Nothing concerns me here. I'm just trying to understand your position. You're sort of all over the place. You previously said occasional, responsible use has no adverse effects. When I posted this study, you then said any use by a developing brain is problematic (and the brain develops into young adulthood). Now you're saying six joints a week is not "occasional" (which misstates what the study actually says) so you dismiss the findings of this study.
Here is what it actually says about the frequency of use:
"Half of the group said they used marijuana at least once a week, and the other 20 had not used the drug in the past year, and reported using it less than five times in their life.
Among the group that did smoke, the median use was about six joints per week."
I am all over the place because it's a complex topic in which I cannot make blanket statements. I think it's healthy, I think high doses of THC have robust health consequences. I am trying to be honest and explain the nuance to you. The thing is the body and brain have an endocannabinoid system, which is located in the limbic (amygdala) an cortex. Now the amydala is a key center for fear and emontionality. Low and high doses of THC have paradoxical effects, low increases serotonin, high decreases. It also exerts it's effects via modulation.
I didn't dismiss the findings, the found what they found, I disagree with the conclusion. Also, why are we discussing this? you aren't even educated on this? I mean they are describing neuroadaptation, WHOAA
"["Neuroadaptation" in long-term cannabis abuse. A clinical and electroencephalographic case study].
[Article in German]
Winterer G1, Schmidt LG, Frick K, Ulrich G.
Author information
Abstract
This report is about electroencephalographic changes in a twenty-eight year old patient with longterm heavy cannabis use. He was admitted to our hospital after he had developed a depressive-apathetic syndrome. Two days after the last cannabis-intake, the patient had recovered from initial psychopathology and his EEG was completely inconspicuous at this day. Some days later however the patient's behavior became increasingly impulsive and unstable, while his EEG showed a marked disturbed regulation of vigilance. In the following weeks his impulsiveness became less and his EEG returned to normal. We suggest that these alterations may reflect a discontinuation of the initial neuroadaption of the central nervous system to the drug.
"
there were changes induced by the drug and they caused withdrawal and return.
Also, the above is research, yours is an article, you may prefer someone explain this stuff to you but I prefer reading it for myself as I can understand it just fine.
http://bjp.rcpsych.org/content/178/2/101.longThis paper highlights the negatives of MJ, it's a review of the literature. Have a read.
There is also the complete difference in motor functioning, cognitive tasks etc when acute versus chronic .
So they found "chronic MJ uses induces neuroadaptation, but we can't say anything other then there was a change". That's all they found, the area is well known.
"Neuropharmacology. 2014 Apr 5. pii: S0028-3908(14)00109-9. doi: 10.1016/j.neuropharm.2014.03.014. [Epub ahead of print]
Prior stimulation of the endocannabinoid system prevents methamphetamine-induced dopaminergic neurotoxicity in the striatum through activation of CB2 receptors.
Nader J1, Rapino C2, Gennequin B1, Chavant F3, Francheteau M1, Makryiannis A4, Duranti A5, Maccarrone M6, Solinas M1, Thiriet N7.
Author information
Abstract
Methamphetamine toxicity is associated with cell death and loss of dopamine neuron terminals in the striatum similar to what is found in some neurodegenerative diseases. Conversely, the endocannabinoid system (ECS) has been suggested to be neuroprotective in the brain, and new pharmacological tools have been developed to increase their endogenous tone. In this study, we evaluated whether ECS stimulation could reduce the neurotoxicity of high doses of methamphetamine on the dopamine system. We found that methamphetamine alters the levels of the major endocannabinoids, anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) in the striatum, suggesting that the ECS participates in the brain responses to methamphetamine. Δ9-tetrahydrocannabinol (THC), a cannabis-derived agonist of both CB1 and CB2 cannabinoid receptors, or inhibitors of the main enzymes responsible for the degradation of AEA and 2-AG (URB597 and JZL184, respectively), blunted the decrease in striatal protein levels of tyrosine hydroxylase induced by methamphetamine. In addition, antagonists of CB2, but not of CB1, blocked the preventive effects of URB597 and JZL184, suggesting that only the former receptor subtype is engaged in neuroprotection exerted by ECS stimulation. Finally, we found that methamphetamine increases striatal levels of the cytokine tumor necrosis factor alpha, an effect that was blocked by ECS stimulation. Altogether, our results indicate that stimulation of ECS prior to the administration of an overdose of methamphetamine considerably reduces the neurotoxicity of the drug through CB2 receptor activation and highlight a protective function for the ECS against the toxicity induced by drugs and other external insults to the brain. This article is part of a Special Issue entitled 'CNS Stimulants'.
Oh my god it's protects da brain? it dun stop da neurotoxicity, but they said it changes the brain.
Mini Rev Med Chem. 2009 Apr;9(4):448-62.
Endocannabinoid system: emerging role from neurodevelopment to neurodegeneration.
Basavarajappa BS1, Nixon RA, Arancio O.
Author information
Abstract
The endocannabinoid system, including endogenous ligands ('endocannabinoids' ECs), their receptors, synthesizing and degrading enzymes, as well as transporter molecules, has been detected from the earliest stages of embryonic development and throughout pre- and postnatal development. ECs are bioactive lipids, which comprise amides, esters and ethers of long chain polyunsaturated fatty acids. Anandamide (N-arachidonoylethanolamine; AEA) and 2-arachidonoylglycerol (2-AG) are the best studied ECs, and act as agonists of cannabinoid receptors. Thus, AEA and 2-AG mimic several pharmacological effects of the exogenous cannabinoid delta9-tetrahydrocannabinol (Delta(9)-THC), the psychoactive principle of cannabis sativa preparations like hashish and marijuana. Recently, however, several lines of evidence have suggested that the EC system may play an important role in early neuronal development as well as a widespread role in neurodegeneration disorders. Many of the effects of cannabinoids and ECs are mediated by two G protein-coupled receptors (GPCRs), CB1 and CB2, although additional receptors may be implicated. Both CB1 and CB2 couple primarily to inhibitory G proteins and are subject to the same pharmacological influences as other GPCRs. This new system is briefly presented in this review, in order to put in a better perspective the role of the EC pathway from neurodevelopment to neurodegenerative disorders, like Alzheimer's disease, Parkinson's disease, Huntington's disease, and multiple sclerosis. In addition, the potential exploitation of antagonists of CB1 receptors, or of inhibitors of EC metabolism, as next-generation therapeutics is discussed.
Its role in nervous system development is quite complex, I suggest you learn about g coupled proteins first.
This study had different results.
Neuropsychopharmacology. 2014 Mar 17. doi: 10.1038/npp.2014.67. [Epub ahead of print]
Long-Term Effects of Cannabis on Brain Structure.
Battistella G1, Fornari E2, Annoni JM3, Chtioui H4, Dao K4, Fabritius M5, Favrat B6, Mall JF7, Maeder P1, Giroud C5.
Author information
Abstract
The dose-dependent toxicity of the main psychoactive component of cannabis in brain regions rich in cannabinoid CB1 receptors is well known in animal studies. However, research in humans does not show common findings across studies regarding the brain regions that are affected after long-term exposure to cannabis. In the present study, we investigate (using Voxel-based Morphometry) gray matter changes in a group of regular cannabis smokers in comparison with a group of occasional smokers matched by the years of cannabis use. We provide evidence that regular cannabis use is associated with gray matter volume reduction in the medial temporal cortex, temporal pole, parahippocampal gyrus, insula, and orbitofrontal cortex; these regions are rich in cannabinoid CB1 receptors and functionally associated with motivational, emotional, and affective processing. Furthermore, these changes correlate with the frequency of cannabis use in the 3 months before inclusion in the study. The age of onset of drug use also influences the magnitude of these changes. Significant gray matter volume reduction could result either from heavy consumption unrelated to the age of onset or instead from recreational cannabis use initiated at an adolescent age. In contrast, the larger gray matter volume detected in the cerebellum of regular smokers without any correlation with the monthly consumption of cannabis may be related to developmental (ontogenic) processes that occur in adolescence.Neuropsychop
harmacology advance online publication, 16 April 2014; doi:10.1038/npp.2014.67.
Again no permenant conseqeunces.
