Can Dual N Back minimize this problem?
"I am an Ivy-league bound student that is extremely concerned"
Carl Sagan used cannabis regularly, often when he needed help understanding the heavy concepts he contemplated.
Although I am currently not using cannabis (fiscal concerns), I smoked daily for almost seven years. My IQ scores did not change at all during that time (I regularly tested myself).
Anecdotal, but sometimes when the research has still left doubts in our minds, an anecdote or two can flesh it out.
Carl Sagan used cannabis regularly, often when he needed help understanding the heavy concepts he contemplated.
Although I am currently not using cannabis (fiscal concerns), I smoked daily for almost seven years. My IQ scores did not change at all during that time (I regularly tested myself).
Anecdotal, but sometimes when the research has still left doubts in our minds, an anecdote or two can flesh it out.
Heterosapiens | 3 years ago
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Gone unmentioned here is the fact that people are different and respond differently to the same thing for a wide variety of reasons.
This is a funny absence in the general discussion on (illegal) drug use, especially when "your results may vary" is so readily acknowledged for prescription medicine.
I for one know of at least one person who feels quite dim and out of sorts after smoking marijuana. But I don't think that this necessarily means _all_ people do. I can readily believe that other people might be made _more_ clever by it.
Just pay attention to how you react. If it doesn't work for you, don't do it. And don't think that just because it's one way for one person means that it will be the same way for you.
This is a funny absence in the general discussion on (illegal) drug use, especially when "your results may vary" is so readily acknowledged for prescription medicine.
I for one know of at least one person who feels quite dim and out of sorts after smoking marijuana. But I don't think that this necessarily means _all_ people do. I can readily believe that other people might be made _more_ clever by it.
Just pay attention to how you react. If it doesn't work for you, don't do it. And don't think that just because it's one way for one person means that it will be the same way for you.
jimmydean9 | 3 years ago
Reply
I suffer from Crohn's disease and having been going through a major flare.Many of the medications,that I am currently on, have horrible effects on the brain.There is no kind of substance that can account for the unspeakable effects Prednisone has on the brain and body.I will be implementing marijuana once a week into my therapy because in the past it has been the one thing that has saved my intestines.I understand the counter intuitive effects it has on the brain, but it is far less then this destructive "medicine" called Prednisone.This leads me to the question I ask of you.Can a daily regime of Dual-N back tasks minimize the effects of once a week marijuana consumption?I am an Ivy-league bound student that is extremely concerned.Your responses are greatly appreciated.
knickerbocker309 | 3 years ago
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IMO ... as an occasional drug user -- mostly psychedelics and cannabis -- and I do not regret their use in the slightest, they have benefited me and will continue to do so ...
... and now also a doctoral candidate in philosophy (it requires incredible intellectual rigor, if you don't know ;)) at a Top 5 School ... I wouldn't worry too much. If you notice disturbances of memory/cognition, then lay off. Sleep, learn, meditate, exercise, stimulating environments, etc.
One mechanism by which cannabis seems to stress hippocampal cells, causing with heavy/extended use reversible changes similar to those caused by e.g. stress, lack of sleep, depression, mania, glutamate-related excitotoxicity; is induction of the caspase-3 enzyme, which promotes apoptosis.
So as far as supplements go, this is one angle. The supplement citicoline (aka CDP-choline) is nootropic and potently neuroprotective against a wide variety of neurotoxic insults (a wealth of literature is available by google), and has been found to inhibit the expression of caspase-3. I take 1000mg daily whether I am smoking or not.
Most people I know (though in other cultures the modes of use are different) that use marijuana to cognitively destructive heights are depressed in the first place, or otherwise out of sorts.
All things in moderation ... moderation too.
... and now also a doctoral candidate in philosophy (it requires incredible intellectual rigor, if you don't know ;)) at a Top 5 School ... I wouldn't worry too much. If you notice disturbances of memory/cognition, then lay off. Sleep, learn, meditate, exercise, stimulating environments, etc.
One mechanism by which cannabis seems to stress hippocampal cells, causing with heavy/extended use reversible changes similar to those caused by e.g. stress, lack of sleep, depression, mania, glutamate-related excitotoxicity; is induction of the caspase-3 enzyme, which promotes apoptosis.
So as far as supplements go, this is one angle. The supplement citicoline (aka CDP-choline) is nootropic and potently neuroprotective against a wide variety of neurotoxic insults (a wealth of literature is available by google), and has been found to inhibit the expression of caspase-3. I take 1000mg daily whether I am smoking or not.
Most people I know (though in other cultures the modes of use are different) that use marijuana to cognitively destructive heights are depressed in the first place, or otherwise out of sorts.
All things in moderation ... moderation too.
gorelando | 3 years ago
Reply
related:
I am no doctor, so I don't have an answer. But you are talking about drugs that alter the chemical balance in your brain, of which all the side effects may not be completely understood, so there is *always* a risk involved.
A quick search on Scholar gave a study on cognitive function following prolonged cannabis use finding that "a partial recovery of function but the past duration of cannabis use continued to have an adverse effect on the ability to effectively reject complex irrelevant information."
Now I don't know what your treatment entails, but if you haven't gotten a second opinion, get one. If you did, get a third.
You may also try Ask Alice, and/or your health counselor, which I'm guessing you will soon have access to.
A quick search on Scholar gave a study on cognitive function following prolonged cannabis use finding that "a partial recovery of function but the past duration of cannabis use continued to have an adverse effect on the ability to effectively reject complex irrelevant information."
Now I don't know what your treatment entails, but if you haven't gotten a second opinion, get one. If you did, get a third.
You may also try Ask Alice, and/or your health counselor, which I'm guessing you will soon have access to.
cognitivefun | 3 years ago
Reply
cognitivefun | 3 years ago
Reply
"a study on cognitive function following prolonged cannabis use finding that "a partial recovery of function but the past duration of cannabis use continued to have an adverse effect on the ability to effectively reject complex irrelevant information."
"
cognitivefun | 3 years ago
Reply
From my understanding,all of these studies with significant detrimental effects have monitored Marijuana Abuse.This usage of it therapeutically is considerably moderate and far outweighs the killing of brain cells that Prednisone inflicts.Also,considering I would only be partaking in such an endeavor for the time span of two months,this was the time that it took previously to fully heal my stomach in past,is a great deal ensuring.After countless research and considering the neuroscience of plasticity ,I am indefinitely confident that Dual-N Back can minimize the effects.I'm just very curious of other opinions.
knickerbocker309 | 3 years ago
Reply
As a daily user of both marijuana and dual n-back, I can confidently say that regular n-back practice more than makes up for whatever supposed loss of short term memory marijuana causes. And with you only using it once a week for only two months, it is incredibly unlikely that your intelligence will be negatively impacted in the long run. Just don't smoke before you do N-back.
dogrothenberg | 3 years ago
Reply
J Clin Pharmacol. 2002 Nov;42(11 Suppl):41S-47S.Click here to read Links
Cognitive measures in long-term cannabis users.
Harrison GP Jr, Gruber AJ, Hudson JI, Huestis MA, Yurgelun-Todd D.
Biological Psychiatry Laboratory, McLean Hospital/Harvard Medical School, Belmont, Massachusetts 02478, USA.
The cognitive effects of long-term cannabis use are insufficiently understood. Most studies concur that cognitive deficits persist at least several days after stopping heavy cannabis use. But studies differ on whether such deficits persist long term or whether they are correlated with increasing duration of lifetime cannabis use. The authors administered neuropsychological tests to 77 current heavy cannabis users who had smoked cannabis at least 5000 times in their lives, and to 87 control subjects who had smoked no more than 50 times in their lives. The heavy smokers showed deficits on memory of word lists on Days 0, 1, and 7 of a supervised abstinence period. By Day 28, however, few significant differences were found between users and controls on the test measures, and there were few significant associations between total lifetime cannabis consumption and test performance. Although these findings may be affected by residual confounding, as in all retrospective studies, they suggest that cannabis-associated cognitive deficits are reversible and related to recent cannabis exposure rather than irreversible and related to cumulative lifetime use.
I was under the impression cannabis produced reversible deficits. If used during adolescence (
Cognitive measures in long-term cannabis users.
Harrison GP Jr, Gruber AJ, Hudson JI, Huestis MA, Yurgelun-Todd D.
Biological Psychiatry Laboratory, McLean Hospital/Harvard Medical School, Belmont, Massachusetts 02478, USA.
The cognitive effects of long-term cannabis use are insufficiently understood. Most studies concur that cognitive deficits persist at least several days after stopping heavy cannabis use. But studies differ on whether such deficits persist long term or whether they are correlated with increasing duration of lifetime cannabis use. The authors administered neuropsychological tests to 77 current heavy cannabis users who had smoked cannabis at least 5000 times in their lives, and to 87 control subjects who had smoked no more than 50 times in their lives. The heavy smokers showed deficits on memory of word lists on Days 0, 1, and 7 of a supervised abstinence period. By Day 28, however, few significant differences were found between users and controls on the test measures, and there were few significant associations between total lifetime cannabis consumption and test performance. Although these findings may be affected by residual confounding, as in all retrospective studies, they suggest that cannabis-associated cognitive deficits are reversible and related to recent cannabis exposure rather than irreversible and related to cumulative lifetime use.
I was under the impression cannabis produced reversible deficits. If used during adolescence (
studentmedical | 3 years ago
Reply
Prog Neuropsychopharmacol Biol Psychiatry. 2007 Jun 30;31(5):1054-63. Epub 2007 Mar 16. Links
Cannabis induces different cognitive changes in schizophrenic patients and in healthy controls.
Jockers-Scherübl MC, Wolf T, Radzei N, Schlattmann P, Rentzsch J, Gómez-Carrillo de Castro A, Kühl KP.
Department of Psychiatry and Psychotherapy Charité Universitätsmedizin Berlin, Campus Benjamin Franklin, Eschenallee 3, Berlin, Germany. maria.jockers@charite.de
It is known that 60 to 80% of schizophrenic patients show deficits in cognition. There may be an increase in these deficits as a result of additional regular use of cannabis. The aim of the study was to evaluate the effect of chronic cannabis consumption on the cognitive functions of schizophrenic patients and healthy control subjects after a minimum abstinence time of 28 days. The study sample consisted of 39 schizophrenics (19 cannabis-abusers and 20 non-abusers) and 39 healthy controls (18 cannabis-abusers, 21 non-abusers). In a 2x2-factorial design (Diagnostic Groups [healthy controls, schizophrenic patients]xCannabis abuse [without, with]) with diagnostic group and cannabis consumption considered between-subject factors) we tested the hypothesis that dually diagnosed patients (i.e. suffering both from schizophrenia and cannabis abuse) perform worse in neuropsychological tests than schizophrenic patients without cannabis abuse. On the whole, schizophrenic patients performed worse than healthy control subjects. Surprisingly, rather than deteriorating neuropsychological performance, regular cannabis abuse prior to the first psychotic episode improved cognition in some tests. This was even more pronounced when regular consumption started before the age of 17. On the other hand, cannabis use deteriorated test performance in healthy controls, especially in cases when regular consumption started before the age of 17. To sum up, regular cannabis abuse has a different effect on cognitive function in schizophrenic patients and healthy controls.
Cannabis is a weird one... I think cannabinoids can be either excitatory or inhibitory, depending on the brain region of interest. In some subpopulations cannabis can improve some aspects of cognitive function.
Psychopharmacology (Berl). 2006 Nov;188(4):425-44. Epub 2006 Sep 26. Links
The acute effects of cannabinoids on memory in humans: a review.
Ranganathan M, D'Souza DC.
Schizophrenia Biological Research Center, VA Connecticut Healthcare System, West-Haven, CT 06516, USA.
RATIONALE: Cannabis is one of the most frequently used substances. Cannabis and its constituent cannabinoids are known to impair several aspects of cognitive function, with the most robust effects on short-term episodic and working memory in humans. A large body of the work in this area occurred in the 1970s before the discovery of cannabinoid receptors. Recent advances in the knowledge of cannabinoid receptors' function have rekindled interest in examining effects of exogenous cannabinoids on memory and in understanding the mechanism of these effects. OBJECTIVE: The literature about the acute effects of cannabinoids on memory tasks in humans is reviewed. The limitations of the human literature including issues of dose, route of administration, small sample sizes, sample selection, effects of other drug use, tolerance and dependence to cannabinoids, and the timing and sensitivity of psychological tests are discussed. Finally, the human literature is discussed against the backdrop of preclinical findings. RESULTS: Acute administration of Delta-9-THC transiently impairs immediate and delayed free recall of information presented after, but not before, drug administration in a dose- and delay-dependent manner. In particular, cannabinoids increase intrusion errors. These effects are more robust with the inhaled and intravenous route and correspond to peak drug levels. CONCLUSIONS: This profile of effects suggests that cannabinoids impair all stages of memory including encoding, consolidation, and retrieval. Several mechanisms, including effects on long-term potentiation and long-term depression and the inhibition of neurotransmitter (GABA, glutamate, acetyl choline, dopamine) release, have been implicated in the amnestic effects of cannabinoids. Future research in humans is necessary to characterize the neuroanatomical and neurochemical basis of the memory impairing effects of cannabinoids, to dissect out their effects on the various stages of memory and to bridge the expanding gap between the humans and preclinical literature.
For most, however, Mary Jane makes you a dunderhead with an overactive limbic system and an impaired frontal cortex, and can predispose to psychosis.
Biol Psychiatry. 2007 Jun 1;61(11):1281-9. Epub 2007 Jan 17. Links
Dorsolateral prefrontal cortex N-acetylaspartate/total creatine (NAA/tCr) loss in male recreational cannabis users.
Hermann D, Sartorius A, Welzel H, Walter S, Skopp G, Ende G, Mann K.
Central Institute of Mental Health, Mannheim, Germany.
BACKGROUND: Cannabinoids present neurotoxic and neuroprotective properties in in vitro studies, inconsistent alterations in human neuroimaging studies, neuropsychological deficits, and an increased risk for psychotic episodes. METHODS: Proton magnetic resonance spectroscopy ((1)H-MRS), neuropsychological testing, and hair analysis for cannabinoids was performed in 13 male nontreatment-seeking recreational cannabis users and 13 male control subjects. RESULTS: A significantly diminished N-acetylaspartate/total creatine (NAA/tCr) ratio in the dorsolateral prefrontal cortex (DLPFC) was observed in cannabis users (p = .0003). The NAA/tCr in the putamen/globus pallidum region correlated significantly with cannabidiol (R(2) = .66, p = .004). Results of the Wisconsin Card Sorting test, Trail making Test, and D2 test for attention were influenced by cannabinoids. CONCLUSIONS: Chronic recreational cannabis use is associated with an indication of diminished neuronal and axonal integrity in the DLPFC in this study. As chronic cannabis use is a risk factor for psychosis, these results are interesting because diminished NAA/tCr ratios in the DLPFC and neuropsychological deficits were also reported in schizophrenia. The strong positive correlation of NAA/tCr and cannabidiol in the putamen/globus pallidum is in line with neuroprotective properties of cannabidiol, which were also observed in in vitro model studies of Parkinson's disease.
For the love of all things cognitively related, ***DO NOT*** mess with the dorsolateral PFC!!!
Cannabis induces different cognitive changes in schizophrenic patients and in healthy controls.
Jockers-Scherübl MC, Wolf T, Radzei N, Schlattmann P, Rentzsch J, Gómez-Carrillo de Castro A, Kühl KP.
Department of Psychiatry and Psychotherapy Charité Universitätsmedizin Berlin, Campus Benjamin Franklin, Eschenallee 3, Berlin, Germany. maria.jockers@charite.de
It is known that 60 to 80% of schizophrenic patients show deficits in cognition. There may be an increase in these deficits as a result of additional regular use of cannabis. The aim of the study was to evaluate the effect of chronic cannabis consumption on the cognitive functions of schizophrenic patients and healthy control subjects after a minimum abstinence time of 28 days. The study sample consisted of 39 schizophrenics (19 cannabis-abusers and 20 non-abusers) and 39 healthy controls (18 cannabis-abusers, 21 non-abusers). In a 2x2-factorial design (Diagnostic Groups [healthy controls, schizophrenic patients]xCannabis abuse [without, with]) with diagnostic group and cannabis consumption considered between-subject factors) we tested the hypothesis that dually diagnosed patients (i.e. suffering both from schizophrenia and cannabis abuse) perform worse in neuropsychological tests than schizophrenic patients without cannabis abuse. On the whole, schizophrenic patients performed worse than healthy control subjects. Surprisingly, rather than deteriorating neuropsychological performance, regular cannabis abuse prior to the first psychotic episode improved cognition in some tests. This was even more pronounced when regular consumption started before the age of 17. On the other hand, cannabis use deteriorated test performance in healthy controls, especially in cases when regular consumption started before the age of 17. To sum up, regular cannabis abuse has a different effect on cognitive function in schizophrenic patients and healthy controls.
Cannabis is a weird one... I think cannabinoids can be either excitatory or inhibitory, depending on the brain region of interest. In some subpopulations cannabis can improve some aspects of cognitive function.
Psychopharmacology (Berl). 2006 Nov;188(4):425-44. Epub 2006 Sep 26. Links
The acute effects of cannabinoids on memory in humans: a review.
Ranganathan M, D'Souza DC.
Schizophrenia Biological Research Center, VA Connecticut Healthcare System, West-Haven, CT 06516, USA.
RATIONALE: Cannabis is one of the most frequently used substances. Cannabis and its constituent cannabinoids are known to impair several aspects of cognitive function, with the most robust effects on short-term episodic and working memory in humans. A large body of the work in this area occurred in the 1970s before the discovery of cannabinoid receptors. Recent advances in the knowledge of cannabinoid receptors' function have rekindled interest in examining effects of exogenous cannabinoids on memory and in understanding the mechanism of these effects. OBJECTIVE: The literature about the acute effects of cannabinoids on memory tasks in humans is reviewed. The limitations of the human literature including issues of dose, route of administration, small sample sizes, sample selection, effects of other drug use, tolerance and dependence to cannabinoids, and the timing and sensitivity of psychological tests are discussed. Finally, the human literature is discussed against the backdrop of preclinical findings. RESULTS: Acute administration of Delta-9-THC transiently impairs immediate and delayed free recall of information presented after, but not before, drug administration in a dose- and delay-dependent manner. In particular, cannabinoids increase intrusion errors. These effects are more robust with the inhaled and intravenous route and correspond to peak drug levels. CONCLUSIONS: This profile of effects suggests that cannabinoids impair all stages of memory including encoding, consolidation, and retrieval. Several mechanisms, including effects on long-term potentiation and long-term depression and the inhibition of neurotransmitter (GABA, glutamate, acetyl choline, dopamine) release, have been implicated in the amnestic effects of cannabinoids. Future research in humans is necessary to characterize the neuroanatomical and neurochemical basis of the memory impairing effects of cannabinoids, to dissect out their effects on the various stages of memory and to bridge the expanding gap between the humans and preclinical literature.
For most, however, Mary Jane makes you a dunderhead with an overactive limbic system and an impaired frontal cortex, and can predispose to psychosis.
Biol Psychiatry. 2007 Jun 1;61(11):1281-9. Epub 2007 Jan 17. Links
Dorsolateral prefrontal cortex N-acetylaspartate/total creatine (NAA/tCr) loss in male recreational cannabis users.
Hermann D, Sartorius A, Welzel H, Walter S, Skopp G, Ende G, Mann K.
Central Institute of Mental Health, Mannheim, Germany.
BACKGROUND: Cannabinoids present neurotoxic and neuroprotective properties in in vitro studies, inconsistent alterations in human neuroimaging studies, neuropsychological deficits, and an increased risk for psychotic episodes. METHODS: Proton magnetic resonance spectroscopy ((1)H-MRS), neuropsychological testing, and hair analysis for cannabinoids was performed in 13 male nontreatment-seeking recreational cannabis users and 13 male control subjects. RESULTS: A significantly diminished N-acetylaspartate/total creatine (NAA/tCr) ratio in the dorsolateral prefrontal cortex (DLPFC) was observed in cannabis users (p = .0003). The NAA/tCr in the putamen/globus pallidum region correlated significantly with cannabidiol (R(2) = .66, p = .004). Results of the Wisconsin Card Sorting test, Trail making Test, and D2 test for attention were influenced by cannabinoids. CONCLUSIONS: Chronic recreational cannabis use is associated with an indication of diminished neuronal and axonal integrity in the DLPFC in this study. As chronic cannabis use is a risk factor for psychosis, these results are interesting because diminished NAA/tCr ratios in the DLPFC and neuropsychological deficits were also reported in schizophrenia. The strong positive correlation of NAA/tCr and cannabidiol in the putamen/globus pallidum is in line with neuroprotective properties of cannabidiol, which were also observed in in vitro model studies of Parkinson's disease.
For the love of all things cognitively related, ***DO NOT*** mess with the dorsolateral PFC!!!
medicalstudent | 3 years ago
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studentmedical | 3 years ago
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