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DontRunMeOver · 10-19-2005, 10:46 AM

Here's an excerpt from
'Effects of cannabis on health: an update of the literature since 1996', Harold Kalant, University of Toronto, Progress in Neuro-Psychopharmacology and Biological Psychiatry, 28 (2004) 849-863.

"This review of the literature since 1996, concerning adverse health effects of cannabis smoking, does not alter in a major way the conclusions reached in an earlier review of the literature up to 1996. The principal additions to, or modifications of, those earlier conclusions are as follows:

• The potential role of cannabis in driving accidents has been further supported by analytical data showing the presence of THC in the blood and saliva of injured or impaired drivers with a higher frequency than probably occurs in the general public or in non-injured, non-impaired drivers. The data on culpability of drivers under the influence of cannabis are not conclusive, but are strongly suggestive because of the relationship to cannabis dosage.
• The frequency of chronic bronchial inflammatory changes and precancerous alterations in the bronchial epithelium of long-term heavy smokers of cannabis has been clearly demonstrated, and one well-designed epidemiological study is strongly suggestive of a causal role of cannabis smoking in upper airways cancer in young adults.
• The possibility of a contribution of cannabis smoking to chronic obstructive pulmonary disease is still not clear, but cannot be dismissed.
• Much new statistical information indicates a substantial involvement of cannabis use in various psychiatric disorders, including schizophrenic relapse, major depression, anxiety or panic disorders, and behavioral disorders in young people, and there is stronger evidence to suggest that cannabis use contributes to the production of these disorders than there is that these disorders contribute to cannabis use.
• Use of sophisticated statistical analytical techniques in a New Zealand long-term follow-up study has yielded evidence to support the idea that regular heavy use of cannabis by young adolescents is causally linked to poor psychosocial outcomes.
• Much new statistical information attests to the widespread occurrence of dependence in regular heavy users of cannabis. There is good, but still not conclusive, evidence of the occurrence of what appears to be a withdrawal syndrome, that impairs the ability to stop use in a significant proportion of cases.
• A small number of case reports suggest that cannabis use may, under certain circumstances, increase the risk of potentially serious cardiovascular disorders in predisposed individuals.
• Independent new data are consistent with the earlier evidence that maternal use of cannabis during pregnancy may give rise to subtle but significant developmental problems in the offspring, detectable in early school years and adolescence."

---

Also, from 'What causes the onset of psychosis?', Schizophrenia Research
Volume 79, Issue 1 , 1 November 2005, Pages 23-34.

"This is increasing evidence that heavy use of cannabis in adolescence can increase the risk of later schizophrenia (Arseneault et al., 2004) and that effects on dopamine also mediate this. A recent study (Caspi et al., in press) has shown that liability to psychosis induced by cannabis is strongly influenced by a polymorphism in the COMT gene that determines the rate of catabolism of frontal dopamine."

---

And 'The ecogenetics of schizophrenia: a review', Schizophrenia Research
Volume 32, Issue 2 , 27 July 1998, Pages 127-135.

"Use of cannabis is a likely risk factor for schizophrenia (Andreasson et al., 1987). Not only are there genetically determined differences in the individual psychotropic effects produced by cannabis (Lyons et al., 1997), but use of cannabis itself is also influenced by genetic factors (Tsuang et al., 1996). Thus, part of the genetic contribution to schizophrenia may be mediated by the use of cannabis and its subjective effects (genotype–environment correlation and interaction). McGuire and colleagues found that the risk for schizophrenia in the first-degree relatives of schizophrenic patients who screened positive for cannabis was increased more than 10-fold compared to those of schizophrenic patients who screened negative (McGuire et al., 1995). These results are suggestive of a mechanism of genotype–environment interaction and/or genotype–environment correlation, as in both instances the first-degree relatives of cases exposed to the environmental risk factor should have higher rates of illness (Ottman, 1996; Marcelis et al., 1998b)."

---
That's for those of your without access to your own online library

So what the last article is suggesting is that the cannabis-schizophrenia link works in both directions. Cannabis use may contribute to the development of schizophrenia and likewise schizophrenic personalities may be more likely to use cannabis. People often seem confused about the fact that this is a scientific point, that the links and causality or non-causality are something that either exists or does not exist and that its not a case for debate, just emotionless and unbiased research. Its science and they haven't made up their minds yet because they still don't have enough concrete evidence either way. Undoubtably an association has been made between weed and going or being schizo, but the exact nature of this link is yet to be confirmed.

10-19-2005, 10:46 AM	#49 (permalink)
DontRunMeOver They call me Tundra Boy Join Date: Sep 2005 Location: In your linen cupboard. Posts: 1,157	Here's an excerpt from 'Effects of cannabis on health: an update of the literature since 1996', Harold Kalant, University of Toronto, Progress in Neuro-Psychopharmacology and Biological Psychiatry, 28 (2004) 849-863. "This review of the literature since 1996, concerning adverse health effects of cannabis smoking, does not alter in a major way the conclusions reached in an earlier review of the literature up to 1996. The principal additions to, or modifications of, those earlier conclusions are as follows: • The potential role of cannabis in driving accidents has been further supported by analytical data showing the presence of THC in the blood and saliva of injured or impaired drivers with a higher frequency than probably occurs in the general public or in non-injured, non-impaired drivers. The data on culpability of drivers under the influence of cannabis are not conclusive, but are strongly suggestive because of the relationship to cannabis dosage. • The frequency of chronic bronchial inflammatory changes and precancerous alterations in the bronchial epithelium of long-term heavy smokers of cannabis has been clearly demonstrated, and one well-designed epidemiological study is strongly suggestive of a causal role of cannabis smoking in upper airways cancer in young adults. • The possibility of a contribution of cannabis smoking to chronic obstructive pulmonary disease is still not clear, but cannot be dismissed. • Much new statistical information indicates a substantial involvement of cannabis use in various psychiatric disorders, including schizophrenic relapse, major depression, anxiety or panic disorders, and behavioral disorders in young people, and there is stronger evidence to suggest that cannabis use contributes to the production of these disorders than there is that these disorders contribute to cannabis use. • Use of sophisticated statistical analytical techniques in a New Zealand long-term follow-up study has yielded evidence to support the idea that regular heavy use of cannabis by young adolescents is causally linked to poor psychosocial outcomes. • Much new statistical information attests to the widespread occurrence of dependence in regular heavy users of cannabis. There is good, but still not conclusive, evidence of the occurrence of what appears to be a withdrawal syndrome, that impairs the ability to stop use in a significant proportion of cases. • A small number of case reports suggest that cannabis use may, under certain circumstances, increase the risk of potentially serious cardiovascular disorders in predisposed individuals. • Independent new data are consistent with the earlier evidence that maternal use of cannabis during pregnancy may give rise to subtle but significant developmental problems in the offspring, detectable in early school years and adolescence." --- Also, from 'What causes the onset of psychosis?', Schizophrenia Research Volume 79, Issue 1 , 1 November 2005, Pages 23-34. "This is increasing evidence that heavy use of cannabis in adolescence can increase the risk of later schizophrenia (Arseneault et al., 2004) and that effects on dopamine also mediate this. A recent study (Caspi et al., in press) has shown that liability to psychosis induced by cannabis is strongly influenced by a polymorphism in the COMT gene that determines the rate of catabolism of frontal dopamine." --- And 'The ecogenetics of schizophrenia: a review', Schizophrenia Research Volume 32, Issue 2 , 27 July 1998, Pages 127-135. "Use of cannabis is a likely risk factor for schizophrenia (Andreasson et al., 1987). Not only are there genetically determined differences in the individual psychotropic effects produced by cannabis (Lyons et al., 1997), but use of cannabis itself is also influenced by genetic factors (Tsuang et al., 1996). Thus, part of the genetic contribution to schizophrenia may be mediated by the use of cannabis and its subjective effects (genotype–environment correlation and interaction). McGuire and colleagues found that the risk for schizophrenia in the first-degree relatives of schizophrenic patients who screened positive for cannabis was increased more than 10-fold compared to those of schizophrenic patients who screened negative (McGuire et al., 1995). These results are suggestive of a mechanism of genotype–environment interaction and/or genotype–environment correlation, as in both instances the first-degree relatives of cases exposed to the environmental risk factor should have higher rates of illness (Ottman, 1996; Marcelis et al., 1998b)." --- That's for those of your without access to your own online library So what the last article is suggesting is that the cannabis-schizophrenia link works in both directions. Cannabis use may contribute to the development of schizophrenia and likewise schizophrenic personalities may be more likely to use cannabis. People often seem confused about the fact that this is a scientific point, that the links and causality or non-causality are something that either exists or does not exist and that its not a case for debate, just emotionless and unbiased research. Its science and they haven't made up their minds yet because they still don't have enough concrete evidence either way. Undoubtably an association has been made between weed and going or being schizo, but the exact nature of this link is yet to be confirmed.