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Ganja talk

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Messenger: GARVEYS AFRICA Sent: 1/25/2019 5:57:38 AM
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I am here to dispel the line of no substantial toxicity


Messenger: GARVEYS AFRICA Sent: 1/25/2019 6:01:39 AM
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Regional brain abnormalities associated with long-term heavy cannabis use.

Yücel M, et al. Arch Gen Psychiatry. 2008.

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Abstract

CONTEXT: Cannabis is the most widely used illicit drug in the developed world. Despite this, there is a paucity of research examining its long-term effect on the human brain.

OBJECTIVE: To determine whether long-term heavy cannabis use is associated with gross anatomical abnormalities in 2 cannabinoid receptor-rich regions of the brain, the hippocampus and the amygdala.

DESIGN: Cross-sectional design using high-resolution (3-T) structural magnetic resonance imaging.

SETTING: Participants were recruited from the general community and underwent imaging at a hospital research facility.

PARTICIPANTS: Fifteen carefully selected long-term (>10 years) and heavy (>5 joints daily) cannabis-using men (mean age, 39.8 years; mean duration of regular use, 19.7 years) with no history of polydrug abuse or neurologic/mental disorder and 16 matched nonusing control subjects (mean age, 36.4 years).

MAIN OUTCOME MEASURES: Volumetric measures of the hippocampus and the amygdala combined with measures of cannabis use. Subthreshold psychotic symptoms and verbal learning ability were also measured.

RESULTS: Cannabis users had bilaterally reduced hippocampal and amygdala volumes (P = .001), with a relatively (and significantly [P = .02]) greater magnitude of reduction in the former (12.0% vs 7.1%). Left hemisphere hippocampal volume was inversely associated with cumulative exposure to cannabis during the previous 10 years (P = .01) and subthreshold positive psychotic symptoms (P < .001). Positive symptom scores were also associated with cumulative exposure to cannabis (P = .048). Although cannabis users performed significantly worse than controls on verbal learning (P < .001), this did not correlate with regional brain volumes in either group.

CONCLUSIONS: These results provide new evidence of exposure-related structural abnormalities in the hippocampus and amygdala in long-term heavy cannabis users and corroborate similar findings in the animal literature. These findings indicate that heavy daily cannabis use across protracted periods exerts harmful effects on brain tissue and mental health.





IN OTHER WORDS: GANJA REDUCES THE VOLUME OF THE MEMORY PORTION OF THE BRAIN

- Well we all knew that!

Not only is the Amygdala and Hippocampus involved in memory but also Psychosis. This next study speaks to what ALL ganja smokers deny to themselves:




Hippocampal and amygdala volumes according to psychosis stage and diagnosis: a magnetic resonance imaging study of chronic schizophrenia, first-episode psychosis, and ultra-high-risk individuals.

Velakoulis D, et al. Arch Gen Psychiatry. 2006.

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Abstract

CONTEXT: Magnetic resonance imaging studies have identified hippocampal volume reductions in schizophrenia and amygdala volume enlargements in bipolar disorder, suggesting different medial temporal lobe abnormalities in these conditions. These studies have been limited by small samples and the absence of patients early in the course of illness.

OBJECTIVE: To investigate hippocampal and amygdala volumes in a large sample of patients with chronic schizophrenia, patients with first-episode psychosis, and patients at ultra-high risk for psychosis compared with control subjects.

..............

RESULTS: Patients with chronic schizophrenia displayed bilateral hippocampal volume reduction. Patients with first-episode schizophrenia but not schizophreniform psychosis displayed left hippocampal volume reduction




Messenger: GARVEYS AFRICA Sent: 1/25/2019 6:09:01 AM
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The Pan African Medical Journal
(YES WE PANAFRICANS ARE HIGHLY INTELLIGENT RESEARCH BEINGS)

African Field Epidemiology Network

Late onset epilepsy associated with marijuana abuse: a case report with MRI findings

Yannick Fogoum Fogang, Massaman Camara, [...], and Kamadore Touré

Additional article information

Abstract

Marijuana is the most widely used illicit substance in the world. The relation between marijuana use and epileptic seizures is still controversial. We report a case of late onset epilepsy associated with marijuana abuse, with brain magnetic resonance imaging (MRI) findings. A 44-year-old patient was admitted for 03 isolated episodes of secondary generalized tonic-clonic seizures. He had a history of 26 years regular marijuana smoking. On admission, we found a tachycardia, psychomotor slowing, asymmetric hyperreflexia, bilateral Babinski sign without weakness. Laboratory work-up showed a high level of urine of Δ;;-9-tétrahydroxycannabinol. Electroencephalogram was normal. Brain MRI revealed abnormal signal intensities in the right frontal lobe and basal ganglia. Seizures cessation was obtained with anti-epileptic treatment. We suggest that marijuana abuse through vascular and toxic mechanisms could explain seizures in this case.

Keywords: Symptomatic epilepsy, intracerebral haemorrhage, marijuana, Magnetic Resonance Imaging

Introduction

Marijuana is a naturally growing plant, with many chemical constituents. Approximately 60 cannabinoids and 260 non cannabinoid constituents have been identified [1]. Marijuana is the most widely used illicit substance in the world [2]. It is generally smoked, but may also be ingested. Acute administration produces diverse cognitive, perceptual, and cardiovascular effects [3]. The association between marijuana and epileptic seizures is still controversial and clinico-radiological case reports are seldom. Interestingly, some evidence suggests that marijuana and its active cannabinoids have antiepileptic effects, especially for focal or tonic-clonic seizures [4–5]. We describe here a case of late-onset epilepsy associated with marijuana abuse, with magnetic resonance imaging (MRI) correlations.

Patient and observation

The patient was a 44-year-old man, single and jobless who was admitted in the neurology department for three isolated episodes in five hours, of secondary generalized left body side tonic-clonic seizures lasting less than ten minutes each. He presented 08 months before this admission a severe headache of abrupt onset during a period of heavy smoking of marijuana, associated with one generalized tonic-clonic seizure. He consulted at a Health Dispensary where he was prescribed, without any brain imaging phenobarbital: 100 mg/day and paracetamol for pain, but his compliance to treatment was poor. However, he did not have any seizure until this consultation. He had a history of regular marijuana smoking for 26 years, but no history of recurrent headache or seizures in childhood and in his family. There was no notion of alcohol intake, or head trauma before the onset of symptoms. On admission, one day after the last seizure, his general state was good, vital signs revealed a blood pressure of 110/80 mmHg, a pulse rate of 104 beats per minute, a respiration rate of 18 breaths per minute, a temperature of 37.2°C, a weight of 56 kg and a height of 1.62 m. Neurologic examination revealed an arouse patient, with psychomotor slowing. Pupils were equal and reactive. We found a bilateral and asymmetric hyperreflexia predominant on the left body side, bilateral Babinski sign, but the muscle strength was normal. The cardiac examination revealed a regular tachycardia without murmurs.

Urine analysis showed a high level of Δ;;-9-tétrahydroxycannabinol (Δ;;-9-THC), superior to 150 ng/ml. Full blood count, Erythrocyte Sedimentation Rate, C-reactive protein level, fasting blood sugar, serum urea and creatinin levels, liver function test, serum levels of sodium, potassium, calcium and magnesium, HIV and syphilis serologies were all normal. Cerebro-spinal fluid analysis was also normal.

An electrocardiogram was done and showed a sinus tachycardia with a heart rate of 102 beats per minute.

An electroencephalogram performed four days after the last seizure was normal.

A brain MRI on day six after the last seizure revealed on FLAIR images, focal hyperintensity of the right sub-cortico-frontal region (Figure 1) and right insular cortex (Figure 2), bilateral and symmetric hyperintensity of striatum (Figure 2). T2*images showed hypointensity of the right fronto-polar region (Figure 3). Brain MRI angiography did not reveal any vascular malformation.

Figure 1

Brain MRI showing focal hyperintensity of the right sub-cortico-frontal region on FLAIR image

Figure 2

Brain MRI showing bilateral and symmetric hyperintensity of striatum and hyperintensity of the right insular cortex on FLAIR image

Figure 3

Brain MRI showing hypointensity of the right fronto-polar region on T2*image

On admission, patient was boarded on carbamazepine: 200 mg bid, and clobazam: 5mg bid for two weeks. A psychiatric consultation was done for marijuana withdrawal. The patient was discharged after twenty days of admission with carmazepine 200mg bid. After three months of follow-up he did not present any epileptic seizure, and the pulse rate became normal.

Discussion

Our patient presented with late onset epileptic seizures associated with chronic marijuana use. The duration and frequency of marijuana smoking, the presence of tachycardia, diffuse hyperreflexia and psychomotor slowing are features of drug abuse. The detection of high level of Δ;;-9-THC in urine indicates marijuana smoking within the last couple of weeks. The asymmetric pattern of hyperreflexia can be attributed to the presence of focal brain lesions. The presence of cortical and subcortical hyperintensities around the right frontal lesion in the peri-ictal period could correspond to transient peri-ictal MRI abnormalities (TPMA). These abnormalities are located around epileptic foci during the peri-ictal period on MRI [6]. Canas and colleagues reported a clinical, electroencephalographic and TPMA concordance in 38.6% of cases [6]. Symmetric and bilateral striatum hyperintensity can be attributed to a toxic effect of marijuana, given the high sensitivity of basal ganglia to toxic and metabolic disturbances. A follow-up brain MRI could have permitted us to follow these abnormalities after marijuana withdrawal, but it was not performed due to economic reasons.

Questions concerning the mechanism of the right frontal lesion and its link with marijuana abuse are addressed. The sudden onset of symptoms is in favour of a vascular mechanism. The T2□;; hypointensity in this lesion suggests and old bleeding, either a spontaneous lobar haematoma or hemorrhagic transformation of an ischemic stroke. However, a traumatic brain injury cannot be formally ruled out, even if there is no clinical evidence of head trauma.

Rare cases of hemorrhagic and ischemic strokes attributed to acute use of high doses of marijuana have been described in the literature [7–8]. Chronic marijuana smoking is also considered as a cerebrovascular risk factor [9]. Stroke in marijuana abusers occurs mostly in young adults without other cardiovascular risk factors, who are not taking other drugs, and who have recently increased their use of marijuana [8]. The onset of symptoms during a period of high marijuana consumption, age, and the absence of other cardiovascular risk factors in this case, corresponds to the clinical characteristics of marijuana-induced stroke. The incriminated mechanism of marijuana induced stroke is a toxic cerebral angiopathy with vasospasm, associated with or without hypotension or hypertension [8–9].

Conclusion

In conclusion, marijuana abuse can lead to various brain abnormalities. We suggest that marijuana abuse, through a combination of vascular and toxic effects on brain could explain epilepsy and other neurological signs in this case. Marijuana should then be used with caution even for therapeutic purposes, given the risk of brain damage.

Competing interests

The authors declare no competing interest.

Authors’ contributions

All the authors contributed in drafting and reviewing the manuscript. All the authors have read and approved the final version of the manuscript.



Messenger: Nesta1 Sent: 1/25/2019 6:28:31 AM
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Oops. Here we go with semantic bickering again. Allow me to re-rephrase from "no....substantial toxicity" to "... extremely low relative toxicity". i know: "relative" to what? Relative to the range of known toxins considered by toxicologists.

i thought we agreed to be done with this silly toxicological debate?

It's just not possible to cause ganja to undergo a latter-day conversion, via scientific studies or journal articles, into some horrible, dangerous --even "substantially" toxic-- substance. There's simply too much history and common experiential knowledge to permit the propagation of such a misconception.

i (and my past years of abundant ganja use) am walking proof of "no substantial toxicity" based upon my definition and usage of the word "substantial". But i grant you that it's all in how you define the word.


Messenger: GARVEYS AFRICA Sent: 1/25/2019 6:39:35 AM
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I literally have pages of evidence in the form of large patient sample studies peer reviews meta reviews etc on the harmful effects of ganja. I have focused on cancer a few days ago and today on the brain. Next time maybe on the lungs.

Ganja is as if not more harmful overall than cigarettes.


Many many many people smoke cigarettes daily and heavily and have no cancer and need no inhaler. That doesn't prove anything. We are talking about relative risks. And one can't use a 1 person sample size to refute multiple issues of 20, 70, 100, 40000 based sample sized studies.

But yeah I don't want to get caught into semantics here. This thread is to SIMPLY talk about the u talked about and give the half that's is never told and never reviewed HONESTLY among ganja using Rastafari.

I will continue to post the evidence in this thread.

Give thankhs


Messenger: Nesta1 Sent: 1/25/2019 7:12:27 AM
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This is not really the forum to examine extremely ponderous toxicological considerations such as modality of exposures, mechanisms of toxicity, co-factors, describing & quantifying synergies, dose-response mechanism, yada, yada, yada.... Suffice to say that each individual case of substance exposure requires its own health assessment to be properly understood, and that toxicological risk information removed from the context of the variety of voluntary risks everyone submits to throughout the course of everyday life is relatively meaningless. i would never discourage anyone from smoking ganja on a sensible basis if they found it to be beneficial. Thankfully, exposure frequency, duration and dosing for a typical ganja smoker are rarely even close to comparable to those related to routine cigarette use for the majority of cigarette smokers.
As with anything we do, common sense and the risk/benefit trade-offs we make as humans must rule the day.


Messenger: GARVEYS AFRICA Sent: 1/25/2019 10:25:21 AM
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Rastafari


 Full text

One Minute of Marijuana Secondhand Smoke Exposure Substantially Impairs Vascular Endothelial Function.

Wang X, et al. J Am Heart Assoc. 2016.

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Abstract

BACKGROUND: Despite public awareness that tobacco secondhand smoke (SHS) is harmful, many people still assume that marijuana SHS is benign. Debates about whether smoke-free laws should include marijuana are becoming increasingly widespread as marijuana is legalized and the cannabis industry grows. Lack of evidence for marijuana SHS causing acute cardiovascular harm is frequently mistaken for evidence that it is harmless, despite chemical and physical similarity between marijuana and tobacco smoke. We investigated whether brief exposure to marijuana SHS causes acute vascular endothelial dysfunction.

METHODS AND RESULTS: We measured endothelial function as femoral artery flow-mediated dilation (FMD) in rats before and after exposure to marijuana SHS at levels similar to real-world tobacco SHS conditions. One minute of exposure to marijuana SHS impaired FMD to a comparable extent as impairment from equal concentrations of tobacco SHS, but recovery was considerably slower for marijuana. Exposure to marijuana SHS directly caused cannabinoid-independent vasodilation that subsided within 25 minutes, whereas FMD remained impaired for at least 90 minutes. Impairment occurred even when marijuana lacked cannabinoids and rolling paper was omitted. Endothelium-independent vasodilation by nitroglycerin administration was not impaired. FMD was not impaired by exposure to chamber air.

CONCLUSIONS: One minute of exposure to marijuana SHS substantially impairs endothelial function in rats for at least 90 minutes, considerably longer than comparable impairment by tobacco SHS. Impairment of FMD does not require cannabinoids, nicotine, or rolling paper smoke. Our findings in rats suggest that SHS can exert similar adverse cardiovascular effects regardless of whether it is from tobacco or marijuana












Altered striatal reward processing in abstinent dependent cannabis users: Social context matters.

Zimmermann K, et al. Eur Neuropsychopharmacol. 2019.

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Abstract

Public perception of cannabis as relatively harmless, alongside claimed medical benefits, have led to moves towards its legalization. Yet, long-term consequences of cannabis dependence, and whether they differ qualitatively from other drugs, are still poorly understood. A key feature of addictive drugs is that chronic use leads to adaptations in striatal reward processing, blunting responsivity to the substance itself and natural (non-drug) rewards. Against this background, the present study investigated whether cannabis dependence is associated with lasting alterations in behavioral and neural responses to social reward in 23 abstinent cannabis-dependent men and 24 matched non-using controls. In an interpersonal pleasant touch fMRI paradigm, participants were led to believe they were in physical closeness of or touched (CLOSE, TOUCH) by either a male or female experimenter (MALE, FEMALE), allowing contextual modulation of the perceived pleasantness and associated neural responses. Upon female compared to male touch, dependent cannabis users displayed a significantly attenuated increase of pleasantness experience compared to healthy controls. Controls responded to female as compared to male interaction with increased striatal activation whereas cannabis users displayed the opposite activation pattern, with stronger alterations being associated with a higher lifetime exposure to cannabis. Neural processing of pleasant touch in dependent cannabis users was found to be intact. These findings demonstrate that cannabis dependence is linked to blunted striatal processing of non-drug rewards and suggest that these alterations may contribute to social processing deficits.

Copyright © 2019 Elsevier B.V. and ECNP. All rights reserved.







Messenger: Nesta1 Sent: 1/25/2019 10:48:15 AM
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I see we're back to bombarding a group of non-epidemiologists, and non- toxicologists with impressive sounding esoteric studies that tell us very little unless we understand their complete contexts, methodologies, and limitations. This is a form of sensationalism which i think is beneath you, G.A.

I reiterate: "each individual case of substance exposure requires its own health assessment to be properly understood, and that toxicological risk information, if removed from the context of the variety of voluntary risks everyone submits to throughout the course of everyday life, is relatively meaningless." There are terribly scary sounding studies regarding motor vehicle exhaust emissions, yet, people from urban & suburban populations who've been exposed to exhaust constituents every day for their entire whole lives routinely live into the 80s. You wouldn't try to tell those people to stay away from driving on roads if they wanted to go somewhere, would you?

Here's a documentary by a group which was also concerned about the potential adverse effects of ganja. We found out later that some of their concerns may have been overstated.

https://www.youtube.com/watch?v=zhQlcMHhF3w

But seriously, it's really not terribly ethical to propagandize using the kind of material you are reproducing here without providing the other side of the equation: That most people who use ganja do not develop any chronic or fatal conditions from smoking it, the ratio of lethal dose to effective dose is quite large (virtually never attained through normal consumption), and it is still generally regarded as a relatively low toxicity substance as compared to say ethanol or a number of commonly prescribed pharmaceuticals.

Balance, I believe the concept of balance came up at one point. Let's strive to achieve that here. It benefits your own credibility while maintaining a scientifically accurate portrayal of overall risk in order communicate knowledge that facilitates informed (not paranoid) risk/benefit decision-making.


Messenger: The BANNED -- Hemphill Sent: 1/25/2019 12:13:51 PM
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Nesta1: "This is not really the forum to examine....."

Why is it that people, especially nesta1, continually say that this forum is not for this or that? What kind of mentality is that? Its like saying: "I am the supreme commander of this forum and I SAY your topic is NOT ALLOWED"... Wtf? Who does that? Its called free speech there bud.. (even though that is relative as I have been hit with banned topics and messages)
Bottom line is, Ras Tafari is reality. Therefore, anything and everything that happens should be discussed as a contributing factor to reality.. NOT 'ohh, that doesn't fit the group think, that makes me think outside of the echo chamber, that doesn't belong on this forum..' Thats a pretty pathetic approach. Really


Messenger: Eleazar Sent: 1/25/2019 12:19:27 PM
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Iman say Legalization to the Ganjah Herb you can take your alcohol and tobacco. For every anti-herb scientrickfikal study you post I could post 1,000 more for the death causing effects of tobacco and alcohol. Ganjah can be eaten for those that don't wish to smoke.


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