Soviet pharmacologists searched for a better compound than BROMANTANE to expand their military/space medicine applications, and created CHLODANTANE
It had a much wider spectrum of defense:
hypoxia, freezing cold, toxic chemical exposures, pronounced immune/antioxidant effects..
gaezv retweeted
if you are on amphetamines and want to prevent long term issues, a simple blood pressure medication will go a long way
not many people know this but several long term issues with amphetamines are NOT about dopamine, instead its linked to the AT1R receptor
- AT1R contributes to amphetamine induced oxidative stress and damage
- amphetamines increase astrocyte reactivity in the PFC, an effect reduced by AT1R inhibition
- amphetamines can enlarge blood vessels while reducing their growth in the PFC, through AT1R
- long term amphetamine abuse can impair memory, AT1R blockers can protect against these
- AT1R regulates dopamine production and release while amphetamines can change AT1R activity
the AT1R blockers called telmisartan and candesartan are what you are looking for and are what you want to use in combination with amphetamines
importantly, amphetamines do not bind directly to AT1R, the effects are downstream
Most people will benefit from an antibiotic cycle + notice it
- Cytokine suppression
- Inflammasome regulation
- Insulin sensitivity
- Neuroprotect
- Antioxidant
- Hormone balance
- Anti apoptosis/tumor
- Anti bone resorption/growth
Some:
- Cyclines
- Penicillins
- Ceftriaxone
Trimetazidine helps shift the GABA:Glutamate ratio
- restores depleted hippocampal/cortical GABA
- reduces elevated glutamate, upregulating astroglial transporters, GLT-1, GLAST
- increases GABA synthase (levels went up)
- preserves ATP production, restores glutamate homeostasis
Pregnenolone for neuroprotection, basic but still decent
- anti apoptotic
- suppresses M1 microglial activation through TLR2
- potentiates NMDA at sigma-1
- helps sleep
- supports memory consolidation
- neurogenesis
- glutamate excitotoxicity protection
- pro myelin synthesis
Now that everyone talking bout Cialis again
cGMP build up in osteoblasts due to PDE5Ai, activates PKG2, cells stop dividing and start mineralizing the bone, also suppressing osteoclasts
Telmisartan is a good addition, blocks AT1R on osteoblasts, RANKL drops so less resorption
Sacubitril, a BP drug, can make you TALLER, with open growth plates
By blocking neprilysin, the enzyme that degrades CNP.
CNP accumulates at the growth plate hitting NPR-B receptors on chondrocytes, then bunch of things happen like cGMP PKG goes up, MAPK down, and bone enlarges
PA-915, is also fascinating for elevated CORTISOL cases, an antagonist of PAC1 receptor (amygdala, mPFC..) REGULATING STRESS
The PACAP–PAC1 pathway is a modulator of HPA axis
- Normalizes corticosterone
- Restores dendritic spine density (like Ket)
- Antidepressant + anxiolytic
Instead of taking ashwaganda you should take phosphatidylserine
Ashwaganda lowers basal cortisol levels. The really painful thing here is that people deploy it despite never actually getting their cortisol tested. "I'm stressed. I need to lower my cortisol" well did you get your cortisol tested? "No but I just feel like it's high"
Utter brain death
Phosphatidylserine acts in a much more elegant manner by modulating stress-induced cortisol responses by reducing ACTH release and subsequent adrenal cortisol secretion induced by things like exercise or other stressful activity. This makes it an excellent, non-stimulating, pre-workout ergogenic
PS also acts as a component of neuronal membranes and can even improve memory under certain conditions. It also influences cholinergic signaling and acetylcholine release. Ashwaganda does not do anything for your cognition
I find that most people supplement something based on pure vibes and end up doing something retarded in the long run and waste a ton of money. The only use case for ashwaganda is to attenuate chronically elevated cortisol levels, confirmed by an actual cortisol test, and even then there are better options. Do better
INT131 mogs pioglitazone to death
- 2mg Same HbA1c drop as 45mg Pio
- Less water retention / None at 1mg
- Less weight gain / None at 1mg
- Less edema / None at 1mg
- 20x higher PPARγ affinity (partial)
- Neuroprotective
- Helps w AGEs
- Metabolism benefit
- Insulin sensitivity
Dose MEMANTINE 2.5mg EOD
HL is 65h, if you take more, it builds up quickly
Goal is to reach a concentration of ~22 nM to target extrasynaptic GluN2B (excitotoxicity)
Higher dose, block synaptic GluN2A (needed for memory formation + LTP, brain fog) and hit unwanted D2 receptors
tiktok.com/@humanupgraded/ph…
Full tiktok breaking it down, i cannot break it down in a whole tweet, i do not have premium lol, but yeah that guy breaks it down pretty well




























