is this true about Tren?

[heavyiron]

Complete agreement on bloodwork. A few questions in regards to the study if I may:

1) do you have full access or just the abstract? I ask bc it says a 140mg implantation which sounds like a 1-time dose to me. Does extended dosing patterns affect the results (prolactin specifically) differently? Also I believe most of us would take a higher dose than 140mg/wk so is it dose dependent on when prolactin starts to rise (like a minimum effective dose but to raise prolactin)? Also I'd love to see the methodology and design of the study

2) in regards to AAS, there's not much difference between an IM injection and a Sub-Q injection right? The study was done with sub-q.

3) how is the endocrine system of a sheep similar and different than in humans? Could this have something to do with prolactin failing to change?

I have not read the full study so no idea on the methodology. These were likely pellet implants as that was/is common with farm animals.

SubC likely has a bit slower onset of action but in the end its pretty similar to IM as far as effect.

Your 3rd question is the bottom line. That's why we both want these guys to get labs and see for themselves. I have asked guys to do this in the past and they had completely normal Prolactin and Progesterone levels. I also have seen labs on guys off steroids with high Prolactin. So labs before you medicate with ancillaries is my mantra. =)

 

[juced_porkchop]

Prolactin is what induces lactation not "gyno". Gyno is ductal hyperplasia which is caused by estrogen or estrogen dominance in relation to progesterone and the ducts are what Hold the milk. Progesterone can be a factor but not the root cause. Too much progesterone will cause alveolar hyperplasia and the alveoli secrete the milk. Progesterone is one thing that can help "tip" the scales to the onset of gyno but so are GH and IGF-1. Without these precursors in minimal quantities gyno is very unlikely to happen. Prolactin serum levels are raised by 19-noes such as tren and prolactin is what causes milk to start forming/secreting from the breast. Caber and prami are dopamine agonists which will reduce prolactin and lactation but will not do much for estrogen or progesterone if at all.

it dose induce gyno AND lactation and estrogen will induce gyno . both will grow the glands but pro is the main factor in the milk production.
IGF1 and gh may play a related role but it DOES NOT CAUSE gyno.

its like saying gh causes cancer... no it doesn't.. but if you have cancer it will come into play as a factor.

 

[juced_porkchop]

I have not read the full study so no idea on the methodology. These were likely pellet implants as that was/is common with farm animals.

SubC likely has a bit slower onset of action but in the end its pretty similar to IM as far as effect.

Your 3rd question is the bottom line. That's why we both want these guys to get labs and see for themselves. I have asked guys to do this in the past and they had completely normal Prolactin and Progesterone levels. I also have seen labs on guys off steroids with high Prolactin. So labs before you medicate with ancillaries is my mantra. =)

YEP!

blood work before or you DON'T really know what your levels are for your norm or what is or is not working!
BUT I can tell you rui's prami is GTG (got bottle now) as are the other compounds I have researched from them before.

 

[JimiThing]

There is more misinformation in this sibgle thread about tren, orami, progesterone and prolactin than I have seen in a long time. I dont know how you guys deal with idiots posting stff like this and saying a product is bad. Obviously there is much ignorance in this thread.
Get bloodwork before shotgunning and changing things. Oh and also before you use some bro scriene bs speculation Id get my facts staright before saying a sponsirs product is bad. Do you have any idea how stupid this whole thread is ?

 

[juced_porkchop]

so will i be ok just using the letro and b6 if prami is bunk or should get another prami

personally i feel like you should stop and do alot of research before you do this again.

how many cycles have you done? whats your stats?



ps. run letro at around 0.6mg eod.. dont go crazy on dose it will take a couple weeks to notice change in letro dose... letro/ Aromatase inhibitor (AI) is enough for me. i have prami on hand now just to be save.
but i also dont get "deca dick" and am just as horny... not everyone is the same.

 

[DreDay187]

it dose induce gyno AND lactation and estrogen will induce gyno . both will grow the glands but pro is the main factor in the milk production.
IGF1 and gh may play a related role but it DOES NOT CAUSE gyno.

its like saying gh causes cancer... no it doesn't.. but if you have cancer it will come into play as a factor.

View attachment 551836

Prolactin is another anterior pituitary hormone integral to breast development. Prolactin is not only secreted by the pituitary gland but may be produced in normal mammary tissue epithelial cells and breast tumors (40, 68). Prolactin stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobulo-alveolar differentiation only with concomitant progesterone.

http://www.endotext.org/male/male14/male14.pdf


View attachment 551837

^^^^high prolactin is hyperprolactinemia.


Hyperprolactinemia

CLINICAL MANIFESTATIONS OF HYPERPROLACTINEMIA

The symptoms associated with hyperprolactinemia may be due to several factors: the direct effects of excess prolactin, such as the induction of galactorrhea or hypogonadism; the effects of the structural lesion causing the disorder (i.e. the pituitary tumor), leading to, for example, headaches, visual field defects, or external ophthalmoplegia; or associated dysfunction of secretion of other anterior pituitary hormones.

The incidence of galactorrhea in hyperprolactinemic patients is between 30% and 80%, depending on the skill of the examiner and the degree of estrogen deficiency. Approximately 50% of women with galactorrhea, however, have normal prolactin and, as mentioned below, it is particularly those patients with very high prolactin levels, i.e. greater than 100ng/mL (2000mU/L), who often have no galactorrhea - thus, it is a poor marker of hyperprolactinemia. Normal prolactin levels are below 18ng/mL (360mU/L).

Women with hyperprolactinemia usually present with menstrual abnormalities - amenorrhea or oligomenorrhea - or regular cycles with infertility. Occasionally, patients may present with menorrhagia. Menstrual disorders are often not seen with mild hyperprolactinemia but it is unusual for there to be no menstrual problems if the prolactin is greater than 180 ng/l (3,600 mU/L).

In contrast, men often present late in the course of the disease with symptoms of expansion of their pituitary tumor (i.e. headaches, visual defects, and external ophthalmoplegia) or symptoms from secondary adrenal or thyroid failure. These men, however, have usually been impotent for many years before their presentation. Because the disease is occult for many years men present late in the course of their disease and thus in contrast to women where microprolactinomas are most commonly seen, macroprolactinomas in men are usually found and the serum prolactin levels are usually much higher than those in women.

Occasionally, the syndrome may occur in prepubertal or peripubertal children, when it may present with delayed or arrested puberty or with headache and/or visual field defects or with growth arrest. Children and adolescents often present with aggressive prolactinomas, perhaps reflecting a different mechanism(s) of tumorigenesis rather than disease duration; it should not be forgotten that the rate of cell proliferation at this stage of the life cycle is greater.

Chapter*6.*Hyperprolactinemia

Hyperprolactinemia is not believed to play a direct role in gynecomastia, although pro- lactin receptors have recently been demon- strated in gynecomastia tissue.8 Most patients with gynecomastia have normal serum pro- lactin levels.9 Moreover, not all patients with hyperprolactinemia have gynecomastia. Elevated prolactin levels may, however, sup- press gonadotropin release, producing sec- ondary hypogonadism, which then contributes to the development of gynecomastia.

http://www.ccjm.org/content/71/6/511.full.pdf

^^^if prolactin does play a role in gyno, it is an EXTREMELY INDIRECT role and should not be considered a CAUSE for gyno.

DRUGS
A significant percentage of gynecomastia is caused by medications or exogenous chemicals that result in increased estrogen effect. This may occur by several mechanisms: 1) they possess intrinsic estrogen- like properties, 2) they increase endogenous estrogen production, or 3) they supply an excess of an estrogen precursor (e.g. testosterone or androstenedione) which can be aromatized to estrogen.

LABORATORY EVALUATION
All patients who present with gynecomastia should have serum testosterone, estradiol, LH and HCG measured (Fig 2). Further testing should be tailored according to the history, physical examination and the results of these initial tests. An elevated HCG or a markedly elevated serum estradiol suggests neoplasm and a testicular ultrasound is warranted to identify a testicular tumor, keeping in mind, however, other non-testicular tumors can also secrete HCG. A low testosterone level, with an elevated LH and normal to high estrogen level indicates primary hypogonadism. If the history suggests Klinefelter's Syndrome, then a karyotype should be performed for definitive diagnosis. Low testosterone, low LH and normal estradiol levels imply secondary hypogonadism, and hypothalamic or pituitary causes should be sought. If testosterone, LH and estradiol levels are all elevated, then the diagnosis of androgen resistance should be entertained. Liver, kidney and thyroid function should be assessed if the physical examination suggests liver failure, kidney failure, or hyperthyroidism, respectively. Furthermore, if examination of breast tissue suggests malignancy, a biopsy should be performed. This is of particular importance in patients with Klinefelter's syndrome, who have an increased risk of breast cancer. On the other hand, if the examination finding is compatible with breast abscess, then fine needle aspiration for microscopy, acid-fast bacilli and culture is warranted (37

http://www.endotext.org/male/male14/male14.pdf

^^^no mention of prolactin causing drug induced gyno. It's about estrogens. The laboratory evaluations don't even really check for "prolactin induced" gyno.

In summary, gynecomastia is a relatively common disorder. The causes of its development range vastly from benign physiologic processes to rare neoplasms. Thus, in order to properly diagnose the etiology of the gynecomastia, the clinician must understand the hormonal factors involved in breast development. Parallel to female breast development, estrogen, along with GH and IGF-1 is required for breast growth in males. Since a balance exists between estrogen and androgens in males, any disease state or medication that can increase circulating estrogen or decrease circulating androgen, causing an elevation in the estrogen to androgen ratio, can induce gynecomastia.

http://www.endotext.org/male/male14/male14.pdf

^^^^ I never said GH or IGF-1 CAUSED gyno. I said they were necessary CONCOMITANT factors. You cannot develop gyno in the absence of GH or IGF-1 and sudden/extreme changes in serum concentration of them along with other factors can certainly increase the likelihood of developing gyno.

I would like to see your thoughts and JimiThing's on this and will have an open mind for sure, I definitely respect you both. You're a great mods and valuable sources of information but unless there's something I overlooked in that wall of text lol or something else you can point me to, I stand behind my statements .

 

[Dreaded Pirate Roberts]

Yes men baring milk. true if allowed to get to the point

 

[DreDay187]

I'm also trying to find the link and quote where I read the following:

In ~15-25% of cases of gynecomastia, there is no medical explanation for the root cause. Methodology and studies performed up to this point have FAILED to find a root cause for the onset of gyno. That's with prolactin being investigated.

^^^^im not trying to use this as evidence bc as I said I can't find the link and quote to reference myself but it could be helpful in understanding why some cases of gyno are just unexplainable, Regardless of epidemiology. Maybe prolactin could be a cause but where we are now, it has not been shown with the technology available and therefor one cannot say prolactin causes gyno; a cause and effect relationship HAS NOT BEEN SHOWN in all the medical literature I've researched. If anyone has any tips on where to look, I'd be interested in some leads.

 

[tkasch30]

wow im more confused after reading these threads. i dont know what to think. you can tell me im stupid for not doing research but i have and everyone tells you something different just like this

 

[juced_porkchop]

wow im more confused after reading these threads. i dont know what to think. you can tell me im stupid for not doing research but i have and everyone tells you something different just like this

point is with or without prami you can get gyno while on cycle! worse if you let prog build and have high estrogen yes, but the issue can be there even if you take a tone of prami. but NOT taking prami with this issues is not optimal.

also just because we dont know every mechanism for each hormone doesn't mean the effect is not there! I know from personal exp prog and E IS related to gyno. but I would worry more about my Aromatase inhibitor (AI) then my prami on cycle.
You have no experience with this and I feel you think its bunk. but it is not, I have used it, got some here now AND I have used RUI for years with out ANY quality issue.

 

[juced_porkchop]

View attachment 551836



http://www.endotext.org/male/male14/male14.pdf


View attachment 551837

^^^^high prolactin is hyperprolactinemia.


Hyperprolactinemia

Chapter*6.*Hyperprolactinemia

Hyperprolactinemia is not believed to play a direct role in gynecomastia, although pro- lactin receptors have recently been demon- strated in gynecomastia tissue.8 Most patients with gynecomastia have normal serum pro- lactin levels.9 Moreover, not all patients with hyperprolactinemia have gynecomastia. Elevated prolactin levels may, however, sup- press gonadotropin release, producing sec- ondary hypogonadism, which then contributes to the development of gynecomastia.

http://www.ccjm.org/content/71/6/511.full.pdf

^^^if prolactin does play a role in gyno, it is an EXTREMELY INDIRECT role and should not be considered a CAUSE for gyno.




http://www.endotext.org/male/male14/male14.pdf

^^^no mention of prolactin causing drug induced gyno. It's about estrogens. The laboratory evaluations don't even really check for "prolactin induced" gyno.




http://www.endotext.org/male/male14/male14.pdf

^^^^ I never said GH or IGF-1 CAUSED gyno. I said they were necessary CONCOMITANT factors. You cannot develop gyno in the absence of GH or IGF-1 and sudden/extreme changes in serum concentration of them along with other factors can certainly increase the likelihood of developing gyno.

I would like to see your thoughts and JimiThing's on this and will have an open mind for sure, I definitely respect you both. You're a great mods and valuable sources of information but unless there's something I overlooked in that wall of text lol or something else you can point me to, I stand behind my statements .

"not belived to play a direct role"

I never said its the ONLY role but it play a roel and I have NEVER leaked from nipple while on aas that was not prog based, but i HAVE with prog based !
it play a role, it should be controlled if you have issues, that is my point.

an Aromatase inhibitor (AI) and prami is the way to go, I NEVEr said just prami. but prami does play a role and will help in most cases. also for your Hyperprolactinemia argument, it doesn't translate well. they are not on aas, they dont have other high estrogen's being an issue, they don't have ALTERED FORMS OF prog ( deca for eg.) running through there veins... I see your point but i do not fully agree with you.

 

[juced_porkchop]

Well, you usually dont lactate until you have full blown gyno. If you feel the need to let it go untreated, i'm sure you will lactate eventually

not true i caught mine early when i was new and fixed it, but it was not full blown glands, just starting, and liquid was coming...

 

[juced_porkchop]

really? so should i stick with just letro? suggestions please

letro 0.25mg- 0.6mg eod till post cycle therapy (pct) is what I use but it can differ.

 

[juced_porkchop]

from your other thread:
"i di did one cycle of test c 500mg a week and got gyno. i knew i was prone because i got it before i ever used gear. i took .5mg adex from the pharmacy everyday and still got it."

link: http://www.steroidology.com/forum/anabolic-steroid-forum/647880-all-my-gear-garbage.html


you should have gotten blood work long ago and before cycle.... your bashing a product I know and love, when you have used pharm grade and STILL had issues..... nuff said..

Sorry but I am a bit irritated by this thread...