Finasteride induced Gynecomastia: Case report and Review of the Literature.
There are several paths to inducing Gyno
At essense the root cause of Gynecomastia is an imbalance between stimulatory and inhibitory inputs on Breast Tissue.
Estrogen is one of several Stimulatory Inputs
DHT is an Inhibitory Input
ie
Raise the Stimulatory Inputs and you raise your risk of Gyno
or
Lower the Inhibitory inputs ie Block DHT and you raise your risk of Gyno.
Its needs to be pointed out here that the reported rate of Gyno is low in Naturals. Reports on gynecomastia prevalence after DHT Blocking treatment do vary significantly. The highest % I have seen is 2.3% with dutasteride (0.5 mg/day)
That risk MUST escalate in the Enhanced as we raise stimulatory inputs, agreed I have no evidence to support that belief rather its based purely on logic Enhancement raises Stimulatory Inputs and so we must raise Inhibitory Inputs to balance the equation.
For our Tribe the principal takeaway here is simply this..
Its NOT Estrogen that causes Gyno.. its the imbalance between Stimulatory and Inhibitory Inputs on Breast Tissue
Raise the Stimulatory Inputs and you raise your risk of Gyno
or
Lower the Inhibitory inputs ie Block DHT and you raise your risk of Gyno.
Gynecomastia is the result of an imbalance of the Hormonal stimulatory inputs and the inhibitory inputs on Breast Tissue
Finasteride Induced Gynecomastia
Reoccurrence of Gynecomastia following Subcutaneous Mastectomy Surgery?
Is it true that following Glandular Tissue Removal by Subcutaneous Mastectomy Surgery that you no longer have to worry about Gyno recurring ?
Any Evidence to support this?
Gyno is the result of an imbalance between the stimulatory and inhibitory inputs on Male Breast Tissue.
More here on how it happens
https://victorblackmasterclass.com/gynecomastia-is-the-result-of-an-imbalance-of-the-hormonal-stimulatory-inputs-and-the-inhibitory-inputs-on-breast-tissue/
https://victorblackmasterclass.com/using-melatonin-in-collaboration-with-noladex-might-be-more-effective-at-treating-gynacomestia/
Study to support this Post
In this 2019 study they looked at the risk of recurrence with continued DHT Blocking following Surgery for Gyno caused by Finasteride Use.
Using Systemic DHT Blockers raises the risk of Gyno in Naturals by a large enough margin its a documented side effect in Finasteride Use its use in the Enhanced significantly increases that risk again.
The findings of this study support the idea that complete excision of Mammary Glandular Tissue by Subcutaneous Mastectomy Surgery means that you no longer have to worry about Gyno recurring.
Yes caveat being “complete excision”
Influence of Postoperative Finasteride Therapy on Recurrence of Gynecomastia After Mastectomy in Men Taking Finasteride for Alopecia September 25, 2019
https://doi.org/10.1177/1557988319871423
1557988319871423
Halotestin (Fluoxymesterone) sold under the Brand name Androxy.
Don’t believe everything you read on the Internet
Like virtually everyone in our community initially when I first wanted to learn more about PIEDs I started by reading the few books that where available on the subject. Later as the Internet developed we felt blessed by the emergence of websites that took up that role ( or at least complimented various books ) and for a time I felt rather confident that I understood with a fair degree of expertise these Compounds, the risks attached to their use and ” how to use them”.. based on my reading of and understanding of these resources.
But eventually, as I dug deeper and deeper I came to be confused by noticing a difference between what you read on these sites and what you read in the Clinical Literature from the Research Community.
As I am 30 days out from the first competition of Season A 2019 and in another 15 days I will start to use Halotestin, let me offer this drug as an example.
Go looking for information on Halotestin on one or more of the more popular AAS websites today and you will find snippets of information like this.
from
https://www.steroid.com/Halotestin.php
On the Estrogenic Side-effects on Halotestin
” Although a testosterone derived anabolic steroid, Halotestin does not aromatize and will not produce estrogenic related side effects. Water retention and gynecomastia are impossible with this steroid. “
that word jumps out ” impossible” – strong words
But ok ” no water retention” ” ” no gyno” – impossible.. noted
https://www.steroidal.com/steroid-profiles/halotestin/
On the Estrogenic Side-effects on Halotestin
” Because of its chemical modifications mentioned in the introduction to this profile, Halotestin side effects do not include any measure of Estrogenic activity or Estrogen-related side effects what so ever at any dose.
It is unable to interact with the aromatase enzyme in order to form Estrogens through the conversion process, and therefore all of the side effects normally associated with Estrogen should not present themselves from Halotestin alone.
Estrogenic side effects include the following: water retention and bloating, blood pressure elevations (as a result of the water retention), increased possible fat retention/gain, and ” gynecomastia.
This time ” no X side effects what so ever at any dose ” – noted
What about Bill Llewellyn’ Anabolic Guide
https://anabolic.org/halotestin-fluoxymesterone/
On the Estrogenic Side-effects on Halotestin
Fluoxymesterone is not aromatized by the body, and is not measurably estrogenic. An anti-estrogen is not necessary when using this steroid, as gynecomastia should not be a concern even among sensitive individuals.
OK, so what I read here in general is Halotestin cant cause Gyno or water retention right ?
Do you agree ? Is that what you read ?
Well why then does the Product insert that comes with the Drugs from Pharmaceutical Manufacturers state
” Due to sodium and water retention, edema with or without congestive heart failure may be a serious complication in patients with preexisting cardiac, renal, or hepatic disease. In addition to discontinuation of the drug, diuretic therapy may be required. If the administration of fluoxymesterone is restarted, a lower dosage should be used.”
and
” Gynecomastia frequently develops and occasionally persists in patients being treated for hypogonadism. “
There must be a reason for this. Right ?
The manufacturers inserts says possible
Water Retention and Gynocomastia
Learning Point
Use of fluoxymesterone, can absolutely lead to irreversible and persistent gynaecomastia and water rentention 100 percent !
Certain adverse effects have been associated with this drug. Among them are included hepatotoxicity, psychological disturbances, virilization, reduced spermatogenesis, gynaecomastia and cardiovascular complications.
The underlying molecular mechanisms of the side effects remain unknown. Therapeutic doses of testosterone can be aromatized to oestrogen peripherally and cause gynaecomastia. Non-aromatisable androgens such as methyltestosterone and dihydrotestosterone can also cause gynaecomastia via other unknown mechanisms.
Read that again.
Non-aromatisable androgens such as methyltestosterone and dihydrotestosterone can also cause gynaecomastia via other unknown mechanisms, I will explain the water rentention in another post cause that one we understand ” why”
Case Study ? Sure here is one..
bcr-2014-207474 (2)
Biochemical and hormonal tests to rule out pathological causes of gynaecomastia were normal (table 1). Breast mammography showed normal glandular breast and normal breast tissue on biopsy. Abdominal ultrasound revealed normal liver, pancreas, kidneys and prostate. Based on the clinical history, temporal relationship between drug initiation and appearance of gynaecomastia and the absence of pathological causes, the patient was diagnosed to have drug-induced (fluoxymesterone) gynaecomastia.
Takeways for the Bros
You can absolutely get Gyno and Water Retention from Halotestin ” conditionally yes .. all the evidence support this.. conditionally? yes sure.. but hey everything we do is ” conditional.. all of it.
2. If all your knowledge comes from ” Steroid websites”
I guarantee when you open your mouth to speak.. some of it its going to be ” Bro Science” ..
Victor Black
Genetic variants of Estrogen Beta and Leptin receptors may cause Gynecomastia
Sometimes our Tribe can be extremely judgemental.. with limited understanding of ” how” an adverse AAS exposure event might occur
I sometimes see individuals calling out conditions like Gynecomastia in such as way as you would think its a condition that affects everyone in exactly the same way.
No, just no.
Some individuals are simply affected to a greater or lesser degree than others really by all potential adverse events from AAS , from acne to hair loss to prostate BHP to gyno and and and
I have never ever had any problems with acne, never not as a teenager and not as an AAS use, I am simply one of those guys that are not affected by this condition.
Now do not get me wrong, I believe that Acne is massively influenced by environmental and behavioral factors and I could easily argue that well I don’t create an environment in which that condition can flourish, sure but the point here is that there is a genetic component.. there just is
And Gynecomastia is exactly the same – two guys can follow exactly the same behaviors and protocols and see totally different responses, due to biological inter-variability.
Yes Estrogen levels play a role, yes of course but Estrogen Receptor beta gene polymorphism and Leptin receptor polymorphism may massively increase susceptibility to gynecomastia.
In biology polymorphism is the occurrence of two or more clearly different morphs or forms in the population of a species
So be a little more understanding when you see someone ” battling” with the condition.. cause we are not all the same… we don’t all respond the same way to the same inputs.
Look at the bloodwork between these two groups of Young Men, one group experiencing Gyno the other no condition – no these are not AAS users.. we dont always have the data we would like to see available to us in the way we would like to see it..
You can’t just say ” they are doing a bad job” at Testerone and or Estrogen Control.. that is grossly oversimplifying the issue.
The median E2 level was 12.41 (5.00-65.40) pg/ml in the control group and 16.86 (2.58-78.47) pg/ml in the study group (p<0.001). The median T level was 2.19 (0.04-7.04) ng/ml in the control group and 1.46 (0.13-12.02) ng/ml in the study group (p=0.714).
Genetic variants of estrogen beta and leptin receptors may cause
