A Thread Devoted To Gynecomastia

[Sworder]

Trazodone treatment increases plasma prolactin concentrations in depressed patients.
Trazodone treatment increases plasma prolactin concentrations in depressed patients. - Abstract - UK PubMed Central
m-Chlorophenylpiperazine (m-CPP), which is a metabolite of trazodone, is a serotonin agonist. To examine for the possibility that m-CPP is involved in biochemical effects during treatment with the parent compound, prolactin response to trazodone treatment (150 mg at bedtime for 3 weeks) was studied in 12 depressed patients. The means +/- S.D. of plasma prolactin concentrations before treatment, 12 h, and 1, 2 and 3 weeks after initiation of treatment were 9.1 +/- 5.6, 14.7 +/- 9.1, 15.3 +/- 8.5, 13.2 +/- 7.0 and 13.0 +/- 7.0 ng/ml, respectively. The mean prolactin concentrations at 12 h (p < 0.01), 1 week (p < 0.001) and 2 weeks (p < 0.05) were significantly higher than that before treatment. The present study thus shows that trazodone treatment increases prolactin concentrations, suggesting that m-CPP is involved in biochemical effects during treatment with the parent compound.

 

[Sworder]

Breast development and breast milk production are two different things, yet cross paths clearly. I have not doubt that estogen is essential for breast tissue development, as well as prolactin to what ever degree, but the prolactin has to rise to make the milk.. So this is my logic that prolactin is in play when gyno QUICKLY FLARES. Tissue development is not an ovenight game. Quick changes are usually associated with inflection/temp related inflammation, or cancer (as abnormal growth rate which is still much slower that gyno stocking with fluid in a week). This is not to say that general rises in estrogen can not create general inflammation site specific unclear. But This is why I go with prolactin with I apply a drug/stimulus, and get gyno activity. You can also clearly feel the difference is not a new growth, the the expansion of the previously "deflated" breast type Gland or duct. Again I lean toward prolactin.

You further point out YOUR BB. The reason exactly your BB is not at bay is because you are using an AI, which inhibits estrogen activity. Your BB is probably again Prolactin related which in that case the only way to stop is Caber, Bromo, or remove the Trazadone. One stop short of the Caber would be a SERM. This can help as it will block estrogen at the breast tissue effectively, and thus inhibit prolactin activity somewhat. Further, I dont believe in AIs, as while the cut down circulating estrogen, who is to say that the end tissues are not getting every bit as much estrogen as they want.? Also who is to say that perhaps it may ENCOURAGE them to cling on to the estrogens that the are interacting with currently whilst they further cannibalize into E3 and become a carcinogen its self.

Just thoughts.

I agree completely. Although the BB remains and so does my elevated e2. I am on 1mg Caber/week and also as soon as a BB flares I frontload 120mg Nolvadex and continue 20mg/day as well as adjusting my AI(letrozole) dose. Recently ran out of my letrozole and had to use arimidex meanwhile. That bottle got used up quickly and luckily I got some more letro today. Gonna blast some letrozole as I am off cycle so once I get my e2 down to a certain point I am should be able to discontinue use. I usually tell overnight, I wake up the next morning looking pretty lean and ripped.

 

[Michael Scally MD]

Alesini D, Iacovelli R, Palazzo A, et al. Multimodality Treatment of Gynecomastia in Patients Receiving Antiandrogen Therapy for Prostate Cancer in the Era of Abiraterone Acetate and New Antiandrogen Molecules. Oncology 2012;84(2):92-9. Multimodality Treatment of Gynecomastia in Patients Receiving Antiandrogen Therapy for Prostate Cancer in the Era of Abiraterone Acetate and New Antiandrogen Molecules

Gynecomastia is a pathological enlargement of male breasts due to hormonal imbalance and elevation of estrogens at the expense of testosterone. It is very important to diagnose this disease precociously because it can be the expression of different underlying pathologies. Besides genetic, chromosomal or chronic diseases, drugs often represent the principal cause of this hormonal disequilibrium. In the elderly population, antiandrogen therapy for prostate cancer frequently induces gynecomastia, thus negatively affecting the patients' compliance to treatment because of physical and psychological discomfort deriving from this condition; gynecomastia can in fact be associated with severe breast pain, and it can modify how patients see their own body. During the past decades and even today, many different surgical, radiotherapeutic or clinical approaches have been proposed to prevent or treat this hypertrophy. This article focuses on gynecomastia associated with antiandrogen-based hormonal treatment and shortly reviews the currently most often used therapeutic options for preventing and treating this pathology.

 

[BBC3]

This is a good post. And it again highlights in my mind the importance of this thread. Your post rings relevance AS if it takes a lifetime to develop a hormone based disease like PC, and then of course we see the side effects of the current medication well thats not nice. But when you consider that Hormone modulation/deprivation is a common current treatment for hormone based disease, then it drives home - What about the other diseases that are hormone driven and even estrogen based as a primary(perhaps and jury not in of course), then what are you doing to your other systems with the SAME excess estrogen that potentially merits the existance of this thread! One of the points of my discussion here, was that estrogen driven Gyno in males is NOT an overnight occurrence. It is years in the development and on cellular levels not necessarily physically detectible by normal senses in action. Further, my concern was that body buiding or TRT related Gyno which can potentially develop in many cases whereas OTHERWISE it would have taken another 40 years to get to that stage. So what if prostate disease IS indeed as directly related to excess or cumulative estrogen exposure just the same as gyno development is?! So, if potentially you just juiced yourself to gyno that you would not have had otherwise till 70, Then what could you possibly be doing to your prostate?!!?!?!? Marveling redundancy technique indeed.. LOL

Alesini D, Iacovelli R, Palazzo A, et al. Multimodality Treatment of Gynecomastia in Patients Receiving Antiandrogen Therapy for Prostate Cancer in the Era of Abiraterone Acetate and New Antiandrogen Molecules. Oncology 2012;84(2):92-9. Multimodality Treatment of Gynecomastia in Patients Receiving Antiandrogen Therapy for Prostate Cancer in the Era of Abiraterone Acetate and New Antiandrogen Molecules

Gynecomastia is a pathological enlargement of male breasts due to hormonal imbalance and elevation of estrogens at the expense of testosterone. It is very important to diagnose this disease precociously because it can be the expression of different underlying pathologies. Besides genetic, chromosomal or chronic diseases, drugs often represent the principal cause of this hormonal disequilibrium. In the elderly population, antiandrogen therapy for prostate cancer frequently induces gynecomastia, thus negatively affecting the patients' compliance to treatment because of physical and psychological discomfort deriving from this condition; gynecomastia can in fact be associated with severe breast pain, and it can modify how patients see their own body. During the past decades and even today, many different surgical, radiotherapeutic or clinical approaches have been proposed to prevent or treat this hypertrophy. This article focuses on gynecomastia associated with antiandrogen-based hormonal treatment and shortly reviews the currently most often used therapeutic options for preventing and treating this pathology.

 

[Michael Scally MD]

Physiopathology Of Gynecomastia

Gynecomastia derives from an alteration of the normal ratio of estrogens and testosterone, with a pathological imbalance on behalf of the former ones; this increases the peripheral conversion of circulating androstenedione (most of all by the aromatases of the adipose tissue) to estrone, which is in turn transformed into estradiol, the hormone responsible for glandular hypertrophy. The imbalance between estrogens and testosterone also provokes a reduction in the normal inhibiting feedback carried out by the latter on the hypothalamus and mammary glands. In fact, this hormone physiologically induces a blockade of hypothalamic LHRH release and a reduction in glandular duct proliferation. Therefore, the reduction in testosterone-circulating levels overloads the alterations due to the associated hyperestrogenism.

 

[Michael Scally MD]

Akgul S, Kanbur N, Gucer S, Safak T, Derman O. The histopathological effects of tamoxifen in the treatment of pubertal gynecomastia. J Pediatr Endocrinol Metab 2012;25(7-8):753-5. The histopathological effects of tamoxifen in the treatment of pubertal gynecomastia

Pubertal gynecomastia is the glandular proliferation of male breast tissue. It is regarded as a physiological phenomenon, arising due to a presumed transient imbalance in the ratio of free androgen to free estrogen. Treatment with tamoxifen, a selective estrogen receptor blocker, has been shown to effectively reduce the disc size and is generally considered for treatment when the disc diameter is > 3-4 cm. For severe or persistent cases, surgery is considered the mainstay of treatment. We present three cases who reported dissatisfaction with the results of tamoxifen treatment and were therefore submitted to adenectomy by Webster's technique preceded by liposuction. Pathology results showed adipose tissue alone, with no evidence of intraductal epithelial proliferation. The results showing a lack of residual glandular breast tissue after treatment using tamoxifen proves that it is effective in histopathologically eliminating pubertal gynecomastia.

 

[BBC3]

This is good in that it is more of a HIGH GRADE RIDDLE worth of being uttered by the Batman Character.... It is in line for the microscope and translator.. With special note to the inclusion of the chart presented...

Physiopathology Of Gynecomastia

Gynecomastia derives from an alteration of the normal ratio of estrogens and testosterone, with a pathological imbalance on behalf of the former ones; this increases the peripheral conversion of circulating androstenedione (most of all by the aromatases of the adipose tissue) to estrone, which is in turn transformed into estradiol, the hormone responsible for glandular hypertrophy. The imbalance between estrogens and testosterone also provokes a reduction in the normal inhibiting feedback carried out by the latter on the hypothalamus and mammary glands. In fact, this hormone physiologically induces a blockade of hypothalamic LHRH release and a reduction in glandular duct proliferation. Therefore, the reduction in testosterone-circulating levels overloads the alterations due to the associated hyperestrogenism.

 

[BBC3]

So they get $225 for this Volume Issue? I wonder do they provide the DETAILS of the actual STUDY they are discussing in these things, and as LAB DATA and proceedure, or just their own presented qualifications for what is worthy. What kind of a fundamental dance would this be if medical science were charging (a) one group to conduct test/gather data, (b) another group to analyze sight UNSEEN, (c) and the third group being the ones who publish and attempt to DEFINE/INFLUENCE standards based on their own statistical light show... I wonder.. IS this my own lack of understanding, or the epitome of failure of a system in fundamental paradigm as an end product of hyperfocus, groupthink, and a massive series of wrong turns!?. It really almost challenges a full analysis of the fundamentals of the publication - just to be sure mind ya... How we love the sound of our own horns once self-adorned for just a momentary gleem..

So here is what I intially gather...:

But can I assume the the INFAMOUS "BB" has a technical name? And that it is DISK...? Cause I kinda like the sound of "BB" better... Perhaps Bro Science and Medical Science should collide for just a moment. Give us one, and maybe we will let YOU go... LOL

Akgul S, Kanbur N, Gucer S, Safak T, Derman O. The histopathological effects of tamoxifen in the treatment of pubertal gynecomastia. J Pediatr Endocrinol Metab 2012;25(7-8):753-5. The histopathological effects of tamoxifen in the treatment of pubertal gynecomastia

Pubertal gynecomastia is the glandular proliferation of male breast tissue. It is regarded as a physiological phenomenon, arising due to a presumed transient imbalance in the ratio of free androgen to free estrogen. Treatment with tamoxifen, a selective estrogen receptor blocker, has been shown to effectively reduce the disc size and is generally considered for treatment when the disc diameter is > 3-4 cm. For severe or persistent cases, surgery is considered the mainstay of treatment. We present three cases who reported dissatisfaction with the results of tamoxifen treatment and were therefore submitted to adenectomy by Webster's technique preceded by liposuction. Pathology results showed adipose tissue alone, with no evidence of intraductal epithelial proliferation. The results showing a lack of residual glandular breast tissue after treatment using tamoxifen proves that it is effective in histopathologically eliminating pubertal gynecomastia.

 

[Michael Scally MD]

Li C-C, Fu J-P, Chang S-C, Chen T-M, Chen S-G. Surgical Treatment of Gynecomastia: Complications and Outcomes. Annals of Plastic Surgery 2012;69(5):510-5. Surgical Treatment of Gynecomastia: Complications and Outcom... : Annals of Plastic Surgery

Gynecomastia is defined as the benign enlargement of the male breast. Multiple surgical options have been used to improve outcomes. The aim of this study was to analyze the surgical approaches to the treatment of gynecomastia and their outcomes over a 10-year period. All patients undergoing surgical correction of gynecomastia in our department between 2000 and 2010 were included for retrospective evaluation. The data were analyzed for etiology, stage of gynecomastia, surgical technique, complications, risk factors, and revision rate. The surgical result was evaluated with self-assessment questionnaires. A total of 41 patients with 75 operations were included. Techniques included subcutaneous mastectomy alone or with additional ultrasound-assisted liposuction (UAL) and isolated UAL. The surgical revision rate for all patients was 4.8%. The skin-sparing procedure gave good surgical results in grade IIb and grade III gynecomastia with low revision and complication rates. The self-assessment report revealed a good level of overall satisfaction and improvement in self-confidence (average scores 9.4 and 9.2, respectively, on a 10-point scale). The treatment of gynecomastia requires an individualized approach. Subcutaneous mastectomy combined with UAL could be used as the first choice for surgical treatment of grade II and III gynecomastia.

 

[Michael Scally MD]

Kasielska A, Antoszewski B. Surgical Management of Gynecomastia: An Outcome Analysis. Ann Plast Surg. Surgical Management of Gynecomastia: An Outcome Analysis : Annals of Plastic Surgery

BACKGROUND: The aim of the study was to evaluate the surgical management of gynecomastia focusing on techniques, complications, and aesthetic results. The authors also proposed an evaluation scale of the cosmetic results after the treatment.

METHODS: We conducted a retrospective analysis of 113 patients undergoing the surgery for gynecomastia in our department. Preoperative clinical evaluation included the grade of gynecomastia, its etiology, and side, whereas postoperative analysis concerned histologic findings, complications, and cosmetic results.

RESULTS: Operative techniques included subcutaneous mastectomy through circumareolar approach in 94 patients, subcutaneous mastectomy with skin excision in 9 patients, inverted-T reduction mastopexy with nipple-areola complex (NAC) transposition in 6 subjects, and breast amputation through inframammary fold approach with free transplantation of NAC in 4 cases. Complications occurred in a total of 25 patients and did not differ statistically within Simon stages.

CONCLUSIONS: The operative technique appeared to be the crucial determinant of good aesthetic outcome. The postoperative result of shape and symmetry of the NAC was not as satisfactory as postoperative breast size and symmetry. We showed that subcutaneous mastectomy using a circumareolar incision without additional liposuction provides a good or very good aesthetic outcome in patients with Simon grades I to IIa gynecomastia and that it is challenging to achieve a very good or even a good aesthetic outcome in patients with Simon grades IIb to III gynecomastia.

 

[Michael Scally MD]

Unilateral Gynecomastia In A Tennis Player

We report on a 26-year-old male patient who was a tennis player and developed unilateral breast enlargement after puberty. He began to notice unilateral breast enlargement by the age of 18, and underwent surgery at the age of 26 because there was no spontaneous regression. He had no known familial history or medication history such as anabolic steroid use. There was no discharge from the nipples, tenderness or pain in the nipple-areolar complex.

He was a professional tennis player for more than 10 years. His body mass index (BMI) was 21.9 kg/m2, which was in normal range. Anamnestic information on breast enlargement was elicited from the patient and the age of notable breast enlargement, age of maximal breast enlargement, and breast size changes after playing tennis were noted.

Using Simon’s classification, with division into four grades, grade IIA gynecomastia of the right breast was noted. Endocrinal function tests were within normal hormonal range. He underwent subcutaneous mastectomy under general anesthesia. Through the periareolar incision, glandular tissue was removed by meticulous dissection.


Kang SG, Song WJ, Kim CH, Kim JW, Tark MS. Unilateral gynecomastia in a tennis player. Arch Plast Surg 2012;39(6):675-8. http://e-aps.org/Synapse/Data/PDFData/2023APS/aps-39-675.pdf

 

[BBC3]

More than likely in these days he used steroids, but wont admit. Even so, it should be clearly noted that the sport of tennis utilizes ONLY one Pectoral muscle (unless he is playing a retarded Jimmy Connors two handed backhand - LOL). SO... It would speak volumes to know whether he was a right handed or left handed player. My money would be that it developed in the pec on the side he used if onset at the end of his really active career. But knowing the incideous TRUE SLOW nature of development like gyno, I am wagering it occurred for him in the side he does not use for tennis...

Again reading the primer, I see it started at 18. Therefore it would be even more interesting if occurring in the active side. This case could speak volumes about both genetics as well as hormone disposition throughout the body as a unilateral and/or BILATERAL association of duplicity by biology as:
1. If occurring in the side he does not use, it begs the question;
a) Is there a "bilateral call" for hormones as a basic essential by the body's wiring inherent". SO did testosterone go the other pec based on the call to the active one, and only there was not as much androgen generation on that side leaving the other?
b) Is it evidence of just a plain and simply genetic predisposition for gyno, and thus he proved that it all hinged on the active use of one side to prevent?
2. If occurring on the side he used, you have to wonder;
a) Clearly active use of the active side would have summonzed the excess hormones and thus proves that androgenic development of muscle is not any type of "safety" against gyno.
b) I think this case would be also more likely evidence of steroid use, and would wonder what type he used...

Odds of a "lefty" are slim. But my money is on he did NOT play a two handed backhand and that it occurred on the null side regardless..

Unilateral Gynecomastia In A Tennis Player

We report on a 26-year-old male patient who was a tennis player and developed unilateral breast enlargement after puberty. He began to notice unilateral breast enlargement by the age of 18, and underwent surgery at the age of 26 because there was no spontaneous regression. He had no known familial history or medication history such as anabolic steroid use. There was no discharge from the nipples, tenderness or pain in the nipple-areolar complex.

He was a professional tennis player for more than 10 years. His body mass index (BMI) was 21.9 kg/m2, which was in normal range. Anamnestic information on breast enlargement was elicited from the patient and the age of notable breast enlargement, age of maximal breast enlargement, and breast size changes after playing tennis were noted.

Using Simon’s classification, with division into four grades, grade IIA gynecomastia of the right breast was noted. Endocrinal function tests were within normal hormonal range. He underwent subcutaneous mastectomy under general anesthesia. Through the periareolar incision, glandular tissue was removed by meticulous dissection.


Kang SG, Song WJ, Kim CH, Kim JW, Tark MS. Unilateral gynecomastia in a tennis player. Arch Plast Surg 2012;39(6):675-8. http://e-aps.org/Synapse/Data/PDFData/2023APS/aps-39-675.pdf

 

[BBC3]

A study relating to treatment of Male breast cancer.

Endocrine therapy for male breast cancer: rates of toxicity and adherence

And some .GOV 2012 data...
Male Breast Cancer Treatment (PDQ®) - National Cancer Institute

Lasly for now...:
http://monographs.iarc.fr/ENG/Monographs/vol100A/mono100A-13.pdf
4.2.2 Estrogen-receptor-mediated
mechanismExperimental evidence increasingly supports
the importance of estrogen-receptor-mediated
gene regulation as the mechanism responsible
for the differential action of tamoxifen in distinct
tissues (Wu et al., 2005). Selective estrogenreceptor
modulators such as tamoxifen have
tissue-specific estrogenic activity. Tamoxifen is an
estrogen-receptor antagonist in the breast but an
estrogen-receptor agonist in the bone and uterus.
The two main forms of the estrogen receptor,
estrogen receptor-? and estrogen receptor-?, have
different tissue expression profiles. The uterus
predominantly expresses estrogen receptor-?
but the observation of increased cell proliferation
and excessive response to estrogen in estrogenreceptor-
?-knockout mice has suggested that
estrogen receptor-? could modulate estrogen
receptor-? in the uterus, and have an antiproliferative
role (Lecce et al., 2001). Tamoxifen stimulates
proliferation of the human endometrial
epithelium (Mourits et al., 2002). Tamoxifenliganded
estrogen receptors associate with
multiple co-activator proteins, which together
determine tamoxifen binding and transactivation
activity (Shang, 2006). Tamoxifen regulates
gene transcription in epithelial cells from type I
endometrial carcinomas (Wu et al., 2005), and
transcriptional responses have been identified
in epithelial cells but not in stromal cells (Pole
et al., 2004). There is also evidence that the genes
targeted by tamoxifen differ from those targeted
by estrogen (Pole et al., 2005).

(For what that last sentence is worth??)

 

[Michael Scally MD]

 

[BBC3]

Yur killin me.... Lol. !!!!!!

 

[pumpingiron22]

I had this growing up and just now getting surgery it was induced by puberty and add medicine.(Thanks Mom!) I find it crazy that so many people have it. What I don’t understand is during the summer you see all these kids have boobs even the skinny one. It makes me wonder if the chemicals in foods these days are inducing it. I know there are hormones in milk and meat. But I wonder if there something else that is causing all this?
Also why does the insurance company find this a health?
Risk and not cover it.
and doctor find this to be a risk if cancer is not found?

 

[idmd]

I had this growing up and just now getting surgery it was induced by puberty and add medicine.(Thanks Mom!) I find it crazy that so many people have it. What I don’t understand is during the summer you see all these kids have boobs even the skinny one. It makes me wonder if the chemicals in foods these days are inducing it. I know there are hormones in milk and meat. But I wonder if there something else that is causing all this?
Also why does the insurance company find this a health?
Risk and not cover it.
and doctor find this to be a risk if cancer is not found?

I think a lot of chubby little bastards have pseudogynecomastia and not true growth of breast tissue. At my heaviest I had big boobies but it was all adipose and not glandular. At the gym I see very few guys who I'd guess have true gyno although I'm not tweaking their nips to check so who knows.

 

[BBC3]

Personally, I like to KNOW that if I tweek mine enough, I can get a nice little fat mixture to crest. It means I'm ALIVE .. LOL

I think a lot of chubby little bastards have pseudogynecomastia and not true growth of breast tissue. At my heaviest I had big boobies but it was all adipose and not glandular. At the gym I see very few guys who I'd guess have true gyno although I'm not tweaking their nips to check so who knows.

 

[BBC3]

Now here is an interesting forum:

https://www.gynecomastia.org/smf/38/gyne-problem-and-low-testosterone/

 

[BBC3]

Here is a video of a Beverly Hills Plastic Surgeon Removing what I would have put as a 50/50 shot at Psuedo vs. Glandular/true gyno. At first, it looks like he is simply going to butcher the breast tissue (if there is any) with his lypo-wand, bt then he goes on to expound that he is removing "Glandular" as well and gets to that with a scalpel. On the one hand, he never early on stated he thought the patient had glanular (unless I skimmed that), and on the other SAME hand, the chuncks he carves out with his blade from behind the nips were never presented to the camera up close to convict as heavy glandular. Its a GRAPHIC VIDEO..

We have to acknowledge that probably 30% of ALL MEN post puberty are going to have some duct development at some point, if not just elementary and not even visible. WHETHER OR NOT what remained behind this guys nips will remain a mystery as to whether this doc could have just trimmed up to it, and left whatever was directly behind the nip untouched. This would have been a tough call just checking a fellow in the gym via line of site as to which way I would have gambled...