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Answers To Curing Anhedonia/numbness/apathy, No. 1


itstrevor

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Telsig11, thanks for posting. I understand a lot of the things you said firsthand. I have watched someone with anhedonia living a very functional life in spite of her condition. While those around her recieve her brightness, her hugs, her compassion, she is still devoid of any emotional reward in return. I have watched her go from month after month of just laying around in the suffering and emptiness , to being active and having days filled with purpose, albeit emotionally empty. The process or path that I think made the difference for her was to join a gym and start being active. The body is receiving the endorphin release from the excercise though the brain does not recognize it. The social interaction, putting yourself in front of other humans, will eventually lead to conversations, that given time may lead to

Friendships. It's not a cure, it's a way to fill the space from waking up to going to bed. It has been amazing. To see her today compared to the last two years, flat amazing. I wish you well. I hope you find interesting things to do. It will be something you have to force yourself to do sometimes but it does change you for the better. Anything is better than four walls.

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Thanks lastdance. rocked up to the psych hospital today. they have (and i knew from the website) three options: one outpatient program 3 days per week for 3 hours, an intensive outpatient program six days a week from 9a-330p, and an inpatient program. i was thinking the intensive inpatient one, they recommended inpatient, which i refused on the grounds of: they require you to take medication (same prereq for the intense outpatient). i've had such a bad experience with it, and have read enough online to know that before i take any meds i have to try the natural way first: proper sleep, diet and exercise, routine, and social support. like i mentioned, that's what i really felt i needed anyway, the meeting other people who are CRAZY (just kidding - you know, who are struggling, who have issues). so support groups are what i am looking at now. tried a bipolar one a few years ago, didn't meet anyone i could relate to, but i'm going to try a few, just printed out a list of them.

my anhedonia is bad, but i'm making it worse with my food addiction, inactivity and isolation. i feel good about staying away from the psych hospital for now, just that alone is a bit invigorating. i am able to feel some things..not like i used to, but that's the thing i'm going to try to develop. i have to share my story with other people and, as you said, (and i knew before but did not appreciate enough) be active.

i'm on a waitlist for the less intense outpatient program - not sure if i'll do it or not. will try some support groups for depression, bipolar, overeating, see how that goes.

"There is no greater agony than bearing an untold story inside you." - Maya Angelou

another quote i learned recently is that it's easier to act your way into a new way of thinking than think your way into a new way of acting. like this.

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Proud of you man. I hope you can get your feet on the ground and just keep moving. I'm not talking "Forest Gump" running across the country or anything, I just have seen that it's true, a body in motion is better than one not. For what it's worth, I recently found a book on cancer,"Radical Remission".

It has found a common thread amongst people diagnosed with cancer that made changes and became cancer free. I'm not saying it will cure anhedonia but, the life changes this group of people applied, certainly would be good for your physical self. And since that's where your brain lives, it couldnt hurt to spruce up the place a bit!

If you know what I mean. Best wishes, if you can find the Will where none exists, your doing good.

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yeah, another thing i have read that gives me some hope is that our brains are quite fungible. every experience we have changes it a bit. we can change the structure of our brain through work, meditation, thinking, doing things. this is my only hope (and social interaction). well not my only hope. perhaps i may need to take medication again in the future but i will only do so if i'm completely desperate, or if we develop some med that we know, with more reliability than we do now, what it will do. if people are reading this and are being helped by medication, i'm jealous! i know they can help. but ideally we'd like to go without it, right? that's what i'm going to try first. and properly try. it feels kinda good to express myself here. i have a lot more good advice that i've found..don't want to overload people but if you're interested in understanding our brains and want advice on getting things done check these out (can you tell that i've wanted to share this stuff with someone?). for me, these can certainly help, but what we all struggle with here is the lack of positive reinforcement, right? it was helpful for me to learn about reward and punishment, just in the last week. all these things can be helpful, but they don't do the work for us, i have to remind myself. anyway, i'll come back and give updates.

btw i'm going to do the three times per week for three hours a day outpatient program at the psych hospital next week, and check out some support groups. we'll see how it goes. thanks for listening y'all.

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Hey tesig11, good for you. You can talk at me anytime. Seriously. Medications are frightening. I've seen them take someone in psychosis to normal in three hours. That's scary and wonderful. Anhedonia is truly living torture for those swallowed in it. Anyone who claims they understand it without ever experiencing it sadly cannot. I cannot. I can only be a friend to the friendless. I can only ask you to keep on keeping on. Anhedonia for me is torture from a different perspective. I love my wife, would die for her, I would give my soul for her release from anhedonia, but I cannot claim I understand it. You give your best telsig 11, what ever that is. You need to talk, do so. Their are great people on here suffering like you. Some very intelligent folks who all want the same thing, relief from this nothingness. I wish you well my friend. Keep us in the loop !

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Interesting information regarding dopamine..

Depression, Anhedonia, and Psychomotor Symptoms: The Role of Dopaminergic Neurocircuitry

Faculty Affiliation and Disclosure

Dr. Stein is professor in and chair of the Department of Psychiatry and Mental Health at the University of Cape Town in South Africa, and is also on faculty at the Mount Sinai School of Medicine in New York City.

Faculty Disclosures: Dr. Stein has received grant support/honoraria from AstraZeneca, Eli Lilly, GlaxoSmithKline, Lundbeck A/S, Orion, Pfizer, Pharmacia, Roche, Servier, Solvay, Sumitomo, and Wyeth.

Funding/Support: Dr. Stein receives support from the Medical Research Council of South Africa.

Authors’ note: This case is based on an amalgam of the author’s experience.

Abstract

The heterogeneity of major depression suggests that multiple neurocircuits and neurochemicals are involved in its pathogenesis. Anhedonia and psychomotor symptoms are, however, particularly characteristic features of major depression and may provide insights into its underlying psychobiology. Importantly, these symptoms appear to be mediated by dopaminergic mesolimbic and mesostriatal projections, the function of which is, in turn, influenced by key gene variants and environment stressors. Indeed, there is growing evidence of the way in which the dopaminergic system is associated with cognitive-affective disturbances in depression, and provides a useful target for therapeutic interventions. At the same time, a range of other systems are likely to contribute to the psychobiology of this condition.

Case Report

Rachel is a 43-year-old woman who presented for treatment to her primary care physician. She complained of depressed mood, not finding pleasure in her life, and of feeling slower and slower. She had a range of other classical symptoms of depression, including poor concentration, decreased appetite, and insomnia. On mental status examination, her speech was slowed, and there was evidence of psychomotor retardation. Her primary care physician initiated bupropion, increasing the dosage to 100 mg TID. After several weeks of treatment, she demonstrated a good response to treatment. Rachel was particularly delighted to report that she was enjoying life again, and had the sense that she was moving around more quickly and more responsively.

Cognitive-Affective Neuroscience

Depression is a heterogenous condition characterized by multiple symptoms and subtypes. Different symptoms (eg, poor concentration, disturbed sleep) and subtypes (eg, melancholic, seasonal) are likely mediated by different neurocircuitry and neurochemistry,1-3 and may or may not be present, in any particular individual with depression. Depression may be characterized by an increase or a decrease in certain of its symptoms (eg, hyperphagia, hypophagia), further complicating attempts to explore its psychobiology.

Nevertheless, anhedonia—or loss of pleasure—appears to be a particularly central feature of major depression.4-6 Reward is mediated by dopaminergic projections to the nucleus accumbens, suggesting that mesolimbic neurocircuitry plays a crucial role in the pathogenesis of depression.7,8 Furthermore, other dopaminergic projections (ie, mesostriatal, mesocortical) may play a role in mediating additional symptoms of depression that appear to lie at the core of this disorder (eg, psychomotor symptoms, loss of motivation)9,10 and its melancholic subtype.11

Neuroanatomy/Neurochemistry

Basic research on the brain reward and motivation systems and animal models of anhedonia and psychomotor symptoms12-15 have provided a foundation for investigating the role of dopaminergic and associated neurocircuitry in the pathogenesis of depression. Complementary work16,17 has shown that neurological lesions in this circuitry can result in anhedonia or psychomotor symptoms. Finally, neuroimaging studies9,10,18-22 of anhedonic and psychomotor symptoms in depression have contributed to delineating the neurocircuitry and neurochemistry of this disorder.

Anhedonia, for example, was positively correlated with ventromedial prefrontal cortex and negatively correlated with amygdala/ventral striatal activity in response to happy stimuli (Figure 1).19 In another study,20 trait anhedonia was positively correlated to ventromedial prefrontal cortex activity during the processing of positive information, and inversely correlated with anterior caudate volume (Figure 2). Psychomotor symptoms have also been associated with frontal and caudate abnormalities in depression,9,10,23 and fatigue may involve related regions.2,24

Stein1small.jpg

Stein2small.jpg Molecular imaging studies8,25,26 provide partial support for the role of the dopaminergic system in mediating depression, particularly depression with psychomotor symptoms.27-29 Functional brain imaging during a dopaminergic challenge has emphasized that dopaminergic circuitry is involved in altered reward processing in anhedonia (Figure 3).30 Electroconvulsive therapy and prefrontal transcranial magnetic stimulation result in increased dopamine release,8,31 and deep brain stimulation to the reward circuitry is able to relieve anhedonia in treatment-resistant depression.32

Stein3small.jpg

Depression involves a range of other circuits and chemicals, and the extent to which anhedonia, psychomotor symptoms, and other features associated with reduced positive affect are specifically linked to dopaminergic dysfunction is debatable.33,34 Several other systems and molecules that play an important role in mediating depression intersect closely with the dopaminergic system; these include serotonin,35 glutamate,36 opioids,37 the hypothalamic-pituitary-adrenal axis,38 and neurotrophic factors.39,40 However, certain depressive symptoms may be more specifically linked to one of these systems.2,41

Gene/Environment

The heritability of anhedonia and psychomotor symptoms deserves further study.42,43 Response to early maternal separation and to other stressors is mediated in part by dopaminergic circuitry,15,44 and dopaminergic gene variants and their interactions with environmental stressors play a role in the pathogenesis of depression.45,46 Still, a range of other gene-environment mechanisms are also likely to play a role in this condition.47,48 Research on the relationship between dopaminergic receptor variants, cortico-striatal activation, and responsivity to reinforcers,49 may ultimately be relevant to understanding the pathogenesis of depression.

Evolutionary Approaches

A range of evolutionary theories have been put forward to explain anhedonia and psychomotor symptoms in depression.50,51 Nesse,50 for example, notes that low mood increases ability to cope with situations in which effort to pursue a major goal will likely result in danger, loss, bodily damage, or wasted effort. Similarly, others51 have argued that depression represents an adaptive response to the perceived threat of exclusion from important social relationships. Some evolutionary theories have focused specifically on the importance of anhedonia.52

Clinical Implications DSM-IV-TR Diagnosis

Anhedonia and psychomotor symptoms seem to be particularly core features of major depression, and also characterize its melancholic subtype.5,9,53 Other important symptoms of depression may also fall under the rubric of reduced positive affect (eg, lack of energy).33 Nevertheless, it is important to emphasize that symptoms such as anhedonia and psychomotor symptoms occur in a broad range of other medical conditions, including psychotic disorders, Parkinson’s disease, and illegal drug withdrawal.

Assessment/Evaluation

There are a number of scales of anhedonia including the Snaith-Hamilton Pleasure Scale, the Fawcett-Clark Pleasure Capacity Scale, and the Revised Chapman Physical Anhedonia Scale, and these do not completely overlap.54 The Salpêtrière retardation rating scale, the CORE Assessment of Psychomotor Change, and the Motor Agitation and Retardation Scale, are observer-rated measures to assess psychomotor abnormalities, and a range of more sensitive experimental performance measures is also available.10,55

Pharmacotherapy/Psychotherapy

Dopaminergic agents have a useful role to play in the treatment of depression and treatment-resistant depression.8,56,57 Both dopamine agonists and low-dose atypical antipsychotics (which increase extracellular levels of dopamine and norepinephrine, but not serotonin, in the prefrontal cortex) appear effective in the pharmacotherapy of treatment-resistant depression.2 Although effective antidepressants tend to be useful across the range of depressive symptoms, there is some evidence10,33 that dopaminergic agents are particularly useful for reduced positive affect and for psychomotor symptoms.

Conclusion

Depression is universally described as a “down” rather than an “up” feeling. Similarly, there is a common association between depression, anhedonia (feeling down), and psychomotor retardation (slowing down). There is growing evidence that dopaminergic mesolimbic and mesostriatal projections play an important role in mediating these symptoms. Functioning of the dopamine system is impacted on by particular gene variants as well as environmental stressors, and also by its interactions with a range of other systems. As always, researchers hope that a better understanding of these mechanisms will ultimately lead to better treatments.

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Dopamine seems to be only a part of the puzzle, as the feeling I got from dopamine enchancing drugs does not fully encompass the "emotional" "empathetic" experience. It does increase reward salience and potentiates reward, but quickly stops working, and does not really increase empathy, just interest. We know that after chronic use of SSRIs or serotonergics such as MDMA, anhedonia can follow. Receptors upregulate and the serotonin transporter density comes back to normal after about a year: http://bjp.rcpsych.org/content/194/4/355.full.pdfGene expression controls the serotonin transporter. Not really sure where else to take this, but it seems to not be permanent at least (if receptors, neurotransmitter function/level, vitamin d levels, transporter density, and rem sleep latency are any indicators).The only reason I could possibly see it being persistent is if it is perpetuated somehow and prevented from healing and taking it's natural course. The brain really has to "calm down" in order to start recovering - excessive NMDA neurotransmission/activity is associated with the anhedonia/anxiety/depression. Not really sure what causes it to persist other than the limiting factor of how fast the sert density can return to normal and receptors upregulate. I think serotonin synthesis returns to normal (tryptophan hydroxylaze or however you spell it) too, but I'm not sure.

Guess there is longer-term effect on serotonin synthesis that might in part cause post-serotonergic dysfunctions and be related to anhedonia in general: http://www.ncbi.nlm.nih.gov/pubmed/11901216 These data demonstrate that in addition to the known short-term action as an uptake blocker, sertraline also exerts a long-term effect on the serotonin neurotransmission by enhancing serotonin synthesis. A similar effect was observed with another SSRI, fluoxetine, but not with the non-SSRI chlorpromazine. The up-regulation of TPH gene expression by sertraline was attenuated by the protein kinase A (PKA) inhibitor N-[2-(p-bromocinnamylamine)-ethyl]-5-isoquinolinesulfonamine, suggesting that a mechanism involving the PKA signaling pathway might at least in part mediate the long-term therapeutic action.

Edited by itstrevor
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I've been directed to the topic by a friend and have read a bit of it but not all. He thinks that maybe I have anhedonia as i'm starting to not be able to enjoy things very much. I can get very very sad but not really happy, even when I try to do things like play with the kids or go out with friends there is no real happiness there at all and i'm quick to be sad again.

I'm losing interest in most things now and sleeping an awful lot. I'm on 40mg of Citalopram and worry that if I come off it I will get even worse as was very suicidal before and when I first started taking it.

Basically HELP. As I can't carry on feeling like this :verysad3:

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I finally finished up reading through this thread and have some thoughts on some of the recurrent themes within.

1. While it's important to not obsess over your own blunted emotions and hedonic incapacity, as taking a "hands on" approach does, paradoxically, just doing nothing doesn't work for me either. My physiology has shown me no promise in heeling itself over isolated, extended periods of just sucummbing to, or even embracing, the apathy. In fact, I saw it mentioned that some sort of chemical intervention is necessary for those of us with this condition, by defintion, to feel something and I highly agree. Instead, I believe that building positive momentum is the only way out of this. By positive momentum, I mean the "windows" or more extended periods of remission from anhedonia that add to one's personal experience. These windows are necessary not only because it's so easy to forget what it's like to feel real emotions and hedonism after years of being anhedonic, but because you need to know the goal before you can possibly know attainment of it. For me, drugs and medication are the only way to that end. Yes it's hard to play ameteur psychiatrist, but then again, it's even harder to find a competent doctor who understands this condition, or any mental illness really, beyond a clinical, empirical sense.

2. I've adopted the mindful, "impartial observer" in all of my thoughts without even trying to do so. If one is truly emotionally blunted, how can your thoughts, even in regards to planning out suicide, be anything but neutral?

3. I've started experimenting with chronic low dose Salvia Divinorum, as previously I had only used it in hallucinatory doses, and believe it may have promise. I'm familiar with the mechanism of kappa agonism and it's downstream effects, but anecdotal evidence for it's efficacy seems to be uncommon and lacking in detail.

4. In my case, NMDA antagonism via dextromethorphan works temporarilly. I can still remember the first 3rd-plateau trip I ever achieved and the realistic envisioning of a future life for me that it showed me. That sort of anticipation, let alone with any sort of feelings attached, was something that had been alien to me since I originally became depressed at age 11. The afterglow of a good DXM dosage is also pro-hedonic for around 1-2 days afterwords. Like all chemical treatments, the issue is in finding the right dosage and schedule, as in the case of DXM, and with the terrible inactive ingredients in 98% of cough syrups and loczenges, this is a potentially side-effect heavy way to go.

Edited by Dichotohmy
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Nearly 3000 posts and still no concrete answer , just vague replies,. I started reading with so much enthusiasm that i would find my answers but was so 'dissapointed' that if i could feel i would have hit my computer screen with a hammer.

Now i would like to start point to point discussion for the sake of everyone who have spent so much time on this thread.

Does antipsychotic/ssri induced anhedonia resolve with time ?

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Hey itstrevor,

Aren't dopamine agonists able to somewhat reverse PSSD?

"Dopamine agonists have been shown to facilitate the sexual reflex. In the brain there are a series of sexually inhibitory and sexually excitatory neurotransmitters. The sexual inhibitory neurotransmitters are serotonin and another one is prolactin. The ones that are sexual facilitators are dopamine, oxytocin and norepinephrine.

So strategies that raise the facilitators would allow somebody who had a low interest, low orgasm, low lubrication to improve that status."
Source:

Dr. Goldstein, How Does Dopamine Fit In With Pharmacology?

http://youtu.be/miLyeiUJAn4?t=3m30s

http://www.empowher.com/reproductive-system/content/out-all-pharmacology-strategies-how-does-dopamine-fit-dr-goldstein-video

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All of my research seems to indicate that anhedonia is a temporary condition that abates within around 3 years (depending on severity, but most cases seem to abate within 1 year). Studies repeatedly show the brain coming back to baseline after a variety of traumas, but it does take a while, and excessive stress (NMDA overactivity in certain regions of the brain) and use of drugs can perpetuate or prolong the healing period. Healthy distractions (living a normal life, exercise, making progress in life) can make recovery faster.

I've had more windows since coming off of my last antidepressant, and have noticed increased emotional lability after getting up extremely early and doing heavy exercise (this has been shown to upregulate dopamine receptors and increase BDNF which both directly relate to anhedonia). Sometimes I have a deep heavy feeling of depression followed by a window. If the depression feels too intense, eating legumes (possibly in a burrito) and small amounts of inositol seems to help alleviate it (or at least tone it down a bit).

One cannot simply "not do" something. One has to replace "not doing" something with "doing" something. You can't just not think about something, because in your attempt to not think about it, you are thinking about it, but if you replace that something with something else, it becomes a bit easier. Sometimes hitting rock bottom is the only way. You have to expect the numbness, but be neutral about it and know that it goes away eventually. I had to actually find scientific evidence and first-hand accounts to get myself to believe this and make the anxiety about it go away. Emotions can't be stuffed, and people with expectations should be avoided when possible (you will recover even if you don't). You don't have to DO anything to recover, you have to simply let it happen, but it takes a long time. Don't get involved in relationships until you are ready and FEEL GOOD about it. Expect it to take a while, but the given time frame should give you a ballpark estimate (timeline posted earlier in thread). Not everybody fits into the neat little times. Some people take 2 months, some take 6, some take 8, some take a year, and a few 2 years - sometimes 3. But after a while, you are able to live without thinking about it.

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RECENT HOPEFULNESS SHOT DOWN.

Although my earlier post on this topic was extremely despondent, due to my daughter's pregnancy both my therapist and I had hopes that my becoming a grandmother and holding a newborn baby in my arms would elicit a biologically based emotional response.

My grandson was born May 29th and mother, father, and baby are all doing wonderfully.

I visited them all at the hospital on May 30th and got a chance to hold my grandson for about 20 minutes. Then other visitors began to arrive.

However, yesterday I was able to spend 7 hours with my daughter and grandson. It was uninterrupted time, no other visitors as there were at the hospital. I got to hold my grandson for hours. He is the spitting image of both of my kids as newborns.

While the experience brought back memories os when my children were young, and it was a nice experience, I was NOT flooded with feelings of joy, happiness, even love. I didn't feel a thing, not a single thing.

Here I am spending wonderful, quality time with this little miracle of life, and my response to him was NOTHING.

I am truly despondent. It seems that if anything in life could or would or even should trigger a positive emotional reaction, holding your newborn grandson would be it.

Talk about depressing.

Last hope - gone.

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Dopamine agonists (I tried Mirapex/Pramipexole and Amantadine) did not seem to help with anhedonia in any way whatsoever. I've heard that they are supposed to work from anecdotal reports because they downregulate or desensitize presynaptic receptors (the "brakes"), but I'm still skeptical because they aren't exactly known to make people feel euphoric and such, and I tried both myself. They lower prolactin, but prolactin is a part of the "release" that terminates the desire/arousal/release loop. In some cases, excessive gambling and hypersexuality have been reported, however, but this seems to only occur rarely and does not mean that hedonia will be induced in the way that most people probably are looking for.

Mirapex just made me sleepy and amantadine made me a bit jittery, if I can recall correctly. This is probably related to other receptors the two molecules hit or something, but I don't really remember. I wouldn't mess with them and possibly dysregulate the dopamine circuits.

Also, expect that you will feel empty/anhedonic. If you expect to feel great during the healing process, you will just create anxiety/depression spikes.

Edited by itstrevor
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To make anhedonia go away:

BDNF UP

NMDA DOWN

PHASIC DOPAMINE UP

PHASIC SEROTONIN UP

ENDORPHINS UP

ENKEPHALINS UP

DOPAMINE RECEPTOR UP

REM LATENCY DOWN

PROTEIN, EXERCISE, LIMIT STRESS, ROUTINE, NEUTRAL OBSERVER, KEEP ACTIVE, GET UP EARLY TO WORK, EXPECT TO FEEL NUMB, ABSTINENCE FROM PSYCHOTROPICS, WAIT

...or whatever you can do to help with the list of items above (using something like amphetamine, though, for example, will DOWNREGULATE receptors which is not desired)

Also, phasic serotonin firing causes a RELEASE of oxytocin (5HT1A receptor) and prolactin, I believe, is part of the "afterglow." Dopamine works primarily with DESIRE and Norepinepherine is mostly for AROUSAL. All of these neurotransmitters are important for proper functioning. You can't just focus on dopamine or norepinepherine and think it will work the way you want. You can try it, like I did, but I don't think you will get what you want.

Dopamine increases interest, but WILL NOT give you that "touchy-feely" empathetic feeling you might be looking for. Phasic serotonin spikes (like those created from the use of XTC) produce that sort of social/pair bonding and empathy that dopaminergics will not provide. Dopaminergis also have terrible comedowns. In addition, norepinepherine-enchancing drugs can create anxiety, panic attacks, rapid pulse, and lots of other nasty things - you will feel more aroused and everything, but it's more physical and "adrenaline-like" in my opinion than something that makes you hedonic. I'm not sure about how to target oxytocin - I haven't read much about it. I did try bremelanotide - didn't have any effect.

Edited by itstrevor
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This is a massive and very interesting thread.

I have schizophrenia and also have anhedonia. When I was psychotic, I experienced emotions really intensely (delusions, severe anxiety, reactions to voices), some euphoria during that time too. But even then, when my dopamine was high, I still had anhedonia to what I call "interesting emotions" - emotions that refresh you and make life more interesting; the way I used to feel up to about age 19. The way I describe them is "feeling the essence of things"; the essence of a person, the essence of a commercial, the essence of a nature scene, anything which lets you know that that what you're experiencing gives off its own unique essence/gestalt.

I think what really kick-started my anhedonia is listening to a "spiritual teacher" named Adyashanti, who talked about how everything is one and has the same essence of "truth", which made put all my experience up to that standard, denying that everything I experienced can feel different and blocking those experiences, if that makes sense. Also he gave me the impression that enlightenment is about no longer feeling emotions. I think his teachings (which I believed and tried to implement so obsessively) may be the cause of my anhedonia.

Other probable causes of my anhedonia are my body's reaction to too much anxiety and stress, shutting me down to give me a break from it, but failing to re-start again. Also, it could be the anti-psychotic that I am on. However, even before I was on the dopamine lowering antipsychotics, I still had anhedonia, so I don't think its purely a low dopamine problem.

What has helped me though is Sarcosine, an NMDA agonist which is a Glycine-transport inhibitor, increasing the concentration of glycine. It's been shown in studies to help the negative symptoms of schizophrenia (such as apathy, anhedonia, blunted-affect, social-interaction difficulties, cognitive deficits). They found out that NMDA agonism can help these symptoms because people taking PCP showed schizophrenia symptoms (both positive and negative) and PCP is an NMDA antagonist, Also, sarcosine outperformed Citalopram in a study treating depression. Maybe people without schizophrenia also have an NMDA hypofunction issue, I don't know. But what I noticed since taking 2g of sarcosine daily is increased motivation for sure and increased feelings of excitement. This alone helped me to not think about my anhedonia so much, but the "essence of things" experiences did not return, however. I am hopeful though that coming off my antidepressant will help. This is contrary to what Trevor says about treating anhedonia by making NMDA go down, but it helped me.

Another thing I noticed is that taking L-theanine, which is a GABA-agonist, seems to make me feel less emotion and enhances the feeling of blankness probably because of its inhibitory effects on glutamate. So maybe GABA antagonism can help with feeling more emotion.. which is why I'm trying Pregnenolone next, a GABA antagonist which is also shown to help sz negative symptoms.

Edited by Supernothing
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yes i am pretty sure GABA plays a big role there and i could think antagonism of that receptor could be beneficial... also what trevor said is niecly summed up and i believe that BDNF played a big role in my improvement: both tianeptine and testosterone/gonadotrophin in particular.

what austin said is also true: 3000 pages and theres no pattern, only vague directions. I think, as a person who is not particularly scared of trying new things and supplement, that a collective trial&error approach with different OTC supplements could be beneficial to the "community": but that would need a structured database and methodic approach, for which i lack (partly) time and energy. Yohimbine for example, but theres a miriad of others

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Yes, L-theanine made me feel pretty flat and gave me a "brain buzz" heavy-headed feeling.

Supernothing, thanks for your interesting post about the negative symptoms of schizophrenia - which include anhedonia-like symptoms. I ordered a bag of glycine powder two weeks ago to help with my sleep. I've only been taking 1 gram every night, but might try taking 10 grams in the morning now, since I have it. See if it does anything.

http://schizophrenia.com/glycinetreat.htm

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