Cannabis Is Neuroprotective

A fascinating new study shows that cannabis offers some neuroprotection to young people who engaged in binge drinking episodes. The binge drinkers were young – aged 16-19. This is an age at which the effects of drugs on the brain may be particularly bad, since the brain is continuing to develop.

What was shocking was that binge drinking in adolescents caused the type and degree of damage that it did. Binge drinking caused actual losses of white matter in the brain, similar to the damage seen with drugs like cocaine and methamphetamine.

Briefly, white matter is the axons that connect brain cells to each other. Grey matter consists of the connections and also the cells themselves. So heavy drinking in adolescence causes actual damage to the connections between brain cells. That’s pretty serious stuff. It’s not known if the damage repairs later, or at all. However, connections between cells can grow back.

If the damage does not repair, then a Hell of a lot of adults are walking around with significant brain damage from binge drinking in adolescence. If this is the case, then clearly the brain can handle this sort of damage, since most such folks, assuming they are damaged in this way, are able to function well both cognitively and psychologically.

The study was fascinating because if the adolescents used cannabis in addition to binge drinking, the damage was notably less than if they binge drank alone. Therefore, cannabis use was somewhat neuroprotective to the brain in terms of the damage caused by binge drinking.

This does not mean that cannabis use is good for your brain, or that it does not damage the brain. But no study of cannabis use has ever found anything as dramatic as extensive white matter losses in the brain (that’s a pretty serious type of damage). So, if anything, binge drinking in adolescence (which many adolescents do) is remarkably worse for your brain than using cannabis in adolescence, which is an amazing thing to say right there.

But that’s not exactly what the anti-drug moralfags and fuckwits tell us, is it? In their view, binge drinking is a necessary evil, while cannabis use, especially in adolescence, is a moral and public health catastrophe. God, what a load of shit that is.

Cannabis and Brain Damage: Structural Evidence

Repost from the old site.
The original post in its native form was far too long, so I broke it up into seven different posts, in addition to this post. The separate sections are listed below.
The original post, what is left of it, is here.
For an analysis of neuropsychological batteries of cannabis users to determine whether or not they suffer brain damage, see here.
For an analysis of EEG testing of cannabis users to discover evidence of brain damage, see here.
For an analysis of studies looking at cerebral blood flow in cannabis users to determine brain damage, see here.
For an admittedly impressionistic analysis of whether or not cannabis causes schizotypal symptoms in users, see here.
For a summary comparing the effects of cannabis on the brain compared to other drugs, see here.
For a summary of the findings of cannabis and brain damage, see here.
A major charge against cannabis is that it causes actual structural damage to the brain, that is, damage to the brain cells, axons and dendrites themselves. In this post, we will look at this charge. In other posts, we will look at other charges relating to cannabis and brain damage.
A frequent charge is that marijuana causes “changes to the hippocampus,” which may or may not be permanent.
A new study released in early June 2008 suggested that use of more than 5 joints/day for more than 10 years (average of 20 years) caused shrinkage of the hippocampus and the amygdala in the brain. The hippocampus of the cannabis users was 12% smaller, and the amygdala was 7.1% smaller. The cannabis users also did poorer on a word recall test.
Nadia Solowij of Australia was involved in this study, and her studies, for whatever reason, almost always find serious harm from cannabis, even at low doses (see below).
However, four other studies found no hippocampal damage from cannabis. An MRI study from 2005 of very heavy cannabis users who had used cannabis on average of 20,100 times found no damage to the hippocampus at all. A study of cannabis-using young adults from 2006 found no damage to the hippocampus, or to any other structure. And a third study also found no hippocampal damage .
The study of users from 2006 also found no damage to the amygdala. This study actually found that the hippocampus-amygdala was 5% larger in the cannabis users than in the non-users, but the difference was not thought to be significant.
For what it is worth, 15-18 year olds with alcohol abuse (extremely common at that age) and alcohol dependence also showed hippocampal shrinkage. Even chronic stress such as is seen in Post-traumatic Stress Disorder causes shrinkage of the hippocampus. Such shrinkage is also a completely normal part of aging for all humans, and probably becomes apparent first around age 40.
Another study released in March 2008 found that heavy cannabis use beginning in early adolescence caused loss of white matter in the corpus callosum, the part of the brain that separates the left from the right hemispheres. White matter is composed of the connections between neurons, or axons.
This alarming study implies loss of axons in the corpus callosum separating the prefrontal cortex in early adolescent heavy cannabis users. This adds to a body of damage suggesting the heavy cannabis use in adolescence, especially in early adolescence, may be particularly risky.
Yet another study found a marker for what they felt was a loss of axonal and neuronal integrity (this implies damage to brain cells and their connections) in the dorsolateral prefrontal cortex (perhaps the most highly evolved region of our brains) in recreational cannabis users.
Finally, a study found elevated nerve growth factor (NGF) blood concentrations in cannabis-using schizophrenics. This can be a marker for neuronal damage. The suggestion was that cannabis caused brain damage in schizophrenics who used it. How this relates to non-schizophrenics is uncertain.
However, another study showed a variety of differences in brain structure with heavy cannabis users.
Heavy cannabis users had less gray matter (brain cells) in the right parahippocampal gyrus and less white matter (axons) in the left parietal lobe.
However, they also had more gray matter (brain cells) near the precentral gyrus and the right thalamus and had more white matter (axons) in the left parahippocampal gyrus and the left fusiform gyrus. Only more grey matter (brain cells) in the left precentral gyrus was associated with duration of use.
This study is very confusing and implies that heavy cannabis use damages some parts of the brain while growing more cells and connections in other parts of the brain. Subjects had fewer brain cells in one region but more in two others. They also had fewer axons in one region and more in two others.
Another study found something similar – in this case they found fewer axons (white matter) in the left parietal lobe and increased axons around the left parahippocampal gyrus and left fusiform gyrus. Increased years of cannabis use was associated with increased axons in the left precentral gyrus. So, while one area appeared to be damaged, three other areas appeared to be improved by cannabis.
As might be expected, postmortem examination of the brains of cannabis users found down-regulation of cannabinoid receptors in various parts of the brain, including the caudate nucleus, the putamen, the accumbens nucleus, the globus pallidus, the ventral tegmental area and the substantia nigra pars reticulata. The effects of such down-regulation were not known.
One of the most frightening studies so far used DTI, a new method of looking at the brain that is better than MRI. This study found an altered development of the arcuate fasciculus in adolescent heavy cannabis users. This structure is a bundle of fibers connecting the Wernicke’s and Broca’s Areas of the brain, one involved in the production of language and the other involved in the reception of language.
Damage to the arcuate fasciculus is associated with a particular type of aphasia, Conduction Aphasia, where language can be produced and comprehended well, but if you say something to the sufferer, they cannot repeat what you just said. They also have a hard time reading aloud, transpose sounds and morphemes in words, and substitute phonemes with similar-sounding phonemes when they talk.
The arcuate fasiculus is still developing in early adolescence, but it is not known if it continues growing through late adolescence. In this study, lower volume was seen on the left side of the arcuate fasiculus in adolescent marijuana users.
The revelation of this damage is quite disturbing, but the significance of this altered development is not yet known. Surely cannabis users do not have conduction aphasia, the typical result of damage to this structure. But this study adds weight to evidence that people should at least wait until they are 18 to start using cannabis. Cannabis use by minors is not a good idea and needs to be discouraged.
Further studies using DTI have not found any abnormalities whatsoever in any part of the brains of adolescent heavy cannabis users. In fact, if anything, adolescent cannabis users tended to have larger brains, with more brain cells (white matter) than the controls. However, this study did not look specifically at the arcuate fasiculus.
That doesn’t mean that using cannabis in adolescence makes you smart, but it surely rules out significant global brain damage.
The damage to the arcuate fasciculus in this study is absurdly being played up as being evidence for cannabis causing schizophrenia, since this structure is also damaged, though more extensively, in schizophrenia.
There are serious problems with the notion that problems with this structure could cause schizophrenia, not to mention with the whole idea of cannabis causing schizophrenia. I deal with the question of whether or not cannabis causes schizophrenia here.
So at the moment, the issue of whether or not heavy cannabis use causes damage to either the hippocampus, the amygdala, the corpus callosum or the prefrontal cortex is up in the air.
There is one study suggesting damage to the amygdala, but another study found no amygdala damage. There is one study suggesting that cannabis damages the hippocampus, but three other studies found no damage.
There is one study suggesting damage to the corpus callosum in early adolescent cannabis users and another suggesting damage to brain cells and connections in the prefrontal cortex. Neither has been confirmed.

Cannabis and Brain Damage: Cerebral Blood Flow Findings

Repost from the old site.
The original post in its native form was far too long, so I have decided to break it up into seven different posts, in addition to this post. The separate sections are listed below.
The original post, what is left of it, is here.
For an examination of the evidence of whether or not cannabis causes actual structural damage to brain cells, axons or dendrites, see here.
For an analysis of neuropsychological batteries of cannabis users to determine whether or not they suffer brain damage, see here.
For an analysis of EEG testing of cannabis users to discover evidence of brain damage, see here.
For an admittedly impressionistic analysis of whether or not cannabis causes schizotypal symptoms in users, see here.
For a summary comparing the effects of cannabis on the brain compared to other drugs, see here.
For a summary of the findings of cannabis and brain damage, see here.
With the use of SPECT and MRI, we can now measure changes in blood flow in various parts of the brain. Permanent changes in blood flow, especially low blood flow, are said to be indicative of brain damage.
Recently, some new SPECT studies have come out of Britain, and were published in the Journal of Psychoactive Drugs, appearing to show reduced CBF activity in certain areas of the brain with long-term heavy use of “skunk weed”, which is extremely potent marijuana. However, the part in the article where they talk about a user’s brain being “pitted and scarred” is nonsense. These are just areas of reduced activity.
One user was a 16-year-old who had smoked every day for two years, another an 18-year-old who had smoked several times a week for two years and the third was a 28-year-old who had smoked for 10 years.
Whether or not areas of reduced activity can be said to be “damaged” is an extremely difficult proposition to make. If the reduced activity is permanent, we can say that, but if it is temporary, it’s simply not “damage.”
A report also indicated that a similar study showed an effect even after one month post-use in teenagers.
Another study, this time using MRI to look at cerebral blood flow, actually found increased blood flow in the right frontal lobe, left temporal lobe and the cerebellum in chronic, long-term daily cannabis users. This means increased activity in these areas.
If the British study is being used to say that cannabis damages the brain on basis of low cerebral blood flow, then this study can be used to say that cannabis improves the brain based on cerebral blood flow. Furthermore, this study would seem to contradict the British study.
Yet another study concluded that very heavy cannabis use may be harmful, while more moderate or light use may be less deleterious. This study found that perfusion deficits in cerebrovascular flow attenuated in light to moderate users after one month’s absence, while persisting in heavy users. Moderate use was defined as 2.5-10 joints/day, while heavy use was defined as 11-50 joints/day.
This study completely contradicts the British study that got so much media attention.
The CBF findings may be related to dose. One study found an effect at 7.5 joints+/day, but found no effect at 5 joints/day or less. According to this study, it would be prudent to limit oneself to 5 joints a day or less.
The finding of this study, of reduced activity in the frontal cortex combined with increased activity in the cerebellum, is a fairly common one in recent studies. Rather than damage, this appears to be a neuroadaptation to the effects of cannabis use on the brain.
Yet another CBF study found changes in CBF in abstinent cannabis users on a stroop test. They found low CBF in the left perigenual anterior cingulate cortex and the left lateral prefrontal cortex and excessive flow in the hippocampus. The two regions with low blood flow are said to be involved in something called executive function, which I do not completely understand.
The cannabis users scored the same as controls on the stroop test, but they used a different brain style than the one people typically use to  complete the test. Since the scores were the same, the significance of this study is called into question.
There is an increasing body of literature showing that cannabis users utilize alternate brain networks than those normally employed, possibly to compensate for the effects of cannabis.

Cannabis and Brain Damage: Summary

The original post in its native form was far too long, so I have decided to break it up into seven different posts, in addition to this post. The separate sections are listed below.
The original post, what is left of it, is here.
For an examination of the evidence of whether or not cannabis causes actual structural damage to brain cells, axons or dendrites, see here.
For an analysis of neuropsychological batteries of cannabis users to determine whether or not they suffer brain damage, see here.
For an analysis of EEG testing of cannabis users to discover evidence of brain damage, see here.
For an analysis of studies looking at cerebral blood flow in cannabis users, see here.
For an admittedly impressionistic analysis of whether or not cannabis causes schizotypal symptoms in users, see here.
For a summary comparing the effects of cannabis on the brain compared to other drugs, see here.
Original monkey and later rat studies indicating structural brain damage have generally not panned out when conducted in humans, but a recent study from 2008 found damage to the hippocampus and amygdala. The hippocampus findings are contradicted by three earlier studies finding no damage, and the finding on the amygdala was contradicted by an earlier study.
Another study found damage to the corpus callosum in early adolescent users. And another found damaged axons and brain cells in the prefrontal cortex. These findings have not yet been replicated. Yet another study found damage to two areas but improvements in four other areas of the brain. The consequences of this are not known.
At the moment, whether or not cannabis causes structural damage or even improvements to the limbic system, corpus callosum, prefrontal cortex or other areas of the brain is somewhat up in the air.
Neuropsychological studies of long-term users have been somewhat contradictory, but in general have not found significant brain damage, although they did find a “very small effect” on learning and memory. Apparently they did not think it was significant enough to be called brain damage.
New studies show that chronic long-term users perform worse than controls in memory, learning and recall, and the effect worsens as use progresses. These effects last up to one week after the last use. Therefore, daily marijuana users are always going to be somewhat impaired in these areas.
Some EEG studies found some interesting changes in theta waves in users who had used heavily and daily for 15-30 years. The significance of these findings is not yet known; one suggestion that is that the increased theta may be indicative of organic damage. But here again we do not have any clinical correlates of the organic theta change either.
Even this study did not find permanent effects from sporadic or occasional use of marijuana.
Another found problems with screening out external stimuli after five years of use, but it is possible that two attempts to replicate that study may have failed.
A SPECT studies out of Britain showed low CBF in three heavy cannabis users. Another found that low CBF did not clear up in adolescent users even after one month. However, they have been contradicted by two other studies, one showing that the CBF deficits clear up after three months, and another showing increases in CBF as opposed to decreases.
A new study using DTI found damage to the left side of the arcuate fasiculus in adolescent heavy cannabis users. This is one of the most disturbing findings to date, and adds weight to evidence that cannabis should not be used by adolescents, since the arcuate fasiculus is still developing in early adolescence. Nevertheless, no clinical significance has yet been attached to this finding.
But another DTI study looking at the entire brain found no evidence of generalized damage, and if anything, found that teenage cannabis users have less brain atrophy and more brain cells than non-users. We would expect a clinical correlate of this to be more intelligent teenage potheads, but no one is suggesting that.
Unless clinical correlates can be discovered, all findings of damage or enhancement of the brain via marijuana should be viewed with a critical eye.
So the evidence on permanent brain damage from long-term heavy marijuana use is rather contradictory and is still somewhat up in the air.
It looks like cannabis can be used for up to five years, or possibly up to 15 years, even on a daily basis, without any permanent harm to the brain. Beyond that, there may effects, but they appear to be more subtle than profound.