I heard and read about weed increases estrogen in small amounts but it blocks HGH too along with alcohol and Xany bars! I did not know this shit! I don't drink (religious reasons) so I'am not concerned about the alcohol, but I love weed after training because of the anti inflammatory affects I get tired of taking motrin. I have been known to take a xany bar on occasion too.
GABA has been purported to increase the amount of the Human Growth Hormone. The results of those studies have been seldom replicated and have recently been in question since it is unknown if GABA can pass the blood-brain barrier.
Drugs that affect GABA receptors:
* alcohol (ethanol)[2][3][4]
* avermectins—doramectin, selamectin, ivermectin
* barbiturates
* bicucullines
* benzodiazepines
* baclofen
* tramadol
* opiates
* cannabinoids
* carbamazepines
* cyclopyrrolone derivatives—eszopiclone, zopiclone
* fluoroquinolones
* gabazine (SR-95531)
* gamma-hydroxybutyrate (GHB)[5]
* imidazopyridines—zaleplon, zolpidem, zopiclone
* muscimol
* phenytoin
* picrotoxin
* progabide
* propofol
* phenibut
* thujone—GABA antagonist
* valproate
Drugs that affect GABA in other ways:
* tiagabine—potentiates by inhibiting uptake into neurons and glia
* vigabatrin—potentiates by inhibiting GABA-T, preventing GABA breakdown
* tetanospasmin—primary toxin of tetanus bacteria, blocks release of GABA
http://www.ncbi.nlm.nih.gov/sites/en...&dopt=Abstract
Depression of growth hormone and cortisol response to insulin-induced hypoglycemia after prolonged oral delta-9-tetrahydrocannabinol administration in man.
Six hospitalized volunteer male subjects were given insulin, 0.15 U/kg, before and after 14 days of administration of delta-9-tetrahydrocannabinol (THC) at a dose of 210 mg/day. A
diminished maximal serum human growth hormone (GH) increase followed the prolonged THC ingestion. The mean maximal GH response was: 52.6 ng/ml +/- 8.7 (+/-SE) before THC and 18.8 ng/ml +/- 6.7 (+/-SE) during THC, P less than 0.01; corresponding cortisol responses were 20.1 mug/dl +/- 3.0 before THC and 10.0 mug/dl +/- 1.1 during THC, P less than 0.05. The data suggest suppression of the hypothalamic-pituitary axis after prolonged high dose THC use. This is consistent with other reported endocrine effects of marijuana in man.
Gamma-aminobutyric acid B receptor 1 mediates behavior-impairing actions of alcohol in Drosophila: adult RNA interference and pharmacological evidence.
Department of Psychiatry, Psychiatric Institute, University of Illinois, Chicago, IL 60612, USA.
In addition to their physiological function, ****botropic receptors for neurotransmitter gamma-aminobutyric acid (GABA), the GABA(B) receptors, may play a role in the behavioral actions of addictive compounds. Recently, GABA(B) receptors were cloned in fruit flies (Drosophila melanogaster), indicating that the advantages of this experimental model could be applied to GABA(B) receptor research. RNA interference (RNAi) is an endogenous process triggered by double-stranded RNA and is being used as a tool for functional gene silencing and functional genomics. Here we show how cell-nonautonomous RNAi can be induced in adult fruit flies to silence a subtype of GABA(B) receptors, GABA(B)R1, and how RNAi combined with pharmacobehavioral techniques (including intraabdominal injections of active compounds and a computer-assisted quantification of behavior) can be used to functionally characterize these receptors.
We observed that injection of double-stranded RNA complementary to GABA(B)R1 into adult Drosophila selectively destroys GABA(B)R1 mRNA and attenuates the behavioral actions of the GABA(B) agonist, 3-aminopropyl-(methyl)phosphinic acid. Moreover, both GABA(B)R1 RNAi and the GABA(B) antagonist CGP 54626 reduced the behavior-impairing effects of ethanol, suggesting a putative role for the Drosophila GABA(B) receptors in alcohol's mechanism of action. The Drosophila model we have developed can be used for further in vivo functional characterization of GABA(B) receptor subunits and their involvement in the molecular and systemic actions of addictive substances.
