Posted by Larry Hoover on December 30, 2002, at 9:53:37
In reply to Beardedlady, 2 marijuana/schizo links for you, posted by comftnumb on December 26, 2002, at 11:49:57
> http://www.healthscout.com/static/news/510418.html
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> http://www.xpresssites.com/buffalo/buffalo/xpspecialsections/healthandwellness/story_318702.asp
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> Summary:
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> Smoking pot increases the risk of the psychiatric disorder by about 30 percent (1st article, Swedish study). There is genetic evidence that marijuana use can result in schizophrenia or a significantly increased risk of schizophrenia (2nd article, Japanese Study). Cannabis used before age 18 raises the risk of schizophrenia six-fold (2nd article, Swedish Study).
The Japanese study noted above provides clear evidence of a genetic abnormality in endogenous cannibinoid activity in schizophrenics.From the second link:
"The hallucinogenic properties of marijuana, the researchers explained, are linked to a biochemical found abundantly in the brain. The chemical, called cannabinoid receptor protein, studs the surfaces of brain cells and latches onto the active chemical within marijuana known as THC.
"These sites are where marijuana acts on the brain," Ujike said.
Ujike and his team examined the gene for the marijuana receptor in 121 Japanese patients with schizophrenia and an average age of 44.
When they compared this gene in schizophrenics with the same gene in 148 normal men and woman of the same average age, they found distinct abnormalities in DNA sequences called nucleotides among the schizophrenics.
Some of their nucleotides in the marijuana receptor gene appeared significantly more often than normal while others appeared less frequency.
"This finding is the first to report a potential abnormality of the cannabinoid system in schizophrenia," said clinical neuroscientist Carol Tamminga at the University of Maryland in College Park."
The researchers have identified a clear and unequivocal difference in the *genetic* makeup of schizophrenics. The genetic difference *must* have been present before marijuana use, unless we are to accept that marijuana use can change the genes found throughout the entire body of its users. The researchers could not possibly have sampled the brains of these subjects, for ethical reasons. The samples were probably from blood draws or skin cells. Now, how can you possibly infer that marijuana caused schizophrenia in those with inborn genetic errors in cannibinoid receptors?What these researchers may have stumbled on is one of the regulatory mechanisms which predisposes one to positive symptom schizophrenia, mediated by the neurotransmitters known as anandamides, which are the natural brain chemicals which bind to what has been called the cannibinoid receptor. By the way, research into regulators of the anandamide system as treatments for anxiety and depression is under way.
Anandamides are produced from the long-chain poly-unsaturated fatty acid, arichidonic acid.
Vitam Horm 2002;65:225-55
Endocannabinoids and their actions.
Maccarrone M, Finazzi-Agro A.
Department of Experimental Medicine and Biochemical Sciences, University of Rome Tor Vergata, I-00133 Rome, Italy.
Endocannabinoids are a new class of lipid mediators, which includes amides and esters of long-chain polyunsaturated fatty acids. Anandamide (I) and 2-arachidonoylglycerol (II) are the main endogenous agonists of cannabinoid receptors, able to mimic several pharmacological effects of delta 9-tetrahydrocannabinol (III), the active principle of Cannabis sativa preparations such as hashish and marijuana. The pathways leading to the synthesis and release of anandamide and 2-arachidonoylglycerol from neuronal and nonneuronal cells are rather uncertain. Instead, evidence has accumulated showing that the activity of these compounds at their specific receptors is limited by cellular uptake through a specific membrane transporter, followed by intracellular degradation by a fatty acid amide hydrolase. Here, the endocannabinoids and the endocannabinoid-like compounds most relevant for human physiology will be discussed, along with the synthetic and degradative pathways of anandamide and 2-arachidonoylglycerol and their molecular targets on the cell surface. The main actions of the endocannabinoids in human cells and tissues will also be reviewed, focusing on the activities most recently discovered in the central nervous system and in the periphery.
Getting back to the correlation between cannabis and schizophrenia, more reasonable (in my humble opinion) reviews have been recently published.
Curr Psychiatry Rep 2002 Jun;4(3):191-6
Cannabis and psychosis.Degenhardt L, Hall W.
National Drug and Alcohol Research Centre, University of New South Wales, Sydney, Australia, 2502. l.degenhardt@unsw.edu.au
There has been considerable debate about the reasons for the association observed between cannabis use and psychosis in both clinical and general population samples. Among the hypotheses proposed to explain the association are the following: 1) common factors explain the co-occurrence; 2 cannabis causes psychosis that would not have occurred in the absence of cannabis use; 3) cannabis precipitates psychosis among persons who were vulnerable to developing the disorders; 4) cannabis use worsens or prolongs psychosis among those who have already developed the disorder; and 5) that persons with psychosis are more likely to become regular or problematic cannabis users than persons without psychosis. This article evaluates the evidence on each of these hypotheses, including recent research on the role of the cannabinoid receptor system in schizophrenia. The evidence suggests that common factors do not explain the comorbidity between cannabis use and psychosis, and it is unlikely that cannabis use causes psychosis among persons who would otherwise not have developed the disorder. The evidence is more consistent with the hypotheses that cannabis use may precipitate psychosis among vulnerable individuals, increase the risk of relapse among those who have already developed the disorder, and may be more likely to lead to dependence in persons with schizophrenia.
In the following study, you will see that alcohol abuse and tobacco use are more strongly correlated to schizophrenia than is cannabis, but they don't fit into the "war on drugs" "reefer madness" concept.Actas Esp Psiquiatr 2002 Mar-Apr;30(2):65-73
[Relevance of drug use in clinical manifestations of schizophrenia][Article in Spanish]
Arias Horcajadas F, Sanchez Romero S, Padin Calo JJ.
Unidad de Psiquiatria, Fundacion Hospital Alcorcon, Alcorcon, Madrid, Spain. farias@fhalcorcon.es
OBJECTIVES: To study the association between drugs use with schizophrenia clinical manifestations. MATERIAL AND METHODS: The sample consists of 82 out-patients with schizophrenia, between 18 and 45 years old. They were evaluated with Addiction Severity Index (ASI) and with Positive and Negative Syndrome Scale (PANSS). A 6 months follow up was carried out. RESULTS: 37,8% patients had lifetime drug dependence (including alcohol and others drugs except for tobacco). The prevalence of dependence for the different drugs were: opioids 9,8%, cocaine 11%, alcohol 29,3%, cannabis 24,4%, tobacco 68,3%, caffeine 15,9%. Drug dependent had more family and legal problems. At the multiple regression analysis it was observed that cannabis and tobacco dependence was associated with a decrease in the PANSS negative symptoms subscale, and on the contrary, alcohol dependence produces a similar intensity increase at that scoring. We don't detect any clinical relevance effects over positive symptoms. CONCLUSIONS: Cannabis and tobacco may improve schizophrenia negative symptoms or neuroleptic secondary effects or patients with few negative symptoms may have more predisposition to the use, on the contrary alcohol use can impairment those symptoms.
I hope my views are not overwhelming, but will instead stimulate debate about the subject.Lar
poster:Larry Hoover
thread:133136
URL: http://www.dr-bob.org/babble/20021230/msgs/133788.html