PCT Didn't Work. Help.

Pharma
21

[quote]Jscott8220 wrote:

[quote]chasek77 wrote:
Jscott8220 - Testosterone 38 L should be 241-827 ng/dl
Estradiol 26 should be < 0r = 39 pg/ml

Do I need a more complete panel for LH, etc?[/quote]

I was refering to checking your progesterone levels.[/quote]

Progesterone itself wouldn’t be the problem. Progesterone isn’t that bad as it supports your cortisol production line, which your body uses preferentially over sending it downstream.

It’s downstream hormone (prolactin) would be the issue. This is possible, but it is much more likely his HPTA is still suppressed due to the PCT being ran too early.

If you can test for everything, it would be a good idea just to put things in perspective, but probably isn’t a deal breaker IMO.

Yes it will be worth while to get LH. Also add in FSH and Prolactin if you wish. I would suggest some others, but they will be so low it will be useless to run them (mainly your T metabolites).

22

I was told to go with this firm to get a better handle of where I am:

BASELINE LABS:

COMPREHENSIVE METABOLIC PROFILE (INCLUDES 'LYTES, BUN. BS, KIDNEY, LFT, LIPID PROFILE)

CBC W/ DIFF

FSH

LH

PROLACTIN

TSH

IRON/FERRITIN

TOTAL TESTOSTERONE (TT)

ESTRADIOL

SEX HORMONE BINDING GLOBULIN (SHBG)

PSA (Optional)

VITAMIN D

23

This may sound stupid, but will masterbation help or hurt my chances of my HPTA getting in gear?

24

From what I understand, Tren should only wreak havoc with progesterone/prolactin levels while it is still active in the blood stream since it affects the receptors, not the source. Once it’s cleared your system the issues should resolve (though the gyno might be permanent).

Since it doesn’t sounds like he had any prolactin/progesterone related gyno, one would hope he’s in the clear. Elevated prolactin could explain his problem busting a nut, but I think the low T (which we KNOW is an issue) is the more likely culprit. Admittedly I don’t know a whole lot about the Tren/Deca and prolactin/progesterone connection, and I don’t think there’s really a consensus among the steroid community either.

Here’s more info:

Kurt-

I would run the SERM PCT again and see if that doesn’t fix the issue. You didn’t “maybe” start it too early, you definitely started it too early. Cyp/Enth take at least 2 weeks to clear your system. You finished your last PCT right about when you should have been starting. Most of what you did was worthless.

I think starting back up with test+HCG is a bad idea. I know you said you had high sex drive before, but at 44 you are really pushing it in terms of recovery. At this point I don’t think shutting yourself down even longer is wise, especially if you are strongly opposed to TRT.

Personally if it was me I’d just get on TRT. I’m going to anyway when I get to 35-40, the inconvenience is minor compared to the benefits.

26

overstand - Trenbolone Acetate is in your system for 5 months. Testosterone is about 3 months. The biggest issue with TRT is you are going to be on shots for life! If you start at 40 and you live to 80, then that is 480 months x how much a month for a doctor to prick you once a week? It’s always a LAST ditch alternative when everything else has failed. Now, if you are dropping as you get older, then it may make sense, but it’s best to hold off on these things.

bushidobadboy - I will check to see how to get the panel done for you guys to evaluate before jumping into any PCT. I found a source to get me clomid and nolvadex via UGL. I should have it soon.

Last night, I got hard for a good 30 minutes, balls are still small, but I came finally, so I wonder if my work out and getting off the anti-biotics helped. I still need help, but more encouraged then yesterday.

27

Your timelines are not really accurate. Metabolites of the drugs will be present in your body for that amount of time probably, but its active life is directly related to the esters in question. Acetate has about a 2-3 day half life, I believe. About 6 half lives are considered to be inactive.

So after 2 weeks, you are completely clear of Tren Ace. Enanthate with is 7 day half life is done right at the 1.5 month mark.

Note that this does not correspond to levels at which you are no longer suppressed (i.e. this active life should not be the determination of when you start PCT).

28

good point! I was just saying how long I guess it would be in your system for a test to detect it, but it may not be effecting your body, which is totally different.

29

[quote]chasek77 wrote:
good point! I was just saying how long I guess it would be in your system for a test to detect it, but it may not be effecting your body, which is totally different. [/quote]

Dont be scared of HCG. If you do something retarded like shoot 10,000 iU then yes theres a risk of desensitisation. At the correct dosage you will have no problems whatsover

I have personally ran 300iU of HCG per day, after recovering from a steroid cycle, for one month. I had my test levels checked once during the hcg and twice after. They were perfectly normal. Theres a paper somewhere that I saw this dosage protocol in that confirmed that no desensitisation of leydig cells takes place with this dosage and time frame.

I do wonder why people are afraid of castrating themselves with HCG when you took exactly the same risk by taking steroids.

To get you back into shape I would try this:

Day 1: 100mg nolva/500iu HCG
Day 2-30: 20mg nolva/250 iu HCG
Day 3-60: 10mg nolva

You can use clomid instead of nolva if need be.

If that doesnt get you back in shape ill be very suprised.

30

I think that is some very good advice on HCG. Doesn’t HCG mimic the LH, so taking nolvadex or clomid at the same time would be useless? I got my lab work done yesterday and will have results within 72 hours.

31

[quote]chasek77 wrote:
Doesn’t HCG mimic the LH, so taking nolvadex or clomid at the same time would be useless? [/quote]

Correct. I do not think they should be taken at the same time. IMO, it would be best to use HCG for a short time then discontinue and move to a SERM. This will act in two parts, the first turning your nuts back on, the second turning your pituitary back on with the nuts still working.

33

Lab Results are in from blood work done on 1/19/2012

Tests Results Flag Units Reference Interval
CBC With Differential/Platelet
WBC 8.3 x10E3/uL 4.0-10.5
RBC 5.33 x10E6/uL 4.10-5.60
Hemoglobin 15.9 g/dL 12.5-17.0
Hematocrit 45.9 % 36.0-50.0
MCV 86 fL 80-98
MCH 29.8 pg 27.0-34.0
MCHC 34.6 g/dL 32.0-36.0
RDW 14.6 % 11.7-15.0
Platelets 281 x10E3/uL 140-415
Neutrophils 74 % 40-74
Lymphs 21 % 14-46
Monocytes 4 % 4-13
EOS 0 % 0-7
Basos 1 % 0-3
Neutrophils (Absolute) 6.1 x10E3/uL 1.8-7.8
Lymphs (Absolute) 1.8 x10E3/uL 0.7-4.5
Monocytes (Absolute) 0.3 x10E3/uL 0.1-1.0
Eos (Absolute) 0.0 x10E3/uL 0.0-0.4
Baso (Absolute) 0.1 x10E3/uL 0.0-0.2
Immature Granulocytes 0 % 0-2
Immature Grans (Abs) 0.0 x10E3/uL 0.0-0.1

Comp. Metabolic Panel (14)
Glucose, Serum 88 mg/dL 65-99
BUN 14 mg/dL 6-24
Creatinine, Serum 0.98 mg/dL 0.76-1.27
eGFR If NonAfricn Am 93 mL/min/1.73 >59
BUN/Creatinine Ratio 14 9-20
Sodium, Serum 141 mmol/L 134-144
Potassium, Serum 4.0 mmol/L 3.5-5.2
Chloride, Serum 103 mmol/L 97-108
Carbon Dioxide, Total 23 mmol/L 20-32
Calcium, Serum 9.3 mg/dL 8.7-10.2
Protein, Total, Serum 6.8 g/dL 6.0-8.5
Albummin, Serum 4.2 g/dL 3.5-5.5
Globulin, Total 2.6 g/dL 1.5-4.5
A/G Ratio 1.6 1.1-2.5
Bilirubin, Total 0.5 mg/dL 0.0-1.2
Alkaline Phosphate, S 77 IU/L 25-150
AST (SGOT) 16 IU/L 0-40
ALT (SGPT) 19 IU/L 0-55
Testosterone, Serum 588 ng/dL 348-1197
LH 4.5 mIU/mL 1.7-8.6
FSH 5.5 mIU/ml 1.5-12.4
Prolactin 4.6 ng/mL 4.0-15.2
Estradiol 55.5 HIGH pg/mL 7.6-42.6
Roche ECLIA methodology
Sex Horm Binding Glob, Serum 30.4 nmol/L 16.5-55.9

Questions:

  1. It looks like my testosterone has finally bounced back, but so has my estogen. Why do I do now? I am still waiting on my shipment of HCG, Clomid, and Nolvadex. It looks at the very least I need to do some Nolvadex to get the estrogen down?

  2. If my testosterone is so high, then why are my balls still so small? Estrogen? Prolactin?

  3. Would doing a round of Clomid and Nolvadex hurt? or should I just stay with a do nothing approach, which seems to be working other then the high estrogen issue.

34

Everything looks good except the estrogen. You do not need a SERM for that, you need an AI. It is possible your liver does not process estrogen correctly and allows it to pool in your body. You may want to consider some sort of liver support or resveratrol to help it. But an AI would certainly be effective (and would also boost your Total T).

Why do you think you need a round of clomid/nolva? Your LH/FSH are fine, so what would you hope to accomplish?

35

[quote]bushidobadboy wrote:

[quote]MassiveGuns wrote:
I do wonder why people are afraid of castrating themselves with HCG when you took exactly the same risk by taking steroids.

[/quote]
Not at all. Excess HCG/LH might desensitize leydig cells. AAS are going to have ne effect on leydig cells in that respect so the two are in no way comparable really.

BBB[/quote]

My point was that the end result of abusing either is the same; hypogonadism.

Permanently screwing up your HPTA or your leydigs cells has the same net result.

36

[quote]VTBalla34 wrote:

[quote]chasek77 wrote:
Doesn’t HCG mimic the LH, so taking nolvadex or clomid at the same time would be useless? [/quote]

Correct. I do not think they should be taken at the same time. IMO, it would be best to use HCG for a short time then discontinue and move to a SERM. This will act in two parts, the first turning your nuts back on, the second turning your pituitary back on with the nuts still working.
[/quote]

I believe there are two reasons for using nova and clomid whilst using hCG.
Armoatase activity in the testes mean that high levels of estrogen are produced when you use hCG (and the treatment is successful), the nova and clomid will help protect against issues such as gyno. An AI cannot do this - because it will not enter the testes in a high enough concentration to have any impact on estrogen production. It will also negate the impact (at least somewhat) of estrogen on the hypothalamus and pituitary glands - reducing the “degree” of negative feedback.
A second reason would be that nova has been shown (in the lab) to prevent desensitisation of the leydig cells of rats with high doses of hCG.

37

I decided to do another round ( 3 weeks) of clomid and nolvadex to get my balls to fill up, because they are really small.

I plan on doing blood work on my testosterone, estrogen, LH at the end of 3 weeks of my 2nd attempt of PCT.

I will then wait about 3-4 weeks post PCT and run the same bloodwork again to see what natural levels I have leveled off to.

My test was 588 on a natural bounce back atfer the first attempt at PCT, so lets see how much the clomid and nolvadex helps the test and LH, while hopefully keeping the high estrogen at bay.

The HCG doesn’t seem like an option at this time due to my body natually producing testosterone. Sure, it would fill up my balls faster then clomid and nolvadex, but it’s not worth shutting down my natural production of testosterone again. I think the atrophy of the balls over time should come back naturally and with the clomid come back faster then naturally, but not as fast as HCG. Comments?

38

[quote]Cymru wrote:

I believe there are two reasons for using nova and clomid whilst using hCG.

Armoatase activity in the testes mean that high levels of estrogen are produced when you use hCG (and the treatment is successful), the nova and clomid will help protect against issues such as gyno. An AI cannot do this - because it will not enter the testes in a high enough concentration to have any impact on estrogen production. [/quote]

This is irrelevant unless you are taking stupidly high doses, which nobody here advocates. You aren’t going to get gyno from a 250 iu dose 2-3x/week.

Are you saying an AI will negate the impact on the hypothalmus/pituitary? How? SERMs themselves aren’t actually estrogen either, but bind to those receptors to induce feedback. Lowering ACTUAL E2 with an AI only gives the SERM less competition. I’m not sure what you are saying here.

Again, irrelevant since we are not using high doses of HCG. Also, please link to this study. I am not aware of studies involving SERMs and HCG (two products that are not FDA approved for use in men) together in men. This would be a good read.

39

To the above;

Point 1.

The high estrogen from hCG occurs because of high T in the testes, this means more collisions are occurring in the testes between T and aromatase, hence far more estrogen produced. This is why estrogen in blood is higher from hCG than it it is when compared to estrogen in blood from the same blood concentration of exogenous T.

Point 2 - my grammar or your misreading - I am say YOU SHOULD USE A SERM AS IT HELPS INHIBIT the negative feedback of E on the brain. I am not suggesting the use of an AI.

Point 3
Clin Endocrinol Metab 1980 Nov;51(5):1026-9

Tamoxifen suppresses gonadotropin-induced 17 alpha-hydroxyprogesterone accumulation in normal men.

Smals AG, Pieters GF, Drayer JI, Boers GH, Benraad TJ, Kloppenborg PW.

Intramuscular administration of 1500 IU hCG daily for 3 days induced a transient accumulation of 17 alpha-hydroxyprogesterone (17 OHP) relative to testosterone (T) in normal men, reaching its maximum 24 h after the first injection (17 OHP to T ratio, 1.7 +/- 0.3 times baseline; P < 0.01). Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone). These data indirectly suggest that, in man, the hCG-induced steroidogenic lesion might be mediated through its estrogen-stimulating effect.

Andrologia 1991 Mar-Apr;23(2):109-14

Effect of an antiestrogen on the testicular response to acute and chronic administration of hCG in normal and hypogonadotropic hypogonadic men: tamoxifen and testicular response to hCG.

Levalle OA, Suescun MO, Fiszlejder L, Aszpis S, Charreau E, Guitelman A, Calandra R.

Division Endocrinologia, Hospital Carlos Durand, Instituto de Biologia y Medicina Experimental, Buenos Aires, Argentina.

The effect of the antiestrogen tamoxifen (Tx) on the acute and chronic hCG administration was evaluated in patients with hypogonadotropic hypogonadism (HH) and in normal men. An hCG test (5000 IU hCG) was performed before, after two months of hCG administration (2000 IU hCG three times weekly) and after two months of hCG + Tx (2000 IU hCG three times weekly plus 20 mg/day of tamoxifen). Blood samples were obtained before and following 24 and 72 h of every test to determine T, E, 17OHP and SHBG. T increased only in HH with both treatments (X +/- SEM: Basal: 97.9 +/- 19.7; hCG: 237.7 +/- 43.2; hCG +/- Tx: 204.7 +/- 10.7 ng/100 ml). 17OHP rose with hCG alone, but not with hCG + Tx in both groups. E, SHBG and 17OHP/T ratio did not change after treatments. hCG tests: E increased 24 h following hCG administration in every test. The ratio 17OHP/T rose at 24 h in the first and second test but in the third test it did not change. These results support the role of E in the acute hCG-induced Leydig cell desensitization. However, the association of Tx does not improve T serum levels, suggesting that E might not be the unique factor involved in the mechanisms for testicular desensitization.

40

OP, just to be sure, you were waiting for your order of SERMs to be shipped and got bloodwork done in the meantime and the results say everything is fine (except estrogen levels) without running anything else?