Cannabigerol/CBG For PSSD/Libido (5-HT1A Modulatio)

[Lokzo]

It started off as a quest to reverse the damage done by a year or more of ashwagandha usage, but its turned into a quest to get my brain chemistry to exist in the "sweet spot." What Hans refers to as the ?"high dopamine personality." His articles, along with Haidut's supplements, have been nothing short of life-changing for me. After a couple weeks of cypro/meter, I felt changes taking place in my perception of reality and social interactions with people....improvements. I am an INTP on the myers briggs and have been borderline autistic the majority of my life.... cypro/meter have seemed to reverse this... completely it seems. Other supps have help me make significant improvements, most noticeably uridine, 9mbc, cerebrolysin, and 7,8 DHF. And Semax. But none of this have been quite as profound as cypro/meter. I think I had a severely ****88 up serotonin system from birth, exacerbated byt drug usage throughout my late teens and 20s, especially a particularly horrifying experience where i took way too much LSD and had a terrifying trip for 12 hours.

I am my own worst enemy. To complicate everything, I recently started running Test Cyp at 600 mg weekly to try and get some gains (I'm on TRT normally), and its been a b**** trying to get my AI dosage right. What initially motivated me to try it was the addition of androsterone to my supplemental arsenal. I was running it on my TRT dose of test and finding it had no sides other than sedation, However, I quickly found out that it is not near strong enough to contro9l estrogen on supraphysiological dosages of testosterone (I dont even think it was controlling it on my TRT dose) so i've had to switch back to exemestane. Anyways, my libido is ****88 right now but i cant tell if its the high/low estro or something else (the cypro).

Thats why I'm going to drop the cypro tomorrow, to see if my libido comes back online (your post about cypro interfering with your libido caught my eye - I had assumed that the low serotonin state brought about by cypro would increase libido).

Incredible story man.

Thanks for sharing.

Where are you at with the experiments these days?

 

[CalmAmygdala]

Still trying to find that elusive sweet spot and just stay the **** there. I've lowered my test dose to 200 and have stopped exemestane. Its almost like a cruel joke, but high and low estro symptoms are almost indistinguishable from one another, which makes it damn near impossible to control estrogen on a steroid cycle without at least a few blunders. You assume its too high, but its actually too low, so you take an exemestane and it annihilates your circulating estrogen for the next 72 hours and you go so low your knuckles start bleeding from being so dry.

Anyway I am currently trying to see if I can cruise on 200 mg test cyp and do nothing but supp peaty to control estro (meter or cypro, taurine, glycine, butea superba, creatine, vitamin D, E). Trying to play with exemestane to get the levels right has proven to be impossible for me and I've finally given up.

In regards to paxil, ive finally weaned myself off it completely, and when ive got that test/estro ratio nailed i feel great, but if estro goes either too high or low i get near suicidal its so awful.

You have any opinions on controlling estrogen with 200 mg test weekly

 

[CalmAmygdala]

Also, any updates on CBG? Is it an antagonist at any other serotonin receptors? Also, I think the fact CBG is an agonist at the A2 adrenoreceptor means it can actually decrease sympathetivc nervous activity (clonidine is an a2 agonist). Its the beta adrenoreceptor agonists that cause the major sympathetic sides (like clenbuterol)

 

[TMCMac]

Also, any updates on CBG? Is it an antagonist at any other serotonin receptors? Also, I think the fact CBG is an agonist at the A2 adrenoreceptor means it can actually decrease sympathetivc nervous activity (clonidine is an a2 agonist). Its the beta adrenoreceptor agonists that cause the major sympathetic sides (like clenbuterol)

Interested as well. So should it help calm down the nervous system? I have some CBG extract. But now sure the long terms so I'm just waiting it out for now.

 

[CalmAmygdala]

From my understanding of A2 agonism it should calm/lower BP, but ive anecdotaL reports ive read of those who have used it describe a stimulating, caffeine like effect, could be due to other pharmacological activity of CBG

 

[OccamzRazer]

It's been a few weeks that I started vaping CBG flower (often mixed with CBD flower, sometimes a little regular bud too). I like the effects this far, very clear headed indeed. However I often feel some mild body high the next day, usually in morning and late afternoon.

Good stuff!

You might like raw hemp/cannabis flower even more, if you can get your hands on it somehow. Both chemotypes will be rich in CBGa and CBG when young and still growing.

Some ancient cultures used to eat raw cannabis to ward off parasites, presumably for its CBGa content. The 'raw,' non-decarboxylated cannabinoids and terpenes are said to be very good for gut health.

 

[CalmAmygdala]

Just want to give an update. I have experienced massive improvement on the following stack. I had written this huge long post and then accidently deleted it and now im ******* pissed because it was ******* beautiful.

Of course, the fact I'm feeling angry at all is evidence of the substantial improvements ive made in every area of PSSD - anhedonia, motivation, mood, libido, excitement, anticipatory anxiety....

The real turning point in all this was when i realized what i was actually suffering from was PSSD.... rather than "SSRI discontinuation syndrome" Once I Started targeting PSSD things started getting bettter FAST

I was at the grocery store today and opened this girl and i felt the most intense, euphoric wave of excitement and thrilling attraction down to my balls and throughout my whole body. It felt like I was 13 again pre SSRIs. Orgasms are 80% now.

First off, I got back off the paxil and things immediately got better. the paxil was making it worse. I then got on 50 mg trazodone (it has a favorable profile pharmacologically - 5ht1a agonism, 5ht2a/2c antagonism, and a1 antagonism - which can lead to priapism). I felt better since starting it but the real magic started when i started the stack I'm about to list below. Still, wanted to mention trazodone as it may be a player.

Here's the stack:

Rhodiola (3% salidrosides) 500 mg 2x daily
St. John's Wort (.3% hypericin) 500 mg 2x daily
Bromantane 50-75 mg once daily
L Carnitine L Tartrate - 1 g 2x daily (androgen receptor upregulation)
Phospholipid Complex - 1x daily (helps facilitate receptor binding)

Also been taking tianeptine sulfate 25 mg 2x daily but it was only giving me very minor improvements.... things didnt start getting alot better til I started taking the above 5.

I also ran CBG for a week and stopped yesterday....didnt notice anything from it though. Ive also been redlighting my balls with LLLT (800 nm light).

But the real MVPs are the 5 supps listed above and I am confident they will be enough to substantially liberate anyone from the suicidal, nightmarish hellscape that is PSSD.

Good luck to everyone out there and I hope this helps someone

 

[Mauritio]

CBG seems interesting man . Are you still using it ?
I just read a lost from someone who said his anxiety and autism got like 75%better with CBG .

 

[OccamzRazer]

CBG seems interesting man . Are you still using it ?

CBG is great, but raw, young cannabis or hemp plants are even better. They contain:

CBGa
THCa
CBDa
THCv
CBDv
Terpenes
Flavonoids
Etc etc etc


LEAFLY:

What do you think the future of cannabis research holds?

LUMIR HANUS, who discovered anandamide:

I can see two different directions. One will focus on production of derivatives of active compounds that could be patented and sold in order to make as much money as possible. The other direction puts patients before profit and focuses on the use of the whole plant and synergistic effects of its compounds.

 

[Mauritio]

Yeah I think that's called the entourage effect .
On the other hand CBG, CBD and THC have opposite effects on some receptors so it might be better for some people to use an isolated product.

As always: experiment is the only true method of knowledge, so I ordered some...

 

[Mauritio]

The Pharmacological Case for Cannabigerol

Medical cannabis and individual cannabinoids, such as Δ9-tetrahydrocannabinol (Δ9-THC) and cannabidiol (CBD), are receiving growing attention in both the media and the scientific literature. The Cannabis plant, however, produces over 100 different cannabinoids, and cannabigerol (CBG) serves as...

jpet.aspetjournals.org

Neuroprotective properties of cannabigerol in Huntington's disease: studies in R6/2 mice and 3-nitropropionate-lesioned mice - PubMed

Different plant-derived and synthetic cannabinoids have shown to be neuroprotective in experimental models of Huntington's disease (HD) through cannabinoid receptor-dependent and/or independent mechanisms. Herein, we studied the effects of cannabigerol (CBG), a nonpsychotropic phytocannabinoid...

pubmed.ncbi.nlm.nih.gov

Beneficial effect of the non-psychotropic plant cannabinoid cannabigerol on experimental inflammatory bowel disease - PubMed

Inflammatory bowel disease (IBD) is an incurable disease which affects millions of people in industrialized countries. Anecdotal and scientific evidence suggests that Cannabis use may have a positive impact in IBD patients. Here, we investigated the effect of cannabigerol (CBG), a...

pubmed.ncbi.nlm.nih.gov

 

[Mauritio]

The alpha 2 agonism of cbg is also interesting. It should inhibit part of the stress response and work similar to clonidine, which is also alpha 2 adrenergic agonist.


"Alpha2 adrenergic agonist can also be used to treat anxiety and panic, such as Generalized Anxiety Disorder, Panic Disorder or PTSD. Alpha2-adrenergic receptor agonists, such as clonidine and guanfacine, act at noradrenergic autoreceptors to inhibit the firing of cells in the locus ceruleus, effectively reducing the release of brain norepinephrine.[4] Clonidine has shown promise among patients with Anxiety, Panic and PTSD in clinical trials and was used to treat severely and chronically abused and neglected preschool children. It improved
disturbed behavior by reducing aggression, impulsivity, emotional outbursts, and oppositionality.[5] Insomnia and nightmares were also reported to be reduced."

Sympatholytic - Wikipedia

en.m.wikipedia.org

CBG is also a CB-1 antagonist ,which might very well lead to weight loss :

"The endocannabinoid system (ECS) plays a critical role in obesity development in both central and peripheral functions related to energy metabolism11. At the central level, endocannabinoids act as retrograde neuromodulators of synaptic plasticity, and participate in many physiological processes including pain regulation, learning and memory, appetite and food intake, lipogenesis, and cravings12,13. At the peripheral level, endocannabinoids exert a tonic action on lipogenesis and fat accumulation. Therefore, CB1 blockade may result in a food intake-independent decrease in fat mass through lipolysis14. In fact, CB1 blockade has been shown to be effective in ameliorating obesity and related metabolic disorders15. In addition, the endocannabinoid 2-AG prevent myotube formation in a manner antagonized by CB1 knockdown and by CB1 antagonists, which per se, instead, stimulate differentiation16. Moreover, antagonism of CB1 receptor reduced human satellite cell proliferation and enhanced the formation of myotubes representing an adjuvant therapy of muscle dystrophies17."

Caloric restriction, physical exercise, and CB1 receptor blockade as an efficient combined strategy for bodyweight control and cardiometabolic status improvement in male rats - Scientific Reports

Obesity is critically associated with the development of insulin resistance and related cardiovascular and kidney diseases. Several strategies for weight loss have been developed but most of them exhibit a post-intervention rebound effect. Here, we aimed to design combined weight-loss strategies...

www.nature.com

"Cannabinoid type 1 receptor (CB1r) antagonists can effectively treat obesity and associated metabolic alterations... "

Energy balance regulation by endocannabinoids at central and peripheral levels - PubMed

Dysregulation of the endocannabinoid system (ECS) is a universal and, perhaps, causative feature of obesity. Central nervous system (CNS) circuits that regulate food intake were initially believed to be the targets for dysregulation. However, it is increasingly evident that endocannabinoids...

pubmed.ncbi.nlm.nih.gov

 

[Mauritio]

A little addition to the study on CB1 and alpha 2 adrenoreceptors: that was in vitro. It has not been shown (to my knowledge) that the same is true in vivo , so we have await further studies .


This study is an in vivo study and shows that CBD and CBG reduce the neutrophils recruited through endotoxin by a about 50%.
Interestingly a mix of CBD and CBG did NOT work.
Which shows that they have partially antagonistic function.

The anti-inflammatory effects of cannabidiol and cannabigerol alone, and in combination - PubMed

In conclusion, this study has provided evidence that CBD and CBG formulated appropriately exhibit anti-inflammatory activity. Our observations suggest that these non-psychoactive cannabinoids may have beneficial effects in treating diseases characterised by airway inflammation.

pubmed.ncbi.nlm.nih.gov

 

[Aad]

Would CBG work against premature ejaculation, Mauritio?

 

[Mauritio]

Would CBG work against premature ejaculation, Mauritio?

If it does indeed antagonize 5ht1a in vivo in humans then it looks very promising.
If the theory that it 5ht1a activation increases premature ejaculation ,then it would actually be a good test to see if it helps with it in humans. If it helps then we'd know CBG likely antagonizes 5ht1a in humans.

"5-Hydroxytryptamine (5-HT or serotonin) is involved in ejaculatory control, with its ejaculation-retarding effects likely to be attributable to activation of 5-HT1B and 5-HT2C receptors, both spinally and supraspinally. By contrast, stimulation of 5-HT1A receptors precipitates ejaculation. "
(5-Hydroxytryptamine in premature ejaculation: opportunities for therapeutic intervention - PubMed)


Also check out these posts by hans on PE:

5-HT1A appears to be involved in premature ejaculation. Reduced 5-HT1A function can cause you to struggle to orgasm. This is one way how SSRI drugs cause sexual function. Some SSRI drugs actually upregulate the 5-HT1A post-synaptic receptors, which could then cause premature ejaculation.

Lower serotonin can resensitize the 5-HT1A receptor, which promotes ejaculation. So using a 5-HT1A antagonist might be helpful. Also, overstimulation of the sympathetic nervous system promotes ejaculation, so if you're too excited, you won't last very long.

 

[Aad]

Thank you Mauritio! Very interesting stuff indeed!

 

[Mauritio]

Thank you Mauritio! Very interesting stuff indeed!

Np :)

This is a great summary of CBG's effects.

CBG | GH Medical

ghmedical.com

 

[Aad]

One last question, what about a cbd/cbg duo combo? Would it also help for PE and fat loss?

 

[Mauritio]

One last question, what about a cbd/cbg duo combo? Would it also help for PE and fat loss?

For fast loss I dont know ,for PE not as CBD is a 5ht1a agonist .

 

[Mauritio]

Here's another goodie showing CBG ,but not CBD decreases intestinal inflammation. CBG is known to work for gastrointestinal issues such as IBS .

"CBG, but not CBD, given by oral gavage, ameliorated DNBS-induced colonic inflammation."
(Efficacy of combined therapy with fish oil and phytocannabinoids in murine intestinal inflammation - PubMed)