Pot and Brain Shrinkage

One hopes that the medicinal aspects of Marijuana can be separated from the negative impacts. I know that the straight M.J. causes significant memory impairment and sloth (personal observation…) but now there’s some more detailed study.

One must remember that the presence of a “receptor” on a cell surface for a chemical does not tell you what the receptor does. It can turn on a growth hormone, or turn it off. It can cause cell proliferation, or cell death. That there are a thousand receptors for a chemical doesn’t tell you if it does good, bad, or some of each (as a receptor can do different things on different cell types).

Even then, in the brain, there are times you WANT a bit of brain shrinkage. The brain forms by extensive wiring up, then the “pruning” of selected connections to establish the best function. Inhibition of that needed shrinkage can be as bad as too much shrinkage later on.


Marijuana Use May Shrink the Brain
Smoking Pot Could Have Lasting Effects on the Brain

By Jennifer Warner
WebMD Health News Reviewed by Louise Chang, MD

I find it refreshing that the “reviewer” is listed…

June 2, 2008 — Long-term marijuana use may actually shrink certain parts of the brain and have lasting effects on mental health.

A new study shows heavy marijuana use over several years was associated with structural differences in at least two different regions of the brain, the hippocampus and amygdala.

Researchers found that the hippocampus, which is thought to regulate memory, was an average of 12% smaller among marijuana users, compared with people who didn’t smoke pot. The amygdala, involved in emotion and memory, was an average of 7% smaller.

The study also suggests that long-term marijuana users were more likely to report symptoms associated with mental disorders, although the strength of their symptoms didn’t meet the criteria for diagnosis of mental illness.
In the study, researchers used high-resolution magnetic resonance imaging to compare the brain structure of 15 men who smoked more than five joints of marijuana daily for more than 10 years with images from 16 men who did not smoke pot.

The participants also took a verbal memory test and were evaluated for symptoms of mental disorders.

The results showed men who smoked pot regularly had significantly lower brain tissue volumes in the hippocampus and amygdala areas, as well as more symptoms of mental disorders.

Researchers say marijuana users also performed significantly worse on the verbal learning test, but these differences did not correlate with brain volumes in either group.

I observed that after a relatively short exposure interval (about a year, irregularly) it took between 6 months and year to mostly recover full memory function. I have no idea what longer term exposure or more intense exposure would do, or if it is recoverable then.

OTOH, it might be individual idiosyncratic. I know of at least two folks who smoked heavily in college and went on to get an MBA and Law Degree, respectively, from U.C. Berkeley. Both seemed to remember things fairly well. Enough to pass…

Then there is the “gender” effect

It is also different in women than in men, so gender changes the effect of the receptors too.


Gender effects on amygdala morphometry in adolescent marijuana users

Tim McQueeny,a Claudia B. Padula,a Jenessa Price,a Krista Lisdahl Medina,b Patrick Logan,c and Susan F. Tapertd,e,*

Note that the amygdala is involved both here, and in memory. One brain center, two impacts.

Adolescent developments in limbic structures and the endogenous cannabinoid system suggest that teenagers may be more vulnerable to the negative consequences of marijuana use. This study examined the relationships between amygdala volume and internalizing symptoms in teenaged chronic marijuana users. Participants were 35 marijuana users and 47 controls ages 16–19 years. Exclusions included psychiatric (e.g., mood and anxiety) or neurologic disorders. Substance use, internalizing (anxiety/depression) symptoms and brain scans were collected after 28 days of monitored abstinence. Reliable raters manually traced amygdala and intracranial volumes on high-resolution magnetic resonance images. Female marijuana users had larger right amygdala volumes and more internalizing symptoms than female controls, after covarying head size, alcohol, nicotine and other substance use (p<0.05), while male users had similar volumes as male controls. For female controls and males, worse mood/anxiety was linked to smaller right amygdala volume (p<0.05), whereas more internalizing problems was associated with bigger right amygdala in female marijuana users. Gender interactions may reflect marijuana-related interruptions to sex-specific neuromaturational processes and staging. Subtle amygdala development abnormalities may underlie particular vulnerabilities to sub-diagnostic depression and anxiety in teenage female marijuana users.
Human adolescent studies document aberrant structural morphometry among brain areas that are associated with the cognitive sequelae of marijuana [39]. Irregularities are observed in the prefrontal cortex, hippocampus and cerebellar vermis as well as white matter organization in teenage marijuana users compared to non-using peers, and these abnormalities were associated with poorer neurobehavioral outcomes [40–44].

Gender may represent a differential risk factor for acquiring psychopathology. There is evidence which suggests female adolescent substance users experience negative consequences of drug use earlier than male peers and are more likely to suffer from an internalizing disorder whereas male substance abusers have more externalizing behaviors [45]. The neurocognitive bases for gender-related risk factors for marijuana use and drug use consequences remain relatively unclear. Adolescent girls and boys also differ in the timing of neuromaturational sequences, hormone exposure and neuronal organization [46, 47], thus, male and female teens may be susceptible to gender-specific brain changes resulting from chronic marijuana exposure. In addition, female teens exhibit elevated CB desensitization relative to same-aged males as well as adult men and women [48], suggesting that the endocannabinoid may have a stronger regulatory role in girls. Therefore, marijuana-related brain changes may differ by gender through interactions with adolescent neuromaturational processes.
Specifically, smaller right amygdalas were linked to worse mood and anxiety symptomatology in the whole sample. Plotting the relationship between right amygdala volume versus internalizing symptom scores revealed that the inverse relationship between amygdala and mood/anxiety was driven by female controls and males (see Figure 3). In contrast, female marijuana users show the opposite brain-behavior pattern: larger amygdala volumes were linked to worse internalization scores. Independent of amygdala morphology, marijuana users had higher internalizing composite scores, and female marijuana users endorsed the greatest depression and anxiety symptoms.
These findings are consistent with our laboratory’s previous studies on different samples of marijuana using teens [43, 44]. For example, Medina and colleagues [42] reported larger prefrontal cortex volumes in female marijuana using adolescents, and larger volumes were linked to poorer executive function. Subclinical depression symptoms have also been reported in conjunction with reduced white matter volumes in teenage marijuana use [44], which reflects a similar pattern of neurobehavioral links with internalizing problems as in the current study. Our findings also align with previous literature connecting depression and anxiety to smaller amygdala size in both clinical samples [49, 66, 69] and in normal healthy teens [70]. However, one study of adult marijuana users found smaller amygdala volumes [27] and evidence for altered amygdala morphometry in depressed samples is mixed [72]. If replicated, these results carry important public health implications as interventions targeting teenage marijuana use may mediate risks for developing substance use disorders and comorbid internalizing problems.

Discrepancies between adult and adolescent structural MRI findings could be related to the disruption of neuromaturation by early chronic marijuana use. Brain size increases through adolescence with decreasing volumes observed over the course of adulthood [46]. Exogenous cannabinoid administration is associated with altered astrocyte functioning, and astrocytes play a critical role in eliminating weaker connections and maintaining neuronal health [73, 74]. By interfering with these support processes, marijuana exposure during adolescence may impair typical pruning, which could ultimately result in larger regional brain volumes. Chronic exposure to marijuana may also compromise neurogenesis, as reduced levels of nerve growth factor and brain derived neurotrophic factor have also been reported among adult marijuana users [75, 76], and this effect may have a greater impact after the pruning stage is primarily complete. Taken together, marijuana use may impact brain development such that interrupted pruning (i.e., maturational delay) is followed by accelerated aging (reduced neurogenesis). Therefore, larger right amygdala volumes could be expected among adolescent marijuana users, whereas continued exposure through adulthood may be related to smaller volumes eventually [47].

There’s a lot more in that article. Especially about how M.J. has more effect on women than on men, that it can vary with hormonal cycles, etc. etc. FWIW, the two M.J. users who went on to success, noted above, were both post puberty males…

Overall, it looks like if you wait until after puberty, and are male, it may not be “too bad”, but use as a developing adolescent, and especially among girls, can have negative effects lasting a lifetime. Then the question becomes “Do the negatives outweigh the positives?”, which I doubt can be answered at our present level of understanding.

FWIW, this all tends to match my personal observations of M.J. prolonged users. A bit “ditzy” and more emotional. Don’t remember detail as well, and tend to emotional rather than logical fact based arguments. No, not all. There’s a lot of variation. And, frankly, some folks could benefit from being more emotional and less fact based. Many jobs don’t require a lot of long term memory and folks may not want to remember a lot of a painful life. So again, observing an effect does not tell you if it is for good or bad.

Generally, though, I’d vote for avoiding heavy use at all times, and most or all use during the developmental years. Or maybe I just don’t like the idea of something messing with my brain volume…

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About E.M.Smith

A technical managerial sort interested in things from Stonehenge to computer science. My present "hot buttons' are the mythology of Climate Change and ancient metrology; but things change...
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7 Responses to Pot and Brain Shrinkage

  1. omanuel says:

    Thanks for an intriguing report. I have often wondered if marijuana might be a substitute for psychotropic drugs.

    If the report you cite is valid, marijuana might increase rather than decrease mental illness.

    But I also suspect the same might be true of prescription psychotropic drugs.

  2. John F. Hultquist says:

    Just thinking of the “now” — If I’m not in control of me, who is?

  3. E.M.Smith says:


    IMHO, most psychotropic drugs are problematic an have high individual variation. Basicalyy, you have to try it to know.

    For example, M.J. mostly has me go to sleep. So much so that I can’t even join friens in it at parties as I just sleep. Others get happy.

    Alcohol has a deserved reputation for releasing your basic nature. So folks get mean, I get happy and nice.

    Many anti depressants make folks unworried. Some unworried about murder or suicide. An unfortunate number of mass shootings have an underlaying use or antidepressants or ADHD drugs like ritaline, yet that doesn’t hit the news, the gun does. So a drug that lists suicidal ideation as a known side effect, and nobody asks why the shooter was suicidal…

    So basically you need a trip observer to record your results and find out what it does to you.


    Who says control exists?

  4. Petrossa says:

    my problem with these kinds of studies is indeed ‘what is a control’. Those preferring to use use MJ may have a pre-existing condition which leads/was already present . Those not using MJ might have lack of such pre existing conditions. Chicken and egg all over again. There is no way to have a real control population without doing a full life time workup from birth.

  5. E.M.Smith says:


    IMHO, there is room for the “just observe and react” mode. I drink coffee, I get more aware, energized and think faster (and mostly clearer ;-), my spouse gets nervous and hyper and feels bad with some stomach upset. So I drink coffee and she does not. M.J. makes me sleep and dulls my memory strongly. My Friend has a great time, is alert and engaged, and next day at work does fine. So I don’t use it, and he does.

    “Studies” are an exercise in trying to find the average response, and since each of us is a unique combination of enzymes and systems, that “average” by definition ignores all our unique characteristics and responses. The result are great medicines for “the average” genetic composition (or food intake or…) but “side effects” up to and including death for those of us not “average”. Much of medicine is devoted to finding which drug works best for a given individual and trying to avoid the worst negative reactions in those of us not “average”.

    Favism is one example. Don’t increase oxidative stress in folks with the genes for favism (via things like eating Fava Beans) as they are on the marginal limit of oxidative stress. (It is protective against malaria parasites). Me? I can eat all the fava beans I want… and take high oxidative stress just fine.

    So while I’d not advise taking a glass of arsenic tea just to see what happens (as it’s pretty clear all of us are at somewhere near 100% risk of death and / or injury); for those drugs with relatively mild effects, a little dabble will do ya ;-) At least, that works for me.

    One other set of examples: The spouse gets stomach bleeds with aspirin, I can eat it like chocolate. She can’t take a couple of antibiotics without going to the hospital, I have no issues with any antibiotics. She can eat all the corn she wants, I eat corn and spend the night “on the pot”… Any drug can have that wide a range of responses. Or more.

    Just for grins, read the package insert on drugs or browse the PDR (Physicians Desk Reference) for side effects. It’s just amazing how many bad things happen with even good drugs. Often there are warnings about “for people with {foo variation} don’t use (or use double or…)” and “for people with {bar variation} do not combine with {list of stuff}”. M.D.s are very aware that we are all unique mixes of traits, and know that any drug they prescribe, no matter how well tested, is a bit of a crap shoot. They expect occasional “adverse reactions”. A long winded way to say: Drugs? YMMV.

  6. DonM says:

    Some like it, some don’t .

    Would the “long term effects” show up anyway? Does the “I like it …” type of person have the brain chemistry that is pre-determined (typically or on average) to reflect the … [NEVERMIND, I just finished reading Petrossa as I was typing and he says it better… ]

    Cause and Effect, or Effect and Cause. From the people I know, and have known, I think its primarily an Effect and Cause type of thing. (But I also know there are exceptions)

  7. cdquarles says:

    Oh, nice find. Medicine is, as you say, the art of applying statistics (since there is much that we know, much that we don’t know, much we know that we can’t know now, much that we know that we’ll never know and much that what we think we no, just isn’t so, for some set of conditions) to a single sample complicated by the fact that many conditions have multiple causes funneled into one or a few final common pathways.

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