28 replies to this topic

[medievil]

Cannabinoids have therapeutic potential in a variaty of disorders, personally my adhd is resistant to stimulant treatment but i have read case reports of people that dont respond to them find relief with cannabis wich made me look into it more.

Available cannabinoids are:
Cannabis
AM2201
MAM2201
AKB48
UR-144
And more.

They all have differened affinity's for the cannabinoid receptors, ur-144 is a selective CB2 agonist, its been discussed more in debt in this thread:
http://www.longecity...ve-cb2-agonism/

Some evidence behind their therapeutic potential:

Treating depression with cannabinoids
Kurt Blass
Lindengasse 27/10, 1070 Vienna, Austria
Abstract
Although a variety of drugs are available for the treatment of depression, therapy is not effective in
all cases and finding alternative options is desirable. Results from animal studies, anecdotal experience reported by patients using cannabis and observations from clinical studies where cannabinoids were used in serious diseases suggest an anti-depressive potential of cannabinoid receptor agonists. From 2003 to 2006, 75 patients suffering from depression, stress and burnout syndrome were successfully treated in a practice for general medicine with the cannabis ingredient
dronabinol, alone or in combination with other antidepressants. Two case studies will be presented. The presented observations suggest that dronabinol has an antidepressive potential that can
readily be used in medical practice.
Key words: Depression, burnout, cannabinoid, cannabis, dronabinol

Case 1
Ms. H. came to my practice six years ago, at the age of
48. She had a long psychiatric record with episodes of
depression and the abuse of alcohol and drugs, particularly of benzodiazepines. A former teacher, she is now
retired but continues to work as an actress.
At the onset of the therapy the patient was in a difficult
situation. Her father had recently passed away; she was
highly depressed, sometimes even suicidal. Heavy
abuse of drugs, such as oxazepam, and of alcohol further complicated her situation. Following an extensive
discussion a treatment with oral dronabinol of 5 – 7.5
mg per day was started.
After 6 years of using dronabinol Ms. H. is now very
experienced with the use of the drug. Depending on her
symptoms, she takes between 2 and 4 capsules of 2.5
mg per day. She is no longer addicted to benzodiazepines and does currently not drink alcohol. As supplementary therapy she takes 2.5 mg per day of olanzapin
(an atypical neuroleptic), 25 mg of venlafaxin (an
SNRI) and, if needed, trazodon, SSRI. She reports that
the dronabinol therapy has improved her quality of life
significantly. She feels more stable than before and the
chronically reoccurring episodes of depression are less
severe. Her speed of reaction when operating a vehicle
is impaired. Before extended car trips she has thus
periodically suspended dronabinol for typically one
week, which has resulted in psychological withdrawal
symptoms.
Case 2
Ms. F. first visited our practice at the age of 22 where
she received treatment over a 12-month period. At that
time, the patient suffered from stress related headaches,
migraine, asthma, neurodermatitis and an instable emotional personal disorder. Most prominent was an acute
depressive syndrome, for which Ms. F. had already
received treatment in the psychiatric clinic at Vienna
General Hospital.After repeatedly dropping out of school and frequent
job changes the patient tried, despite a lack of family
contacts, to improve her dismal social and physical
conditions. She was also rather unhappy with her having to consume up to ten prescription medications. In
addition to anti-depressants, such as fluoxetine and
mianserin, neuroleptics, such as prothipendyl, sedatives
and anti-allergic agents, such as hydroxyzine, NSAR,
such as diclofenac, proton pump inhibitors, such as
rabeprazole, analgesics, such as propyphenazone and
tramadol, she daily consumed anti-asthmatics, such as
terbutaline sulfate as prescribed by several other physicians.
Because the patient did not want to continue this multidrug treatment she came to our practice in search for a
more simple and natural treatment, involving no more
than two drugs. Primary objective of the treatment was
to improve her acutely depressive condition, which had
not improved despite the use of multiple drugs. Following an extensive consultation the patient opted for a
monotherapy with dronabinol. After several days the
initial dose of 2.5 mg was raised to 7.5 mg daily. After
several days of treatment we observed a significant
improvement of her depressive condition and of the
concurrently occurring illnesses.
During the first month of therapy the daily dronabinol
dose was raised to 10 mg and 12 month after starting
her therapy the physical and psycho-social condition of
the patient had stabilized at that dose. Subsequently,
the patient resumed relationships with her family, relocated to a different state and left our practice.

http://www.letfreedomgrow.com/cmu/depression_2008_02_2.pdf

Cannabis improves symptoms of ADHD
Peter Strohbeck-Kuehner, Gisela Skopp, Rainer Mattern
Institute of Legal- and Traffic Medicine, Heidelberg University Medical Centre, Voss Str. 2, D-69115 Heidelberg, Germany
Abstract
Attention-deficit/hyperactivity disorder (ADHD) is characterized by attention deficits and an altered activation level. The purpose of this case investigation was to highlight that people with
ADHD can benefit in some cases from the consumption of THC. A 28-year old male, who showed
improper behaviour and appeared to be very maladjusted and inattentive while sober, appeared to
be completely inconspicuous while having a very high blood plasma level of delta-9-
tetrahydrocannabinol (THC). Performance tests, which were conducted with the test batteries
ART2020 and TAP provided sufficient and partly over-averaged results in driving related performance. Thus, it has to be considered, that in the case of ADHD, THC can have atypical effects
and can even lead to an enhanced driving related performance.

http://www.cannabis-med.org/english/journal/en_2008_01_1.pdf

Improvement in Refractory Obsessive Compulsive Disorder With Dronabinol

To the Editor: It has been reported that 40%–60% of patients with obsessive-compulsive disorder (OCD) do not respond to first-line treatment. Treatment options for these patients include switching to another agent or augmentation (1). We report on two patients with treatment-resistant OCD and comorbid axis I disorders who responded to an augmentation with the cannabinoid dronabinol.

“Mrs. L” was a 38-year-old woman who was admitted with recurrent major depression and OCD (Yale-Brown Obsessive Compulsive Scale score: 20) after outpatient treatment with paroxetine (60 mg) for 8 months and cognitive behavioral therapy (CBT) were not efficacious. Switching to clomipramine (300 mg) resulted in partial response after 12 weeks of treatment. Based on the patient’s report that smoking marijuana usually relieved her symptoms, an augmentation with dronabinol (2.5%; 10 mg t.i.d.) was started. The prior medication was continued. While undergoing treatment with dronabinol (2.5%), the patient’s OCD symptoms decreased significantly within 10 days (Yale-Brown Obsessive Compulsive Scale score: 10).

“Mr. K” was a 36-year-old man with schizophrenia and OCD who was admitted for deterioration of psychotic and obsessive symptoms (Yale-Brown Obsessive Compulsive Scale score: 23). During his course of illness, Mr. K had been treated with antipsychotics (including haloperidol, olanzapine, risperidone, quetiapine, and aripiprazole), both in monotherapy and in combination with selective serotonin reuptake inhibitors. His OCD symptoms in particular remained predominately treatment resistant. Treatment with clozapine (400 mg), which he had already received for more than 1 year (in combination with paroxetine [60 mg] for 13 weeks) resulted only in partial response of his psychotic and OCD symptoms. Switching paroxetine to clomipramine (for another 10 weeks), followed by an additional course of 18 electroconvulsive therapy treatments (right unilateral high dose), did not improve the patient’s psychotic or OCD symptoms significantly. After the addition of dronabinol to ongoing treatment with clomipramine (150 mg) and clozapine (400 mg), a significant reduction of OCD symptoms was observed within 2 weeks (Yale-Brown Obsessive Compulsive Scale score: 15). In order to prevent psychotic deterioration, dronabinol (2.5%) was carefully increased to 10 mg b.i.d.

Apart from anticholinergic symptoms that preceded the addition of dronabinol (patient 1: dry mouth, constipation; patient 2: constipation, hypotension), both patients reported no side effects. In particular, there was no deterioration of psychotic or mood disorder symptoms.

Based on data from case reports and small clinical trials suggesting that cannabinoids can reduce symptoms of tic disorder (2) and on findings from genetic studies linking tic disorder with OCD (3), we hypothesized that cannabinoids might also reduce OCD symptoms. Moreover, there is evidence suggesting that besides serotonergic and dopaminergic systems, glutamatergic hyperactivity is involved in the pathophysiology of OCD (4, 5). This view is supported by data suggesting the efficacy of glutamate modulating drugs, such as topiramate, memantine, riluzole, or N-acetylcysteine, in the treatment of OCD (6). It has been reported that cannabinoids inhibit glutamate release in the CNS (7, 8). Additionally, cannabinoid type 1 (CB₁) receptors are distributed abundantly in the striatum (8), a brain region frequently associated with OCD. Hence, it can be speculated that the anti-obsessive effect observed in our patients may have been a consequence of the glutamate modulation of the cannabinoid dronabinol. Since it is well known that cannabinoids may trigger psychotic symptoms in patients with schizophrenia (8), caution is warranted when prescribing for patients with a history of the disorder.
1.Kaplan A, Hollander E: A review of pharmacologic treatments for obsessive-compulsive disorder. Psychiatr Serv 2003; 54:1111–11182.Müller-Vahl KR, Schneider U, Prevedel H, Theloe K, Kolbe H, Daldrup T, Emrich HM: Delta-9-tetrahydrocannabinol (THC) is effective in the treatment of tics in Tourette syndrome: a 6-week randomized trial. J Clin Psychiatry 2003; 64:459–4653.Shavitt RG, Hounie AG, Rosário Campos MC, Miguel EC: Tourette’s syndrome. Psychiatr Clin North Am 2006; 29:471–4864.Arnold PD, Sicard T, Burroughs E, Richter MA, Kennedy JL: Glutamate-transporter gene SLC1A1 associated with obsessive-compulsive disorder. Arch Gen Psychiatry 2006; 63:769–7765.Chakrabarty K, Bhattacharyya S, Christopher R, Khanna S: Glutamatergic dysfunction in OCD. Neuropsychopharmacology 2005; 30:1735–17406.Pittenger C, Krystal JH, Coric V: Glutamate-modulating drugs as novel pharmacotherapeutic agents in the treatment of obsessive-compulsive disorder. NeuroRx 2006; 3:69–817.Fujiwara M, Egashira N: New perspectives in the studies on endocannabinoid and cannabis: abnormal behaviors associate with CB1-receptor and development of therapeutic application. J Pharmacol Sci 2004; 96:363–3668.Pacher P, Bátkai S, Kunos G: The endocannabinoid system as an emerging target of pharmacotherapy. Pharmacol Rev 2006; 58:389–462

I just tried some ur-144 may have been to much as it gave me a potent stoned feeling, was lying down needing to pee urgently for an hour as i was to lazy to get up, def wasnt therapeutic, also didnt seem recreational to me it just pasted me to the floor.

[medievil]

Just ingested the most miniscule dose of AKB48 possible, little speck then licked a cod liver oil capsule and put it on there, this oral method worked for ur144.

CB1 agonism is what makes it therapeutic for ADHD so well see what it does.

[medievil]

I just realised i can focus better and my mind isnt as scattered, the effect is mild tough but i did underdose and could be placebo, will keep testing, looks like my adhd may respond to cannabinoids instead of stims like some others perhaps, well see

[medievil]

Seems like they can help alzheimer too, especially CB2 agonists, also i propose them to be usefull for autoimume and inflammatory disorders.

[kevinseven11]

Very interesting, these cannabinoids are legal you say?

[medievil]

not in the USA, they made everything illegal with the analogue act in throw ppl in jail for more then 2 months if you sell harddrugs, they see it as a extreme criminal act.

[kevinseven11]

http://www.ncbi.nlm....les/PMC2882689/
This study is interesting
The us will change thier position soon becuase look at colorado and washington!

[medievil]

Oh yeah california i read about, docs prescribing cards for ADHD and other disorders, beyond excellent for a country like the US, i lived in belguim were we could just take the train to holland to buy it legally in the shops in the city's there, there's its completely legal.

[medievil]

CBD is a strong antipsychotic and cb1 and 2 antagonist, rimonabant has antipsychotic activity too but can induce depression, i wonder wheter adding in a CB2 agonist, (wich also is antipsychotic and causes simular moodlift) dramatically potentiates this wile abolishing the side effects, cbd is as effective as amisulpiride, this combo may be extremely interesting, also for anxiety and other things (pure CB1 agonism as with selective synthetics induces paranoia and anxiety quite easily in overdose.

Also i wonder wheter low dose rimonabant with a synthetic makes something superior to weed by far (full agonism by synthetics compared to 50% of weed) CB2 is left open and as reported by that guy in the other thread the addition of a low dose abolishes tolerance, theoretically simular to weed with CBD.

Endogenious cannabinoids block LTP, while other things in the brain potentiates it wich clearly shows that the addition of something can easily reverse its negative effects.

"Curr Pharm Des. 2012;18(32):5045-54.
Neural mechanisms for the cannabinoid modulation of cognition and affect in man: a critical review of neuroimaging studies.
Bhattacharyya S, Atakan Z, Martin-Santos R, Crippa JA, McGuire PK.
Source
Department of Psychosis Studies & Psychosis Clinical Academic Group, King's College London, Institute of Psychiatry, 6th Floor, Main Building, PO Box 067, De Crespigny Park, SE5 8AF, London, UK. sagnik.2.bhattacharyya@kcl.ac.uk.
Abstract
Pharmacological challenge in conjunction with neuroimaging techniques has been employed for over two decades now to understand the neural basis of the cognitive, emotional and symptomatic effects of the main ingredients of cannabis, the most widely used illicit drug in the world. This selective critical review focuses on the human neuroimaging studies investigating the effects of delta-9- tetrahydrocannabinol (THC) and cannabidiol (CBD), the two main cannabinoids of interest present in the extract of the cannabis plant. These studies suggest that consistent with the polymorphic and heterogeneous nature of the effects of cannabis, THC and CBD have distinct and often opposing effects on widely distributed neural networks that include medial temporal and prefrontal cortex and striatum, brain regions that are rich in cannabinoid receptors and implicated in the pathophysiology of psychosis. They help elucidate the neurocognitive mechanisms underlying the acute induction of psychotic symptoms by cannabis and provide mechanistic understanding underlying the potential role of CBD as an anxiolytic and antipsychotic. Although there are ethical and methodological caveats, pharmacological neuroimaging studies such as those reviewed here may not only help model different aspects of the psychopathology of mental disorders such as schizophrenia and offer insights into their underlying mechanisms, but may suggest potentially new therapeutic targets for drug discovery."

Full text please!!!

"Prog Neuropsychopharmacol Biol Psychiatry. 2012 Jul 2;38(1):36-50. Epub 2012 Jan 20.
Interactions between the cannabinoid and dopaminergic systems: evidence from animal studies.
El Khoury MA, Gorgievski V, Moutsimilli L, Giros B, Tzavara ET.
Source
Institut National de la Santé et de la Recherche Médicale (INSERM) UMRS-952, Université Pierre et Marie Curie, 9 quai St Bernard, 75005 Paris, France.
Abstract
There is a prominent role of the cannabinoid system to control basal ganglia function, in respect to reward, psychomotor function and motor control. Cannabinoid dysregulations might have a pathogenetic role in dopamine- and basal ganglia related neuropsychiatric disorders, such as drug addiction, psychosis, Parkinson's disease and Huntington's disease. This review highlights interactions between cannabinoids, and dopamine, to modulate neurotransmitter release and synaptic plasticity in the context of drug addiction, psychosis and cognition. Modulating endocannabinoid function, as a plasticity based therapeutic strategy, in the above pathologies with particular focus on cannabinoid receptor type 1 (CB1 receptor) antagonists/inverse agonists, is discussed. On the basis of the existing literature and of new experimental evidence presented here, CB1 receptor antagonists might be beneficial in disease states associated with hedonic dysregulation, and with cognitive dysfunction in particular in the context of psychosis. It is suggested that this effects might be mediated via a hyperglutamatergic state through metabotropic glutamate activation. Indications for endocannabinoid catabolism inhibitors in psychiatric disorders, that might be CB1 receptor independent and might involve TRPV1 receptors, are also discussed."

This too

If anyone has full text acces please pm so i can request full texts and post my findings here.

[medievil]

Thx for full texts!

Got alot more good shit to post:)

As discussed above, CB1 agonists dose dependently modulate hippocampal
ACh release bidirectionally, in a DA dependent manner.
Only the D2 mediated ACh suppressant effect of the high dose has
been associated with memory impairment (Nava et al., 2000). Inversely,
low cannabinoid doses mobilize D1-mediated responses, in
the septo-hippocampal pathway, that are rather pro-cognitive than
detrimental to learning and memory (Hersi et al. 1995). Thus, memory
deficits induced by high cannabinoid doses could be attributed
to a detrimental overactivation of hippocampal D2 receptors through
massive CB1R occupancy, which disrupts the spatiotemporal specificity
of endocannabinoid-mediated fine-tuning of synaptic plasticity, as
proposed previously (Carlsson et al., 2002)

[Cephalon]

Hey Medi

Didn't expect you to jump an the jwh train, thought your point on cannabinoids was clear.
How are you getting along with your research?
I have tried AM2201 and while it feels prety similar to weed I don't see a reason to use it other then saving some bucks. Weed having the more favourable sideeffect profile is my first choice though.
RC's cannabinoids are supposed to cause some nasty withdrawl

[medievil]

Ive got the canabinoid blend sonic boom, haha just like the blends more then in powder form its easy to take.

 

I have no acces to marihuana in the UK, id like to try it as its only a partional agonist and has cananbidiol so its most likely differened, i used to smoke it when i was younger tough.

 

I take propranol, it prevents the cognitive side effects.

[medievil]

Hey Medi

Didn't expect you to jump an the jwh train, thought your point on cannabinoids was clear.
How are you getting along with your research?
I have tried AM2201 and while it feels prety similar to weed I don't see a reason to use it other then saving some bucks. Weed having the more favourable sideeffect profile is my first choice though.
RC's cannabinoids are supposed to cause some nasty withdrawl

My response is entirely differened since i recovered from what a beleive predromal shizoprenia, i never could tolerate it but i feel far better then i did my whole life, as a kid i allways had the tought crossing ppl can read my mind, bot that i really beleived that, thats typical of shizoprenia haha.

 

Anyway benzos work for me now too.

 

Either way i have to take it with promathiazine and klonopin dunno why bit without prom its unpleasant, nothing like the paranoia, without the high effects i used to get from it.

[gamesguru]

I wonder if some of these synthetics may be far more damaging than natural cannabis. Too many apparently healthy people who seem able to handle cannabis for years at a time, are being handled by synthetics and complaining of danger: long lasting mood disturbances and disorganized thinking, some erosion of the intelligence and personality are some of the outwardly visible symptoms.

[medievil]

Have you got links to reports of that? i dont think that occurs for the majority but would like to read some anecdotes.

[gamesguru]

Try searching "am 2201 overdose" or "am 2201 damage", you'll see many scary reports. And as for the clinical evidence: there's not much. But I liken some of these drugs to MDMA or DOx amphetamines, both rather damaging to the brain. Anyone who says they are relatively harmless needs to re-evaluate their sense of drug harm. Even less toxic/harmful drugs, cannabis and LSD, contribute to mental illness, I know they have made me more anxious/neurotic and paranoid/delusional, and during periods of heavier abuse, they have contributed to emotional and intellectual destabilization.

[medievil]

Cannabidioids can cause shizoprenia to come out sooner because of increases in endogenious cannabidiods and CB1 upregulation if im correct that doesnt mean its neurotoxic but the adaptive changes can indeed contribute to mental illness.

 

With LSD its i think the induction of psychosis i beleive wich is why it contributes to mental illness, however daily low doses of lsd, doses that arent psychedelic at all, are very therapeutic for many ppl.

 

I cant look it up my laptop broke (why i disapeared) and those sites are blocked in the library.

am 2201 is auite horrendous, ppl reporting problems dont have issues with other cannabinoids as an aside i dont rule it out tough but it doesnt represent other cannabinoids for the most part.

[gamesguru]

In at least one way, cannabis is harmful to more of the population than just schizophrenics (http://www.ncbi.nlm....pubmed/22385967). Obviously, there is short-term damage to the memory. The question research has yet to answer is whether prolonged abuse might lead to permanent damage or lingering effects...my opinion is that it likely will.

[Reformed-Redan]

Use cannabis that has higher CBD ratio. Preferably no THC. Check ACDC strain or Valentine X.

[medievil]

Poly drug use is associated with cognitive decline, when controlling cannabis mdma didnt cause cognitive long term side effects anymore.

 

Its still with regards to polydrug use but your right caution is advicedm that said cannabinoids are highly therapeutic for some ppl with ADHD, for them it doesnt appear to inhibit cognition read the abstract in the first post.

Use cannabis that has higher CBD ratio. Preferably no THC. Check ACDC strain or Valentine X.

It sucks being stuck on that stupid island called the uk, cant take the train to holland to buy weed in the coffeeshop haha.

[gamesguru]

Poly drug use is associated with cognitive decline, when controlling cannabis mdma didnt cause cognitive long term side effects anymore.

 

Its still with regards to polydrug use but your right caution is advicedm that said cannabinoids are highly therapeutic for some ppl with ADHD, for them it doesnt appear to inhibit cognition read the abstract in the first post.

Please, link me to your study showing that mdma alone is not damaging, only mdma+thc is damaging. The studies I have read seem to suggest the opposite conclusion (see reference). I wonder if other drugs could be damaging on their own, without cannabis, alcohol, etc. I suspect many drugs are very damaging. I wish there were more pure groups and less poly drug users, then we could better profile individual drugs.

 

As for the ADD, I was diagnosed with it during high school, and while I've done well in college and at my job as a daily stoner, it definitely still takes a toll. I'm curious why biochemically it might impair ADD patients' memory/cognition less than healthy people.

Circumstantial evidence correlating total lifetime dose of MDMA with cognitive measures does imply that MDMA is more likely to be the culprit than interaction with cannabis, but in the absence of evidence from pure groups this cannot be known for certain.

→ source (external link)

[medievil]

Ive been experimenting with various cannabinoid blends, the current blend doesnt feel as recreational but is anti anxiety, relaxing and kinda feels like a benzo, much to a CB2 selective compound i tried in the past, it must be more selective for this receptor.

 

I feel both rimonabant and cannabinoids have use when both used depending on the ocasion, rimos half life is too long to really switch around tough.

I gues it would be anxiolytic, antipsychotic, anti "relationship paranoia", psychosis, nootropic.

Ill elaborate when i have time dasheenster.

[medievil]

"personally my adhd is resistant to stimulant treatment"

 

I have found the solution for this, it werent cannabinoids i cant really reveal it but id send the stuff in capsules to volenteers with simular issues and document their experiences.

[medievil]

Cannabinoids are powerfull aphrodisiacs in my experience and provide comparable vasodilation to viagra IME.

[medievil]

Cannabis: Potent Anti-depressant In Low Doses, Worsens Depression At High Doses

A new neurobiological study has found that a synthetic form of THC, the active ingredient in cannabis, is an effective anti-depressant at low doses. However, at higher doses, the effect reverses itself and can actually worsen depression and other psychiatric conditions like psychosis.


It has been known for many years that depletion of the neurotransmitter serotonin in the brain leads to depression, so SSRI-class anti-depressants like Prozac and Celexa work by enhancing the available concentration of serotonin in the brain. However, this study offers the first evidence that cannabis can also increase serotonin, at least at lower doses.
Laboratory animals were injected with the synthetic cannabinoid WIN55,212-2 and then tested with the Forced Swim test -- a test to measure "depression" in animals; the researchers observed an antidepressant effect of cannabinoids paralleled by an increased activity in the neurons that produce serotonin. However, increasing the cannabinoid dose beyond a set point completely undid the benefits, said Dr. Gabriella Gobbi of McGill University.
"Low doses had a potent anti-depressant effect, but when we increased the dose, the serotonin in the rats' brains actually dropped below the level of those in the control group. So we actually demonstrated a double effect: At low doses it increases serotonin, but at higher doses the effect is devastating, completely reversed."
The anti-depressant and intoxicating effects of cannabis are due to its chemical similarity to natural substances in the brain known as "endo-cannabinoids," which are released under conditions of high stress or pain, explained Dr. Gobbi. They interact with the brain through structures called cannabinoid CB1 receptors. This study demonstrates for the first time that these receptors have a direct effect on the cells producing serotonin, which is a neurotransmitter that regulates the mood.
Dr. Gobbi and her colleagues were prompted to explore cannabis' potential as an anti-depressant through anecdotal clinical evidence, she said. "As a psychiatrist, I noticed that several of my patients suffering from depression used to smoke cannabis. And in the scientific literature, we had some evidence that people treated with cannabis for multiple sclerosis or AIDS showed a big improvement in mood disorders. But there were no laboratory studies demonstrating the anti-depressant mechanism of action of cannabis."
Because controlling the dosage of natural cannabis is difficult -- particularly when it is smoked in the form of marijuana joints -- there are perils associated with using it directly as an anti-depressant.
"Excessive cannabis use in people with depression poses high risk of psychosis," said Dr. Gobbi. Instead, she and her colleagues are focusing their research on a new class of drugs which enhance the effects of the brain's natural endo-cannabinoids.
"We know that it's entirely possible to produce drugs which will enhance endo-cannabinoids for the treatment of pain, depression and anxiety," she said.
The study, published in the October 24 issue of The Journal of Neuroscience, was led by Dr. Gabriella Gobbi of McGill University and Le Centre de Recherche Fernand Seguin of Hôpital Louis-H. Lafontaine, affiliated with l'Université de Montréal. First author is Dr. Gobbi's McGill PhD student Francis Bambico, along with Noam Katz and the late Dr. Guy Debonnel* of McGill's Department of Psychiatry.

[medievil]

Neural Plast. 2016;2016:9364091. doi: 10.1155/2016/9364091. Epub 2016 Jan 12.
The Endocannabinoid System as a Therapeutic Target in Glaucoma.
Cairns EA1, Baldridge WH2, Kelly ME3.
Author information

Abstract
Glaucoma is an irreversible blinding eye disease which produces progressive retinal ganglion cell (RGC) loss. Intraocular pressure (IOP) is currently the only modifiable risk factor, and lowering IOP results in reduced risk of progression of the disorder. The endocannabinoid system (ECS) has attracted considerable attention as a potential target for the treatment of glaucoma, largely due to the observed IOP lowering effects seen after administration of exogenous cannabinoids. However, recent evidence has suggested that modulation of the ECS may also be neuroprotective. This paper will review the use of cannabinoids in glaucoma, presenting pertinent information regarding the pathophysiology of glaucoma and how alterations in cannabinoid signalling may contribute to glaucoma pathology. Additionally, the mechanisms and potential for the use of cannabinoidsand other novel agents that target the endocannabinoid system in the treatment of glaucoma will be discussed.
ote


Que
Endogenous and Synthetic Cannabinoids as Therapeutics in Retinal Disease.
Kokona D1, Georgiou PC2, Kounenidakis M2, Kiagiadaki F2, Thermos K2.
Author information

Abstract
The functional significance of cannabinoids in ocular physiology and disease has been reported some decades ago. In the early 1970s, subjects who smoked Cannabis sativa developed lower intraocular pressure (IOP). This led to the isolation of phytocannabinoids from this plant and the study of their therapeutic effects in glaucoma. The main treatment of this disease to date involves the administration of drugs mediating either the decrease of aqueous humour synthesis or the increase of its outflow and thus reduces IOP. However, the reduction of IOP is not sufficient to prevent visual field loss. Retinal diseases, such as glaucoma and diabetic retinopathy, have been defined as neurodegenerative diseases and characterized by ischemia-induced excitotoxicity and loss of retinal neurons. Therefore, new therapeutic strategies must be applied in order to target retinal cell death, reduction of visual acuity, and blindness. The aim of the present review is to address the neuroprotective and therapeutic potential of cannabinoids in retinal disease.
PMID:

26881135

[Pub
Que
Front Neurol. 2016 Jan 28;7:5. doi: 10.3389/fneur.2016.00005. eCollection 2016.
Microglial Cells as a Link between Cannabinoids and the Immune Hypothesis of Psychiatric Disorders.
Lisboa SF1, Gomes FV2, Guimaraes FS1, Campos AC1.
Author information

Abstract
Psychiatric disorders are one of the leading causes of disability worldwide. Although several therapeutic options are available, the exact mechanisms responsible for the genesis of these disorders remain to be fully elucidated. In the last decade, a body of evidence has supported the involvement of the immune system in the pathophysiology of these conditions. Microglial cells play a significant role in maintaining brain homeostasis and surveillance. Dysregulation of microglial functions has been associated with several psychiatric conditions. Cannabinoids regulate the brain-immune axis and inhibit microglial cell activation. Here, we summarized evidence supporting the hypothesis that microglial cells could be a target for cannabinoid influence on psychiatric disorders, such as anxiety, depression, schizophrenia, and stress-related disorders.
some more info

[medievil]

Try searching "am 2201 overdose" or "am 2201 damage", you'll see many scary reports. And as for the clinical evidence: there's not much. But I liken some of these drugs to MDMA or DOx amphetamines, both rather damaging to the brain. Anyone who says they are relatively harmless needs to re-evaluate their sense of drug harm. Even less toxic/harmful drugs, cannabis and LSD, contribute to mental illness, I know they have made me more anxious/neurotic and paranoid/delusional, and during periods of heavier abuse, they have contributed to emotional and intellectual destabilization.

Thank you for report on the negative effects you experienced, we need to be very objective on this subject, also posting the potential risks, that said 30% of the youth smokes cannabis and most of them are fine.

 

AM 2201 is extremely strong with a dose of 1mg, i think that a massive overdose of any drug can cause severe effects and possible long term damage.

 

Also long term negative effects doesnt really mean damage, for example prozac permanenty changes serotonin firing in the brain, this is a adaptive change, which can occur as everything has downstream effects, i need to study cannabinoids more and find out exactly how they act on the brain, they have a very complex mechanism of action.

 

I allways tought that ppl having long term issues, this is supported by some evidence have mental issues that have appeared yet or not but would appear some time anyway such as shizophrenia, have you got any mental issues?

[gamesguru]

damage i take as persistent dysfunction; a wound time won't heal, worse than scar tissue.

i've got a lot of mental issues, but some of my symptoms can't be explained by existing factors.

to name a few: slightly impaired memory, speech, and imagination.  the more i examine myself, the more i find it impossible to deny street drugs have cumulative and erosive effects on the rational faculties.

Edited by gamesguru, 28 February 2016 - 11:37 PM.

[medievil]

I beleive that mdma only causes noticeble issues when you only use that, which i did in the past i heavily abused mdma without anything else no alcohol or weed, when studies controlled cannabis use the long term effects of mdma werent found, that said it definatly does induce small structural changes in the brain.

 

This is only true for healthy ppl, after i triggered shizo i developped forum anxiety after taking mdma once, i basicly feel anxious logging in fora and posting which is why i barely posted for ages, one of the reasons