28 replies to this topic

[Derin105]

Hey guys, Haven't posted for awhile.

 

Basically I abused marijuana for over a year. When I Quit, for about 6 weeks straight I had crippling anxiety/depression/ocd Thoughts. This was over a year ago.

 

To this day I Still feel sort of an empty feeling inside, Like I walk around and I'm not really connected with myself or my environment.

 

It is very hard to enjoy things. I feel almost robotic in nature with very little positive emotion or positive mood.

 

I have been tried on several antidepressants (SSRI) with no success including Wellbutrin

 

Here is what I have noticed:

 

Any Choline source causes me very bad depressive symptoms. I took Aniracetam at 400mg and it made me extremely robotic and mood was worse.

 

CDP Choline Makes me worse, even at 250mg.

 

Tried Deprenyl at low Doses (2.5mg-5mg).  Made me very robotic.

 

Tried Tianeptine for several weeks, all it did was flatten my mood and caused my orgasms to be weak as Shi*

 

Also, for about 8 months now I've had a very high pitched but low volume ringing in my right ear only, Its constant 24/7.

 

 

I am very healthy, Hormones are in range. I eat very well and exercise 5-6 times a week doing Aerobic exercise. Physical exercise makes me feel worse as well, I don't know how this is possible at all (Acetylcholine release?)

 

How I would describe my current situation is this sort of feeling of dread, Like I cant relax ever, I Physically look around at my environment and it literally looks shitty/no color or enjoyment.... I'm also never ever tired no matter how much I work out, or study, or do physical activity, Yet I still fall asleep if I Try.

But the sleep is never deep.

 

 

I'm at a complete dead end in what to do next.

 

What I'm assuming is an issue with Glutamate excitotoxicity/Low Gaba. Mixed with a High Acetylcholine level. Its probably not as simple as I put it.

 

Again, Just an assumption.

 

Does anyone have any ideas or opinions to throw in? Any are appreciated

 

 

 

Edited by Derin105, 01 October 2015 - 04:33 AM.

[gamesguru]

Yes, yes, the issue is desensitized glutamate autoreceptors and hypersensitive gaba autoreceptors.  Not sure acetylcholine has been elevated or reduced long-term.  I'm leaning toward a decrease, in which case, Bacopa would be helpful.  In addition to acetylcholine, it also boosts^[1] dopamine, serotonin, and GABA (which all three tend to be anxiolytic), while decreasing glutamate^[2] and norepinephrine^[3] (which both contribute to anxiety).

 

For example, curcumin, which inhibits glutamate release^{[4], [5], [6]}, may help resensitize glutamate autoreceptors, thereby negatively modulating release, and finally affecting an upregulation on the post-synatpic receptors and restoring the system to the desired balance.

 

As well, though GABA agonists or releasing agents are condemned on the grounds of receptor downregulation, they also have a use in autoreceptor downregulation, which is precisely the problem seeming to afflict you.

Theanine, picamilon, perhaps taurine, ashwagandha, valerian, kava, and more may have some utility in this case.

Edited by gamesguru, 01 October 2015 - 02:41 PM.

[Derin105]

Thanks for the response! What dosage curcumin and for how long? Do you recommend combining bacopa and curcumin? I've heard some interesting things about NAC as well

Yes, yes, the issue is desensitized glutamate autoreceptors and hypersensitive gaba autoreceptors. Not sure acetylcholine has been elevated or reduced long-term. I'm leaning toward a decrease, in which case, Bacopa would be helpful. In addition to acetylcholine, it also boosts^[1] dopamine, serotonin, and GABA (which all three tend to be anxiolytic), while decreasing glutamate^[2] and norepinephrine^[3] (which both contribute to anxiety).

For example, curcumin, which inhibits glutamate release^{[4], [5], [6]}, may help resensitize glutamate autoreceptors, thereby negatively modulating release, and finally affecting an upregulation on the post-synatpic receptors and restoring the system to the desired balance.

As well, though GABA agonists or releasing agents are condemned on the grounds of receptor downregulation, they also have a use in autoreceptor downregulation, which is precisely the problem seeming to afflict you.
Theanine, picamilon, perhaps taurine, ashwagandha, valerian, kava, and more may have some utility in this case.

[gamesguru]

They combine well, but watch out for gastrointestinal side effects and perhaps stimulation/insomnia.  Gradually taper the dosage up to minimize these.

I do nearly but not quite a ¼ tsp, with a little less ground black pepper to boot, perhaps ⅙ or ⅛ tsp.

Bacopa, 300mg 45%

 

NAC is more for hypoglutamatergic states^[1], but if the problem is a upregulated autoreceptors and reduced transmission, it may also help downregulate those and restore normal activity/transmission.

Hypothesis: is infantile autism a hypoglutamatergic disorder? Relevance of glutamate - serotonin interactions for pharmacotherapy.
N-acetylcysteine for treatment of autism, a case report
--------------------------------------------------------------------------------------------------------------------------------------------------------------------------
[Hypoglutamatergic hypothesis of schizophrenia: evidence from genetic studies].
N-acetylcysteine in psychiatry: current therapeutic evidence and potential mechanisms of action
N-Acetyl Cysteine as a Glutathione Precursor for Schizophrenia—A Double-Blind, Randomized, Placebo-Controlled Trial
NAC amino acid offers a potential therapeutic alternative in psychiatric disorders

[sthira]

Why not continue marijuana, but moderately? Marijuana is a solid medicine, and it's harmless in moderation, like coffee or chocolate or red wine or broccoli sprouts. And it's dose dependent just like any other medicine. Maybe respectfully approach your pot behavior this time with wisdom gained? For example, view it as less of a wild party sensation, and more as a healthy addition to your life? Respect and moderation are key.

[gamesguru]

One thing I noticed about Cannabis: if i go a day or two without, the effects aren't as pleasurable or relaxing, they are overwhelmingly anxious and intense.

And even so, even so it was unpleasant, then I am just as tempted to toke up the following morning as if I had been chiefing 24/7 for the last year.

I definitely have an addictive personality or tendencies to impulsive and reckless behavior (I took 80 LSD trips in 6 months: case, point, set and match).

 

And what if it has the effect of elevating baseline anxiety, or making you anxious, then what, is it not wise to fully abstain or keep it very infrequent?

[Derin105]

I can't smoke anymore, even a half of one hit sends me into panic, I don't understand it.... I'm more looking to just get back to my baseline self, without the war ringinging and constant worry
Also am now confused on the whole up regulation not enough transmission for glutamate? I would assume that glutamate is predominant over gaba causing the ear ringing so then which would work better curcumin or NAC?

[gamesguru]

Probably you had anxiety or depression prior to the PTSD, as this greatly increases susceptibility or predisposition.

It is confusing.  I have to take a second every time I think of the subject, though I also have a mild dyslexia. 

 

THC inhibits GABA release, which induces autoreceptor upregulation.  It enhances glutamate release^{[1], [2]}, which induces autoreceptor downregulation.

Upregulated autoreceptors ⇒ diminished neurotransmitter release ⇒ receptors try to compensate reduced activity via postsynaptic upregulation [this is thought of as a superior or stable equilibrium, hyperGABAergic]

Downreglated autoreceptors ⇒ enhanced neurotransmitter release ⇒ receptors try to compensate increased activity via postsynaptic downregulation [this is thought of as an inferior or unstable equilibrium, hypoGlutamatergic]

 

That is to suggest: THC induces favorable changes to GABA pathways, and unfavorable changes to glutamate pathways.  So THC decreases glutamate activity and increases GABA activity, which of its own accord, further decreases glutamate activity.  Need I remind you of the hypoglutamatergic hypothesis of schizophrenia^[2]?

Especially autoreceptors tend to be stubborn at renormalizing and tend to need an agonist or antagonist to induce timely (otherwise you could wait forever for this thing that would never happen) down- or upregulation. 

So I think your problem is mostly downregulated glutamate autoreceptors.  Green tea would actually be bad long-term, cause of inducing 4-AP dependent glutamate release.  Curcumin would be a choice, but I feel there is something more specific and potent which is slipping my mind.

Maybe upregulate GABA(B) autoreceptors with antagonists? [well you may say THC inhibits GABA and this is favorable long-term, but yes...  for this purpose, find something which does not also release too much glutamate!]  But this is getting kind of far-fetched, even by my standards...

Pre-synaptic GABA(B) receptors inhibit glutamate release through GIRK channels in rat cerebral cortex.

Neuronal G protein-gated inwardly rectifying potassium (GIRK) channels mediate the slow inhibitory effects of many neurotransmitters post-synaptically. However, no evidence exists that supports that GIRK channels play any role in the inhibition of glutamate release by GABA(B) receptors. In this study, we show for the first time that GABA(B) receptors operate through two mechanisms in nerve terminals from the cerebral cortex. As shown previously, GABA(B) receptors reduces glutamate release and the Ca(2+) influx mediated by N-type Ca(2+) channels in a mode insensitive to the GIRK channel blocker tertiapin-Q and consistent with direct inhibition of this voltage-gated Ca(2+) channel. However, by means of weak stimulation protocols, we reveal that GABA(B) receptors also reduce glutamate release mediated by P/Q-type Ca(2+) channels, and that these responses are reversed by the GIRK channel blocker tertiapin-Q. Consistent with the functional interaction between GABA(B) receptors and GIRK channels at nerve terminals we demonstrate by immunogold electron immunohistochemistry that pre-synaptic boutons of asymmetric synapses co-express GABA(B) receptors and GIRK channels, thus suggesting that the functional interaction of these two proteins, found at the post-synaptic level, also occurs at glutamatergic nerve terminals.

 

An ‘exciting’ spin on cannabinoid signalling

It has long been appreciated that cannabinoid administration alters cognitive functioning, including learning and memory. These effects are thought to arise, at least in part, from alterations in synchronous activity in the cortex and hippocampus. The synaptic mechanisms underlying these effects, however, have not been clearly delineated. In recent years, the endogenous cannabinoid system has emerged as a powerful mechanism for regulating the release of neurotransmitter from presynaptic terminals (reviewed in Kano et al. 2009). The type 1 cannabinoid (CB1) receptor, which may be the most highly expressed G protein-coupled receptor in the brain, is found throughout the neuraxis, with particularly high levels in the hippocampus, neocortex, cerebellum and basal ganglia. At the subcellular level, the CB1 receptor is predominantly found in presynaptic terminals. Initial localization studies focused on the high levels of CB1 expression in a subset of GABAergic interneurons that co-express the peptide cholecystokinin (CCK). Recent studies have revealed that CB1 receptors are also expressed widely in glutamatergic terminals, as well as in some cholinergic, noradrenergic, and serotonergic terminals. In fact, CB1 receptor-mediated regulation of glutamate release, rather than GABA release, plays a central role in mediating the classic tetrad of behavioural and physiological responses to systemic cannabinoid administration (Monory et al. 2007). Endocannabinoid signalling is involved in a diverse range of physiological as well as pathophysiological processes, and identifying the underlying synaptic mechanisms and the relevant neuronal populations is important for the development of novel therapeutic strategies targeting the endocannabinoid system.

Edited by gamesguru, 01 October 2015 - 10:15 PM.

[Derin105]

I Definately did have issues before, a few years back I had pure ocd obsessive thoughts that I was gay, but I knew I wasn't, but had recurrent intrusive thoughts about it.

When I quit weed I was hyper vigilant, severely depressed and had constanttttttt intrusive thoughts of all types, these thoughts have dumbed down but what remains if this feeling of nothing I do or try gives me any comfort.

For example, I go to school and am like ok shit this is really stessful and for no particular reason. Now when school is over, you'd think ok I'm gonna go home, relax, but this doesn't happen for me, I am absolutely not satisfied with anything and it's horrible.

Sorry I should have clarified in more detail


Could the tinnitus be a seratonin issue? I have tried l tryptophan and at 500mg on an empty stomach I feel like my mind goes numb and my whole body doesn't want to move. It really doesn't help..

Probably you had anxiety or depression prior to the PTSD, as this greatly increases susceptibility or predisposition.
It is confusing. I have to take a second every time I think of the subject, though I also have a mild dyslexia.

THC inhibits GABA release, which induces autoreceptor upregulation. It enhances glutamate release^{[1], [2]}, which induces autoreceptor downregulation.
Upregulated autoreceptors ⇒ diminished neurotransmitter release ⇒ receptors try to compensate reduced activity via postsynaptic upregulation [this is thought of as a superior or stable equilibrium, hyperGABAergic]
Downreglated autoreceptors ⇒ enhanced neurotransmitter release ⇒ receptors try to compensate increased activity via postsynaptic downregulation [this is thought of as an inferior or unstable equilibrium, hypoGlutamatergic]

That is to suggest: THC induces favorable changes to GABA pathways, and unfavorable changes to glutamate pathways. So THC decreases glutamate activity and increases GABA activity, which of its own accord, further decreases glutamate activity. Need I remind you of the hypoglutamatergic hypothesis of schizophrenia^[2]?
Especially autoreceptors tend to be stubborn at renormalizing and tend to need an agonist or antagonist to induce timely (otherwise you could wait forever for this thing that would never happen) down- or upregulation.
So I think your problem is mostly downregulated glutamate autoreceptors. Green tea would actually be bad long-term, cause of inducing 4-AP dependent glutamate release. Curcumin would be a choice, but I feel there is something more specific and potent which is slipping my mind.
Maybe upregulate GABA(B) autoreceptors with antagonists? [well you may say THC inhibits GABA and this is favorable long-term, but yes... for this purpose, find something which does not also release too much glutamate!] But this is getting kind of far-fetched, even by my standards...

Pre-synaptic GABA(B) receptors inhibit glutamate release through GIRK channels in rat cerebral cortex.
Neuronal G protein-gated inwardly rectifying potassium (GIRK) channels mediate the slow inhibitory effects of many neurotransmitters post-synaptically. However, no evidence exists that supports that GIRK channels play any role in the inhibition of glutamate release by GABA(B) receptors. In this study, we show for the first time that GABA(B) receptors operate through two mechanisms in nerve terminals from the cerebral cortex. As shown previously, GABA(B) receptors reduces glutamate release and the Ca(2+) influx mediated by N-type Ca(2+) channels in a mode insensitive to the GIRK channel blocker tertiapin-Q and consistent with direct inhibition of this voltage-gated Ca(2+) channel. However, by means of weak stimulation protocols, we reveal that GABA(B) receptors also reduce glutamate release mediated by P/Q-type Ca(2+) channels, and that these responses are reversed by the GIRK channel blocker tertiapin-Q. Consistent with the functional interaction between GABA(B) receptors and GIRK channels at nerve terminals we demonstrate by immunogold electron immunohistochemistry that pre-synaptic boutons of asymmetric synapses co-express GABA(B) receptors and GIRK channels, thus suggesting that the functional interaction of these two proteins, found at the post-synaptic level, also occurs at glutamatergic nerve terminals.

An ‘exciting’ spin on cannabinoid signallingIt has long been appreciated that cannabinoid administration alters cognitive functioning, including learning and memory. These effects are thought to arise, at least in part, from alterations in synchronous activity in the cortex and hippocampus. The synaptic mechanisms underlying these effects, however, have not been clearly delineated. In recent years, the endogenous cannabinoid system has emerged as a powerful mechanism for regulating the release of neurotransmitter from presynaptic terminals (reviewed in Kano et al. 2009). The type 1 cannabinoid (CB1) receptor, which may be the most highly expressed G protein-coupled receptor in the brain, is found throughout the neuraxis, with particularly high levels in the hippocampus, neocortex, cerebellum and basal ganglia. At the subcellular level, the CB1 receptor is predominantly found in presynaptic terminals. Initial localization studies focused on the high levels of CB1 expression in a subset of GABAergic interneurons that co-express the peptide cholecystokinin (CCK). Recent studies have revealed that CB1 receptors are also expressed widely in glutamatergic terminals, as well as in some cholinergic, noradrenergic, and serotonergic terminals. In fact, CB1 receptor-mediated regulation of glutamate release, rather than GABA release, plays a central role in mediating the classic tetrad of behavioural and physiological responses to systemic cannabinoid administration (Monory et al. 2007). Endocannabinoid signalling is involved in a diverse range of physiological as well as pathophysiological processes, and identifying the underlying synaptic mechanisms and the relevant neuronal populations is important for the development of novel therapeutic strategies targeting the endocannabinoid system.

[gamesguru]

Serotonin is involved^[1], certainly with PTSD generally.

I know LSD can induce in some abusers permanent hyperacusis (yeah, I remember the important information in life) and this is probably also a result of altered serotonin transmission.

 

You said you tried SSRIs including wellbutrin.  Did this reduce tinnitus?

ctrl f 'ssri' http://www.science20...stress_disorder

I don't blame you for staying natural, but SSRIs would also reduce OCD and anxiety (not by as much as depression)

 

Candidate genes: https://books.google...FsxQZEC&pg=PA50

 

Melatonin?

https://books.google...czpRS4C&pg=PT82

 

CBD?

1a) Cannabinoid CB1 Receptor Agonists Do Not Decrease, but may Increase Acoustic Trauma-Induced Tinnitus in Rats

1b) Are cannabidiol and Δ(9)-tetrahydrocannabivarin negative modulators of the endocannabinoid system? A systematic review.

 

2a) Systematic Screening of the Serotonin Receptor 1A (5-HT1A) Gene in Chronic Tinnitus

2b) Agonistic properties of cannabidiol at 5-HT1a receptors.

[Derin105]

Ssris made me experience almost 0 emotion, but that's still a issue right now honestly.

I'd be fine with ocd and anxiety as I'd had these before but never couldn't enjoy anything if you get me?

If I take a 5mg adderall I'll regain my emotions and some sort of motivation but I'll crash reallyyyyyyyy hard after about 3 hours.

Again, stuck.... :(

I'd love to be able to enjoy things again. I mean I can get some feeling out of masturbation but the feeling is fleeting then I'm right back to reality. But mostly the need or want to be with others and empathy, complex emotions that I desperately want to regain.

I use to be very smart, and even with ocd and anxiety I could function socially. I don't have social anxiety I can talk to people just fine, but it's just the "connecting" to people and things that is missing ...

Serotonin is involved^[1], certainly with PTSD generally.
I know LSD can induce in some abusers permanent hyperacusis (yeah, I remember the important information in life) and this is probably also a result of altered serotonin transmission.

You said you tried SSRIs including wellbutrin. Did this reduce tinnitus?

ctrl f 'ssri' http://www.science20...stress_disorder

I don't blame you for staying natural, but SSRIs would also reduce OCD and anxiety (not by as much as depression)

Candidate genes: https://books.google...FsxQZEC&pg=PA50

Melatonin?
https://books.google...czpRS4C&pg=PT82

CBD?
1a) Cannabinoid CB1 Receptor Agonists Do Not Decrease, but may Increase Acoustic Trauma-Induced Tinnitus in Rats

1b) Are cannabidiol and Δ(9)-tetrahydrocannabivarin negative modulators of the endocannabinoid system? A systematic review.

2a) Systematic Screening of the Serotonin Receptor 1A (5-HT1A) Gene in Chronic Tinnitus

2b) Agonistic properties of cannabidiol at 5-HT1a receptors.

[Derin105]

When I was on lexapro I had no tinnitus but also felt way worse because all I wanted to do was sleep, and the lack of emotions/anhedonia was 1000x worse


There must be some way to facilitate some sort of repair of overall brain structures?

Serotonin is involved^[1], certainly with PTSD generally.
I know LSD can induce in some abusers permanent hyperacusis (yeah, I remember the important information in life) and this is probably also a result of altered serotonin transmission.

You said you tried SSRIs including wellbutrin. Did this reduce tinnitus?

ctrl f 'ssri' http://www.science20...stress_disorder

I don't blame you for staying natural, but SSRIs would also reduce OCD and anxiety (not by as much as depression)

Candidate genes: https://books.google...FsxQZEC&pg=PA50

Melatonin?
https://books.google...czpRS4C&pg=PT82

CBD?
1a) Cannabinoid CB1 Receptor Agonists Do Not Decrease, but may Increase Acoustic Trauma-Induced Tinnitus in Rats

1b) Are cannabidiol and Δ(9)-tetrahydrocannabivarin negative modulators of the endocannabinoid system? A systematic review.

2a) Systematic Screening of the Serotonin Receptor 1A (5-HT1A) Gene in Chronic Tinnitus

2b) Agonistic properties of cannabidiol at 5-HT1a receptors.

Edited by Derin105, 01 October 2015 - 11:31 PM.

[gamesguru]

OK, you could try ginkgo or uridine [vasodilators], melatonin, or CBD... probably none will be nearly as effective as lexapro.

Overall repair on the causes of tinnitus?  First off we don't know the causes clearly, so we can't treat it clearly.  It's kind of a miracle that lexapro could be so effective.  Not much I can recommend (I'd have to do more researches on PTSD) besides nutritious diet, exercise, general supplements (alcar/ps, ginkgo, green tea, ginseng, bacopa, kava, ash)

It's hard to say what is wrong just based on your improved response to adderall. It affects dopamine and norepinephrine levels, to a lesser degree, serotonin, histamine, and epinephrine levels, and not so much glutamate.  My guess therefore would be both the amotivation and the anhedonia are dopaminergic (this is a guess I also arrived at by independent reasoning in another thread... technically i only narrowed it down to glutamate and dopamine, here dopamine is suggestive.  but again, just a guess)

And it also suggests perhaps no downregulation of dopamine autoreceptors, cause this would result in chronic depletion of dopamine, and leave none for amphetamine to release.  But still in this case, it is favorable to upregulate receptors, not neurotransmitter.

 

Antidepressant-like effects of Trichilia catigua (Catuaba) extract: evidence for dopaminergic-mediated mechanisms

• Acute oral treatment with the extract of T. catigua produced antidepressant-like effects in the forced swimming model in both mice and rats. Anti-immobility actions of T. catigua extract in mice were significantly reversed by haloperidol or by chlorpromazine, but not by pimozide, ketanserin, spiroxatrine or p-chlorophenylalanine. In vitro, T. catigua extract concentration-dependently inhibited the uptake and increased the release of serotonin, and especially of dopamine, from rat brain synaptosomal preparations.

Mucuna^[1]

Rhodiola (MAO-B)

^^^all these things I suspect increase dopamine levels and decrease dopamine receptors

------------------

these are more natural choices, favoring homeostasis and equilibrium (pay special attention to the upregulators of DA receptors)

Inducers of PH (phenylalanine hydroxylase):

Lamiaceae^[1]??

Simple diet^[2]

Exercise^[3]

Iron^[4]

High ORAC foods^[5]

 

Inducers of TH (tyrosine hydroxylase):

Horny goat weed^[1]

Lithium

Ginkgo

Bacopa^[2]

Green tea^[3]

 

Upregulators of receptors (dopamine):

Caffeine^[1]

Bacopa^[2]

Exercise^[3]

Antidepressants^{[4], [5]}

It could be mild depression [which cannabis does worsen, but not to the same degree as it worsens anxiety or psychosis], sounds like you usually have this slightly low mood, and some days you have motivation and interest in things.  Could also be just a flat or blunted affect, related to glutamate/dopamine.  I would suggest reading this:

Blunted affect is very similar to anhedonia, the decrease or cessation of all feelings of pleasure (which thus affects enjoyment, happiness, fun, interest, and satisfaction). In the case of anhedonia, emotions relating to pleasure will not be expressed as much or at all because they are literally not experienced or are decreased. Both blunted affect and anhedonia are considered negative symptoms of schizophrenia, meaning that they are indicative of a lack of something. There are some other negative symptoms of schizophrenia which include avolition, alogia and catatonic behaviour.

Closely related is alexithymia – a condition describing people who "lack words for their feelings. Indeed, they seem to lack feelings altogether, although this may actually be because of their inability to express emotion rather than from an absence of emotion altogether".^[25] Alexithymic patients however can provide clues via assessment presentation which may be indicative of emotional arousal.^[26]

"If the amygdala is severed from the rest of the brain, the result is a striking inability to gauge the emotional significance of events; this condition is sometimes called 'affective blindness'".^[27] In some cases, blunted affect can fade, but it's not 100% sure why it does.

https://en.wikipedia...elated_symptoms

 

Connecting to people is more a social cognition than social anxiety issue.  Like Flex, I think it comes down to downregulated glutamate and dopamine, which feed into the mPFC, which is like our cognitive processing center or executive function cortex.  So basically it makes you dumber, less sharp, more forgetful.  Though he mentions a lot more than glutamate/dopamine, including FosB antigenes.

And as you mention you used to be smart, this impairment in social cognition is part of the bigger issue of cannabis-induced generalized cognitive impairment.  Which is probably due in large part to decreased glutamate/dopamine activity.  Just focus on the healthy lifestyle for tonight, maybe tomorrow I can think of ways to re-regulate dopamine and glutamate.  Yet I have mentioned a few ways.  And courtesy of area-1255 I'm reminded of inositol and forskolin[!].

 

 

Found this paper recently and it made me wonder that the effects arent well researched and that the effects of Cannabis might have chronic consequences even to those who havent smoked in the adolescence:

 

Decreased dopamine brain reactivity in marijuana abusers is associated with negative emotionality and addiction severity

We found that marijuana abusers display attenuated dopamine (DA) responses to MP, including reduced decreases in striatal distribution volumes. These deficits cannot be unambiguously ascribed to reduced DA release (because decreases in nondisplaceable binding potential were not blunted) but could reflect a downstream postsynaptic effect that in the ventral striatum (brain reward region) might contribute to marijuana’s negative emotionality and addictive behaviors.

http://www.pnas.org/...1/30/E3149.full

 

MP = Methylphenidate

 

I will try to find some targets and corresponding supplements that might (sigh) reverse something

and post it + I will report the results.

 

There are several papers that have to be read regarding:

- the cause of the  decrease of tyrosine hydroxylase

- the reason of decreased dopamine activation/response, release and synthesis in the Striatum.

-> according to one paper, it could be a downstream problem and I believe to read something about fos antigenes

- any other related problem like, altered plasticity.

 

Dont get me wrong, I´m aware that I´m just an amateur but a desperate one..

my problems are: affect i.e. mutism and avolition in social interactions, introverty, cognition, memory retrieval & a few others.

So You might allready assume that my social life was, is and will be bad, means no wife no childern & etc. if this goes on.

So I need a solution !

Lets see how far this goes. Perhaps some questions cant be answered even by the scientists up to this date.

 

I´m happy for any thoughts and inputs

-----------------------

-----------------------

-----------------------

Yes its afaik not know whether those alteration will relieve to a great extend. This sentences sounds concerning:

Structural and Functional Imaging Studies in Chronic Cannabis Users: A Systematic Review of Adolescent and Adult Findings

However, overall the results suggest that long-term cannabis use may result in persistent alterations in brain function and morphology that would extend beyond the period of intoxication [28], [31], and that earlier onset of use may be associated with greater detrimental effects [32], [33].

http://www.ncbi.nlm....les/PMC3563634/

 

I´m still affected and havesome doubts on the body owns healing capacity

because I´ve smoked from the age of 15 to 22, had 2 Years a break because of Risperdal (which was a "bright idea" from my psychiatrist)

and kept on from 24 untill 26. I had since then, here and there, some sessions but rather random and I havent smoked pot from Sept 2013 untill recently

As You see, I had long breaks but no big improvements in terms of affect.

Those problems are actually exact the same as the negative symptoms of Schizophrenia, exept the lack of emotion

 

A short summary of a list of negative symptoms are:

    lack of emotion - the inability to enjoy regular activities (visiting with friends, etc.) as much as before [of this, Flex doesn't complain you mention SSRIs: https://www.google.c...ack of emotion]
    Low energy - the person tends to sit around and sleep much more than normal
    lack of interest in life, low motivation
    Affective flattening - a blank, blunted facial expression or less lively facial movements, flat voice (lack of normal intonations and variance) or physical movements.
    Alogia (difficulty or inability to speak)
    Inappropriate social skills or lack of interest or ability to socialize with other people
    Inability to make friends or keep friends, or not caring to have friends
    Social isolation - person spends most of the day alone or only with close family

http://www.schizophr...diag.php#common

 

The long break did improve the emotions and the interrest in socializing but not the ability (funny huh?).

And everything other stayed more or less the same, unless when taken something like EGCG & etc.

 

I have to add that I´ve experimented 2 years ago with Ethyphenidate + various stuff like Amisulpride and L-dpoa

and this fried my brain which resulted into Depressions and somewhat lower emotions and decrease of libido and euphoria,

but I dont believe that it affected my skills too much.

 

Admittely my affect was not that great before but ok and a near relative who smoked randomly, dont have those problems as I.

 

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[Derin105]

What's weird is that through my entire year of abuse, my tolerance never increased, well... my tolerance was always actually really low, I could take a hit and be gone show.  But constant excersice may have helped. Would it hurt to give curcumin a 6 week trial or would increased dopamine from it cause down regulation?

 

 

 

 

Like I said any choline source makes me actually feel worse, I've tried uridine as well..
I've also been taking krill oil daily, as well as a rainbow multi vitamin. Wouldn't low dopamine mean fatigue?  Balance issues? Temors? None of which I have. So what's going on with my dopamine?

 

Is it possible that excess glutamate over Gaba would effect my other feel good chemicals IE. Endorphins? opioids?. This would explain why I don't feel any better with exercise.

I have take a single dose of 20mg IR Adderall and experienced manic/euphoric behavior. Like I was on speed
 

OK, you could try ginkgo or uridine [vasodilators], melatonin, or CBD... probably none will be nearly as effective as lexapro.
Overall repair on the causes of tinnitus? First off we don't know the causes clearly, so we can't treat it clearly. It's kind of a miracle that lexapro could be so effective. Not much I can recommend (I'd have to do more researches on PTSD) besides nutritious diet, exercise, general supplements (alcar/ps, ginkgo, green tea, ginseng, bacopa, kava, ash)

It's hard to say what is wrong just based on your improved response to adderall. It affects dopamine and norepinephrine levels, to a lesser degree, serotonin, histamine, and epinephrine levels, and not so much glutamate. My guess therefore would be both the amotivation and the anhedonia are dopaminergic (this is a guess I also arrived at by independent reasoning in another thread... technically i only narrowed it down to glutamate and dopamine, here dopamine is suggestive. but again, just a guess)
And it also suggests perhaps no downregulation of dopamine autoreceptors, cause this would result in chronic depletion of dopamine, and leave none for amphetamine to release. But still in this case, it is favorable to upregulate receptors, not neurotransmitter.

Antidepressant-like effects of Trichilia catigua (Catuaba) extract: evidence for dopaminergic-mediated mechanisms

• Acute oral treatment with the extract of T. catigua produced antidepressant-like effects in the forced swimming model in both mice and rats. Anti-immobility actions of T. catigua extract in mice were significantly reversed by haloperidol or by chlorpromazine, but not by pimozide, ketanserin, spiroxatrine or p-chlorophenylalanine. In vitro, T. catigua extract concentration-dependently inhibited the uptake and increased the release of serotonin, and especially of dopamine, from rat brain synaptosomal preparations.

Mucuna^[1]
Rhodiola (MAO-B)
^^^all these things I suspect increase dopamine levels and decrease dopamine receptors
------------------
these are more natural choices, favoring homeostasis and equilibrium (pay special attention to the upregulators of DA receptors)

Inducers of PH (phenylalanine hydroxylase):
Lamiaceae^[1]??
Simple diet^[2]
Exercise^[3]
Iron^[4]
High ORAC foods^[5]

Inducers of TH (tyrosine hydroxylase):
Horny goat weed^[1]
Lithium
Ginkgo
Bacopa^[2]
Green tea^[3]

Upregulators of receptors (dopamine):
Caffeine^[1]
Bacopa^[2]
Exercise^[3]
Antidepressants^{[4], [5]}

It could be mild depression [which cannabis does worsen, but not to the same degree as it worsens anxiety or psychosis], sounds like you usually have this slightly low mood, and some days you have motivation and interest in things. Could also be just a flat or blunted affect, related to glutamate/dopamine. I would suggest reading this:

Blunted affect is very similar to anhedonia, the decrease or cessation of all feelings of pleasure (which thus affects enjoyment, happiness, fun, interest, and satisfaction). In the case of anhedonia, emotions relating to pleasure will not be expressed as much or at all because they are literally not experienced or are decreased. Both blunted affect and anhedonia are considered negative symptoms of schizophrenia, meaning that they are indicative of a lack of something. There are some other negative symptoms of schizophrenia which include avolition, alogia and catatonic behaviour.
Closely related is alexithymia – a condition describing people who "lack words for their feelings. Indeed, they seem to lack feelings altogether, although this may actually be because of their inability to express emotion rather than from an absence of emotion altogether".^[25] Alexithymic patients however can provide clues via assessment presentation which may be indicative of emotional arousal.^[26]
"If the amygdala is severed from the rest of the brain, the result is a striking inability to gauge the emotional significance of events; this condition is sometimes called 'affective blindness'".^[27] In some cases, blunted affect can fade, but it's not 100% sure why it does.
https://en.wikipedia...elated_symptoms

Connecting to people is more a social cognition than social anxiety issue. Like Flex, I think it comes down to downregulated glutamate and dopamine, which feed into the mPFC, which is like our cognitive processing center or executive function cortex. So basically it makes you dumber, less sharp, more forgetful. Though he mentions a lot more than glutamate/dopamine, including FosB antigenes.
And as you mention you used to be smart, this impairment in social cognition is part of the bigger issue of cannabis-induced generalized cognitive impairment. Which is probably due in large part to decreased glutamate/dopamine activity. Just focus on the healthy lifestyle for tonight, maybe tomorrow I can think of ways to re-regulate dopamine and glutamate. Yet I have mentioned a few ways. And courtesy of area-1255 I'm reminded of inositol and forskolin[!].

Found this paper recently and it made me wonder that the effects arent well researched and that the effects of Cannabis might have chronic consequences even to those who havent smoked in the adolescence:

Decreased dopamine brain reactivity in marijuana abusers is associated with negative emotionality and addiction severity
We found that marijuana abusers display attenuated dopamine (DA) responses to MP, including reduced decreases in striatal distribution volumes. These deficits cannot be unambiguously ascribed to reduced DA release (because decreases in nondisplaceable binding potential were not blunted) but could reflect a downstream postsynaptic effect that in the ventral striatum (brain reward region) might contribute to marijuana’s negative emotionality and addictive behaviors.
http://www.pnas.org/...1/30/E3149.full

MP = Methylphenidate

I will try to find some targets and corresponding supplements that might (sigh) reverse something
and post it + I will report the results.

There are several papers that have to be read regarding:
- the cause of the decrease of tyrosine hydroxylase
- the reason of decreased dopamine activation/response, release and synthesis in the Striatum.
-> according to one paper, it could be a downstream problem and I believe to read something about fos antigenes
- any other related problem like, altered plasticity.

Dont get me wrong, I´m aware that I´m just an amateur but a desperate one..
my problems are: affect i.e. mutism and avolition in social interactions, introverty, cognition, memory retrieval & a few others.
So You might allready assume that my social life was, is and will be bad, means no wife no childern & etc. if this goes on.
So I need a solution !
Lets see how far this goes. Perhaps some questions cant be answered even by the scientists up to this date.

I´m happy for any thoughts and inputs
-----------------------
-----------------------
-----------------------
Yes its afaik not know whether those alteration will relieve to a great extend. This sentences sounds concerning:
Structural and Functional Imaging Studies in Chronic Cannabis Users: A Systematic Review of Adolescent and Adult Findings
However, overall the results suggest that long-term cannabis use may result in persistent alterations in brain function and morphology that would extend beyond the period of intoxication [28], [31], and that earlier onset of use may be associated with greater detrimental effects [32], [33].
http://www.ncbi.nlm....les/PMC3563634/

I´m still affected and havesome doubts on the body owns healing capacity
because I´ve smoked from the age of 15 to 22, had 2 Years a break because of Risperdal (which was a "bright idea" from my psychiatrist)
and kept on from 24 untill 26. I had since then, here and there, some sessions but rather random and I havent smoked pot from Sept 2013 untill recently
As You see, I had long breaks but no big improvements in terms of affect.
Those problems are actually exact the same as the negative symptoms of Schizophrenia, exept the lack of emotion

A short summary of a list of negative symptoms are:
lack of emotion - the inability to enjoy regular activities (visiting with friends, etc.) as much as before [of this, Flex doesn't complain you mention SSRIs: https://www.google.c...ack of emotion]
Low energy - the person tends to sit around and sleep much more than normal
lack of interest in life, low motivation
Affective flattening - a blank, blunted facial expression or less lively facial movements, flat voice (lack of normal intonations and variance) or physical movements.
Alogia (difficulty or inability to speak)
Inappropriate social skills or lack of interest or ability to socialize with other people
Inability to make friends or keep friends, or not caring to have friends
Social isolation - person spends most of the day alone or only with close family
http://www.schizophr...diag.php#common

The long break did improve the emotions and the interrest in socializing but not the ability (funny huh?).
And everything other stayed more or less the same, unless when taken something like EGCG & etc.

I have to add that I´ve experimented 2 years ago with Ethyphenidate + various stuff like Amisulpride and L-dpoa
and this fried my brain which resulted into Depressions and somewhat lower emotions and decrease of libido and euphoria,
but I dont believe that it affected my skills too much.

Admittely my affect was not that great before but ok and a near relative who smoked randomly, dont have those problems as I.

Edited by Derin105, 02 October 2015 - 02:15 AM.

[sthira]

Lots of info here. But back to weed, the strain really matters. Like, I can't do much sativa because it totally freaks me out and I have panic attacks. But the various indica strains and mixes do me right. I guess I'm still suggesting marijuana not because I'm a pothead -- I'm not -- but it's frankly way, way better and safer than just about all the other compounds mentioned here in your thread. Have you tried getting specific with what you're smoking, and working with dosages? Because really just saying "marijuana" as one broad compound isn't very informative. How many hundreds of different strains are out here now, each and every one producing totally different effects for ya?

[gamesguru]

This is a good point.  I have a qp (well close to 3oz now) which induces inexplicable psychosis, totally caught me off guard.  I sent a gram to the lab with $40, turns out it has lots of CBN, not as much THC as i hoped, and virtually no CBD.  CBN = more potent psychotomimitic than THC... with no CBD to balance it out.  No bueno.

 

Probably, yes, your brain was rejecting cannabis, getting to its tipping point, the camel's back about to break... who knows if you can get permanently stoned, who wants to find out?
But there's a lot going on besides dopamine/glutamate receptors, eg proteins (FosB), neurotrophins (trkB & NGF down)... some of it good, like reduced cytokines/inflammation, reduced excitotoxicity, antioxidative protection.  THC upregulates 58 and downregulates 36 genes, so there's a big story to be told.

 

avoid choline then? a little tea, perhaps less polyphenolic, more watery [as the caffeine upegulates dopamine receptors which is good, but the EGCG releases gluatamate and downregulates NMDARs/mGluRs which is harmful in the case of downregulated autoreceptors]

look up anything you buy to see if it's cholinergic.  for example bacopa is slightly, but only slightly, so i would give it a try.

if you want to know my anti-cannabis stack, it's basically that: bacopa, tea, turmeric, and good food (not very sophisticated, i admit)

 

depends which region

striatal dopamine is associated with emotions and motivation, of which you claim to have none, or very little.

The other guy, Londonscouser, had anhedonia but no amotivation... that I can't explain, not at my current level of thinking. Because if this isn't a peculiar/individual biochemical reaction, it suggests not both are dopaminergic.  I'm very sure amotivation is dopamine related, less sure about anhedonia.

 

krill oil isn't a bad thing, but i look at WildPlanet sardines or tuna, or wild salmon...whole unprocessed fish, and the word that leaps to mind is "superior"... even flaxseed, cheaper, perhaps just as anti-inflammatory.  you could even keep taking the krill and add flax on top, for pennies per day.  Andrew Weil said something like... 'if you're not eating flax, you're a drop out... anytime a culture is shifted and begins to incorporate flax, their productivity and longevity increase, when they shift away from flax, their productivity and longevity wane.'

[Area-1255]

When I was on lexapro I had no tinnitus but also felt way worse because all I wanted to do was sleep, and the lack of emotions/anhedonia was 1000x worse


There must be some way to facilitate some sort of repair of overall brain structures?

Use betahistine + Ginkgo Biloba for Tinnitus and both raise dopamine and histamine which is good for emotions and libido and relieving anhedonia. Betahistine can be bought at internationaldrugmart.com - has a nootropic effect too but don't use more than 60 mg a day or you won't sleep...16 mg x 3 - too much raises histamine too much you will be itching the soles of your feet for hours...            (in other words use 16 mg 2x or 3x a day any more can produce adverse effects)

Betahistine in the treatment of tinnitus in patients with vestibular disorders.

[Article in English, Portuguese]

Ganança MM1, Caovilla HH, Gazzola JM, Ganança CF, Ganança FF.

Author information

 

Abstract

Betahistine is a medicine used to treat vestibular disorders that has also been used to treat tinnitus.

AIM:

To assess the effects of betahistine on tinnitus in patients with vestibular disorders.

MATERIAL AND METHOD:

Retrospective data were collected from patient records for individuals presenting with vestibular dysfunction and tinnitus. Patients included had received betahistine 48 mg/day and clinical outcomes were compared with a control group comprising individuals who were unable to receive betahistine due to gastritis, ulcers, pregnancy, asthma or hypersensitivity to the drug. Patients underwent control of any aggravating factors and also standard vestibular exercises as a basis for treatment. The intensity, frequency and duration of tinnitus were assessed on the first day of dosing and after 120 days of treatment. Clinical improvement was defined as a total or partial reduction of tinnitus after treatment.

RESULTS:

Clinical improvement was observed in 80/262 (30. 5%) of patients treated with betahistine and 43/252 (17. 1%) of control patients. Betahistine significantly (p<0. 0001) improved tinnitus in treated individuals.

CONCLUSIONS:

The daily dosage of 48 mg of betahistine during 120 consecutive days is useful to reduce or eliminate tinnitus in patients with vestibular disorders.

PMID:   21860977   [PubMed - indexed for MEDLINE]    Free full text+

 

 

 

 

 

Ginkgo biloba extract in the treatment of tinnitus: a systematic review

Alexander von Boetticher

Author information ► Article notes ► Copyright and License information ►

This article has been cited by other articles in PMC.

Abstract

Tinnitus is a symptom frequently encountered by ear, nose, and throat practitioners. A causal treatment is rarely possible, and drug and nondrug treatment options are limited. One of the frequently prescribed treatments is Ginkgo biloba extract. Therefore, randomized, placebo-controlled clinical trials of Ginkgo biloba extract preparations were searched for and reviewed systematically. There is evidence of efficacy for the standardized extract, EGb 761® (Dr Willmar Schwabe GmbH & Co KG Pharmaceuticals, Karlsruhe, Germany), in the treatment of tinnitus from three trials in patients in whom tinnitus was the primary complaint. Supportive evidence comes from a further five trials in patients with age-associated cognitive impairment or dementia in whom tinnitus was present as a concomitant symptom. As yet, the efficacy of other ginkgo preparations has not been proven, which does not necessarily indicate ineffectiveness, but may be due to flawed clinical trials. In conclusion, EGb 761®, a standardized Ginkgo biloba extract, is an evidence-based treatment option in tinnitus.

Keywords: tinnitus, Ginkgo biloba, EGb 761®, systematic review

 

 

A number of uncontrolled (e.g ^.4−8) or controlled but non-randomised clinical trials (e.g ^.9,10,11] suggest that the regular medication with ginkgo biloba is effective in the treatment of tinnitus. As such trials are open to bias and tend to over-estimate the effect size, ¹²this systematic review was aimed at summarising all randomised controlled trials on this subject.

Go to:

Abstract

Tinnitus is a symptom frequently encountered by ear, nose, and throat practitioners. A causal treatment is rarely possible, and drug and nondrug treatment options are limited. One of the frequently prescribed treatments is Ginkgo biloba extract. Therefore, randomized, placebo-controlled clinical trials of Ginkgo biloba extract preparations were searched for and reviewed systematically. There is evidence of efficacy for the standardized extract, EGb 761® (Dr Willmar Schwabe GmbH & Co KG Pharmaceuticals, Karlsruhe, Germany), in the treatment of tinnitus from three trials in patients in whom tinnitus was the primary complaint. Supportive evidence comes from a further five trials in patients with age-associated cognitive impairment or dementia in whom tinnitus was present as a concomitant symptom. As yet, the efficacy of other ginkgo preparations has not been proven, which does not necessarily indicate ineffectiveness, but may be due to flawed clinical trials. In conclusion, EGb 761®, a standardized Ginkgo biloba extract, is an evidence-based treatment option in tinnitus.

Keywords: tinnitus, Ginkgo biloba, EGb 761

 

Fundam Clin Pharmacol. 1995;9(2):169-74.

Stress-induced 5-HT1A receptor desensitization: protective effects of Ginkgo biloba extract (EGb 761).

Bolaños-Jiménez F1, Manhães de Castro R, Sarhan H, Prudhomme N, Drieu K, Fillion G.

Author information

 

Abstract

The effects of sub-chronic cold stress on the functioning of hippocampal 5-HT1A receptors in old isolated rats and the possible protective effects of Ginkgo biloba extract (EGb 761) were investigated. Cold exposure during five days, produced a significant reduction of the inhibitory effect of 8-hydroxy-2-(di-n-propylamino)tetraline (8-OH-DPAT) on forskolin-stimulated adenylyl cyclase activity. In contrast, neither the affinity nor the density of hippocampal [3H]8-OH-DPAT binding sites were affected indicating that the reduced sensitivity of 5-HT1A receptors induced by stress is probably due to a modification of their coupling mechanisms to adenylyl cyclase. The stress-induced desensitization of 5-HT1A receptors was prevented by the administration of EGb 761 (50 mg/kg per os/14 days). These results clearly indicate that 5-HT1A receptors are desensitized by stress and point out the reduced capacity of old rats to cope with the adverse effects of a chronic stressor. EGb 761 appears to restore the age-related decreased capacity to adapt to a chronic stressor.

PMID:   7628830   [PubMed - indexed for MEDLINE]

 

Edited by Area-1255, 02 October 2015 - 04:00 AM.

[Londonscouser]

Yeh dude i basically got the same problem.

 

I quit approximately just over 10 weeks ago, however i did abuse it for like 5 years.

 

My biggest issues are ; inability to connect with other individuals on an emotional level. If i had to rephrase that, i would say i don't feel like i am on the same wavelength when socializing.

 

Also, lack of emotion. I guess i am anhedonic to an extent, but not fully.

 

I don't want to sound like a dick, but i do have a feeling this could be semi-permanent ... Although its always best to try everything you can to fix problem. I think being proactive, socializing/meeting new people (even though it doesn't feel right), encountering new environments and this may sound weird, but reading books.

 

Anyways, to leave on an optimistic note, I read about somebody who had similar issues, albeit not the exact same, nevertheless he stated it took him 3-4 years to feel '100%' normal.

 

Good luck, and if you do find a solution, please tell me lol !

[gamesguru]

London, on a scale of 1-10, how much would you say you're putting yourself out there, or making effort to get in social situations?  Even despite your handicap

[jaiho]

try nsi-189. 

[Londonscouser]

London, on a scale of 1-10, how much would you say you're putting yourself out there, or making effort to get in social situations?  Even despite your handicap

 

Most likely in the ranges of 5-6. I think i could try harder, but its also difficult to go out with the same friends regularly if you can't build any sort of 'relationship, connection' ect.

 

However my urge and motivation to socialize is more or less there.

 

At the minimum, i go out twice a week.

[PeaceAndProsperity]

Why not continue marijuana, but moderately? Marijuana is a solid medicine, and it's harmless in moderation, like coffee or chocolate or red wine or broccoli sprouts. And it's dose dependent just like any other medicine. Maybe respectfully approach your pot behavior this time with wisdom gained? For example, view it as less of a wild party sensation, and more as a healthy addition to your life? Respect and moderation are key.

 

It's amusing and peculiar when someone tries to defend a drug with many serious side-effects and whose "therapeutic potential" is easily matched with drugs whose side-effects are minimal or even none in comparison.

 

Cannabis is not a "wonder drug," it's used for recreational purposes - because it dulls and makes parties and social gatherings more enjoyable or more easily handled.

Cannabis is also addictive and this probably explains the constant attempt to defend this drug.

 

Don't forget why it was legalized - it was legalized to make it less appealing, because many teenagers were consuming it solely for its illegality, and it could be financially exploited if it was legal. Now it is claimed that its use has gone down and this supposedly proves the success of its legalization.

 

If there are drugs more safe and better than a specific drug, why continue to take that specific drug? The only explanation I can find is addiction or ignorance.

(There's no need for hostility or Reddit-like downvoting.)

[gamesguru]

Most likely in the ranges of 5-6. I think i could try harder, but its also difficult to go out with the same friends regularly if you can't build any sort of 'relationship, connection' ect.

However my urge and motivation to socialize is more or less there.

At the minimum, i go out twice a week.

 

Were you connecting better before you became pothead?  Or were you already somewhat handicapped?  I was, and it made it three times worse.  I literally haven't gone out or hung out since May, all I do is read .

 

 

Why not continue marijuana, but moderately?

 

Addictive personalities are not super compatible with the idea of moderation.  I think if you can stick to it, <0.25g is the therapeutic range, and it won't hurt you motivationally or socially.

[Londonscouser]

 

Most likely in the ranges of 5-6. I think i could try harder, but its also difficult to go out with the same friends regularly if you can't build any sort of 'relationship, connection' ect.

However my urge and motivation to socialize is more or less there.

At the minimum, i go out twice a week.

 

Were you connecting better before you became pothead?  Or were you already somewhat handicapped?  I was, and it made it three times worse.  I literally haven't gone out or hung out since May, all I do is read .

 

 

Why not continue marijuana, but moderately?

 

Addictive personalities are not super compatible with the idea of moderation.  I think if you can stick to it, <0.25g is the therapeutic range, and it won't hurt you motivationally or socially.

 

 

Before i started smoking cannabis, and even throughout the first 1-2 years of abusing it, i was literally a social butterfly. I got along with pretty much everybody, thats why i can see the stark difference between me of the past and the present me.

 

The only 'issues' i had, i was a little shy when talking to beautiful ladies, however i think that's fairly normal.

 

I don't even want to sound arrogant, but throughout my school years i was one of the most popular individuals in either of my 2 schools. I attribute this to being very talented at sports.

 

But yeh,,,i just knew how to make other people laugh ect.

[jaiho]

i personally think that cannabis has triggered an underlying mental disorder. family history of depression at all?

[Londonscouser]

i personally think that cannabis has triggered an underlying mental disorder. family history of depression at all?

 

My mum is a little depressed sometimes, however my dad is perfectly healthy and always happy.

 

In terms of triggering an underlying mental disorder, the only condition i believe i have obtained from my abuse of cannabis is a mild-sometimes moderate case of social anxiety. (its more of a background feeling rather than overwhelming).

 

I've never been depressed in my entire life, i have no idea what depression feels like to be honest. I've never had any mental health issues apart from the social anxiety and this case of emotional numbness.

 

The only thing i can think of in regards to family history, is that i have 2-3 uncles on my dads side who got diagnosed with schizophrenia at a very young age....therefore i could possibly be experiencing negative symptoms and its a waiting game for the positive symptoms to manifest ? 

[sthira]

I think well, yeah, if you think marijuana ain't going well for you then don't do it. It's certainly not for everyone, and affects all of us in our unique snowflakey ways. When it stops being friendly and positive, then let it go. Find what'll work better for your own biology and history. Realize, too, that your body chemistry is changing all the time as you move through life. And marijuana itself is also changing -- not necessarily in the mystical sense -- but new powerful strains are being crafted all the time. Some of these are great, some good, some neutral, some bad, and some strains are weird, some are terrifyingly horrible and may activate laten schizophrenic gene tendencies.

[Blackkzeus]

Try piracetam. It's been helping a lot with my anhedonia. I finally feel like have the Emotional range Of a normal human being. Just supplement with a good amount of choline the night before you take piracetam. I'd say about like 2-4gs.

[Area-1255]

Try piracetam. It's been helping a lot with my anhedonia. I finally feel like have the Emotional range Of a normal human being. Just supplement with a good amount of choline the night before you take piracetam. I'd say about like 2-4gs.

Yo check your PMs!