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  1. #1
    1luv's Avatar
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    puffy fat nipple not gyno, but what???

    ok bros ive determined yesterday that i do not have gyno.....but after posting pics members say they think its just water retention or possibly estrgenic fat deposits...now, what can i do?!?!?! i need to get rid of them as quik as possible, and yes im on nolva and ldex ED and b6.....what can i do??

  2. #2
    jmp51483's Avatar
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    Some people say Yohimburn works.. Although I've never tried it.. Might want to give that a shot.

  3. #3
    1luv's Avatar
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    yohimburn? never heard of it? legal? where can i get it, what doses and how much? lol

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    I think im in the same boat as you. Normally they look a little puffy to me but when they get cold it goes away. I think its just loose skin maybe from shrinking after a cycle. Try doing more incline to lift and stretch the skin.

  5. #5
    1luv's Avatar
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    ive been bulking, so its not. how about preperation H??? ive heard that works for stuff like this? what exactly does it do?

  6. #6
    Dally's Avatar
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    shrinks stuff up...

    dont put it on your wang!

    yohimburn .. I dunno... do a google search... I will too.

    if you wanna get rid of fat .. run some clen ... ITS WICKED. I'm on clen and boy oh boy does it work.

    Its totally helpin my teet issue.

    GL

  7. #7
    1luv's Avatar
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    is there anything i can do within the next 7 days??? how about a over the conter diuretic "water-shed" pill?

  8. #8
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    i've had the same problem.. nothign under the nipple but puffy all the time unless the nipple becomes cold.. i noticed from personal experience that as my chest grows it becomes less and less visible. but i'm gonna give preperation H a try.. another suggestions?

  9. #9
    jmp51483's Avatar
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    Do a search :-D Yohimburn.com

  10. #10
    nate da gr8 is offline Associate Member
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    Talking

    Quote Originally Posted by Dally
    shrinks stuff up...

    dont put it on your wang!

    yohimburn .. I dunno... do a google search... I will too.

    if you wanna get rid of fat .. run some clen ... ITS WICKED. I'm on clen and boy oh boy does it work.

    Its totally helpin my teet issue.

    GL
    Teets!

  11. #11
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    ive never heard of preparation h.....does it actually work? and do you just apply it to your nipple? if so how often

  12. #12
    Dally's Avatar
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    Quote Originally Posted by thunder20
    ive never heard of preparation h.....does it actually work? and do you just apply it to your nipple? if so how often

    its for hemmoroids man. It shrinks up the "distended veins from the anus"

    ahahhah

    I'm not reading that off the package or anything .. I just find myself saying that little sentance every now and again.

    It may work!


  13. #13
    1luv's Avatar
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    i tried it last nite and when i woke up my nips seemed to have went down a lil.....ill keep u updated

  14. #14
    MrDezel is offline Banned
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    Well first off I would like to say WELCOME TO MY WORLD OF PUFFY NIPS!

    What is your bf%? Try lowering that and see if it sticks around.

  15. #15
    1luv's Avatar
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    lol, my bf is under 7%...and it seems the prep H worked well....very well...i dunno how long it will last tho

  16. #16
    1luv's Avatar
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    wow....im looking at them now....it worked GREAT!!!! i am going to keep applying like twice a day.....

  17. #17
    MrDezel is offline Banned
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    I think I shall try this preperation H stuff. Does it burn or anything on em?

  18. #18
    1luv's Avatar
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    no...if anything its a tingle....

  19. #19
    1luv's Avatar
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    bump for vets and mods.....how long will the effects of the prep H last? if i stop applying, hjow long after will my nipples become puffy again?

  20. #20
    EastCoaster's Avatar
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    This is interesting

  21. #21
    SAUCYgator is offline Junior Member
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    Quote Originally Posted by 1luv
    bump for vets and mods.....how long will the effects of the prep H last? if i stop applying, hjow long after will my nipples become puffy again?
    bump, im curious as well

  22. #22
    smalldogbigdogbrain is offline Junior Member
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    Man i have never laughed so much.. hahaha.. Hey i hear of people putting it under thier eyes to help out with the bags. BUT< I myself have those darn puffy nips with no gyno, and I think i got it from smoking way too much herb! But now that im on a cycle im trying to stop that bad stuff, and hope like hell the puffy nips go away!

  23. #23
    1luv's Avatar
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    im convinced, it works great dude...im still looking for some serious info on others with experience...i think it was either johnny b, da bull, or pheedno that said somethin about prep h...

  24. #24
    1luv's Avatar
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    bump

  25. #25
    peaker's Avatar
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    Puffy nipple syndrome is the ****en worst!! i had a thread about this awhile back how to make my nips erect all the time so my chest can look good with my shirt on and off!

  26. #26
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    bump how long will prep H keep the nips from being puffy??

  27. #27
    spound's Avatar
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    bump

  28. #28
    EastCoaster's Avatar
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    lol... Still Interesting

  29. #29
    smalldogbigdogbrain is offline Junior Member
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    i have had them most of my life,, its way weird when some freak chick starts sucking on them while your banging. IM thinking B#tch, im not your momma!

  30. #30
    1luv's Avatar
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    **** im really sorry that no one could respond with some knowledge on this matter...not just for me but for everyone else out there having the same problem...i know the prep H has worked for me great...but i dont know how long it will last or what exactly it has done..

  31. #31
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    Hope this helps. Peace

    Posted: Feb 14 2003, 07:34 AM



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    I read a lot of stuff on this board and other boards about Gyno during PH/PS cycles. From what I read the following are some of the more common symptoms to watch out for:

    1. Itchy nipples.
    2. Puffy nipples.
    3. Tender/sensitive/sore nipples.

    I have been doing a 6 week SuperOne/Boldione cycle. I have not had any of the symptoms listed above, but I have some questions about Gyno.

    1. Do you guys worry about Gyno if you are not having any of the symptoms listed above?

    2. Should I do periodic checks even if I do not have any of the symptoms above?

    3. Do any of you guys do periodic checks even if no symptoms are present?

    4. Are there any other symptoms that are not listed above tha I should be worried about? I think I pretty much remembered all of them, but may have forgotten some.

    I have not been doing any periodic checks and I am 5 weeks into my 6 week cycle. The reason I have not done any checks is I have not had any of the symptoms listed above. I'm sure I have nothing to worry about, but I just wanted to see what your answers to my questions would be.



    nightop Posted: Feb 14 2003, 08:31 AM



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    In general, yes, itchy, puffy, and tender/sensative nipples are common symptoms. However, I know individuals who claim to have minor glandular growth despite no symptoms; this is consistent with my current understanding/research, but it still holds that significant gynecomastia development will almost always be accompanied by such symptoms.

    1. Can't really answer your question because I do not use PH/AAS (currently...), but in general, some people are very "gyno-aware" and constantly worry about it, while others do not.

    2. I assume that you mean "periodic checks" as "feeling for gyno" or something along those lines. There is evidence that excessive touch/aggrevation of the nipples and underlying tissue can actually stimulate prolactin response; whether this occurs easily in the average male BB'er or not and whether such would substaintially worsen or proliferate a gyno situation, remains unknown (for now...). If it was me, I would once a day (prolly in the evening before bed), feel for any changes in the nipple area.

    3. [see number 2, and yes some people can't keep their hands off their chest even when there are no symptoms]

    4. That is [essentially] it.

    If you had/have any significant gyno development during your cycle, you will probably already know about it (the attitude of "if you have to ask if you have it or not, you don't..." often holds some truth). While gynecomastia is defined as "development [or growth] of the male breast" (which would involve both glandular/mammary aspects and adipose [fat]), numerous men simply store chest fat quickly/easily and a high alpha-2 density in the area (similiar to the love handle trouble spots) is to be blamed. I myself have a minor propensity for chest fat, and I just want to underline the distinction between gynecomastia and simple (fairy even) fat storage across the chest; some call this pseudo-gyno....

    Some people also read posts such as mine and begin thinking and worrying unnecessarily (sp?) about their chest and begin building the idea that they have gyno in their head/mentaly, when in reality, there is very little or nothing to be concerned with.

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    rhafley Posted: Feb 15 2003, 07:34 AM



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    QUOTE (nightop @ Feb 14 2003, 08:31 AM)
    I know individuals who claim to have minor glandular growth despite no symptoms

    I recently experienced this while on super one+. My nipples have always been "puffy" and I never felt the itching so I wasn't worried. Then I checked it one day and what do you know, I've got gyno. Sucks.

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    nightop Posted: Feb 15 2003, 09:54 AM



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    Yep. This seems to be consistent with a percentage of pubertal cases as well (~13 year olds); growth without symptoms. Another thing is that for people with pre-existing gyno, I think the risk for slow/minor growth w/o symptoms is higher than for people who do not have it to begin with, when using PH/AAS... there are a ton of variables (as with everything), naturally.

    Another thing is that even in individuals not on cycle, who have gyno, there can be a fluctuation (both growth and reduction) without any real symptoms as their diet/nutrition, training, and hormonal profile changes (i.e. during a prolonged bulk or cut, etc.); although I believe substaintial changes to coincide with symptoms (here is an odd one, I know people that claim they've had a stinging or pain sensation that occured as their gyno reduced...).

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    Dio Posted: Feb 15 2003, 10:24 AM



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    QUOTE (nightop @ Feb 15 2003, 09:54 AM)
    Yep. This seems to be consistent with a percentage of pubertal cases as well (~13 year olds); growth without symptoms. Another thing is that for people with pre-existing gyno, I think the risk for slow/minor growth w/o symptoms is higher than for people who do not have it to begin with, when using PH/AAS... there are a ton of variables (as with everything), naturally.

    I've noticed this in the stuff I've come across as well. I think in many of these cases there is either a hormonal imbalance or greater sensitivity to the female sex hormones (greater receptor density?)

    If you look at the successful gyno treatment studies there's always boys/men who rebound after the treatment is over. To me this always implied that those people had a permanent imbalance (in the case of older men, low test/DHT levels) while those that recovered, experienced transitory imbalances.



    nightop Posted: Feb 15 2003, 11:02 AM



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    QUOTE (Dio @ Feb 15 2003, 10:24 AM)
    I've noticed this in the stuff I've come across as well. I think in many of these cases there is either a hormonal imbalance or greater sensitivity to the female sex hormones (greater receptor density?)

    If you look at the successful gyno treatment studies there's always boys/men who rebound after the treatment is over. To me this always implied that those people had a permanent imbalance (in the case of older men, low test/DHT levels) while those that recovered, experienced transitory imbalances.

    There are a ton of possibilities and what makes it hard in regards to researching/concluding things from some of the studies is that a number of them involved people who most likely (when its not mentioned) had other more complicating problems (i.e. 5-AR deficiency, etc... like you said), but the greater receptor density theory is something that I have been trying to nail down, as it would help explain why some people are geneticly more prone to gyno than others with the same serum hormonal profiles.

    I also want to add that I believe a great deal of the rebound in the studies done on people who would more closely resemble a normal/healthy BB'er is significantly due to the mechansims of whatever drug was used. For instance, with SERMs you have a quick receptor upregulation (I believe I have seen the numbers occuring withing a couple of days actually), and over time many things take place (some good, some bad in regards to chances for gyno regrowth/rebound). What I really want to figure out is exactly what mechansims for homeostasis regulate aromatase (and such, in relationship to ER/estrogen activity)... if there is an exploitable weakpoint in the system (lol, starting to sound like Star-Trek here) then a specific drug could be chosen (aromasin is what I have my eye on, have not looked near enough though) that would probably have a much lower rate of rebound.

    I have even seen one study, and I think I linked it on this board a while ago (I can try to find it again if anyone wants) that actually showed a lasting change (for the better) in 1 out of 7 participant's test:estrogen ratios... I believe this was measured at something like 1 year post treatment, but I can think of a few reasons how that could be flawed.

    Here is another study done with DHT administration, which is cool because it has both ER-blocking effects as well as aromatase inhibiting effects (although its more complicated than that and I'm having to learn as I go in my digging, but that is basically what DHT does initially). This study is old and sort of bare-bones so to speak and only has 4 boys undergoing treatment, but its still relevant:

    "1: J Pediatr 1986 Jul;109(1):144-9 Related Articles, Links


    Treatment of persistent pubertal gynecomastia with dihydrotestosterone heptanoate.

    Eberle AJ, Sparrow JT, Keenan BS.

    Four boys with persistent pubertal gynecomastia were given intramuscular dihydrotestosterone heptanoate (DHT-hp) at 2 to 4-week intervals for 16 weeks. By the end of treatment, breast size in all four boys had decreased 67% to 78%. Initial plasma levels of gonadotropins, estradiol, testosterone , and dihydrotestosterone (DHT) were normal. Mean plasma DHT concentration rose with the injections of DHT-hp, and remained elevated throughout the treatment period. Estradiol, LH, FSH, and testosterone decreased during treatment, as did 24-hour urinary LH and FSH. No regrowth of breast tissue was observed 6 to 15 months after treatment, although hormone concentrations had returned to near pretreatment values by 2 months after the last injection. DHT-hp has potential to be an effective medical therapy for persistent pubertal gynecomastia.
    PMID: 3088241 [PubMed - indexed for MEDLINE] "

    BTW- I have been meaning to share some notes/ideas on this with you Dio and ask a few things, will PM you later

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    Dio Posted: Feb 15 2003, 11:36 AM



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    I was also thinking about local aromatase levels as another possibility, but honestly haven't had a chance to look into it.

    As far as avoiding rebound from SERMs, I think an answer might be to switch the mechanism at the end. For example while tapering from nolva, add an aromatase inhibitor at a low-moderate dose and then taper that as well. This would obviously have to occur relatively quickly, or you'd have the same problem all over again.

    I thought the permanent modification in the hormone ratios was from arimidex (I saw the study a while back) and I remember someone on meso-rx talking about using it for that reason (elevating test -- not gyno) and getting some permanent results.

    I've seen that study you posted before. I always thought that pubertal gyno resulted from temporary fluctuations, which is why there's less rebound with it. That study shows that estradiol levels were in the normal range at the beginning of the study.

    I look forward to the idea exchange



    nightop Posted: Feb 15 2003, 12:07 PM



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    QUOTE
    I was also thinking about local aromatase levels as another possibility, but honestly haven't had a chance to look into it.




    That is funny you should mention that because I ran across this yesterday: although, these don't really offer as much info as we need. Also, aside from any specificly abnormal gyno/endocrine aspects, we know that the more adipose tissue you have = the more aromatase production...

    "1: Endokrinologie 1982 Oct;80(2):173-80 Related Articles, Links


    Role of human adipose tissue in the production and metabolism of steroid hormones.

    Feher T, Bodrogi L, Vallent K, Ribai Z.

    Radioimmunological methods have been employed for the simultaneous determination of dehydroepiandrosterone, androstenedione, testosterone, oestrogens (oestradiol + oestrone), progesterone, 17 alpha-hydroxyprogesterone and cortisol in human adipose tissue and peripheral blood to compare the hormone pool of adipose tissue with that in the general circulation. Extremely high steroid concentrations in the adipose tissue and hormone pool in the fat of obese subjects were observed. For adipose tissue/serum steroid ratios, the highest values were obtained for dehydroepiandrosterone and the lowest ones for cortisol. A preliminary study showed a great accumulation of steroids in adjacent adipose tissue of breast tumors. Striking differences were observed in the adipose tissue steroid concentrations between benign and malignant mammary tumors. The present findings revealed that blood hormone determinations may be insufficient to consider the steroid hormone availability in various endocrinopathies or steroid responsive tumors, especially when the endocrine state of extremely obese subjects is observed.

    PMID: 6218984 [PubMed - indexed for MEDLINE] "

    and (this one is a little better)

    " Clin Chim Acta 1982 Dec 9;126(2):135-41 Related Articles, Links


    A comparative study of steroid concentrations in human adipose tissue and the peripheral circulation.

    Feher T, Bodrogi L.

    Using radioimmunological methods, levels of cortisol, dehydroepiandrosterone, androstenedione, testosterone, oestrogens (oestradiol + oestrone), progesterone and 17 alpha-hydroxyprogesterone were determined in adipose tissue and peripheral blood obtained during surgical treatment of patients with non-endocrine diseases. The steroid content of human adipose tissue was observed to be extremely high relative to that in the general circulation, giving a tissue/serum ratio of 0.4 to 13.2. The concentration of steroids decreased in the following order: dehydroepiandrosterone greater than cortisol greater than androstenedione greater than progesterone greater than testosterone greater than 17 alpha-hydroxyprogesterone greater than oestradiol + oestrone. This sequence is different from that found in blood. When anthropometric variables were taken into consideration, the adipose tissue mass of severely obese subjects contained a steroid pool far greater than that in the total blood volume.

    PMID: 6217923 [PubMed - indexed for MEDLINE] "

    QUOTE
    As far as avoiding rebound from SERMs, I think an answer might be to switch the mechanism at the end. For example while tapering from nolva, add an aromatase inhibitor at a low-moderate dose and then taper that as well. This would obviously have to occur relatively quickly, or you'd have the same problem all over again.



    That is a very good idea, I tried this on a short term cycle on myself the first time I used nolvadex (can't really compare it to nolva alone in regards to rebound because it was my first and only time to use it)... I wonder as to whether the primary mechanism for ER regulation is the presence of an antagonist or agonist; OR not. For instance a simpler model would be; "if there are significant blockers present you get ER upregulation, if there are significant agonists present you get ER downregulation, and if there is neither present, do the ERs upregulate because there is no transcription occuring or would they down regulate because nothing is there?" .. theres of course alot more to it than that, but if the later is the case then that would help explain why/how a specific use of aromtase inhibitor post nolva therapy (I would prolly start it right before stopping the nolva rather... thats what I did) would work. I think we've talked about a similiar use for preventing A-2 rebound (such as after a long LD-Y cycle) and have a few windows open right now with search results/studies possibly relevant to that....

    QUOTE
    I thought the permanent modification in the hormone ratios was from arimidex (I saw the study a while back) and I remember someone on meso-rx talking about using it for that reason (elevating test -- not gyno) and getting some permanent results.



    That is pretty cool; I've heard (getting mythical here) that Teslac is noteably capable of this.

    QUOTE
    I've seen that study you posted before. I always thought that pubertal gyno resulted from temporary fluctuations, which is why there's less rebound with it. That study shows that estradiol levels were in the normal range at the beginning of the study.



    Very good point, I have to be careful when extrapolating data from purely pubertal studies. However, in that study, they use the term "persistant" so I don't know if that would mean it would be more applicable or not, we also don't know the age of the subjects (the full text would be nice...), so its sort of shady to begin with. (The andractim related study that I posted on the hung on gyno thread was a different one I believe?)

    QUOTE
    I look forward to the idea exchange




    EDIT: I forgot to ask, do you think it would be necessary to taper the arimidex (or anti-aromatase drug) when using it as discussed to prevent post nolva rebound? I'm thinking that it might not due to the half-life and mechanism of aromtase regulation (this is really where I need to focus my reading on, surely some of these questions can be partially answered with a simple endocrinology text book).

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    Dio Posted: Feb 15 2003, 02:59 PM



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    Those first two studies look interesting. Have you seen the full papers with the hormone breakdowns. I know the second study shows the estrogens to be at the bottom in concentration, which seems odd given what we've been assuming. I ran across something similar when looking at enzymes in adipose tissue.

    QUOTE
    hat is a very good idea, I tried this on a short term cycle on myself the first time I used nolvadex (can't really compare it to nolva alone in regards to rebound because it was my first and only time to use it)... I wonder as to whether the primary mechanism for ER regulation is the presence of an antagonist or agonist; OR not. For instance a simpler model would be; "if there are significant blockers present you get ER upregulation, if there are significant agonists present you get ER downregulation, and if there is neither present, do the ERs upregulate because there is no transcription occuring or would they down regulate because nothing is there?" .. theres of course alot more to it than that, but if the later is the case then that would help explain why/how a specific use of aromtase inhibitor post nolva therapy (I would prolly start it right before stopping the nolva rather... thats what I did) would work. I think we've talked about a similiar use for preventing A-2 rebound (such as after a long LD-Y cycle) and have a few windows open right now with search results/studies possibly relevant to that....


    I'd guess it's the lack of transcription that signals the lack of local estrogen, but there may be other mechanisms. It's worth looking into. Storm, from the Syntrax board, claims that testolactone does not show upregulation of aromatase. I have not been able to find a reference supporting this though. I still think that aromatase upregulation is likely. I agree that some overlap time would be good --- probably some time during the taper. Again you'd have to be careful here because using it too long would result in aroma upregulation and then you'd be right where you started.

    QUOTE
    Very good point, I have to be careful when extrapolating data from purely pubertal studies. However, in that study, they use the term "persistant" so I don't know if that would mean it would be more applicable or not, we also don't know the age of the subjects (the full text would be nice...), so its sort of shady to begin with. (The andractim related study that I posted on the hung on gyno thread was a different one I believe?)


    Actually I think those studies are useful for our purposes since the gyno is probably the result of a temporary stimulus. Kinda like supplementing with exogenous hormones Still, I agree that we need full studies to know for sure.

    QUOTE
    EDIT: I forgot to ask, do you think it would be necessary to taper the arimidex (or anti-aromatase drug) when using it as discussed to prevent post nolva rebound? I'm thinking that it might not due to the half-life and mechanism of aromtase regulation (this is really where I need to focus my reading on, surely some of these questions can be partially answered with a simple endocrinology text book).


    Depends on the length used -- the shorter the better. Half-life would be drug specific, but I'm not aware of any that are really long. I think tapering is probably a good idea in this situation too -- it definitely couldn't hurt.



    nightop Posted: Feb 15 2003, 03:52 PM



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    Too lazy to cut and paste quotes for my reply, each space between what I say corresponds with each point/quote from your reply.

    Haven't seen the full papers yet.

    Interesting, I will add that to my list of stuff to run down (about Storm and teslac).

    And you are right and I know what you mean about pubertal studies in relation to the average BB'er's gyno problems; physiologic cases are in general better than pathologic cases for this reason; I'm just saying that the propsenity for rebound can be different in pubertal cases (dealing with the younger age group) than with grown BB'ers.

    Good point, wouldn't hurt...

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    nightop Posted: Feb 15 2003, 06:10 PM



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    Did a quick HighWire search for teslac and aromatase and found the following:

    "Medline Abstract

    N Itoh, Y Kumamoto, H Maruta, T Tsukamoto, Y Takagi, N Mikuma, A Nanbu, and H Tachiki
    [Therapeutic efficacy of testolactone (aromatase inhibitor) to oligozoospermia with high estradiol/testosterone ratio]
    Nippon Hinyokika Gakkai Zasshi, February 1, 1991; 82(2): 204-9.

    --------------------------------------------------------------------------------

    Department of Urology, Sapporo Medical College.

    To our knowledge, the action of estradiol which is produced from testosterone by aromatase on human spermatogenesis has not been fully clarified. In oligozoospermia, with high values of E2/T ratio, it is considered that the role of estradiol is suppressive to spermatogenesis. In this study, alteration of spermatogenesis was evaluated when serum estradiol levels were decreased by suppression of aromatase activity. Nine male infertile patients were treated with testolactone (Teslac: 1.0 g/day, for 3 months), one of the aromatase inhibitors. Four of them had an increase in sperm count (more than 10 x 10(6)/ml relative to base line). In endocrinological findings, serum estradiol levels and E2/free T ratio were significantly decreased after treatment. Serum free testosterone levels were significantly increased in all cases, presumably from decreased sex hormone binding globulin (SHBG) levels. These findings suggested the effectiveness of the administrated aromatase inhibitor. In particular four patients whose sperm counts were improved after testolactone treatment had high values of basal serum estradiol levels and E2/free T ratio before treatment, and these values were normalized after treatment. In conclusion we suggest that an aromatase inhibitor may be effective to male infertile patients with high serum estradiol levels."

    really wish I could get the full text on that one.

    Although this seems to tell a different story...

    "Medline Abstract


    RV Clark and RJ Sherins
    Treatment of men with idiopathic oligozoospermic infertility using the aromatase inhibitor, testolactone. Results of a double-blinded, randomized, placebo-controlled trial with crossover.
    J Androl, May 1, 1989; 10(3): 240-7.

    --------------------------------------------------------------------------------

    Section of Internal Medicine, Emory University Clinic, Atlanta, Georgia 30322.

    The hypothesis that increased estradiol production may be the cause of impaired spermatogenesis in infertile men with idiopathic oligozoospermia was tested by administering the aromatase inhibitor, testolactone, and by assessing its effects on sperm output and fertility. Our study was a randomized, placebo-controlled double-blind crossover trial. Subjects (n = 25) with infertility due to unexplained oligozoospermia were given testolactone (2 g/day) or placebo for 8 months followed by crossover to the other treatment for an additional 8 months. Total estradiol and testosterone levels during testolactone exposure did not change from basal and placebo values. However, sex hormone-binding globulin binding capacity consistently decreased (30%, p less than 0.01) and free testosterone levels increased (36%, p less than 0.01). Free estradiol values increased but not significantly. Additionally, LH and FSH serum levels increased by 15% and 20%, respectively (p less than 0.05), and 17 alpha-hydroxyprogesterone values increased by 90% (p less than 0.05) during drug administration. Sperm output and semen quality remained unchanged during either testolactone or placebo treatment, and no pregnancies occurred during the 16-month study. These data suggest that chronic administration of testolactone at this dose fails to maintain aromatase inhibition despite depression of 17,20-desmolase activity with elevated 17 alpha-hydroxyprogesterone and depressed SHBG binding capacity with elevation of free testosterone. Testolactone is not efficacious in the treatment of idiopathic oligozoospermic infertility."

  32. #32
    barbarian's Avatar
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    good post bro..but oh so very long lol

  33. #33
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    ok maybe i jsut need it in plain english but how long will the effects of prep H last, are they just temporary in reducing the puffiness of the nipple??

  34. #34
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    Bro, this explains that what you are experiencing is a precursor to gyno. I read a lot of stuff on this board and other boards about Gyno during PH/PS cycles. From what I read the following are some of the more common symptoms to watch out for:

    1. Itchy nipples.
    2. Puffy nipples.
    3. Tender/sensitive/sore nipples.

  35. #35
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    i'm on 20mg of nolva and .5mg ldex everyday during my current cycle.. the puffiness i have currently was from gyno during puberty so i was wondering whether the prep H will work for that or not.

  36. #36
    ripped525 is offline Junior Member
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    i have puffy nipples with a lil extra soft fat between them and my rock hard pecs...haha.....i was thinkin of platis surgery any other suggestions

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    bumpage from hell

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    jojo2002 is offline Associate Member
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    mod vet some one.... bumb for info on how long to run prep h.

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    jojo2002 is offline Associate Member
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    bump

  40. #40
    vitor is offline Anabolic Member
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    The effect of Prep h will only be temporary ofcourse.

    The puffy nipple syndrom can be b/c of, glanduar tissue under the nipple, estrogenic fat, loose skin around the nipple/aroela area.

    I would look into to plastic surgery if you have any of the problems above, nothing else will cure it imo.

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