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 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 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 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.
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