Tianeptine solutions for anhedonia

[MelaninWarlord]

Stablon is a brand name for the antidepressant tianeptine, and it may help with anhedonia, which is the inability to feel pleasure. Research indicates that tianeptine acts on the brain's reward system differently than traditional antidepressants like SSRIs, which are often less effective against anhedonia. Some evidence suggests that tianeptine can increase dopamine levels and has shown promise in treating depression-related anhedonia, particularly when combined with other medications.

What is anhedonia?

• Anhedonia is a core symptom of depression where a person loses interest or pleasure in activities they once enjoyed.
• It can manifest as a lack of motivation, joy, or general feeling of "being alive".
• For many with depression, it can be a long-lasting and difficult-to-treat symptom.

How Stablon (tianeptine) relates to anhedonia

• Different mechanism: Tianeptine works on the brain's reward pathways differently than selective serotonin reuptake inhibitors (SSRIs).
• Dopamine and motivation: Research suggests tianeptine can increase extracellular dopamine, which is linked to the motivation ("wanting") aspect of reward.
• Potential for anhedonia treatment: Because anhedonia is often associated with a lack of dopamine function, tianeptine has been explored as a potential treatment.

 

[MelaninWarlord]

Scientific Rationale: Preclinical studies show tianeptine reverses stress-induced neuronal damage in brain regions like the hippocampus, amygdala, and nucleus accumbens (a key "hedonic hotspot" for pleasure). It promotes synaptic plasticity and protects against glutamate excitotoxicity, which is implicated in depression and anhedonia.

Clinical data supports its efficacy for MDD symptoms, including anxious depression, but direct trials on anhedonia are limited.

User Experiences: Anecdotal reports from communities like Reddit (e.g., r/anhedonia, r/depressionregimens) are largely positive for low-dose therapeutic use. Users describe partial restoration of motivation, reduced emotional blunting, and "pieces of the old self" returning, often without the sedation or worsening of symptoms seen with SSRIs.

For instance:
One user reported it as "fucking amazing" for anhedonia, outperforming other antidepressants without exacerbating symptoms.

 

[MelaninWarlord]

@Asgard

 

[Asgard]

How does it interact with sleep? I can't seem to sleep more than 5 hours for some reason unknown to me.

 

[MelaninWarlord]

How does it interact with sleep? I can't seem to sleep more than 5 hours for some reason unknown to me.

Common Effects on Sleep

Low to moderate therapeutic doses (12.5 mg × 3/day, the standard antidepressant dose)

Generally neutral to mildly positive on sleep architecture in depressed patients.
Improves sleep continuity (fewer awakenings, longer total sleep time) in many studies on major depression.

Does not strongly suppress REM sleep (unlike most SSRIs/SNRIs). Some studies even show slight REM increase.

Can reduce early-morning awakening, a classic symptom in melancholic depression.

 

[MelaninWarlord]

How does it interact with sleep? I can't seem to sleep more than 5 hours for some reason unknown to me.

I can't get REM sleep hence I can't dream

 

[Asgard]

I can't get REM sleep hence I can't dream

Why?

 

[MelaninWarlord]

Why?

Idk my brain is ruined from traumatic life and bad people and lack of romantic partner

 

[Suigin Trismegistus]

Idk my brain is ruined from traumatic life and bad people and lack of romantic partner

Sounds like pineal gland dysfunction/calcification, given lack of REM sleep and anhedonia.

 

[Suigin Trismegistus]

From Grok...

There is an emerging but still indirect and preliminary link between anhedonia (the inability to feel pleasure) and the pineal gland, primarily through the pineal's role in producing melatonin and regulating circadian rhythms. Here's what the research landscape looks like as of 2025:

Main Pathways Connecting the Pineal Gland to Anhedonia​

1. Melatonin and Dopamine Interaction
   • The pineal gland is the primary source of melatonin.
   • Melatonin receptors (MT1/MT2) are expressed in dopamine-rich areas such as the ventral tegmental area (VTA) and nucleus accumbens — the core of the brain's reward system.
   • High melatonin levels (e.g., at night or in seasonal affective disorder) suppress dopaminergic firing in the reward pathway. Multiple rodent studies show that melatonin administration reduces dopamine release in the nucleus accumbens, producing an anhedonia-like state (e.g., reduced sucrose preference, a classic animal model of anhedonia).
   • Conversely, pinealectomy (removal of the pineal gland) in animals increases dopamine release and can reverse depression-like behaviors in some models.
2. Circadian Disruption and Anhedonia
   • Almost all major depressive disorder (MDD) patients with prominent anhedonia show disrupted circadian rhythms (delayed sleep phase, blunted melatonin amplitude, etc.).
   • Human studies using agomelatine (an antidepressant that is an MT1/MT2 agonist and 5-HT2C antagonist) show particularly strong effects on anhedonia scores (SHAPS, DIMD) compared with SSRIs, suggesting that directly targeting melatonin receptors can improve pleasure processing independently of pure serotonin reuptake inhibition.
3. Pineal Calcification and Psychiatric Correlates
   • Heavy pineal calcification (visible on CT scans) correlates with lower melatonin output.
   • Some (controversial) studies report higher rates of pineal calcification in schizophrenia and bipolar disorder patients who have severe anhedonia, but causation is completely unproven and most researchers consider this association weak or coincidental.
4. Seasonal Affective Disorder (SAD) and Winter Anhedonia
   • The clearest clinical example: in winter-type SAD, prolonged melatonin secretion due to shorter daylight strongly predicts anhedonia severity. Bright-light therapy (which suppresses melatonin) rapidly improves hedonic tone, often within days, faster than its effect on sad mood.

Current Evidence Summary (2025)​

Evidence Type	Strength of Link to Anhedonia	Notes
Animal studies (melatonin administration, pinealectomy)	Strong	Direct causal evidence in rodents
Agomelatine clinical trials	Moderate–Strong	Specifically improves anhedonia
Circadian disruption in MDD	Strong	Correlational but very consistent
Pineal calcification studies	Weak	Mostly negative or contradictory
Direct pineal pathology → anhedonia in humans	Very weak	Rare pineal tumors can cause psychiatric symptoms, but anhedonia is not the dominant feature

Bottom Line​

There is a biologically plausible and increasingly supported link between pineal gland function (via melatonin and circadian regulation) and anhedonia, especially in mood disorders with circadian components. However, the pineal gland is not considered a primary driver of anhedonia in most cases — dopamine hypoactivity in the mesolimbic system remains the central mechanism. The pineal connection is more of a modulator, and one that becomes clinically relevant in seasonal depression, delayed sleep-phase syndromes, and certain treatment-resistant cases where agomelatine works well.

So: Yes, a link exists — strongest through melatonin’s inhibitory effect on reward circuitry and circadian misalignment — but it is one piece of a much larger puzzle.

 

[Suigin Trismegistus]

You got the melanin, but you need some of that melatonin.

 

[Asgard]

Idk my brain is ruined from traumatic life and bad people and lack of romantic partner

I’m telling you guys, anything is possible. Don’t ever get up, keep grinding, keep hustling, shoot for your dreams.

You can do anything you want, I promise you. You just have to take that first step, take that hard step of actually doing something.

 

[Asgard]

You got the melanin, but you need some of that melatonin.

Keep grindin', keep hustlin'... I promise you anything is possible.