Marijuana Linked to Schizophrenia, Retardation; Affects Memory, Attention, Speech, Thinking


Smoking marijuana can cause a person to acquire brain damage to the point of retardation...

There is a causal relationship between cannabis use and schizophrenia (psychotic disorders).

Marijuana's well-known effects on short-term memory may be the result of misfiring brain cells, according to neuroscientists. Scientific American reported Nov. 20 that David Robbe of Rutgers University and colleagues found that rats given THC -- the active ingredient in marijuana -- and a synthetic cannabinoid experienced disruptions in the synchronous brain-cell firing that causes memories to be formed. The drugs also slowed brain-wave activity, notably theta and fast-ripple waves but also gamma waves. This is provoked by its main component, cannabinol.

Theta and gamma waves are believed to be involved in short-term memory formation, while the fast-ripple waves are thought to play a role in moving such memories into long-term storage.

At very high doses, the drugs appeared to prevent learning altogether.

"Overall, our findings indicate that under the influence of cannabinoids, neurons are liberated from population control," the researchers wrote in the online version of the journal Nature Neuroscience.

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Researchers at Rutgers University have found that the marijuana's active ingredient, tetrahydrocannabinol (THC), interferes with the synchronized activity between neurons in the hippocampus of rats and decreases brain waves, impairing this way memory formation.

The hippocampus is a brain part playing a central part in memory and spatial navigation. How exactly the weed acts on memories, attention and speech, among other things, has never been well understood. Normally, hippocampus neurons in that region form groups that trigger action potentials, or nerve impulses, together, especially theta waves.

When the researchers injected THC directly into the hippocampus, the synchronized pattern (tendency to occur at the same time) of the firing neurons was disrupted: even if they fired as much as before, it was in a more random pattern. Synchrony was also disturbed in other types of brain neurons, such as interneurons and pyramidal cells, although, interestingly, they were actually overactivated (explaining the random nature of thoughts provoked by the drug consumption).

Animals with less synchronized neural activity under the drug performed less well in a standard test of memory, thus synchronized neural firing is a must for normal hippocampal function. "Overall, our findings indicate that under the influence of cannabinoids, neurons are liberated from population control." The drug decreased significantly certain brain waves: the theta (4-12 hertz) and fast ripple (100-200 hertz) waves, whereas gamma (30 to 80 hertz) waves were slightly less affected.

Theta and gamma waves are thought to be crucial in creating and storing short-term memories, and fast ripple oscillations may turn short-term memories into long-term storage. If they are stopped, the rats will miss memories. Rats trained to do specific tasks turned very dazed after intravenous injections with marijuana. At the highest doses of THC, the rats failed to discover the right sequence of turns altogether. Thus, over a certain doses, the drug entirely prohibits learning.

The following are some of the common side effects of using marijuana:

* Trouble remembering things
* Slowed reaction time
* Difficulty concentrating
* Sleepiness
* Anxiety
* Paranoia (feeling that people are "out to get you")
* Altered time perception
* Red, bloodshot eyes

Using marijuana for a long time makes some people lose interest in school, work, relationships and other activities. It may also cause legal problems. Using marijuana can be especially dangerous in certain situations, such as when you are driving, because your reaction time is slower. This make it more difficult to react to a dangerous situation, which could cause an accident.

The following are some of the common physical effects of marijuana:

* Tremors (shaking)
* Nausea
* Headache
* Decreased coordination
* Breathing problems
* Increased appetite
* Reduced blood flow to the brain
* Changes in the reproductive organs

Marijuana and Schizophrenia

Working in a psychiatric ward you will very often see patients with a first onset of paranoia or other psychotic symptoms after a chronic use of cannabis. A recent research paper discussed the following hypotheses for a possible relationship:

* There is a causal relationship between cannabis use and schizophrenia (psychotic disorders).
* The cannabis use precipitates schizophrenia in vulnerable persons.
* Cannabis use exacerbates schizophrenia -> symptoms are more severe.
* Patients with psychotic disorders are more liable to abuse cannabis

This Australian study found a rise in the prevalence of cannabis use and a decrease of the age at the beginning of regular cannabis consumption over the last 30 years. They found no clear increase of the prevalence of schizophrenia in Australia in this time span. We know that cannabis abuse is rather common among patients with schizophrenia, maybe sometimes a rather bad attempt to cope with psychotic symptoms or irritability or hallucinations.

So the authors of this study think that cannabis use is not the main causal factor for the incidence of schizophrenia, but seems to precipitate the onset of psychotic symptoms / paranoia for vulnerable persons. So if you have a high vulnerability for schizophrenia the abuse of cannabis will most likely lead to severe paranoia and a worse outcome!

The co-occurrence of substance abuse and schizophrenia is one of the worst problems in psychiatry! It is very difficult to offer a good treatment approach for this group of patients. Special treatment programs are available for schizophrenic patients with cannabis dependence or other types of substance abuse.

Many of these research studies indicate that the risk is higher when the drugs are used by people under the age of 21, a time when the human brain is developing rapidly and is particularly vulnerable.

People with any biological predisposition towards schizophrenia are at the highest risk -- unfortunately its impossible to accurately identify this predisposition beforehand ( a family history of mental illness is just one indicator of such a predisposition). [see causes and prevention of schizophrenia for more information on all risk factors linked to a person developing schizophrenia]

Researchers in New Zealand found that those who used cannabis by the age of 15 were more than three times (300%) more likely to develop illnesses such as schizophrenia. Other research has backed this up, showing that cannabis use increases the risk of psychosis by up to 700% for heavy users, and that the risk increases in proportion to the amount of cannabis used (smoked or consumed). Additionally, the younger a person smokes/uses cannabis, the higher the risk for schizophrenia, and the worse the schizophrenia is when the person does develop it. Research by psychiatrists in inner-city areas speak of cannabis being a factor in up to 80 percent of schizophrenia cases.

Professor Robin Murray (London Institute of Psychiatry) has recently (2005) completed a 15-year study of more than 750 adolescents in conjunction with colleagues at King's College London and the University of Otago in New Zealand.

Overall people were 4.5 times more likely to be schizophrenic at 26 if they were regular cannabis smokers at 15, compared to 1.65 times for those who did not report regular use until age 18.

Many researchers now believe that using the drug while the brain is still developing boosts levels of the chemical dopamine in the brain, which can directly lead to schizophrenia.

Professor John Henry, clinical toxicologist at Imperial College London said research has shown that people with a certain genetic makeup who use the drug face a ten times (1000%) higher risk of schizophrenia. (for example - if your risk of schizophrenia was 6% (due to a family history of mental illness) prior to taking cannabis, it could be 60% -- or more likely than not - after taking cannabis). Every person is different (i.e. has different genes and different environments) - so this "10 Times Higher Risk with cannabis use"- is just a generalization, and it may or may not apply to a given person.

The increased risk applies to people who inherit variants of a gene named COMT and who smoked cannabis as teenagers. About a quarter of the population have this genetic make-up and up to 15 per cent of the group are likely to develop psychotic conditions if exposed to the drug early in life. Neither the drug nor the gene raises the risk of psychosis by itself.

A recent Dutch study showed that teenagers who indulge in cannabis as few as five times in their life significantly increase their risk of psychotic symptoms.

The increase in evidence during the past decade could be tied to the increased potency of marijuana. A review by the British Lung Association says that the cannabis available on the streets today is 15 times more powerful than the joints being smoked three decades ago.

Schizophrenia can sometimes be triggered by heavy use of hallucinogenic drugs, especially LSD; but it appears that one has to have a genetic predisposition towards developing schizophrenia for this to occur. There is also some evidence suggesting that people suffering from schizophrenia but responding to treatment can have an episode as a result of use of LSD. Methamphetamine and PCP also mimic the symptoms of schizophrenia, and can trigger ongoing symptoms of schizophrenia in those who are vulnerable.

Melbourne University's Professor David Castle stated in a February, 2005 interview that heavy drug use during formative times of life, such as the years at school, could affect the way a teenager or young adult thought, impairing cognitive ability and having a long-term impact on job prospects. Victorian studies had revealed that regular use of cannabis by adolescent girls could trigger long-term depression. And for those vulnerable to a psychotic disorder, even a small amount of cannabis could pose a threat.

Professor Castle, author of the book Marijuana and Madness, has said that those people with this "psychotic proneness" were those who had a family history of mental illness or who had had a bad response on their first use of cannabis or to a tiny amount. Others at risk included those who had experienced a psychotic episode where they had paranoid thinking or heard a voice calling their name. Professor Castle said experiencing such a one-off episode was far more common than people thought.

"People with such a vulnerability should avoid cannabis like the plague," he said.

Without the effects of the drug, such a person might live their whole life without ever experiencing mental health problems. It has been estimated, for example, that between 8% and 13% of people that have schizophrenia today would never have developed the illness without exposure to cannabis.

Professor Castle compared the effect to feeding sweets to a diabetic. While high sugar content foods did not cause too many problems for most people in the short term, they could be catastrophic for diabetics.

He said there was an accumulative effect when it came to cannabis use and schizophrenia. Those who used the drug more than once a week were more prone to needing hospitalisation and often suffered other associated problems such as the breakdown of relations with their family, isolation, crime and violence.

* Cannabis impacts on neurotransmitters that regulate how arousal and stress are managed in the brain. Cannabis takes a long time to metabolise, and can quickly build up to high levels in the body. Once you get to this point, there is a real risk of depression or schizophrenia being triggered.

* A Swedish study of 50,000 military conscripts found heavy use of cannabis increased the risk of suicide by four times (400%). A Victorian study of 2332 adolescents found weekly use increased the risk of suicide attempts among females by five times. Weekly use as a teenager doubled the risk of depression and anxiety. Daily use at the age of 20 boosted the risk of depression and anxiety by five times (500%).

Helpful Actions: If you want to avoid getting schizophrenia - research suggests that the number one thing you should avoid are street drugs (especially marijuana/cannabis - but because you never know what someone has put into a street drug, all of them are dangerous). By avoiding use of all street drugs research suggests that you can greatly reduce the chance (by as much as 50% to 80% if you are biologically predisposed) that you'll develop schizophrenia. Avoiding marijuana after developing schizophrenia also helps reduce relapse rates. Some people with schizophrenia suggest that it makes them feel better, but if depression is an issue we recommend these people talk to their Psych-Doc about possible anti-depressant use rather than street drugs.

Do not use even small amounts of cannabis if you have any family history of mental illness, have had an episode of paranoid thinking or hearing voices or had a bad response when first using cannabis or when using a small amount.

Other street drugs are also very dangerous - partly because they are produced in home laboratories with virtually any possible combination of additional substances mixed in with the drugs. See: Crystal Meth & Schizophrenia

Schizophrenia and Cannabis Video Report:

A recent Internet video report on schizophrenia and cannabis has recently become available. To play the video go to the following link - and then click on "Play" button to view any of the 6 different sections of the video report: Messing with Heads: New Research into the longterm effects of Cannabis (Internet Video, 2005) from the Australian Broadcasting Company (ABC).

Science Suggests Smoking Pot Raises Risk of Testicular Cancer, Schizophenia and Infertility - and Lowers IQ

Pot Smoking May Double Risk of Testicular Cancer

Today’s headline was pretty bold: Smoking pot leads to double the risk of developing testicular cancer. Testicular cancer is on the rise, and experts have been trying for awhile to figure out why. Now, after comparing groups of young men who smoked and those who didn’t, there’s a possible answer. Those who smoked pot recreationally were twice as likely to develop testicular germ cell tumors, or nonseminomas, the most common kind in men under 35, says a study in Cancer. Nonseminomas are faster growing and harder to treat – a deadly combination – say researchers at the University of Southern California.

This study, though small, is actually the third study to link testicular cancer to pot use; the first two were also published in Cancer. The first word of the connection came out in 2009 from research out of the Fred Hutchinson Cancer Center in Seattle. That study found an even higher risk increase: 70 percent. The pot use researchers studied was described as “once a week or more”, and it’s important to note that many smokers toke up every day. No studies have contradicted the link, experts point out. It’s important to note that the risk of testicular cancer is relatively low, slightly more than 1 percent.

Pot Smoking May Lower IQ

Last week’s headline was at least as alarming as this week’s. Researchers followed a group of youngsters from age 13 to age 38, and found that the IQs of regular pot smokers fell up to 8 points during the 25-year period, compared with the IQs of those who didn’t smoke pot, which stayed the same. The study, published in the Proceedings of the National Academy of Sciences, also found an increase in memory and attention problems among those deemed marijuana-dependent.

Pot Smoking May Trigger Schizophrenia

There should have been headlines, “Marijuana May Make You Psychotic” at least a couple times over the past few years, but somehow the studies documenting this issue haven’t gotten as much attention as you might expect. Maybe it’s because this link is much harder to prove, which it is. That’s because the association could work backward: Those who smoke pot could be self-medicating for symptoms of schizophrenia that hasn’t become full-blown yet.

Supporting News (a sample):

* Recent news on Marijuana / cannabis and schizophrenia (from newsblog)
* Marijuana Doubles Risk of Schizophrenia - March, 2005
* Interview with Dr. Andrew Campbell on Schizophrenia and Cannabis - Feb, 2005
* 25% of cannabis users faces a ten-fold higher risk of mental illness - Jan, 2005
* True Story of Cannabis-Induced Schizophrenia - January, 2005
* Marijuana and Psychosis Link - December, 2004
* Another Study Links Marijuana to Schizophrenia - News, April 2004
* Psychotic Symptoms More Likely with Cannabis - New Scientist, 2004
* The Link between Cannabis and Psychosis - Robin Murray, MD
* Cannabis link to mental illness strengthened - New Scientist Magazine
* If cannabis is safe, why am I psychotic? - Times Online
* My Son and Cannabis - a anecdotal story from a parent convinced that his son's use of cannabis caused the development of schizophrenia. BBC News, June 2005
* Drug Abuse and Risk of Developing Schizophrenia - (News)
* Marijuana and Schizophrenia - (News)
* Cannabis mental health risks 'must be taught' - Guardian Newspaper
* Powerpoint Presentation "Canabis: The Facts" by British Toxicology Society
* Review shows that cannabis use is a risk factor for schizophrenia
* Psychiatrists say "No" to Marijuana
* The National Institute on Drug Abuse Adds Warning of Major Depressive Disorders (MDD’s) Experienced by Marijuana Users
* Causal association between cannabis and psychosis: examination of the evidence. (British Journal of Psychiatry, 2004)
* Cannabis use as a probable causative factor in the later development of schizophrenia
* Cannabis and neurological soft signs in schizophrenia: absence of relationship and influence on psychopathology
* Self reported cannabis use as a risk factor for schizophrenia in Swedish conscripts of 1969: historical cohort study
* Cannabis and schizophrenia: impact on onset, course, psychopathology and outcomes
* Marijuana Mental Disturbances

Marijuana as a Teratogen

Marijuana and Fertility

Long term use of marijuana does affect fertility in both men and women. For men, marijuana causes a lower sperm count and smaller volume of seminal fluid, that is about half of the normal amount. However, Marijuana also causes abnormalities in the existing sperm. The problem comes from timing. In normal sperm, hyperactivation occurs when the sperm is in the cervix, close to the egg. In the sperm affected by THC, hyperactivation occurs too early, and the sperm “burn themselves out”. (DeNoon, 2003) The sperm is only able to stay hyperactivated for a few hours, to push through the egg. When this occurs to early, the sperm are not able to break through the egg and therefore unable to fertilize the egg. At the same time, men that smoke marijuana are able to get women pregnant. It is thought that the effects of marijuana use are most clearly seen among males who already are borderline- infertile. The problem is that many men do not know if they are borderline infertile or not, and the general consensus is that if marijuana does contribute to infertility in general. (DeNoon, 2003) Marijuana use can also lead to erectile dysfunction due to its ability to suppress hormones that important to the male reproductive system. (Kuhn, 2003)

There has been much less research done on women’s use of marijuana and fertility. However, it has been found that even traces of THC in the women’s vaginal fluids can affect the sperm negatively. When sperm comes into contact with the vaginal fluid it can then absorb the THC and show the same sort of effects that come from the man using marijuana. (DeNoon, 2003) There is also evidence that large amounts of marijuana after awhile can create an irregular menstrual cycle. (Kuhn, 2003)

There is still the question of the ability to reverse the effects of marijuana over time. It seems as if things will go back to normal but it may take a long time. (Otis, 2007)THC is stored in fat deposits and the process to which it leaves can be very slow. (About, 2003)

Marijuana and Breastfeeding

Though a child might already by born, if it is breastfeeding, it still has a significant connection to the mother, and to her body. When a mother is exposed to marijuana, her breastmilk is also exposed. Some studies have shown that it actually concentrates in breastmilk, and the infant is exposed to a higher level than the mother(Perez-Reyes & Wall, 1982). Others suggest a more moderate exposure (Committee, 1991). Either way, an infant who does not yet have all their brain functions fully developed is exposed to a mind-altering drug. In animal studies it has been shown that marijuana use by breastfeeding mothers can decrease the productivity of milk in the mammary glands(Perez-Reyes & Wall, 1982).

Another study suggests that exposure to marijuana through a mother's breastmilk within the first month of life can cause a delayed motor response at one year (Astley & Little, 1990). Babies who are exposed to marijuana through breastfeeding are also more oftern lethargic, feed less and feed for shorter period of times. Exposure to marijuana during the first few months of life is partiuclarly concerning because a baby's brain has not fully developed until much later in development, and exposure to a mind-altering drug could have a significant effect on that development.

Longterm Effects of Prenatal Exposure to Marijuana

Upon birth, many children who were exposed to marijuana prenatally have lowered response to light stimuli, lowered habituation to the same, less "self-quieting" behavior (thumb-sucking, etc.), more tremors are startled more easily, and they also have more high-pitched cries. These symptoms of exposure to marijuana gradually even out as the infant gets older, however there are a few long term effects of prenatal marijuana exposure that continue on into the child's life.

One of the major effects is a smaller head circumference. The smaller head circumference is usually noted at birth, though it becomes much more concerning when the child reaches adolescence and the head circumference difference does not correct itself (Fried, Waatkinson, & Gray, 1999). Though there are some physical longterm effects, the behavioral longterm effects seem to be more lasting. A study done by Goldschmidt, Day, & Richardson (2000) found that prenatal marijuana exposure led to increased hyperactivity, impulsivity, and increased delinquency.

Cognitive skills may also be effected by prenatal exposure to martijuana. A study found that women who exposed themselves to marijuana in their first and second trimesters had children who scored much lower on intelligence tests at age three (Day et al., 1994). The tests did improve greatly however with the attendence at day-care or preschool. These children are put at a disadvantage from birth because of a possible difference in development and physiology caused by their early exposure to marijuana.

Teratogenic and Neurological Effects

There is some evidence that marijuana can have teratogenic and neurological effects at various dosings, based on experimental animal studies and corellational studies of humans.

Marijuana is evidenced to cause reproductive abnormalities at several different junctures. Though not all of its effects are strictly teratogenic, in the sense that they cause developmental abnormalities directly by marijuana's interaction with the unborn child, they nevertheless result in unpleasant consequences.

Even before conception, marijuana has the potential to affect the pregnancy-- in several ways. In men, chronic marijuana use has been corellated with lower sperm quantity and quality (Bloch, 1983, National Academy of Science, 1982; Wenger et al, 1992). While this may not technically count as a teratogenic effect, a mutant sperm might contribute mutant DNA to the child and cause deformities or other abnormalities in that way. Interestingly, this effect seems to be a result of a dual action on the part of THC (the active ingredient in marijuana): on the testes themselves, which produce the sperm, and on hypothalamic secretions that interact with the testes (Wenger et al, 1992). These effects are especially pronounced for younger users of cannabis, and heavy chronic users with existing reproductive problems (Hollister, 1986). Bloch (1983) is of the opinion that a similar phenomenon occurs in women, also due to hypothalamic effects, resulting in overall lower reproductive function.

The second way in which marijuana may affect future pregnancies is a mugagenic effect. Cannabis smoke "has been ... associated with chromosomal aberrations ... such as hypoploidy, mutagenicity in the Ames test ... " (Bloch, 1983, p413). Smoking marijuana is in fact probably the most common means of consumption; THC must be "activated" by heat before it is in its effective form, and so it is typically smoked. These genetic changes brought on by the smoke may be permanent, and so could be passed on to the sperm, and then to the egg, and so on, resulting in a abnormalities in the early stages of development, which may not be significant to the already developed adult, but very significant for the still-developing conceived child.

Actual teratogenic effects of marijuana are "resorption, growth retardation, and malformations" in mice, rats, rabbits, and hamsters (Bloch, 1983, p406), with resorption and retardation more consistently reported than malformations (Abel, 1985). However, these effects have typically necessitated very large doses of crude marijuana extract. Marijuana has also been found to produce lower birth weights in mammals. This effect however, may not be direct. There are studies with mammals that have shown that this could be mediated by a reduction in appetite of the animals involved. Furthermore, this effect was found to decrease the closer in the evolutionary tree the animals were to humans, primates being the most human.

Undesirable neonatal effects of marijuana that are not mechanically teratogenic include: lowered response to light stimuli, lowered habituation to the same, less "self-quieting" behavior (thumb-sucking, etc.), more tremors and increased startling, and more "cri du chat" (high-pitched cries).

Marijuana and Tubal Pregnancy

The Vanderbilt University Medical Center has experimented with mice and has found that excessive cannabis intake can result in less pregnancies; specifically, these mice had an increased number of tubal pregnancies. CB1 is a cannaboid-receptor which assists muscle contractions that moves the embryo down to the uterus, and when this receptor is blocked, over-stimulated, or not present, tubal pregnancies occur more often in mice (Snyder, 2004). It has not been concluded if these results would occur in humans, but it is advised that women who are trying to become pregnant should avoid marijuana usage. There is also an anti-obesity drug which seems to have the same effect in mice (Snyder, 2004).

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