c a n n a b i s e r a

Cannabis ger inte upphov till hjärnskador!

Myten om att cannabis skulle ge upphov till hjärnskador är ett mysterium hur den ens uppkom och har inte mycket seriös forskning bakom sig.

På sjuttiotalet gjordes det studier som pekade på att apor, som konstant blev tvungna att röka cannabis fick hjärnskador. Man sa då att det var cannabisen som gav upphov till dessa skador, när det troligtvis i själva verket var bristen på ren syre under exponeringstiden.
Denna forskning har också motbevisats vid senare tillfällen.¹

Även Sveriges egna "centralförbund för alkohol- och narkotikaupplysning" har en presentation på sin hemsida där de erkänner att cannabis inte dödar hjärnceller.²

Det finns faktiskt forskning som tyder på att vissa ämnen i cannabis (s.k. cannabinoider) kan ha positiva effekter på hjärnan och hjärnceller, till skillnad mot nästan alla andra droger.^{3, 4}

Dock finns det vissa saker som pekar på att ungdomars och barns hjärnfunktioner kan, vid tungt cannabisanvändande påverkas i en negativ riktning. Försökspersonerna hade tyvärr intagit alkohol under testperioden så en riktig analys på enbart cannabis kunde inte göras.⁵

Självklart ska aldrig ungdomar och barn använda cannabis, på samma sätt som de inte ska röka tobak, dricka alkohol eller köra bil.
En reglerad marknad skulle lättare kunna hålla koll på vilka som köper och ge en mer trovärdig bild av skadorna av cannabis.

Det de flesta i stället menar när man säger permanenta hjärnskador är de bieffekter som tungt användande kan ha. T.ex. sämre korttidsminne och sämre kognitiv förmåga osv. Detta är debatterade tillstånd men är heller inga bestående skador, till skillnad från vad tung alkoholkonsumtion kan ha.^{6, 7}

Källor:

1: For the in vitro study, THC was added (1-100 nM) to membranes prepared from different regions of the rat brain and muscarinic cholinergic (MCh) receptor binding was measured. For the acute in vivo study, rats were injected IP with vehicle, 1, 3, 10, or 30 mg THC/kg and sacrificed 2 h later. For the chronic study, rats were gavaged with vehicle or 10 or 20 mg THC/kg daily, 5 days/week for 90 days and sacrificed either 24 h or 2 months later. Rhesus monkeys were exposed to the smoke of a single 2.6% THC cigarette once a day, 2 or 7 days a week for 1 year. Approximately 7 months after the last exposure, animals were sacrificed by overdose with pentobarbital for neurochemical analyses. In vitro exposure to THC produced a dose-dependent inhibition of MCh receptor binding in several brain areas. This inhibition of MCh receptor binding, however, was also observed with two other nonpsychoactive derivatives of marijuana, cannabidiol and cannabinol. In the rat in vivo study, we found no significant changes in MCh or other neurotransmitter receptor binding in hippocampus, frontal cortex or caudate nucleus after acute or chronic exposure to THC. In the monkey brain, we found no alterations in the concentration of neurotransmitters in caudate nucleus, frontal cortex, hypothalamus or brain stem.
Chronic marijuana smoke exposure in the rhesus monkey. IV: Neurochemical effects and comparison to acute and chronic exposure to delta-9-tetrahydrocannabinol (THC) in rats.
2: Det finns inget bevis att cannabis skadar hjärnceller.
"Drugs and the brain"
3: The effects of HU210 on adult hippocampal neurogenesis were quantified in freely moving rats and were correlated with behavioral testing. We show that 1 month after chronic HU210 treatment, rats display increased newborn neurons in the hippocampal dentate gyrus and significantly reduced measures of anxiety- and depression-like behavior.
Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects
4: Thus, cannabinoids appear to be the only illicit drug whose capacity to produce increased hippocampal newborn neurons is positively correlated with its anxiolytic- and antidepressant-like effects.
Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects
5: Our results support the hypothesis that heavy cannabis use during adolescence may affect the trajectory of normal brain maturation. Due to concurrent alcohol consumption in five HCU subjects, conclusions from this study should be considered preliminary, as the DTI findings reported here may be reflective of the combination of alcohol and marijuana use. Further research in larger samples, longitudinal in nature, and controlling for alcohol consumption is needed to better understand the pathophysiology of the effect of cannabis on the developing brain.
Diffusion abnormalities in adolescents and young adults with a history of heavy cannabis use
6: At days 0, 1, and 7, current heavy users scored significantly below control subjects on recall of word lists, and this deficit was associated with users' urinary 11-nor-9-carboxy-9-tetrahydrocannabinol concentrations at study entry. By day 28, however, there were virtually no significant differences among the groups on any of the test results, and no significant associations between cumulative lifetime cannabis use and test scores.
Neuropsychological Performance in Long-term Cannabis Users (Archives of General Psychiatry; October 2001)
7: We do know that heavy drinking may have extensive and far–reaching effects on the brain, ranging from simple “slips” in memory to permanent and debilitating conditions that require lifetime custodial care.
U.S. department of health and human services: Alcohol alert (October 2004)