Please Scroll Down to See Forums Below
napsgear
genezapharmateuticals
domestic-supply
puritysourcelabs
UGL OZ
UGFREAK
napsgeargenezapharmateuticals domestic-supplypuritysourcelabsUGL OZUGFREAK

Calling Bill Llewellyn!!

HCG and Clomid.

Just got his anabolic 2000

Bill you are the man. I do not completely agree with you about everything, but then again who the hell am I.

You did a great job on the book. I started reading it about 8 last night and didn't finish it until 4 this morning.

Good Job and Thanks for the effort you put into it
Nautica

One more question Bill. Do you have any or know of anybooks out there that have more infor on half-lives and detection times. Thanks.
 
Thanks Nautica,

Actually I am more fond of HCG plus Nolvadex lately. Nolvadex is better all around. I'd only go for Clomid if it were unavailable..

I hope you mean Anabolics 2002.. It's out, and much better than the old b&w 2000 edition... If its in good condition you could prob return it..

Off hand I can't recommend a book on drug detection, but I think one covered the subject specifically some years back. Forget the name, and never read it.. I may look into doing something on this in the future perhaps..

- Bill
 
w_llewellyn said:
Thanks Nautica,

Actually I am more fond of HCG plus Nolvadex lately. Nolvadex is better all around. I'd only go for Clomid if it were unavailable..

- Bill

Bill: If I understand you correctly, you say that

a) HCG should be used POST-CYCLE (thus introducing synthetic LH and downregulating your body's endogenous production potentially slowing HPTA recovery)

b) Clomid POST-CYCLE is not necessary if nolva and HCG are used POST-CYCLE?

(note I'm talking all about POST-cycle, not MID-cycle, in which case I agree with you).

Pls elaborate on that...
 
DaMan said:
Bill: If I understand you correctly, you say that

a) HCG should be used POST-CYCLE (thus introducing synthetic LH and downregulating your body's endogenous production potentially slowing HPTA recovery)

b) Clomid POST-CYCLE is not necessary if nolva and HCG are used POST-CYCLE?

(note I'm talking all about POST-cycle, not MID-cycle, in which case I agree with you).

Pls elaborate on that...

HCG is important because the testicles get atrophied during longer cycles. With this loss in mass also comes a loss in the ability to respond properly to LH with increased testosterone production once the cycle is over. Even if Nolvadex/Clomid will help to get LH levels elevated, the testicles won't respond to it well.. HCG provides a bolus dose of LH, to help shock them back into shape faster than a slight elevation would. Post-cycle I actually think Nolvadex's main purpose is to block any excess estrogen from the HCG shots, as once the drugs are gone you don't have much estrogen or androgen to deal with until T release from the testicles catches up.

Clomid is essentially Nolvadex, just not as strong. The thought that one is an anti-estrogen and the other a T stimulating drug is incorrect.

- Bill Llewellyn
 
Last edited:
w_llewellyn said:


HCG is important because the testicles get atrophied during longer cycles. With this loss in mass also comes a loss in the ability to respond properly to LH with increased testosterone production once the cycle is over. Even if Nolvadex/Clomid will help to get LH levels elevated, the testicles won't respond to it well.. HCG provides a bolus dose of LH, to help shock them back into shape faster than a slight elevation would. Post-cycle I actually think Nolvadex's main purpose is to block any excess estrogen from the HCG shots, as once the drugs are gone you don't have much estrogen or androgen to deal with until T release from the testicles catches up.

Clomid is essentially Nolvadex, just not as strong. The thought that one is an anti-estrogen and the other a T stimulating drug is incorrect.

- Bill Llewellyn

Whoa. So you ARE saying Nolva can be used vs Clomid post-cycle... that's a pretty significant proposition and contrary to much of what this board believes (I don't have the background to discuss this with you, but others do). I hope you don't mind if I start a separate thread on this, it's bound to get some attention. It will point to this thread.

Thx for your feedback!!!
 
w_llewellyn said:
Thanks Nautica,

Actually I am more fond of HCG plus Nolvadex lately. Nolvadex is better all around. I'd only go for Clomid if it were unavailable..

I hope you mean Anabolics 2002.. It's out, and much better than the old b&w 2000 edition... If its in good condition you could prob return it..


I just bought it 2 days ago. I did not realize there was 2002 out yet. Give me a site and I will order it also.

Thanks
Nauitca
 
Bill Llewellyn, I don't know who you are, but this board has taken a turn for the better since you got here! Anyway, I'm definitely buying your book.

In a related thread you stated that "if possible you would minimize your anti-estrogen regime while on cycle" - having to do with blood glucose or something.

My question is specifically about my present cycle, which is 250 mg of test enanthate every three days + dbol in an ascending pattern 20mg/day wk 1, 30 mg/day wk 2, 40 mg/day wk 3, then tapering off in wk 4 and no dbol from weeks 5-9. Winny will be used in weeks 6 thru 9.

I was taking arimidex at .25mg daily. Would you think gains & muscle recovery would be improved by going to .25mg EOD.

I'd be reluctant to drop it entirely.
 
The reason is that estrogen has been shown to support an important pathway in which glucose is utilized by the muscle. This is the same reason women tend to notice less muscle damage than men for similar levels of exercise.

But if using an arom-inhibitor for a specific purpose, such as maximizing the androgen to estrogen ratio for fat loss, you really can't have it both ways.

A middle ground is a hormone like Boldenone though, which has less estrogen conversion but seemingly enough to aid growth. Prob a lot easier than trying to guess what dosage of an inhibitor suppresses it "just enough".

- Bill Llewelyn

BTW-Nautica, you can grab 2002 off a link on my website below.
 
Bill do you recommend smaller doses of HCG rather than one big dose?? I mean like say 1000 iu's a day for 5 days rather than one big shot (that may give ya gyno). I have been on low dose test for awhile, my "boys" are about normal sized but I'm wondering if I can just shock them before my next heavy cycle.
 
While speaking of Nolvadex... can anybody tell me the detection time for Tamoxifen Citrate?
I know a lot of BB use it pre-contest due to lower water retention and thereby better hardness of the muscles.
 
Di'Sastre said:
While speaking of Nolvadex... can anybody tell me the detection time for Tamoxifen Citrate?
I know a lot of BB use it pre-contest due to lower water retention and thereby better hardness of the muscles.


It's not scheduled so I see no reason for them to test for it.
 
Mr Llewellyn if possible could you post a baseline dose for Nolvadex post cycle? I've seen your comments frequently on the use of Nolva over Clomid, but never exact doses.
 
talonracer said:
Bill do you recommend smaller doses of HCG rather than one big dose?? I mean like say 1000 iu's a day for 5 days rather than one big shot (that may give ya gyno). I have been on low dose test for awhile, my "boys" are about normal sized but I'm wondering if I can just shock them before my next heavy cycle.


Bump for thoughts...I always have found that smaller more frequent injections worked better.
 
Bill, I am a newbie to the AS world. Nevertheless, I will have to say that Anabolics 2002 has been the most informative source to me thus far. You made a post that Nolvadex is a stronger form of Clomid... I must be honest with you that in AN. 2002 you make this point a little unclear. Once seeing some of your post it is a little more clear now. Adding on to the base dose of Nolvadex asked for above..... what would you recommend for someone using a combination of strong of Test Prop. and Deca. I am sure you understand why I am asking this question. I am taking into consideration your commit about every individual being different. Thanks and keep up the hard work... Your truly making it a safer place for us all.
 
w_llewellyn said:


HCG is important because the testicles get atrophied during longer cycles. With this loss in mass also comes a loss in the ability to respond properly to LH with increased testosterone production once the cycle is over. Even if Nolvadex/Clomid will help to get LH levels elevated, the testicles won't respond to it well.. HCG provides a bolus dose of LH, to help shock them back into shape faster than a slight elevation would. Post-cycle I actually think Nolvadex's main purpose is to block any excess estrogen from the HCG shots, as once the drugs are gone you don't have much estrogen or androgen to deal with until T release from the testicles catches up.

Clomid is essentially Nolvadex, just not as strong. The thought that one is an anti-estrogen and the other a T stimulating drug is incorrect.

Excellent post and I agree with it 100%.
 
I am also in the begining of a long cycle.
could someone please post dosages for hcg and nolvadex/
Thank you Bill for the outstanding info.

God bless all
 
Great thread. I look forward to going with this approach next cycle. Additional information on amounts used would be even more helpful.
 
I will have to disagree that hcg and novaldex will do more for hpta resoration than clomid. Hcg does not provide a bolus dose of LH, it mimics LH it is not LH. It will stimulate the production of testosterone for a short time, but will do nothing to restore the hpta. It may have it's use in making the testes more 'available' for Lh stimulation, however at the same time it will produce just as much estrogen in your body as it will testosterone.

The novaldex, was such a wonderful breast cancer drug, and was revolutionary in teh field when discovered becasue it's BREAT TISSUE SPECIFIC. Not all encompasing the way clomid is, hence it will not bind to the hypothalamus, as well as clomid, and stimulate natural LH productionl.

e2.jpg

 
I want to bump this again....

Bill can you list the amount of Nolvadex and HCG to use? i.e. lay out and exact plan for people to follow at the end of the cycle. I have some ideas but I would like to see something solid.
 
I grazed over pub med for some studies trying to prove that nolvadex does in fact stimulate natural test production. I found conflicting ideas. My thoughts are either clomid or nolvadex would work fine at restoring HPTA. I don't see how one is really better than the other.


Both clomid and nolvadex stimulate test production

Clomiphene or tamoxifen for idiopathic oligo/asthenospermia.

Vandekerckhove P, Lilford R, Vail A, Hughes E.

Institute of Epidemiology, University of Leeds, 34 Hyde Terrace, Leeds, Yorkshire, UK, LS2 9LN. [email protected]

BACKGROUND: Oligo-astheno-teratospermia (sperm of low concentration, reduced motility and increased abnormal morphology) of unknown cause is common and the need for treatment is felt by patients and doctors alike. As a result, a variety of empirical, non-specific treatments have been used in an attempt to improve semen characteristics and fertility. The administration of anti-oestrogens is a common treatment because anti oestrogens interfere with the normal negative feedback of sex steroids at hypothalamic and pituitary levels in order to increase endogenous gonadotropin-releasing hormone secretion from the hypothalamus and FSH and LH secretion directly from the pituitary. In turn, FSH and LH stimulate Leydig cells in the testes, and this has been claimed to lead to increased local testosterone production, thereby boosting spermatogenesis with a possible improvement in fertility. There may also be a direct effect of anti-oestrogens on testicular spermatogenesis or steroidogenesis. This review considers the available evidence of the effect of both Clomiphene citrate and tamoxifen, both of which have a predominant anti-oestrogenic effect, for idiopathic oligo and/or asthenospermia. OBJECTIVES: The objective was to assess the effects of treating subfertile men with anti-oestrogens (clomiphene or tamoxifen) on pregnancy rates among couples where subfertility has been attributed to idiopathic oligo- and/or asthenospermia. SEARCH STRATEGY: The Cochrane Subfertility Review Group specialised register of controlled trials was searched". SELECTION CRITERIA: Randomised trials of anti-oestrogen therapy for 3 months or more compared to placebo or no placebo for subfertile males among couples where subfertility is attributed to male factor. DATA COLLECTION AND ANALYSIS: Data were extracted independently by two reviewers. Any differences were resolved with a third reviewer. MAIN RESULTS: Ten studies involving 738 men were included. Five of the trials did not specify method of randomisation. Anti-oestrogens had a positive effect on endocrinal outcomes, such as serum testosterone levels. In trials with secure randomisation there was no difference in the pregnancy rate between the anti-oestrogen groups and the control groups (odds ratio 1.26, 95% confidence interval 0.99 to 1.56). The overall pregnancy rate for these five trials was 15.4% compared to the spontaneous rate of 12.5% in the control groups. These odds increased to 1.56 (95% confidence interval 0.99 to 2.19) when all 10 trials were included, but this result is likely to be artificially inflated. REVIEWER'S CONCLUSIONS: Anti-oestrogens appear to have a beneficial effect on endocrinal outcomes, but there is not enough evidence to evaluate the use of anti-oestrogens for increasing the fertility of males with idiopathic oligo-asthenospermia.


Evidence of tamoxifen restoring HTPA, and shows no decrease in LH-releasing hormone as clomid does.

Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.

Vermeulen A, Comhaire F.

The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development.


Evidence against tamoxifen restoring HPTA consistently

Short- and long-term hormonal effects of a single dose of 50 mg tamoxifen administered to normal males.

Fauser BC, Dony JM, Doesburg WH, Thomas CM, Rolland R.

To five potentially fertile males, a single dose of 50 mg tamoxifen was administered orally to explore the short- and long-term hormonal effects on the hypothalamic-pituitary-gonadal axis. Blood specimens were obtained through an integrated sampling technique for the first two hours after the intake of the drug. Then, samples were taken daily throughout one week, and twice weekly for the next two weeks. Hormone measurements of luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone and oestradiol were obtained by specific RIA. All the subjects showed different response patterns. No general characteristic of the hormonal changes in the investigated group could be given. A consistent correlation between the within-individual levels of gonadotrophin and sex steroid changes could not be observed. It is concluded, within the limits of the used experimental design, that in healthy males a single administration of tamoxifen does not result in consistent changes in serum levels of either gonadotrophins or sex steroid hormones.

As far as HCG goes, I don't see the point in using something that will keep you shut down post cycle.
 
E2 said:
I will have to disagree that hcg and novaldex will do more for hpta resoration than clomid. Hcg does not provide a bolus dose of LH, it mimics LH it is not LH. It will stimulate the production of testosterone for a short time, but will do nothing to restore the hpta. It may have it's use in making the testes more 'available' for Lh stimulation, however at the same time it will produce just as much estrogen in your body as it will testosterone.

HCG mimics LH of course, which is why it is able to provide a bolus dose (of LH STIMULATION if you want to be pedantic). It allows the testes to notice a level of stimulation far greater than endogenous LH will do on its own. Plus you have to remeber that post cycle your body is already in a physiological state that favors heightened LH levels. Estrogen levels are lower than normal because you have shunted the normal T>E2 pathway, and androgen levels are in the toilet. Your body is already primed for ample levels of LH, and studies show that they do return to normal much more quickly than T does because of the atrophy issue (in fact we often see rebound overcompensation because at first T is not raised well to offer a counterbalance).

Clomid (or Nolvadex) alone is simply not capable of offering much benifit here. For too long people have been assuming that because they work well in the normal state that they must also in the recovery window, which is a MUCH different place to be.


The novaldex, was such a wonderful breast cancer drug, and was revolutionary in teh field when discovered becasue it's BREAT TISSUE SPECIFIC. Not all encompasing the way clomid is, hence it will not bind to the hypothalamus, as well as clomid, and stimulate natural LH productionl.

Nolvadex is not specific to breast tissue, and acts as an anti-estrogen in many other tissues inclusing the pituitary and hypothalamus. Clomid acts as a weak estrogen at the Pituitary, which represents a slight although admittedly more technical disadvantage over the more pure AE tamoxifen.
 
5,000-7,000 U of HCG per week for three weeks ( I recommend 2,000 U three times per week, non consecutive days). Begin HCG during last week of cycle. Nolvadex 20mg daily for 6 weeks, beginning the last week of the cycle or continue Nolvadex if using it during the cycle. My $0.02
 
Hey doc, wouldn't using the much mid cycle hurt your gains? I assume that you are just worried about anti-e in this case would arimidex be better mid cycle and save the novadex for after the cycle?

Also 6 weeks on the Ndex seems a bit long. (at 20 mgs?)
 
Top Bottom