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

[SPUNK]

You cant just say "Heroin is worse that weed, or weed is worse that heroin." There are many factors that must be taken into account that could potentially swing this opinion either way.

1- Marijuana is not neurotoxic on any significant (or even noticeabl) level until it's been used chronically for multiple years (even Paradoxle's evidence supports the claim that it takes 7-10 years). So in a case where someone has used heroin consistently for many years versus an occasional pot smoker, heroin is more dangerous.

2- Part of what makes heroin unhealthy it the way with which it is administered. Reusing needles, missed shots, and contiunal injections in th same spots are bad for the veins no matter what drug is used. So for a person who occasionaly snorts, smokes, or even occasional shoots up, heroin may be less harmful that someone who smokes 5 blunts per day. The same concept applies for marijuana, injesting weed by stomach is healthier than the act of smoking, regardless of neurotoxicity levels (obviously).

my point is just that it's silly to sit around and argue over which one is simply "more bad." It is however, interesting to compare the two drugs in areas less vague than "good or bad." Such areas could include looking at each drug on a sociological level and the chemical (makeup) level.

 

[gloggawogga]

From the studies paradoxcycle and gloggawogga posted, it sounds like marijuana is more damaging. Perhaps there are valid studies on responsible heroin users showing damage, but it seems like none were posted. Paradoxcycle showed valid entries of studies of marijuana causing damage, specifically, nueron damage.

Perhaps you overlooked the studies that I posted on morphine. Heroin is converted into morphine in the body, right? Let me post them agian, and a few more:

J Neurosci. 2002 Sep 1;22(17):7650-61.
Neuronal apoptosis associated with morphine tolerance: evidence for an opioid-induced neurotoxic mechanism.

Mao J, Sung B, Ji RR, Lim G.

Massachusetts General Hospital Pain Center, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.

Tolerance to the analgesic effect of an opioid is a pharmacological phenomenon that occurs after its prolonged administration. Activation of the NMDA receptor (NMDAR) has been implicated in the cellular mechanisms of opioid tolerance. However, activation of NMDARs can lead to neurotoxicity under many circumstances. Here we demonstrate that spinal neuronal apoptosis was induced in rats made tolerant to morphine administered through intrathecal boluses or continuous infusion. The apoptotic cells were predominantly located in the superficial spinal cord dorsal horn, and most apoptotic cells also expressed glutamic acid decarboxylase, a key enzyme for the synthesis of the inhibitory neurotransmitter GABA. Consistently, increased nociceptive sensitivity to heat stimulation was observed in these same rats. Mechanistically, the spinal glutamatergic activity modulated morphine-induced neuronal apoptosis, because pharmacological perturbation of the spinal glutamate transporter activity or coadministration of morphine with the NMDAR antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate affected both morphine tolerance and neuronal apoptosis. At the intracellular level, prolonged morphine administration resulted in an upregulation of the proapoptotic caspase-3 and Bax proteins but a downregulation of the antiapoptotic Bcl-2 protein in the spinal cord dorsal horn. Furthermore, coadministration with morphine of N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (a pan-caspase inhibitor) or acetyl-aspartyl-glutamyl-valyl-aspart-1-aldehyde (a relatively selective caspase-3 inhibitor) blocked morphine-induced neuronal apoptosis. Blockade of the spinal caspase-like activity also partially prevented morphine tolerance and the associated increase in nociceptive sensitivity. These results indicate an opioid-induced neurotoxic consequence regulated by the NMDAR-caspase pathway, a mechanism that may have clinical implications in opioid therapy and substance abuse.

Int J Neurosci. 2004 Aug;114(8):1001-11.

Opioid neurotoxicity: comparison of morphine and tramadol in an experimental rat model.

Atici S, Cinel L, Cinel I, Doruk N, Aktekin M, Akca A, Camdeviren H, Oral U.

Department of Anesthesiology & Reanimation, Mersin University School of Medicine, Mersin, Turkey.

Histopathologic changes in rat brain due to chronic use of morphine and/or tramadol in progressively increased doses were investigated in this study. Thirty male Wistar rats (180-220 g) were included and divided into three groups. Normal saline (1 ml/kg) was given intraperitoneally as placebo in the control group (n = 10). Morphine group (n = 10) received morphine intraperitoneally at a dose of 4 mg/kg/day for the first 10 days, 8 mg/kg/day between 11-20 days, and 12 mg/kg/day between 21-30 days. The tramadol group (n = 10) received the drug intraperitoneally at doses of 20, 40, and 80 mg/kg/day in the first, second, and the third 10 days of the study, respectively. All rats were decapitated on the 30th day and the brain was removed intact for histology. The presence and the number of red neurons, which are a histologic marker of apoptosis, were investigated in the parietal, frontal, temporal, occipital, entorhinal, pyriform, and hippocampal CA1, CA2, CA3 regions. Red neurons were found in morphine and tramadol groups but not in the control group. The total number of red neurons was not different in morphine and tramadol groups, but the numbers of red neurons were significantly higher in the temporal and occipital regions in tramadol group as compared with the morphine group (p < .05). In conclusion, chronic use of morphine and/or tramadol in increasing doses is found to cause red neuron degeneration in the rat brain, which probably contributes to cerebral dysfunction. These findings should be taken into consideration when chrome use of opioids is indicated.

Activity of adenylyl cyclase and protein kinase A contributes to morphine-induced spinal apoptosis.

Lim G, Wang S, Lim JA, Mao J.

Pain Research Group, Division of Pain Medicine, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, Suite WACC 324, 15 Parkman Street, Boston, MA 02114, USA.

Our previous study has shown that chronic morphine exposure induces neuronal apoptosis within the spinal cord dorsal horn; however, the mechanisms of morphine-induced apoptosis remain unclear. Here we examined whether adenylyl cyclase (AC) and protein kinase A (PKA) would play a role in this process. Intrathecal morphine regimen (10mug, twice dailyx7 days) that resulted in antinociceptive tolerance induced spinal apoptosis as revealed by in situ terminal deoxynucleotidyl transferase (TdT)-UTP-biotin nick end labeling (TUNEL). The TUNEL-positive cells were detected primarily in the superficial laminae of the spinal cord dorsal horn, which was associated with an increase in the expression of activated caspase-3 and mitogen-activated protein kinase (MAPK) within the same spinal region. Co-administration of morphine with a broad AC inhibitor (ddA), a PKA inhibitor (H89), or a MAPK inhibitor (PD98059) substantially reduced the number of TUNEL-positive cells, as compared with the morphine alone group. The results indicate that the spinal AC and PKA pathway through intracellular MAPK may be contributory to the cellular mechanisms of morphine-induced apoptosis.

Toxic effects of opioid and stimulant drugs on undifferentiated PC12 cells.

Oliveira MT, Rego AC, Morgadinho MT, Macedo TR, Oliveira CR.

Institute of Biochemistry, Faculty of Medicine and Center for Neuroscience and Cell Biology of Coimbra, University of Coimbra, 3004-504 Coimbra, Portugal.

Cell death and reactive oxygen species production have been suggested to be involved in neurodegeneration induced by the drugs of abuse. In this study we analyze the toxicity of the following drugs of abuse: heroin, morphine, d-amphetamine, and cocaine in undifferentiated PC12 cells, used as dopaminergic neuronal models. Our data show that opioid drugs (heroin and morphine) are more toxic than stimulant drugs (d-amphetamine and cocaine). Toxic effects induced by heroin are associated with a decrease in intracellular dopamine, an increase in DOPAC levels, and the formation of ROS, whereas toxic effects induced by amphetamine are associated with a decrease in intracellular dopamine and in ATP/ADP levels. In contrast with cocaine, both amphetamine and heroin induced features of apoptosis. The data suggest that the death of cultured PC12 cells induced by the drugs of abuse is correlated with a decrease in intracellular dopamine levels, which can be associated with an increased dopamine turnover and oxidative cell injury.

Neuropharmacology. 2002 May;42(6):829-36.

Morphine induces apoptosis of human microglia and neurons.

Hu S, Sheng WS, Lokensgard JR, Peterson PK.

Neuroimmunology Laboratory, Minneapolis Medical Research Foundation, Minneapolis, MN 55404, USA.

Apoptosis plays a critical role in normal brain development and in a number of neurodegenerative diseases. Recently, opiates have been shown to promote apoptotic death of cells of the immune and nervous systems. In this study, we investigated the effect of morphine on apoptosis of primary human fetal microglial cell, astrocyte and neuronal cell cultures. Exposure of microglia and neurons to 10(-6) M morphine potently induced apoptosis of these brain cells (approximately fourfold increase above untreated control cells). In contrast to microglia and neurons, astrocytes were completely resistant to morphine-induced apoptosis. Concentration-response and time-course studies indicated that neurons were more sensitive than microglia to morphine's effect on apoptosis. Naloxone blocked morphine-induced apoptosis suggesting involvement of an opiate receptor mechanism. Potent inhibition (>70%) of apoptosis by an inhibitor of caspase-3 as well as co-localization of active caspase-3 and DNA fragmentation in microglia or neurons treated with morphine indicated that caspase-3 is involved in the execution phase of morphine-induced apoptosis. The results of these in vitro studies have implications regarding the potential effect of opiates on fetal brain development and on the course of certain neurodegenerative diseases.

Int J Dev Neurosci. 1986;4(3):293-302.

Effects of opiates on the growth of neuron-enriched cultures from chick embryonic brain.

Sakellaridis N, Mangoura D, Vernadakis A.

Department of Pharmacology, University of Colorado School of Medicine, Denver 80262.

Neuron-enriched cultures derived from 6-day-old chick embryo cerebral hemispheres were treated with morphine or methadone, 10(-5) M or 10(-6) M, on days 4-6 or 6-8 in culture and were evaluated morphologically and biochemically at day 9 using phase contrast microscopy and choline acetyltransferase activity (ChAT) as a cholinergic marker. The treatment of the cultures with morphine markedly affected their growth pattern; specifically, we observed an increased number of flat cells presumptively glia, and aggregates sided by flat cells and devoid of thick bundles of neuritic processes that normally characterize neuron-enriched cultures. These morphologic changes were reflected in a drastic decrease of ChAT activity in cultures treated from day 4 to day 6 but not from 6 to 8. In contrast to morphine, exposure to 10(-6) M methadone from day 4 to day 6 resulted in reduced ChAT activity but the growth pattern of the cultures remained morphologically intact. We suggest that morphine exerts a general neurotoxic effect whereas methadone may affect some specific cholinergic function.

Neurol Res. 2000 Oct;22(7):733-7.

Opioid neurotoxicity: role of neurotransmitter systems.

Kofke WA, Garman RH, Garman R, Rose M.

Department of Anesthesiology, West Virginia University, Morgantown 26506-9134, USA.

We hypothesized that blockade of synthesis or release of several categories of neurotransmitters would ameliorate opioid neurotoxicity. Rats were randomly assigned to one of six groups in two sequential protocols: vesamicol (VES, n = 10), alpha-fluoromethylhistidine (FMH, n = 10), reserpine (RES, n = 10), BW1003C87 (BW, n = 7), lamotrigine (LAM, n = 10), or one of two control groups (CON, n = 19). Physiologically controlled rats received fentanyl (fen) i.v., loading dose 800 micrograms kg-1 followed by maintenance dose 32 micrograms kg-1 min-1 for 2 h. Drug dosing: CON, isovolemic (between rats) 0.9% saline i.v.; BW, 20 mg kg-1 i.v. 15 min pre-fen; LAM, 16 mg kg-1 i.v. 30 min pre-fen; VES, 2.5 mg kg-1 i.p. 60 min and 30 min pre-fen then infused 3.75 mg kg-1 during fen; FMH, 20 mg kg-1 i.p. 2 h pre-fen; RES, 0.75 mg kg-1 i.p. 18 h pre-fen. Seven days later all rats underwent cerebral perfusion fixation, followed by histologic grading (0-5, 0 = normal). Pathological data was analyzed by Wilcoxen's Signed rank test (two-tailed) for pathologic scores summated across all brain areas (overall severity score) and for scores of areas previously associated with opioid neurotoxicity. Compared to CON, overall severity was decreased by RES (p = 0.05) with an effect suggested by VES (p = 0.10). Compared to CON, lesions were decreased: (a) in the amygdala with VES (p = 0.03) and RES (p = 0.05) with a trend suggested by BW (p = 0.06); (b) in the subiculum by VES (p = 0.02) and RES (p = 0.008) with a trend suggested by FMH (p = 0.06); and (c) in the entorhinal cortex by VES (p = 0.004) and RES (p = 0.008) with a trend suggested by FMH (p = 0.07). The data indicate that brain acetylcholine and catecholamines contribute to opioid neurotoxicity, and suggest a possible role of glutamate and histamine in opioid neurotoxicity.

All of these studies indicate morphine neurotoxicity in rats and test tubes, just as paradoxcycle's posts showed THC neurotoxicity in rats and test tubes. None of these show neurotoxicity in human beings. How is the evidence against pot more damming? At this point, its a tie.

And, here are two cases of morphine neurotoxicity in humans:

J Pain Symptom Manage. 2005 May;29(5):520-4.

Neurotoxicity from chronic opioid therapy after successful palliative treatment for painful bone metastases.

Broadbent A, Glare P.

Braeside Hospital, Prairiewood, Sydney, Australia.

A 64-year-old man with severe bone pain secondary to pathological fracture of a vertebra required large doses of morphine to obtain pain relief. After receiving effective palliative anti-tumor treatment, he developed chronic opioid neurotoxicity. We postulate that the gradual reduction in pain over a period of time precipitated the development of toxicity that presented as cognitive failure. Delayed opioid toxicity is a potential consequence of effective disease-modifying therapies that needs to be recognized and treated appropriately when it occurs. The increasing use of community-based palliative care after hospitalization means that the community practitioner also needs to be aware of the development of chronic opioid toxicity at home. Optimal timing for going back down the ladder of opioid doses, after reduction of the noxious stimulus, requires clinicians to recognize different types of symptoms and signs and to consider the effect of other treatments and time on the noxious stimulus. A suggested protocol warrants consideration as a means of improving clinical practice; however, it requires prospective evaluation in the clinical setting.

Neuroradiology. 2000 Nov;42(11):845-8.

Unusual pattern of leukoencephalopathy after morphine sulphate intoxication.

Nanan R, von Stockhausen HB, Petersen B, Solymosi L, Warmuth-Metz M.

Children's Hospital, University of Wurzburg, Josef-Schneider-Str. 2, 97080 Wurzburg, Germany.

We report a 14-year-old girl with an unusual pattern of leukoencephalopathy after intentional intoxication with morphine sulphate tablets. Toxicological analysis showed exceedingly high levels of morphine and its metabolites. MRI disclosed a leukoencephalopathy with high signal from the centrum semiovale, corpus callosum and cerebellar white matter on T2-weighted images. These findings could be only partially explained by a hypoxic-ischaemic event; neurotoxic effects must be considered in this atypical leukoencephalopathy.

So now we have documented cases of pharmecuetical grade morphine neurotoxicity in humans, and we know that heroin converts to morphine in the body. We have no known cases of THC neurotoxity in humans. How exactly is the evidence suggest pot more damming?

I was pretty sure paradoxcycle posted some articles about research conducted on humans showing that marijuana conclusively caused neuron damage.

No he did not. He posted studies on rats and test tubes and subjective cognitive tests on humans that were not repeated in humans. He did not post one single case study of THC damage in humans. Above I just posted two case studies of morphine damage in humans, and we all know heroin converts to morphine in the body.

 

[gloggawogga]

all of the following posted by CreativeRandom

gloggawogga, I'm also a bit put off by your personal attacks...

You idiots who say stupid shit like

are just fucking retards. Such comments provide no insight at all besides your blatant stupidity

...Again, you thickheaded numbskulls.

...How the fuck can you be so retarded?

You know, I don't want this to personal any more than the next guy. I asked paradoxcycle to stop baiting me with personal remarks and since then he hasn't. One good thing I can say about both paradoxcycle and my self is that we don't resort to the sort of vulgar and offensive language that you resort to. He and I both show a little bit or restraint. Perhaps you should learn to as well.

 

[Blowmonkey]

Bilzor, I never said there were a lot of HUMAN toxicity studies, I merely said that there was indeed toxicity information, regardless of whether or not it was in humans or not.

So, perhaps I'm not the one who needs to read threads more thoroughly. I don't mean to be rude, I just think that was a bit uncalled for.

Right, I don't think it was.. I'll just stop coming to this thread entirely, because I've got the impression that people are just NOT READING (again).

I'm not Bilz0r. 8)

 

[BilZ0r]

I am though. I think this thread has been complicated by a lack of a definition for neurotoxicity (at least as far as I could see). Cannabis almost certainly causes semi-long term neurochemical changes, but so do all neuroactive compounds.

Does cannabis cause brain cell death in vivo? Almost certainly not, there is almost no evidence for this, and there is certainly no evidence for this in humans.

I know no one made the arguement explicitly, but just because a compound is neuroprotective, doesn't mean it can't be neurotoxicity too. DXM is neuroprotective and neurotoxic in rats. MPTP protects against MDMA-induced serotonergic deficits, but it is patently neurotoxic.

The problem with all of these things is that animal models and in vitro models can tell you a lot about the human condiiton, but only when they are done properly: Done one way capsaicin (the hot oil in chillis) can be grossely neurotoxic, kill all pain fibres all the way to the spinal cord. I eat hot curries, yet I can still feel pain in my mouth. These studies aren't pertenent. It's worth noting that animals given massive doses of THC for huge perioids of times do become just fucked, and seizures all the time and are behaviourally damage to fuck.

Also, there is a distinct lack of good animal or human studies. There no good primate studies investigating THC-induced neurotoxicity, rodent studies could does for longer. Human studies (like the costa rican study cited above) need to be coupled to (f)MRI, and better dose-deficit correlations need to be conducted.

 

[CreativeRandom]

SPUNK, things like missed shots, reusing needles, sharing needles, and unsterile equipment, are not involved in all cases of using heroin. I've been using heroin for a year, and I do admit I sometimes get lazy, but I never have shared needles, rarely ever miss shots, and rarely resuse needles. My equipment is kept sterile.

These traits should not be attributed with heroin. Perhaps the cliche junkie lifestyle, or the risk associated with the heroin underground, but not all users or heroin usage. Some of us are responsible with our drug use. This may seem like an oxymoron to some, but what I mean is that we administer our drugs safely to ourselves.

gloggawogga, neat studies you posted. I stand corrected. It seems as heroin can induce neurotoxicity and is damaging.

I was sure paradoxcycle posted studies of THC damage on human brains, but apparently you have read more thoroughly through this thread than I have. I guess I am corrected again.

Hahaha, neat observations on me gloggawogga. I was a bit put off on personal comments you made on paradoxcycle, specifically about someone helping him use. Some of my insults were crude and vulgar, but I don't take them back. Some of the comments made were stupid.

Oh, and some of the more vulgar comments I made were just merely jokes against the person who I was responding too. Good use of copy, paste, and edit.

So, it seems like both prolonged heroin use and prolonged marijuana use can cause permanent neurotoxicity and brain damage. Both appear to be slight, and do not cause noticeable differences in people. As SPUNK said of marijuana, it seems that both are not neurotoxic on a noticeable or any significant level.

Both marijuana and heroin cause minimal damage that is not noticeable or significant. What a relief.

 

[Blowmonkey]

So, it seems like both prolonged heroin use and prolonged marijuana use can cause permanent neurotoxicity and brain damage.

No.

I was sure paradoxcycle posted studies of THC damage on human brains, but apparently you have read more thoroughly through this thread than I have. I guess I am corrected again.

Yes.

Both appear to be slight, and do not cause noticeable differences in people. As SPUNK said of marijuana, it seems that both are not neurotoxic on a noticeable or any significant level.

Make up your mind already.

Both marijuana and heroin cause minimal damage that is not noticeable or significant. What a relief.

Damage equals neurotoxicity. If it's not neurotoxic, no damage is done.

Changes in brain chemistry are NOT neurotoxic, as previously noted.

Oh, and some of the more vulgar comments I made were just merely jokes against the person who I was responding too.

Great kind of humour you have!

Good use of copy, paste, and edit.

Yes, it is.

 

[Fujicrow]

having read all the abstracts, I'd rather put my mind off these "cientific data" and look at the facts.

paradoxcycle is obviously an addict in denial, and I bet my testicles that a few years from now, heroin WILL catch with you, as does with everyone, and you will spiral down into a dark dark place like I've seen many people go to.

Also, you have to observe the lifestyles that come attached to both drugs.

Cannabis: the worst thing that can happen, is that you'll be a lazy fat fuck, with fucked up short term memory, BUT when you quit, even if you've been smoking everyday for years, in a few month's time you'll be good as new.

Heroin: Malnutrition, isolation and other very dark things can happen to you and your body, even if not a DIRECT result from the neurochemical reactions in your brain. I agree that, in itself, heroin is not damaging by itself, like cannabis, but the lifestyle attached to heroin is VERY damaging. Also, when quitting, as with any other downer drug, carries with itself a rebound neural excitatory effect that may induce neurotoxicity.

you can't really compare the two drugs.

 

[paradoxcycle]

Originally posted by Fujicrow
paradoxcycle is obviously an addict in denial, and I bet my testicles that a few years from now, heroin WILL catch with you, as does with everyone, and you will spiral down into a dark dark place like I've seen many people go to.

Excuse me?
I have had it with the personal attacks and insults in this thread. This is my final warning. I will not hesitate to close or just move the whole thing to WOB.

 

[Fujicrow]

no direct offense meant man, it's just what happens...wait a few months/years and then you'll tell me. I hope not, but it'sjust the way things go.

 

[paradoxcycle]

I took it as a direct offense. You have no idea how long I've been using the drug and you have absolutely no idea what my life is like.