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Research Chemical SciencesUGFREAKeudomestic
napsgeargenezapharmateuticals domestic-supplypuritysourcelabsResearch Chemical SciencesUGFREAKeudomestic
Great article. Always thought it should be a week to wait for Test P to clear before PCT though...
 
Ok, I looked these studies over and I'm confused as to what they are saying the exact mechanism may be. It looks as if they are saying that increasing the Glutamate to GABA ratio is what increases the LH/Testosterone production. But, this doesn't make any sense from a standpoint of Dermacrine making one "feel better" which is what is reported. Glutamate is an exitatory neurotransmitter which increases feelings of anxiety, nervousness, etc. It doesn't make sense from a logical standpoint. Does Dermacrine increase or decrease this ratio? There are anti-siezure studies for Passion Flower as well, which would indicate a decrease in Glutamate. I'm confused.

This is complicated by the fact that there are more than one type of GABA receptor. There are pharmacueticals, Gabapentin and Campral, that affect the Glutamate/GABA ratio in favor of higher GABA. These have a calming effect. I wonder if there may be an anabolic effect as well?

The 7,8-benzoflavone comes from passionflower, which has been used as an aphrodisiac for thousands of years.

There really isnt any peer-reviewed, placebo-controlled human studies examining pure 7,8-benzoflavone. But there is research with passionflower (passiflora incarnta) used in humans for increasing libido, and it’s been postulated that most of this aphrodisiac effect is from the 7,8-benzoflavone content.

Some of these reffs are not directly related to 7,8-benzoflavone, but are tied together with the nuero-active GABA agonistic/antagonistic activity that is likely the mechanism behind the testosterone and sex drive boosting effects.

-Eric

Die Bedeutung der Passionsblume in der Heilkunde.
Lutomski J et al.
Pharmazie in unserer Zeit 1981;10:45-49.

Drug/substance reversal effects of a novel trisubstituted benzoflavone moiety (BZF) isolated from Passiflora incarnata Linn. - a brief perspective
KAMALDEEP DHAWAN et al.
Addiction Biology (December 2003) 8, 379 - 386

Prevention of chronic alcohol and nicotine-induced azospermia, sterility and decreased libido, by a novel tri-substituted benzoflavone moiety from Passiflora incarnata Linneaus in healthy male rats.
K Dhawan and et al.
Life Sci, Nov 2002; 71(26): 3059-69.

Neuroactive flavonoids interacting with GABAA receptor complex.
F Wang, M Shing, Y Huen, SY Tsang, and H Xue
Curr Drug Targets CNS Neurol Disord, Oct 2005; 4(5): 575-85.

Passiflora: a review update.
Dhawan K, Dhawan S, Sharma A.
J Ethnopharmacol. 2004 Sep;94(1):1-23. Review.

A gamma-aminobutyric acidB agonist reverses the negative feedback effect of testosterone on gonadotropin-releasing hormone and luteinizing hormone secretion in the male sheep.
Endocrinology. 2000 Nov;141(11):3940-5.

Drug/substance reversal effects of a novel tri-substituted benzoflavone moiety (BZF) isolated from Passiflora incarnata Linn. – a brief perspective.
Dhawan, et al.
Addiction Biology 379-386

Anticonvulsant effects of aerial parts of Passiflora incarnata extract in mice: involvement of benzodiazepine and opioid receptors.
Nassiri-Asl M, Shariati-Rad S, Zamansoltani F.
BMC Complement Altern Med. 2007 Aug 8;7:26.

Effects of Dialyzing γ-Aminobutyric Acid Receptor Antagonists into the Medial Preoptic and Arcuate Ventromedial Region on Lutienizing Hormone Release in Male Sheep.
Suzie A, et al.
Biology of Reproduction 58, 1038-1046 (1998)

Antiandrogen Microimplants into the Rostal Medial Preoptic Are Decrease γ-Aminobutyric Acidergic Neuronal Activity and Increase Luteinizing Hormone Secretion in the Intact Male Rat.
David R et al.
Endocrinology, Vol. 137 No. 10 (1996)

Non-classical estrogen modulation of presynaptic GABA terminals modulates calcium dynamics in gonadotropin-releasing hormone (GnRH) neurons.
Nicola Romano, et al.
Endocrinology, 10.1210/en.2008-0424 (2008)

Restoration of the Luteinizing Hormone Surge in Middle-Aged Female Rats by Altering the Balance of GABA and Glutamate Transmission in the Medial Preoptic Area
Genevieve S, et al.
Biol Reprod, Jul 2008; 10.1095/biolreprod.108.069831.
 
Ok, I looked these studies over and I'm confused as to what they are saying the exact mechanism may be. It looks as if they are saying that increasing the Glutamate to GABA ratio is what increases the LH/Testosterone production. But, this doesn't make any sense from a standpoint of Dermacrine making one "feel better" which is what is reported. Glutamate is an exitatory neurotransmitter which increases feelings of anxiety, nervousness, etc. It doesn't make sense from a logical standpoint. Does Dermacrine increase or decrease this ratio? There are anti-siezure studies for Passion Flower as well, which would indicate a decrease in Glutamate. I'm confused.

This is complicated by the fact that there are more than one type of GABA receptor. There are pharmacueticals, Gabapentin and Campral, that affect the Glutamate/GABA ratio in favor of higher GABA. These have a calming effect. I wonder if there may be an anabolic effect as well?

Those reffs are related to 7,8 benzoflavone with reffs on GABA control over LH, FSH and testosterone production. The Dermacrine makes people feel good because of the DHEA and pregnenolone and not so much the 7,8 benzoflavone.

The benzo helps increase GnRH release from the hypothalamus probably via an agonistic action on GABA-b. Just remember, there is a lot going on with GABA receptors -- alpha, beta, gamma, delta receptors – pre and post synaptic interactions – receptor ligands, ect

BTW, 7,8 benzoflavone actually has anti-anxiety effects, but no drowsiness. (possibly effects on the opioid or endorphin receptor too)

-Eric
 
Doesn't DHEA convert to estrogen more so than testosterone? I remember buying a bottle not too long ago and as usual did a little more research and found that. Threw that one in the garbage!
 
FWIW I will say that PP has never smacked of bullshit marketing hype, and I cannot say that of some other past EF sponsors that evaded more questions than they answered. I'm pretty sure I was the first woman to ever try Dermacrine and the stuff won me over.
 
Those reffs are related to 7,8 benzoflavone with reffs on GABA control over LH, FSH and testosterone production. The Dermacrine makes people feel good because of the DHEA and pregnenolone and not so much the 7,8 benzoflavone.

The benzo helps increase GnRH release from the hypothalamus probably via an agonistic action on GABA-b. Just remember, there is a lot going on with GABA receptors -- alpha, beta, gamma, delta receptors – pre and post synaptic interactions – receptor ligands, ect

BTW, 7,8 benzoflavone actually has anti-anxiety effects, but no drowsiness. (possibly effects on the opioid or endorphin receptor too)

-Eric

Thanks Eric. It is not my intent for my questions to come off as skepticism, so I hope they did not. I like that you always take the time to answer technical questions intelligently and backed up by research. My questions are mainly prompted by obsessive curiosity.:evil::evil::evil:

This is interesting stuff. I'm still confused regarding the one reference where it says that Glutamate was responsible more for the increase in LH. But, that confusion stems more from the impression I had that the 7,8-Benzoflavone was the key ingredient responsible for the "feel good" effects of Dermacrine.
 
Doesn't DHEA convert to estrogen more so than testosterone? I remember buying a bottle not too long ago and as usual did a little more research and found that. Threw that one in the garbage!

Not really.

It may convert more readily to E1 from Adione, but that is a weaker estrogen that E2, so it’s basically a wash.

-Eric
 
Great Thread!



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