HEXEDRONE
pharmaphile, neurophile, hedonophile
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reupload needed formatting + new info
D O P A M I N E
Dopamine is an essential neurotransmitter that greatly benefits us in terms of survival through its effect on motivation. However, it also has effects on testosterone and growth hormones.
LOCATIONS WHERE DOPAMINE HITS
So, in general, from what I managed to dig up, which might explain some of the confusing studies and info:
Boost Testosterone: Activation of D1 receptors
Lower Testosterone: Activation of D2 receptors
Boost GH: Activation of D1 receptors with GHRH
Lower GH: Activation of D2 receptors
More precisely:
dopa is complex
The relaxing neurotransmitter. That also boosts GROWTH HORMONE!!!!!!
SHORT-TERM STRESS MAY BE BENEFICIAL FOR HORMONES
The increase in GH from diazepam seems to be linked to GABA reducing dopamine’s inhibition on GH release, making it easier for GH to be secreted. Either way, it seems that benzodiazepenes can be useful for acutely spiking GH, yet it isn't sustainable due to addiction and withdrawal.
GABA’s effects on GH seem to depend on the context, such as whether it’s acutely increasing dopamine release or blocking its inhibitory effects
thoughts?
D O P A M I N E
These are the dopamine receptors -
GPT FOR FORMATTING TABLE
cAMP = cyclic Adenosine Monophosphate
↑ cAMP
↓ cAMP
| DOPAMINE RECEPTOR | TYPE | EFFECT | ROLE | DIRECT MODULATORS | INDIRECT MODULATORS |
| D1 | Excitatory | ↑ cAMP | Drive, reward, movement | Agonist: Fenoldopam, Apomorphine Antagonist: SCH‑23390 | L‑DOPA (precursor), Amphetamines, Modafinil |
| D5 | Excitatory | ↑ cAMP | Hormone control, memory | Agonist: Apomorphine Antagonist: N/A | L‑DOPA, Modafinil |
| D2 | Inhibitory | ↓ cAMP | Prolactin ↓, reward, motor function | Agonists: Bromocriptine, Pramipexole, Ropinirole Antagonists: Haloperidol, Sulpiride | L‑DOPA, Amphetamines |
| D3 | Inhibitory | ↓ cAMP | Cravings, addiction, novelty seeking | Agonists: Pramipexole, SB‑277011 Antagonists: U-99194, BP 897 | Ropinirole, Cocaine (transporter blocker) |
| D4 | Inhibitory | ↓ cAMP | Risk-taking, attention, emotional balance | Agonists: N/A Antagonists: L‑745,870, Clozapine, Quetiapine | Aripiprazole (partial agonist), Amphetamines (indirect) |
cAMP = cyclic Adenosine Monophosphate
- Tells cells how much to activate certain pathways
↑ cAMP
- stimulates neurons
- boosts alertness
- boosts motivation
- boosts memory
↓ cAMP
- calms neurons
- decreases prolactin
- regulates mood and hormone release
Dopamine is an essential neurotransmitter that greatly benefits us in terms of survival through its effect on motivation. However, it also has effects on testosterone and growth hormones.
LOCATIONS WHERE DOPAMINE HITS
Hypothalamus
- Dopamine inhibits GnRH (Gonadotropin-Releasing Hormone) neurons indirectly → ↓ LH → ↓ Testosterone
Pituitary
- Dopamine (via D2 receptors) suppresses prolactin
- Less prolactin = ↑ Testosterone and ↑ GH / IGF-1 (since prolactin normally suppresses GnRH/LH)
Testes
- Dopamine stimulates Leydig cells indirectly → ↑ steroidogenesis → ↑ Testosterone
- This happens even without a surge in LH
Therefore, boosting dopamine WITHOUT inhibiting GnRH neurons is essential.
DOPAMINE & TEST
- Rats were given a dopamine agonist and an antagonist to compare how it influences GnRH and whether it boosts testosterone levels
- "BRO", the agonist bromocriptine, increased GnRH mRNA in certain brain cells (neurons) by 67%, showing dopamine's importance in increasing testosterone and androgen levels.
DOPAMINE & GH
- Dopamine boosts GH secretion, particularly when combined with GHRH (growth hormone-releasing hormone), by inhibiting somatostatin
- Saline = ~1.7 ng/mL·h
- Dopamine = ~13.2
- GHRH = ~14.7
- GHRH + Dopamine = ~29.8
- With oral dopamine agonist, GH doubled compared to placebo
L-DOPA FOR TEST
- Chronic L-DOPA therapy in male patients did not significantly change plasma testosterone or LH levels
- Therefore, this shows that not in all cases does extra dopamine boost test
- The participants might've had baseline hormonal levels already, and the extra dopamine served no extra benefit, possibly inhibiting GnRH
- There is a chance that there was a short-term benefit, and the "chronic" therapy led to receptor downregulation, diminishing benefits
MUCUNA PRURIENS FOR TEST
- Treatment with Mucuna pruriens also helped to restore androgens and even fix the HPTA, but only in infertile men
- ↑ Dopamine, Testosterone, LH
- ↓ FSH, Prolactin
- This is the primary pathway for the production of dopamine in the body:
- L-Phenylalanine → L-Tyrosine → L-DOPA → Dopamine
- By skipping the first 2 rate-limiting steps, increasing dopamine through L-DOPA is more efficient and faster
- L-DOPA passes the brain blood barrier more easily than dopamine itself
- Mucuna also contains antioxidants that protect the dopamine neurons
So, in general, from what I managed to dig up, which might explain some of the confusing studies and info:
Boost Testosterone: Activation of D1 receptors
Lower Testosterone: Activation of D2 receptors
Boost GH: Activation of D1 receptors with GHRH
Lower GH: Activation of D2 receptors
Dopamine D1-D2 receptor heteromer signaling pathway in the brain: emerging physiological relevance - Molecular Brain
Dopamine is an important catecholamine neurotransmitter modulating many physiological functions, and is linked to psychopathology of many diseases such as schizophrenia and drug addiction. Dopamine D1 and D2 receptors are the most abundant dopaminergic receptors in the striatum, and although a...doi.org
More precisely:
- D1, D5 (Excitatory): These receptors generally boost testosterone and GH by increasing cAMP and stimulating hormonal processes
- D2, D3, D4 (Inhibitory): These receptors tend to lower testosterone by reducing cAMP and inhibiting GnRH, while they also have inhibitory effects on GH and prolactin depending on the receptor subtype
CONCLUSION
| Receptor | cAMP | Action |
|---|---|---|
| D1/D5 | ↑ | ↑ GH & T via GHRH & GnRH stimulation |
| D2/D3/D4 | ↓ | ↓ Prolactin → ↑ LH/T (short-term) but ↓ GnRH if overstimulated |
- Avoid oxidative damage to Leydig cells
- Avoid long-term cortisol elevation
- Avoid D2 overactivation (can ↓ T)
- Don’t downregulate receptors
- Cycle L-DOPA/mucuna (if taking. better use other dopa meds)
- Support with L-Tyrosine, B6, Rhodiola
- Keep baseline dopamine levels stable
dopa is complex
G A B A
- There are 2 types of GABA receptors, with many different subtypes, but those aren't really important
| Feature | GABA-A | GABA-B |
|---|---|---|
| Type | Ion channel (lets ions flow through) | A receptor that signals inside cells |
| Speed | Fast acting with shorter effects | Slow acting with longer effects |
| Main Roles | Makes you relaxed, calms anxiety, controls seizures, relaxes muscles, makes you fall and stay asleep | Relaxes muscles, influences sleep, stress, sometimes aggression, pain relief, can influence blood pressure and heart rate by relaxing muscles around blood vessels |
| Drugs | Benzodiazepines, alcohol, barbiturates | Baclofen, GHB |
The relaxing neurotransmitter. That also boosts GROWTH HORMONE!!!!!!
GABA BOOSTS GH...
- Used 5g of oral GABA in the study
- GABA stimulates dopamine, which in turn promotes GH release
- Blocking dopamine with pimozide blunts this GH increase
- Prolactin is not involved in this GABA-induced GH spike
GABA AND CORTISOL
- Low doses of GABA can lower cortisol, but high doses may raise it
- Low-dose GABA (10 mg/kg) decreased corticosterone levels
- Higher doses (100–500 mg/kg) increased them
- Chronic cortisol exposure turns hippocampal neurons more GABAergic
- The brain is adapting to stress short term by increasing sensitivity to GABA
- Long term, it can cause issues with memory, sleep and mood
- Glucocorticoids (like cortisol) also boost GABA release but suppress glutamate, often via endocannabinoids
- This may help acutely spike GH
SHORT-TERM STRESS MAY BE BENEFICIAL FOR HORMONES
DIAZEPAM & GH
- Blocking dopamine with pimozide cuts this GH increase by 50%
- Valproate, another GABA-enhancer, blunts GH response by 50%
- GABA seems to be inhibitory for GH overall
- The first assumed pathway is this:
- Diazepam → GABA-A activation → Dopamine release ↑ → GH ↑
DIAZEPAM & GH, HOWEVER...
- Combining diazepam with L-DOPA or apomorphine (dopamine boosters) reduced GH release. This suggests that GABA can reduce dopamine’s inhibition on GH release, thus promoting GH secretion in certain contexts
- So the pathway is now this -
- Diazepam → GABA-A activation → ↓ Dopamine activity → Less dopamine inhibiting GH → GH ↑
The increase in GH from diazepam seems to be linked to GABA reducing dopamine’s inhibition on GH release, making it easier for GH to be secreted. Either way, it seems that benzodiazepenes can be useful for acutely spiking GH, yet it isn't sustainable due to addiction and withdrawal.
GABA’s effects on GH seem to depend on the context, such as whether it’s acutely increasing dopamine release or blocking its inhibitory effects
GABA = PROLACTIN?
- In humans, acute oral GABA administration elevates plasma growth hormone levels
- Prolonged treatment blunts growth hormone response and enhances prolactin response to insulin-induced hypoglycemia
Basically, over prolonged use of GABA, instead of releasing GH during hypoglycemic metabolic states (during fasting, after exercise, etc), the balance shifts to more prolactin being released
CONCLUSION
| Acute GABA | ↑ GH |
| Chronic GABA | ↓ GH, ↑ PROLACTIN |
| Low dose | ↓ CORTISOL |
| High dose | ↑ CORTISOL |
- Avoid daily use or cycle the GABA, don't take high doses
- Optimise with GABA, valerian root, l-theanine, taurine
- Short-term stress, like arguments, deadlines, presentations, competition, and physical exertion, is beneficial to hormones
- Short-term stress increases GABA, which can spike GH
thoughts?
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