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kopplingen mellan ventrikelseptumdefekter (hjärtfel med ofullständig kammarvägg)<br />

hos nyfödda och mödrarnas livsstil bland annat i fråga om rökning <strong>av</strong> marijuana.<br />

Bakgrunden var att man under de gångna 30 åren sett en signifikant ökning <strong>av</strong> denna<br />

missbildning i USA. För cannabisrökande mödrar var risken att föda ett missbildat<br />

barn fördubblad. Risken ökade med rökningens intensitet.<br />

Missbildningar på grund <strong>av</strong> cannabisorsakade kromosomskador<br />

Missbildningar kan också framkallas på annat sätt än genom toxisk påverkan direkt<br />

på fostret. Gifter med förmåga att påverka arvsanlagen kan genom att skada an lagen<br />

hos någon <strong>av</strong> föräldrarna framkalla missbildningar på genetisk väg. Man har inte<br />

kunnat visa att THC har sådana egenskaper och risken har <strong>av</strong>visats i flera<br />

forskningsöversikter (Marijuana and Health, 1982; Hollister, 1986; Hall, et al., 1994).<br />

— Jan Ramström, Folkhälsoinstitutet - Skador <strong>av</strong> hasch och marijuana [28]<br />

Hall skriver i sin rapport från 1994 om svårigheterna att identifiera faktorer som ger falska svar:<br />

The animal evidence indicates that in sufficient dosage cannabis can "produce<br />

resorption, growth retardation, and malformations" in mice, rats, rabbits, and<br />

hamsters (Bloch, 1983, p406). Growth esorption and growth retardation h<strong>av</strong>e been<br />

more consistently reported than birth malformations (Abel, 1985). There are also<br />

several c<strong>av</strong>eats on the evidence that cannabis increases rates of malformations. The<br />

doses required to reliably produce malformations h<strong>av</strong>e been very high (Abel, 1985),<br />

and such effects h<strong>av</strong>e been observed more often after the administration of crude<br />

marijuana extract than pure THC, suggesting that other cannabinoids may be<br />

involved in producing any teratogenic effects. There h<strong>av</strong>e also been doubts expressed<br />

about whether these teratogenic effects can be directly attributed to THC. Some h<strong>av</strong>e<br />

argued, for example, that the malformations may be a consequence of reduced<br />

nutrition caused by the <strong>av</strong>ersive properties of the large doses of cannabis used in<br />

these studies (Abel, 1985; Bloch, 1983).<br />

“<br />

Hollister (1986) has also discounted the animal research data, arguing that "virtually<br />

every drug that has ever been studied for dysmorphogenic effects has been found to<br />

h<strong>av</strong>e them if the doses are high enough, if enough species are tested, or if treatment<br />

is prolonged" (p4). Similar views h<strong>av</strong>e been expressed by Abel (1985) and by Bloch<br />

(1983), who concluded that THC was unlikely to be teratogenic in humans because<br />

"the few reports of teratogenicity in rodents and rabbits indicate that cannabinoids<br />

are, at most, weakly teratogenic in these species" (p416).<br />

...<br />

Even when large sample sizes h<strong>av</strong>e been obtained, there are difficulties in<br />

interpreting any associations found between adverse pregnancy outcomes and<br />

cannabis use. Cannabis users are more likely to use tobacco, alcohol and other illicit<br />

drugs during their pregnancy. They also differ from non-users in social class,<br />

education, nutrition, and other factors which predict an increased risk of<br />

experiencing an adverse outcome of pregnancy (Fried, 1980, 1982; National<br />

Academy of Science, 1982; Tennes et al, 1985). These sources of confounding make it<br />

difficult to unequivocally attribute any relationship between reproductive outcomes<br />

and cannabis use to cannabis use per se, rather than to other drug use, or other<br />

variables correlated with cannabis use, such as poor maternal nutrition, and lack of<br />

prenatal care. Sophisticated forms of statistical control provide the only way of<br />

assessing to what degree this may be the case, but its application is limited by the<br />

small number of cannabis smokers identified in most studies.<br />

Given these difficulties, and the marked variation between studies in the proportion<br />

of women who report cannabis use during pregnancy, the degree of agreement<br />

between the small number of studies is more impressive than the disagreement that<br />

seems at first sight to such be a feature of this literature. There is reasonable<br />

consistency (although not unanimity) in the finding that cannabis use in pregnancy is<br />

associated with foetal growth retardation, as shown by reduced birth weight (e.g.<br />

”<br />

442

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