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Which is more damaging; Cannabis or Heroin? [split from DC]

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^^Glutamate is a major excitatory neurotransmitter. It's only neurotoxic under certain conditions--prolonged exposure to abnormally high concentrations for example during injury and periods of ischemia. It's not toxic under normal conditions. I don't think the role of anandamine is clearly understood, but it has been shown to be an endogenous ligand involved in forming short term memory. There's no way any endogenous neurotransmitter or neuromodulator is going to be neurotoxic under normal physiological conditions. (I"m not counting cell death during developement and programmed cell death and other normal situations.) It would be impossible for survival of the organism.
 
socko said:
There's no way any endogenous neurotransmitter or neuromodulator is going to be neurotoxic under normal physiological conditions.

You said it yourself, normal conditions. This is in vitro if I'm not mistaken.

And if you wanna turn off smilies, click the box "disable smilies in this post".. ;)
 
It was in vitro. They put THC and some other drugs on samples from a neuroblastoma cell culture. For those who don't know, a neuroblastoma is a kind of cancer. Cell culture studies like this use cells that are extremely abnormal. It's not realistic to say that results from studies like this apply to pot smokers. But it would have been more informative if paradoxcycle had listed the drug concentrations this study used.
 
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^I want to see some conclusive evidence that heroin is neurotoixc then. Not vague, flawed, subjectivity.

And I want to see some conclusive evidence that THC is neurotoixc. Not vague, flawed, subjectivity. ;)
 
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Thnks for that link glog. Very interesting stuff. I think that if I ever get cancer, I'll take up pot smoking. I wonder if it would be more effective than traditional chemotherapy? At least it would be a more pleasant way to go out.
 
socko said:
Thnks for that link glog. Very interesting stuff. I think that if I ever get cancer, I'll take up pot smoking. I wonder if it would be more effective than traditional chemotherapy? At least it would be a more pleasant way to go out.

I didn't read the link, but my understanding (from previously read, haze-ily remembered articles) is that marijuana greatly inhibited a certain type of herpes from RNA transcription and this type of herpes is the catalyst for a couple major types of cancer. Someone else be the search engine for once I'm going to go chase the dragon and inject some pure THC right into my fucking brain. Peace.
 
Originally posted by gloggawogga
And I want to see some conclusive evidence that THC is neurotoixc. Not vague, flawed, subjectivity.


Why? I already have numerous times; as shown above. THC can be neurotoxic in vitro, and in humans cannabis use is associated with neuronal loss, as determined by MRI studies. the neurotoxic profile of THC may be dependent on the phase of neuronal development though.
Always have to have the last word Glogga, even when you've been proven wrong.
 
paradoxcycle, what MRI study are you referring to? i couldn't find it in your previous posts, but you cited a lot of stuff, so i could have missed it. from what i've seen in this thread, nobody cited any in vivo studies that convincingly demonstrate cannabis neurotoxicity. could someone please indulge me and (re)cite just the one or two articles that best demonstrate this?

IMO, and in the opinion of professional, respected scientists, such as the one i cited in an earlier post, the in vitro work is--at best--of questionable relevency to the human cannabis user.
 
Why? I already have numerous times;

No you haven't. The evidence you posted about THC is no more conclusive than the evidence that we posted about heroin. In fact, its less conclusive.


as shown above. THC can be neurotoxic in vitro

We also showed that morphine can be neurotoxic in vitro. Anything can be neurotoxic in vitro. It does not prove neurotoxicity in vivo in humans. I also posted studies regarding neurprotective properties of THC, and that cannabanoids can stimulate and regulate neuronal growth, and you completely ignore it.

and in humans cannabis use is associated with neuronal loss, as determined by MRI studies.

Bull shit.. I just searched this entire thread and I found no such study. The MRI studies showing neuronal loss in humans were on heroin users.

Always have to have the last word Glogga, even when you've been proven wrong.

You haven't proven me wrong, not one person in this thread is agreeing with you. Moreover, "paradoxcycle", you are a fucking hipocrite. You posted the following in OD:

http://www.bluelight.ru/vb/showthread.php?postid=3393967#post3393967
http://www.bluelight.ru/vb/showthread.php?postid=3394698#post3394698

the only reason my use is under control is because I allow someone else to control it for me. That is really the only way I can guarantee moderation.

I trust her 100%, I know that she has amazing self-control and when Saturday rolls around she's going to make sure we both get high.

So you tell us heroin is no more dangerous than pot yet you need another person to control your own craving for heroin. Obviously, your passion for the drug is strong enough you can't think objectively about it either.
 
These are the human MRI and lesion studies in question:

CMAJ \u2022 January 25, 2000; 162 (2)
© 2000 Canadian Medical Association or its licensors
ReviewSynthèse
Chasing the dragon - neurological toxicity associated with inhalation of heroin vapour: case report
Michael D. Hill*, Perry W. Cooper{dagger} and James R. Perry*

From the Divisions of *Neurology and {dagger}Neuroradiology, Sunnybrook and Women's College Health Sciences Centre, Sunnybrook Site, Toronto, Ont.

Case

A 33-year-old white man was admitted to a Toronto hospital after being found in an unresponsive state by his sister. He was a known drug abuser and had a history of heroin and cocaine use. It was known that he took his heroin not by injection but by inhalation of heated heroin vapours, a method known as "chasing the dragon." He had last been seen well 3 days previously and had spent the intervening period in bed for unknown reasons.

The patient was intubated at the scene by paramedics and had a Glasgow coma score of 6 upon admission. He was tachypneic (38 breaths/min) but hemodynamically stable, with blood pressure of 150/95 mm Hg, normal sinus rhythm and temperature of 38°C. Neurological examination revealed that he was comatose, unresponsive to verbal or painful stimuli. His pupils were both 4 mm in diameter and reactive, and the fundi were normal. Eye movements were conjugate but roving. Corneal reflexes were present bilaterally. The face was symmetric. The breathing pattern was fast but regular. Motor examination revealed axial myoclonus involving the neck flexors, the pectoral muscles and the abdominal musculature. The patient was diffusely hypotonic, and the limbs withdrew symmetrically on painful stimuli. Reflexes were 1+ throughout, but bilateral Babinski signs were present. General examination revealed no cardiac murmurs, a clear chest and normal abdomen. No needle marks were seen.

Head CT revealed bilateral hypoattenuated regions in the pallidum. Brain MRI demonstrated diffusely abnormal areas of increased T2 signal intensity involving the deep white matter of both cerebral hemispheres and the cerebellum (Fig. 1). Magnetic resonance angiography demonstrated normal proximal cerebral circulation. Electroencephalography demonstrated diffuse bilateral moderate-voltage theta and delta activity without epileptiform abnormalities. Carbon monoxide was undetectable in the serum. Lumbar puncture showed entirely normal cerebrospinal fluid indices. Chest radiography revealed no pulmonary disease. Creatine kinase was significantly elevated, to 32 930 U/L, with no myoglobinuria. The result of HIV serologic testing was negative. The heroin metabolites O6-monoacetylmorphine and morphine were present in the urine.1 Results of tests for cocaine metabolites and other toxic agents were negative.




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Neural activity associated with cognitive regulation in heroin users: A fMRI study.

Lee TM, Zhou WH, Luo XJ, Yuen KS, Ruan XZ, Weng XC.

Neuropsychology Laboratory, The University of Hong Kong, Hong Kong, PR China.

Previous research has found heroin addicts to be impulsive. This study employed functional magnetic resonance imaging technology to investigate the differences between heroin addicts and normal controls in neural activity associated with cognitive regulation of behavior. Twenty-one Chinese men participated in this study, 11 of whom were newly admitted heroin-addicted patients and 10 of whom were healthy volunteers. In the experimental task, the subjects were required to first identify the correct directions of arrowheads and then give the opposite answers. Behaviorally, the heroin-dependent patients took a much shorter time to complete the more demanding second part of the task but committed more errors than the normal controls. This pattern of behavior, characteristic of people who are disinhibited and who tend to be impulsive, was consistent with previous reports of impulsivity observed in people who have abused heroin. The neural activity of the patients that was associated with performing the experimental task of cognitive regulation was different to that of the normal controls in terms of the pattern of prefrontal activation, the attenuation of activity in the anterior cingulate, and the additional recruitment of the right inferior parietal region. This study is the first that seeks to understand the neural activity associated with impulsive behavior in people who abuse heroin. The pattern of imaging data obtained resembled the pattern of data observed in immature brains attempting to exercise cognitive control of behavior. Further theoretical and clinical implications of the findings are discussed.



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"Forensic Sci Int. 1999 May 31;102(1):51-9.
Related Articles, Links
_
Hypoxic/ischaemic brain damage, especially pallidal lesions, in heroin addicts.

Andersen SN, Skullerud K.

"Institute of Pathology, National Hospital, University of Oslo, Norway. [email protected]

The occurrence of pallidal lesions with or without other hypoxic/ischaemic brain injuries was evaluated in 100 intravenous (i.v.) heroin addicts. The brains were collected consecutively from forensic autopsies during the period from January 1995 to June 1996. The autopsies were required by the police and performed at The Institute of Forensic Medicine, The National Hospital, Oslo. There were 21 women and 79 men, median age 32 (range 21-47) and 34 (19-60) years, respectively. Of 38 brains with abnormalities, twenty-five cases showed isolated or combined lesions of hypoxic/ischaemic origin. Pallidal lesions were found in nine brains; six lesions were old, one was subacute (a couple of weeks), and two were part of recent, generalized hypoxia/ischaemia. Six persons had old infarcts in the hippocampal formation, and one of them in combination with old pallidal infarcts. In seven brains small and old infarcts were found in watershed areas in the cerebellum. Between five and ten percent of i.v. heroin addicts might have pallidal infarcts, either as the sole lesion, or combined with other manifestations of hypoxic/ischaemic brain injury. This might give severe mental disturbances in the affected persons.

PMID: 10423852 [PubMed - indexed for MEDLINE]"


These are real life case studies of nuerotoxicity in human heroin addicts. There are many more on pub med, I can post them if you wish. I'd like to see the same on pot heads.
 
Originally posted by gloggawogga
You haven't proven me wrong, not one person in this thread is agreeing with you. Moreover, "paradoxcycle", you are a fucking hipocrite. You posted the following in OD:

So you tell us heroin is no more dangerous than pot yet you need another person to control your own craving for heroin. Obviously, your passion for the drug is strong enough you can't think objectively about it either.


So you're turning this into a personal attack now? You're setting a great example, glogga. I have no interest in continuing this discussion if you feel the need to resort to this.
 
^^^

You are the one spreading a horrible example by blatently twisting the facts over a drug that you need another person to control your cravings for. Studies show brain lesions and other neural damage in human heroin users, not cannabis users as you claimed. Sorry if you I'm being too personal, but don't accuse me of "getting the last word in" while blatently turning the facts completely upside down in the same post.
 
Originally posted by gloggawogga
twisting the facts over a drug that you need another person to control your cravings for.


How is that relative to our discussion, twisting the facts? Another cheap, personal attack.

Originally posted by gloggawogga
Studies show brain lesions and other neural damage in human heroin users, not cannabis users as you claimed. Sorry if you I'm being too personal, but don't accuse me of "getting the last word in" while blatently turning the facts completely upside down in the same post.


The two areas of motor control and memory are where the effects of cannabis are directly and irrefutably evident. cannabinoids, depending on the dose, inhibit the transmission of neural signals though the basal ganglia and cerebellum. At lower doses, canabinoids seem to stimulate locomotion while greater doses inhibit it, most commonly manifested by lack of steadiness (body sway and hand steadiness) in motor tasks that require a lot of attention. Other brain regions, like the cortex, the cerebellum, and the neural pathway from cortex to striatum, are also involved in the control of movement and contain abundant cannabinoid receptors, indicating their possible involvement as well.

One of the primary effects in humans is the disruption of short-term memory, which is consistent with the abundance of CB1 receptors on the hippocampus. The effects of THC at these receptor sites produce what is called a "temporary hippocampal lesion." As a result of this lesion, several neurotransmitters like acetylcholine, norepinephrine, and glutamate, are released that trigger a major decrease in neuronal activity in the hippocampus and its inputs. In the end, this procedure leads to the blocking of cellular processes that are associated with memory formation.

References:

1) Pharmacology of Cannabinoid CB1 and CB2 Receptors, by R.G. Pertwee, Pharmacology and Therapeutics, 1997, 129-180

2) The Merck Manual of Medical Information (Home Edition), by R. Berkow MD et al, 1997. 449
 
. The effects of THC at these receptor sites produce what is called a "temporary hippocampal lesion." As a result of this lesion, several neurotransmitters like acetylcholine, norepinephrine, and glutamate, are released that trigger a major decrease in neuronal activity in the hippocampus and its inputs. In the end, this procedure leads to the blocking of cellular processes that are associated with memory formation.

References:

1) Pharmacology of Cannabinoid CB1 and CB2 Receptors, by R.G. Pertwee, Pharmacology and Therapeutics, 1997, 129-180

2) The Merck Manual of Medical Information (Home Edition), by R. Berkow MD et al, 1997. 449 [/B]
I'm not sure if you understand what that phrase (tempory lesion) means. The way I read what you've posted, you are implying that it means neurotoxicity. Neurotoxicity being neuron death or severe injury. In the text that you've quoted or paraphrased, term "temporary hippocampal lesion" is jargon for temporalily inhibited activity of hippocampal neurons. It can be thought of as a simulated lesion. It's not permanent. It doesn't indicate that the tissue was acutually injured. No neurotoxicty has been observed here. You go on to mention that other neurotransmitters are released that further decrease neural activity. Again, this is not a real pathological lesion.
fMRI studies sometimes induce temporary lesions in the test subjects. They'll do things like inject cold fluid ( I think) or do some kind of magnetic stimulation into part of the brain to block normal funcitoning of the targeted brain areas.. This shuts down the activity in the affected neurons. It doesn't cause permanent damage, but it is another way to induce a "temporary lesion."
 
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Sorry, I dind't mean for my post to sound like a personal attack against paradoxcycle. I won't post in this thread again.
 
i'm not interested in any personal attacks, but i would like to see this thread get back on track. i'm genuinely interested in reading some evidence of lasting cannabis neurotoxicity.

sure it pisses me off at first when someone argues vehemently against my personal point of view, but in retrospect i'm usually happier to learn that i was wrong about something--or at least not entirely correct--than i am to receive perfect confirmation of my beliefs.

IMO very strong views are often the result of ignorance. few issues are simple enough to have clear correct interpretations. i wouldn't be surprised if i'm missing some key piece of info on the neurotoxicity debate, and if i am, i'd really like to know what it is so i can carry on more informed discussions in the future.
 
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