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03-09-2010, 05:59 PM #41
Excellent thread Swifto.
Things discussed here, ive seen you talk about for quite some time.
I need an update on my sticky, might have to use this, considering it offers the best explanation of new SERMs use in PCT, and their effectiveness.
Kudos again.
My regards,
-WAR
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03-10-2010, 04:42 AM #42
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I need confirmation, you repeatedly say that all serms raise IGF levels, but link no studies to prove that tamox can do this. Where are the studies that show igf and gh response with tamox and the other serms?
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03-10-2010, 05:07 AM #43
Where do I say this?
Tamoxifen increases IGF-1 binding proteins. But lowers plasma IGF-1.
Second, I dont have ALL the answers. I research pubmed/medline and other journals, thats where I research.
Rather than demand studies on various subjects. Do your own research and formulate your OWN opinoin.Last edited by Swifto; 03-10-2010 at 05:10 AM.
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03-10-2010, 07:31 AM #44
Still a bit confused both of them are almost alike i mean clomid and nolva so why take them together if i see that someone says they will be using just nolva they get hammered sayin it is a weak pct and a serm and ai is a no go so can someone let me know why use two of the same thank you and swifto you write good stuff man thank you ....
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03-10-2010, 07:53 AM #45
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03-11-2010, 03:16 AM #46
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both bolded items led me to think you said tamo increased igf,
This is interesting about protein binding, can you tell me more? Do other serms increase the protein binding?
Sorry for making you feel uncomfortable, I was just hoping you had some info I could never find. I honestly spent months trying to read studies about serms and have found not too much to make me feel any better using clomid over tamo, so I just use tamo to avoid the clomid sides.Last edited by elfin1mf; 03-11-2010 at 03:18 AM.
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03-11-2010, 03:26 AM #47
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potential problems with nolva are -
nolva can apparently lead to oestrogen rebound unlike clomid because of the oestrogen mimicking effect in the pituitary --edit - some think this is not going to be a problem for a usual pct
nolva will lower gh and igf levels unlike clomid -- edit - apparently this is wrong and some studies show that tamox lowers igf, but actually increases gh
Nolva does nothing to help stimulate the release of GnRH from the hypothalamus, unlike clomid --edit- I am looking into this, this may not be true, I have not seen enough evidence yet to confirm this.
Many think these effects warrant the use of clomid instead of nolva and NOT in addition to, because clomid does not have any of these problems as far as any studies I have ever seen can show.Last edited by elfin1mf; 03-11-2010 at 06:58 PM.
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03-12-2010, 01:54 PM #48
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03-12-2010, 02:00 PM #49
Both Tamoxifen and Clomid and SERMs can lead to an extrogen rebound. They only blocks its effects at the receptor, they dont lower total estrogen levels. So if E is high and you take the blocking effects away your going to get estrogenic sides if E is high already.
I havent actually seen much on Clomid and GH/IGF. It may not be the same as Tamoxifen because Tamox is more an an overall antagonist than Clomid is. Tamoxifen is more of an ANTI-estrogen than Clomid is.
Tamoxifen does stimulate the hypothalmus to secrete GnRH. Thats exactly how it stimulates testosterone production. ER inhibition in the hypothalamus. You statement on that is nonsense.
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03-12-2010, 04:31 PM #50
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http://www.ncbi.nlm.nih.gov/pubmed/9364247 This study actually says that tamox "induced a transient increase in GH levels" after 1 month of use but decreased igf-1 slightly.
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03-12-2010, 04:34 PM #51
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Other studies on igf levels reveal that even in cancer patients who are PURPOSELY attempting to lower igf levels, tamox (obviously combined with other cancer treatments) only lowered igf 12%, 20% at highest in 2 years of heavy treatment. These levels are not ANY concern to aas users. The increase in gh is FAR outweighing any slight decrease in igf which will really not show us a negative effect.
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03-12-2010, 06:29 PM #52
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can you explain to me how the testosterone production of tamoxifen can only be explained by a stimulated raising of pulsatile GnRH from the hypothalamus?
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03-13-2010, 06:33 AM #53
You need to first understand how the endocrine system, in regards to testosterone production, works.
The hypothalamus sends down a signal (GnRH) to the putuitary which then sends down signals (LH and FSH) to the testis, which then manufacturer testosterone (leydig cells) and sperm (steroli/germ cells).
By using a SERM and blocking/inhibiting the ER inside the hypothalamus, the hypothalamus senses a decreased estrogen level and increases ganadotropins to reach homeostasis again. Its very similar to AI's increasing enodgenous testosterone by manipulating the androgen:estrogen ratio.
I explain this in my PCT thread/sticky.
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03-13-2010, 06:36 AM #54
To my knowledge, all SERMs raise testosterone via ER inhibition at the hypothalamus.
SERM (Selective Estrogen Receptor Modulators) are selective in the tissues they exert agonistic and antagonistic properties.
The 4 in regards to this thread all exert antagonistic effects in the hypothalamus. Whereas others are more agonistic in bones than others imporving bone mineral density.
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03-15-2010, 04:30 PM #55
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03-16-2010, 05:36 AM #56
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03-16-2010, 06:52 AM #57
thanks----will b on gh thru pct aswell
last pct i felt kind of depressed and low libido---thought caber might help from reading dukkits thread on caber
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03-16-2010, 07:16 AM #58
jeez, sounds like I should take Nolva everyday!
so many benefits.
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03-16-2010, 04:07 PM #59
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thanks for the great thread, tons of information.
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03-24-2010, 10:48 AM #60
Swifto I got a question for you. I realize this probably hasn't been studied so you prob dont have the answer but I figured if anyone knew you prob would... Do any SERMS act as agonist on the AR? I have heard that estrogen can upregulate the ar so this would be very useful if one of them did.
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03-24-2010, 12:44 PM #61
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very good pct information on this thread, thanks swifto
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03-24-2010, 04:48 PM #62
Thats a very good question.
SERMs such as Rolaxifene, can exert apoptosis in androgen-responsive human cells (prostate). But do so in an androgen independant manner (neither up regulation/down regulation of the AR).
I'm going to come back to this as its 10.47pm here and its been a long day.
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03-26-2010, 02:14 PM #63
Some SERMs such as Tamoxifen and Toremifene act by reducing AR gene transcription. But only in certain cell types, such as prostate cells, as stated in this study.
To quote from the study, "These results highlight the anti-androgenic aspect of anti-estrogens and estrogens in regard to the AR-mediated transcription of the relevant genes in prostate cancer."
But thats for prostate cells and cancer cells. Not the AR in muscle.
I think I know where your going with your question and taking SERMs wont boost AR gene-transcription when on cycle, I dont think. The only data I've seen is of the contrary. That they will reduce AR gene-transcription in specific tissues.
Estrogen is needed and aromotasation is responsible for the increase in GH and IGF we get when taking exo. testosterone . I think thats what matters more, not whether SERMs increase or decrease AR gene transcription.
I hope that sheds more light on your question.
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03-26-2010, 02:36 PM #65
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03-26-2010, 02:45 PM #66
Oh, thats where your going...
Well...
Here's something on L-carnitine L-tartrate showing "upregulation of AR content".
Human Performance Laboratory, Department of Kinesiology, University of Connecticut, Storrs, CT 06269-1110, USA. [email protected]
PURPOSE: The purpose of this investigation was to determine the effects of 3 wk of L-carnitine L-tartrate (LCLT) supplementation and post-resistance-exercise (RE) feeding on hormonal and androgen receptor (AR) responses. METHODS: Ten resistance-trained men (mean+/-SD: age, 22+/-1 yr; mass, 86.3+/-15.3 kg; height, 181+/-11 cm) supplemented with LCLT (equivalent to 2 g of L-carnitine per day) or placebo (PL) for 21 d, provided muscle biopsies for AR determinations, then performed two RE protocols: one followed by water intake, and one followed by feeding (8 kcal.kg body mass, consisting of 56% carbohydrate, 16% protein, and 28% fat). RE protocols were randomized and included serial blood draws and a 1-h post-RE biopsy. After a 7-d washout period, subjects crossed over, and all experimental procedures were repeated. RESULTS: LCLT supplementation upregulated (P<0.05) preexercise AR content compared with PL (12.9+/-5.9 vs 11.2+/-4.0 au, respectively). RE increased (P<0.05) AR content compared with pre-RE values in the PL trial only. Post-RE feeding significantly increased AR content compared with baseline and water trials for both LCLT and PL. Serum total testosterone concentrations were suppressed (P<0.05) during feeding trials with respect to corresponding water and pre-RE values. Luteinizing hormone demonstrated subtle, yet significant changes in response to feeding and LCLT. CONCLUSION: In summary, these data demonstrated that: 1) feeding after RE increased AR content, which may result in increased testosterone uptake, and thus enhanced luteinizing hormone secretion via feedback mechanisms; and 2) LCLT supplementation upregulated AR content, which may promote recovery from RE.
Androgenic responses to resistance exercise: effec...[Med Sci Sports Exerc. 2006] - PubMed Result
Hows that?
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04-11-2010, 01:11 AM #67
This deserves a bump for all to read.
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09-15-2010, 07:37 AM #68
Sticky in the PCT section maybe?
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09-15-2010, 08:36 AM #69
Good stuff!
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04-04-2012, 02:15 PM #70
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bump
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04-04-2012, 08:38 PM #71
Thanks for bumping this Dan. Great thread.
Thanks Swifto! As always.
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hi swifto - amazing amount of info, there has been talk on the forums about using a serm to increase test levels for those not wanting to go through AAS, more from a wellbeing viewpoint, of course with the added benefit of increased muscle mass etc.
Its well known the testosterone increases are not as high as an AAS cycle but this isnt the purpose.
can you reccomend a dosage protocol for those wanting to embark upon a serm only cycle, paying attention to coming off cycle , limiting any sides that might be expected. eg higher than normal estrogen levels.
thanks , your posts are always good reading
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bump
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07-07-2012, 01:19 AM #74
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Probably one of the best write-ups I've seen on the net on SERMs. You did an excellent job especially at collecting and interpreting the relevant studies.
Though I would add to it by correcting this minor issue:
I don't know why it is written all over every bodybuilding site about Clomid: that it is estrogenic "in the brain", which is why it increases emotionality at higher doses. The only reason I can think of is the stereotype of estrogen being a "female hormone" (a gross oversimplification of complex biology), and since females are more emotional, well...there. This is just inaccurate.
First off...understand that it is low estrogen in key emotional centers of the brain that causes hyperemotionality in both males and females. High estrogen, in males in particular, is actually associated with emotional detachment and irritability.
All SERMs exert an agonistic effect, strictly speaking, in all parts of the brain as well as body. That's because they are simply weak estrogens. In certain areas the body where estrogen receptors have naturally low exposure to estrogen, SERMs act as agonists, raising overall estrogen signaling. In areas where the ER experiences high natural estrogen exposure, a SERM will compete for the receptor with the numerous estrogen ligands already present, but upon binding exert less estrogenic activity than the natural ligand would have, thereby causing an overall decrease in estrogenic activity in said area. This is how, ironically, weak estrogen agonists can ultimately end up being antagonists.
In the brain in particular, certain areas have high exposure to the enzyme aromatase (and therefore estrogen) and some almost none. Clomid, as you may imagine, would have an antagonistic effect to estrogen signalling in regions of the former category and an agonistic effect to regions of the latter. In the male brain, most areas that control emotion have high aromatase. Because estrogen blunts emotion and reduces MAO activity in these parts of the brain, Clomid thereby increases emotionality. Simple.
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07-07-2012, 06:32 AM #75
This is a brilliant thread, Swifto. I've been saying this stuff for YEARS. For years I have been telling people tha tamoxifen is far more effective at restoring HPTA function than clomid is, and most people shrugged it off not believing me (or the medical studies that demonstrated as such). People kept going around parroting that clomid was far more effective.
As far as I am concerned, clomid is old and outdated. It is useless, TOTALLY useless, as nolvadex and toremifene do everything clomid does, and they do it far better.
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07-07-2012, 05:18 PM #76
Fantastic read and i must say i am back to the drawing board. I will be doing a cycle sometime late this year or next year who knows and through research and questions here people recommend Nolva/Clomid but after reading this im screwed up lol. Anyways i will be reading this thing a few more times so it can sink in and change my future PCT. Swifto you are the man!!!
Keep up the good work!!! Greatly appreciated!!!
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09-21-2012, 03:27 PM #77
Bump
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Love this guy, great write up Swifto!!!!
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09-21-2012, 05:08 PM #79
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09-21-2012, 09:20 PM #80
is there any thread from swifto that is not sticky-worthy?
maybe we should move this to the Educational subforum, where important things like this don't get washed off the first page too quickly.
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