Bloodwork, Crashed Estradiol, & PCT Recommendation?

[KoDa]

Finishing a basic cycle of 600mg/wk Test-E (300mg E3.5D), this is week 12 with the last injection tomorrow.

Bloodwork (attached, and left to right), was taken pre-cycle, after 10th injection (week 5) and yesterday (23rd injection, week 12).

Anastrazole taken 0.5mg twice a week for first 5 weeks.

Mid-cycle showed estradiol level a bit high, needed to get that cut about in half I figured. Unfortunately first time with an AI, I upped to 0.5mg EOD as planned and kinda freaked later after running out of one supplier's anastrazole and switching to another... I started taking BP around this time and it was consistently high after a week of switching, the taste was so different from the other, etc... wondering if it was bunk or underdosed- I upped to 0.5mg ED and after awhile started to feel more and more like shit. I stopped this past weekend and got bloodwork yesterday confirming my stupidity; AI was fine, 0.5mg EOD was probably the sweet spot.

So question no. 1, I'm figuring I'll stay off the AI for at least the next two weeks, does that sound about right? Is there any way of predicting estradiol level recovery time?

Second is PCT. The original plan was the typical taking a break for two weeks (AI as needed, obviously not now) clomid/nolva/aromasin for 4 weeks.

I've been reading the comprehensive guide and I guess this makes a lot of sense.

What's been confusing is the exogenous test- start PCT when it falls to roughly 50mg. Should be in line with my starting level of ~550ng/dl. Then you have:

A 12wk cycle of test e at 500mg per week will put ex Test at around 1000mg
(500mg+250+125+62.5+31.25 etc = 1000mg)

This means it will take 5 half lives to reach ex test at or below 50mg therefore time between last injection and start of PCT is 35 days.

12 week cycle at 600mg/wk, ex test at around 1200mg, will still be 5 half lives (if assuming 7 days), and PCT start at 35.

Of course I have no interest in ballparking this based on a 600mg/wk number based on a supposed concentration written on a bottle. I have bloodwork showing peak levels were somewhere around 2300ng/dl.

So I guess my question is, where does this line up with exogenous test, how can I know where I'm starting to even ballpark a number of 7day half-lifes to drop to 50mg?

I've seen multiple claims on this forum and a linked radio interview claiming 500-600mg/wk puts you in the 4000-5000ng/dl ballpark. Yet the commonly referenced study showed 600mg yielded a mean of 2,370 ng/dl, which nearly dead on with the results I have.

So I guess, knowing I'm starting at ~2300ng/dl... I can make an assumption of half-life at 7 days and where does that put me in the 500ng/dl ballpark?

I know bloodwork can be done in a couple weeks, which I may end up doing. But let's say I want to follow the following protocol:

HCG 2000iu E3D for 14 days before pct start date

PCT start

1-35 Clomiphene 50mg morning and night
1-45 Tamoxifen 20mg morning and night

1-45 low dose of Exemestane 12.5mg E3D (Optional)

Obviously I have everything on hand to do this (as it's identical to my plan other than the start date) but HCG. If it's the way to go I'll pick some up and have it ready. But obviously I can't pull bloodwork in 3 weeks and find out I need to start PCT about then also be hittin' HCG 14 days prior to PCT start. It would be too late at that point. I'd either PCT alongside HCG for 14 days, or I'd HCG for 14 days and then start PCT... given what HCG does, I'm not sure if it's a huge deal?

I suppose it's not going to be perfect the first time through, and that's what this experience yields. But I'd just like to understand the best assumptions to make given the actual data I have on hand with bloodwork.

Ideas?

 

[Michael Scally MD]

What is the source for the TE?

 

[KoDa]

What is the source for the TE?

PEP, unfortunately. This is what I had posted with the first set of bloodwork:

For full disclosure source is PEP, purchased right before the fan was hit; upon inspection there were zero floaters, though I did filter through Whatman 0.22µm anyway. I have no interest in purchasing from him again, or promoting the product due to the way everything was handled, hence it was left out of the title- but I'm not going to lie about what it is.

I guess that's part of the confusion- because the source went bad folks jumped on the gear as if it were bunk; obviously bloods (multiple people) showed otherwise, but then there's still the matter of dosing. Some are saying significantly underdosed, and maybe that is correct. But of course the most referenced study showed a mean of 2370ng/dl for 600mg/week, so I've reached no conclusion on that front. For me my results showing 2300ng/dl is still a great cycle, it's of no consequence to me for a first time learning experience; the source is dead and I have no interest in promoting them so I try to leave it mentioned as little as possible (apologies for missing that in this post though).

It's just a matter of trying to understand what assumptions to make with this information. For example, should I assume underdosed to a 300mg/week range based on what's been claimed (about 600mg yielding 4000-5000ng/dl)?

 

[Michael Scally MD]

It does make a big difference for PCT. It could be the difference between success and failure. [Un]Fortunately, you have labs. Be back shortly..

 

[KoDa]

Much appreciated, Michael. Thank you.

 

[Michael Scally MD]

The obvious reason as you noted was the TT was much lower than expected for 600 mg per week. In fact, about 50% lower. If the TE had been true, there would be a wait again as you noted for about one month+.

I was curious why the last lab did not have a value as did the middle. Regardless, the level is probably about the same. Using the level ~2500 ng/dL, it will take about three weeks for the conditions to be right for HPTA function.

The PCT is fine. hCG 1,000 IU will be adequate. There is no need to do SERMs at the same time as hCG except for the final week. I prefer one week to load.

 

[KoDa]

Last lab was purely for an estradiol check- I really had no reason to believe TT would differ significantly from the week 5 labs, and so the more expensive test that gives results over 1500 wasn't really necessary. Same gear, same 1ml injections week 1-12, so I think the assumption is fairly safe?

Everything looks great, and as I said I appreciate the advice. I do want to make sure I'm understanding correctly: the original plan was hCG 2000iu E3D for 14 days prior to PCT (SERMs from there on out).

What you're saying is:

Week 12: last injection
Week 13: nothing
Week 14: hCG 1,000 IU (E3D?)
Week 15: hCG 1,000 IU
Week 16-19: SERMs

When you say you prefer one week to load are you meaning a SERM load (week 15) or an hCG load (week 13)?

Also, any thoughts on exemestane alongside at any point? Just curious about the estradiol rebound since I'm dropping anastrazole. Or a good point in the next 7weeks to pull another set of bloodwork?

 

[corageon]

Last lab was purely for an estradiol check- I really had no reason to believe TT would differ significantly from the week 5 labs, and so the more expensive test that gives results over 1500 wasn't really necessary. Same gear, same 1ml injections week 1-12, so I think the assumption is fairly safe?

Everything looks great, and as I said I appreciate the advice. I do want to make sure I'm understanding correctly: the original plan was hCG 2000iu E3D for 14 days prior to PCT (SERMs from there on out).

What you're saying is:

Week 12: last injection
Week 13: nothing
Week 14: hCG 1,000 IU (E3D?)
Week 15: hCG 1,000 IU
Week 16-19: SERMs

When you say you prefer one week to load are you meaning a SERM load (week 15) or an hCG load (week 13)?

Also, any thoughts on exemestane alongside at any point? Just curious about the estradiol rebound since I'm dropping anastrazole. Or a good point in the next 7weeks to pull another set of bloodwork?

So what you had low E2 for a while??? What did you feel like?

 

[tacohuman]

So what you had low E2 for a while??? What did you feel like?

You get really fatigued, sleep alot, dry skin, brain fog, difficulty concentrating on complex tasks, seem to recover slower, lifts go down, get kinda bitchy, etc. Pretty horrible. Happened to me a few weeks back. I'm assuming that test bottoms out at <5.1 since that's what mine said as well.

 

[KoDa]

Yep, taco nailed it. There's no telling how low it is, since it doesn't read below there.

How long did it take for things to recover/level out for you?

 

[corageon]

You get really fatigued, sleep alot, dry skin, brain fog, difficulty concentrating on complex tasks, seem to recover slower, lifts go down, get kinda bitchy, etc. Pretty horrible. Happened to me a few weeks back. I'm assuming that test bottoms out at <5.1 since that's what mine said as well.

Low Estrogen is a big Cipher...some people (like me) love having low estrogen.
For others, I guess it depends on other factors as well..maybe adrenal gland function, and what you do during the prime hours.

The body/brain are very interesting....interesting how "homeostasis" works...
It seems the wiring looks similar on both ends but with minor differences.
It's all just a "keep-up" mechanism I guess...

For example - Estrogen induces/activates Dopamine Beta-Hydroxylasehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3077094/ ((1)), leading to more dopamine converting into norepinephrine (not necessarily a good thing), yet estrogen also blocks excessive norepinephrine binding to alpha-1-receptors (vasoconstrictive, fight or flight)(2).
Estrogen also increases alpha-2-receptor activity (lowering norepinephrine).

With this regard - high estrogen = high norepinephrine and yet lower alpha-1-activity except higher alpha-2 activity = less norepineprhine.
Then I would say this - Beta-Adrenergic activation/FAVOR is highly LIKELY but yet possibly UNLIKELY with high Estrogen.

Now with low estrogen...depending on other factors influencing DBH (Dopamine Beta Hydroxylase)...like Vitamin D, Copper and Zinc levels for example. Let's just assume those are "all good"...you still have a net decrease in DBH levels due to Estrogen deficiency. Now you have less norepinephrine - but OH LOOK!!!
Less Estrogen PLUS High DHT will also lead to DOUBLY MORE ALPHA-1-ADRENERGIC ACTIVITY!!!

High DHT Low Estrogen PhenoType


Also since Estrogen INCREASES alpha-2-receptor expression...
Now deficient levels and high DHT - assuming you have High DHT = low alpha-2, but yet high Alpha-1 receptor expression. Since estrogen, again, normally does the opposite of what DHT does in that regard (to adrenergic influence).

So by having low estrogen the problem is nitric oxide deficiency, too much alpha-1-stimulation...and too little norepinephrine in general???

The point is more this ---- yes you have low levels of NE/NA whilst having low estrogen...but it's still going to be produced (as a normal rhythmical, natural response).AND YET - it might still maintain high levels or adrenaline/norepi whilst having low estrogen AS IF YOU HAD HIGH ESTROGEN!!! Due to that less Alpha-2 feedback!!!

Norepinephrine is also going to shockwave when you increase it during exercise or any other activity. Having too MUCH alpha-1 activity creates an ANXIETY provoking atmosphere, and less oxygen delivery due to too much vasoconstricton...and also attention problems from the SAME or SIMILAR mechanisms!!!!!!

THUS, HIGH AND LOW ESTROGEN create similar HYPER-ADRENERGIC states...except that high Estrogen also causes GLUTAMATE, and HISTAMINE increases / excess as well.
Whereas with low estrogen I would presume you would have high Epi/NorEpi but low histamine, and possibly low glutamate!**

The other BIG DIFFERENCE between HIGH and LOW estrogen is ELECTROLYTE distribution and the the resultant changes in NeuroTransmitter activity ....!
For example calcium channels and potassium channels change when estrogen becomes low.

Specifically **all that extra potassium in your diet might not do SHIT for your blood pressure if you have LOW estrogen**. Yet your calcium channels go crazy having low estrogen...! I would presume then since calcium channels are CONTRACTILE...that this is yet another mechanism behind the HYPER-ADRENERGIC state of low estrogen...AS DESCRIBED in my ARTICLE AND SOURCES!!!




Oestrogen modulates vascular adrenergic reactivity of the spontaneously hypertensive rat
Abstract BACKGROUND:
Male spontaneously hypertensive rats (SHRs) show an increased vascular neurogenic response compared with normotensive Wistar-Kyoto (WKY) control rats.
OBJECTIVE:
To study the vascular adrenergic response in hypertensive and normotensive female rats, with a focus on the influence of oestrogen.
METHODS:
Female SHRs and WKY rats were allocated randomly to a control group or to groups to undergo ovariectomy or ovariectomy combined with oestrogen supplementation (17beta-oestradiol 150 microg/kg per day) for either 1 day (group 1E2) or 10 days (group 10E2). Mean arterial pressure (MAP) was recorded and small mesenteric arteries were mounted in a Multi Myograph 610M. Vascular reactivities to transmural nerve stimulation (TNS), exogenous noradrenaline and acetylcholine were analysed.
RESULTS:
MAP was significantly greater in SHRs than in WKY rats in all groups studied. Sensitivity to cumulative TNS (0.12-32 Hz) did not differ between vessels from control SHRs and WKY rats, expressed as the frequency giving 50% of maximal neurogenic response (Ef(50): 4.1 +/- 1.1 and 4.0 +/- 1.6 Hz, respectively). However, there was a greater reactivity to TNS in ovariectomized SHRs than in ovariectomized WKY rats (Ef(50) 1.8 +/- 0.7 and 6.8 +/- 2.2 Hz, respectively; P < 0.05). Oestradiol treatment significantly decreased the sensitivity to TNS in ovariectomized SHRs (P < 0.05), and after 10 days the frequency-response curves were almost identical (Ef(50) 6.3 +/- 1.9 Hz for group 10E2 SHRs and 5.6 +/- 0.8 Hz for group 10E2 WKY rats). The increased adrenergic reactivity in ovariectomized SHRs was inhibited by prazosin, an alpha(1)-adrenergic antagonist, and could not be explained by differences in endothelial function or sensitivity to applied noradrenaline.
CONCLUSION:
Increased adrenergic reactivity is not present in small arteries from female SHRs. The findings of this study suggest that oestrogenacts on prejunctional mechanisms, reducing full expression of hypertension and peripheral vascular pathology.

Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta.
The ability of estradiol to affect phenylephrine-induced contraction and the subsequent increase in resting tone, associated with capacitative Ca(2+) entry across the plasma membrane, was evaluated in rat aortic rings incubated in Ca(2+)-free solution. The incubation with estradiol (1-100 nM, 5 min) inhibited both the phenylephrine-induced contraction and the IRT. Neither cycloheximide (1 microM; inhibitor of protein synthesis) nor tamoxifen (1 microM; blocker of estrogenic receptors) modified the effects of estradiol. Estradiol (100 microM) also blocked the contractile response to serotonin (10 microM) but not to caffeine (10 mM). In addition, estradiol (100 microM) inhibited the contractile responses to cyclopiazonic acid (1 microM; selective Ca(2+)-ATPase inhibitor) associated with capacitative Ca(2+) influx through non-L-type Ca(2+) channels. Finally, estradiol inhibited the Ca(2+)-induced increases in intracellular free Ca(2+) (after pretreatment with phenylephrine) in cultured rat aorta smooth muscle cells incubated in Ca(2+)-free solution. In conclusion, estradiol interfered in a concentration-dependent manner with Ca(2+)-dependent contractile effects mediated by the stimuli of alpha(1)-adrenergic and serotonergic receptors and inhibited the capacitative Ca(2+) influx through both L-type and non-L-type Ca(2+) channels. Such effects are in essence nongenomic and not mediated by the intracellular estrogenic receptor.
The effects of 17?-oestradiol on increased ?(1)-adrenergic vascular reactivity induced by prolonged ovarian hormone deprivation: the role of voltage-dependent L-type Ca channels.

Valencia-Hernández I1, Reyes-Ramírez JA, Urquiza-Marín H, Nateras-Marín B, Villegas-Bedolla JC, Godínez-Hernández D.



The present study investigated the hypothesis that the duration of ovarian hormone deprivation before reintroduction of oestrogen affects the role ofoestrogen as a mediator of the contractile function of ?(1)-adrenergic receptors. Rats underwent ovariectomy (OVX) or were sham-operated, and the OVX rats were treated with vehicle (corn oil) or 17?-oestradiol (E(2)) for 5 days either 10, 28 or 60 days after OVX. The OVX increased phenylephrine- and Ca(2+)-induced contractions. Interestingly, the phenylephrine-induced contractions were increased at each of the three time points, whereas the Ca(2+)-induced contractions were only increased in the 60-day group. E(2) had biphasic effects on phenylephrine- and Ca(2+)-induced contractility. Indeed, E(2) increased contractions in the 10-day group and diminished contractions in the other groups (the increased contractions were avoided by verapamil). These results indicate that E(2) controls ?(1)-adrenergic receptor-mediated contractility through effects on L-type Ca(2+) channels in a way that depends on the timing in which the treatment with E(2) is initiated.
Copyright © 2012 S. Karger AG, Basel.

 

[corageon]

You get really fatigued, sleep alot, dry skin, brain fog, difficulty concentrating on complex tasks, seem to recover slower, lifts go down, get kinda bitchy, etc. Pretty horrible. Happened to me a few weeks back. I'm assuming that test bottoms out at <5.1 since that's what mine said as well.

Low Estrogen is a big Cipher...some people (like me) love having low estrogen.
For others, I guess it depends on other factors as well..maybe adrenal gland function, and what you do during the prime hours.

The body/brain are very interesting....interesting how "homeostasis" works...
It seems the wiring looks similar on both ends but with minor differences.
It's all just a "keep-up" mechanism I guess...

For example - Estrogen induces/activates Dopamine Beta-Hydroxylasehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3077094/ ((1)), leading to more dopamine converting into norepinephrine (not necessarily a good thing), yet estrogen also blocks excessive norepinephrine binding to alpha-1-receptors (vasoconstrictive, fight or flight)(2).
Estrogen also increases alpha-2-receptor activity (lowering norepinephrine).

With this regard - high estrogen = high norepinephrine and yet lower alpha-1-activity except higher alpha-2 activity = less norepineprhine.
Then I would say this - Beta-Adrenergic activation/FAVOR is highly LIKELY but yet possibly UNLIKELY with high Estrogen.

Now with low estrogen...depending on other factors influencing DBH (Dopamine Beta Hydroxylase)...like Vitamin D, Copper and Zinc levels for example. Let's just assume those are "all good"...you still have a net decrease in DBH levels due to Estrogen deficiency. Now you have less norepinephrine - but OH LOOK!!!
Less Estrogen PLUS High DHT will also lead to DOUBLY MORE ALPHA-1-ADRENERGIC ACTIVITY!!!

High DHT Low Estrogen PhenoType​

Also since Estrogen INCREASES alpha-2-receptor expression...
Now deficient levels and high DHT - assuming you have High DHT = low alpha-2, but yet high Alpha-1 receptor expression. Since estrogen, again, normally does the opposite of what DHT does in that regard (to adrenergic influence).

So by having low estrogen the problem is nitric oxide deficiency, too much alpha-1-stimulation...and too little norepinephrine in general???

The point is more this ---- yes you have low levels of NE/NA whilst having low estrogen...but it's still going to be produced (as a normal rhythmical, natural response).AND YET - it might still maintain high levels or adrenaline/norepi whilst having low estrogen AS IF YOU HAD HIGH ESTROGEN!!! Due to that less Alpha-2 feedback!!!

Norepinephrine is also going to shockwave when you increase it during exercise or any other activity. Having too MUCH alpha-1 activity creates an ANXIETY provoking atmosphere, and less oxygen delivery due to too much vasoconstricton...and also attention problems from the SAME or SIMILAR mechanisms!!!!!!

THUS, HIGH AND LOW ESTROGEN create similar HYPER-ADRENERGIC states...except that high Estrogen also causes GLUTAMATE, and HISTAMINE increases / excess as well.
Whereas with low estrogen I would presume you would have high Epi/NorEpi ACTIVITY but low histamine, and possibly low glutamate!**

The other BIG DIFFERENCE between HIGH and LOW estrogen is ELECTROLYTE distribution and the the resultant changes in NeuroTransmitter activity ....!
For example calcium channels and potassium channels change when estrogen becomes low.

Specifically **all that extra potassium in your diet might not do SHIT for your blood pressure if you have LOW estrogen**. Yet your calcium channels go crazy having low estrogen...! I would presume then since calcium channels are CONTRACTILE...that this is yet another mechanism behind the HYPER-ADRENERGIC state of low estrogen...AS DESCRIBED in my ARTICLE AND SOURCES!!!

IN SUMMARY, I have found that because having low estrogen itself induces sympatholytic like activity, because of DBH levels becoming low - but yet that you commonly have high DHT when you have low e2 (unless you have taken Propecia/Finasteride or take MASSIVE amounts of Zinc - or have genetically low DHT activity), that DHT maintains HIGH alpha-1 activity leading to an adrenal crash and vasoconstriction / HBP!!!!

ONE FINAL THOUGHT - Low Estrogen is VERY likely to make you DEPENDANT on STIMULANTS...whereas HIGH ESTROGEN - you may seek ALCOHOL and have too much FUN with HALLUCINOGENS....

Then when you stimulate while having low estrogen (TO GET RID OF THE LETHARGY), you get an ENDORPHIN boost because of the super powered alpha-activity from HIGH DHT (that downstream activates Serotonin receptor TYPE 1-A) and then you feel GREAT for a while...til you CRASH HARDER...AND HARDER...AND HARDER!!!


Oestrogen modulates vascular adrenergic reactivity of the spontaneously hypertensive rat
Abstract BACKGROUND:
Male spontaneously hypertensive rats (SHRs) show an increased vascular neurogenic response compared with normotensive Wistar-Kyoto (WKY) control rats.
OBJECTIVE:
To study the vascular adrenergic response in hypertensive and normotensive female rats, with a focus on the influence of oestrogen.
METHODS:
Female SHRs and WKY rats were allocated randomly to a control group or to groups to undergo ovariectomy or ovariectomy combined with oestrogen supplementation (17beta-oestradiol 150 microg/kg per day) for either 1 day (group 1E2) or 10 days (group 10E2). Mean arterial pressure (MAP) was recorded and small mesenteric arteries were mounted in a Multi Myograph 610M. Vascular reactivities to transmural nerve stimulation (TNS), exogenous noradrenaline and acetylcholine were analysed.
RESULTS:
MAP was significantly greater in SHRs than in WKY rats in all groups studied. Sensitivity to cumulative TNS (0.12-32 Hz) did not differ between vessels from control SHRs and WKY rats, expressed as the frequency giving 50% of maximal neurogenic response (Ef(50): 4.1 +/- 1.1 and 4.0 +/- 1.6 Hz, respectively). However, there was a greater reactivity to TNS in ovariectomized SHRs than in ovariectomized WKY rats (Ef(50) 1.8 +/- 0.7 and 6.8 +/- 2.2 Hz, respectively; P < 0.05). Oestradiol treatment significantly decreased the sensitivity to TNS in ovariectomized SHRs (P < 0.05), and after 10 days the frequency-response curves were almost identical (Ef(50) 6.3 +/- 1.9 Hz for group 10E2 SHRs and 5.6 +/- 0.8 Hz for group 10E2 WKY rats). The increased adrenergic reactivity in ovariectomized SHRs was inhibited by prazosin, an alpha(1)-adrenergic antagonist, and could not be explained by differences in endothelial function or sensitivity to applied noradrenaline.
CONCLUSION:
Increased adrenergic reactivity is not present in small arteries from female SHRs. The findings of this study suggest that oestrogenacts on prejunctional mechanisms, reducing full expression of hypertension and peripheral vascular pathology.

Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta.
The ability of estradiol to affect phenylephrine-induced contraction and the subsequent increase in resting tone, associated with capacitative Ca(2+) entry across the plasma membrane, was evaluated in rat aortic rings incubated in Ca(2+)-free solution. The incubation with estradiol (1-100 nM, 5 min) inhibited both the phenylephrine-induced contraction and the IRT. Neither cycloheximide (1 microM; inhibitor of protein synthesis) nor tamoxifen (1 microM; blocker of estrogenic receptors) modified the effects of estradiol. Estradiol (100 microM) also blocked the contractile response to serotonin (10 microM) but not to caffeine (10 mM). In addition, estradiol (100 microM) inhibited the contractile responses to cyclopiazonic acid (1 microM; selective Ca(2+)-ATPase inhibitor) associated with capacitative Ca(2+) influx through non-L-type Ca(2+) channels. Finally, estradiol inhibited the Ca(2+)-induced increases in intracellular free Ca(2+) (after pretreatment with phenylephrine) in cultured rat aorta smooth muscle cells incubated in Ca(2+)-free solution. In conclusion, estradiol interfered in a concentration-dependent manner with Ca(2+)-dependent contractile effects mediated by the stimuli of alpha(1)-adrenergic and serotonergic receptors and inhibited the capacitative Ca(2+) influx through both L-type and non-L-type Ca(2+) channels. Such effects are in essence nongenomic and not mediated by the intracellular estrogenic receptor.
The effects of 17?-oestradiol on increased ?(1)-adrenergic vascular reactivity induced by prolonged ovarian hormone deprivation: the role of voltage-dependent L-type Ca channels.

Valencia-Hernández I1, Reyes-Ramírez JA, Urquiza-Marín H, Nateras-Marín B, Villegas-Bedolla JC, Godínez-Hernández D.



The present study investigated the hypothesis that the duration of ovarian hormone deprivation before reintroduction of oestrogen affects the role ofoestrogen as a mediator of the contractile function of ?(1)-adrenergic receptors. Rats underwent ovariectomy (OVX) or were sham-operated, and the OVX rats were treated with vehicle (corn oil) or 17?-oestradiol (E(2)) for 5 days either 10, 28 or 60 days after OVX. The OVX increased phenylephrine- and Ca(2+)-induced contractions. Interestingly, the phenylephrine-induced contractions were increased at each of the three time points, whereas the Ca(2+)-induced contractions were only increased in the 60-day group. E(2) had biphasic effects on phenylephrine- and Ca(2+)-induced contractility. Indeed, E(2) increased contractions in the 10-day group and diminished contractions in the other groups (the increased contractions were avoided by verapamil). These results indicate that E(2) controls ?(1)-adrenergic receptor-mediated contractility through effects on L-type Ca(2+) channels in a way that depends on the timing in which the treatment with E(2) is initiated.
Copyright © 2012 S. Karger AG, Basel.

 

[KoDa]

The obvious reason as you noted was the TT was much lower than expected for 600 mg per week. In fact, about 50% lower. If the TE had been true, there would be a wait again as you noted for about one month+.

I was curious why the last lab did not have a value as did the middle. Regardless, the level is probably about the same. Using the level ~2500 ng/dL, it will take about three weeks for the conditions to be right for HPTA function.

The PCT is fine. hCG 1,000 IU will be adequate. There is no need to do SERMs at the same time as hCG except for the final week. I prefer one week to load.

Last lab was purely for an estradiol check- I really had no reason to believe TT would differ significantly from the week 5 labs, and so the more expensive test that gives results over 1500 wasn't really necessary. Same gear, same 1ml injections week 1-12, so I think the assumption is fairly safe?

Everything looks great, and as I said I appreciate the advice. I do want to make sure I'm understanding correctly: the original plan was hCG 2000iu E3D for 14 days prior to PCT (SERMs from there on out).

What you're saying is:

Week 12: last injection
Week 13: nothing
Week 14: hCG 1,000 IU (E3D?)
Week 15: hCG 1,000 IU
Week 16-19: SERMs

When you say you prefer one week to load are you meaning a SERM load (week 15) or an hCG load (week 13)?

Also, any thoughts on exemestane alongside at any point? Just curious about the estradiol rebound since I'm dropping anastrazole. Or a good point in the next 7weeks to pull another set of bloodwork?

Any thoughts on this? I'm just curious about "SERMs at the same time as hCG the final week" is that meaning an overlap of a week or just that the last hCG pin coincides with the first day of SERMs?

Then "one week to load", I saw in the comprehensive guide thread it was commented on that a lower dose (500iu 2x/wk) prior to the 2 week full dose (1000iu E3D) may be a better approach- is that what is being referenced by "load" here?

 

[KoDa]

The obvious reason as you noted was the TT was much lower than expected for 600 mg per week. In fact, about 50% lower. If the TE had been true, there would be a wait again as you noted for about one month+.

I was curious why the last lab did not have a value as did the middle. Regardless, the level is probably about the same. Using the level ~2500 ng/dL, it will take about three weeks for the conditions to be right for HPTA function.

The PCT is fine. hCG 1,000 IU will be adequate. There is no need to do SERMs at the same time as hCG except for the final week. I prefer one week to load.

Update, coming to the end of the three weeks here. Took one week off, 2nd week started 1000iu hCG e3d- took 4th dosing Wed night, and bloodwork Thurs morning so I'd get results today:



Have one more (5th) 1000iu dosing, and then should I start PCT this upcoming week or do I need to wait longer?

 

[Michael Scally MD]

There should be 10 injections for a total of 30 days. I would start SERMs during the 7-10 hCG injections.

 

[KoDa]

Roger that. I've got another 5000iu on hand. Will continue e3d and start SERMS in about a week. Much appreciated.

 

[KoDa]

18 days out from last PCT, just checkin' in with some bloods. Everything looks to be on track here?

I'll probably get them done again in another 2-3 weeks?

 

[Michael Scally MD]

18 days out from last PCT, just checkin' in with some bloods. Everything looks to be on track here?

I'll probably get them done again in another 2-3 weeks?

 

[KoDa]

~16 weeks after PCT, prepping for next cycle. Thoughts? Both test/est seem a little on the low side.

 

[eryximachus]

you're in range. Most are stuck at that level after cycling. I was that way before cycling. It's the price we pay.