operating under guidelines established in September of 2003: Adult marijuana patients with the approval of a San
Diego County doctor may keep up to 1 pound of marijuana and grow up to 24 plants. Under the measure,
caregivers can keep up to 2 pounds of marijuana and grow up to 48 plants for as many as four patients. Are
these still acceptable guidelines?

The suit by the County of San Diego to avoid issuing medical marijuana ID cards has now moved to appellate
court. It is our view that this suit has a slim chance of being decided in the County’s favor. What action
can we expect on ID cards from the City/County after this ruling?

Thank you

Anecdotal Evidence for Treatment of Bipolar with Cannabis

Scientific and medical research of medical cannabis has been limited by the Food and Drug Administration's (FDA) classification of marijuana as a Schedule I drug. A schedule I drug is one with a high potential for abuse and NO MEDICAL VALUE. Crack, PCP, heroin and meth are schedule II drugs. This category is reserved for drugs with a potential for abuse but with legitimate medical uses. Psilocybin (magic mushroom) is another Schedule I drug. The FDA is telling us marijuana and mushrooms are much more dangerous than Crack, PCP, heroin and meth. If you don't believe me read it for yourself,

FDA Drug Schedule / DEA Shopping List


So why are California doctors recommending medical marijuana if it has no value? Why are they not recommending a drug our government thinks has medical value... medical meth perhaps? The answer lies in anecdotal evidence. When you get past the rhetoric and talk to actual bipolar sufferers you find a surprising number who medicate with marijuana. Cannabis is by no means a panacea for everyone with bipolar disorder. But anecdotal evidence clearly shows that it gives significant relief to sufferers of bipolar.

The scientific/medical community sees it as a chicken and the egg question. Do sufferers of depression smoke marijuana because they are depressed or are they depressed because they smoke marijuana? It's an easy question to answer for most people.... marijuana provides relief for their symptoms. For those who feel they are depressed because they are smoking marijuana there are a huge number of well-funded organizations out there to help them. Here is a very small sample:

Marijuana Addiction Drug Rehab
Marijauna Addiction Treatment
How to Stop Smoking Marijuana.com
Marijuana Anonymous


Clearly there are a huge number of free resources available to anyone who feels marijuana is detrimental to their health. Those who experience a benefit from medical marijuana are not so lucky. The 70-year prohibition of marijuana in America has made it difficult for many patients to be honest with their doctors about their use. However, that hasn't stopped them from searching out other patients on the internet. Bipolar sufferers in particular have sought to build the knowledge of cannabis as a treatment method. The following are examples of that effort:

"Numerous patients report significant improvement and stabilization with their bipolar disorder when they utilize adjunctive therapy with medical cannabis. While some mental health professionals worry about the impact of cannabis on aggravating manic states, most bipolar patients trying cannabis find they "cycle" less often and find significant improvement in overall mood. Bipolar disorders vary tremendously in the time spent in the depressive versus manic states. Those who experience extended depressive episodes are more likely to be helped with cannabis.

Patients who use cannabis to "relax" may be treating the anxiousness sometimes associated with depression. Cannabis aids the insomnia sometimes present in depression and can improve appetite. Better pain control with cannabis can reduce chronic pain related depression. While cannabis cannot yet be considered a primary treatment of major depression it may improve mood when used under physicians supervision and in combination with therapy and/or SSRI’s.

There is currently a debate as to which "strain" of cannabis is most appropriate for the adjunctive treatment of depression. Since symptoms are so individualistic it is hard to determine what strain is right expect empirically. In general Sativa dominant strains tend to be more "up" and Indica dominant strains more relaxing.

Patients themselves are often the best judges of whether or not cannabis helps relieve the symptoms of depression. A poorly educated or narrow-minded physician may think any use of cannabis to be a substance abuse related aspect of depression. More enlightened psychiatrists (i.e. Lester Grinspoon of Harvard Medical School) appreciate the often beneficial aspects of cannabis therapy.

Perhaps the most reliable yardstick of the efficacy of medical cannabis in the treatment of depression is whether or not specific aspects of functionality improve. Functionality includes aspects such as self-care ability, job or school attendance, social interaction, normal sleeping, and cognitive skills." source

"I find marijuana the right drug for me, because it helps lower my BP, prevents me from being quite so obsesive and relaxes me. I have Epilepsey, stress related seizures and Bipolar Disorder NOS and last but not least, Post Tramatic Stress Disorder. I believe it helps me control all of my disorders."

"Good for Mania, not for Depression I am fortunate enough to live in a state that allows medical Cannabis. I use it for the severe nausea of Menieres Disease and have to smoke it several times a day. I also am manic depressive though considered what they call,"borderline". I find that great when I need to chill out and calm down from a mania phase. However if you've ever smoked pot, you should remember that when you are high...it makes you think a lot. Sometimes thinking about your problem over and over can make you feel worse. Pot can make you do just that. So beware. Also count on being treated like a second class citizen if you choose to medicate with cannabis. In some counties of California, they actually do arrest and take away all a patients medicine......and feel it is up to the courts to figure it out. So expect to be treated like a criminal no matter where you live.....except San Francisco." source


"I use cannabis as a herbal alternative to pills. I suffer from acute depression or clinical depression aka bipolar disorder (anxiety, mood swings). Also suffer from recurring pain in my lower back and both knees from a car crash. One... What state should I move to? To get a medical card.. Two what strains would be the best for treatment? Three.. does anyone else suffer from bipolar disorder?"

"I also use cannabis as a safer alternative to the pills. In Alaska it is legal to own/cultivate for personal use. If you are goin for medical strains, i would suggest bubblegum, jock horror, or white widow.... anything with an abundance of THC... Hey good luck, and i know what its like to be bipolar.. this shit really helps doesn't it!"


"That is exactly what I use cannabis for. I hate taking pills."

"My wife is bi-polar and has taken so many meds over the years I can't remember them all. Right now she is down to Clonazapam and smoking AK47. This seems to be working well at this time. She has also used Cinderella 99. Both strains create a positive mental attitude...we live in Oregon and you can get a medical card here."


"I am extremely bi-polar, diagnosed at age 12 with the rapid cycling type of disease. Seroquel helps more than anything, I take 500mg a day. But weed definetly helps with the depression part." source

Medicinal Cannabis as Treatment for Bipolar

Many patients who have have attended Hope Unlimited meetings in 2008 discuss their use of cannabis as a mood stabilizer in bipolar disorder. Some use it to treat mania, depression, or both. Some use it as a substitute to lithium others combine the two. Their have been at least 6 bipolar patients with San Diego medical cannabis ID cards at this year's hope gatherings.



Want to read more about using cannabis as a treatment for bipolar disorder:

Treatment of Bipolar Disorder - Medical Marijuana - Wikipedia

Peer-Reviewed Medical Cannabis Studies

The use of cannabis as a mood stabilizer in bipolar disorder: anecdotal evidence and the need for clinical research. - L Grinspoon

Steve Francis attends Hope Unlimited meeting

Candidate for mayor Steve Francis was in attendance at last night's Hope Unlimited meeting. He pledged to re-establish the dialog between police and medical marijuana patients if elected. The previous council under mayor Murphy voted to accept guidelines established by the city's medical marijuana task force. This work has stalled under mayor Sanders.

Full story coming soon.

Medical Marijuana Voting Guide for City Attorney

The June 3rd election for San Diego City Attorney is the one of the most contentious in years. Five candidates, Mike Aguirre, Amy Lepine, Jan Goldsmith, Brian Maienschein, and Scott Peters are vying for the seat. If no one candidate wins 50% of the vote, the top two vote getters will run against each other in a November run-off election. Hope Unlimited has been seeking to gather public opinions from the candidates on medical marijuana. The following voter guide has been prepared based on the response to our inquires and research of past medical marijuana legislation.

We will update as we hear new information from the candidates.

Grading the City Attorney candidates on medicinal marijuana

Jan Goldsmith B+

-Superior Court Judge, endorsed by Republican party, former State Assemblyman for North County

Goldsmith was a State Assemblyman when Proposition 215 came before California voters in 1995. Prop 215 became Bill 1529 when it reached Assembly. It passed committee by a vote of 5 to 2. The bill then went before the full assembly where it narrowly passed 41 to 30. Goldsmith was one of the 41 who voted in favor of implementing prop 215 guidelines. However, he has been labeled an anti-drug Republican, and when bill 1529 came back to the Assembly for a second vote Goldsmith was absent or abstained.

Scott Peters B-

- Represents District 1 and is currently president on City Council, Democrat, attorney

Peters sat on the San Diego City Council in 2003 when recommendations from San Diego's Medical Cannabis Task Force came up for vote. The measure authorizing medical patients to possess a pound of tried cannabis or 24 plants was a milestone in San Diego. It passed 6 to 3, Peters was one of the 6 voting in favor of adopting local medical marijuana guidelines. More recently in 2006 he was criticized by San Diego Americans for Safe Access (ASA) for obstructing them in getting a resolution docketed for City Council.


Mike Aguirre F

- Current city attorney, claims office should be used to "serve the public interest", Democrat

Aguirre has never been in a position to put himself on the record with a yes or no vote on a medical marijuana initiative. Hope Unlimited has contacted him repeatedly to give him a chance to state his views on medical marijuana but neither his campaign or his city office have responded. Judging from his recent attempt to shutdown "smoke shops" shows his motivations. Publicly he told City Beat he was going after crack and meth pipes. The actual letter sent out to smoke shops had the following passages underlined and asterisked: "bongs", "otherwise introducing into the body a controlled substance", & "marijuana, ... hashhish, & hashhish oil". Aguirre seems to have been caught in a lie on this one.



Brian Maienschein F

- Represents District 5 on City Council, Republican, attorney


Maienschein also sat on San Diego City Council for the 2003 vote. He was one of 3 who voted against implementing medical marijuana guidelines. When this item was voted on it took about 7 hours to hear everyone who wanted to speak on the issue. Many passionate cases were made for individual's medical need of marijuana. Maienschein made a point at the time to speak out against the guidelines.


Amy Lepine ?

- Former Deputy City Attorney under Aguirre, quit and filed suit claiming sexism



Has no taken no public stance on the issue to the best of our knowledge.

Marc Emery Extradition Trial Update

The BC3 still needs your help. The next hearing in the extradition trial is scheduled for April 9th 2008. The latest reports are that a tentative plea bargain has been reached. The deal would see Michelle Rainey and Greg Williams go free, while Marc Emery serves a 5-10 year sentence. However, one of Emery's stipulations, that he be allowed to spend more than half his sentence in a Canadian prison, has caused the deal to hit a snag. A 5 year sentence for selling marijuana seeds does not fit within Canada's sentencing guidelines. Essentially the Canadian government is saying they cannot agree to the plea because the sentence is illegal under Canadian law.

The BC3 need your help more than ever in their battle with the DEA.

Please call the Canadian Minster of Justice at (613) 957-4222 to tell them it would be "cruel and unjust", and an insult to Canada's sovereignty, to extradite Canadians Marc Emery, Michelle Rainey and Greg Williams to the United States to face life in US prison.

If you can help with money please donate to the BC3 Legal Defense Fund .