Will Trisorbagen change a PCT protocol due to its effects?

[temper35]

Since Trisorbagen apparently increases both absorption and prolongs the activity of a PH/PS in the bloodstream, would this call for a more thorough PCT due to the possibility of increased suppression?

Example, something mild like Halo/Bold, Epi/Prop that people often run with OTC PCT.

Would the use of Trisorbagen alongside a PH cycle make an OTC PCT less of a good idea?

[Sampson]

good question, I would like to know the answer to this as well.

[dinoiii]

I cannot offer an answer to your question with certainty as I have little experience with both the product and one of the potential ingredients: Emblica officinalis. But, we can however, pontificate a little, so please indulge me and I will address each ingredient one-by-one.

Emblica

While a 50% extract of Emblica officinalis (EO) seems to exert a hepatoprotective effect, its relationship to the steroidal nucleus with cycles is unclear. There seems to be the most research available with the anti-tuberculosis subset of drugs (rifampicin, isoniazid, and pyrazinamide), which don’t translate identically. For instance, there are 3 mechanisms hypothesized for aiding EO’s effects:
(1) membrane stabilization
(2) antioxidative properties
(3) Cytochrome p450 2E1 inhibition

The first two are suggested as least likely and the cytochrome effects do NOT involve 3A4 (predominate offering in AAS metabolism) so I am uncertain it would offer any type of aid in that regard and have no blood test backing here.

I am unaware after visiting toxicology reports if any directly occur secondary to use of the EO itself. And a rather neat thing is that the Estrogen-channeler is present in EO (ascorbigen - which is actually I3C + Vitamin C), which actually might make it more viable on cycle for aromatizable agents (unsure).

I don’t care for the tannins present (Emblicanin A&B) which are the hypothesized anti-oxidants due to how they work and if you do NOT possess asthma, the rationale for this agent seems likely moot overall.


Bioperine

This agent is tricky as when used with certain compounds, it increases absorption…yet others it DECREASES it. I am unaware of quality research with steroid molecules for adequate appraisal, but it certainly seems like companies put this in virtually everything these days for the sake of what it does.

Piperine strongly inhibits hepatic arylhydrocarbon hydroxylase and UDP-glucuronyl transferase activities, thus prolonging hexabartital sleeping time and zoxazolamine paralysis time in mice, but again the translation to humans is very limited. Piperine enhanced the bioavailability of oxyphenylbutazone and thereby potentiated its anti-inflammatory activity in rats – again, you might start to see a theme.

Now, there are some nutrients (some basic vitamins/minerals) that it has been shown to increase the absorption of, but the translation to steroidal nuclei is so much less clear.


DHB

This may be the most important and/or minimally most-directly related item in the formula, however – those that have tried it concurrently with cycles don’t tend to report phenomenal results.

5 furocoumarins isolated from grapefruit juice were evaluated at different concentration on cytochrome P450 3A4, cytochrome P450 2C9, and cytochrome P450 2D6 isoenzyme activity. Among the 5 furocoumarins tested, the inhibitory potency was in the order of paradisin A > dihydroxybergamottin > bergamottin > bergaptol > geranylcoumarin at 0.1 μM to 0.1 mM concentrations. The IC50 value was lowest for paradisin A for CYP3A4 with 0.11 μM followed by DHB for CYP2C9 with 1.58 μM, so I think there is significant application – however, the translation into what a real-world IN VIVO dose would include is unclear.



D_

[dinoiii]

It may very well follow that pardisin A (3A4) is the ingredient with more rationale for employment here rather than DHB (2C9).


D_