20 replies to this topic

[JChief]

Here is the study .

We found that NGF serum levels were significantly reduced in cannabis abusers as compared to healthy subjects. These findings indicate that NGF may have a role in the central action of cannabis and potentially in the neurotoxicity induced by this drug. These data also suggest that chronic cannabis consumption may be a risk factor for developing psychosis among drug users.

This is troubling news (for people like me anyway! lol)

Discuss.

[computeTHIS]

Well, for one thing, this study and most studies dealing with cannabis are specifically addressing "abusers" or "light users". What constitutes abuse and light use is rather subjective, studies with statistically large sample populations are also needed. Even then, it's my opinion that most cannabis use would probably be categorized as abuse since most instances seem to be people who smoke it - which is much more efficient at getting the stuff in your bloodstream.

Ark shared this document which shows cannabis increasing BDNF levels in healthy controls, while having no effect on "light users" and furthermore, users showed lower basal BDNF levels. (https://docs.google....r2/fulltext.pdf)

I think the fact that it increased BDNF in healthy controls is enough to demonstrate that it has efficacy at some level. Most of the studies also fail to consider consumption of the other cannabinoids, many of which are present in the female plants, and some of which are marketed in perfectly legal "hemp supplements".

[spider]

Damn! Oh well, just neutralize this with some mushroom. :p

Seriously, I'm thinking of using cannabis to reset my brain. This will be necessary about 2 times a month. I think for me and my goal 1-1.2 gram of cannabis will be sufficient. NB, this is a very moderate dosage.

I like to compare cannabis use with the use of alcohol. In both cases one can use it stuppidly or one can use it wisely. One or two glasses of an alcohol beverage used daily is very healthy, cardiovascular wise but also for some neurodegenerative diseases like alzheimer. I guess the same is true for cannabis use, light cannabis use is probably healthy but use too much and you will become a pot head.

[Ark]

I will list some other studies later , offering a counter point to this study.

[Ark]

Most of the studies I've seen had chronic usage causing a boost in BDNF while first or light light users caused a drop in there BDNF levels.


After work, I'll do my best to gather the reseach and see which is right and what is wrong.

[Luminosity]

Smoking anything is bad for your lungs. Further, there are resins in pot that gum up your system. I would stay away from it, especially if you have a health, or mental health, issue. It lessens your memory, ambition and drive. It makes some people angry, flaky and sulky when not high, or even if they are. I see more compulsive/addictive pot use now than before. Something about people now is more addiction-prone. There's better ways to reset your brain that don't involve substances or vices.

[Raptor87]

Never heard that cannabis causes neurotoxicity. But then again they say potentially. I think that the reasons for their findings are due to atrophy. A person who is constantly intoxicated wont learn shit and the brain will follow.

[Ark]

J Psychopharmacol. 2003 Dec;17(4):439-45.
Chronic cannabis abuse raises nerve growth factor serum concentrations in drug-naive schizophrenic patients.

Jockers-Scherübl MC, Matthies U, Danker-Hopfe H, Lang UE, Mahlberg R, Hellweg R.

Source

Department of Psychiatry and Psychotherapy, Charite-University Medicine Berlin, Campus Benjamin Franklin, Berlin, Germany. maria.jockers@medizin.fu-berlin.de

Abstract

Long-term cannabis abuse may increase the risk of schizophrenia. Nerve growth factor (NGF) is a pleiotropic neurotrophic protein that is implicated in development, protection and regeneration of NFG-sensitive neurones. We tested the hypothesis that damage to neuronal cells in schizophrenia is precipitated by the consumption of cannabis and other neurotoxic substances, resulting in raised NGF serum concentrations and a younger age for disease onset. The NGF serum levels of 109 consecutive drug-naive schizophrenic patients were measured and compared with those of healthy controls. The results were correlated with the long-term intake of cannabis and other illegal drugs. Mean (+/- SD) NGF serum levels of 61 control persons (33.1 +/- 31.0 pg/ml) and 76 schizophrenics who did not consume illegal drugs (26.3 +/- 19.5 pg/ml) did not differ significantly. Schizophrenic patients with regular cannabis intake (> 0.5 g on average per day for at least 2 years) had significantly raised NGF serum levels of 412.9 +/- 288.4 pg/ml (n = 21) compared to controls and schizophrenic patients not consuming cannabis (p < 0.001). In schizophrenic patients who abused not only cannabis, but also additional substances, NGF concentrations were as high as 2336.2 +/- 1711.4 pg/ml (n = 12). On average, heavy cannabis consumers suffered their first episode of schizophrenia 3.5 years (n = 21) earlier than schizophrenic patients who abstained from cannabis. These results indicate that cannabis is a possible risk factor for the development of schizophrenia. This might be reflected in the raised NGF-serum concentrations when both schizophrenia and long-term cannabis abuse prevail.

http://www.ncbi.nlm....pubmed/14870957

[JChief]

Whoever gave this thread 1 star needs to be spanked.

[spider]

Reduced serum concentrations of nerve growth factor, but not brain-derived neurotrophic factor, in chronic cannabis abusers.

Angelucci F, Ricci V, Spalletta G, Pomponi M, Tonioni F, Caltagirone C, Bria P.
Source

IRCCS Santa Lucia Foundation, Department of Clinical and Behavioural Neurology, Rome, Italy. f.angelucci@hsantalucia.it
Abstract

Chronic cannabis use produces effects within the central nervous system (CNS) which include deficits in learning and attention tasks and decreased brain volume. Neurotrophins, in particular nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), are proteins that serve as survival factors for CNS neurons. Deficits in the production and utilization of these proteins can lead to CNS dysfunctions including those associated with cannabis abuse. In this study we measured by enzyme-linked immunosorbent assay (ELISA) the NGF and BDNF serum levels in two groups of subjects: cannabis-dependent patients and healthy subjects. We found that NGF serum levels were significantly reduced in cannabis abusers as compared to healthy subjects. These findings indicate that NGF may have a role in the central action of cannabis and potentially in the neurotoxicity induced by this drug. These data also suggest that chronic cannabis consumption may be a risk factor for developing psychosis among drug users. PMID: 18774699 [PubMed - indexed for MEDLINE]

Reading this abstact gives me the feeling that it is highly biased against cannabis. Maybe money or more likely their strong ethics have muddled their objectivity. Unfortunately, I have been reading in the media more-and-more that scientists being accussed of using false data interpretations and arguments. The following sentences smell a bit fishy, especially because they state it so factual.

Chronic cannabis use produces effects within the central nervous system (CNS) which include deficits in learning and attention tasks and decreased brain volume.

Cannabis does not always cause deficits in learning and attention. On the contrary, cannabis IMPROVES learning in schizophrenia and bipolar patients.

The neuropsychological correlates of cannabis use in schizophrenia: lifetime abuse/dependence, frequency of use, and recency of use.

This study examined the relationship between neuropsychological performance and three different indices of cannabis use in schizophrenia. These indices were DSM-IV lifetime abuse/dependence, frequency of use, and recency of use. Sixty males with schizophrenia/schizoaffective disorder and 17 healthy males were recruited. The two groups were matched for age, years of education, and premorbid IQ. Medical history, substance use, and psychiatric symptoms were assessed. A neuropsychological battery was also administered to assess attention/processing speed, executive functions, memory, and perceptual organisation. Substance use within 24 hours of cognitive assessment was screened by urine analysis, and a range of confounds were controlled. In the schizophrenia group, 44 participants met DSM-IV criteria for lifetime cannabis abuse/dependence. In addition, there were three mutually exclusive frequency-of-cannabis-use subgroups comprising "high" frequency users (n=11), "medium" frequency users (n=7), and "low" frequency users (n=34) over the preceding year. There were also four mutually exclusive recency-of-cannabis-use categories comprising "cannabis abuse/dependence in the past week" (n=11 users), "non-dependent cannabis use in the past week" (n=7 users), "non-dependent cannabis use in the past month, but prior to the past week" (n=7 users), and "non-dependent cannabis use prior to the past month" (n=9 users). The control group performed better than the schizophrenia group in all cognitive domains. Within the schizophrenia group, a larger proportion of participants with lifetime cannabis abuse/dependence demonstrated better performance than those without lifetime abuse/dependence on a component of psychomotor speed. Frequency and recency of cannabis use were also associated with better neuropsychological performance, predominantly in the domains of attention/processing speed and executive functions. In conclusion, cannabis use is associated with enhanced cognitive functioning in schizophrenia. Implications of the results, limitations of the study, and directions for future research are discussed.

And what about decreased brain volume? More likely most cannabis users are self-medicating to treat their symnptoms of depression. Depression causes decrease in brain volume, esp. The hippocampus.

These findings indicate that NGF may have a role in the central action of cannabis and potentially in the neurotoxicity induced by this drug.

Cannabis causes neurotoxicity? Again, a statement which I have never heard of before. Below a study which indicates cannabis reduces/protects against neurotoxicity.

Cannabidiol and (−)Δ⁹-tetrahydrocannabinol are neuroprotective antioxidants

The neuroprotective actions of cannabidiol and other cannabinoids were examined in rat cortical neuron cultures exposed to toxic levels of the excitatory neurotransmitter glutamate. Glutamate toxicity was reduced by both cannabidiol, a nonpsychoactive constituent of marijuana, and the psychotropic cannabinoid (−)Δ⁹-tetrahydrocannabinol (THC). Cannabinoids protected equally well against neurotoxicity mediated by N-methyl-d-aspartate receptors, 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid receptors, or kainate receptors. N-methyl-d-aspartate receptor-induced toxicity has been shown to be calcium dependent; this study demonstrates that 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid/kainate receptor-type neurotoxicity is also calcium-dependent, partly mediated by voltage sensitive calcium channels. The neuroprotection observed with cannabidiol and THC was unaffected by cannabinoid receptor antagonist, indicating it to be cannabinoid receptor independent. Previous studies have shown that glutamate toxicity may be prevented by antioxidants. Cannabidiol, THC and several synthetic cannabinoids all were demonstrated to be antioxidants by cyclic voltametry. Cannabidiol and THC also were shown to prevent hydroperoxide-induced oxidative damage as well as or better than other antioxidants in a chemical (Fenton reaction) system and neuronal cultures. Cannabidiol was more protective against glutamate neurotoxicity than either ascorbate or α-tocopherol, indicating it to be a potent antioxidant. These data also suggest that the naturally occurring, nonpsychotropic cannabinoid, cannabidiol, may be a potentially useful therapeutic agent for the treatment of oxidative neurological disorders such as cerebral ischemia.

Edited by spider, 15 December 2011 - 07:19 AM.

[matter_of_time]

Most of the studies I've seen had chronic usage causing a boost in BDNF while first or light light users caused a drop in there BDNF levels.


After work, I'll do my best to gather the reseach and see which is right and what is wrong.

I never liked Cannabis, I can't understand why people smoke it. I can't communicate with anyone any more and get paranoid immediately.

I wonder what other supplement do in the long run. Most supplements are studied for a few weeks but nobody knows what happens after taking them for years.

[evo]

Well, I agree that the discussion seems a bit biased against Cannabis, however the data is nevertheless interesting.

Ark--the study you posted is referenced in the full text (Angelucci et al., 2008), however it is also noted that in that study, the Cannabis-dependent subjects showed schizophrenic and/or positive psychotic symptoms. I think the link between NGF production and and reparative/neuro-protective brain function has been clearly established, as well as the link between Schizophrenia and abnormal NGF synthesis, so I'm guessing these elevated serum levels are caused more by the underlying psychotic disorder in conjunction with the Cannabis than by the Cannabis alone.

I think it's equally interesting that BDNF levels in this study were significantly increased. While I don't have a medical background (this is pure speculation), it is my current understanding that NGF is primarily associated with neuro-protective function while BDNF is the primary neurotrophin responsible for controlling synaptic plasticity and integration of learned knowledge into fluid and crystallized intelligence. The lack of a corresponding significant decrease in BDNF in the Cannabis-dependent patients NOT showing positive psychotic symptoms makes me think that this study warrants more consideration before any conclusions are drawn...

Edited by lmlj, 15 December 2011 - 09:10 PM.

[Ark]

This paper here puts everything in retrospect for ya, give it a whirl.


http://www.springerl...r2/fulltext.pdf

Δ9-THC increased BDNF levels; this was driven by
the control group. Thus, at +145 min, i.e., at the end of the
20-min intravenous infusion of Δ9-THC, there were group
differences in serum BDNF levels (F1,95=4.83, p=0.03)


also

It is also possible that

spillover into serum.


Δ9-THC

induces changes in serum BDNF levels via direct effects on peripheral cells known to release BDNF. Future studies will need to be conducted to localize the source of


Δ9-THC-induced increases in serum BDNF levels.

Alternatively, increases in serum BDNF may be related


to the effects ofΔ9-THC on platelets (Fujimura et al. 2002;

Radka et al.


1996),

[Ark]

Smoking anything is bad for your lungs. Further, there are resins in pot that gum up your system. I would stay away from it, especially if you have a health, or mental health, issue. It lessens your memory, ambition and drive. It makes some people angry, flaky and sulky when not high, or even if they are. I see more compulsive/addictive pot use now than before. Something about people now is more addiction-prone. There's better ways to reset your brain that don't involve substances or vices.

seems a bit harsh

[computeTHIS]

Smoking anything is bad for your lungs. Further, there are resins in pot that gum up your system. I would stay away from it, especially if you have a health, or mental health, issue. It lessens your memory, ambition and drive. It makes some people angry, flaky and sulky when not high, or even if they are. I see more compulsive/addictive pot use now than before. Something about people now is more addiction-prone. There's better ways to reset your brain that don't involve substances or vices.

I would echo the part about smoking things. As to the other statements, it reminds me of what David Pearce (of biopsychiatry.com) had to say about it:

By contrast to today's opioids, marijuana isn't usually addictive in the traditional sense of the term. It can still be habit-forming. Marijuana has euphoriant, psychedelic and sedative properties. Experiments with stoned rats suggest that cannabis use reduces the amount of corticotrophin-releasing factor (CRF) in the amygdala. Excess secretion of CRF is associated with abnormalities in the HPLA axis and depression. The rebound surge of CRF on ceasing cannabis-use correlates with increased vulnerability to stress and a withdrawal-reaction, arguably one good reason not to stop in the first instance. Stress-induced endocannabinoid deficit in the brain may induce melancholic depression in users and non-users alike. A dysfunctional response to stress, linked to a chronically overactive HPLA axis, causes anxiety disorders and depression; CRH-type 1 receptor antagonists like antalarmin are being investigated as potential anxiolytics and antidepressants. The deeper roots of our malaise lie buried in the evolutionary past.

The primary psychoactive ingredient in marijuana is THC, tetrahydrocannabinol. Smoking or eating marijuana and its complex cocktail of compounds may rarely trigger episodes of depersonalisation, derealisation and psychosis. Sometimes it can induce paranoia, particularly in advocates of The War Against Drugs. More commonly, marijuana just leaves the user pleasantly and harmlessly stoned. It's fun. Sleepiness, pain-relief and euphoria are typical responses. Cannabinoid CB(1) receptor agonists are potential antidepressants. Indeed cannabinoids may be neuroprotective against the effects of stress. Conversely, cannabinoid CB(1) receptor antagonists/inverse agonists, like the new EC-licensed diet-drug rimonabant (Acomplia), may cause depression and anxiety. Indeed the first brain-derived substance found to bind to our cannabis receptors was christened "anandamide", a derivative of the Sanskrit word for internal contentment. Getting high may thus serve as an innocent recreational pastime in an uncaring world.

Yet marijuana is not a wonderdrug. Cognitive function in the user is often impaired, albeit moderately and reversibly. Marijuana interferes with memory-formation by disrupting long-term potentiation in the hippocampus. One of the functions of endogenous cannabinoids in the brain is to promote selective short-term amnesia. Forgetting is not, as one might have supposed, a purely passive process. Either way, choosing deliberately to ingest an amnestic agent for long periods is scarcely an ideal life-strategy. It's especially flawed given the centrality of memory to human self-identity. Some artists and professional bohemians, it is true, apparently do find smoking grass an adjunct to creative thought. For persons of a more philistine temperament, on the other hand, it's hard to see such a drug as a major tool for life-affirmation or the development of the human species. This shortcoming does not, one ought scarcely need to add, suggest marijuana users should be persecuted and criminalised. Indeed the marijuana compound THC may actually be superior to commercially licensed products at blocking the formation of mind-rotting amyloid plaques of the memory-destroying Alzheimer's disease.

He also mentions JDTic, a promising kappa-opioid receptor antagonist.

[JChief]

The last paragraph said it well. Daily use for years and years isn't ideal. I do wish I could better recall a lot of that period in my life when I was using it chronically. I think occasional use (even moreso if it were legal or prescribed) is ideal though. No doubt!

[JChief]

I never liked Cannabis, I can't understand why people smoke it. I can't communicate with anyone any more and get paranoid immediately.

Yeah a buddy of mine I remember freaking out thinking his heart was going to beat out of his chest and got all freaked out. Told him to breathe.. that he wasn't gonna die haha. But I have always loved it. All through latter part of junior high and "high" school, college.. perhaps it was to medicate on some level? High school was a time I was on all sort of meds for depression, anxiety, and low motivation you name it. Even got diagnosed as bipolar at one point. Depakote etc. It was a mess of a time. But cannabis was one of the substances that always seemed to help.. but there are side effects with everything as was explained above quite well I must say. And btw I recently discovered that piracetam seemed to mitigate much of the short term side effects for me. Reduced anxiety and paranoia were noted.

Edited by JChief, 16 December 2011 - 12:45 PM.

[Ark]

Smoking anything is bad for your lungs. Further, there are resins in pot that gum up your system. I would stay away from it, especially if you have a health, or mental health, issue. It lessens your memory, ambition and drive. It makes some people angry, flaky and sulky when not high, or even if they are. I see more compulsive/addictive pot use now than before. Something about people now is more addiction-prone. There's better ways to reset your brain that don't involve substances or vices.

I would echo the part about smoking things. As to the other statements, it reminds me of what David Pearce (of biopsychiatry.com) had to say about it:

By contrast to today's opioids, marijuana isn't usually addictive in the traditional sense of the term. It can still be habit-forming. Marijuana has euphoriant, psychedelic and sedative properties. Experiments with stoned rats suggest that cannabis use reduces the amount of corticotrophin-releasing factor (CRF) in the amygdala. Excess secretion of CRF is associated with abnormalities in the HPLA axis and depression. The rebound surge of CRF on ceasing cannabis-use correlates with increased vulnerability to stress and a withdrawal-reaction, arguably one good reason not to stop in the first instance. Stress-induced endocannabinoid deficit in the brain may induce melancholic depression in users and non-users alike. A dysfunctional response to stress, linked to a chronically overactive HPLA axis, causes anxiety disorders and depression; CRH-type 1 receptor antagonists like antalarmin are being investigated as potential anxiolytics and antidepressants. The deeper roots of our malaise lie buried in the evolutionary past.

The primary psychoactive ingredient in marijuana is THC, tetrahydrocannabinol. Smoking or eating marijuana and its complex cocktail of compounds may rarely trigger episodes of depersonalisation, derealisation and psychosis. Sometimes it can induce paranoia, particularly in advocates of The War Against Drugs. More commonly, marijuana just leaves the user pleasantly and harmlessly stoned. It's fun. Sleepiness, pain-relief and euphoria are typical responses. Cannabinoid CB(1) receptor agonists are potential antidepressants. Indeed cannabinoids may be neuroprotective against the effects of stress. Conversely, cannabinoid CB(1) receptor antagonists/inverse agonists, like the new EC-licensed diet-drug rimonabant (Acomplia), may cause depression and anxiety. Indeed the first brain-derived substance found to bind to our cannabis receptors was christened "anandamide", a derivative of the Sanskrit word for internal contentment. Getting high may thus serve as an innocent recreational pastime in an uncaring world.

Yet marijuana is not a wonderdrug. Cognitive function in the user is often impaired, albeit moderately and reversibly. Marijuana interferes with memory-formation by disrupting long-term potentiation in the hippocampus. One of the functions of endogenous cannabinoids in the brain is to promote selective short-term amnesia. Forgetting is not, as one might have supposed, a purely passive process. Either way, choosing deliberately to ingest an amnestic agent for long periods is scarcely an ideal life-strategy. It's especially flawed given the centrality of memory to human self-identity. Some artists and professional bohemians, it is true, apparently do find smoking grass an adjunct to creative thought. For persons of a more philistine temperament, on the other hand, it's hard to see such a drug as a major tool for life-affirmation or the development of the human species. This shortcoming does not, one ought scarcely need to add, suggest marijuana users should be persecuted and criminalised. Indeed the marijuana compound THC may actually be superior to commercially licensed products at blocking the formation of mind-rotting amyloid plaques of the memory-destroying Alzheimer's disease.

He also mentions JDTic, a promising kappa-opioid receptor antagonist.

I should note the tone of the above paper you've quoted is biased

[computeTHIS]

I should note the tone of the above paper you've quoted is biased

For, or against? It wouldn't surprise me if David Pearce currently uses it, or has in the past. He's professed to trying a number of things, regardless of legality. One of his pages was recently shutdown (by his ISP) due to pressure from the DEA concerning a list he compiled of global pharmacies offering different opioids.

The section I quoted is actually part of the webpage at biopsychiatry.com.

[Thorsten3]

This has no relevance to NGF but when I was previously a stoner I would notice (after a nightly binge) that I would feel completely stress free. I think cannabis has been spoken about before with certain restorative effects it has within the hippocampus (although isn't going to benefit memory that's for sure).

However it could also make me feel very stupid and extremely paranoid (which was very detrimental to brain health alone).

I once experimented with low dosage cannabis each day (one small spiff) and it felt great for a couple of weeks but it soon became quite laborious, demotivating and very tiresome (yes you kind of get sick of being high the whole time).

I eat it very occasionally nowadays in the form of cookies. I gave up smoking it due to my obsession with longevity.

[Ark]

on a side note, looking to fight MRSA then think THC http://news.injurybo...googleid=246942