A Thread Devoted To Gynecomastia

[Michael Scally MD]

[OA] Nuttall FQ, Warrier RS, Gannon MC. Gynecomastia and drugs: a critical evaluation of the literature. Eur J Clin Pharmacol. http://link.springer.com/article/10.1007/s00228-015-1835-x/fulltext.html

PURPOSE: A large number of medications have been implicated in the genesis of gynecomastia. However, gynecomastia is common in men, asymptomatic, increases with age, and is considered to be due to an increased estradiol/testosterone ratio.

This complicates the interpretation of medication-related gynecomastia. Therefore, we have reviewed the literature in order to assess the data relating gynecomastia onset with utilization of specific medications.

METHODS: The literature was searched in PubMed and the Ovid/Medline databases from the 1946 to January 2015 with the search terminology of "gynecomastia, drugs/medications." A few other articles were found and included.

RESULTS: One hundred ten publications were reviewed. Sixty-three were single case reports. There were 24 population-based studies of which 8 were HIV-infected patients treated with antiretroviral agents.

Among the case reports, 49 were for individual medications, and 2 were reports of antineoplastic or antiretroviral drug regimens. In the great majority, mastodynia with or without breast enlargement was present and referred to as gynecomastia.

Generally, hormonal profiles could not explain the breast enlargement. The pain/tenderness and breast enlargement resolved spontaneously over time.

CONCLUSION: Many different medications have been associated with the presence of "gynecomastia." Generally, it presents as a syndrome characterized by a single painful/tender breast (mastodynia) associated with breast enlargement and is transient. We suggest that these cases be referred to as an acute gynecomastia syndrome. This syndrome also occurs independent of medication use. Thus, in an individual patient, whether it is medication induced often remains uncertain. The pathogenesis remains unknown.

 

[bdg77]

One idea that comes to mind is the administration of serms and other anti-gyno meds. I wonder if any benefit could be obtained if these drugs were injected directly to site, i.e. subcutaneously directly behind nipple. Just an idea, but maybe one that should be researched. It seems they might be more effective delivered directly to problem area rather than taken systemically.

 

[BBC3]

Its not a bad question - IMO... Medical science is so "Smart" and sure of its self that they overlook more opportunity than can be imagined I am certain. I often harp on the follies of "group-think, hyper-focus, and poor diversification of mind".. It is a DANGEROUS combination. Something about "that left turn of Albuquerque"... ... And once you found the bend the REST is the PAST... And we have no time machine yet...

As I am sure you are aware these drugs all work systemically and to do the job as they were intended. But this is also how they are TRIALED and tested. So even if there were a change on a molecular level from interaction with the body in route from stomach - to brain, site, or system, this is the mode of operation. The result may be completely different UNTIL the drug is taken up "Systemically" as intended. It could be a different as aggravating tissue POSSIBLY unnecessarily to some pretty good pain I would imagine.

I am not familiar with all the latest anti-gyno meds out there. I would assume they mostly fall in Breast cancer treatment category. My guess would be that "Gyno" is considered somewhat "NORMAL" by medical science with a given probability & "harmless preponderance" / and to go tinkering with all those who would otherwise just have to live with a live extra lovin with no further issue would be to beg a problem where not.

I suspect you could get a really skilled plastic surgeon for $3500-5k to do the job right is always going to be surest bet. I do wonder how the OUTCOME IN PHYSICAL APPEARANCE varies from doc to doc, and procedure specifics considers. WHAT would you be getting for the money...!??

Not to hijack your post. There may be preparations of drugs for local application to combat breast tissue activity. I don't know.

Here is a new one called a S.E.R.D... Still an IM general injection and looks kind permanent... Dont have any idea how it MIGHT apply..

http://en.wikipedia.org/wiki/Fulvestrant

One idea that comes to mind is the administration of serms and other anti-gyno meds. I wonder if any benefit could be obtained if these drugs were injected directly to site, i.e. subcutaneously directly behind nipple. Just an idea, but maybe one that should be researched. It seems they might be more effective delivered directly to problem area rather than taken systemically.

 

[Michael Scally MD]

Lo TE, Andal ZC, Lantion-Ang FL. Fluoxymesterone-induced gynaecomastia in a patient with childhood aplastic anaemia. BMJ Case Rep.2015. http://casereports.bmj.com/content/2015/bcr-2014-207474.abstract

Gynaecomastia is a benign condition characterised by enlargement of the male breast. Drug-induced gynaecomastia merits deep consideration as it may account for as many as 25% of all cases of gynaecomastia in adults.

Although the mechanism is not fully clear, some mechanisms include oestrogen-like activities, stimulation of testicular production of oestrogens, inhibition of testosterone synthesis or blockade of androgen action. Anabolic steroids, in particular when used during the pubertal stage, may cause significant irreversible gynaecomastia.

We report a case of 28-year-old Filipino man with persistent gynaecomastia from fluoxymesterone used for aplastic anaemia during his prepubertal stage. Hormonal work ups for gynaecomastia all turned out normal, thus isolating the drug as the cause. The patient was unable to undergo breast reconstruction surgery due to haematological contraindications, but eventually referred to psychiatry for counselling.

This case will highlight the paradoxical effect of androgenic steroid used during childhood on male breast proliferation during puberty.

 

[Michael Scally MD]

ACR Appropriateness Criteria Evaluation of the Symptomatic Male Breast
[For Full-Text Email mike.scally@asih.net (Include Title)]

Most male breast problems are benign, and men with typical symptoms of gynecomastia or pseudogynecomastia do not usually need imaging. When a differentiation between benign disease and breast cancer cannot be made on the basis of clinical findings or when the clinical findings are suspicious for breast cancer, imaging is indicated.

Mammography is useful in both identifying cancer and obviating the need for biopsy in patients for whom a benign mammographic impression confirms the clinical impression. However, because of the relationship of breast cancer to increasing age, age-based protocols that do not include mammography have been developed.

For men with an indeterminate palpable mass, begin with ultrasound if the patient is <25 years of age, because breast cancer is highly unlikely.

Mammography should be performed if ultrasound is suspicious. For men >/=25 years of age or having a highly concerning physical examination, usually begin with mammography; ultrasound is useful if mammography is inconclusive or suspicious.

The ACR Appropriateness Criteria are evidence-based guidelines for specific clinical conditions that are reviewed every 3 years by a multidisciplinary expert panel. The guideline development and review include an extensive analysis of current medical literature from peer-reviewed journals, and the application of a well-established consensus methodology (modified Delphi) to rate the appropriateness of imaging and treatment procedures by the panel. In instances in which evidence is lacking or not definitive, expert opinion may be used to recommend imaging or treatment.

Mainiero MB, Lourenco AP, Barke LD, Argus AD, Bailey L, et al. ACR Appropriateness Criteria Evaluation of the Symptomatic Male Breast. J Am Coll Radiol. https://www.sciencedirect.com/science/article/pii/S1546144015001878

 

[Michael Scally MD]

Ahmed M, Kanji A, Begum T. Gynaecomastia: an unusual presenting symptom of bladder cancer. BMJ Case Rep. 2015. http://casereports.bmj.com/content/2015/bcr-2015-210649.abstract

A 74-year-old man presented to the outpatient clinic with painful gynaecomastia. A detailed physical examination to sort out possible causes of the gynaecomastia, including intracranial tumour, liver cirrhosis, hyperthyroidism, and adrenal and testicular tumour, was negative.

No offending agent was found in his medication list. A CT scan of the head and ultrasound of the scrotum did not show any mass lesion.

His serum beta-human chorionic gonadotropin (beta-hCG) and oestradiol levels were elevated.

A CT scan of the abdomen and pelvis revealed bladder wall thickening with soft tissue mass. A cystoscopic biopsy confirmed transitional cell carcinoma with muscle invasion. The patient was started on chemotherapy but responded poorly.

This case report describes the beta-hCG and oestradiol-secreting transitional cell carcinoma of the bladder presenting as gynaecomastia in an older man.

 

[Michael Scally MD]

Benign and Malignant Male Breast Diseases: Radiologic and Pathologic Correlation

Male breast disease is often under recognized owing in part to its rarity and also to a lack of awareness. Although male breast disease is most often benign, cancer of the vestigial male breast does occur.

Currently, breast cancer is 1 of the most infrequent cancer types in men and comprises <1% of all male cancers and 0.65% of all breast cancers. Prognostic factors and current treatment regimens have been extrapolated from experiences gathered from female breast cancer.

No current guidelines exist regarding screening mammography of asymptomatic men at any age. Thus almost all male patients present with a clinical symptom such as breast pain or palpable mass.

In this article, we describe and characterize a series of both benign and malignant male breast disease processes encountered at our institution over the past 8 years (2005-2013) by correlating the radiological and pathological appearances.

Yen PW, Sinha N, Barnes P, Butt R, Iles S. Benign and Malignant Male Breast Diseases: Radiologic and Pathologic Correlation. Can Assoc Radiol J. https://www.sciencedirect.com/science/article/pii/S0846537115000108

Gynecomastia is unilateral or bilateral enlargement of the male breast caused by a proliferation of dense connective tissue and ductal epithelial hyperplasia in response to an increased estrogen to testosterone ratio. This is the most common benign breast pathology in men and has been found in up to 55% of male breasts in 1 autopsy specimen series.

There are many pathological causes of elevated estrogen, which can lead to gynecomastia (Table 1). Normally, breast tissue develops identically in both sexes from birth until puberty.

Physiologic gynecomastia can occur at 3 stages of life: the neonatal period secondary to maternal estrogen, during pubertal gonadotropin surge, and finally in senescence due to a drop in the testosterone level.

Three radiographic patterns have been described:

Nodular: Initially, there is ductal epithelial hyperplasia with periductal stromal edema in the retroareolar region, also described as the florid phase. Mammography shows well-circumscribed homogeneously radiodense disc shaped retroareolar densities.

Dendritic: This appears as a heterogeneous retroareolar soft tissue density with extensions radiating into the adipose tissue with a ‘‘flame-shaped’’ appearance. Histologically, this represents the fibrous phase of gynecomastia characterized by minimal proliferation of the ductal epithelium and periductal stromal fibrosis. This form of gynecomastia is irreversible.

Diffuse: The mammographic appearance of diffuse glandular gynaecomastia is similar to that of the female breast. There is an overall increase in breast size by heterogeneous breast tissue.

 

[Michael Scally MD]

Mieritz MG, Lau Raket L, Hagen CP, Nielsen JE, Talman M-LM, et al. A Longitudinal Study of Growth, Sex Steroids and Insulin-like Growth Factor I in boys with Physiological Gynaecomastia. The Journal of Clinical Endocrinology & Metabolism. http://press.endocrine.org/doi/abs/10.1210/jc.2015-2836

Context: Physiological gynaecomastia is common and affects a large proportion of otherwise healthy adolescent boys. It is thought to be caused by an imbalance between estrogen and testosterone, though this is rarely evident in analyses of serum.

Objective: This study aimed to describe the frequency of physiological gynaecomastia, and to determine possible etiological factors (e.g. auxology and serum hormone levels) in a longitudinal set-up.

Design, Settings and Participants: A prospective cohort study of 106 healthy Danish boys (5.8–16.4 years) participated in the longitudinal part of “the COPENHAGEN Puberty Study”. The boys were examined every six months during an eight year follow-up. Median number of examinations was 10 (2–15).

Main outcome measurements: Blood samples and analysed for FSH, LH, testosterone, estradiol, SHBG, inhibin B, AMH, IGF-I and IGFBP-3 by immunoassays. Auxological parameters, pubertal development and the presence of gynaecomastia were evaluated at each visit.

Results: 52 of 106 boys (49 %) developed gynaecomastia of which 10 (19 %) presented with intermittent gynaecomastia. Boys with physiological gynaecomastia reached peak height velocity at a significantly younger age than boys who did not develop gynaecomastia (13.5 vs 13.9 years, p = 0.027), and they had significantly higher serum levels of IGF-I (p = 0.000), estradiol (p = 0.013), free-testosterone (p < 0.001) and FSH (p = 0.030) during pubertal transition.

However, no differences in serum LH or in the estradiol to testosterone ratio were found.

Conclusions: Gynaecomastia is frequent in pubertal boys. Increased IGF-I levels and pubertal growth appear to be associated, whereas changes in estrogen to testosterone ratio seem negligible.

 

[Michael Scally MD]

Koklu E, Arslan S, Yuksel IO, Bayar N, Demirci D. Nebivolol-induced gynecomastia. J Pharmacol Pharmacother. 2015;6(3):166-8. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4544141/

Adverse drug reactions play a substantial role in the etiology of gynecomastia. Gynecomastia as an adverse drug reaction, related to some cardiovascular drugs, has been reported in literature.

Nebivolol is a third generation beta-blocker, and gynecomastia as an adverse effect on the consumption of this drug has not been reported in any article yet.

We herein present the case of a 42-year-old male, who developed bilateral gynecomastia following nebivolol use and complete regression after discontinuation of nebivolol.

Other reasons causing gynecomastia were excluded.

Discontinuation of the responsible drug is quite sufficient with regard to the treatment of drug-induced gynecomastia, without any pharmacological or surgical treatment.

 

[BBC3]

????!!!! Fuck N A/ Did you just say Bystolic causes gyno...!!! They are giving this one out in samples like paxil in the 1990's... My current occasional BP drug too. I was just sitting here denoting my liver hurting and have taken a couple this week including last night...

And I really want to know HTF they differentiate a "Drug induced Gyno" vs. a "Steriod Induced", WHICH REALLY IS SAME BUT PHRASED LIKE THAT YOU CAN SEE CONFUSION CREATED... Now take the opposite they are probably referring which would be genetic preponderance and you got one that wont stop-Right??

But then WHY should anyone worry about steroid related Gyno if all "Drug Induced Gyno's" go away on their own... !! ?? LOL

Koklu E, Arslan S, Yuksel IO, Bayar N, Demirci D. Nebivolol-induced gynecomastia. J Pharmacol Pharmacother. 2015;6(3):166-8. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4544141/

Adverse drug reactions play a substantial role in the etiology of gynecomastia. Gynecomastia as an adverse drug reaction, related to some cardiovascular drugs, has been reported in literature.

Nebivolol is a third generation beta-blocker, and gynecomastia as an adverse effect on the consumption of this drug has not been reported in any article yet.

We herein present the case of a 42-year-old male, who developed bilateral gynecomastia following nebivolol use and complete regression after discontinuation of nebivolol.

Other reasons causing gynecomastia were excluded.

Discontinuation of the responsible drug is quite sufficient with regard to the treatment of drug-induced gynecomastia, without any pharmacological or surgical treatment.

 

[Michael Scally MD]

Gynecomastia and Psychological Functioning

Highlights
· Gynecomastia involves excess breast tissue growth in males.
· Gynecomastia is estimated to affect 30–70% of males at some point in their life.
· While often transient in nature, 10% of cases remain permanent.
· Associated consequences include depression, anxiety, and poor body image.
· Surgery is the primary form of treatment for gynecomastia and its symptoms.

Ordaz DL, Thompson JK. Gynecomastia and psychological functioning: A review of the literature. Body Image. 2015;15:141-8. https://www.sciencedirect.com/science/article/pii/S1740144515000996

Gynecomastia is defined as excess glandular growth of breast tissue in males. It is a noticeable physical difference that commonly affects males in adolescence and old age.

While often transient in nature, gynecomastia persists indefinitely in 10% of cases.

Much of the literature on gynecomastia has focused on etiology and management.

Little research has been done regarding the impact of gynecomastia on one's mental health and quality of life; however, some studies have suggested various psychosocial and psychological consequences related to gynecomastia.

These consequences include but are not limited to depression, anxiety, disordered eating, body dissatisfaction, and reduced self-esteem.

The aims of this paper are to review the current gynecomastia literature, bring awareness to an understudied but troubled population, and discuss directions for future work, including offering extant models of body image to guide researchers.

 

[Michael Scally MD]

Schroder L, Rudlowski C, Walgenbach-Brunagel G, Leutner C, Kuhn W, Walgenbach KJ. Surgical Strategies in the Treatment of Gynecomastia Grade I-II: The Combination of Liposuction and Subcutaneous Mastectomy Provides Excellent Patient Outcome and Satisfaction. Breast Care (Basel) 2015;10(3):184-8. http://www.karger.com/Article/Abstract/381152

BACKGROUND: Gynecomastia (GM) is a benign condition with glandular tissue enlargement of the male breast. GM is classified into 4 grades of increasing severity. We describe a series of GM grade I-II, diagnosed, treated surgically and analyzed regarding feasibility, complication rate, and satisfaction.

METHODS: From 2005 to 2012, a chart review was performed for 53 patients. Preoperative examination included endocrine and urological examination and exclusion of other pathological conditions. The surgical technique consisted of liposuction through an inframammarian-fold incision and excision of the glandular tissue by a minimal periareolar approach.

RESULTS: A total number of 53 male patients with 104 breasts were available for analysis. By liposuction, a median of 300 ml (range: 10-1000 ml) was aspirated from each breast and 25.1 g (range: 3-233 g) gland tissue was resected. Surgery lasted between 25 and 164 min per patient (median: 72 min). 2 postoperative hemorrhages occurred (n = 2, 3.8%). 2 patients underwent re-operation due to cosmetic reasons (n = 2, 3.8%).

CONCLUSIONS: This analysis demonstrates that treatment of GM grade I-II can easily be performed by liposuction combined with subcutaneous resection of the glandular tissue as a minimally invasive and low-impact surgical treatment with a low rate of complications and excellent patient satisfaction. Preoperative workup is important to rule out specific diseases or malignancy causing the GM.

 

[Michael Scally MD]

Young DB. 6'6'' United States Marine Seeks Treatment for Gynecomastia Only to Learn It Is All in His Head. Mil Med 2015;180(12):e1290-e2. 6'6″ United States Marine Seeks Treatment for Gynecomastia Only to Learn It Is All in His Head. - PubMed - NCBI

Growth Hormone (GH) excess is an uncommon cause of gynecomastia encountered in primary care. Adults with GH excess (acromegaly) have a 72% increase in mortality compared with the general population, which is reversible with early detection and intervention. Currently, however, the diagnosis of acromegaly is often delayed up to 12 years because of the subtle onset of symptoms. We present an active duty male diagnosed with acromegaly after presenting to his primary care provider with chronic gynecomastia. The most common cause of GH excess is a pituitary somatotroph adenoma; however, it is important to remember that magnetic resonance imaging of the pituitary does not distinguish between functioning and nonfunctioning tumors. Subsequently, the diagnosis of GH excess is based on biochemical studies, not imaging.

 

[Michael Scally MD]

Shirol SS. Orange Peel Excision of Gland: A Novel Surgical Technique for Treatment of Gynecomastia. Ann Plast Surg. Orange Peel Excision of Gland: A Novel Surgical Technique fo... : Annals of Plastic Surgery

INTRODUCTION: Gynecomastia is a common aesthetic problem faced by men with reported incidence as high as 65% with serious psychosocial impact. Although various techniques of liposculpture combined with glandular excision is the standard of treatment, many of the glandular excision techniques have inherent limitations and complications such as leaving a long scar, long operative time, contour abnormalities, and increased risk of hematoma. Here, we describe an innovative "the orange peel excision of gland (OPEG) technique" which overcomes these limitations with excellent cosmetic results.

METHODS: A total of 38 breasts were operated in 20 patients (18 bilateral and 2 unilateral). All the patients underwent suction-assisted liposuction and glandular excision under general anesthesia by our OPEG technique.

RESULTS: The average operative time per breast was 60 minutes. One patient had a small hematoma which did not require evacuation. The patient satisfaction rate was 95%.

CONCLUSION: The technique has reduced operative time and avoids residual gland and hematoma with excellent aesthetic outcome.

 

[Reddog82e]

This is a great read all the way through. Great set of info. Thanks

 

[Michael Scally MD]

J&J to Pay $70M to Teenage Boy Who Developed Breasts After Taking Risperdal.
J&J must pay $70 million to male teen who took Risperdal and developed large breasts - STAT

In a blow to Johnson & Johnson, the company was ordered last Friday to pay $70 million to a male Tennessee teenager who claimed its Risperdal antipsychotic pill caused him to grow enlarged breasts.

The finding by a Pennsylvania state court jury was not only the latest, but it is the biggest defeat to date in what has become another sprawling litigation over the drug.

In reaching its decision, the jury found that J&J failed to properly warn Risperdal could cause gynecomastia, which is the abnormal development of large mammary glands in males.

Moreover, the jury also determined that the company “intentionally falsified, destroyed, or concealed records” that Risperdal could cause boys to develop breasts.

Last week’s verdict, which only included compensatory damages, dwarfs the $2.5 million that was awarded last year to an Alabama man, who sued J&J after he developed size 46 DD breasts.

The latest case was brought by Andrew Yount, who was born in 1998, and was given Risperdal in 2003 to treat a psychiatric problem, according to one of his attorneys.

…

 

[Mushroomsnmuscles]

Yup, absolutely horrible what ''evidence'' was concealed in that matter. It's also equally an issue that the risks of the medication themselves were not weighed against the other medications which are equally effective and produce far less side-effects!

 

[Michael Scally MD]

Gynaecomastia

What you need to know
· Gynaecomastia typically results from an imbalance between the level or action of oestrogen and androgen
· Physiological gynaecomastia is common in newborns, adolescents, and older men and most do not require investigation
· Removal of the underlying cause often leads to resolution of gynaecomastia
· Early treatment with tamoxifen (unlicensed) is the most effective medical option in men with symptoms
· Surgery is the only effective treatment option once gynaecomastia becomes fibrotic

Thiruchelvam P, Walker JN, Rose K, Lewis J, Al-Mufti R. Gynaecomastia. BMJ 2016;354. Gynaecomastia | The BMJ

 

[Rupling]

I used .5mg ED of Arimidex for 30 days after my first Dbol cycle (wasn't even that heavy) back when I was 27....I only did one more Dbol cycle after that, before sticking to just Winny and Var, and now have been sticking to just Var as my only oral for years now. Arimidex is a Godsend. People think Nolva is awesome compared to Clomid. Well, let me tell you--Arimidex blows even Nolva away!!! virtually no sides, either!

 

[BBC3]

A POINTER.... (with respect to an edeavoring youngster)...

AND YOU ARE BORDERING ON FUCKING WITH UNIVERSES. FYI... And not unlike a Loose Cannon..

So an AI SImply reduces aromatase enzyme so estrogen can not be converted as readily. THIS MEANS THE ESTROGEN IS NOT METABOLICALLY CAPABLE OF CONVERTING TO ESTROGEN AT THE TISSUE END POINT DUE TO LACK OF LIVER GENERATED ENZYMATIC CATALYST. More than likely the body adjusts fairly quickly. Of course it does...

SermS (Nolva/Clomid) simply stop the estrogen from INVOLVING with certain tissues. Primarily, and "ON LABEL", they specifically stop estrogens with normal enzyme function from making it to CERTAIN final point destinations. More like STOP THEM from involving with said tissues. WHICH ARE DESIGNED AS BREAST TISSUE BLOCKERS..

** A more important form of SERMS is that they suppress the NORMAL Reception and Creation of Estrogen at these SAID tissues (among others). What this does in turn is tells the brain that there is NOT ENOUGH estrogen AROMATIZATION going on. Hence it can force the body by TRICKING IT into thinking there is not enough testosterone available. AND SOLELY VIA THE FACT THAT IT DOES NOT SEE THE CORRECT or ENOUGH (based on current tissue profile) ESTROGEN in the system and thus tricking the "reverse feedback loop"... The function of the body..... IT IS A BITCH and a BLESSING at the same time...!

- So now we circle back to the whole grand issue. WHAT IS THE VALUE OF SERMS IN TRT AND AAS...?!!! (which you so lightly trample on... LOL).!

There has long been a quandary as to WHAT IS THE VALUE OF TRT and HOW TO DO IT... Typically AI's are utilized on-label (I GUESS) to suppress estrogen conversion in different given scenarios. SERMS BLOCK the involvement of ESTROGEN at LOCAL TISSUE SITES.. ITS IMPORTANT TO KNOW THAT THIS ACTION VARIES AND UNBENOUNCED SOMEWHAT.. There is actually some documentation on this around here by BILL PHILLIPS back when he was last around in 2009 and to the specific actions of SERMS and WHERE they work. NOTE THAT the UNUSUAL THING about SERMS is that they BOTH Block and Encourage Estrogen involvement at Local tissues DEPENDING (ON WHAT??) WHO THE FUCK KNOWS.. REALLY..!?!?!?!?!?!? But apparently is depends on the particular SERM as to WHERE it acts as EITHER an ANTAGONIST OR AGONIST...!

SO... How does this relate to YOU.?!??? WHICH SERMS HAVE YOU TRIED...?

AND THE FUNDAMENTAL ISSUE WHICH YOU ARE TREADING ON IS THE VALUE OF SERMS TO RESTART THE HTPA via it's primary action of Lowering total estogen count OR getting said local tissue to not report to the brain that it is being aromatized (or NOT). We won't even get into the old school primitive notion that SERMS act DIRECTLY on the brain.. THE POINT that different serms actions at different local tissues PROVES that the action is LOCAL ONLY and merely acting as a "report to the brain".. (That's an oldy-but-goody.. LOL) Its classic BULLSHIT... As once you look deeper, the various DIFFERENT TISSUEs that SERMS affect VARIES depending on the SERM. Some of them block more or less estrogen involvement at prostate, bone, muscle, etc. AND DEPENDING ON THE SERM. AS WELL AS BREAST TISSUE.. But the one thing you can bet, is that they will ALWAYS BLOCK AT BREAST TISSUE..! Thus they are SERMS... POLITICALLY/MEDICALLY SPEAKING....

BACK ON TRACK - SERMS VS. AI's...

It's a question of IS THERE a double and IMPORTANT advantage to choosing a SERM over an AI... Do SERMS restart the HPTA, and better than an AI, OR SIMPLY JACKING OFF!!??? LOL.... Cause either way you slice it - THERE's GONNA BE HELL TO PAY..!

**** BOTH will obviously have a reverse feedback effect. SO DO SERMS ONLY HAVE A SUPERIOR VALUE IN AAS WHEN CONSIDERING THAT MOST AAS USERS WHEN INVOLVING SERMS ARE GOING RIGHT BACK ON CYCLE..!!!! ????? Well as far as I am concerned its a matter of WHO THE FUCK CARE's. Cause I dont cycle with "Steroids".. At least not yet... So FOR ONCE, I CAN say I can not speak from my own ANECDOTAL EXPERIENCE (they love that TERM around here... LOL) So either will block estrogen aromatization EFFECTIVELY AT TISSUE LOCAL POINTS. From an overall perspective.
** The question of Reverse feedback time loop now applying with regard to OVERALL EFFICACY of ESTROGEN REDUCTION AT TISSUE LOCAL SITEs NOW APPLYING... (MANY have hypothesized the VALUE of AI's as a RESTART MECHANISM. The question holds MERIT but unfortunately "Medical Science" has not cared to endeavor the actions/results/consequeses/true action/ and for the purpose of RESTART. (yes pussy bitchez and LIARS). It should be noted here that - ANECDOTAL EVIDENCE - LOL ALSO kinda also proves the LOCAL FEEDBACK TO BRAIN as the effective mechanism from tissue. AND NOT as a "body don't see estrogen", but body don't see estrogen coming from said receptors (Breast etc.. TISSUE SENSITIVE) ALSO NEITHER WORKING DIRECTLY ON BRAIN. (STILL NOT FINALLY RULED OUT THOUGH)..!

AND NO...! After a first AAS experience. You could sit on a log and your body would recover in 30-60 days...! Don't get cocky..!

YOU POST IS A GREAT ONE..!. These are the kind of "Statementalized QUESTIONS" like I used to PRESENT/ASK..! I LIKE IT.. I LOVE IT.. Keep in mind YOU ARE NEVER MAKING A STATEMENT AND ALWAYS ASKING/PROBING as QUESTION. Be humble and you will LEARN AND GO FAR... For some reason I see the potential in you that some saw in me...! (Based on that post alone and I have seen no others.)

POINT - Someone could come along next and say that guy is an idiot based on this or the other in the very next post. THIS IS STILL A LEARNING MECHANISM. You get salt here.. OUTSPOKEN IS ALWAYZ GOOD..! ONLY IF OPEN..>!

Enough... For now... The CUNT CALLZ...

I used .5mg ED of Arimidex for 30 days after my first Dbol cycle (wasn't even that heavy) back when I was 27....I only did one more Dbol cycle after that, before sticking to just Winny and Var, and now have been sticking to just Var as my only oral for years now. Arimidex is a Godsend. People think Nolva is awesome compared to Clomid. Well, let me tell you--Arimidex blows even Nolva away!!! virtually no sides, either!