Going through very rare obsessive complaints

Hello everyone,

So excited that my account has now been activated. I'm currently going through very 'rare' and 'strange' situation. I suppose that the members of this forum can understand my problem (because you know how it goes if I see a psychiatrist, profiting from mental-ill health and there's a reason psychiatrists prescribe drugs rather than talking therapy). Anyway, due of my insomnia last two years I started with sleeping pills temazepam, and now I'm slowly tapering off with valium. I've gotten ever since my first panic attack in july 2019, and I was brought to the ER (i thought i was dying). After that everything changed.. I developed 'generalized anxiety disorder'. In december 2019 when I switched from sleeping pills to valium I started with some supplements and amino acids after doing long research for alleviating of 'withdrawal symptoms'. And one them was Magnesium + Vitamin B6. As you know magnesium is a NMDA antagonist. So one month after I started with magnesium I developed OCD .. the obsessive thoughts that I have are so irrational and stupid, generally it's about my sleep. Rationally speaking I love sleep and dreams, but there's one thought that grabs my mind whole day (it's so strange). Its like: "'why i lose my my conscious during asleep". It's so laughable, i know. But it just doesn't go away. I can't go to bed like a baby. What's going on here? I swear I'm able to give my everything if you can help me, I'm so desperate.

Age: 24
Medications I take: Valium 2,5 mg (currently tapering off)
Supplements/ Amino acids: Few days ago stopped with Magnesium + Vitamin B6, same day when I stopped taking Magnesium + Vitamin B6 started with:
* NAC 1,4 g
* Valerian + Melissa
* Bacopa

What are your thoughts? Let me know. Take care

Protector wrote:Hello everyone,

So excited that my account has now been activated. I'm currently going through very 'rare' and 'strange' situation. I suppose that the members of this forum can understand my problem (because you know how it goes if I see a psychiatrist, profiting from mental-ill health and there's a reason psychiatrists prescribe drugs rather than talking therapy). Anyway, due of my insomnia last two years I started with sleeping pills temazepam, and now I'm slowly tapering off with valium. I've gotten ever since my first panic attack in july 2019, and I was brought to the ER (i thought i was dying). After that everything changed.. I developed 'generalized anxiety disorder'. In december 2019 when I switched from sleeping pills to valium I started with some supplements and amino acids after doing long research for alleviating of 'withdrawal symptoms'. And one them was Magnesium + Vitamin B6. As you know magnesium is a NMDA antagonist. So one month after I started with magnesium I developed OCD .. the obsessive thoughts that I have are so irrational and stupid, generally it's about my sleep. Rationally speaking I love sleep and dreams, but there's one thought that grabs my mind whole day (it's so strange). Its like: "'why i lose my my conscious during asleep". It's so laughable, i know. But it just doesn't go away. I can't go to bed like a baby. What's going on here? I swear I'm able to give my everything if you can help me, I'm so desperate.

Age: 24
Medications I take: Valium 2,5 mg (currently tapering off)
Supplements/ Amino acids: Few days ago stopped with Magnesium + Vitamin B6, same day when I stopped taking Magnesium + Vitamin B6 started with:
* NAC 1,4 g
* Valerian + Melissa
* Bacopa

What are your thoughts? Let me know. Take care

Hi man, I don't know exactly what causes obsessions, however I have some thoughts. You probably right, it could be a glutamate issue (can I ask you to answer why you think so?). Another thought is vit. b6 itself can cause some stupid worrying from my experience, so it's alright you stopped it. I have seen some modern papers on ocd with remedies, so will put them here when at home. My additional thought is probably long term lecithin can offer some improvements at least in checking if you have it. Also for mild nmda stimulation you can look for sarcosine. See area1255 blog for some other remedies. For example it is mentioned there that magnolia officinalis removed some ocd symptoms. For insomnia there some thing to try too, since gaba modulators is very unsafe way to calm yourself, you know.

kpavel wrote:

Protector wrote:Hello everyone,

So excited that my account has now been activated. I'm currently going through very 'rare' and 'strange' situation. I suppose that the members of this forum can understand my problem (because you know how it goes if I see a psychiatrist, profiting from mental-ill health and there's a reason psychiatrists prescribe drugs rather than talking therapy). Anyway, due of my insomnia last two years I started with sleeping pills temazepam, and now I'm slowly tapering off with valium. I've gotten ever since my first panic attack in july 2019, and I was brought to the ER (i thought i was dying). After that everything changed.. I developed 'generalized anxiety disorder'. In december 2019 when I switched from sleeping pills to valium I started with some supplements and amino acids after doing long research for alleviating of 'withdrawal symptoms'. And one them was Magnesium + Vitamin B6. As you know magnesium is a NMDA antagonist. So one month after I started with magnesium I developed OCD .. the obsessive thoughts that I have are so irrational and stupid, generally it's about my sleep. Rationally speaking I love sleep and dreams, but there's one thought that grabs my mind whole day (it's so strange). Its like: "'why i lose my my conscious during asleep". It's so laughable, i know. But it just doesn't go away. I can't go to bed like a baby. What's going on here? I swear I'm able to give my everything if you can help me, I'm so desperate.

Age: 24
Medications I take: Valium 2,5 mg (currently tapering off)
Supplements/ Amino acids: Few days ago stopped with Magnesium + Vitamin B6, same day when I stopped taking Magnesium + Vitamin B6 started with:
* NAC 1,4 g
* Valerian + Melissa
* Bacopa

What are your thoughts? Let me know. Take care

Hi man, I don't know exactly what causes obsessions, however I have some thoughts. You probably right, it could be a glutamate issue (can I ask you to answer why you think so?). Another thought is vit. b6 itself can cause some stupid worrying from my experience, so it's alright you stopped it. I have seen some modern papers on ocd with remedies, so will put them here when at home. My additional thought is probably long term lecithin can offer some improvements at least in checking if you have it. Also for mild nmda stimulation you can look for  sarcosine. See area1255 blog for some other remedies. For example it is mentioned there that magnolia officinalis removed some ocd symptoms. For insomnia there some thing to try  too, since gaba modulators is very unsafe way to calm yourself, you know.

Dear brother, really I appreacite your message. I thought this forum was no longer active anymore, however forunately I have gotten your message. I used my insight and I found an interesting detail about my problem. I smoked weed for a week or so (for my insomnia), the last time that I smoked I started to get really paranoid, it was insane. About six hours I was in a hell. And since then I'm dealing with that rare obsessive thoughts that I had mentioned above. What do you think, is it possible that my obsessive toughts are 'cannabis induced'?

Actually I think yes. And the text below says something about it.
https://pubmed.ncbi.nlm.nih.gov/19166390/
Delta-9-tetrahydrocannabinol (THC) is the primary psycho-active ingredient in Cannabis spp., the most widely used illicit drug in the United States. THC is an exogenous agonist of the central cannabinoid receptor (CB1), one of the most abundant G-coupled receptors in the mammalian brain. Although CB1 receptors are distributed throughout the brain, they are found at very high levels in the cerebellum. Despite the variety of disturbances associated with acute cannabis intoxication, including altered short-term memory, dissociation of thoughts, motor impairments, and paranoia, among others, a reliable index of cannabinoid system function has in large part eluded scientists. Thus, there is a demand in contemporary clinical neuroscience for methods sensitive to cannabinoid system function, not only for assessing how cannabis use influences human information processing, but also to assess the involvement of the endocannabinoid system (ECS) in clinical disease and evaluate the effects of CB1-based drug therapies. The purpose of the present article, therefore, is to address this current need by integrating two separate literatures. The first literature demonstrates that the ECS mediates synaptic plasticity, specifically, long-term depression (LTD) of parallel fibers at the parallel fiber-Purkinje junction in the cerebellar cortex. The second literature suggests that LTD at this junction is necessary for the acquisition of the primary dependent variable in delay eyeblink conditioning (EBC)--the exhibition of temporally measured conditioned responses. These two literatures are integrated by proposing an updated EBC circuit that incorporates the CB1 receptor and the endogenous cannabinoids. Finally, the implications of the model is discussed in consideration of recent evidence from CB1 knockout mice, human cannabis users, and schizophrenia patients, with the expectation that translational research on the cannabinoid system will be advanced.

kpavel wrote:Actually I think yes. And the text below says something about it.
https://pubmed.ncbi.nlm.nih.gov/19166390/
Delta-9-tetrahydrocannabinol (THC) is the primary psycho-active ingredient in Cannabis spp., the most widely used illicit drug in the United States. THC is an exogenous agonist of the central cannabinoid receptor (CB1), one of the most abundant G-coupled receptors in the mammalian brain. Although CB1 receptors are distributed throughout the brain, they are found at very high levels in the cerebellum. Despite the variety of disturbances associated with acute cannabis intoxication, including altered short-term memory, dissociation of thoughts, motor impairments, and paranoia, among others, a reliable index of cannabinoid system function has in large part eluded scientists. Thus, there is a demand in contemporary clinical neuroscience for methods sensitive to cannabinoid system function, not only for assessing how cannabis use influences human information processing, but also to assess the involvement of the endocannabinoid system (ECS) in clinical disease and evaluate the effects of CB1-based drug therapies. The purpose of the present article, therefore, is to address this current need by integrating two separate literatures. The first literature demonstrates that the ECS mediates synaptic plasticity, specifically, long-term depression (LTD) of parallel fibers at the parallel fiber-Purkinje junction in the cerebellar cortex. The second literature suggests that LTD at this junction is necessary for the acquisition of the primary dependent variable in delay eyeblink conditioning (EBC)--the exhibition of temporally measured conditioned responses. These two literatures are integrated by proposing an updated EBC circuit that incorporates the CB1 receptor and the endogenous cannabinoids. Finally, the implications of the model is discussed in consideration of recent evidence from CB1 knockout mice, human cannabis users, and schizophrenia patients, with the expectation that translational research on the cannabinoid system will be advanced.

Really thank you so much! So (apparently) if that was the reason how can we upregulate these CB1 receptors? Thank you in advance

Protector wrote:

kpavel wrote:Actually I think yes. And the text below says something about it.
https://pubmed.ncbi.nlm.nih.gov/19166390/
Delta-9-tetrahydrocannabinol (THC) is the primary psycho-active ingredient in Cannabis spp., the most widely used illicit drug in the United States. THC is an exogenous agonist of the central cannabinoid receptor (CB1), one of the most abundant G-coupled receptors in the mammalian brain. Although CB1 receptors are distributed throughout the brain, they are found at very high levels in the cerebellum. Despite the variety of disturbances associated with acute cannabis intoxication, including altered short-term memory, dissociation of thoughts, motor impairments, and paranoia, among others, a reliable index of cannabinoid system function has in large part eluded scientists. Thus, there is a demand in contemporary clinical neuroscience for methods sensitive to cannabinoid system function, not only for assessing how cannabis use influences human information processing, but also to assess the involvement of the endocannabinoid system (ECS) in clinical disease and evaluate the effects of CB1-based drug therapies. The purpose of the present article, therefore, is to address this current need by integrating two separate literatures. The first literature demonstrates that the ECS mediates synaptic plasticity, specifically, long-term depression (LTD) of parallel fibers at the parallel fiber-Purkinje junction in the cerebellar cortex. The second literature suggests that LTD at this junction is necessary for the acquisition of the primary dependent variable in delay eyeblink conditioning (EBC)--the exhibition of temporally measured conditioned responses. These two literatures are integrated by proposing an updated EBC circuit that incorporates the CB1 receptor and the endogenous cannabinoids. Finally, the implications of the model is discussed in consideration of recent evidence from CB1 knockout mice, human cannabis users, and schizophrenia patients, with the expectation that translational research on the cannabinoid system will be advanced.

Really thank you so much! So (apparently) if that was the reason how can we upregulate these CB1 receptors? Thank you in advance

Honestly I don't think you should upregulate the receptors. What you need is to get rid of symptoms, right? You may consider trying cbd oil, pregnenolone, niacin in high doses, changes in diet. If you eat too much fat or too low it can contribute to your symptoms, as ketogenic diet was researched in psychosis symptoms and, on the other hand, anandamide which is thought to high in people with schizo symptoms is a fatty acid derivative.
See the links
https://www.healtheuropa.eu/cbd-and-psychosis-new-study-shows-cannabidiol-alters-brain-activity/97236/
https://www.forbes.com/sites/daviddisalvo/2018/08/31/study-cbd-from-marijuana-may-reset-the-brain-to-counteract-symptoms-of-psychosis/#7bbdc7816a36
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6843725/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652467/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5447368/
https://www.reddit.com/r/Psychiatry/comments/djvt3e/cbd_for_psychosis/
For details I recommend to do some search on reddit, I'm sure there are some experienced guys there.