I lost nearly all my SD gains using Nolva as PCT!!!
- 08-15-2005, 07:03 PM
I lost nearly all my SD gains using Nolva as PCT!!!
I did a 3.5 week cycle of SD using liquid Nolva as a PCT. I am starting my third week off and lost all but 2lbs of my gains. At the end of my cycle I was 198 lbs. (up 10), now I am 190 lbs. (up 2). I lost 90% of it during the week that I was off. I was expecting to lose half at the most but this is nearly all of it.
I think its from taking a break right after the SD but I had to take one cuz my muscles were starting to ache from six weeks of lifting with no breaks. I had no symptoms besides back pumps at the end. I also used fish oil, milk thistle and hawthorne berry on cycle.
Could I get some opinions on what I should do next time? I am having trouble knowing what week to start a cycle after a break and when I should take my break after a cycle.
I know its the first week back in the gym but my strength is down about 15lbs (on bench) from what I was before cycle. I'll see how everything else goes during the week.
Diet was good on and off cycle. Lots of fish, veggies, chicken, beans, fiber. Got it all.
Other than this I feel great. Test levels feel like they are back again.
Week 1 - 10mg
Week 2 - 10mg
Week 3 - 20mg
Week 4 - 20mg/end cycle/start PCT Nolva 40mg
Week 5 - Nolva 40mg/Rest from gym
Week 6 - Nolva 20mg/Back in the gym
- 08-15-2005, 07:10 PM
You're likely to get this thread shut down because you are only 20. But while it is still alive and breathing I'll suggest that you my want to look at your diet. Most people will gain a transient 8-10lbs from SD just from the glycogen retention (muscle volume/pumps) it produces. The key to keeping that weight on is in your post cycle diet and training. Nolva did not make you loose the weight. You need to eat at least as much (in surplus) as you did while on cycle, for the first few weeks, and train about as regualrly as you did when on as well. Time off right after a cycle is not the best time to take it. A couple few weeks of solid training at the begining of PCT is advisable...then take a few days off to get some rest.The fool says in his heart “There is no God."
I vehemently support your right to take offense to anything I post.
- 08-15-2005, 07:18 PM
I'm actually 26.....i never put the right dates and stuff when i register. I just put crap information. fixed it now
but anyway....i know nolva didnt make me loose it cuz my test levels are great. what i really want opinions on is when to start SD after a break and when to take a break after. I can really never go beyond 6 or 7 weeks of training without a break.
What i did with this cycle is start 3 weeks after my last break. Should I start earlier??
btw my supp experience is only m1t a few years ago (gained 15...kept 10)
08-16-2005, 01:47 PM
In your case, start immediately after a break, use for three weeks, then break 4 weeks after discontinuation of SD. A break is good every once in a while, but try taking a few days off and getting back into the gym, rather than a week off evey 6 weeks.
Like B stated, keep the calories up!
08-16-2005, 02:19 PM
08-16-2005, 04:41 PM
what do u mean a break? how long?are you doing a 3 day split or what? Im confused on how you cant lift for more then 6 weeks at a time sounds like a dedication problem ! if it is that then no substance is going to help in the long run
08-16-2005, 07:25 PM
08-16-2005, 08:08 PM
That topic has been beaten to death. Let's just say there are those who hate Clomid, and those who don't.
08-16-2005, 08:28 PM
Well I for one love clomid, but always rely on nolva to carry me through PCT. I just use clomid for the first week or so to jump start my balls, haha.
08-16-2005, 11:18 PM
as said, this has been beaten to death, and although nolva seems to have won over clomid from a scientific literature stand point, i stand by clomid because i've always felt that it got my test back up better.Originally Posted by Addiction
traditionally clomid has always been the favored pct drug, and nolva was an anti-gyno drug. so thats the way i use each respectivly. call me old-fashioned.
08-17-2005, 12:04 AM
also a lot of people bitch about clomids side effects. this is probably because people have always been told to mega dose clomid the first day of pct at 300mg and then 100mg for a week. i tried this once and i experianced bad sides and recovery wasn;t any better.
just dose 100mg ed week 1, split into 2 50mg doses, and 50mg ed for the second week.
i have never experianced a bad side doing it this way.
08-17-2005, 08:33 AM
Have you guys used clomid alone for PCT then, just asking for clarification. I would like to try this, but have always been afraid it might not work as well as nolva for restoring natty test. Now with raloxifene out, I may just give that a try.
08-17-2005, 12:10 PM
Nolva doesn't increase/restore natural test levels.
Clomid leads to the production of FSH and LH, thereby increasing natural test production.
08-17-2005, 12:21 PM
The fool says in his heart “There is no God."
I vehemently support your right to take offense to anything I post.
08-17-2005, 01:21 PM
Short oral only cycles aren't that great even with good bulkers like m1t or SD.
Many shy away from this topic even after losing 80% post-pct but its the truth. Its difficult to keep an extra 10lbs on of lean mass on an already stacked frame.
The good news is that gaining back the 'lost' mass is faster probably due to muscle memory.
08-24-2005, 11:29 PM
Well, I was reading your case and the only supplement you listed for PCT is Nolva. Did you take any of the side supplements during your SD cycle? Such as, CoQ10, Red Yeast Rice, Odorless Garlic, Pro liver, Hawthorn, and Policosanol. You will need to add these supplements to your SD cycle and continue these supplements through your PCT cycle.
You might want to add HMB, Lean Xtreme, DHEA, Glutamine, BCAA, Flax/Fish Oil, and CEE/Creatine on your next PCT cycle because these supplements will help you keep some or all of your gains.
I did a four week cycle of SD and a five week cycle of PCT. I have kept my SD gains and gained a couple of extra muscle weight and size. I will be ending my PCT cycle this week. I don't know what my post PCT results will be but this is the info I have right now.
Did you drop your calories? How much carbs and protein did you consume during PCT?
Originally Posted by Budweiser Frogg
09-10-2005, 01:27 PM
Or you might not, Nolva didn't cause you to lose your gains... your lack of diet/training increase after getting off SD compared to while on caused you to lose your gains. Get your diet right before you try pH's, and 20 is to young anyway.Originally Posted by QUICKRYDE
09-10-2005, 03:06 PM
yea i did take hawthorne, garlic, proliver, glutamine and creatine.
to the guy who was saying that it will probably be easier to gain back the lost muscle mass it seems like it was. I did gain 2-3 lbs since the end of PCT and my strength has been going up without much of a diet change (the usual).
09-10-2005, 03:51 PM
For test raising abilities Clomid is weaker than Nolva, but Clomid makes you balls plump up faster, so people equate that to them producing test. Since when is testicle size related to how much test they put out?Originally Posted by Addiction
3rd paragraph under characteristics :
Nolvadex is clearly the stronger component of the two
First paragraph :
Clomiphene citrate is usually used for preventing aromatization ( but is not as effective as Arimidex or Nolvadex in this field )
09-10-2005, 04:10 PM
They are both SERMs. They both take up estrogen receptors (ER). Estrogen is the negative feedback to the hypothalamus which leads to test production via the HPTA. Estrogen comes from test, so when these SERMs are taking up ERs at the hypothalamus, the hypothalamus "thinks" the body is low on test. So it kicks out GnRH. When the pituitary sees GnRH it kicks out LH, and when the testicles see LH, the Leydig cells in the testes kick out test.Originally Posted by anabolicfreak
09-10-2005, 04:18 PM
It is very wise to take a break for 1-2 weeks every so often so you can let your body heal up...especailly for ectomorphs who have a lot of recovery problems as is. Not only does this allow for physical recovery, but it also allows for mental recovery as far as dedication/motivation goes.Originally Posted by scarfacebling
09-10-2005, 05:37 PM
If you gained 10 lbs assuming most was tissue, your maint. calories went up about 150-200 calories. Did you acount for this post cycle? If you don't feed the new muscle it will go bye bye really quick.
09-12-2005, 03:15 PM
09-12-2005, 03:51 PM
never take a break right after your cycle, and keep those cals high, as mentioned. Breaks are necessarry, but you need to keep nutrition and workouts solid (albeit slightly altered) when your test levels are low and you are recovering.
09-12-2005, 04:16 PM
The studies Bill referenced showed over a 6 month period.Originally Posted by B5150
Nolva takes many months to causes a significant increase in LH and FSH, whereas Clomid is almost immediate. Clomid therapy over a longer period however (such as for several months), actually lowers LH and FSH. Thus, it is recommended that clomid be discontinued after several weeks (i.e. 3 or 4) of usage. Nolvadex will do virtually nothing to help testosterone levels in that time period.
The reason is that these compounds are site specific. That's the "S" part of "SERM" refers to. Nolvadex binds almost entirely to estrogen receptors in breast tissue. Clomid binds almost exclusively around the pituitary and hypothalmus. Both have SOME systemic binding. To my knowledge IIRC relox is mostly systemic which is why it is effective for osteoperosis.
This is the reason that Clomid does not work to prevent or stop gynecomastia. It is also the reason why Nolvadex is never used as a fertility drug.
Before I learned this, I had been suspicious of something to this regard due to personal experience. Nolvadex alone did positively nothing to help my recovery, whereas Clomid worked quite well. The thing is, both together have purpose in PCT. The reason being that many are more susceptible to gyno during that time. So Nolva should be used as it is always used; to prevent gyno, and Clomid should be used as the primary agent to increase FSH and LH. When going off for an extended period, to ensure full recovery, one can continue using Nolvadex over the course of several months to ensure a more thorough recovery since it takes that long for Nolvadex to have that effect on FSH and LH.
I have seen data that suggests that low dose arimidex is also beneficial during PCT in addition to Clomid and Nolvadex.
09-12-2005, 04:50 PM
Originally Posted by GhostingOriginally Posted by GhostingIs this another my balls got bigger faster post or I could feel my test rising in my blood stream things? Or are you dropping some bro science on us?Originally Posted by Nullifidian
09-12-2005, 04:59 PM
Read the studies that William Llewellyn mentioned. They show that Nolvadex took 6 months before significant elevations in FSH and LH could be detected.
What makes SERMs different is what they do in different tissues. After reading more into ralox, it appears that raloxifene is an agonist in bone tissue (more powerful than natural estrogens), moderately potent in the liver (about as powerful or more powerful than natural estrogens), and moderately antagonistic (FAR weaker than natural estrogens) in breast tissue. It is curretnly not well known ralox's effects on the hypothalmus. Thus, what IS known is that in women it has shown a decrease in spinal fracture caused by osteoperosis (bone), increased bone density (bone), improved lipid profile (liver), slight decrease in breast size (breast), and a decreased likelihood of contracting breast cancer over placebo (breast).
I should correct myself regarding tamoxifen. Aparently it is used sometimes as a fertility treatment but typically only in conjunction with Clomid. Once again though it is a situation where success is typicaly not seen until many months of therapy. Clomid however is still the first choice due to its very pronounced and almost immediate effect on FSH levels in particular.
Ralox is only just starting to be looked at as a possible fertility treatment.
Btw, regarding Clomid being inneffective for prevent gyno; Clomiphene is only slightly weaker than estrogen in breast tissue. Prolonged Clomid use can actually CAUSE gyno in men.
09-12-2005, 05:23 PM
I respectively disagree. The first week of PCT, I believe that training will only hurt your chances at keeping gains. Your T levels are low, and LH doesn't even begin to rise until the latter part of the first week. This will lead to serious overtraining. If you cannot recover, then you should not train. I've implemented this into my PCT and have been able to keep more of my gains this way. And then in the latter weeks of PCT, I will still only train every third day.Originally Posted by scarfacebling
Maintenance is key here, not gaining. But if it has worked for you, that's great....but I would bet that 90% of trainees will only benefit from taking the first week off and reducing training frequency in general.
09-12-2005, 05:26 PM
To the original poster, I do not think that taking a break was the primary factor...I believe that it was indeed your diet and loss of glycogen storeage from the SD. Gotta keep those cals high during PC. I believe even moreso than what they were on cycle. I always increase a minimum of 300 over when in PC.
This is also the main reason why oral only cycles aren't the way to go here...especially in regards to these big mass-gainers like SD, dbol, drol ,etc..
The body is more capable of keeping newly added muscle when it has a chance to get used to it. Gaining 12lbs. in 3 weeks is not long enough to keep new muscle....that is why it is always suggested to run an injectable cycle past the orals for awhile longer in order for your body to get accustomed to the newly added lbs.
09-12-2005, 05:26 PM
Originally Posted by Nullifidian*sigh*Originally Posted by Nullifidian
Umm...ok, the HPTA in your body must work different than everybody elses.
Ghosting dont be an idiot. Look at Bills studies. His study on LH and FSH is the end all, be all of studies. Plus Ghosting, you are welcome to feel my balls after PCT on Clomid. My testiscle size is proof.
Despite that they are alike in structure, Clomids starting dose is 150mg and Nolva is only 40mg. You still want to claim Clomid rocks for PCT? Oh ya, Bills study. I cant believe this is even a consideration for PCT if it werent for the size of your nuts. Other than that, it should be confined for fertiality.
BTW, I never once mentioned Ralox, so Im not sure why you included it, but thanks for telling me about PCT.
Last edited by Ghosting; 09-12-2005 at 05:54 PM.
09-12-2005, 05:30 PM
I also didnt get into this for a pissing contest, but to point out you were and are incorrect.
09-12-2005, 05:49 PM
2nd paragraph in the conclusion from Bills study, incase there is any doubt.
Nolvadex would seem to provide a better and more stable increase in testosterone levels
09-12-2005, 08:41 PM
Why are you being an ******* about this? And no, I'm not spouting "bro-telligence" at you. I get tested during EVERY PCT, and I can tell you with fact I was below baseline after 4 weeks of Nolva, but above baseline after 4 weeks of Clomid from two different cycles of THE SAME COMPOUNDS.Originally Posted by Ghosting
As for studies...
Credit to Blown_SC at ironforlife for these:
Tamox vs Clomid
Am J Physiol 1983 Feb;240(2):E125-30
Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro.
Adashi EY, Hsueh AJ, Bambino TH, Yen SS.
The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin.
Br J Pharmacol 1978 Apr;62(4):487-93
Differential depletion of cytoplasmic high affinity oestrogen receptors after the in vivo administration of the antioestrogens, clomiphene, MER-25 and tamoxifen.
Kurl RN, Morris ID.
1 The in vivo actions of the oestrogen antagonists, MER-25 and tamoxifen upon the cytosol oestrogen receptors prepared from amygdala, hypothalamus, pituitary and uterus of rats were studied 24 h after drug administration. 2 There was a dose-related depletion of cytosol oestrogen receptors. However, the uterine and pituitary receptors were consistently affected at a lower dose than were those from the brain. 3 The ratios of the combined central ED50 to the combined peripheral ED50 were clomiphene 169 greater than MER-25 19.2 greater than tamoxifen 2.13. 4 The receptor changes were not related to biological activity monitored by serum luteinizing hormone levels and uterotrophic response. 5 The possible role of these drug effects in the induction of ovulation and future developments are discussed.
Case for Clomid
J Clin Endocrinol Metab 1985 Nov;61(5):842-5
Evidence for a role of endogenous estrogen in the hypothalamic control of gonadotropin secretion in men.
Winters SJ, Troen P.
To examine the mechanism by which endogenous estrogens inhibit gonadotropin secretion in men, blood samples were drawn every 10 min for 12 h in five men before and at the completion of 3 weeks of treatment with the estrogen antagonist clomiphene citrate (50 mg twice daily). Samples were analyzed for LH and alpha-subunit by RIA. Clomiphene produced a 3-fold rise in circulating LH levels, which was associated with a 80% increase in pulse frequency and a 70% increase in pulse amplitude. Immunoreactive alpha-subunit secretion was also pulsatile before and after clomiphene treatment. Mean alpha-levels rose 70%, together with a 39% increase in pulse frequency and a 41% increase in pulse amplitude. Circulating testosterone and estradiol levels increased 2-fold and FSH levels increased 3-fold after clomiphene treatment. Insofar as each LH and uncombined alpha-subunit pulse reflects a LHRH secretory episode, our data indicate that endogenous estrogens tonically restrain the hypothalamic release of LHRH. From these results and those of previous studies, we conclude that estrogens as well as androgens are important in the testicular feedback inhibition of the hypothalamic oscillator that governs pulsatile gonadotropin secretion.
J Androl 1991 Jul-Aug;12(4):258-63
The effects of normal aging on the response of the pituitary-gonadal axis to chronic clomiphene administration in men.
Tenover JS, Bremner WJ.
Department of Medicine, University of Washington School of Medicine, Seattle.
Serum androgens decline with age in normal men, despite normal or elevated bioactive serum gonadotropins, suggesting that primary testicular dysfunction occurs with aging. The authors further assessed the question of age-related testicular dysfunction by evaluating whether raising serum gonadotropins above the normal serum range for an extended time in healthy elderly men might result in bringing their gonadal function to a level similar to that found in young adult men. Five elderly (65 to 85 years old) and five young adult men (26 to 33 years old) were given 50 mg of clomiphene citrate (CC) twice a day for 8 weeks to stimulate gonadotropin production. During that time, testosterone (T), non-sex hormone-binding globulin bound T, and estradiol increased significantly in both age groups, while serum inhibin increased significantly only in the young adult men. The increases in serum androgens with CC administration were significantly greater in the young adult men than in the elderly men. These hormone changes occurred in the setting of serum gonadotropins that increased significantly in both age groups, although there was a tendency for the elderly men to have a smaller increase in luteinizing hormone. Despite 8 weeks of stimulation of the pituitary-gonadal axis by CC administration, the elderly men demonstrated significantly diminished testicular responses compared with the young adult men. Sertoli cell function, as determined by inhibin production, was more diminished in the elderly men than was Leydig cell function. These data strengthen the hypothesis that normal aging in men is accompanied by a decline in testicular function.
Urology 1991 Oct;38(4):317-22
Possible hypothalamic impotence. Male counterpart to hypothalamic amenorrhea?
Guay AT, Bansal S, Hodge MB.
Section of Endocrinology, Lahey Clinic Medical Center, Burlington, Massachusetts.
Twenty-one men with erectile complaints who were found to have a low level of serum testosterone without a reciprocal elevation of the serum levels of luteinizing hormone were evaluated to identify whether the defect was of hypothalamic or of pituitary origin. Patients underwent a luteinizing hormone (LH)-follicle-stimulating hormone (FSH)-releasing hormone stimulation test that showed a normal but sluggish increase in LH and FSH levels, thus ruling out a pituitary defect and suggesting a suprapituitary abnormality. This was confirmed when, in response to clomiphene, patients had a normal increase in gonadotropin and testosterone levels. Although the basal as well as clomiphene and gonadotropin releasing hormone-stimulated levels of total testosterone and gonadotropins were identical in men less than and more than fifty years old, the elevation of free testosterone levels in response to clomiphene was higher in patients younger than fifty. This suggested that although the primary abnormality found in these patients is altered secretion of gonadotropin hormone-releasing hormone from the hypothalamus, an age-related decline in the responsivity of Leydig cells to LH may make it more manifest in older patients. Elevation of testosterone levels from a subnormal to a normal range in response to clomiphene administered for seven days suggests that the defect is functional and reversible and that the drug may be useful in treatment of sexual dysfunction in this group of patients.
Effect of clomiphene citrate on hormonal profile in male hemodialysis and kidney transplant patients.
Martin-Malo A, Benito P, Castillo D, Espinosa M, Burdiel LG, Perez R, Aljama P.
Department of Nephrology, Hospital Universitario Reina Sofia, Cordoba, Spain.
The aim of this study was to evaluate the role of clomiphene citrate (CC) therapy in the hypothalamus-pituitary-gonadal axis of male uremic subjects. Thirty-four patients on hemodialysis (HD) and 8 successful kidney transplant subjects (RT) were evaluated. Nine healthy males were used as controls (C). At baseline, zinc, testosterone (TEST), prolactin (PRL), FSH, LH and estradiol plasma concentrations were measured. All subjects were treated with CC (100 mg/day) for a week. The aforementioned parameters were determined again on the seventh day of CC therapy, and 3 days after drug withdrawal. Following CC, there was a rise in FSH, LH and TEST levels in all subjects (p < 0.05); it is interesting to stress that TEST became normal in HD. In addition, we observed a decrease of PRL after CC only in HD patients (p < 0.01). In summary, CC was able to partially correct most of the hormonal disturbances of the gonadal axis in uremic patients.
nolvadex aka tamoxifen studies:
Arch Gynecol Obstet 1993;252(3):143-7
Tamoxifen treatment of oligozoospermia: a re-evaluation of its effects including additional sperm function tests.
Sterzik K, Rosenbusch B, Mogck J, Heyden M, Lichtenberger K.
Abteilung Frauenheilkunde, Geburtshilfe der Universitat, Ulm, Germany.
Because of previous contradictory results, we reevaluated the effects of tamoxifen on 29 men presenting with idiopathic oligozoospermia. To determine whether a possible increase in sperm concentration might be correlated with an improvement of sperm quality, the hamster ovum penetration (HOP) test and the hypo-osmotic swelling (HOS) test were included as additional tests of sperm function. Patients were treated with tamoxifen (20 mg/day) for 3 months. From 4 weeks until the end of the study, tamoxifen had no significant effect (P > 0.05) on blood levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (T), or estradiol (E2). There was no significant improvement (P > 0.05) of conventional semen parameters (volume, concentration, motility, morphology), and of HOP and HOS test results. The lack of correlation between a rise in hormone levels and improvement of sperm quality suggests that tamoxifen is of questionable value in men with idiopathic oligozoospermia.
Asian J Androl 2001 Jun;3(2):115-9
Effect of intermittent treatment with tamoxifen on reproduction in male rats.
Gill-Sharma MK, Balasinor N, Parte P.
Department of Neuroendocrinology, Institute for Research in Reproduction, ICMR, Parel, Mumbai, India. email@example.com
AIM: To identify the antifertility effect of intermittent oral administration of tamoxifen in male rat. METHODS: Tamoxifen was administered orally at a dose of 0.4 mg x kg(-1) x d(-1) with an intermittent regime for 120 days. Treated and control rats were mated with cycling female rats on days 60, 90 and 120 of treatment. The mated males were sacrificed and the weights of reproductive organs were recorded, and the serum levels of LH, FSH, testosterone and estradiol estimated by radioimmunoassay. In the female rats, the numbers of implantation sites, corpora lutea, and numbers of normal and resorbed foetuses were recorded on d 21 of gestation. The potency, fecundity, fertility index, litter size and post-implantation loss were then calculated. RESULTS: The fecundity of male rats was completely suppressed by tamoxifen while the potency was maintained at the control level. The fertility index was significantly decreased. No viable litters were sired. Post implantation loss, indicative of non-viable embryos, was observed but was not significantly increased above the control level. The weights of the testes, epididymides, ventral prostate and seminal vesicles were significantly reduced. The blood LH and testosterone levels were significantly decreased, but not FSH and estradiol. CONCLUSION: Intermittent oral tamoxifen administration completely suppressed the fecundity of adult male rats with reserved potency.
Case study showing benefit to FSH, LH, and testosterone from tamox- Notice administration duration
Treatment of idiopathic and post varicocelectomy oligozoospermia with oral tamoxifen citrate.
BJU Int 1999 Apr; 83: 646-8
Kadioglu TC KĂ¶ksal IT TunĂ§ M Nane I Tellaloglu S
[see related articles]
Department of Urology, Faculty of Medicine, Istanbul University, Istanbul, Turkey.
OBJECTIVE: To identify a subgroup of men who may benefit from tamoxifen citrate (a widely prescribed drug for male infertility) among those with normogonadotrophic and hypergonadotrophic oligozoospermia, either idiopathic or after varicocelectomy. PATIENTS AND METHODS: The study included infertile men with oligozoospermia, 136 referred to our outpatient clinic and 84 infertile after varicocelectomy. All patients received tamoxifen citrate (10 mg twice daily); semen analysis and hormone tests were repeated at the end of 3 and 6 months of treatment, the values being compared with those before treatment. RESULTS : The levels of follicle-stimulating hormone, luteinizing hormone and testosterone increased in all groups receiving tamoxifen citrate. Normogonadotrophic patients had a significant increase in sperm count and concentration, while the slight increase detected in the hypergonadotrophic group was statistically insignificant. CONCLUSION: In patients with normogonadotrophic oligozoospermia, tamoxifen citrate may be offered as a practical and economic alternative before using any assisted reproduction techniques. However, double-blind placebo-controlled trials are needed to confirm the findings of this preliminary study.
09-12-2005, 09:30 PM
LOL. I didnt even read your studies, not to mention you didnt provide links to where they came from. If any are from Lancet i'll probably die laughing. You win Clomid is weaker, but it raises test levels better than Nolva. Im a big fan of bro-lore.
09-12-2005, 09:40 PM
Glancing over your studies I want to know why detectable LH and (FSH) is so important to you. Levels of LH are hardly worth mentioning when we are concerned with test. Bottom line, not how much LH, trying to imply the LH will cause a boost in test. Also why you are concerned with sperm production. Testicle size and test production is not a good indication. Now Im an ******* for telling the truth. LOL
09-12-2005, 09:46 PM
Test production matters for PCT, not the size of your testicles , amount of sperm, or levels of LH. *groan*
09-13-2005, 12:27 AM
Dude, stop being a little bitch, and stop accusing ME of "bro-telligence" when you don't even read the studies I posted.Originally Posted by Ghosting
I'm trying to discuss this in a civilized manner, and all you are doing is backtalking to me and calling names. If you have anything to offer other than Bill's 6 month study, then as far as I'm concerned you DO NOT have enough evidence backing your side of the story. You aparently don't know anything about SERMs or you would recognize that tissue specific action is the key reason they don't prescribe the same SERM for everything.
I also recognized that Nolvadex has its uses in PCT, but only for longer term recovery, not short term. The one study you cling to with such fervor supports this. You'd have to mega dose the tamoxifen for it to be as effective as clomiphene in the same amount of time with respect to increasing FSH and LH levels. The toxicity at that dose would make Clomid look tame. As it is tamox isn't as nice as a lot of people like to think. And in case you didn't notice FSH and LH are exactly the primary concerns where SERMs are AIs are concerned with PCT. Keeping testicles sensitive to LH and thus able to produce test is only accomplished via HCG, preferably oncycle via Swale's Protocol since HCG itself suppresses endogenous LH production.
09-13-2005, 03:14 AM
Ok, you win. Clomid is the best. Next PCT all I will care about is LH levels forget test. Youve shown me the error of my ways. Geezus. I know the endocrinolgy in regards to PCT inside and out, so you can stop with the apparently I dont know. Dude, youre right, Im wrong, you are good looking, Im not so good look, and you can spank me in tennis. Plus Im gay and mentally handicapped. Viva la Clomid!! Please stop, you win.Originally Posted by Nullifidian
09-13-2005, 03:51 AM
09-13-2005, 09:58 AM
I'm not looking to "win" and I'm not looking for anyone to "lose." I just wanted to see the evidence you have supporting your claim. I'm interested in truth.
When I first came to anabolicminds, I thought was uninformed about how SERMs work, and just thought blindly tat Clomid was for PCT and that Nolva was for preventing gyno. Then I read Bobo's link to Bill L.'s article about Nolva for PCT. I read the article and felt convinced otherwise.
Since then however I have learned a great deal more about how SERMs work. I saw ralox come to market and thought, hey this is supposedly stronger than Nolva at effective dose, and has fewer sides. Why isn't everyone using it? So I did some reading. I poked around fertility boards, osteoperosis boards, and breast cancer boards. I read some posts by doctors that cited studies. Then I began to understand that with SERMs it isn't just a question of "strength" it is a question of mechanism of action. As I said in previous posts, SERMs act different when they bind to estrogen receptors in different tissues. The reason is that estrogen serves multiple purposes in the body. It effects cholesterol, bones density, IGF1 production, breast tissue growth, and regulates HPTA function by triggering or preventing the release of GnRH.
Estradiol for example improves lipid profile, increases IGF1 production, increases bone density, causes breast tissue growth, and inhibits GnRH. Estradiol binds well in all relevant tissues. Tamoxifen improves lipid profile, increases IGF1, increases bone density slightly, inhibits breast tissue growth, and does virtually nothing for GnRH. Tamoxifen binds primarily in breast and liver cells, and secondarily in bones. The thing is, due to high number of binding sites tamoxifen winds up preventing natural estrogens like estradiol from bdining to a significant degree. This prevents the negative feedback from that estrogen and thus results in less inhibition of GnRH. This however takes several months to happen. Clomid has little effect on lipid profile, almost no effect on IGF1, does nothing for bone density, causes only very slight increase in breast tissue growth, and directly triggers the release of GnRH. It binds primarily only in the suprapituitary region, and only in other sites with prolonged administration. Thus Clomid causes a rise in LH and FSH quickly; in only a couple weeks. The OVERALL increase however is not as great as that seen by Nolvadex administration over the course of several MONTHS. So, Nolva used long term is more effective than Clomid used short term OR long term.
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