Cannabis och hjärnskador

Cannabis ger bestående hjärnskador

Orsakar cannabis skador på hjärnan? Krymper hjärnan av cannabis? Vilka skador ger cannabis på hjärnan?

Ett vanligt argument man kan få höra från lekmän är att man får hjärnskador av cannabis och därmed är drogen neurotoxisk. Detta budskapet hade förbudsförespråkare som huvudargument under 1970-talet och fram till 1990-talet. Det är mer sällan man ser det i "faktaskrifterna" nu för tiden. Det beror på att den främsta forskningen som hela argumentet vilat på har fallit sönder.

Istället pratar förbudsförespråkare numera hellre om morfologiska förändringar av hjärnans volym och struktur. Man lyfter fram att vissa forskningsresultat tyder på att vissa delar av cannabisrökares hjärnor är mindre (eller i vissa fall större), hävdar att detta beror på cannabisexponeringen och drar slutsatsen att det leder till sämre neurokognitiva förmågor. Men det som vanligt inte vetenskapligt solida och underbyggda argument vilket vi skall visa här.

Läs även kapitlet om Cannabis och kognitiva nedsättningar som handlar om huruvida man blir "dum" eller får lägre intelligens av att använda cannabis.

Robert Heaths forskning

Argumentet om hjärnskador uppkom på 1970-talet. Robert Heath vid Tulane University Medical School, New Orleans inledde experiment på apor och resultaten visade tydligt att apornas hjärnor fått stora skador:

1974: Cannabis causes brain damage

New studies in America have revealed that smoking cannabis can cause brain damage.

The US government has funded the cultivation of marijuana in the southern United States for research purposes.


In a laboratory in New Orleans, rhesus monkeys were forced to smoke the equivalent of two cannabis cigarettes a day for nearly a year.

Electrodes implanted in their brains measured brain activity, and the results have indicated major if not permanent damage.

Researchers claim cannabis has a lasting impact - one monkey had not been subjected to the testing for six months, but still showed "disrupted brain wave patterns".

Studies on humans have assessed the effects of cannabis smoking on hormonal disruption, birth defects and severe personality disorders.
— BBC, 1974-10-02[1]

När studien kom så proklamerade president Ronald Reagan att:

The most reliable scientific sources say permanent brain damage is one of the inevitable results of the use of marijuana.
— Ronald Reagan (L.A. Times)[2]

Och detta blev under närmare ett årtionde huvudargumentet mot cannabis.

Tidningen Playboy och intresseorganisationen NORML begärde att få se rapporten, men det tog flera års processande innan all data släpptes[3][4][5]

Heath kritiserades senare hårt av flera tunga institutioner (Institute of Medicine och National Academy of Sciences) p.g.a. forskningens uppenbara brister, ovetenskapliga metoder och felaktiga redovisningar. Bland annat så användes bara 4 apor i studien, de fick inandas rök motsvarande 63 jointar under fem minuter varje dag i tre månader istället för 30 jointar om dagen under en ettårsperiod som Heath först hade rapporterat, detta för att spara pengar. Men kritiken riktas i huvuddrag åt metoden för administreringen. Aporna fick in all rök in i små lufttäta burar runt huvudena där tvingades andades in den koncentrerade röken, med bl.a giftig kolmonoxid som skapas vid förbränning[2]. Eventuellt kan även ett övertryck i kammaren orsakat hjärnskadorna[6].

Senare studier från början av 1990-talet från bl.a National Center for Toxicological Research (NCTR)[7][8] där 64 rhesus-apor fick cannabis dagligen eller varje vecka under ett år kunde inte påvisa strukturella eller neurokemiska skador eller förändringar i hjärnan. SRI International[9] gjorde också en studie där 30 apor fick inhalera cannabis utan att skador påvisades. Det finns även studier på människor som gjordes under 1970-talet som inte kunde påvisa skador[10][11] och i princip alla studier i mordern tid delar åsikten att några strukturella skador som beror på cannabis kan man inte finna.

Heath et al (1979) found that continuous, daily exposure to the equivalent of the smoke from about 3 marijuana cigarettes per day produced abnormal electrical alterations after 2 to 3 months. Additional exposure of up to 3 to 6 months produced electrical abnormalities which persisted for up to 8 months. Heath also conducted histological examinations on brain tissue from the monkeys and found anatomic changes were apparent in the electronmicrographs, suggesting long-lasting changes related to the THC exposure. These changes included widening of the synaptic cleft, clumping of synaptic vesicles and other unspecified changes in morphology of neurones which occurred in monkeys after 6 months of forced cannabis intake and were still evident 6 months after cessation of cannabis use. However, it is unclear from his report whether a methodical evaluation of the supposed histopathology was made which included an independent panel of judges or whether these were his own personal judgements.

The deep sites from which abnormal EEG recordings were recorded are generally believed to be involved in emotional expression and hence affect disorders.2 Heath's earlier work remains somewhat problematic when his experimental setup is examined in more detail. Although his monkeys included controls who were exposed to both very low THC containing marijuana and tobacco smoke alone,3 this research remains highly confounded. The monkeys were strapped into chairs with transparent, sealed plastic boxes surrounding their heads. The smoke, together with oxygen, was pumped into the box for a pre-determined period while EEG recordings were made through permanently implanted deep electrodes. Given that in humans THC can induce panic anxiety attacks and given that monkeys do not like to be restrained, it is impossible to tell whether the abnormal electrical activity recorded in limbic areas was directly induced in the brain by the action of THC or whether this activity was what one would observe when panic is induced in restrained monkeys intoxicated by THC.

Heath describes the monkeys' behaviour.

All displayed dilated pupils and sharp reduction in level of awareness. The monkeys would stare blankly into space, sometimes displaying spontaneous nystagmus, and would become much less attentive or completely unresponsive to environmental stimuli. When their hands or feet were grasped, the clasping response, which was consistently elicited on baseline examinations, was absent. Responses to pain (pinprick) and to sound (hand claps) were minimal to absent. Although the monkeys were not particularly drowsy, spontaneous motor movements were notably slowed, and passive tests of muscle tone suggested a degree of catatonia, although true waxy flexibility never developed (Heath, 1973, p. 4).

This certainly is not the way that the vast majority of human beings react to cannabis intoxication. The behaviour Heath describes appears to be more in line with an animal frozen in panic or manifesting what used to be called 'animal hypnosis'. Hunt (1984), a cognitive psychologist, has called this the "negative capability" and it appears to be part of a neurophysiological mechanism for behavioural and cognitive shutdown when an animal is overwhelmed by, for example, a predator.

Another major problem with Heath's 1973 study was the control of O2 partial pressure (PP) in the head chamber. From tables in his paper one can see that the PP of O2 inside the monkey's "breathing chamber" was 75% greater than room PP in the marijuana run but only 9% above for the control tobacco sequence. The measured serum PP of O2 was 143% above pre-exposure levels as seen in his data for the marijuana sequence as opposed to a rise of only 22.4% in the case of the tobacco run. There is little doubt that high partial pressures of serum O2 will affect brain function and hence the EEG recordings (p. 9). Thus, any comparisons between THC exposure and tobacco exposure in this study are at best spurious. Finally, Heath states that, as the choice of subjects for cannabis studies moves up the phylogenetic scale, it is observed that THC produces a more localised effect in the brain involving fewer areas. In other words, humans show the least generalised reactions to THC. In summary, apart from the confounding factors of behavioural variables and O2 partial pressures in this research, any attempt to generalise from monkeys to humans is fraught with the possibility of committing a logical category error.

As mentioned above, the research of Heath and his colleagues has been widely reported and appears to have been accepted somewhat uncritically by a number of serious researchers as seen in two of the review articles being reported on here (Cohen, 1986; Jones, 1980). This seems to be a recurring theme in much of the cannabis research today. In most research into psychopharmacological effects on EEG reliable conclusions are rarely drawn from so small a number of studies. The interaction of pharmacological agents with brain and behaviour is complex and even the simplest relationships require many experiments in order to delineate the causal connections with any degree of reliability. It appears as though any findings in cannabis research are immediately set upon by the those opposed to it use for the purpose of adding power to already pre-drawn conclusions.
— A Critical Review Of The Research Literature Concerning Some Biological And Psychological Effects Of Cannabis (Nelson, 1993)[6]

Argument från förbudsförespråkare

Jan Ramström ägnar inte Heaths forskning ett enda ord i delarna som handlar om bestående hjärnskador. Den är tydligen inte bra att visa upp i den historiska genomgången av hur man bedrivit forskning om cannabisskador...

Bestående hjärnskador efter cannabisrökning

Med hjärnskador avses här bestående skador som kan påvisas genom röntgenologiska och liknande metoder under livet eller genom mikroskopisk undersökning av hjärnan från avlidna missbrukare. Det finns många kliniska och anekdotiska rapporter om långvarig psykisk funktionsnedsättning vid kroniskt cannabisbruk, inte minst från utvecklingsländerna. Dessa iakttagelser stöds av tidiga vetenskapliga studier (till exempel Chopra, 1976; Soueif, 1976). Även om dessa studier har stora begränsningar på grund av otillfredsställande vetenskaplig design har de starkt bidragit till att frågeställningen om bestående hjärnskador diskuterats sedan lång tid tillbaka. Campbell et al. (1971) skapade viss uppståndelse när gruppen publicerade en undersökning som påvisade hjärnatrofi (förtvining av hjärnan) med hjälp av luftencefalografi hos tio kroniska cannabismissbrukare medan 13 kontroller i samma ålder uppvisade normala förhållanden. Denna studie utsattes för metodologisk kritik på flera punkter och kunde inte heller upprepas av andra forskare. Det har också gjorts ett flertal andra undersökningar med hjälp av datortomografi (skiktröntgen) där man inte heller har kunnat påvisa någon hjärnatrofi hos kroniska cannabismissbrukare (Hannerz & Hindmarch, 1983).
— Jan Ramström, Folkhälsoinstitutet - Skador av hasch och marijuana[12]

Förändrad hjärnmorfologi

Jan Ramström (se ovan) går in mer i detalj på en studie av Yücel & Solowij (2008)[13] som visade en minskning i volymen på hippocampus och amygdala mellan 7 och 12%. Ramström drar samband med schizofrena som också uppvisar mindre volymer av dessa hjärnregioner och driver tesen att det är själva hjärnskadan. En Professor vid New Yorks University reder i en artikel från 2008[14] ut detta och menar att det inte finns någon forskning som stödjer påståendet att cannabis kan orsaka morfologiska förändringar hos friska som leder till schizofreni.

Det finns både forskning som stöder[15][16][17][18][19][20][21] respektive inte stöder[22][10][11][23][24][19][25] teorin att cannabis orsakar bestående förändringar av hjärnans delvolymer. En studie från 2007 rapporterar t.o.m ökad hippocampus-volym hos cannabisbrukare[26]. En metaanalys från 2010[27] går igenom 13 tidigare studier. Inga studier framställer bevis för strukturella förändringar. 6 stycken kan påvisa regionala förändringar. Man drar slutsatsen att det finns stöd för existensen av morfologiska förändringar, även om studierna inte är entydiga och visar olika resultat.

2013[28] publicerades en studie där man noterar minskade volymer för delar av hjärnan som relateras till arbetsminnet, vilket satte ny fart i debatten. SVT rapporterade att "Marijuana krymper hjärnan"[29] och passade även på att inflika en hel del påståenden som inte hade med studien att göra, exempelvis schizofrenirisken och ökad cannabispotens. Nästa gång en studie uppmärksammas har istället delar av hjärnan ökat i volym, och då är detta farligt och tyder på skador...

"Även de som bara röker cannabis ibland ligger i farozonen för beroende och skadliga effekter" rapporterar SVT 2014[30]. Man låter även Thomas Lundqvist uttala sig kring resultatet. Drugnews skriver på Twitter att "även liten cannabisanvändning stör hjärnfunktioner"[31].

Artikeln bygger på en studie från 2014[32]. Forskarna använde magnetisk resonanstomografi för att undersöka hjärnorna hos 20 ungdomar mellan 18-25 år som använde cannabis minst en gång i veckan (medel 3 gånger i veckan) men inte uppfyllde kraven för beroende enligt DSM-IV. Resultaten jämfördes med en kontrollgrupp och man kunde se att cannabisanvändarna uppvisade vissa strukturella abnormiteter. Den grå hjärnsubstansens densitet och volym var högre i vänstra accumbenskärnan. Det fanns även skillnader i formen på vänstra accumbenskärnan och högra amygdala och man såg en association mellan formen och cannabisfrekvensen (skillnaden var signifikant om personen rökte ofta/mycket). Det här är intressant eftersom medelvärdet i studien för antal jointar i veckan var 11 stycken, vilket känns avvikande från vad man borde innefatta i begreppet "röker ibland". Det fanns inga signifikanta förändringar om cannabiskonsumtionen faktiskt var låg. Resultat kan därmed inte påstås återspegla vad som händer med personer som bara röker cannabis ibland.

Forskarna kommer aldrig till någon definitiva slutsatser om skadliga effekter eller störningar av hjärnfunktionerna, utgången här är inte annorlunda mot tidigare studier som räknats upp, ändå kan Lundqvist räkna upp olika störningar som han tycker att studien ger stöd för... När det gäller beroendet så jämförs den ökade volymen och densiteten med liknande förändringar hos personer som använder droger som ökar utsöndringen av dopamin i hjärnan, samt hos personer med med diagnosen cannabisberoende. Forskarna spekulerar därför kring att amygdala kan ha en stor roll i drogberoendets funktion, att förändringen kan vara ett tecken på begynnande beroende. Magnus Callmyr analyserade SVT och Drugnews tolkningar[33] och påpekar också bristen på kausalitet. Med tanke på att majoriteten av all statistik som finns visar att under 10% procent blir beroende av cannabis så finns det inte stöd från verkliga observationer för att den påstådda beroenderisken från sporadiskt bruk stämmer.

Studierna uppvisar en stor spridning kring vilka delar som påverkas och hur de påverkas. Men även om det förekommer volymförändringar, är det samma sak som hjärnskador? "The Interagency Committee on Neurotoxicology" (ICON) har följande definition av neurotoxicitet: "any adverse effect on the structure or function of the central and/or peripheral nervous system by a biological, chemical or physical agent and may result from direct or indirect actions or reflect permanent or reversible changes in the nervous system". En annan definition från "Dorland's Medical Dictionary for Health Consumers" och "Miller-Keane Encyclopedia & Dictionary of Medicine, Nursing, & Allied Health" är "the quality of exerting a destructive or poisonous effect upon nerve tissue". Med andra ord är tolkningen ytterst tveksamt.

Nadia Solowij som är biträdande professor vid University of Wollongong i Australien och som har publicerat egen forskning i området sammanfattar vilka slutsatser man kan dra av forskningen som tyder på mindre volymer av vissa delar av hjärnan. Läs gärna hela artikeln, den går igenom resultatet från många studier:

What might be the implications of structural brain changes in cannabis users?

It is often assumed that alterations in the morphology of the brain may underlie impaired cognition and may indicate neural substrates of risk for the development of psychosis, but there are limited data to support these notions. The interrelationships between cognition and psychopathology, and indeed between brain structure and function, are complex. Few structural brain imaging studies of cannabis users have specifically examined the relationship between brain volumes and cognitive performance measures and most of those that did found no associations (Tzilos et al., 2005 ; Jager et al., 2007 ; Medina et al., 2007b ; Yücel et al., 2008) or isolated relationships (Medina et al., 2007a ; Solowij et al., 2008). An exception to this was the finding of poor white-matter structural integrity being related to poorer cognitive perform-ance in cannabis and alcohol-using adolescents (Bava et al., 2010). The lack of association in most studies might be interpreted as aberrant associations between brain structure and function, as discussed elsewhere (Solowij et al., 2009).
— Solowij (2012)[34]

En studie från 2014[35] studerade hjärnorna hos 48 cannabisrökare (som rökte i genomsnitt tre gånger per dag) med magnetisk resonanstomografisom. Forskarna jämförde resultatet med 62 ickerökare av samma kön och ålder samt justerade för alkohol och tobaksanvändning. Cannabisrökarnas bilaterala orbitofrontala gyri hade mindre volym, men samtidigt uppvisade de högre grad av funktionella kopplingar i orbitofrontala cortex (OFC), och högre grad av strukturella kopplingar i forceps minor. Den funktionella ökningen i OFC assoicerades med tidigare cannabisdebut. Man kunde inte se något samband mellan lägre IQ och morfologiska avvikelser.

Tests reveal that earlier onset of regular marijuana use induces greater structural and functional connectivity. Greatest increases in connectivity appear as an individual begins using marijuana. Findings show severity of use is directly correlated to greater connectivity.

Although increased structural wiring declines after six to eight years of continued chronic use, marijuana users continue to display more intense connectivity than healthy non-users, which may explain why chronic, long-term users "seem to be doing just fine" despite smaller OFC brain volumes, Filbey explained.
— Science Daily 2014-11-10[36]

Bristen på kausalitet påpekas i en artikel som publiceras av brittiska NHS (National Health Service) som är den brittiska motsvarigheten till Folkhälsomyndigheten:

The researchers say that their findings "suggest that chronic marijuana use is associated with complex neuroadaptive processes, and that onset and duration of use have unique effects on these processes".


Although this type of study can identify differences in brain structure and connections between cannabis users and non-users, it cannot show that the differences were caused by cannabis use: people with different brain structures may be more likely to use cannabis, for example.
— NHS 2014-11-11[37]

Paul Armentano från NORML pekar även på andra brister som inverkar i en totalbedömning av vad studien faktiskt kan påvisa och inte[38].

2015 publicerades en studie[39] där både ungdomar (262st) och vuxna (503st) undersöktes. Till skillnad från de flesta tidigare studierna kontrollerade och justerade man för livsstilsfaktorer som kan påverka resultatet, exempelvis bruk av alkohol och tobak, etnicitet, depression, ångest och impulsivt kicksökande beteende. När man tog hänsyn till dessa faktorer kunde inte cannabisbruk associeras med några morfologiska förändringar av hjärnan:

Recent research has suggested that marijuana use is associated with volumetric and shape differences in subcortical structures, including the nucleus accumbens and amygdala, in a dose-dependent fashion. Replication of such results in well controlled studies is essential to clarify the effects of marijuana. To that end, this retrospective study examined brain morphology in a sample of adult daily marijuana users (n 29) versus nonusers (n 29) and a sample of adolescent daily users (n 50) versus nonusers (n 50). Groups were matched on a critical confounding variable, alcohol use, to a far greater degree than in previously published studies. We acquired high-resolution MRI scans, and investigated group differences in gray matter using voxel-based morphometry, surface-based morphometry, and shape analysis in structures suggested to be associated with marijuana use, as follows: the nucleus accumbens, amygdala, hippocampus, and cerebellum. No statistically significant differences were found between daily users and nonusers on volume or shape in the regions of interest. Effect sizes suggest that the failure to find differences was not due to a lack of statistical power, but rather was due to the lack of even a modest effect. In sum, the results indicate that, when carefully controlling for alcohol use, gender, age, and other variables, there is no association between marijuana use and standard volumetric or shape measurements of subcortical structures.
— Weiland (2015)[39]

En Brittisk studie från 2015[40] visade att cannabisanvändare har 2% skillnad i corpus callosums morfologiska struktur jämfört med ickebrukare, vilket media rapporterade som bevis för att cannabis orsakar hjärnskador[41][42][43]. Forskarna jämförde även skillnaden mellan cannabisrökare med och utan psykoshistorik, men kunde inte se någon skillnad mellan dessa grupperna. Forskarna justerade för bruk av alkohol, men inte tobak. Att media så kraftigt vantolkade studiens resultat genom att rapportera om bevis för hjärnskador ledde till en omedelbar motreaktion från NHS (National Health Service):

The Sun's headline, "Scientists warn smoking 'skunk' cannabis wrecks brains", and the Daily Mail's, "Proof strong cannabis does harm your brain", were not based on any evidence.

This type of study cannot prove cause and effect, only suggest a possible link, so "proof" is too strong a term. Also, the study didn't look at how the small changes in the brain associated with skunk affected thoughts or other brain functioning, so it was not fair to say skunk "wrecks" the brain.


This type of study can't prove cannabis causes changes in brain structure or any associated mental health illness


What this study doesn't tell us is whether these structural changes do any harm or cause any negative mental health effects. The study simply didn't look at this, a subtlety much of the news reporting failed to recognise.

The study also can't tell us whether cannabis use is the direct cause of these observed differences, or whether other factors could be having an influence


The effects of cannabis use – both in the short and long term – are not firmly established
— NHS 2015-11-27[44]

En studie från 2015[45] undersökte om associationen kan ha genetiska förklaringar. Genom att jämföra 241 syskonpar där det ena syskonet använt cannabis och det andra inte, så kunde man se att personer som använt cannabis hade mindre amygdala, men att samma storleksförändringar fanns i amygdala hos syskonet som inte använde cannabis:

Small sample sizes in prior studies (generally N < 100) and varied definitions of cannabis exposure may have contributed to these inconsistent findings. Additionally, studies have implied that cannabis causes volumetric alterations, despite typically not controlling for potential confounding effects of shared predispositional factors (eg, genes/rearing environment that contribute to both volumetric differences and cannabis use)


Among 483 study participants, cannabis exposure was related to smaller left amygdala (approximately 2.3%;P .007) and right ventral striatum (approximately 3.5%; P< .005) volumes. These volumetric differences were within the range of normal variation. The association between left amygdala volume and cannabis use was largely owing to shared genetic factors (Pg -0.43;P .004), while the origin of the association with right ventral striatum volumes was unclear. Importantly, brain volumes did not differ between sex-matched siblings discordant for use (fixed effect -7.43;t -0.93,P .35). Both the exposed and unexposed siblings in pairs discordant for cannabis exposure showed reduced amygdala volumes relative to members of concordant unexposed pairs (fixed effect 12.56; t 2.97;P .003).


Importantly, by leveraging the familial design of the HCP, we demonstrated that amygdala volumetric reductions among cannabis users are primarily attributed to familial factors shared by twins/siblings. Overlapping genetic factors (Pg) were the only significant source of covariance; a significant correlation between individual-specific environmental factors (Pe) would be expected if the causal hypothesis were supported. The discordant sibling analyses further confirmed this; even in the absence of cannabis exposure, smaller amygdala volumes were observed among individuals with heightened familial liability, given their sibling’s cannabis use. However, interpretations from our sibling analyses should be tempered by our limited sample size to examine discordant MZ pairs only. This predisposition to smaller brain volumes, even in the absence of manifest cannabis use, casts considerable doubt on hypotheses that cannabis use, at least at the levels noted in this sample, causes reductions in amygdala volumes. Instead, both the exposed and unexposed siblings in discordant pairs and concordant exposed pairs tended to have smaller amygdala volumes than concordant unexposed individuals.
— Pagliaccio (2015)[45]

En studie från 2016 med 111 deltagare visade att hippocampus är mindre hos cannabisrökare som röker cannabis som inte innehåller CBD, men man kunde inte se några volymskillnader hos personer som röker cannabis som innehåller CBD. Man noterade även att volymskillnaden inte är permanent, den återställs vid avhållsamhet och kan inte påvisas hos f.d brukare. Inga justeringar gjordes för eventuellt bruk av legala droger eller social bakgrund:

we show for the first time that both hippocampal volume and neurochemistry are reduced to the greatest extent in users exposed to THC without CBD. In contrast, current users of cannabis containing CBD, as well as former users, show no structural or neurochemical hippocampal differences compared with controls. These findings are consistent with suggestions that CBD may be neuroprotective, perhaps through its role in synaptic plasticity and/or neurogenesis.


Our findings suggest that not all cannabis users experience adverse brain and behavioural outcomes
— Yücel (2016)[46]

2018 publicerades en studie[47] där 14 "tunga" cannabisrökares hjärnor jämförts med ickerökares. Man kunde inte se några förändringar i hippocampus eller amygdala likt tidigare studier, däremot såg man att några andra regioner av hjärnan hade signifikant större volym:

Results: The VBM study revealed that, compared to the control group HC1, the cannabis users did not show cortical differences nor smaller volume in any subcortical structure but showed a cluster (p < 0.001) of larger GM volume in the basal ganglia, involving the caudate, putamen, pallidum, and nucleus accumbens, bilaterally. The subcortical volumetric analysis revealed that, compared to the control group HC2, the cannabis users showed significantly larger volumes in the putamen (p 0.001) and pallidum (p 0.0015).

Conclusions: This study does not support previous findings of hippocampal and/or amygdala structural changes in long-term, heavy cannabis users. It does, however, provide evidence of basal ganglia volume increases.
— Moreno-Alcázar (2018)[47]

Ett forskarlag valde ut 781 ungdomar mellan 14–22 år från en databas med högupplösta bilder tagna med magnetisk resonanstomografi. 147 av dessa var cannabisanvändare. I studien som publicerades 2019[48] kan man inte se några skillader mellan cannabisgruppen och ickeanvändarna.

I en långtidsstudie som publicerades 2019 har man haft tillgång till liknande bilder av hjärnan från tonåringa pojkar och man har tagit uppföljande bilder i vuxen ålder. Inte heller här hittar man några bevis för att cannabisanvändning i tonåren gav bestående förändringar av hjärnans morfologi på de punkter som undersöktes:

We found that adolescent cannabis use was not associated with adult brain structure in a sample of boys followed prospectively to adulthood. Boys were classified into one of four prototypical adolescent cannabis trajectory subgroups based on prospective assessments of cannabis use frequency from age 13–19: infrequent use/no use, desisting use, escalating use, or chronic-relatively frequent use. These subgroups showed different patterns of cannabis use across adolescence and differed in terms of their overall cumulative exposure to cannabis. For example, the infrequent/no use subgroup had used cannabis, on average, on four total days from age 13–19, whereas the chronic-relatively frequent subgroup had used cannabis, on average, on 782 total days from age 13–19. We found no differences in adult brain structure for boys in the different adolescent cannabis trajectory subgroups. Even boys with the highest level of cannabis exposure in adolescence showed subcortical brain volumes and cortical brain volumes and thickness in adulthood that were similar to boys with almost no exposure to cannabis throughout adolescence.

Our findings contribute to already mixed evidence regarding whether adolescent cannabis use is associated with lasting brain differences (Nader and Sanchez, 2018). Case-control studies of adult cannabis users and comparison adults have generally not found an association between an earlier age-of-onset of cannabis use and adult brain structure (Ashtari et al., 2011; Cousijn et al., 2012; Filbey et al., 2015; Gilman et al., 2014; Lorenzetti et al., 2014; Matochik et al., 2005), suggesting that adolescent cannabis use might not have lasting effects on brain structure, consistent with our findings. Relatedly, a number of studies have reported that cannabis-related brain and cognitive differences resolve with abstinence (Fried et al., 2005; Hanson et al., 2010; Hirvonen et al., 2012; Korponay et al., 2017; Schreiner and Dunn, 2012; Scott et al., 2018; Tait et al., 2011). However, animal studies have suggested that cannabis exposure in adolescence may have lasting effects (O’Shea et al., 2004; Rubino et al., 2009; Schneider and Koch, 2003; Verrico et al., 2014). Further, a number of human studies have suggested that adolescent cannabis users show persisting differences in brain structure, brain function, or cognitive functioning (Ashtari et al., 2011; Bolla et al., 2002; Ganzer et al., 2016; Jacobus et al., 2014; Lorenzetti et al., 2014; Medina et al., 2010; Meier et al., 2012; Padula et al., 2007; Pope et al., 2003; Schweinsburg et al., 2008; Tapert et al., 2007). Conflicting findings might be attributable to between-study methodological differences, such as the extent of the sample’s cannabis exposure, length of cannabis abstinence at the time of testing, as well as inadequate control for covariates, such as alcohol use.
— Meier (2019)[49]

Hur påverkar cannabis existerande hjärnskador?

Till förbudsförespråkarnas förtret så har forskarna de senaste 10-20 åren istället märkt av andra effekter cannabis har på hjärnan, nämligen lindringen av olika hjärnsjukdomar och förmågan att förhindra hjärnskador. Upptäckterna har lett till att cannabis används inom dessa områden idag med stor framgång. Om man är intresserad att läsa forskningsrapporter där cannabis anses ha neuroskyddande egenskaper, se referenserna nedan samt kapitlet om Medicinska användningsområden för Cannabis:


Cannabis, alkohol och vit hjärnsubstans

En studie från 2012 visar att bruk av enbart cannabis inte påverkar den vita hjärnsubstansen negativt[80]. Enbart alkohol ger dock en negativ förändring och en annan studie visar även en synergieffekt om alkohol kombineras med cannabis[81]:

Man kan även notera att det är sällsynt att media varnar för att alkoholdoserna som är vanligt förekommande i ungdomarnas festkultur leder till hjärnskador...

A teen who consumes alcohol is likely to have reduced brain tissue health, but a teen who uses marijuana is not, according to a new study.

Researchers scanned the brains of 92 adolescents, ages 16 to 20, before and after an 18-month period. During that year and a half, half of the teens -- who already had extensive alcohol and marijuana-use histories -- continued to use marijuana and alcohol in varying amounts. The other half abstained or kept consumption minimal, as they had throughout adolescence.

The before-and-after brain scans of the teens consuming typically five or more drinks at least twice a week showed reduced white matter brain tissue health, study co-author Susan Tapert, neuroscientist at University of California, San Diego, told HuffPost. This may mean declines in memory, attention, and decision-making into later adolescence and adulthood, she said.

However, the level of marijuana use -- up to nine times a week during the 18 months -- was not linked to a change in brain tissue health. The researchers did not test performance; they only looked at brain scans.
— Huffington Post 2012-12-21[82]

Hjärnskador och kognitiva skador är för övrigt mycket vanligt förekommande bland brukare och missbrukare av alkohol[83][84].


Kapitel 9 "Does cannabis cause lasting brain damage" i boken Marijuana and Madness

Fler studier om cannabis påstådda neurotoxicitet samt motargument: Are Cannabinoids Neurotoxic? by Bilzor, edited by Austior


  1. BBC: On This Day 2 1974: Cannabis causes brain damage
  2. 2,0 2,1 The Emperor Wears No Clothes av Jack Herer
  3. J. W. Harper, R. G. Heath, W. A. Myers. Effects of Cannabis Sativa on Ultrastructure of the Synapse in Monkey Brain. Journal of Neuroscience Research Vol. 3 pp. 87-93. (1977)
  4. R. G. Heath, A. T. Fitzjarrell, R. E. Garey, W. A. Myers. Chronic Marihuana Smoking Its Effects on Function and Structure of the Primate Brain. Marihuana: Biological Effects Analysis, Metabolism, Cellular Responses, Reproduction and Brain. Gabriel G. Nahas, W. D. M. Paton ed. pub. Pergamon Press Oxford (1979)
  5. Heath, R.G., A.T. Fitzjarrell, C.J. Fontana, and R.E. Garey. Cannabis sativa: Effects on brain function and ultrastructure in Rhesus monkeys. (1980)
  6. 6,0 6,1 A Critical Review Of The Research Literature Concerning Some Biological And Psychological Effects Of Cannabis (Nelson, 1993)
  7. William Slikker et al "Behavioral, Neurochemical, and Neurohistological Effects of chronic Marijuana Smoke Exposure in the Nonhuman Primate", pp219-74 in l. Murphy and A. Bartke (eds), Marijuana Neurobiology and Neurophysiology, Boca Raton: CRC press (1992)
  8. Syed F. Ali, Glenn D. Newport, Andrew C. Scallet, Merle G. Paule, John R. Bailey, William Slikker, Jr. "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" Pharmacology, Biochemistry & Behavior, 40: 677-682. (1991)
  9. Charles Rebert & Gordon Pryor - Chronic Inhalation of Marijuana Smoke and Brain Electrophysiology of Rhesus Monkeys, International Journal of Psychophysiology V 14, p.144. (1993)
  10. 10,0 10,1 Absence of cerebral atrophy in chronic cannabis users: Evaluation by computerized transaxial tomography (Co, 1977)
  11. 11,0 11,1 Computed tomographic examination of heavy marijuana smokers (Kuehnle, 1977)
  12. Folkhälsoinstitutet - Skador av hasch och marijuana
  13. Regional Brain Abnormalities Associated With Long-term Heavy Cannabis Use (Yücel, Solowij, 2008)
  14. The Effect of Cannabis on the Brain: Can it cause brain anomalies that lead to increased risk for Schizophrenia? (DeLisi, 2008)
  15. Cerebral atrophy in young cannabis smokers (Campbell, 1971)
  16. Effects of frequent marijuana use on brain tissue volume and composition (Block, 2000)
  17. Brain morphological changes and early marijuana use: a magnetic resonance and positron emission tomography study (Wilson, 2000)
  18. Altered brain tissue composition in heavy marijuana users (Matochik, 2005)
  19. 19,0 19,1 Depressive symptoms in adolescents: associations with white matter volume and marijuana use (Medina, 2007)
  20. Medial temporal structures and memory functions in adolescents with heavy cannabis use. (Ashtari 2011)
  21. Diminished gray matter in the hippocampus of cannabis users: possible protective effects of cannabidiol. (Demirakca, 2011)
  22. Biological aspects of cannabis use (Stefanis, 1978)
  23. Neurological and neuroradiological examination of chronic cannabis smokers (Hannerz och Hindmarsh, 1983)
  24. Effects of frequent cannabis use on hippocampal activity during an associative memory task (Jager, 2007)
  25. Lack of hippocampal volume change in long-term heavy cannabis users (Tzilos, 2005)
  26. Effects of alcohol and combined marijuana and alcohol use during adolescence on hippocampal volume and asymmetry. (Medina, 2007)
  27. Structural MRI findings in long-term cannabis users: what do we know? (Lorenzetti, 2010)
  28. Cannabis-Related Working Memory Deficits and Associated Subcortical Morphological Differences in Healthy Individuals and Schizophrenia Subjects (Smith, 2013)
  29. SVT 2013-12-19: Marijuana krymper hjärnan
  30. SVT 2014-04-16: Även lite cannabis stör hjärnfunktioner
  31. Drugnews Twitterflöde 2014-04-22
  32. Cannabis Use is Quantitatively Associated with Nucleus Accumbens and Amygdala Abnormalities in Young Adult Recreational Users (Gilman, 2014)
  33. Magnus Callmyr 2014-04-23: Visar verkligen forskningen det SvT och Drugnews påstår?
  34. Does cannabis cause lasting brain damage? (Solowij, 2012)
  35. Long-term effects of marijuana use on the brain (Filbey, 2014)
  36. Science Daily 2014-11-10: Marijuana's long-term effects on the brain demonstrated
  37. NHS 2014-11-11: Long-term cannabis users brains 'are different'
  38. AlterNet 2014-11-11: Media Leaping to Extremely Faulty Conclusions from Study on the Effects of Marijuana on the Brain
  39. 39,0 39,1 Daily Marijuana Use Is Not Associated with Brain Morphometric Measures in Adolescents or Adults (Weiland, 2015)
  40. Effect of high-potency cannabis on corpus callosum microstructure. (Rigucci, 2015) pdf-version
  41. The Guardian 2015-11-27: Smoking high-strength cannabis may damage nerve fibres in brain
  42. The Sun 2015-11-27: Scientists warn smoking ‘skunk’ cannabis wrecks brains
  43. Daily Mail 2015-11-27: Proof strong cannabis DOES harm your brain
  44. NHS 2015-11-27: High-strength 'skunk' cannabis linked to brain changes
  45. 45,0 45,1 Shared Predisposition in the Association Between Cannabis Use and Subcortical Brain Structure (Pagliaccio, 2015) pdf-version
  46. Hippocampal harms, protection and recovery following regular cannabis use (Yücel, 2016)
  47. 47,0 47,1 Larger Gray Matter Volume in the Basal Ganglia of Heavy Cannabis Users Detected by Voxel-Based Morphometry and Subcortical Volumetric Analysis. (Moreno-Alcázar, 2018)
  48. Cannabis use in youth is associated with limited alterations in brain structure (Scott, 2019)
  49. Associations between adolescent cannabis use frequency and adult brain structure: A prospective study of boys followed to adulthood (Meier, 2019)
  50. Cannabidiol and (-)Delta9-tetrahydrocannabinol are neuroprotective antioxidants. (Hampson, 1998)
  51. Neuroprotection by Delta9-tetrahydrocannabinol, the main active compound in marijuana, against ouabain-induced in vivo excitotoxicity (van der Stelt, 2001)
  52. The cannabinoids: an overview. Therapeutic implications in vomiting and nausea after cancer chemotherapy, in appetite promotion, in multiple sclerosis and in neuroprotection. (Mechoulam, 2001)
  53. Endocannabinoids and Neuroprotection (Mechoulam, 2002)
  54. Neuroprotection: is it already applicable to glaucoma therapy? (Ritch, 2000)
  55. Cannabinoid CB2 receptors and fatty acid amide hydrolase are selectively overexpressed in neuritic plaque-associated glia in Alzheimer’s disease brains (Benito, 2003)
  56. Cannabinoid CB2 receptors in human brain inflammation (Benito, 2003)
  57. Cannabinoid CB1 and CB2 receptors and fatty acid amide hydrolase are specific markers of plaque cell subtypes in human multiple sclerosis (Benito, 2007)
  58. Cannabinoids as Therapeutic Agents for Ablating Neuroinflammatory Disease (Cabral, 2008
  59. The endocannabinoid system in targeting inflammatory neurodegenerative diseases (Centonze, 2007)
  60. Protective effects of Delta(9)-tetrahydrocannabinol against N-methyl-D-aspartate-induced AF5 cell death (Chen, 2005)
  61. A molecular link between the active component of marijuana and Alzheimer's disease pathology (Eubanks, 2006)
  62. Dual modulation of endocannabinoid transport and fatty acid amide hydrolase protects against excitotoxicity(Karanian, 2005)
  63. Involvement of protein kinase A in cannabinoid receptor-mediated protection from oxidative neuronal injury (Kim, 2005)
  64. Role for neuronal nitric-oxide synthesis in cannabinoid-induced neurogenesis (Kim, 2006)
  65. Drug-induced hypothermia reduces ischemic damage: effects of the cannabinoid HU-210 (Leker, 2003)
  66. The cannabinoids: an overview. Therapeutic implications in vomiting and nausea after cancer chemotherapy, in appetite promotion, in multiple sclerosis and in neuroprotection (Mechoulam, 2001)
  67. Cannabinoids and neuroprotection in basal ganglia disorders (Sagredo, 2007)
  68. Endocannabinoids potently protect the newborn brain against AMPA-kainate receptor-mediated excitotoxic damage (Shouman, 2006)
  69. Cannabinoid activation of PPAR alpha, a novel neuroprotective mechanism (Sun, 2007)
  70. Experimental autoimmune encephalomyelitis disrupts endocannabinoid-mediated neuroprotection. (Witting, 2006)
  71. d9-tetrahydrocannabinol (THC) and AM 404 protect against cerebral ischaemia in gerbils through a mechanism involving cannabinoid and opioid receptors (Zani, 2007)
  72. Modulation of the balance between cannabinoid CB(1) and CB(2) receptor activation during cerebral ischemic/reperfusion injury (Zhang, 2008)
  73. The CB1 cannabinoid receptor mediates excitotoxicity-induced neural progenitor proliferation and neurogenesis (Aguado, 2007)
  74. Endocannabinoids and their implications for epilepsy (Alger, 2004)
  75. Increases in expression of 14-3-3 eta and 14-3-3 zeta transcripts during neuroprotection induced by delta9-tetrahydrocannabinol in AF5 cells. (Chen, 2007)
  76. Cannabinoids and the immune system: Potential for the treatment of inflammatory diseases. (Croxford, 2005)
  77. Neuroprotective effect of (-)Delta9-tetrahydrocannabinol and cannabidiol in N-methyl-D-aspartate-induced retinal neurotoxicity: involvement of peroxynitrite (El-Remessy, 2003)
  78. CB1 cannabinoid receptors are involved in neuroprotection via NF-kappa B inhibition (Panikashvili ,2005)
  79. Cannabinoids inhibit neurodegeneration in models of multiple sclerosis (Pryce, 2003)
  80. Longitudinal Changes in White Matter Integrity Among Adolescent Substance Users (Bava, 2012)
  81. White Matter Integrity Pre- and Post Marijuana and Alcohol Initiation in Adolescence (Jacobus, 2012)
  82. Huffington Post 2012-12-21: Teen Marijuana Use May Show No Effect On Brain Tissue, Unlike Alcohol, Study Finds
  83. Cognitive Brain Deficits Associated With Alcohol Abuse: Treatment Implications (Norton & Halay, 2011)
  84. Wikipedia: Long-term effects of alcohol


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