344 replies to this topic

[Mr Serendipity]

Getting off the Riluzole. 2nd day of trouble getting to sleep, and then my sleep quality was wrecked again.

I need to look into DMAE again, I had mood stabilising effects with it, but also major insomnia. However if I cut the pill into 4 (or was it 8?) I think I could curb this side effect somewhat.

 

Riluzole helped with ocd for sure I noticed. If the pills weren’t so small, I’d rather cut them into 4 (12.5mg) doses, rather than half (25mg) doses. I’m afraid 25mg will be too strong for me. Maybe I’ll try it, before testing DMAE, not sure yet

 

edit:

Ok I decided to try and cut the Riluzole to 1/4 and also took DMAE 1/4.

 

So I’ve taken this morning:

 

2 x Multivitamin

100mg Selenium

1/4 Riluzole (approx 12.5mg give or take)

1/4 DMAE (approx 44mg give or take)

 

I’ll consume cocoa hot drink later, to see how well I can handle it (as cocoa can cause my mood instability).

 

Funnily enough while my sleep quality felt poor, I feel alright now I’ve woken up. Something that selenium has had a good effect on before (daytime tiredness).

 

Let’s see what happens.

 

Edited by Jesus is King, 25 September 2020 - 10:10 AM.

[Mr Serendipity]

Okay some good news. I seem to be “fixed”. In the sense the last couple of days I haven’t taken anything, and felt fine. Now I don’t know whether this is due to my t.gondii killer combo, riluzole, DMAE, hypnosis, etc... But another point could be tiredness, if that brings any inhibiting effect. Anyway I say “fixed” as it’s too early to tell, but my emotions/mood don’t seem out of control at all. I still have anhedonia.

 

Now I was doing some more investigation, and I can now confirm I was taking high doses of ALCAR before my pop:

 

 

I notice a difference. I take about 30 different capsules a day, 10 being fish oil, and 10 borage oil. The rest are high doses of b complex, zinc, vitamin d, multivitamins, and herbs.

 

I've only started my strict regime 10 days ago, and have so much more energy and concentration.

I think my best supplement for body building (and brain), is a teaspoon of acetyl l carnitine with a couple of raw egg yolks. My concentration/motivation in the gym has sky rocketed, I do so many more exercises in a shorter time, and I don't have the feeling to leave because I'm bored until much later on. I also can do more reps, and the lactic acid in my muscles takes a long time to build up, it feels weird but good

 

This was written on 9th Feb 2010, pop happened 3rd Feb 2011.

 

Now there is a year difference, but I found another post where I referred to myself eating 6 raw egg yolks a day on 11th August 2010. No mention of ALCAR, but I could have still been taking it.

 

The last hint is from here when I posted on 27th September 2010 asking whether glutamine is a good way to increase GABA. Which gives me the possibility I may have been taking glutamine, though I can’t find any evidence to back this up.

 

Anyway I decided to go full whammy today. Created my stack as opposed to just taking the multivitamin and selenium in the morning. Also decided to experiment with 500mg ALCAR and 4g of glutamine, just because I’ve been feeling very calm lately. I also increased my dose of riluzole to 25mg, this is because it’s easier to cut in half than a quarter, and it will absorb less when taken with fats, and I’m taking other things for NDMA antagonism, such as NAC, and I think turmeric is one also.

 

So it will be interesting to see what happens by the end of the day. It should be noted ALCAR gave me major insomnia and irritability when I experimented with it a few months back, so I’m hoping with the tweaks since then I’ll be able to handle it (like when I use to take a teaspoon of the stuff), and get it’s wonderful benefits on the amygdala and frontal lobes as the studies a few pages back show.

 

 

Edit note: Also I might have been taking creatine around that time also, and will be looking to add a low dose of it (500mg-1g) to my stack in the future if I can tolerate ALCAR and glutamine first (and then at higher doses).

Edited by Jesus is King, 01 October 2020 - 11:02 AM.

[InfinityExists]

Something about this thread resonated with me and I had to come back and post so I can find it again.

Edited by InfinityExists, 01 October 2020 - 05:35 PM.

[Mr Serendipity]

So I feel I’ve hit a milestone in my mental health. I don’t know whether it was the riluzole, t-gondii combo killer, or hypnosis, but I will note down my observations here.

 

1. My paranoia was most evident and would go into overdrive if I ever got high on weed. Now it’s pretty much non existent. The same with feeling shame/guilt when being high, pretty much non existent. This is a big development because the difference is night and day compared to a month ago.

 

2. OCD - My OCD has lessened a lot. 

 

3. Anhedonia - Still have it, but getting a little pleasure from music.

 

4. Mood swings/Anger - Lately I’ve just been as cool as a cucumber. I seem to handle everything quite well. No anger issues, mood swings, emotional flashbacks. 

 

5. Things that have triggered an emotional flashback in the past, or high/low mood swings, don’t seem to trigger me at all right now. It’s like I handle everything better right now. Doesn’t matter if I eat gluten with tabasco sauce, drink hot cocoa, my mind doesn’t get over excited and then really low.

 

6. I also seem to handle supplements and substances much better now, ones I previously couldn’t take. I use to be so sensitive that many supplements felt stimulating and could cause insomnia even when taken in the morning. Now my body and mind just feel more resiliant. It’s like drinking hot cocoa, or caffeine, I just handle it miles better. 

 

But the main difference is, my brain feels somewhat RESET. This is because lately I’ve not been taking any riluzole or the t.gondii combo, only my normal supps, but even forgot them on days. But the days I don’t take anything at all, I still feel pretty normal and balanced. It’s quite a remarkable change and I hope it continues.

[Mr Serendipity]

https://www.research...erience_in_rats

 

 

 

Abstract

The incidence of psychiatric disturbances is elevated in temporal lobe epilepsy (TLE) patients. Early life stressful events are believed to have a major impact on mental health later in life, and increasing evidence suggests that such stresses may also promote a vulnerability to TLE. This study investigated whether subjecting rats to early life stress exacerbated mood and cognitive disturbances associated with the development of epilepsy. On postnatal days 2-14, rat pups were separated from their dams for either 180 min/day (handling and maternal separation--HMS180, modelling early life stress) or 15 min/day (control handling and maternal separation--HMS15). At 7 weeks, rats were implanted with a bipolar electrode into the left amygdala. Following recovery, one group of rats from each litter underwent rapid amygdala kindling (RAK) epileptogenesis, while another underwent sham kindling. One week following this, rats were subjected to behavioural tests assessing anxiety and cognition. HMS180-exposed rats kindled faster than HMS15 rats (p<0.0001). RAK induced a potent anxiolytic effect as evidenced by increased % time spent in the open arms of the elevated plus maze, compared with sham kindled rats (p<0.0001). This anxiolytic effect was also observed in the open field task, as evidenced by increased time spent in the inner area (p=0.010). Neither RAK nor maternal separation had any effect on cognitive function in the Morris water maze. We conclude that maternal separation stress accelerates limbic epileptogenesis in adult rats, and that RAK induces potent anxiolytic effects that are not influenced by such early life stressful events.

 

[Mr Serendipity]

Dam I feel in a good mood today, like my anhedonia has lessened and I enjoy listening to music. Could be my hypnosis session earlier, but most of that was focused more on getting rid of bad habits.

 

However because of some insomnia yesterday, instead of taking my stack, I just ended up taking sulbutiamine and forskolin.

 

Forskolin being a relatively new supplement to me, only got and tried it the first time this year, maybe 3 months ago. And I definitely noticed a boost in a stimulating energy and a reduction in anxiety. But I have rarely experimented with it as a usual supplement.

 

But today was only forskolin and sulbutiamine. If it wasn't the hypnosis, this combo damn feels like a anhedonia killer, at least partially.

 

I actually hope if I can recreate this mood lift today in the future with these 2 substances, I can drop a lot of my other supplements, and just take these 2, 2 multivitamins, and selenium. And then occasionally like once a week, my t.gondii combo.

 

Anyway writing this now because the mood lift is very noticeable.

Edited by Jesus is King, 22 October 2020 - 02:03 PM.

[Mr Serendipity]

 

Hi,

 

I’ve decided to start experiment with selegiline and PEA, to see what effects it has on me.

 

Now the hypertension risk is something I want to avoid, I have 40mg of propranolol, so I was wondering, would it be possible to use it if I go into hypertension.

 

Now this morning I took:

 

5mg Selegiline (oral)

2 x Multivitamins

Selenium

100mg DLPA

 

I opened the 500mg DLPA capsule and measured 100mg and took it. No effect, so I took the rest (500mg), no effect.

 

Then I got my PEA today in 250mg capsules. I opened and measured 130mg, took it, not much effect, so I took the whole capsule, not much effect.

 

Then I took another 250mg capsule, a bit of body tingling, dilated pupils, clearer vision, but no other effects.

 

Then I took another 250mg capsule, I’m getting some body sweats, less appetite, I felt some nausea when taking a sip of water, but nothing else.

 

So all in all I’ve taken:

 

500mg DLPA

750mg PEA

 

I’m not feeling hypertension. The reason I started with 100mg of the DLPA and PEA, is because I read these low doses can cause hypertension, and cause euphoria. It doesn’t feel like I’m getting any hypertension or euphoria, the main reason for experimenting with the combo to see what effect it has on me, my brain, and anhedonia. 

 

But because I want to be careful, just in case of a hypertension emergency, will taking propranolol stop a hypertensive crisis?

 

 

I just now decided to take 2 capsules, so 500mg at once. Let’s see what happens.

 

So a total of 1250mg of PEA.

 

 

So I just posted the above in a new thread. As you can see I took 5mg selegiline this morning, and I’ve taken 500mg DLPA and 1250mg PEA.

 

The main reason for this, was I wanted to compare the euphoria to my mini pop in 2011 to see if they were related or the same, and whether it could be a problem with my PEA levels. According to many people’s reports, the euphoria has been described as the strongest euphoria they’ve ever felt, more than crack, DMT, and ecstasy.

 

Well I don’t know what’s happened, but I’m not experiencing any hypertension (good thing), or euphoria.

 

I know recently, I think when I started taking selenium (better thyroid, higher gluthinoine levels), or maybe the t.gondii killer combo I was using. But I’ve been tolerating supplements so much better lately.

 

But the fact that I tolerate PEA + selegiline right now, without any euphoria or hypertension is baffling to me. I’m only experiencing clearer vision,appetite suppression, sweating, some body tingling, and a bit of nausea.

 

I plan on to continue experimenting with the combo. I will probably experiment with some higher doses initially to see if anything happens, and then just reduce it to 250mg PEA + 5mg Selegiline in the morning, as it seems I can tolerate it extremely well.

 

 

[Mr Serendipity]

Okay I’ve decided not to experiment any further with higher doses after today.

 

The reason being, the PEA is obviously affecting me, I had:

 

1. sweats at one point

2. a bit of body tingling

3. a bit of nausea

4. pupils are dilated

5. clearer vision

6. vasoconstriction (even though I don’t feel cold, my wifes hands are warm, and she said I feel really cold)

7. some heart beat changes (a bit faster pumping)

8. I feel a bit more in control (I think)

9. appetite suppression

 

So in other words, PEA is in my system, regardless of the fact there was no euphoria or pleasure or reduction of anhedonia or hypertension at such high doses. Which means my reward system is so royally screwed up that even this famous combo doesn’t do anything.

 

I plan on taking just one pill (250mg) of PEA and 5mg of selegiline in the morning, to see if there is any improvement over time. It’s a shame I can’t get hold of any lower doses though, and I can’t be bothered to buy the powder to measure it out every time, but I would prefer doses in the 60-100mg range.

 

Let’s see what happens.

[Mr Serendipity]

And the plans changed again.

I think I’m going to avoid PEA completely. Selegiline by itself has had some positive effects. When I took 10mg yesterday, I actually felt a shaking/build up to an orgasm (remember I suffer from ejaculatory anhedonia), very different then any other time. Also during yesterday I was in an alright mood.

But the biggest problem selegiline causes in me is excessive talking, whether it’s 5mg or 10mg. The other problem is insomnia, however I might be able to get use to this.

But the excessive talking is a problem. I’m wondering if I can combine it with ALCAR (which also gives me insomnia) to see if there is a balancing effect for the dopamine by increasing my acetylcholine at the same time (as well as the other mood benefits of ALCAR).

Problem then is insomnia. Maybe I should look to boost serotonin as well, maybe 5htp. See if I can figure out the right combo.

Edited by Jesus is King, 24 October 2020 - 11:27 PM.

[Mr Serendipity]

https://pubmed.ncbi....ih.gov/6448885/

 

 

 

Antidepressant potentiation of 5-hydroxytryptophan by L-deprenil in affective illness

Abstract

In an open trial study, L-Deprenil, an irreversible selective MAO-B inhibitor without 'chesse effect' was given to 14 patients with unipolar and bipolar depression receiving L-5-Hydroxytryptophan (L-5-HTP) and benzerazide. Ten out of 14 patients showed a good response to the combination of drugs and a correlation was found between the degree of platelet MAO inhibition and clinical response. In a double-blind controlled study, 18 affectively ill patients were randomly allocated to L-Deprenil plus L-5-HTP and benzerazide, 21 patients were treated with L-5-HTP and benzerazide and 19 patients with placebo only. Patients treated with the combination of L-Deprenil and L-5-HTP showed a significantly greater clinical improvement than placebo patients but this was not the case for patients treated with 5-HTP alone. A positive relationship was demonstrated between mood improvement and degree of platelet MAO inhibition in patients treated with L-Deprenil.

Just a quick google search and I find a study on 5htp and selegiline, and it seems very positive. It’s also under the cheese effect, so they were probably using doses under 20mg.

 

So I’m thinking an experiment with selegiline for dopamine, 5htp for serotonin/melatonin, and alcar for acetylcholine is something to experiment with tomorrow.

 

 

Edited by Jesus is King, 24 October 2020 - 11:38 PM.

[Mr Serendipity]

https://www.selegiline.com/noss.html

 

 

 

  Effects of co-administration of a selective serotonin reuptake inhibitor and monoamine oxidase inhibitors on 5-HT-related behavior in rats 
by
Izumi T, Iwamoto N, Kitaichi Y, Kato A, Inoue T, Koyama T.
Department of Psychiatry,
Hokkaido University Graduate School of Medicine,
North 15, West 7, Sapporo 060-8638, Japan. 
Eur J Pharmacol. 2006 Feb 17; 

ABSTRACT

5-hydroxytryptamine (5-HT) syndrome is a dangerous condition of 5-HT excess that can occur in the case of co-administration of a monoamine oxidase (MAO) inhibitor and a serotonin reuptake inhibitor (SSRI). The goal of the present study was to investigate the effects of acute administration of MAO inhibitors and subchronic administration of fluvoxamine on 5-HT-related behaviors (head shaking and 5-HT syndrome) in rats treated with 5-hydroxytryptophan (5-HTP). Administration of the non-selective MAO inhibitor, pargyline, and the selective MAO-A inhibitor, clorgyline, resulted in 5-HT syndrome in 5-HTP-treated rats, and subchronic co-administration of fluvoxamine intensified the syndrome. However, administration of the selective MAO-B inhibitor, selegiline, did not induce 5-HT syndrome with or without subchronic fluvoxamine co-administration. These data suggest that non-selective MAO and selective MAO-A inhibitors can induce 5-HT syndrome in humans when co-administered with SSRI. Further, the risk of 5-HT syndrome may be lower with the selective MAO-B inhibitor, selegiline.

And this study shows selegiline should be safe with 5-htp as in to not cause serotonin syndrome.

[Mr Serendipity]

https://nootropicsex...s-for-adhd-add/

 

 

 

But Deprenyl is the only drug known to selectively enhance a tiny region of the brain called the substantia nigra. This place is rich in dopamine neurons. That’s where problems start that turns into Parkinson’s.

 

So I came across this interesting comment. 

 

https://www.cell.com...(11)00192-5.pdf

 

 

dopaminergic projections from the substantia nigra to areas such as the dorsal striatum, also called caudate putamen. The latter dopaminergic projections may also be involved in anhedonic responses, particularly in individuals suffering from Parkinsonism, which is characterized by gradual de- generation of the substantia nigra dopaminergic projec- tions. 

 

https://psycnet.apa..../1995-09514-001

 

 

 

Anhedonia in schizophrenic, depressed, or alcohol-dependent patients: Neurobiological correlates.

 

Abstract

Anhedonia, dysphoria, and avolition are common symptoms of schizophrenic, depressive, and alcohol-dependent patients during withdrawal. These symptoms may be caused by a functional deficit of dopaminergic transmission in the dopaminergic reward system, ascending from the mesencephalon to the ventral striatum. The dopaminergic reward system is functionally and anatomically closely connected with the ascending extrapyramidal pathways from the substantia nigra to the dorsal striatum. A dysfunction of both ascending dopaminergic pathways is expected to cause psychomotor slowing, dysphoria, and anhedonia. This hypothesis is supported by positron emission tomography and single photon emission computed tomography findings from neuroleptic-treated schizophrenics and from drug-dependent patients. (PsycINFO Database Record © 2016 APA, all rights reserved)

 

https://www.ncbi.nlm...les/PMC6406445/

 

 

 

Conclusion: Paroxetine but not agomelatine was associated with important decreased activity in dopaminergic areas such as the substantia nigra and ventral tegmental areas that could be associated with sexual performance impairment in humans after antidepressant treatment.

 

The known SSRI Paxil sexual dysfunction side effects could be due to decreased activity in the substantia nigra area of the brain.

 

https://www.ncbi.nlm...les/PMC6832699/

 

 

 

More than 80% of subjects from the paroxetine group showed sexual problems in the first week (mainly ejaculation retardation and anorgasmia), while the sexual problems reported by the two agomelatine groups were similar to placebo.

 

So this is all of interest to me because of the sexual buildup I experienced yesterday when I had taken 10mg of selegiline. Which should be noted I never experience.

 

Could selegiline possibly be enhancing the substantia nigra part of my brain, which caused a partial reversal of my ejaculatory anhedonia/anorgasmia yesterday?

 

Also the fact that Paxil decreased activity in the substantia nigra, and that 80% of subjects on Paxil experienced sexual problems which were mainly ejaculation retardation and anorgasmia (in the first week of treatment), be the connection the connection I’m looking for?

 

I might first just experiment with 5htp and selegiline first and forget the ALCAR for now. If the 5htp can help prevent the negative effects of selegiline I experience (insomnia, excessive talking), I might be able to raise my dose higher than 5 or 10mg.

 

The big development here is something happened with 10mg of selegiline, whereas nothing happens with all the other things I’ve experimented with. So I should be looking into why selegiline helped in this area, something I’ve suffered with for 16 years.

Edited by Jesus is King, 25 October 2020 - 12:49 AM.

[Mr Serendipity]

https://www.hindawi....rn/2011/219427/

Several reports have described that selegiline, a monoamine oxidase B (MAO-B) inhibitor, is effective for the treatment of decreased willingness and depressed mood in PD.Tom and Cummings[32] recommended selegiline as the first choice to treat depression in PD patients not exhibiting suicidality. The primary effects of selegiline are inhibition of MAO-B and efficient use of intracranial dopamine. Moreover, selegiline is known to reinforce the intracranial phenylethylamine (PEA) activity [33]. PEA promotes serotonin release to improve symptoms of decreased willingness and depressed mood in PD. Therefore, PEA is particularly effective for apathy and anhedonia complicated with depression.

 

 

More interesting stuff. Selegiline will increase PEA as well.

 

Here is the referred study: https://link.springe...1007/BF01246964

[Mr Serendipity]

https://pubmed.ncbi....h.gov/23904408/

 

 

 

Abstract

It is 16 years since we reviewed anhedonia in depression. Since then, there have been important developments in the study of anhedonia, mainly using the new techniques that neuroimaging made available, which provide very interesting new insights. It is becoming increasingly apparent that anhedonia, with psychomotor retardation, defines a dimension in depressive disorder that seems to be distinct from a dimension encompassing mood plus somatic symptoms. These dimensions can coexist, but may also be present separately. The first appears associated with disturbances (under-functioning) in dopamine function; the other appears to be related to a similar under-functioning in the serotonin system. Furthermore, anhedonia itself increasingly appears to be a composite symptom, consisting of at least two dimensions (i.e. a motivational/appetitive and a consummatory one). Depression appears to be characteristically linked more to the first one, in contrast to what was originally thought. We discuss the significance of the above in the evolving treatment of depression and the potential use of dopamine-targeting drugs.

 

Hmm associated with disturbances with the dopamine function and an under-functioning serotonin system.

 

It will be interesting to experiment with 5-htp and selegiline tomorrow. My idea for the initial experiment is 50mg of 5-htp and 10mg of selegiline, and lets see how I function. If the 5-htp seems to reduce the negatives I experience with selegiline, I can then try experimenting with high doses of selegiline, and if need be 5-htp.

 

 

[Mr Serendipity]

https://www.research...in_rat_midbrain

 

 

 

The vitamin D receptor in dopamine neurons; its presence in human substantia nigra and its ontogenesis in rat midbrain

 

Abstract

There is growing evidence that vitamin D is a neuroactive steroid capable of regulating multiple pathways important for both brain development and mature brain function. In particular, there is evidence from rodent models that prenatal vitamin D deficiency alters the development of dopaminergic pathways and this disruption is associated with altered behavior and neurochemistry in the adult brain. Although the presence of the vitamin D receptor (VDR) has been noted in the human substantia nigra, there is a lack of direct evidence showing that VDR is present in dopaminergic cells. Here we confirm that the VDR is present in the nucleus of tyrosine hydroxylase (TH)-positive neurons in both the human and rat substantia nigra, and it emerges early in development in the rat, between embryonic day 12 (E12) and E15. Consistent evidence based on immunohistochemistry, real-time PCR and western blot confirmed a pattern of increasing VDR expression in the rat midbrain until weaning. The nuclear expression of VDR in TH-positive neurons during critical periods of brain development suggests that alterations in early life vitamin D status may influence the orderly development of dopaminergic neurons.

 

https://www.ncbi.nlm...les/PMC7070325/

Vitamin D Supplementation is Associated with Increased Glutathione Peroxidase-1 Levels in Arab Adults with Prediabetes

Abstract

Vitamin D supplementation may be used to lower oxidative stress. This interventional study aimed to investigate the effects of vitamin D supplementation on glutathione peroxidase 1 (GPx1) levels and other parameters in Arab adults with prediabetes. A total of 203 Saudi adults with prediabetes and vitamin D deficiency [intervention group, N = 146 (53 males and 93 females); control group, N = 57 (25 males and 32 females)] were included in this non-randomized, six-month intervention study. The intervention group received 50,000 international units (IU) cholecalciferol tablets once a week for two months, then twice a month for the next two months, followed by 1000 IU daily for the last two months. The control group received no supplementation. Serum 25(OH)D, lipid profile, glucose, C-reactive protein (CRP) and GPx1 were measured at baseline and after six months. Post-intervention, GPx1 concentrations increased significantly in the intervention group [17.3 (11.5–59.0) vs 26.7 (11.4–59.9) p < 0.01] while no changes were observed in the control group (p = 0.15). This significant increase in 25(OH)D and GPx1 levels persisted after adjusting for age and BMI. Stratification according to sex revealed that this favourable increase in GPx1 was true only for males (p = 0.002). In all groups, baseline GPx1 was inversely correlated with low density lipoprotein (LDL)-cholesterol (r= −0.26, p < 0.01) and body mass index (BMI) (r = −0.20, p < 0.05), while positively correlated with age (r = 0.18, p < 0.05) and systolic blood pressure (r = 0.19, p < 0.05). In conclusion, vitamin D supplementation favourably enhanced GPx1 levels in adult Arabs with prediabetes, particularly in males.

 

 

 

https://www.ncbi.nlm...les/PMC4580407/

 

Vitamin D Deficiency and Depressive Symptomatology in Psychiatric Patients Hospitalized with a Current Depressive Episode: A Factor Analytic Study

Abstract

Background

Low vitamin D levels have been associated with depressive symptoms in population-based studies and non-clinical samples as well as with clinical depression. This study aimed to examine the association of vitamin D levels with the severity and dimensions of depressive symptoms in hospitalized patients with a current episode of depression taking into account confounding variables.

Methods

We investigated 380 patients (mean age 47±12 years, 70% women) who were consecutively hospitalized with a main diagnosis of an ICD-10 depressive episode. All patients self-rated depressive symptom severity with the Hospital Anxiety and Depression Scale (HADS-D), the Beck Depression Inventory-II (BDI-II), and the Brief Symptom Inventory. A principal component analysis was performed with all 34 items of these questionnaires and serum levels of 25-hydroxyvitamin D3 (25-OH D) were measured.

Results

Vitamin D deficiency (<50 nmol/l), insufficiency (50–75 nmol/l), and sufficiency (>75 nmol/l) were present in 55.5%, 31.8% and 12.6%, respectively, of patients. Patients with vitamin D deficiency scored higher on the HADS-D scale and on an anhedonia symptom factor than those with insufficient (p-values ≤0.023) or sufficient (p-values ≤0.008) vitamin D. Vitamin D deficient patients also scored higher on the BDI-II scale than those with sufficient vitamin D (p = 0.007); BDI-II cognitive/affective symptoms, but not somatic/affective symptoms, were higher in patients with vitamin D deficiency (p = 0.005) and insufficiency (p = 0.041) relative to those with sufficient vitamin D. Effect sizes suggested clinically relevant findings.

Conclusions

Low vitamin D levels are frequent in hospitalized patients with a current episode of depression. Especially 25-OH D levels <50 nmol/l were associated with cognitive/affective depressive symptoms, and anhedonia symptoms in particular.

 

 

 

First of all I took this morning:

 

15mg Selegiline

50mg 5-htp

2 x Multivitamins

100mcg Selenium

 

I thought hell lets try a 15mg dose. Well I can confirm the 50mg 5-htp does prevent the side effect of excessive talking I was getting from selegiline.

 

 

Now lets go back to something interesting. I was thinking, what helped me with my general anhedonia most? NAC. If I stop taking it I get that stuck in the rut feeling.

 

As we know NAC helps increase glutathione levels.

 

Then I read the interesting thing about people with Parkinson’s: https://scienceofpar...insons-disease/

 

 

 

The investigator who conducted this study began by analysing levels of glutathione in autopsied human brain. They found that in general glutathione content is significantly lower in the substantia nigra (the region where the dopamine neurons live) than in other brain regions. But when they looked at glutathione levels in the substantia nigra of people who died with Parkinson’s disease, they barely detected any glutathione at all.

 

Now when I got hit by Covid, even though I took most popular supplements under the sun (including NAC), I was hit by it the hardest and off work the longest compared to my wife and father. Also even though I took many supplements, I would always get ill on holidays and stuff while my wife who didn’t take anything didn’t, and it confounded me why my immune system was so weak. After the COVID incident I discovered NAC can exacerbate a selenium deficiency if you already have one, and that COVID severity has been linked to selenium levels.

 

Since I’ve taken selenium, I can tolerate supplements I couldn’t previously, my libido went up, daytime tiredness was eliminated, and I haven’t been ill since.

 

But there was one moment where I was dosing a lot of vitamin D and C during my COVID to try and recover (prior to selenium supplementation), and I noticed a very happy mood lift, and said to myself to investigate higher doses of Vitamin D later on.

 

After reading a comment about Vitamin D increasing glutathione levels, and finding a study on it (2nd one above). And then finding that there are vitamin D receptors in the substantia nigra (1st study above), and that Parkinson’s disease have barely any glutathione levels in the substantia nigra (last study), and that low vitamin d levels are associated with anhedonia (3rd study), and the fact that I was selenium deficient (thus having lower glutathione levels), it makes me think my focus should be to increase glutathione levels in the substantia nigra.

 

So it’s time to focus on the following, here’s my idea:

 

10mg Selegiline

50mg 5-htp

2g NAC

High doses of Vitamin D 10,000 IU and above

100-150mcg Selenium

2 x Multivitamins

1-2g Vitamin C to potentiate the NAC

 

Last point, I was taking Vitamin D in high doses (10,000 UI) when at uni. However my earliest recollection was the year after my mini pop, but I have no way of knowing if this is the case, and my order history from iherb has gone from around that period.

 

 

[zorba990]

Not sure combining Selegiline with 5-HTP is a good idea IRT possible serotonin syndrome. By the time the heart valve(s) damage occurs it may be too late to reverse it.

I would think replacing Selegiline with 2-4G tyrosine n an empty stomach first thing AM would be way safer way to up-regulate dopamine. But them I have a number of sensitivities that would make your stack too much for me... perhaps it will be ok for you.


https://en.wikipedia...otonin_syndrome
"Many cases of serotonin toxicity occur in people who have ingested drug combinations that synergistically increase synaptic serotonin.[8] It may also occur due to an overdose of a single serotonergic agent.[26] The combination of MAOIs with precursors such as L-tryptophan or 5-HTP pose a particularly acute risk of life-threatening serotonin syndrome.["

[Mr Serendipity]

Not sure combining Selegiline with 5-HTP is a good idea IRT possible serotonin syndrome. By the time the heart valve(s) damage occurs it may be too late to reverse it.

I would think replacing Selegiline with 2-4G tyrosine n an empty stomach first thing AM would be way safer way to up-regulate dopamine. But them I have a number of sensitivities that would make your stack too much for me... perhaps it will be ok for you.


https://en.wikipedia...otonin_syndrome
"Many cases of serotonin toxicity occur in people who have ingested drug combinations that synergistically increase synaptic serotonin.[8] It may also occur due to an overdose of a single serotonergic agent.[26] The combination of MAOIs with precursors such as L-tryptophan or 5-HTP pose a particularly acute risk of life-threatening serotonin syndrome.["

 

I refer you to posts 251 and 250.

 

Serotonin syndrome was something I was worried about and researched where I found these 2 studies, and decided it should be safe to take as long as I’m not in cheese effect doses of 20mg and above.

 

https://www.selegiline.com/noss.html

 

And this study shows selegiline should be safe with 5-htp as in to not cause serotonin syndrome.

 

 

https://pubmed.ncbi....ih.gov/6448885/

 

Just a quick google search and I find a study on 5htp and selegiline, and it seems very positive. It’s also under the cheese effect, so they were probably using doses under 20mg.

 

So I’m thinking an experiment with selegiline for dopamine, 5htp for serotonin/melatonin, and alcar for acetylcholine is something to experiment with tomorrow.

 

Side note: I have experienced serotonin syndrome a few years back (around 2016) when taking 5-htp and smoking weed. So it’s definitely something I want to avoid.

 

Also from what I understand, it’s a risk when MAO-A is inhibited. Selegiline inhibits MOA-B but spills over to MAO-A when you take doses of 20mg and above, while low doses don’t inhibit MOA-A.

 

More info: https://en.m.wikiped...amine_oxidase_B

 

 

Differences between MAOA and MAOBEdit

MAO-A is involved in the metabolism of tyramine; inhibition, in particular irreversible inhibition of MAO-A can result in a dangerous pressor effect when foods high in tyramine are consumed such as cheeses (informally known as the "cheese effect"). MAO-A is involved in the metabolism of serotonin, noradrenaline and dopamine whereas MAO-B metabolises the dopamine neurotransmitter.^[7] MAO-B is an enzyme on the outer mitochondrial membrane and catalyzes the oxidation of arylalkylamineneurotransmitters^[8]

 

 

Edited by Jesus is King, 25 October 2020 - 06:24 PM.

[Mr Serendipity]

I'm going to go in another direction, just looking back at my experiences and the information.

 

Selegiline helps with addictions. On it I feel no need to smoke weed or drink alcohol. I probably wouldn't even smoke cigarettes if I didn't currently have a pack of tobacco. It also crushes my appetite which is good, would make losing weight effortless. However I also forget to drink water, or I lack thirst, luckily I recognize it and make sure I do drink, but sometimes I realize I haven't drank anything since the morning, 6 hours later or something. Another problem with it is it's killed my libido. I also get a weird tunnel vision motivation with it, but it's not goal motivation, it's more like I can spend hours reading or doing something, but my brain doesn't register/absorb the information well, like a lack of focus. But the biggest problem is it does absolutely nothing for my anhedonia or mood, I feel emotionally flattened.

 

Now I thought maybe I should be focusing on the D2 receptor. I've had had mood lifting effects from sulbutiamine and forskolin. But with sulbutiamine it's only happened very few times, and I find it harsh on my kidneys (I notice this when urinating). I also don't want to bother experimenting with inositol and raising the doses higher and getting use to the diarrhea.

 

But there is one supplement which sticks out, I tried it by itself once and it's effects were pronounced, and not only was my mood lifted, but my anxiety was non existent and I felt more motivated. Forskolin. Yes forskolin is a D2 upregulator, but I have a feeling it's not a hit and miss supplement either like sulbutiamine for example.

 

Now the benefit of this small selegiline trial was the fact that I needed to take 50mg of 5-htp in the morning to prevent excessive talking (this entry doesn't count). In fact it worked so well for excessive talking, the difference was night and day between the days before I took it (but was on selegiline) and the days after. So I plan to keep on experimenting with it.

 

But the new information I learnt about the substantia nigra, is where I currently think my issues stem from. There are a few studies on forskolin and the substantia nigra, but I can't pretend to understand or interpret them. However the studies on Vitamin D in that area are clear, and also the link between low Vitamin D levels and anhedonia. However increasing vitamin D always causes strong constipation with me, as I found out again by taking 10,000 I.U. yesterday. Also my days of going to extremes with doses are behind me. However due to the vitamin D studies aforementioned (on the substantia nigra and on anhedonia), I will increase my dose to 5000 I.U. a day rather than the 1000 I.U. I have taken this dose in my stack previously without bad constipation effects, though I felt it increased my serotonin too much to the point it made me apathetic, but I'm willing to give it another try. Also lets not forget the glutathione levels connection with the substantia nigra in parkisons disease, and the fact vitamin D raises glutathione levels too.

 

So the base stack I'm thinking of doing for my substantia nigra and glutathione levels (which are the things I believe I should be trying to target), would be something like the following:

 

2 x Multivitamins

100mcg Selenium

5000 I.U. Vitamin D

Forskolin (50mg active forskolin)

500mg NAC

 

They'll probably be other additions, but the above are the main ones, and the ones I'll be experimenting with initially to see its effect.

 

Another thing is I should reiterate what I posted on the 1st of October (post 242). Even before these recent experiments with selegiline and other things, is I still feel partially fixed. This came after my 2 or 3 days I experimented with riluzole. There hasn't been an incident where my emotions have gone out control, had an emotional flashback, or felt triggered. It felt like my brain reset somewhat from that brief stint on riluzole, and one of the reasons I say this, is because I had days where I didn't bother taking any of my supplements and I felt fine. And I'm not sure whether I'm suffering from OCD anymore or not, but that's hard to tell when you're trying different things. But it definitely felt like a milestone. Hell something like 500mg of DLPA which sent me into an emotional flashback I couldn't control jsut recently in September (and the reason I avoided it for awhile), doesn't effect me at all now when I've experimented with it. However I felt no benefits from DLPA even when taking selegiline, so it's not something I'd bother with right now, maybe future experimentation. Also the riluzole may have done it, or maybe I did kill t.gondii in my brain by taking my t.gondii killer combo over a 2 week period, or the fact the multivitamin I've been taking has been covering other nutrients I haven't been supplementing and was deficient in, or the fact it has live bacteria in it, who knows. But around the beginning of October, things didn't effect my mood and emotions negatively as much as they use to, whether on or off supplements.

 

Regardless I'm enjoying these small experiments I'm doing, t.gondii killer, riluzole, selegiline etc... because I feel they are teaching me bits and bobs along the way, such as the 5-htp to counteract increased dopamine/hyper side effects. Then again 5-htp may not be needed if previous experiences with 5000 IU of Vitamin D and serotonin increase are anything to go by, but this is where the next few weeks of experimentation will help.

 

Anyway I've written a lot, I wanted to get all my thoughts down before I forget them. But lets see if I can hone in more on the right supplements, using my experiences and the new studies I've learnt about.

 

 

Edited by Jesus is King, 27 October 2020 - 02:45 AM.

[Mr Serendipity]

Too much Vitamin D, including 5000 IU isn’t great for me, tight muscles and all, insomnia yesetday, but I can deal with day time tiredness. I’m going back to my old stack that worked with a few tweaks. Might try taking my MK4 supplement again to balance the Vitamin D so I can take 5000 IU, I took it this morning and I wasn’t as out brain fog before. Vitamin D really helps with IBS though.

 

I tried my old stack with forskolin and 5000 IU today, and MK4, so I think my stack is really shaping up. Yesterday I was going on a bit of a high when I only took:

 

2 x Multivitamins

100mcg Selenium

5000 I.U. Vitamin D

Forskolin (50mg active forskolin)

500mg NAC

 

However I don’t think I need 5-HTP to balance me, because I took my original stack this morning, and I feel concentrated, no releaving in anhedonia though, but motivation and control. The DMAE and tumeric is best for me with the balancing stack. And also 250mg PEA.

 

In other words I seem to be more stable on things like amphetamine type substances. Like DMAE or PEA and forskolin. So they stable my highs, my mood, and make me avoid addictive behaviour like weed and alcohol. And while my anhedonia is alleviated, the mood balancing effect is great, and the slight motivation.

 

I feel so motivated to lose weight now, and find I pop a PEA when I’m hungry I can go another few hours.

 

I think I may still take selegiline as a once a week thing. Like every Sunday.

 

Anyway here’s my stack I’ll be taking the next couple of weeks:

 

Morning

 

2 x Multivitamin (Higher Nature - Advanced Multi)

1 x Selenium [200mcg] (Natures Aid)

1 x NAC [500mg] (Prowise/Amazon)

1 x Benfotiamine [150mg] (Doctors Best)

1 x Vitamin C [1g] (Any brand is fine as long as it’s ascorbic acid)

1 x Vitamin D [5000 I.U.] (Natures Aid)

1 x Vitamin E (Healthy Origins - E400)

1 x Cod Live Oil [1g] (Natures Aid)

1 x Borage Oil [1g] (Supplemented/Amazon) 

1 x Pycnogenol [30mg] (Natures Aid)

1 x Ginger (Natures Aid or Higher Nature)

1 x Turmeric (Nature’s Aid)

1 x Forskolin [50mg Active Forskolin] (Amazon

1/4 x DMAE [175mg] (Nature’s Aid)

1 x Phenylethylamine/PEA[250mg] (eBay)

1 x Vitamin K2 [5mg MK4] (Carlson)

 

 

So basically whats changed are the following:

 

Added Vitamin K2

Added PEA

Added Forskolin

Upped my Vitamin D from 1000 IU to 5000 IU

Upped my Selenium from 100mcg to 200mcg

 

Whereas before 200mcg Selenium seemed too much, I think my body has adapted and can handle it now, so even if I get insomnia, it doesn’t effect me during the day to function. Also I may plan on upping the DMAE to just one pill for convenience. DMAE also gives me insomnia, as does ALCAR, but it will be interesting to see if I can handle these things, and function during the day.

 

If I had to give any advice to people from my experiences for anxiety or mood balancing effects, Forskolin and DMAE seem to be the ones that work best. Obviously everyones different, but these 2 are mood stablising.

 

[Mr Serendipity]

Okay I definitely hit some sort of milestone. Yesterday I was in a great mood. Here’s what my stack came down to:

 

[] = Dosage of pill, not total dosage

 

2 x Multivitamin (Higher Nature - Advanced Multi)

1 x NAC [500mg] (Prowise/Amazon)

1 x Benfotiamine [150mg] (Doctors Best)

1 x Vitamin C [1g] (Any brand is fine as long as it’s ascorbic acid)

1 x Vitamin E (Healthy Origins - E400)

1 x Cod Live Oil [1g] (Natures Aid)

1 x Borage Oil [1g] (Supplemented/Amazon) 

1 x Pycnogenol [30mg] (Natures Aid)

1 x Ginger (Natures Aid or Higher Nature)

1 x Turmeric (Nature’s Aid)

1 x Forskolin [50mg Active Forskolin) (Amazon)

1/2 x Selenium [200mcg] (Natures Aid)

 

As you can I:

 

1. Cut Selenium to 100mcg again, feels right for me.

2. Dropped DMAE, PEA, Vitamin K2 (MK4), Vitamin D

 

I still get Vitamin D from Cod Liver Oil and Multivitamin, 600 IU in total. I don’t feel right with extra high doses of vitamin D though, even when using vitamin k mk2 to try and balance it, I feel mentally out of it. However I am going to add 1000 I.U. again as I was handling that fine in my stack previously, which would make it 1600 I.U. In total. DMAE actually ended up making me irritable at higher doses, also major insomnia. PEA doesn’t seem to fix anything so no point in supplementing it.

 

Also I take sulbutiamine every now and then, just not every day. So I’m pretty much happy with my stack at this point, and don’t think I’ll be trying many more things in the near future.

 

 

So for results:

 

1. Yesterday I was in a great mood, no anxiety when interacting with people.

2. Feel a bit more umph in life.

3. Enjoy things slightly better, even music.

4. No emotional flashbacks?

 

But I think I’m getting more of a mood lift than a reduction in anhedonia. I think emotions and pleasure are very much separate. As in I’m listening to music and enjoying it a little bit more because I’m in a good mood, rather than the music making me feel better.

 

 

 

 

Edited by Jesus is King, 11 November 2020 - 10:45 AM.

[Mr Serendipity]

I forgot to add I can drink an energy drink now and feel fine, whereas before I would easily get stressed out by everything.

 

Also I’ve been taking glutamine powder some days just like sulbutiamine, usually around 5-10g.

 

So in general, since October 1st where I described myself as sort of fixed, I think I’ve been slowly making progress since then. It’s hard to describe and it’s subtle, but I hope it can continue. I still have OCD btw, sometimes it rears itself, but most of the time not.

 

I think the focus on increasing my glutathione levels via selenium and NAC, as well as forskolin which is great for mood and anxiety, and the new multivitamin I added in the last few months are helping the most, though the former 2 gave me noticeable changes even by themselves. But lets not forget I did a t.Gondi trio combo killer consistently for around 3 weeks back in September, so maybe my brain is readjusting dopamine, assuming I did have t.Gondii.

 

Let’s see what happens.

 

Oh something else. I think I can get a mood boost from amygdala tickling now, but it has to be short and once in the day. I notice I don’t go down in mood loads, and I just end up having a load of nightmares which aren’t scary, which happens when I amygdala tickle, a lot more nightmares, but at least they’re not scary. Anyway I’m thinking of tickling once of a max of 5 minutes before falling asleep, to see if I can get the mood boost for the next day without bad mood/emotional flashbacks, and let the dreams handle the craziness. Hopefully, we’ll see, but I might just put one song or music piece on, and tickle throughout it, and then don’t tickle the rest for that day. Anyway ideas.

[Mr Serendipity]

I’ve been in a brilliant mood most of the day, and totally forgot I had taken sulbutiamine today along with my normal stack, glutamine, and an additional 1000IU of Vitamin D.

 

So sulbutiamine + forskolin I think gives me the best mood boosting effects. Maybe I really need D2 upregulation or something. 

 

Oh and I remember why I dropped DMAE, I decided to try a higher dose which was 2 tablets vs 1/4 of 1 tablet. That day was a bad day, very irritable, bad mood, easily stressed, thoughts racing. Thankfully now I have alternatives, mainly being forskolin, I won’t have to worry about experimenting with DMAE again.

Edited by Jesus is King, 11 November 2020 - 09:16 PM.

[Mr Serendipity]

One thing I want to quickly go into, is the separation of emotion and pleasure. I was thinking about my emotional climax, mini pop, whatever you want to call it back in 2011.

 

The day of that mini pop, I went to a higher level of emotions. There was no hallucinations, no visual or auditory changes, just a higher level of positive emotions. Think happiness vs super happiness. I remember my brain really woke up for the first time, like we’re all drifting through life half asleep. It felt all my subconscious fears collapsed, but not anything specific, just all of them. The only way I can describe it, is imagine you have all these subconscious fears running in the background through every moment of your life, affecting the way you do things, how you feel, the way you behave, but you’re not consciously aware of them. Well all of them collapsed and I experienced super happiness with 0 fear, I emotionally felt everything was going to be alright, whether world war 3 broke out, whether I was tortured, or there was a food crisis, everything was going to be a-okay. It was a great emotion people can’t quite grasp, the feeling of complete utter contentment and 0 worry about anything. Alas it only lasted for 10-15 minutes.

 

Basically I’ve redescribed my mini pop. But I’m the unique case where I haven’t had an orgasm for 16 years, back then it would have been about 7 years I hadn’t experienced one. And after I had that mini pop, there was no change in sexual pleasure afterward, which is contrary to Lingos theory for progress (sexual pleasure and orgasms should increase), but then again if I can’t experience it like normal people, it would have been very lucky if it restored any of it back, let alone enhanced it.

 

But my point is how separate pleasure and emotions are. Someone like me who is pleasure defunct, can still experience higher positive emotions that aren’t felt by normal people. 

 

Now when you experience anhedonia, the line gets blurred between pleasure and emotion. Now I’m starting to feel in better moods, even though there’s no increase pleasure, positive emotions give a sort of pleasure themselves. For example while I don’t feel lots of pleasure from music for example, I’m listening and singing along to it because I’M ALREADY IN A GOOD MOOD, and being in a good mood makes it that bit more fun.

 

So I feel I have my foot in the door a bit. If I just focus on increasing positive emotions rather than pleasure, I might be able to pop again. It’s been 9 years, but I can see the progress I’ve made immensely.

 

Oh and very last thing. Paranoia is little to non existent when smoking weed now, which is remarkable. While I don’t see weed as beneficial to me and try to avoid it, nothing taught me more about how strong my paranoia was, and it’s remarkable decrease in the last couple of months.

[Mr Serendipity]

Okay a bit of an update from yesterdays experience.

 

I had taken glutamine, extra vitamin D, sulbutiamine, and an energy drink.

 

I was in a great mood yesterday, but the insomnia was killer.

 

Things I’ve noticed from past experience:

 

Glutamine - Causes excessive talking

Sulbutiamine - Great for mood, especially when paired with forskolin, but causes major insomnia.

Vitamin D - I already get 600 IU from my stack, adding an extra 1000 IU might help but higher doses in the past have caused insomnia in the past, so I’m going to see how I do with just 600 IU and my mood.

Forskolin - Great for mood, anti anxiety, and probably anhedonia, works even when I take it alone without any other supplements.

Energy drink - I can handle caffeine now, and this along with sulbutiamine and forskolin makes me in a great hyperactive mood, but is not worth going down this route.

 

So one thing I’ve noticed, is taking sulbutiamine in the past for mood is hit and miss. And it has given me insomnia in the past without a mood increase.

 

Forskolin seems to be my favourite supplement right now for mood and anxiety (non existent). It also doesn’t cause problems like excessive talking, and I don’t think it has any effect on sleep/insomnia, in fact I’ve read it has helped people with their insomnia/sleep issues.

 

Now here’s a connection. I remember in the past I threw away my cdp-choline because it would cause major insomnia. But I also remember I had it around the time of my first mini pop, and may have been taking it. The connection with forskolin, cdp-choline, and sulbutiamine is they all help with the D2 receptor.

 

So I’m hoping I can now just supplement forskolin for the mood side of things within my current stack, and not need alternatives like sulbutiamine, cdp-choline, or DMAE. In fact DMAE absolutely sucks for me now when taking higher doses, puts me in a bad mood.

 

But if I can continue to get the mood benefits from forskolin alone in my stack, I’m going to attempt tickling my amygdalas again, and see how I handle it.

 

My biggest problem is the brand. I usually stick to what works, and unfortunately the brand I bought isn’t being sold anymore. I got some from a different brand and will test it eventually. But now forskolin is so beneficial to me, I hope I am able to get the same benefits from other brands.

 

I do wonder if the D2 receptor has anything to do with euphoria though. I’ll do more research later.

[Mr Serendipity]

Okay another update already.

 

So I tried tickling for a little bit today. Well low and behold later on my mind starts getting hyped up, I start talking a lot, my breathing is quicker, and when this usually happens, the “high”, I then end up getting an emotional flashback triggered by some negativity (the low). Well in this case that didn’t happen, but the fact tickling causes this “high” reaction, is not the reaction I’m looking for. It makes me worried I could easily be triggered into a deep low/emotional flashback in this state.

 

But now time for the good news:

 

1. The good news is I didn’t get an emotional flashback. There was a trigger that made me low/sad for like 10 minutes, but I was able to get over it. 

2. I’ve had a smile on my face a lot, even later on in the day.

3. I’ve been way more sociable.

4. Anti addiction. I had no cravings for weed or alcohol.

5. My appetite has been crushed, which is a good thing, will help lose weight. And with the anti addiction quality, I won’t put it back on by getting high and binge eating.

Now to clarify, this wasn’t just from tickling. I decided to take either 3 or 4 forskolins this morning, rather then the 1 usually in my stack.

 

I did a quick search on D2 receptor and addiction, and down regulated D2 seems to be linked with binge eating, and substance abuse. 

 

I haven’t done any research into D2 and mood disorders. But it seems like forskolin has the following effects on me:

 

1. Better mood

2. Reduce/forget addictive cravings

3. Appetite suppression 

4. Vision becomes slightly clearer

5. Short term memory is worse though

6. Anti anxiety

 

So I think I definitely need to look into D2 for myself.

 

While I haven’t gone to sleep yet, I’m definitely tired, and I don’t believe forskolin will give me major insomnia like other D2 agonists I experience with like sulbutiamine or cdp-choline. Though the last time I tried cdp choline was around 2015.

 

So I definitely want to continue to test higher doses of forskolin, as it seems to have a lot of benefits without much negatives. I’m pretty sure I took 3 this morning, so I believe a dose of 2-3 is where I should be. 1 works well, but I have been on weed binges while taking my stack with 1 in it. So I want the anti addictive properties for sure, so hopefully I can get it from 2 but if not keep trying 3.

 

I’m not sure I’ll probably find another D2 upregulator or agonist that has the the same benefits with little side effects, but for now I’ll keep experimenting with forskolin.

Edited by Jesus is King, 13 November 2020 - 12:31 AM.

[Mr Serendipity]

Just ordered some lithium orotate, 5mg.

I remember I experimented with the stuff once in 2011 or 2012 (this was after my mini pop). The first day or two I was in a great mood, after which I became really brain fogged and just dropped the stuff. So I’ve only experimented with it once for like 3 days, and not since then, but it left an impression as I remember how great of a mood it caused in me. Maybe this was an early sign of deficiency?

Regardless, it would be good to experiment along with forskolin. Hopefully I can avoid the brain fog this time round now my stack is more honed in. And if I get great mood results but also brain fog after some time, I’ll definitely look into cycling it this time as opposed to dropping it completely

[Mr Serendipity]

https://www.ncbi.nlm...?report=classic

Increased volume of the amygdala and hippocampus in bipolar patients treated with lithium

Abstract

Previous structural neuroimaging studies of bipolar disorder have reported conflicting findings in limbic structures. Medication heterogeneity of patient samples may have contributed to these in-consistencies. Using structural magnetic resonance imaging we assessed whether lithium treatment was associated with differences in amygdala and hippocampal volumes in a sample of bipolar adults. A total of 49 magnetic resonance imaging scans were collected from patients who were currently treated with or without lithium. Amygdala and hippocampal volumes were analyzed using tensor-based morphometry. Statistical between-group comparisons of deformation maps showed that patients treated with lithium exhibited significantly increased volumes of the amygdala and hippocampus compared with patients who were not taking lithium. Our findings may help to explain previous inconsistencies in the bipolar literature.

Keywords: amygdala, bipolar disorder, emotion, hippocampus, lithium, magnetic resonance imaging, mood disorder

 

 

 

hmm interesting.   
 

Edited by Jesus is King, 13 November 2020 - 02:39 AM.

[Mr Serendipity]

https://www.ncbi.nlm...les/PMC5844774/
 

​Lithium monotherapy associated clinical improvement effects on amygdala-ventromedial prefrontal cortex resting state connectivity in bipolar disorder

Abstract

Background

This study, for the first time, investigated lithium monotherapy associated effects on amygdala-ventromedial prefrontal cortex (vMPFC) resting-state functional connectivity and correlation with clinical improvement in bipolar disorder (BP)

Methods

Thirty-six medication-free subjects − 24 BP (12 hypomanic BPM) and 12 depressed (BPD)) and 12 closely matched healthy controls (HC), were included. BP subjects were treated with lithium and scanned at baseline, after 2 weeks and 8 weeks. HC were scanned at same time points but were not treated. The effect of lithium was studied for the BP group as a whole using two way (group, time) ANOVA while regressing out effects of state. Next, correlation between changes in amygdala-vMPFC resting-state connectivity and clinical global impression (CGI) of severity and improvement scale scores for overall BP illness was calculated. An exploratory analysis was also conducted for the BPD and BPM subgroups separately.

Results

Group by time interaction revealed that lithium monotherapy in patients was associated with increase in amygdala-medial OFC connectivity after 8 weeks of treatment (p = 0.05 (cluster-wise corrected)) compared to repeat testing in healthy controls. Increased amygdala-vMPFC connectivity correlated with clinical improvement at week 2 and week 8 as measured with the CGI-I scale.

Limitations

The results pertain to open-label treatment and do not account for non-treatment related improvement effects. Only functional connectivity was measured which does not give information regarding one regions effect on the other.

Conclusions

Lithium monotherapy in BP is associated with modulation of amygdala-vMPFC connectivity which correlates with state-independent global clinical improvement.

 

 

wowowowo.

 

I’m liking this study here, we have the amygdala, connectivity to the frontal lobes, lithium, and bipolar. And after 8 weeks of lithium treatment connectivity between the amygdala and frontal lobes increased!

 

Could this be the reason why I experience major bipolar symptoms whenever I tickle my amygdalas? I’m lacking lithium.

 

I’m not going to lie, I am majorly excited right now. 

 

Summary:

 

1. I tried lithium orotate once back in uni, for a short period of time. And I remember it putting me in a brilliant mood, but dropped it after a few days because I developed brain fog. Haven’t experimented with it since.

 

2. Over this thread journey over 2 years now, it’s been a process of self discovery and trial and error. When you suffer from certain things, you may not even be aware of them, one of the big self discovery for me was paranoia. I only thought I had OCD and anhedonia, but as I learn, my symptoms also reflect bipolar, highs and lows, irritability, mood swings.

 

3. While I may experience these bipolar symptoms sometimes, and thy can be exacerbated by certain supplements. I can pretty much guarantee them and make they come out in full force whenever I tickle my amygdalas. 

 

4. Now we have a study that shows lithium increases connectivity between the amygdala and frontal lobes after 8 weeks! Meaning a lithium deficiency could cause a lack of connectivity between the two (I assume).

 

5. Also we have a study of bipolar patient treated with lithium enlarges their amygdalas and hippocampus.

 

6. One thing I noticed, this was way back in 2014. Was when you correct the right deficiency, it makes a world of difference compared to taking 100’s of other supplements. I first discovered this with liquid magnesium, and grew a lot of my stack over time (including with this journey) with a lot of supplements which make a difference. A couple of examples was when I first took NAC, and realised how well it helped me with my OCD. Another recent example is selenium, and how that’s helped me in various ways.

 

7. And of course lithium has been used for decades now to treat bipolar and mood disorders, something I should have probably tested early on. But I’m also glad I didn’t, as I was able to hone my stack in for other deficiencies and problems I suffered with.

 

 

I really really hope lithium is the last key component of my puzzle. If I can cure my emotional instability, the rest of my stack is now honed in enough to support the rest of my health.

 

This is probably the most exciting news and may be the last piece of the puzzle. Especially with the fact I’ve experienced lithium probates mood boosting effects before with that short experience back at uni, before I dropped it due to brain fog. And I’m actually hoping my honed stack, specifically the increase in glutathione levels in the brain, may be able to eliminate that brain fog side effect I experienced all those years ago.

 

Very exciting times, now I just have to wait until next week for it to arrive.

 

Edited by Jesus is King, 13 November 2020 - 03:27 AM.

[Mr Serendipity]

Just a quick update:

 

first of all in the last study I posted I highlighted the wrong text red. And also it’s as little as 2 weeks for increased connectivity between the amygdala and frontal lobes.

 

The other thing is I can not take higher doses of forskolin, couldn’t fall asleep until 5am. But since the discovery of lithium, I don’t feel the need to up my forskolin dose now, I’m hoping lithium will be the last key to this. Also high doses made my short term memory really bad, but I did read it increases the enzyme which breaks acetylcholine more.

 

I hope I get my lithium tomorrow so I can start experimenting this Sunday, but who knows.

 

 

[Mr Serendipity]

A post of mine from another forum on 2012-09-27:

 

 

Recently I've been taking this supplement: http://www.iherb.com...0-Tablets/22628

 

Lithium Orotate. 

 

I've never had crippling anxiety or depression, I'm just your normal lad with normal ups and downs in life. However what this supplement has done for me is just out of this world. You feel like your on a constant high, your happy, anxiety vanishes, and you feel like king. Almost like how human beings should feel like everyday. I'm still level headed, think clearly, and rational, but I have a super-confidence that makes me do things I would of be too scared to do normally. It's like your not worried about getting embarrassed, and even when other people on downers, or trying to make you feel down, you logically think you should be hurting, but you aren't. It's like today my friend was giving me some constructive criticism about last night, and usually even if it is genuine advice, it hurts when your told these things, but not today! I'm also taking tyrosine powder to boost it's effects.

 

2013-02-20:

 

 

The lithium I take 1x 5mg tab before bed otherwise it can dumb you down during the day. If you do it before bed, you get the mood lift without the brain fog the next day.

2013-03-12:

 

 

I think I might of jumped the gun on Lithium Orotate. I recently put it in my supp regime again 1 x 5mg tab before bed and had to stop after a couple of weeks. This is because I think it was effecting my clarity of thought a lot the next day (even though I took it before bed), and that it also caused some insomnia at night. Also when I was on it I didn't make the connection that it was effecting my clarity of thought straight away, because the effects are not hugely pronounced that you just think you've had a bad night sleep, or you're just not thinking clearly today. I do get a very subtle air headed almost drugged feeling on it. Some people seem to be really sensitive to lithium and I think I'm one of them. Saying that the mood boosting effects were extremely evident first time I took it, and may have continued to do so, but I wouldn't have noticed.

2013-06-20:

 

 

Tyrosine is a great supplement. It makes me laugh my ass off when I watch something funny. I definitely have a dopamine problem, but the problem with tyrosine is it's effects will not last because your body will lower (down regulate) the enzyme that converts it into dopamine. Also if you take too much of it, you start to get pissed off easily (agitation), and it can cause anxiety. I'm going to have to experiment with it more, but sadly all my supplements are at home at the moment since I'm moving out of this house. 

 

But the supplement lithium is meant to increase (up regulate) the enzyme that converts tyrosine, which is why I previously posted about feeling on top of the world/like a king mindset when on it (because I had more dopamine). Sadly lithium also makes you dumb as fudge, because of the foggy mind/drugged feeling it gives you. Luckily tyrosine doesn't do that, but like I said, you're body will try to adapt by making less enzyme to get that dopamine.

First of all I must say, my memory is really bad, I forget I wrote any of my experiences on this only 7 years ago.

 

I also realise now it wasn’t only a couple of days I was on it. If the dates between my first 2 posts are anything to go by, I might have tried it for around 4 months.

 

I seem to supplement 1 x 5mg before bed because it would give me a mood lift without dumbing me down/causing brain fog the next day, as opposed to taking it in the morning.

 

It seems like I eventually dropped it because it continue to cause this brain fog and also insomnia.

 

I’m not so worried this time around. I was also taking tyrosine at the same time back then, and my stack wasn’t as well rounded as it is today. I’m pretty sure I won’t suffer from brain fog this time round, mainly due to selenium and increasing my glutathione levels in the brain. But if I need to cycle or takes breaks from lithium, this time I will, rather than completely drop it.

 

Anyway still waiting for it to arrive, hopefully I’ll be able to post my results in the coming weeks.

 

Edited by Jesus is King, 15 November 2020 - 02:40 PM.