Morning testosterone spike....

hhajdo....These studies are done on people w/ out gear. Now does the spike also occur on a low dosage of Anavar... As far as I know anavar also suppresses natural test production. So if your natural test is suppressed then the morning test spike doesn’t occur? Or they do but not as much?
 
jyzza said:
hhajdo....These studies are done on people w/ out gear. Now does the spike also occur on a low dosage of Anavar... As far as I know anavar also suppresses natural test production. So if your natural test is suppressed then the morning test spike doesn’t occur? Or they do but not as much?


When you're on cycle, LH amplitude & frequency decrease, so your 24 hour test profile looks more like a straight line - check pic 1...



J Clin Pharmacol 2000 Jul;40(7):731-8 Related Articles, Links


Modeling of circadian testosterone in healthy men and hypogonadal men.

Gupta SK, Lindemulder EA, Sathyan G.

ALZA Corporation, Mountain View, CA 94043, USA.

The testosterone circadian rhythm has been reported extensively in the literature and has been described by a cosine function. Typically, these data are measured at frequent and regular (e.g., hourly) intervals. However, modeling circadian rhythm with data collected sparsely at irregular intervals and/or data that are not collected at the same time in all individuals has not been reported. The population nonlinear mixed-effects approach can handle such data and also allows covariates to be incorporated into the model. Frequent hourly testosterone concentration data available in the literature for young and elderly healthy volunteers were analyzed first. In the elderly, blunted or completely absent circadian rhythm has been reported, but a full circadian model was significantly better than a model containing one or no circadian component. Therefore, data from both the elderly and young were modeled together, and age was included as a categorical variable (young or elderly). Consistent with literature, the rhythm-adjusted mean testosterone concentrations was lower, and the deviation from the mean, especially to the maximum daily value, was less than half in the elderly (7%) compared to young subjects (16%). The testosterone concentration data measured infrequently and at varying intervals in young normal men and hypogonadal men were evaluated next. Although not measured at regular frequency in each individual, the data were obtained at different clock times for different subjects. Since for population mixed-effects analysis, data from all subjects are pooled, there was enough information to profile the 24-hour circadian cycle. In healthy young subjects, the mean Cnadir, Cpeak, Tnadir, and Tpeak values estimated from the model were 420 ng/dL, 577 ng/dL, 21:42 hours, and 0600 hours, respectively, and were similar to the parameters obtained for the frequently sampled young subjects. In hypogonadal men (testosterone concentrations < 300 ng/dL), the mean testosterone concentrations were much lower than the healthy young or elderly men, and a straight-line model was the best descriptor (i.e., no circadian rhythm was detected). It was also shown that with the application of a transdermal testosterone system, the mean testosterone concentrations in the treated men were within the 95% confidence interval for healthy young men. The results presented here suggest that the advantages of the analysis approach--namely, handling of covariates and handling of sparse, infrequently collected data--can be used in characterizing testosterone circadian rhythm or the lack of it.
 
Sorry, i gotta throw a question into this technical and scientific thread. I thought bridging with dbol at 10mg in the AM would allow the body to recover since your body recognizes it as the normal testosterone spike when you awake. If morning testosterone spike isnt significant, and your bridging with dbol, wouldnt your body recognize it as added testosterone, thus not allowing your natural testosterone levels recover?
 
TooPowerful4u said:
I thought bridging with dbol at 10mg in the AM would allow the body to recover since your body recognizes it as the normal testosterone spike when you awake.

That theory doesn't make much sense.
You have a LH/Test spike every two hours, time of administration really isn't important.

Even if you could avoid suppression of one of LH pulses, you would affect several other pulses.... so the level of suppression would be similar regardless of when you take the AS..

Testosterone secretion can't be compared to secretion of GH where you have 70-80 % of GH secreted during sleep...
 
So is that sayin the dbol am bridge is inaccurate? Would it still work and allow your natural levels to recover?
 
hhajdo said:
If you want to fully recover don't use it.

LOL....I found out that it doesn't make a difference if you use anavar, d-bol or primo for a bridge. Your natural test will never fully recover. You natural test will be suppressed but not as much as on 400mg of Test.

My idea of bridge is that a bridge is still a part of your cycle just lower dosages and it does help you by lower dosages and maintaining your mass. Your test will get better but it will not fully recover.

This would be my bridge..

1-4 20mg Nolvadex
1-3 500ius EOD
1-6 200-300mg Primo
1-6 15mg Anavar

hhajdo..what do you think about a bridge like that. It could be used to shock your body after 2-3 months of AS use. After week 6 back on full dosages.
 
If you follow jsut the testosterone graph, look at 8:30 and follow it till midnight. Youll see its slowly goes down. If you take dbol around that highest morning peak (kinda just sneak it in there) I think the half-life would allow the curve to closely mimic this curve.

I dont think 10mg is going to be enough for significant suppresion of LH via neg-feed back either.


Case scenerio, Ive done it, got blood work too. Results, I recovered..not 100% though when comparing with my normal baseline. However, statistically speaking I did recover, as I was well within the ave for my age group. The other factor to add into this, I kept all of my gains and felt great.

JMO only, take it or leave it. I dont own any stock in Dbol yet haha! (just finished a 48hr debate on another board about it lol)

Unless anyone knows how much E2 is produced from this low dosage, and how much it takes for significant suppression, and how much is present by nightfall, I have not been yet convinced its not a possible theory. Well..that and the fact it worked ok for me.
 
I wouldn't recommend it bro..
Even very low doses of 17AA's significantly increase hepatic lipase which causes breakdown of HDL + you can't maintain physiological level of estradiol on a cycle like that which would also neagatively affect plasma lipids...

If you have to take something to maintain your gains, insulin/GH would be a much better option...
 
Billy_Bathgate said:
If you follow jsut the testosterone graph, look at 8:30 and follow it till midnight. Youll see its slowly goes down. If you take dbol around that highest morning peak (kinda just sneak it in there) I think the half-life would allow the curve to closely mimic this curve.

I dont think 10mg is going to be enough for significant suppresion of LH via neg-feed back either.


Case scenerio, Ive done it, got blood work too. Results, I recovered..not 100% though when comparing with my normal baseline. However, statistically speaking I did recover, as I was well within the ave for my age group. The other factor to add into this, I kept all of my gains and felt great.

JMO only, take it or leave it. I dont own any stock in Dbol yet haha! (just finished a 48hr debate on another board about it lol)

Unless anyone knows how much E2 is produced from this low dosage, and how much it takes for significant suppression, and how much is present by nightfall, I have not been yet convinced its not a possible theory. Well..that and the fact it worked ok for me.



It really doesn't take much for significant suppression.

15 mg of Dbol ED for 8 weeks decreased test by 69 % & LH by 50 % in this study:




Acta Endocrinol (Copenh) 1976 Dec;83(4):856-64 Related Articles, Links


Effect of an anabolic steroid (metandienon) on plasma LH-FSH, and testosterone and on the response to intravenous administration of LRH.

Holma P, Adlercreutz H.

Plasma levels of testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) as well as the response of LH and FSH to the intravenous administration of 100 mug of luteinizing hormone releasing hormone (LRH) were measured in 16 well-trained athletes (mean age 30 years) before and after 2 months of daily oral intake of 15 mg of metandienon, and anabolic steroid (Anabolin, 17 alpha-methyl-17beta-hydroxy-1,4-androstadien-3-one, Medica, Finland). All athletes continued to train regularly, just as they had done for several years. During administration of metandienon the mean plasma testosterone level fell 69%, from 29.4 +/- 11.6 nmol/1 to 9.1 +/- 7.5 nmol/1. The mean plasma levels of LH and FSH also fell significantly (P less than 0.001 and P less than 0.01, respectively), both about 50%. Because LH and FSH levels were low after administration of the steroid the maximum stimulation values after LRH administration were also lower than pre-treatment values although the mean increments did not differ significantly before and after administration of the anabolic steroid. However, after treatment, the FSH response curve had a biphasic pattern in most subjects, with peaks at 10 to 20 and 50 to 60 min after the iv injection of LRH. Administration of LRH after the treatment period had no effect on FSH secretion in two subjects and no effect on LH secretion in one. Our results show that administration of an anabolic steroid causes a pronounced lowering of plasma levels of testosterone, LH and FSH but causes no gross alteration in the response of LH secretion to stimulation by LRH. The reason for the biphasic response pattern of FSH to LRH administration in most subjects is not known.


I don't doubt that Human Chorionic Gonadotropin (HCG) + SERM + dbol would get your test up and prevent loss of gains...



(1) Am J Sports Med 1987 Jul-Aug;15(4):357-61

Androgenic-anabolic steroid effects on serum thyroid, pituitary and steroid hormones in athletes.

In this study posted by nandi12 normal men were given a 12 week cycle of test(150mg/wk)+deca(150mg/wk) + dbol(15mg/day) + winny(5 mg/day)

Their baseline LH was 6.8 U/L.
One month after quitting it had risen to 5.2 U/L.
12 weeks after the cycle their LH was 8.0 U/L but their test was still depressed (14nmol/l vs. a baseline of 21.8 nmol/L)


If both your androgen & estrogen levels are low, HPTA stimulation with Clomid can increase your LH to supraphysiological level ..
If you add an androgen, your LH can't be increased nearly as much even if you use a very low dose...

Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse.
Fertil Steril. 2003 Jan;79(1):203-5.


...Just before clomiphene citrate administration, laboratory examination revealed a total T of 71 ng/dL (reference range, 260–1000 ng/dL), free T of 29 pg/dL (reference range, 34–194 pg/dL), bioavailable T of 61 ng/dL (reference range, 84–402 ng/dL), LH of 3.7 miu/mL (reference range, 1.5–9.3 miu/mL), FSH of 2.4 miu/mL (reverence range 1.4–18.1 miu/mL), prolactin of 5 ng/mL (reference range, 2–18 ng/mL), and TSH of 1.36 miu/mL (reference range, 0.40–5.50 miu/mL). Free and total Ts were measured by radioimmunoassay methods. Magnetic resonance imaging did not show any abnormality in the pituitary area. Cortisol and thyroxine were also in the normal ranges. Sperm samples were not collected as the patient declined. Total T levels rather than free or bioavailable T were used for follow-up...

..He was challenged with 100 mg of clomiphene citrate for 5 days. Two weeks later, his total T was 828 ng/dL. The patient reported better moods and return of libido and energy, but still continued on his antidepressant. The patient was followed up, and 2 months after clomiphene citrate challenge, he had a relapse of symptoms including tiredness and loss of libido. At this time, his total T dropped again to 301 ng/dL. A decision was made to continue treatment with clomiphene citrate for 2 months. At the end of 2 months, his total T was 705 ng/dL, and LH was 26.3 miu/L (Fig. 1). The magnetic resonance imaging of the pituitary was repeated and remained normal. Symptoms resolved and the patient continues to be followed up...
 
Ya I seen the 15mg one before, but I dont see how it was administered. Could have been AM though.

I just would like to know how much E2 is going to be produced, and just how much it really takes for suppresion? With the above, I see they didnt experience a total shutdown, which I did still get some when I did it, but not 69% more like 10-15%.

Any chance you have any material on either one of those two questions? You have alot of good material. I havent gotten an exact answer (I agree with you it wont take much though) and would just like to see some numbers to think about for a better analysis.
 
Billy_Bathgate said:
Unless anyone knows how much E2 is produced from this low dosage, and how much it takes for significant suppression, and how much is present by nightfall, I have not been yet convinced its not a possible theory. Well..that and the fact it worked ok for me.


Just ask Big Cat or Bobo. They know all about E2. :p
 
Billy_Bathgate said:
Ya I seen the 15mg one before, but I dont see how it was administered. Could have been AM though.

I just would like to know how much E2 is going to be produced, and just how much it really takes for suppresion? With the above, I see they didnt experience a total shutdown, which I did still get some when I did it, but not 69% more like 10-15%.

Any chance you have any material on either one of those two questions? You have alot of good material. I havent gotten an exact answer (I agree with you it wont take much though) and would just like to see some numbers to think about for a better analysis.

Unfortunately, only the abstract is available online so I don't have any info about their estrogen levels..

I did see one study in which androgel+anastrozole was used, and one in which teslac was administered in combination with 15 mg of test i.v.

LH & LH response to LHRH remained unchanged in those studies but they only lasted for a few days & it can take several days for low dose androgen (like 15 mg OX for example) to affect HPTA.

I've also seen one on prepubertal boys in which test (enanthate) + letrozole was used but the dose of test used was very low (1mg/kg once a month)..


http://jcem.endojournals.org/cgi/content/full/86/10/4887
 
Juice Authority said:
Just ask Big Cat or Bobo. They know all about E2. :p

LMFAO! That was the most fucked up discussion Ive ever been in...

Anyways though, here is what Fonz came up though in responce to them.








The Dball AM Bridge: Proven mathematically and scientifically
Thanks to Blade for showing me this...it proved VERY useful.

Acta Endocrinol (Copenh) 1976 Dec;83(4):856-64 Related Articles, Links


Effect of an anabolic steroid (metandienon) on plasma LH-FSH, and testosterone and on the response to intravenous administration of LRH.

Holma P, Adlercreutz H.

Plasma levels of testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) as well as the response of LH and FSH to the intravenous administration of 100 mug of luteinizing hormone releasing hormone (LRH) were measured in 16 well-trained athletes (mean age 30 years) before and after 2 months of daily oral intake of 15 mg of metandienon, and anabolic steroid (Anabolin, 17 alpha-methyl-17beta-hydroxy-1,4-androstadien-3-one, Medica, Finland). All athletes continued to train regularly, just as they had done for several years. During administration of metandienon the mean plasma testosterone level fell 69%, from 29.4 +/- 11.6 nmol/1 to 9.1 +/- 7.5 nmol/1. The mean plasma levels of LH and FSH also fell significantly (P less than 0.001 and P less than 0.01, respectively), both about 50%. Because LH and FSH levels were low after administration of the steroid the maximum stimulation values after LRH administration were also lower than pre-treatment values although the mean increments did not differ significantly before and after administration of the anabolic steroid. However, after treatment, the FSH response curve had a biphasic pattern in most subjects, with peaks at 10 to 20 and 50 to 60 min after the iv injection of LRH. Administration of LRH after the treatment period had no effect on FSH secretion in two subjects and no effect on LH secretion in one. Our results show that administration of an anabolic steroid causes a pronounced lowering of plasma levels of testosterone, LH and FSH but causes no gross alteration in the response of LH secretion to stimulation by LRH. The reason for the biphasic response pattern of FSH to LRH administration in most subjects is not known.

Thanks for the article:

Ah...now lets delve into mathematics, shall we:

First: 15mg I said 10mg.

15mg lowered test levels by 69%.

LH and FSH by 50%

Now, lets apply some simple math.

15mg dball will be excreted in.......15mg /average 4hr T-life = Average of:

15mg ------ 7.5mg ------ 3.75mg ------ 1.875mg ------- 0.9875mg

So after overgoing 4 Half-life conversion(I'm not even counting the fact that excercise INCREASES dball excretion btw...by quite a margin)

It took the men roughly 16hrs to get to within reasonable Dball(Androgen concentrations), about roughly 1mg.
In case you're wondering, I'm mathematically comparing the suppression seen by 15mg and 10mg of dball in reference to blood levels and time.
(I'm not even going to state that the study doesn't even say they took it all in the AM....they probably didn't. But I'm feeling charitable today so I'll give you guys a break. I'll stipulate they took i all in the AM)

Now, for 10mg.

10mg ------- 5mg --------- 2.5mg --------1.25mg ---------0.625mg

Linearly speaking, it took 3.4 half-lives or roughly 13.6 hrs to get to 1mg.

Thats 85% of the 15mg Dball study.13.6hrs/16hrs = 0.85

So, Free Test should then become 58.7% decrease and LH and FSH 42.5%

This is using the 4hr half-life. The gold standard for dball.

Now lets add Arimidex and Clomid to the mix shall wee?

Arimidex will INCREASE the decrease in test seen by the AM dball administration via less testosterone being converted into estrogen via the aromatase enzyme.

By how much normally? 58% increase in test.(Look the abstracts up. They've been posted a zillion times...I'm not going to do it for you) And also a large decrease in estrogen mind you.

OK. So now, the 58.7% reduction in test seen for the 10mg Dball is FURTHER reduced to (58.7 * (1-0.58)) = 24. 65%

So, low and behold 10mg AM dball+arimidex BY THEMSELVES cause only a 24.65% drop in test levels. Compare this to the 58.7% seen in the Dball only group. This is why arimidex MUST be used, and why I have said it a zillion times.

Now lets add Clomid and Human Chorionic Gonadotropin (HCG) shall we? Good. The math/pharmacology class is proceeding nicely. Clomid will boost both FSH and LH, and Human Chorionic Gonadotropin (HCG) will cause yet ANOTHER surge in endo Test levels through its effects on the Leydig cells.
And low and behold, since we are on arimidex, the increase seen will be test only because the aromatase enzyme is being blocked by the arimidex from converting the test surge caused by the Human Chorionic Gonadotropin (HCG) into estrogen..

By how much?

I don’t know. But what I do know, is that the 24.65% reduction in testosterone will be reduced even further(By the Human Chorionic Gonadotropin (HCG) and the Clomid), and the LH values as well to well less than 45%.

Gee whiz…..am I starting to kill of all the SCIENTIFIC doubters…….. LOL

From my bloodwork(and from other peoples) NOT Clomid and Human Chorionic Gonadotropin (HCG) studies, I came up with an INCREASE in Test levels over pre-main cycle levels and an almost normal LH.(Roughly 80-90%) of normal.

The problem was THAT I could not extrapolate info from ANY Human Chorionic Gonadotropin (HCG) and Clomid studies b/c they were not on the AM Dball routine.

So, I had to test it on myself and get bloodwork done.

And it WORKED. Yes, it WORKED. My test levels INCREASED while on the Dball AM bridge while my LH slowly recuperated, when compared to pre-main cycle levels.

Again, the dball bridge ONLY works if you take the dball in accordance with your bodies circadian rhythm. If you don’t go to sleep at a certain time and sleep for 8 hours and wake up at a certain time(and then take the 10mg dball right away) CONSISTENTLY, The Dball bridge will then not work properly.

As an addendum, if you actually want to BOOST your LH levels to normal while on the bridge, use 25mg proviron 6-8 weeks before your AM Dball Bridge post-cycle therapy, and you will then be able to increase LH levels to normal.(I already proved this with studies at AF…go look them up. Its in the Hall of Fame) You obviously must use the proviron during the Dball bridge as well.

So, the Bridge becomes:

(6-8 weeks) before end of Main cycle: Start 25mg Proviron

End Main Cycle.

AM Dball Bridge cycle: 8 weeks

#1.Start Bridge at 10mg Dball in the AM upon waking up.
#2 Make damn sure you take the 10mg dball at the same damn
time every day. As soon as you wake up. This wake up time
(if 8 or 9 or 10 AM) must be used for the rest of
the bridge(8 weeks)(Circadian Rhythm is VERY important to
the success of the bridge)
#3 Proviron at 25mgs/day(LH booster)
#4 Arimidex at 1mg ED or more.(2mg is as high as I would go).
#5 Human Chorionic Gonadotropin (HCG) at 5000IU’s 2X/week on Weeks 5,6,7,8(Endo Test
Booster)
#6 Clomid at 300mgs Day 1, and then 100mgs/day from then on
until the end of the bridge(LH and FSH Booster)

End result: Test levels HIGHER than pre-main cycle levels…by roughly 20% (Most definately in the normal range), and a normal LH function.
Even better: NO DAMN MUSCLE LOST while coming off the bridge.
Almost EVERY single post-cycle therapy out there causes you to lose muscle(Except for GH/Slin/IGF-1). PERIOD. Well guess what? This one doesn’t.

There, I scientifically and mathematically wise PROVED that the AM Dball Bridge works.

Fonz
 
Billy_Bathgate said:
I just would like to know how much E2 is going to be produced, and just how much it really takes for suppresion? With the above, I see they didnt experience a total shutdown, which I did still get some when I did it, but not 69% more like 10-15%.

http://jcem.endojournals.org/cgi/content/full/85/9/3027

"The mechanism proposed for this divergence between spontaneous pulse height and acute pituitary responsiveness to exogenous GnRH was that clomiphene was having tissue-specific mixed agonist/antagonist effects. The authors concluded that clomiphene was acting as an estrogen antagonist at the hypothalamus, resulting in an increase in endogenous GnRH secretion, but as an estrogen agonist at the pituitary, causing decreased responsiveness to exogenous GnRH"

..."This concept that E2 is a more potent suppressor of LH secretion than is T is supported by studies in both prepubertal boys (42, 43) and adult males (1, 2, 3, 7, 8, 41, 44), indicating that, on a molar basis, the steroid dose required to suppress gonadotropin secretion is approximately 200-fold less for E2 than for T..."

..."From these clinical investigative studies on the impact of aromatase inhibition in NL and GnRH-deficient men, employing frequent blood sampling combined with administration of a GnRH antagonist, we conclude that, in the human male, estrogen has dual sites of negative feedback, acting at the hypothalamus to decrease GnRH pulse frequency and at the pituitary to decrease pituitary responsiveness to GnRH..."
 
I've just logged on to several boards & noticed that the latest Dbol bridge threads have turned into flame wars again...

You really can't apply simple math like it was done in the above post to try to figure out how much your test/LH would be suppressed after a cycle while on dbol+ Human Chorionic Gonadotropin (HCG) +anastrozole...

The anastrozole/SERM studies he mentions were done on normal or IHH men...
After/during the cycle you'll first develop secondary hypogonadism (low LH) , but in some cases a combo of primary + secondary can happen, - although Human Chorionic Gonadotropin (HCG) should help with that...

Your Leydig cell LHR will downregulate...

Your LH response to LHRH will be significantly reduced so if you want to completely recover your goal should be to get your LH to supraphysiological level & that's not going to happen while you're on...

If you want to only partially recover & prevent crash you can use dbol, it really depends on what is your goal...

Another problem is that you're not going to have only dbol in your system, you'll also have test induced by Human Chorionic Gonadotropin (HCG) which will prevent your LH to reach optimal levels for recovery...

Then there's the issue of time of administration which is irrelevant IMO, even if you would want to control your androgen levels at the certain time of day you wouldn't be able to do that while on dbol + Human Chorionic Gonadotropin (HCG) ...

The Human Chorionic Gonadotropin (HCG) will increase your test levels which will with dbol result in low LH...

Even if you could raise your LH to baseline, that's not enough...

Notice that LH went up quick after the cycle in this study posted by nandi12, but even after it became higher than baseline, test was still heavily suppressed...


(1) Am J Sports Med 1987 Jul-Aug;15(4):357-61

Androgenic-anabolic steroid effects on serum thyroid, pituitary and steroid hormones in athletes.

In this study posted by nandi normal men were given a 12 week cycle of test(150mg/wk)+deca(150mg/wk) + dbol(15mg/day) + winny(5 mg/day)

Their baseline LH was 6.8 U/L.
One month after quitting it had risen to 5.2 U/L.
12 weeks after the cycle their LH was 8.0 U/L but their test was still depressed (14nmol/l vs. a baseline of 21.8 nmol/L)
 
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