Flamma77 skrev:
De är tyvärr inte enskilda eller ens utförda på samma individ.
Kopplar jag ihop detta med de farmakologiska och medicinska kunskaper jag har, så har jag bilden klar för mig.
Jag tycker att cannabisbrukare är moffiga i huvudet. Med moffig menar jag trött, seg, frånvarande och en aningen flummiga...
Men det är klart, en vetenskaplig undersökning om så är fallet borde ju vara det korrekta.
Här är en liten del.....av WHO:s rapport intressant just i detta fallet
Adult Motivation
One of the major concerns about the psychological effects of chronic heavy cannabis use has been that it impairs adult motivation. The evidence for an "amotivational syndrome" among adults consists largely of case histories and observational reports (e.g. Kolansky and Moore, 1971; Millman and Sbriglio, 1986). The small number of controlled field and laboratory studies have not found compelling evidence for such a syndrome (Dornbush, 1974; Negrete, 1983; Hollister, 1986). The evidential value of the field studies is limited by their small sample sizes, and the limited sociodemographic characteristics of their samples, while the evidential value of the laboratory studies is limited by the short periods of drug use, the youthful good health of the volunteers, and minimal demands made on volunteers in the laboratory (Cohen, 1982). Some regular cannabis users report a loss of ambition and impaired school and occupational performance as adverse effects of their use (e.g. Hendin et al, 1987) and that some ex-cannabis users give impaired occupational performance as a reason for stopping (Jones, 1984). Nonetheless, it is doubtful that cannabis use produces a well defined amotivational syndrome. It may be more parsimonious to regard the symptoms of impaired motivation as symptoms of chronic cannabis intoxication rather than inventing a new psychiatric syndrome.
Adolescent Development
In the United States in the 1970s and 1980s, cannabis use appears to have increased the risk of discontinuing a high school education, and of experiencing job instability in young adulthood (Newcombe and Bentler, 1988). The apparent strength of these relationships in cross-sectional studies (e.g. Kandel, 1984) has been exaggerated because those adolescents who are most likely to use cannabis have lower academic aspirations and poorer high school performance prior to using cannabis than their peers who do not (Newcombe and Bentler, 1988). It remains possible that factors other than the marijuana use account for apparent causal relations. To the extent they may exist, these adverse effects of cannabis and other drug use upon development over and above the effect of pre-existing nonconformity may cascade throughout young adult life, affecting choice of occupation, level of income, choice of mate, and the quality of life of the user and his or her children.
A major finding of research into the adult consequences of adolescent cannabis use has been the strong evidence of a regular sequence of initiation into the use of illicit drugs among American adolescents in the 1970s in which cannabis use preceded involvement with "harder" drugs such as stimulants and opioids (Kandel et al, 1984; Donovan and Jessor, 1983; Yamaguchi and Kandel, 1984 a, b). The causal significance of this sequence of initiation into drug use remains controversial. The hypothesis that it represents a direct effect of cannabis use upon the use of the later drugs in the sequence is the least compelling. There is better support for two other hypotheses which are not mutually exclusive: that there is a selective recruitment into cannabis use of nonconforming adolescents who have a propensity to use other illicit drugs; and that once recruited to cannabis use, the social interaction with other drug using peers, and exposure to other drugs when purchasing cannabis on the black-market, increases the opportunity to use other illicit drugs (Baumrind, 1983; Goode, 1974; Kandel, 1988).
A Dependence Syndrome
A cannabis dependence syndrome as defined in DSM-IV (American Psychiatric Association, 1994) can occur in heavy, chronic users of cannabis. There is good experimental evidence that chronic heavy cannabis users can develop tolerance to its subjective and cardiovascular effects. There is also suggestive evidence that some users may experience a withdrawal syndrome on the abrupt cessation of cannabis use, although one that is much milder and less marked than that experienced when withdrawing from alcohol or opiates (Compton, Dewey and Martin, 1990; Jones and Benowitz, 1976). DSM-IV notes that "symptoms of possible cannabis withdrawal (e.g. irritable or anxious mood accompanied by physical changes such tremor, perspiration, nausea and sleep disturbances) have been described in association with the use of very high doses, but their clinical significance is uncertain." (American Psychiatric Association, 1994:215).
There is clinical and epidemiological evidence that some heavy cannabis users experience problems in controlling their cannabis use, and continue to use the drug despite experiencing adverse personal consequences of use (Jones, 1984; Roffman et al, 1988; Weller et al, 1984). There is limited clinical evidence for a cannabis dependence syndrome analogous to the alcohol dependence (Kosten et al, 1987). Epidemiological surveys of the prevalence of drug dependence in the general population (e.g. Anthony and Helzer, 1991) show that cannabis dependence, as defined in the diagnostic manuals, is among the most common forms of drug dependence in Western societies by virtue of its high prevalence of use. On the other hand, relatively few users seek treatment for cannabis dependence (American Psychiatric Association, 1994: 220-221).
Cognitive Effects
The weight of the available evidence suggests that even the long term heavy use of cannabis does not produce any severe or grossly debilitating impairment of cognitive function (Carter et al, 1980; Fehr and Kalant, 1983b, Rubin and Comitas, 1975; Wert and Raulin, 1986). If it did research to date should have detected it. There is some clinical and experimental evidence, however, that the long-term use of cannabis may produce more subtle cognitive impairment in the higher cognitive functions of memory, attention and organisation, and the integration of complex information (Page et al, 1988; Solowij et al, 1991, 1992, 1993 and see chapter by Solowij in this volume). While subtle, these impairments may affect everyday functioning, particularly among individuals in occupations that require high levels of cognitive capacity. The evidence suggests that the longer the period that cannabis has been used, the more pronounced is the cognitive impairment (Solowij et al, 1992, 1993). It remains to be seen whether the impairment can be reversed by an extended period of abstinence from cannabis.
Brain Damage
A suspicion that chronic heavy cannabis use may cause gross structural brain damage was provoked by a single poorly controlled study using an outmoded method of investigation which reported that cannabis users had enlarged cerebral ventricles (Campbell et al, 1971). This finding was widely and uncritically publicised. Since then a number of better controlled studies using more sophisticated methods of investigation have consistently failed to demonstrate evidence of structural change in the brains of heavy, long term cannabis users (e.g. Co et al, 1977; Kuehnle et al, 1977). These negative results are consistent with the evidence that any cognitive effects of chronic cannabis use are subtle, and hence unlikely to be manifest as gross structural changes in the brain.
Serious Psychiatric Disorder
There is suggestive evidence that large doses of THC can produce an acute psychosis in which confusion, amnesia, delusions, hallucinations, anxiety, agitation and hypomanic symptoms predominate. The evidence comes from laboratory studies of the effects of THC on normal volunteers and clinical observations of psychotic symptoms in heavy cannabis users which remit rapidly following abstinence (Bernardson and Gunne, 1972; Chopra and Smith, 1974; Edwards, 1976).
There is less support for the hypothesis that cannabis use can cause either an acute or a chronic functional psychosis (Thornicroft, 1990). Such possibilities are difficult to study because of the rarity of such psychoses, and the near impossibility of distinguishing them from schizophrenia and manic depressive psychoses occurring in individuals who also use cannabis (Ghodse, 1986).
There is strongly suggestive evidence from a prospective study that heavy cannabis use may precipitate schizophrenia in vulnerable individuals (Andreasson et al, 1987; Schneier and Siris, 1987; Thornicroft, 1990). This relationship is still only strongly suggestive because in the only prospective study conducted to date (Andreasson et al, 1987) the use of cannabis was not documented at the time of diagnosis, there was a possibility that cannabis use was confounded by amphetamine use, and there are doubts about whether the study could reliably distinguish between schizophrenia and acute cannabis, or other drug-induced, psychoses (Negrete, 1989; Thornicroft, 1990).
There is less support for the hypothesis that cannabis use can cause either an acute or a chronic functional psychosis (Thornicroft, 1990). Such possibilities are difficult to study because of the rarity of such psychoses, and the near impossibility of distinguishing them from schizophrenia and manic depressive psychoses occurring in individuals who also use cannabis (Ghodse, 1986). There is better evidence that cannabis use can adversely affect the course of schizophrenia in affected individuals who continue to use it (Cleghorn et al, 1991; Jablensky et al, 1991; Martinez-Arevalo et al, 1994).
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