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Tickle Your Damn Amygdala's You Neurotic Fools!

amygdala visualization frontal lobes brain exercise

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#211 CalmContact

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Posted 27 August 2020 - 03:17 PM

Omg, reading your journal thoughts came to mind was 'Omg, so much stuff seems to work for this guy, i want these effects too but i don't feel jack shit'!

eg "You feel like your on a constant high, your happy, anxiety vanishes, and you feel like king."

 

Eg 

5 Curcumin pills, i feel no effect at all

1 dmae pill, i feel no effect at all

Other stuff i didn't feel a difference: phenibut, phenylpiracetam, sulbutiaminine, kanna, ashvaghanda, theanine

 

Ok, what i felt so far: kratom, lsd

 

-> i will keep on experimenting with higher dosages (and other compounds)

 

 



#212 Jesus is King

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Posted 27 August 2020 - 09:37 PM

That was from a post I wrote in 2012 on another forum about lithium which I ended up dropping because of brain fog. I’m trying to backtrack on what things worked for me in the past and piece it together for myself. My body and brain chemistry is much different from 8 years ago, and I react differently to a lot of supplements now then I did a decade ago.

 

I wouldn’t go on my experiences either. Everyone’s biology, brain chemistry, and psychology is unique. What might work for me might not for you, and vice versa.

 

Plus supplements aren’t the only thing I’m experimenting with. Instant self hypnosis and amygdala tickling are two psychologically methods I’m messing with too.

 

So I can’t help you, only share my experiences.

 

Good luck with your journey.


Edited by Jesus is King, 27 August 2020 - 09:38 PM.

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#213 Jesus is King

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Posted 30 August 2020 - 12:10 PM

Just to correct my PEA and egg yolk posts as I made a mistake (thank Google search for that).

 

Egg yolks contain palmitoylethanolamide. Cocoa contains phenylethylamine (the thing I’m actually intrested in). Both are abbreviated to PEA and interchangably used by Google when seraching. 

 

Regardless, I’m going to make it my new habit of taking 4 raw egg yolks in the morning and see if I have any improvements. Use to be 6, but taking 4 is more convenient because you can last 3 days when eggs usually come in a dozen or half a dozen (buy 2). 


Edited by Jesus is King, 30 August 2020 - 12:12 PM.


#214 Jesus is King

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Posted 30 August 2020 - 06:45 PM

I definitely think I’m dopamine dominant.

 

Lately I haven’t been taking my stack, and I’ve been testing things individually. Thursday I got my dlpa and had only taken one of those later on and oxiractam in the morning with egg yolks. Later that day I had the first emotional flashback I’ve had in months. I also may have drunk some coke I.e. caffeine. Today I took 4 dlpa (2g) and 4g of vitamin c in the morning, later I drunk some coke, and I am now feeling an emotional flashback worked up feeling coming on, luckily I can control it right now, but I’ve concluded I’m dopamine dominant. I also had a brain zap earlier, which I was getting a lot 2 years ago when I was taking sarcosine. Apparently brain zaps happen when you’re low on serotonin. And obviously OCD which I have, is linked to low serotonin levels. The other thing I noticed since taking 2g of DLPA today is I’ve had a pressure headache, and I never get headaches.

 

Also oxiracetam makes me dumb, I couldn’t think clearly on Thursday (before I had taken the dlpa), and I tested oxiracetam yesterday with egg yolks and the same thing happened.

 

Luckily my current stack I’ve been taking before these experiments have actually improved my clarity of thinking and memory retrieval speed ever since I added selenium and glycine to it.

 

Unfortunately I can’t increase my serotonin beneficially with 5-htp or tryptophan, both making me spaced out throughout the day. The best thing I found for balancing serotonin is turmeric.
 

So this is good news as I’ve pinpointed extra dopamine or its derivatives exacerbated my problems. So I can continue to take my current stack and feel emotionally stable, this includes even if I drink caffeine that day in the form of coke. So no need to mess with serotonin or dopamine precursors anymore. Though a bit saddening as I was hoping I could take DLPA to increase my PEA and help with the anhedonia side of things.

 

The last thing is one positive thing I noticed with oxiracetam without taking my current stack, was I was much more emotionally balanced, though I became dumb. So acetylcholine is something I could also look into experimenting with again, I haven’t done that for years though. What I will be doing though is taking 4 egg yolks in the morning.

 

 



#215 Jesus is King

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Posted 31 August 2020 - 07:58 AM

Ok I actually ended up being triggered and having an emotional flashback yesterday.

 

That’s 2 emotional flashbacks in the space of 4 days, Thursday and Sunday, and I haven’t had any for months. DLPA is definitely the culprit, as I only took that (2g) and 4g of vitamin c yesterday. The other thing I noticed is my pee smelt really bad, like broccoli or asparagus, so I don’t know what compounds I was excreting, but I never usually have a strong smell in my pee.

 

Anyway at least I know to avoid dopamine increasing supplements.

 

One I believe the culprit to be noradrenaline, it’s interesting that a few years ago I tried Wellbutrin for a day, and I felt very emotionally normal, and that’s a NE reuptake inhibitor, so not sure how that makes sense. The only reason I didn’t continue using it was because of the slightly spaced out side effects, and insomnia,  but I think if I can get my hands on some, I’d be willing to test it again.



#216 Jesus is King

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Posted 08 September 2020 - 12:46 AM

So one treatment I’ve never experimented with is killing of parasites. I’ve just learn protozoa means micro parasites. Now I’ve had problems in my gut previously, mainly jock itch years ago which wouldn’t go away until I supplemented probiotics, and then just supplementing zinc and other supplements to keep it in bay. However I was still getting sore skin in that area if I smoked cigarettes, which was largely helped recently by taking selenium (even though I took every other essential nutrient under the sun). Other things with my gut is if I eat pizza or bread, especially with Tabasco sauce, I will get depressed and even triggered an emotional flashback by it once (something I’ve only been able to trigger with amygdala tickling, and recently, with dopamine precursors), i.e. my brain seems to be gluten sensitive. Regardless with all my stack I take I’ve never focused on killing parasites or micro parasites.

 

Now there is an interesting article here: Protozoa Could Be Controlling Your Brain

 

Some protozoa infect the brain of their host, shaping its behavior in ways most suited to the pathogen, even if it leads to the suicide of the host

 

THE ANCIENT DEBATE surrounding the existence of free will appears unresolvable, a metaphysical question that generates much heat yet little light. Common sense and volumes of psychological and neuroscientific research reveal, however, that we are less free than we think we are. Our genes, our upbringing and our environment influence our behaviors in ways that often escape conscious control. Understanding this influence, the advertisement industry spent approximately half a trillion dollars worldwide in 2010 to shape the buying decisions of consumers. And extreme dictatorships, such as that in North Korea, remain in power through the effective use of insidious and all-pervasive forms of propaganda. Yet nothing approaches the perfidy of the one-celled organism Toxoplasma gondii, one of the most widespread of all parasitic protozoa. It takes over the brain of its host and makes it do things, even actions that will cause it to die, in the service of this nasty hitchhiker. It sounds like a cheesy Hollywood horror flick, except that it is for real.

We know that illness in general can slow us down, incapacitate us and, in the worst case, kill us. Yet this organism is much more specific. Natural selection has given rise to pathogens that infiltrate the nervous system and change that system’s wiring to achieve its ultimate purpose, replication—like a computer virus that reprograms an infected machine.

Such is the case with T. gondii. It sexually reproduces only in the intestines of cats yet can maintain itself indefinitely in any warm-blooded animal. Infected cats shed millions of their oocysts in their feces. Taken up by all kinds of animals, including dogs, rodents and humans, they infect muscle and the brain to escape attacks by the host’s immune system. Hidden away, they remain dormant as cysts, surrounding themselves with a tough cell wall. Yet this quiet stage of infection, called toxoplasmosis, is deceptive. Violating all rules of good hospitality, these invaders make the host’s brain do things counterproductive to its own survival.

Toxoplasmosis has been most thoroughly studied in rats and mice. Both species have a deep-seated, innate fear of cats for obvious reasons. Spray a bit of cat urine into a corner, and the rodent will avoid this location, well, like the plague. In contrast, an infected animal loses its innate fear of cats. By some measures, it even appears to be mildly attracted to the smell of felines. This is an unfortunate turn of events for the rodent, because it is now more likely to be successfully hunted by a cat. On the other hand, this is a great deal for T. gondii. When the cat devours the sick critter and its contaminated brain, T. gondii moves into its final host, where it reproduces, completing its life cycle. Not quite what the romantics have in mind when they write about “the circle of life”!

The behavioral manipulation induced by T. gondii is quite specific. The infected rodent doesn’t look sick; its weight is normal; it moves about normally, possibly a bit more frantically than other mice; it grooms itself; and it interacts routinely with its conspecifics. Think how different this case is from what happens in rabies, another nasty infection. The animal loses its instinctual shyness, aggressively attacking others (the proverbial mad dog), thereby spreading the rabies virus through its bite. But because T. gondii can reproduce only in felines, it wants its host to be eaten by cats, not by just any carnivore. And because cats hunt live prey and do not eat carrion, T. gondii must not immediately kill its temporary host.

Rodents Aren’t Superheroes
How does T. gondii effect its insidious changes in the host? Experiments by Joanne P. Webster of Imperial College London, Robert Sapolsky of Stanford University and others have shown that infected rats or mice do not turn into the murine equivalent of Siegfried, the hero of Wagner’s Ring who knew no fear. No, they still avoid open spaces, remain nocturnal creatures, retain their aversion to the urine of other predators and learn to fear a tone associated with a foot shock. Might the protozoa have stunted their smell? After all, if they cannot smell anything anymore, they would not know how to avoid places smelling of cat urine. But infected mice still avoid food if it smells different—an aversion that arose partly because for centuries humans have been trying to control rodents by poison. The infected mice also respond appropriately to the smell of their littermates.

Clues about how the parasites affect the animal come from several observations. First, the density of cysts in the amygdala is almost double that in other brain structures involved in odor perception. Parts of the amygdala have been linked to anxiety and the sensation of fear. Second, the genome of T. gondii contains two genes related to mammalian genes involved in the regulation of dopamine, the molecule associated with reward and pleasure signals in the brain, including in ours. So perhaps the creepy protozoa makes suicidal activities, such as hanging around places frequented by cats, feel more pleasurable for the infected rodent?

What elevates this vignette about evolution and life in the wild to epic proportions for humanity is that about a tenth of the U.S. population is infected by T. gondii (in some countries, such as France, the infection rate is seven to eight times higher, possibly because of the widespread consumption of uncooked and undercooked meat). Human toxoplasmosis is usually considered to be symptom-free (what doctors refer to as asymptomatic). Exceptions are patients with a weakened immune system and the unborn (hence the need for pregnant women to avoid cleaning cat-litter boxes).

Science has known for a long time that schizophrenic patients are two to three times more likely to carry antibodies to T. gondii than are controls who are not schizophrenic. Furthermore, antipsychotic drugs that block the action of dopamine, such as haloperidol, commonly used in the treatment of schizophrenia, are also effective in combating toxoplasmosis in both rats and people. And some infected adults go on to develop psychotic symptoms similar to schizophrenia. Little is known about the mode or site of action of this pathogen in the human brain. The exact link between T. gondii and psychiatric diseases is tantalizing but remains murky.

Recent claims go so far as to argue for a role of T. gondii in shaping distinct cultural habits, depending on the rate of infection in the population. A prospective study tracking the road safety in Czech recruits during their 18 months of compulsory military draft found a rate of accidents six times higher in affected drivers. Are the young men with toxoplasmosis infection simply slowed down? Or do they drive more aggressively?

In my November 2009 column, I described the discovery by cognitive neuroscientists that the feeling of freely willing an action (called authorship or agency) is a subjective, conscious sensation no different, in principle, from the conscious awareness of seeing the azure blue sky or feeling the sharp pain of a toothache. When I engage in a dangerous pursuit, such as taking the end of the rope on a steep section of a granite wall in Yosemite Valley while climbing, I feel as if “I freely decided” to do so, whatever this might mean in a metaphysical sense. Yet my action is most likely caused by an inexhaustible multiplicity of factors not accessible to my conscious introspection, including, yes, possibly some tiny single-celled parasites lodging in my brain and making me act out their silent commands. The wonder of it all.

 

 

So a few things in this article about Toxoplasma gondii interest me:

 

1. A tenth of the US population has it, so that’s around 33 million people. 1 in 10 according to the CDC.

2. The French population has it 7 to 8 times higher.

3. The cysts are double in the amygdala?

4. Those infected have more care accidents which may be caused by them driving more aggressively.

 

Regardless, it’s pretty damn widespread, and can effect the brain.

 

So I’ve just discovered Fenbendazole due to rumours of it curing cancer. There’s even a study of brain cancer being cured or helped by it.

 

Having such a widespread infection rate, and fenbendazole being quite tolerable and doesn’t build drug resistance in the body, so it’s effective the 90th time as the first time you take it (there’s a study on this somewhere). I’m going to see if I can get my hands on some and dose it everyday at 222mg, as I’ve pretty much tried every supplement out there, maybe this might help fight the root cause?

 

Here’s an interesting study on the Protozoa and the amygdala: https://dmm.biologis...content/6/2/516

 

Toxoplasma gondii infection induces dendritic retraction in basolateral amygdala accompanied by reduced corticosterone secretion

 

Pathological anxiety is thought to reflect a maladaptive state characterized by exaggerated fear. Naturally occurring perturbations that reduce fear can be crucial in the search for new treatments. The protozoan parasite Toxoplasma gondii invades rat brain and removes the fear that rats have of cat odors, a change believed to be parasitic manipulation of host behavior aimed at increasing parasite transmission. It is likely that mechanisms employed by T. gondii can be used as a heuristic tool to understand possible means of fear reduction in clinical settings. Male Long-Evans rats were infected with T. gondii and compared with sham-infected animals 8 weeks after infection. The amount of circulating plasma corticosterone and dendritic arborization of basolateral amygdala principal neurons were quantified. Previous studies have shown that corticosterone, acting within the basolateral amygdala, enhances the fear response to environmental stimuli. Here we show that T. gondii infection causes a dendritic retraction in basolateral amygdala neurons. Such dendritic retraction is accompanied by lower amounts of circulating corticosterone, both at baseline and when induced by an aversive cat odor. The concerted effects of parasitism on two pivotal physiological nodes of the fear response provide an animal model relevant to interactions between stress hormones and amygdalar plasticity.

 

 

 

So here we show it has an effect on amygdala neurons and amygdala plasticity. Now in rats it took away fear, but still it effects the amygdala, and is an extremely widespread Protozoa.

 

https://www.cell.com...?code=cell-site

 

Recent studies have revealed that Toxoplasma alters both excitatory and inhibitory neurotransmission in the central nervous system and that these changes lead to unbalanced synaptic activity and seizures.”

 

Something else of interest.

 

https://www.robertsa...oplasmosis.html

 

It takes about 6 weeks for toxo to migrate from the gut to the brain. In the brain it forms cysts in multiple locations, but mainly in the amygdala region. The amygdala is the brain's center for fear and anxiety. It is also the brain center for forming predator aversion pathways. Once in the amygdala toxo is able to take dendritic nerve cell endings and cause them to shrivel up.

 

 

https://www.sciencedaily.com/releases/2011/11/111104102125.htm

 

 

 
Brain parasite directly alters brain chemistry

 

Research shows infection by the brain parasite Toxoplasma gondii, found in 10-20 per cent of the UK's population, directly affects the production of dopamine, a key chemical messenger in the brain.

 

Findings from the University of Leeds research group are the first to demonstrate that a parasite found in the brain of mammals can affect dopamine levels.

Whilst the work has been carried out with rodents, lead investigator Dr Glenn McConkey of the University's Faculty of Biological Sciences, believes that the findings could ultimately shed new light on treating human neurological disorders that are dopamine-related such as schizophrenia, attention deficit hyperactivity disorder, and Parkinson's disease.

This research may explain how these parasites, remarkably, manipulate rodents' behaviour for their own advantage. Infected mice and rats lose their innate fear of cats, increasing the chances of being caught and eaten, which enables the parasite to return to its main host to complete its life cycle.

In this study, funded by the Stanley Medical Research Institute and Dunhill Medical Trust, the research team found that the parasite causes production and release of many times the normal amount of dopamine in infected brain cells.

Dopamine is a natural chemical which relays messages in the brain controlling aspects of movement, cognition and behaviour. It helps control the brain's reward and pleasure centres and regulates emotional responses such as fear. The presence of a certain kind of dopamine receptor is also associated with sensation-seeking, whereas dopamine deficiency in humans results in Parkinson's disease.

These findings build on earlier studies in which Dr McConkey's group found that the parasite actually encodes the enzyme for producing dopamine in its genome.

"Based on these analyses, it was clear that T. gondii can orchestrate a significant increase in dopamine production in neural cells," says Dr McConkey.

"Humans are accidental hosts to T. gondii and the parasite could end up anywhere in the brain, so human symptoms of toxoplasmosis infection may depend on where parasite ends up. This may explain the observed statistical link between incidences of schizophrenia and toxoplasmosis infection."

Dr McConkey says his next experiments will investigate how the parasite enzyme triggers dopamine production and how this may change behaviour.

Toxoplasmosis, which is transmitted via cat faeces (found on unwashed vegetables) and raw or undercooked infected meat, is relatively common, with 10-20% of the UK population and 22% of the US population estimated to carry the parasite as cysts. Most people with the parasite are healthy, but for those who are immune-suppressed -- and particularly for pregnant women -- there are significant health risks that can occasionally be fatal.

The parasite infects the brain by forming a cyst within its cells and produces an enzyme called tyrosine hydroxylase, which is needed to make dopamine. Dopamine's role in mood, sociability, attention, motivation and sleep patterns are well documented and schizophrenia has long been associated with dopamine, which is the target of all current schizophrenia drugs on the market.

The enzyme tyrosine hydroxylase is a crucial step in making L-DOPA (prescribed as levodopa for Parkinson's Disease), a chemical that is readily converted to the neurotransmitter dopamine.

The US-based Stanley Medical Research Institute, which focuses on mental health conditions and has a particular emphasis on bipolar illnesses. Dunhill Medical Trust supports research on diseases of aging.

 

 

Wow. So this article is saying 10-20% of the UK population is infected (relevant to me). Also says 22% of the US population.

 

Not only that but it may increase dopamine. I’ve noticed in recent years I am dopamine dominant, or at least low serotonin, mainly brain zaps and my OCD, and dopamine precursors send me over the edge with anger and can even trigger an emotional flashback.

 

I wonder if all this excessive dopamine is the reason my reward system is so screwed up. I.e. suffer from anhedonia, haven’t had an orgasm in 16 years. Maybe I’m dopamine dominant but very desensitised to it.

 

Time to try and kill some parasites with Fenbendazole whether I may have them or not, and see if anything happens mentally and emotional. Main observation I hope to see improvement in would be any alleviation in my anhedonia, i.e. an increase in pleasure, emotions, and motivation. But first I have to get my hands on the stuff.



#217 Jesus is King

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Posted 08 September 2020 - 10:48 AM

Okay I just found the perfect study which examines which compounds (including natural supplements) which fight against Toxoplasmosis.

 

https://www.ncbi.nlm...les/PMC6747942/

 

 

 
Abstract

Toxoplasmosis, which affects more than a billion people worldwide, is a common parasitic infection caused by the obligate intracellular parasite, Toxoplasma gondii. Current treatment strategies have several limitations, including unwanted side effects and poor efficacy. Therefore, newer therapies are needed for toxoplasmosis. Drug repurposing and screening of a vast array of natural and/or synthetic compounds is a viable option for antiparasitic drug discovery. In this study, we screened 62 compounds comprising natural products (NPs) and FDA-approved (FDA) drugs, to identify the hit compounds that suppress the growth of T. gondii. To determine the parasite inhibitory potential of the compounds, host mammalian cells were infected with a transgenic T. gondii strain, and the viability of the parasite was evaluated by luminescence. Of the 62 compounds, tubericidin, sulfuretin, peruvoside, resveratrol, narasin and diacetoxyscirpenol of the natural product isolates, as well as bortezonib, 10-Hydroxycamtothecin, mebendazole, niflumic acid, clindamycin HCl, mecamylamine, chloroquine, mitomycin C, fenbendazole, daunorubicin, atropine, and cerivastatin of FDA molecules were identified as “hits” with ≥ 40 percent anti-parasite action. Additionally, mitomycin C, radicicol, naringenin, gitoxigenin, menadione, botulin, genistin, homobutein, and gelsemin HCl of the natural product isolates, as well as lomofungin, cyclocytidine, prazosin HCl, cerivastatin, camptothecin, flufenamic acid, atropine, daunorubicin, and fenbendazole of the FDA compounds exhibited cytotoxic activity, reducing the host viability by ≥ 30 percent. Our findings not only support the prospects of drug repurposing, but also indicate that screening a vast array of molecules may provide viable sources of alternative therapies for parasitic infection.

 

 

 

So first points to take from this:

 

1. Toxoplasmosis affects more than a billion people worldwide.

2. Resveratrol is a natural compound  I recognise which is effective against it.

3. Chloroquine, obviously something that's been making rounds recently due to Covid and Trump, is effective against it.

4. Fenbendazole is also effective, which is reassuring as I didn't know before whether it would be as I couldn't find the studies.

 

These 3 are the only compounds I recognize.

 

This makes me think I should also experiment with resveratrol and hydroxychloroquine, especially since hydroxychloroquine is well tolerated. The only problem I may have with resveratrol is I can't take grape seed extract because it seems to lower my iron or haemoglobin too much, I did create a thread here on it. Also I took hydroxychloroquine when I had covid, which I believe I went a bit yellow/jaundice. However I believe the severity of my covid was mainly due to low selenium levels (which has since been corrected), and I've never tested resveratrol itself, only grape seed extract.

 

So I want to try and get hold of some resveratrol and hydroxychloroquine (harder to get hold of), along with fenbendazole, and see if I can take minimum doses of each long term without ill effect, along with my current stack. I'd hope that combo would sort out any parasites I may have, or at least the toxoplasm gondii parasite if I am infected with it.

 

The other possible connection I would want to look into is glutathione levels and whether it protects against this parasite. As I was low selenium and was hit pretty hard by covid (I know covid isn't a parasite). But there may be a connection with low selenium/glutathione levels, toxoplasmosis, and the problems I suffer with.

 

Here's a study I found just now: https://europepmc.or...le/med/32416707

 

 
Evaluation of Glutathione Bioactivity on Toxoplasma Gondii in BALB/c Mice Post Impact of Selenium and Calcium Supplementation.

 

 

Abstract 
Studies have shown that selenium is an essential component of glutathione as an important antioxidant to reduce oxidative stress and inhibit intracellular parasites' growth. In contrast, calcium in cytosol of such parasites plays a key role in entry of the parasite into the host cell and its primary motility. The present study was designed to evaluate and compare glutathione peroxidase bioactivity effects post administration of selenium and calcium in BALB/c mice infected by Toxoplasma gondii (Table 3) Sixty BALB/c mice susceptible to T. gondii were randomly divided into twelve groups of case and control groups. There were six control groups including two positive controls infected only with the paraites either 104 or 5×104 , non-infcetd and untreated groups, Treated controls were received only calcium, selenium, or both respectively. Case groups were infected with 104 or 5×104 parasites. While each set of three case groups separately received minerals alone or together. Mice were orally fed with 200 μg selenium, 50 μg calcium or their combination for 7 days. Mice were infected by parasite's tachyzoites. Sera of mice were kept and the peritoneal macrophages were isolated for counting tachyzoites during infection. The results showed that selenium unlike calcium was significantly effective in reducing Toxoplasma tachyzoites compared to control groups. Moreover, glutathione peroxidase [GPX] activity was elevated in mice treated with selenium and vice versa decreased in mice treated with calcium. Administration of selenium unlike calcium reduced Toxoplasma tachyzoites proliferation by elevating bioactivity of selenium-dependent detoxification enzyme, GPX.

 

 

 

 

BOOM.

 

Goal is to increase glutathione levels which I'm already doing (selenium, NAC, and glycine). And experiment with Fenbendazole, Hydroxychloroquine, and Resveratrol. 

 

Maybe the connection to all of this comes down to Toxoplasmosis causing more oxidative stress and inflammation in the brain, as well as "once in the amygdala toxo is able to take dendritic nerve cell endings and cause them to shrivel up".



#218 Jesus is King

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Posted 08 September 2020 - 09:23 PM

https://www.ncbi.nlm...cles/PMC356918/

 

Toxoplasma seropositivity and depression: a case report

There have been only a few case reports associating toxoplasmosis and psychiatric disorders. There are reports of improvement of psychiatric symptoms with the absorption of retinochoroidal lesion due to toxoplasmosis [1]. In an interesting study the reactivity for toxoplasmin intradermal test, it was found to be highest in the manic depressive patients especially in the depressed patients, and the percentage of such patients increased with mental deterioration [2]. Symptom of toxoplasma chorioretinitis may masquerade as complaint of blurred vision a side effect of psychotropics like imipramine and trifluoperazine [3]. Possibilities of a relationship between toxoplasma infection and the occurrence of schizophrenia [4] and obsessive-compulsive disorder [5] have been suggested. It has been found that the individuals with first-episode schizophrenia had significantly increased levels of IgG, IgM, and IgA class antibodies to toxoplasma proteins, as compared with the control subjects [6]. We are reporting a patient whose depressive syndrome may be associated with the toxoplasmosis.

Case presentation

A 32 years old male presented with sad mood, anhedonia, suicidal ideas, impaired sleep, loss of appetite, multiple somatic complaints for 7 months was diagnosed to have depressive episode and was under treatment with antidepressants without much benefit. His somatic complaints were characterized by positional vertigo, tinnitus, weakness, feeling that the head is moving up and down and reeling of head. He had undergone detailed routine clinical examination in ophthalmology, otorhinolaryngology, endocrinology and neurosurgery departments for these complaints. Specific investigation like CT scan of brain, brainstem auditory evoked response did not show any abnormality. His HIV status was negative. However he was found positive on the serological test for the toxoplasma. He was treated with pyrimethamine and sulphadiazine. He was also prescribed carbamazepine 600 mg, clonazepam 4 mg and sertraline 100 mg per day. He came for regular follow-ups and after 6 months he was found to have recovered completely, and free from any evidence of toxoplasma infection.

Conclusion

The patient responded to the antidepressant therapy after he was treated for the toxoplasmosis. This case bringing to the fore the toxoplasma seropositivity and non-response to depression suggests a probable association between toxoplasmosis and depression. Though there has been strong indication that toxoplasmosis can be associated with various psychiatric disorders, we do agree that for a clearer association more accurate and rigorous proofs are required than those presented in this communiqué.

 

 

 


Edited by Jesus is King, 08 September 2020 - 09:23 PM.


#219 Jesus is King

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Posted 08 September 2020 - 09:25 PM

https://www.ncbi.nlm...les/PMC5364308/

 

Involvement of Host Defense Mechanisms against Toxoplasma gondiiInfection in Anhedonic and Despair-Like Behaviors in Mice

ABSTRACT

Toxoplasma gondii is a pathogen relevant to psychiatric disorders. We recently showed that reactivation of chronic T. gondii infection induced depression-like behaviors in mice. Furthermore, it has been hypothesized that depression-like behaviors are mediated via a host defense mechanism against invading pathogens; proximate mechanisms of this behavioral hypothesis remain unclear. In the present study, we investigate the contribution of indoleamine 2,3-dioxygenase (IDO), inflammation, and interferon gamma (IFN-γ) to anhedonic and despair-related behaviors in T. gondii-infected mice by using sucrose preference and forced-swim tests, respectively. First, we confirmed that BALB/c mice exhibited both sickness and depression-like behaviors during acute infection. Treatment of infected wild-type mice with minocycline (anti-inflammatory drug) abated sickness and anhedonic and despair-like behaviors, whereas in T. gondii-infected mice, treatment normalized kynurenine/tryptophan (Kyn/Trp) ratios in both plasma and brain tissue. Additionally, T. gondii infection failed to induce anhedonic and despair-like behaviors or increase the Kyn/Trp ratio in immunocompromised (IFN-γ−/−) mice, whereas sickness behavior was observed in both immunocompetent and IFN-γ−/− mice following infection. Furthermore, treatment with 1-methyl tryptophan (an IDO inhibitor) did not affect locomotor activity, attenuated clinical scores and anhedonic and despair-like behaviors, and resulted in normal Kyn/Trp ratios in T. gondii-infected wild-type mice. Although low levels of serotonin and dopamine were observed in the brain during acute and chronic infections, anhedonic and despair-like behaviors were not detected in the chronic stage of infection. Collectively, our results demonstrated that immune enhancement in response to infection with T. gondiiresulted in IFN-γ production, IDO activation, and inflammation associated with anhedonic and despair-like behaviors.

 

 

 



#220 Jesus is King

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Posted 08 September 2020 - 09:28 PM

https://www.ncbi.nlm...les/PMC5894522/

 

Positive association between Toxoplasma gondii IgG serointensity and current dysphoria/hopelessness scores in the Old Order Amish: a preliminary study

Abstract

Toxoplasma gondii (T. gondii) IgG seropositivity and serointensity have been previously associated with suicidal self-directed violence (SSDV). Although associations with unipolar depression have also been investigated, the results have been inconsistent, possibly as a consequence of high heterogeneity. We have now studied this association in a more homogeneous population, [that is (i.e.) Old Order Amish (OOA)] with previously reported high T. gondii seroprevalence. In 306 OOA with a mean age of 46.1 ± 16.7 years, including 191 (62.4%) women in the Amish Wellness Study, we obtained both T. gondii IgG titers (by enzyme-linked immunosorbent assay [ELISA]), and depression screening questionnaires (Patient Health Questionnaire [PHQ-9] [n = 280] and PHQ-2 [n = 26]). Associations between T. gondii IgG and dysphoria/hopelessness and anhedonia scores on depression screening questionnaires were analyzed using multivariable linear methods with adjustment for age and sex. Serointensity was associated with both current dysphoria/hopelessness (p = 0.045) and current combined anhedonia and dysphoria/hopelessness (p = 0.043), while associations with simple anhedonia and past/lifelong (rather than current) phenotypes were not significant. These results indicate the need for larger longitudinal studies to corroborate the association between dysphoria/hopelessness and T. gondii IgG-titers. Current hopelessness is a known risk factor for SSDV which responds particularly well to cognitive behavioral therapy, and may be a focused treatment target for T. gondii-positive individuals at high-risk for SSDV.

 

 

 



#221 Jesus is King

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Posted 08 September 2020 - 09:30 PM

https://www.scienced...889159114004188

 

 
Toxoplasma gondii and anxiety disorders in a community-based sample

Abstract

A growing body of literature suggests that exposure to the neurotropic parasite Toxoplasma gondii (T. gondii) is associated with increased risk of mental disorders, particularly schizophrenia. However, a potential association between T. gondii exposure and anxiety disorders has not been rigorously explored. Here, we examine the association of T. gondii infection with both anxiety and mood disorders. Participants (n = 484) were drawn from the Detroit Neighborhood Health Study, a population-representative sample of Detroit residents. Logistic regression was used to examine the associations between T. gondii exposure (defined by seropositivity and IgG antibody levels) and three mental disorders: generalized anxiety disorder(GAD), posttraumatic stress disorder (PTSD) and depression. We found that T. gondii seropositivity was associated with a 2 times greater odds of GAD (odds ratio (OR), 2.25; 95% confidence interval (CI), 1.11–4.53) after adjusting for age, gender, race, income, marital status, and medication. Individuals in the highest antibody level category had more than 3 times higher odds of GAD (OR, 3.35; 95% CI, 1.41–7.97). Neither T. gondiiseropositivity nor IgG antibody levels was significantly associated with PTSD or depression. Our findings indicate that T. gondii infection is strongly and significantly associated with GAD. While prospective confirmation is needed, T. gondii infection may play a role in the development of GAD.

 

 

 



#222 Jesus is King

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Posted 08 September 2020 - 09:33 PM

https://www.nature.c...60681-4?proof=t

 

 

 
Sialylated N-glycan profile during acute and chronic infections with Toxoplasma gondii in mice
Abstract

Toxoplasma gondii is associated with physiological and psychiatric perturbations. The immune response is interrelated to the progress of anhedonia and despair symptoms of T. gondii-infected subjects. We recently reported that serum N-glycans were altered in mice displayed depressive-like behaviors. However, a novel biomarker that correlated to T. gondiiinfection and associated behaviors is demanded. Glycomics has been used to find affected glycoproteins during depression. The objective of this study is to investigate serum N-glycomics changes during infection with T. gondii in BALB/c mice, immunocompetent, or in severe combined immunodeficient mice, and after treatment with an immunostimulant; 1-methyl tryptophan. Glycans were examined through glycoblotting-protocol then investigated by MALDI-TOF/MS. Both depressive and sickness-related behaviors were significantly abundant (P ≤ 0.001 each), during acute T. gondii in immunocompetent mice, compared to controls. Only sickness symptoms were evident in immunodeficient mice infected with T. gondii, as associated with high expression level (P ≤ 0.001) of Peak # 15 (2 × Neu5Gc) compared to controls. The alteration of sialylated N-glycan expressions is important to detect the immune status of animals/humans against T. gondii. Moreover, 1-methyl tryptophan reduced depressive-like behavior (P ≤ 0.001) compared to controls. Therefore, sialylated N-glycan (Neu5Ac/Neu5Gc-terminal) is targeted to be used as a novel biomarker of sickness/depressive-like behaviors.

 

 

 



#223 Jesus is King

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Posted 08 September 2020 - 09:44 PM

Anyway I got hold of some Hydroxychloroquine Sulfate today, 200mg.

 

My Fenbendazole is coming tomorrow, 100g. So is my resveratrol.

 

While I'll test with some of each this week. I won't be able to test fully until the after next week as I'm going away on holiday. Though I may continue to take hydroxycloroquine, and maybe resveratrol. But that's a maybe, depends if I have any gastrointestinal problems taking the 2 initially. Also the fenbendazole would be a pain to dose on holiday as it's powder.

 

So next week holiday either 2 x Multivitamin, or 2 x Multivitamin + 600mg Resveratrol + 200mg Hydroxychloroquine. 

 

I'll try and keep a diary and post here any results.

 

 

 



#224 Jesus is King

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Posted 09 September 2020 - 01:47 AM

https://pdfs.semanti...f22466bf5994.pd

 

“Indeed, FBZ, a widely-used veterinary BZD, has been used to successfully treat intracranial parasites in dogs, emphasizing that FBZ can cross the BBB and is able to reach levels within the CNS adequate for its anti-parasitic action.“


Edited by Jesus is King, 09 September 2020 - 01:54 AM.


#225 Jesus is King

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Posted 09 September 2020 - 01:53 AM

https://www.ingentac...08?crawler=true
 

“One study suggested that once parasitic larvae reach the brain and musculature, they are resistant to anthelminthic agents.1 How- ever, the literature suggests that larvae in the brain are susceptible to FBZ treatment8,13,18,21,22,28,61,62 and that FBZ can penetrate the blood–brain barrier.22 “



#226 Jesus is King

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Posted 09 September 2020 - 10:38 PM

https://www.biorxiv....9.999672v1.full

 

Efficacy of Guanabenz Combination Therapy Against Chronic Toxoplasmosis Across Multiple Mouse Strains Abstract

Toxoplasma gondii, an obligate intracellular parasite that can cause life-threatening acute disease, differentiates into a quiescent cyst stage to establish lifelong chronic infections in animal hosts, including humans. This tissue cyst reservoir, which can reactivate into an acute infection, is currently refractory to clinically available therapeutics. Recently, we and others have discovered drugs capable of significantly reducing brain cyst burden in latently infected mice, but not to undetectable levels. In this study, we examined the use of novel combination therapies possessing multiple mechanisms of action in mouse models of latent toxoplasmosis. Our drug regimens included combinations of pyrimethamine, clindamycin, guanabenz, and endochin-like quinolones (ELQs), and were administered to two different mouse strains in an attempt to eradicate brain tissue cysts. We observed mouse strain-dependent effects with these drug treatments: pyrimethamine + guanabenz showed synergistic efficacy in C57BL/6 mice, yet did not improve upon guanabenz monotherapy in BALB/c mice. Contrary to promising in vitro results demonstrating toxicity to bradyzoites, we observed an antagonistic effect between guanabenz + ELQ-334 in vivo. While we were unable to completely eliminate brain cyst burden, we found that a combination treatment of ELQ-334 + pyrimethamine impressively reduced brain cysts to 95% in C57BL/6 mice, which approaches the limit of detection. These analyses highlight the importance of evaluating anti-infective drugs in multiple mouse strains and will help inform further preclinical cocktail therapy studies designed to treat chronic toxoplasmosis.



#227 Jesus is King

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Posted 10 September 2020 - 12:18 PM

https://pubmed.ncbi....h.gov/12102233/

 

 

 
An in vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi to hydroxychloroquine
Abstract
In this work the susceptibility of mobile and cystic forms of Borrelia burgdorferi to hydroxychloroquine (HCQ) was studied. The minimal bactericidal concentration (MBC) of HCQ against the mobile spirochetes was > 32 microg/ml at 37 degrees C, and > 128 microg/ml at 30 degrees C. Incubation with HCQ significantly reduced the conversion of mobile spirochetes to cystic forms. When incubated at 37 degrees C, the MBC for young biologically active cysts (1-day old) was > 8 microg/ml, but it was > 32 microg/ml for old cysts (1-week old). Acridine orange staining, dark-field microscopy and transmission electron microscopy revealed that the contents of the cysts were partly degraded when the concentration of HCQ was > or = MBC. At high concentrations of HCQ (256 microg/ml) about 95% of the cysts were ruptured. When the concentration of HCQ was > or = MBC, core structures did not develop inside the cysts, and the amount of RNA in these cysts decreased significantly. Spirochetal structures inside the cysts dissolved in the presence of high concentrations of HCQ. When the concentration of HCQ was > or = MBC, the core structures inside the cysts were eliminated. These observations may be valuable in the treatment of resistant infections caused by B. burgdorferi, and suggest that a combination of HCQ and a macrolide antibiotic could eradicate both cystic and mobile forms of B. burgdorferi.

While not t .gondii or a parasite, as I can't find any information yet on HCQ or Fenbendazole getting rid of cysts for t. gondii (latent toxoplasmosis). I've posted this study because HCQ seems to rupture cysts of this bacteria. May have no effect on the cysts formed by t. gondii, but I can only hope it might.

 

I am keeping a diary on my HCQ + Fenbendazole + Resveratrol self experiment. First time I took all 3 yesterday. It's too early to tell, but my mind feels pretty clear today, and I don't feel tired. I've had the feeling of needing to go to the toilet, but nothing like IBS in the past where I have to go right away or disaster. However the new multivitamin I've taken to replace my b-complex includes probiotics, and includes Vitamin D, so my Vitamin D intake is even higher now (cod liver oil 200IU, 1000IU Vitamin D tablet, 400IU multivitamin) and I've noticed with higher amounts of Vitamin D I experience a constipation type effect. I've still been able to go, but even after going my stomach feels unsettled right now, but I'm not worried at the same time as I can handle it.

 

Initial results feel promising. But will have to wait and see.



#228 Jesus is King

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Posted 15 September 2020 - 09:35 AM

Okay it’s been 7 days since I’ve been taking the combo of fenbendazole + hcq + resveratrol.

 

Things I’ve noticed that have changed:

 

I don’t have anxiety during the day.

I feel emotionally balanced at the moment, haven’t had a high then low yet.

I don’t get major paranoia if I smoke weed.

I act pretty emotionally normal when I drink alcohol.

I don’t get major indigestion from eating beef.

I haven’t noticed much change in my OCD or anhedonia.

 

However I must reiterate, I have been taking a new multivitamin as well (replaced my b-complex) which includes probiotics and other micronutrients I don’t supplement in my usual stack. So while I can’t pinpoint whether it’s these parasite killing drugs or not giving me these benefits, I’ll continue to use them in the evening as I don’t seem to get any major side effects from them.

 

Also it’s hard to pinpoint the benefits in certainty, only time will be able to do that for me. For example there hasn’t been enough time to see if I will experience another high and low, or an emotional flashback, etc... So will be interesting to see what happens as we get to 30 days (9th August) and beyond.

As for a summation of how I feel this may have benefited me, I would say mood stabilising. But like I said time will tell.

 

Also I haven’t bothered keeping a diary after the first couple of days, so I’m posting what effects I’ve observed here before I forget them.

 



#229 Jesus is King

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Posted 17 September 2020 - 09:28 PM

Okay I’m having some pretty remarkable results right now, consistent too.

 

But first let me reiterate what I’ve been taking:

 

Morning:

 

2 x Advanced Multivitamin (Higher Nature)

2 x 50mcg Selenium 

 

After evening meal:

 

1 x 600mg Trans resveratrol (Doctors Best)

1 x 200mg Hydroxychloroquine

1 x 222mg Fenbendazole

 

Results:

 

1. Basically, I don’t get any anxiety anymore. I don’t feel anxiety talking to people, interacting with people, that sort of anxiety. This effect is pretty consistent throughout the day.

 

2. I actually felt very peaceful today. I think this comes from my mood being more stable, rather than highs or lows or irritable.

 

3. Highs, lows, and irritability. Now, I have had some, but from what I have observed so far, this has only occured whenever I’ve practice any amygdala tickling. I’ll be observing this more, but I think amygdala tickling is the only or at least the biggest factor, that seems to be triggering any emotional instability. Otherwise refer to results 1 and 2.

 

4. Dare I say it, I had slighlty less anhedonia today, I enjoyed listening to music in the care more so that usual. Just a tad, but exciting non the less.

 

5. OCD is still present, but to what degree it’s hard to tell as I’m currently on holiday, though cleanliness is still somewhat there, I do wonder how much is habit, and how much is my ocd lessening? When I get home I’ll know better, as it will be interesting to see how compelled I feel to check if the doors are locked several times.

 

6. Indigestion. Had a Burger today, no indigestion. Seems like I can tolerate beef well at the moment, like I could with the steak and alcohol 3 days ago. I originally thought this was a thiamine problem, as I swear sulbutiamine and benfotiamine both helped in this area. However currently I haven’t been taking either and seem to be doing quite well.

 

7. Addiction. This will need more observation, but I feel I have more control. Alcohol being my example on this, except on the first day of my holiday, where I drunk a bit, and found it more of an educational experience on how I handled it emotionally. I haven’t felt the need or desire to drink it again. Smoking is my hardest addiction per se, and I have been smoking less, but I’ve also been on holiday where it hasn’t been easy access to smoke all the time. But it will be interesting to see how I do with desires and temptations to weed and alcohol from this moment forward.

 

 

Last points:

 

I do not know where my results are coming from exactly.

 

1. It could be because I’m killing the remenants of T Gondii and it’s cysts in my brain (assuming I have it) by taking fenbendazole, hydroxychloroquine, and resveratrol.

 

2. It could be the fact I’m taking trans resveratrol for the first time ever.

 

3. It could be because of the new multivitamin I’m taking, which also includes probiotics.

 

One thing I know for sure, is because my stack has been reduced recently, there’s a whole list of supplements I know are not contributing to this progress.

 

The other thing I know, is I had been taking the multivitamin just before I even got my HCQ, fenben, and resveratrol, and noted in my first diary entry of being in a better mood than usual. 

 

Here is a link to the multivitamin: https://www.higherna.../advanced-multi

 

 
Two tablets typically provide: 

Vitamin A (800iu) 240µg 
Vitamin D3 (400iu) 10µg 
Vitamin E (90iu) 60.6mg 
Vitamin C 200mg 
Vitamin B1 50mg 
Vitamin B2 50mg 
Vitamin B3 80mg 
Vitamin B5 50mg 
Vitamin B6 6.6mg 
Folic acid 130µg 
Vitamin B12 40µg 
Biotin 50µg 
Vitamin K1 80µg 
Choline 20mg 
Inositol 20mg 
Calcium 342mg 
Iron 10mg 
Magnesium 169mg 
Zinc 10mg 
Chromium 40µg 
Iodine 75µg 
Selenium 30µg 
Manganese 2.6mg 
Molybdenum 30µg 
Beta Carotene 0.8mg 
Becillus Coagulans 0.8mg** 
**In the order of 100 million cfu at the time of manufacture

 

Our Advanced Multi stands out amongst multivitamin and mineral supplements both for the broad spectrum of nutrients it provides and the highly absorbable forms in which they are delivered. When it comes to vitamins and minerals not all forms are equal - some are much better abosrbed and used by the body and we want to make sure you get the best. In this multi we have natural vitamin E, vitamin B12 as methylcobalamin, vitamin B6 as the active co-enzyme form of pyridoxal-5-phosphate, folic acid as methyltetrafolate and with well absorbed calcium from lithothamnion calcarea - a fossilised seaweed. We have improved the fomula and now include a vegan source of the active D3 form of Vitamin D and increased iodine. For better balance we have reduced vitamin A and added beta carotene - an alternative way to get Vitamin A and safe for pregnant women. To complete the formula we have now added live bacteria. This formula really will help you cover all bases! A year-round best seller, the Advanced Multi provides 26 essential nutrients ensuring that you and your family get the nutrition you need. With particularly good levels of iron, calcium, magnesium and B vitamins to support energy and the nervous system, this is a superior multi free from artificial colours, flavourings or preservatives, dairy products, gluten, lactose, soya and wheat.

 

 

Anyway I’ll continue experimenting and see if the progress continues.


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#230 Jesus is King

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Posted 23 September 2020 - 01:22 PM

Just a quick update. I went on a bit of a weed binge the last few evenings, it was weak stuff thought. But I haven’t been able to observe exactly anything emotional wise because of it. I still have paranoia with weed, but it’s so much weaker than what it once was. I don’t know whether this is due to the weed being weak, or my progress, but I have noticed before my paranoia has lessened. Also my cravings to smoke cigarettes are way down.

 

The main thing I will say I’ve noticed, is my libido is WAY UP. This could be due to the multivitamin rather then the other stuff, I’m not sure. But it is WAY up.

 

One thing I’ve noticed, and have to reconsider, is my stack. I’ve been doing quite well on the multivitamin and extra selenium in the morning, and then resveratrol + hcq + fenben with the evening meal. It actually makes me feel I need to start at the bottom again, and work my way up. For example with my libido being so high, I don’t want to take ZMA anymore before bed, and just rely on the multivitamin. Also I may be able to drop benfotiamine because it’s quite stimulating, and my digestion has been normal at the moment, and that was the main reason I would take it. Might even drop extra vitamin D, and maybe even extra 1g of Vitamin C, and even glycine. I’m not sure yet. But my stack is going to be built up slowly again from what it was.

 

Now this experiment isn’t exactly going to be precise anymore. I’m adding something new into the mix. Riluzole!

 

I got my hands on some 50mg of Riluzole recently, and took my first dose this morning. I haven’t taken anything else. I felt my vision was a bit clearer, but not sure. I do feel slight tingling, almost like irritability, but I seem fine.

 

The other thing I added to the mix is practicing hypnosis again, with one suggestion of feeling love and peace where ever I am and whatever the situation. So nothing I take is going to accurately reflect what works and what doesn’t. 

 

I will continue to take my hcq + fenben + resveratrol until I run out of HQC, there’s 60 tablets, I’ve used 13 so far (so 12 days of using the 3 combo). Once they’re finished, I’ll just continue taking fenben + resveratrol. I got 100g of 99% fenben powder, so it should last me around 450 days if a scoop is 222mg, so I won’t run out of that anytime soon.

 

The last point is blood sugar levels. I noticed I possibly go into mood swings if I haven’t eaten for a long time. About 4 years ago I did test prediabetes levels (according to the internet) in a finger blood test, but I was told the levels were too low to worry about by a nurse in the family, so I didn’t do anything. However with my hypnosis, and hopefully riluzole, I will be able to drop my weight. Riluzole has the possible side effect of appetite suppression. No idea if it will happen to me, I’m taking it for OCD, but am mainly using hypnosis to help in the weight loss area.

 

Last point, in my stack I want to reintroduce NAC. Taking 500mg of NAC previously helped my OCD tremendously. However Riluzole is also an NDMA antagonist like NAC. So I will have to test this on a day I have off where I can take both, plus multivitamin and selenium in the morning. Not sure what NAC & Riluzole might cause when taking together, probably nothing bad, but will experiment on a day off.

 

One thing I will note, is I don’t think Riluzole did anything for my anhedonia. But it’s only been one day. 



#231 Jesus is King

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Posted 23 September 2020 - 09:05 PM

Okay a quick update on Riluzole as it was my first day.

 

I’ve been extremely emotionally stable, too peaceful lol

 

I don’t know whether that’s the riluzole or the hypnotic suggestions I gave myself this morning. There is I think, body irritability and stimulation, but either the Riluzole or the hypnotic suggestions are squashing it emotionally.

 

But there is one thing I noticed. My reflexes are down. Like while I’m driving, I find it very hard to take “risks”. When I say risks, I mean knowing I can pull onto a road because the cars on both sides are far enough away, but not doing it, and waiting until the road is really clear. Almost like my automatic reflexes are down. This could also possibly be T.Gondii eradication from my brain with the hcq, fenben, resveratrol combo.

 

The other thing I’ve noticed is I’m more present in the world I think. Especially when driving. Time is longer, I’m less on automatic reflex and more present. I think this is what I attribute to my vision being slightly clearer in my last post but not being certain.

 

So I assume my glutamate in down and GABA is up, something riluzole does.

 

Also I think my OCD has improved somewhat. I left the house this afternoon, and when I got in the car, as I couldn’t remember locking the door, there was a small battle within myself to go check or not, I did eventually check (and it was locked), but that small battle nearly made me leave it.

 

There is no improvement with anhedonia.

 

But one thing is I was tickling my amygdalas with feeling method a little bit, and there was no highs and lows, or emotionally instability later on.

 

Oh and I successfully stuck to my diet today, one meal in the evening, so if prediabetes was a possible factor in my mood swings, it didn’t effect me today. It was also pizza with tabasco sauce, something that’s triggered an emotional flashback in me before due to the gluten.

 

I will say hypnotic suggestions have had a great effect on me in the past, so I can’t put this all down to Riluzole. Regardless I’ll try and keep up with Riluzole and hypnotic suggestions, and see if I can squash this emotionally instability long term, and still tickle my amygdalas without mood swings popping up.

 

I am going to add my multivitamin and selenium tomorrow with Riluzole.

 

So my current stack is basically:

 

Morning:

 

50mg Riluzole

2 x Multivitamins

100mg Selenium

 

With evening meal:

 

222mg Fenbendazole

200mg Hydroxychloroquine

600mg Trans Resveratrol

 

 

Edit: I forgot to mention that my breathing feels a little heavier today, most likely due to Reluzole, but could also be due to smoking and not taking selenium today.


Edited by Jesus is King, 23 September 2020 - 09:18 PM.


#232 Jesus is King

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Posted 23 September 2020 - 09:21 PM

https://pubmed.ncbi....h.gov/20620171/

Riluzole rapidly attenuates hyperemotional responses in olfactory bulbectomized rats, an animal model of depression

 

Abstract

Growing evidence indicates that the glutamatergic neurotransmitter system is central to the neurobiology and treatment of depression. Riluzole, a drug currently used to slow the progression of amyotrophic lateral sclerosis (ALS), directly affects the glutamatergic system. In this study, we investigated the effects of riluzole in olfactory bulbectomy (OBX) rats, an animal model of depression. The olfactory bulbs in rats were removed by suction. The emotionality of rats was measured by scoring their responses to given stimuli, i.e., attack, startle, struggle, and fight responses. The OBX rats chronically treated with vehicle for 7 days at 14 days following surgery showed significant increases in emotionality responses. Single (1st day administration) and subchronic (7th day administration) riluzole treatment (1-10 mg/kg, po) significantly and dose-dependently reduced hyperemotional responses in OBX rats. Both single and subchronic riluzole treatment (10 mg/kg, po) had no significant effects on the emotional responses in sham operated rats. In addition, we demonstrated that single riluzole treatment (10 mg/kg, po) significantly decreased extracellular glutamate levels in medial prefrontal cortex of OBX rats by in vivo microdialysis. We provide the first experimental evidence that riluzole rapidly attenuated hyperemotional responses in OBX rats, an animal model of depression.

 


Edited by Jesus is King, 23 September 2020 - 09:22 PM.


#233 Jesus is King

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Posted 23 September 2020 - 09:24 PM

https://pubmed.ncbi....h.gov/28534874/

Shifting brain inhibitory balance and connectivity of the prefrontal cortex of adults with autism spectrum disorder

 

Abstract

Currently, there are no effective pharmacologic treatments for the core symptoms of autism spectrum disorder (ASD). There is, nevertheless, potential for progress. For example, recent evidence suggests that the excitatory (E) glutamate and inhibitory (I) GABA systems may be altered in ASD. However, no prior studies of ASD have examined the 'responsivity' of the E-I system to pharmacologic challenge; or whether E-I modulation alters abnormalities in functional connectivity of brain regions implicated in the disorder. Therefore, we used magnetic resonance spectroscopy ([1H]MRS) to measure prefrontal E-I flux in response to the glutamate and GABA acting drug riluzole in adult men with and without ASD. We compared the change in prefrontal 'Inhibitory Index'-the GABA fraction within the pool of glutamate plus GABA metabolites-post riluzole challenge; and the impact of riluzole on differences in resting-state functional connectivity. Despite no baseline differences in E-I balance, there was a significant group difference in response to pharmacologic challenge. Riluzole increased the prefrontal cortex inhibitory index in ASD but decreased it in controls. There was also a significant group difference in prefrontal functional connectivity at baseline, which was abolished by riluzole within the ASD group. Our results also show, for we believe the first time in ASD, that E-I flux can be 'shifted' with a pharmacologic challenge, but that responsivity is significantly different from controls. Further, our initial evidence suggests that abnormalities in functional connectivity can be 'normalised' by targeting E-I, even in adults.

 



#234 Jesus is King

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Posted 23 September 2020 - 09:31 PM

https://www.ncbi.nlm...les/PMC5916346/

Riluzole Impairs Cocaine Reinstatement and Restores Adaptations in Intrinsic Excitability and GLT-1 Expression

 

Abstract

Adaptations in glutamate signaling within the brain’s reward circuitry are observed following withdrawal from several abused drugs, including cocaine. These include changes in intrinsic cellular excitability, glutamate release, and glutamate uptake. Pharmacological or optogenetic reversal of these adaptations have been shown to reduce measures of cocaine craving and seeking, raising the hypothesis that regulation of glutamatergic signaling represents a viable target for the treatment of substance use disorders. Here, we tested the hypothesis that administration of the compound riluzole, which regulates glutamate dynamics in several ways, would reduce cocaine seeking in the rat self-administration and reinstatement model of addiction. Riluzole dose-dependently inhibited cue- and cocaine-primed reinstatement to cocaine, but did not affect locomotor activity or reinstatement to sucrose seeking. Moreover, riluzole reversed bidirectional cocaine-induced adaptations in intrinsic excitability of prelimbic (PL) and infralimbic (IL) pyramidal neurons; a cocaine-induced increase in PL excitability was decreased by riluzole, and a cocaine-induced decrease in IL excitability was increased to normal levels. Riluzole also reversed the cocaine-induced suppression of the high-affinity glutamate transporter 1 (EAAT2/GLT-1) in the nucleus accumbens (NAc). GLT-1 is responsible for the majority of glutamate uptake in the brain, and has been previously reported to be downregulated by cocaine. These results demonstrate that riluzole impairs cocaine reinstatement while rectifying several cellular adaptations in glutamatergic signaling within the brain’s reward circuitry, and support the hypothesis that regulators of glutamate homeostasis represent viable candidates for pharmacotherapeutic treatment of psychostimulant relapse.

 


https://www.ncbi.nlm...les/PMC2845177/

Preclinical Evaluation of Riluzole: Assessments of Ethanol Self-Administration and Ethanol Withdrawal Symptoms

 

Abstract
Background

Many of the neurobehavioral effects of ethanol are mediated by inhibition of excitatory N-methyl-d-aspartate (NMDA) and enhancement of inhibitory γ-amino-butyric-acid (GABA) receptor systems. There is growing interest in drugs that alter these systems as potential medications for problems associated with alcoholism. The drug riluzole, approved for treatment of amyotrophic lateral sclerosis (ALS), inhibits NMDA and enhances GABAA receptor system activity. This study was designed to determine the preclinical efficacy of riluzole to modulate ethanol self-administration and withdrawal.

Methods

Male C57BL/6J mice were trained to lever press on a concurrent fixed-ratio 1 schedule of ethanol (10% v/v) versus water reinforcement during daily 16-hour sessions. Riluzole (1 to 40 mg/kg, IP) was evaluated on ethanol self-administration after acute and chronic (2 week) treatment. To determine if riluzole influences ethanol withdrawal-associated seizures, mice were fed an ethanol-containing or control liquid diet for 18 days. The effects of a single injection of riluzole (30 mg/kg) were examined on handling-induced convulsions after ethanol withdrawal.

Results

Acute riluzole (30 and 40 mg/kg) reduced ethanol self-administration during the first 4 hours of the session, which corresponds to the known pharmacokinetics of this drug. Ethanol self-administration was also reduced by riluzole after chronic treatment. Riluzole (30 mg/kg) significantly decreased the severity of ethanol-induced convulsions 2 hours after ethanol withdrawal.

Conclusions

These results demonstrate that riluzole decreases ethanol self-administration and may reduce ethanol withdrawal severity in mice. Thus, riluzole may have utility in the treatment of problems associated with alcoholism.

 



#235 Jesus is King

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Posted 23 September 2020 - 09:35 PM

https://www.ncbi.nlm...les/PMC3473175/

A Pilot Study of Hippocampal Volume and N-Acetylaspartate (NAA) as Response Biomarkers in Riluzole-Treated Patients with GAD

 

Abstract

Anxiolytic benefit following chronic treatment with the glutamate modulating agent riluzole in patients with generalized anxiety disorder (GAD) was previously associated with differential changes in hippocampal NAA concentrations. Here, we investigated the association between hippocampal volume and hippocampal NAA in the context of riluzole response in GAD. Eighteen medication-free adult patients with GAD received 8-week of open-label riluzole. Ten healthy subjects served as a comparison group. Participants underwent magnetic resonance imaging and spectroscopy at baseline and at the end of Week 8. GAD patients who completed all interventions were classified as remitters (n = 7) or non-remitters (n = 6), based on final Hamilton Anxiety Rating Scale (HAM-A) scores ≤ 7. At baseline, GAD patients had a significant reduction in total hippocampal volume compared to healthy subjects (F(1,21) = 6.55, p = 0.02). This reduction was most pronounced in the remitters, compared to non-remitters and healthy subjects. Delta (final – baseline) hippocampal volume was positively correlated with delta NAA in GAD. This positive association was highly significant in the right hippocampus in GAD [r = 0.81, p = 0.002], with no significant association in healthy subjects [Fisher r-to-z p = 0.017]. Across all GAD patients, delta hippocampal volume was positively associated with improvement in HAM-A (rspearman = 0.62, p = 0.03). These preliminary findings support hippocampal NAA and volume as neural biomarkers substantially associated with therapeutic response to a glutamatergic drug.

 



#236 Jesus is King

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Posted 23 September 2020 - 09:39 PM

https://www.ncbi.nlm...les/PMC5742506/

Amygdala Plasticity and Pain

Another recent strategy to mitigate pain-related amygdala hyperactivity is activation of small-conductance calcium-activated potassium (SK) channels in the CeA. SK channels are calcium-sensitive, voltage-insensitive potassium channels that are expressed in somatic and dendritic regions of the neuron in a brain region-specific manner [155158]. Somatically expressed SK channels regulate neuronal excitability by mediating the medium afterhyperpolarization (mAHP) to decrease action potential firing rate [155]. In the amygdala, SK channels regulate action potential firing of neurons in the lateral CeA [159] but not LA [160]. SK channels also regulate dendritic excitability to modulate synaptic transmission and plasticity. In the amygdala, activation of synaptic SK channels in the LA acts as a postsynaptic shunt to reduce excitatory synaptic transmission [161], whereas removal of SK channels from the postsynaptic membrane of LA neurons by a PKA-dependent mechanism facilitates excitatory transmission and synaptic plasticity [162].

 

A clinically available compound that can inhibit SK channels is riluzole, an FDA approved drug for the treatment of amyotrophic lateral sclerosis (ALS) that easily crosses the blood-brain barrier [163164]. It should be noted that other actions of riluzole include inhibition of voltage-gated calcium channels, rapidly inactivating voltage-gated and persistent sodium channels, and glutamate receptor currents [165167]. Systemically applied riluzole had antinociceptive effects in the formalin test [168170], in the carrageenan model of hindpaw inflammation [171], and in neuropathic pain models [172175]. Riluzole also produced pain relief in patients with irritable bowel syndrome [176]. The site and mechanism of pain-related riluzole effects were not identified in these studies. Systemic application of riluzole inhibited emotional responses (audible and ultrasonic vocalizations), but not mechanosensitivity (spinal withdrawal reflexes), in a rodent model of arthritic pain, and these inhibitory effects were reversed by stereotaxic (intra-CeA) administration of a blocker of SK channels (apamin) but not of large-conductance calcium-activated potassium BK channels (charybdotoxin) [177].

 

An interesting observation is that not every intervention targeting the amygdala to inhibit emotional-affective responses to pain affects mechanosensitivity. This is true for riluzole [177] as well as for NPS [142], an mGluR5 antagonist [178], and an SSRI [154], and may suggest differential roles of neurochemically distinct intra-amygdala circuits.

 

 

 

 

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Whats interesting for me, is when I was trying to increase my potassium last year, I tried taking lo-salt. And I had a loopy, emotional instability effect, basically triggered an emotional high. I think the same thing happened when I just tried to increase just sodium around that time as well, though I’m not sure. Not sure what all that means, but electrolytes definitely play a role with my emotions when trying to increase them directly.


Edited by Jesus is King, 23 September 2020 - 09:44 PM.


#237 Jesus is King

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Posted 23 September 2020 - 09:59 PM

https://www.ncbi.nlm...les/PMC3874704/

Riluzole activates TRPC5 channels independently of PLC activity

Abstract
BACKGROUND AND PURPOSE

The transient receptor potential channel C5 (TRPC5) is a Ca2+-permeable cation channel, which is predominantly expressed in the brain. TRPC5 is activated in a PLC-dependent manner by, as yet, unidentified endogenous messengers. Recently, modulators of TRPC5, like Ca2+, pH and phospholipids, have been identified. However, the role of TRPC5 in vivo is only poorly understood. Novel specific modulators of TRPC5 might help to elucidate its function.

EXPERIMENTAL APPROACH

Novel modulators of TRPC5 were identified in a compound screening of approved drugs and natural compounds. The potency and selectivity of TRPC5-activating compounds were determined by fluorometric calcium imaging. The biophysical properties of channel activation by these compounds were analysed using electrophysiological measurements.

KEY RESULTS

Riluzole was identified as a novel activator of TRPC5 (EC50 9.2 ± 0.5 μM) and its mechanism of action was shown to be independent of G protein signalling and PLC activity. Riluzole-induced TRPC5 currents were potentiated by La3+ and, utilizing TRPC5 mutants that lack La3+ binding sites, it was confirmed that riluzole and La3+ activate TRPC5 by different mechanisms. Recordings of excised inside-out patches revealed a relatively direct effect of riluzole on TRPC5.

CONCLUSIONS AND IMPLICATIONS

Riluzole can activate TRPC5 heterologously expressed in HEK293 cells as well as those endogenously expressed in the U-87 glioblastoma cell line. Riluzole does not activate any other member of the TRPC family and could, therefore, despite its action on other ion channels, be a useful pharmacological tool for identifying TRPC5-specific currents in immortalized cell lines or in acutely isolated primary cells.

 

https://www.ncbi.nlm...les/PMC2719954/

Essential role for TRPC5 in amygdala function and fear-related behavior

 

Summary

The transient receptor potential channel 5 (TRPC5) is predominantly expressed in the brain where it can form heterotetrameric complexes with TRPC1 and TRPC4 channel subunits. These excitatory, non-selective cationic channels are regulated by G protein, phospholipase C-coupled receptors. Here, we show that TRPC5−/− mice exhibit diminished innate fear levels in response to innately aversive stimuli. Moreover, mutant mice exhibited significant reductions in responses mediated by synaptic activation of Group I metabotropic glutamate and cholecystokinin 2 receptors in neurons of the amygdala. Synaptic strength at afferent inputs to the amygdala was diminished in P10–P13 null mice. In contrast, baseline synaptic transmission, membrane excitability, and spike timing-dependent long-term potentiation at cortical and thalamic inputs to the amygdala were largely normal in older null mice. These experiments provide genetic evidence that TRPC5, activated via G protein-coupled neuronal receptors, has an essential function in innate fear.

 

 

TRPC5 Expression in the Mouse Brain

Consistent with previous immunocytochemical localization of TRPC5 protein (Strübing et al., 2001), TRPC5-mRNA is abundant in the amygdala (lateral, basolateral, and central nuclei) and hippocampus. High levels of TRPC5-mRNA were detected in the CA1, CA2, and CA3 regions of the hippocampus and dentate gyrus (Figure 1A), areas that regulate fear-related behaviors through projections to the amygdala (Seidenbecher et al., 2003). Regions of the auditory cortex (AuD, Au1, and AuV) that process conditioned stimulus information bound for the LA during auditory fear conditioning (Maren and Quirk, 2004), the somatosensory cortex (S1 and S2 areas) and the parietal insular cortex, regions that transmit somatosensory unconditioned stimulus (US) information to the LA, also contain TRPC5 mRNA (Figure 1A). Finally, TRPC5 is present in the perirhinal cortex (PRh), an area involved in processing CS and somatosensory US information (Lanuza et al., 2004LeDoux, 2000Shi and Davis, 1999Shumyatsky et al., 2005). Interestingly, TRPC5 mRNA was not observed in the auditory thalamus, another auditory CS area (Figure 1B).

 

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Never heard of TRPC5 before, but it is abundant in the amygdala and plays a role in innate fear. Mice without it (genetically removed) have less innate fear. However Riluzole activates it, so would this increase innate fear? But Riluzole has fear extinction, which I guess are learned fears. I do wonder if TRPC5 has anything to do with fear extinction though. All interesting nontheless. 



#238 Jesus is King

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Posted 23 September 2020 - 10:06 PM

https://www.ncbi.nlm...les/PMC6322878/

The TRPC5 channel regulates angiogenesis and promotes recovery from ischemic injury in mice

 

Abstract

Ischemia-related diseases are a leading cause of death worldwide, and promoting therapeutic angiogenesis is key for effective recovery from hypoxia–ischemia. Given the limited success of angiogenic factors, such as vascular endothelial growth factor, in clinical trials, it is important to find more promising angiogenic targets. Here, using both cell- and tissue-based assays and a mouse model of injury-induced ischemia, we investigated the involvement of the transient receptor potential canonical 5 (TRPC5) ion channel in angiogenesis and the effects of a TRPC5 activator, the Food and Drug Administration–approved drug riluzole, on recovery from ischemic injury. We demonstrate that TRPC5 is involved in endothelial cell sprouting, angiogenesis, and blood perfusion in an oxygen-induced retinopathy model and a hind limb ischemia model. We found a potential regulatory link between nuclear factor of activated T cell isoform c3 and angiopoietin-1 that could provide the mechanistic basis for the angiogenic function of TRPC5. Importantly, treatment with riluzole, which can activate TRPC5 in endothelial cells, improved recovery from ischemia in mice. Our study reveals TRPC5 as a potential angiogenic target and suggests riluzole as a promising drug for managing ischemic diseases.

 

 

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Well it’s good to know Riluzole may help build my blood vessels up and combat ischemia-related diseases which are the leading cause of death worldwide.



#239 Jesus is King

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Posted 23 September 2020 - 10:28 PM

https://pubmed.ncbi....h.gov/28843863/

Administration of riluzole to the basolateral amygdala facilitates fear extinction in rats

 

Abstract

A general understanding exists that inhibition of glutamatergic neurotransmission in the basolateral amygdala (BLA) impairs fear extinction in rodents. Surprisingly, we recently found that systemic administration of riluzole, which has been shown to inhibit the glutamatergic system, facilitates extinction learning in rats with a preconditioned contextual fear response. However, the mechanisms underlying this paradoxical effect of riluzole remain unclear. In this study, adult male Wistar rats were bilaterally cannulated in the BLA to examine the effects of intra-BLA administration of riluzole. We also compared the effects of riluzole with those of d-cycloserine, a partial agonist at the glycine-binding region of the N-methyl-d-aspartate (NMDA) receptor. In this study, intra-BLA administration of either riluzole or d-cycloserine facilitated extinction learning of contextual fear in conditioned rats. In addition, both riluzole and d-cycloserine enhanced the acquisition of recognition memory in the same model. However, intra-BLA injections of riluzole, but not d-cycloserine, had a potent anxiolytic-like effect when investigated using an elevated plus-maze test. Our findings suggest that riluzole-induced facilitation of extinction learning in rats with a preconditioned contextual fear reflects an indirect effect, resulting from the intra-BLA administration of the drug, and might not be directly related to inhibition of glutamatergic signaling. Further research is needed to clarify the mechanisms underlying the paradoxical effect of riluzole on fear extinction learning observed in this study.

 


Edited by Jesus is King, 23 September 2020 - 10:29 PM.


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#240 Jesus is King

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Posted 24 September 2020 - 10:18 PM

So my second day of Riluzole, but with the added multivitamin and selenium in the morning.

 

I’ve been amygdala tickling a lot since yesterday, and I drank 2 teaspoons of hot cocoa (which can also cause a high/low mood swing), just to see how well riluzole works. Well I became very talkative, something that happens when I’m going on a high. And I had feelings of irritability on the inside, I felt like I could be triggered, but it seemed like I wasn’t, and remained normal and calm throughout the day (hooray!).

 

Now I don’t know whether I handled it so well because of riluzole or the hypnotic suggestions. However I have used the same hypnotic suggestions in the past, and have still experienced mood swings. So I’m leaning toward the riluzole. 

 

The only problem is I don’t feel after today 50mg is strong enough, as I want to completely eradicate those strong emotions on the inside. But rather than upping the dose, I need to look into adding NAC back into my stack, and maybe look for some other NMDA anatagonists, I think curcumin is one, which I was previously taking before rebuilding my stack recently.

 

The other thing is I find Riluzole makes me a bit apathetic (another reason I tried the cocoa), and I think I’m not drinking water as much as I should (something that’s never been a problem before). Also theres a sort of slight stim feeling in the background, and my focus and thinking isn’t quite all there; it’s not terrible, but a feel a bit less with it. Maybe I’m slightly dissociating? It reminds me of that one day experiement I had with wellbutrin years ago, where I felt stimmed, but calm at the same time. Who knows though.

 

To sum up my 2nd day and general experience of riluzole. You feel stimmed/irritable in the body and inside, but emotions and behaviour remain calm? If that makes sense. The other possibility is Riluzole is increasing hypnotic suggestibility making my hypnosis sessions more effective, and there’s a study showing ketamine increases hypnotic suggestibility.

 

Oh and there was a study that compared ketamine and riluzole for anhedonia. Ketamine helped, riluzole didn’t. So I doubt my 16 years of anhedonia will change much with riluzole.


Edited by Jesus is King, 24 September 2020 - 10:22 PM.






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