GYNO or gynecomastia that wonderfully terrifying growth of female fatty tissue in the male breast is much simpler in most cases than most of us have been led to think.

Where is the solution? As always, the route of the answer lies in the basics of human breast physiology and growth - information that has been available before anabolic steroids were even invented.

1. Estradiol (E2) goes up - you knew that. But...Estradiol when it is elevated causes negative feedback to the knew that...and the pituitary...ok - so you knew that...then LH goes down - you probably knew that too...then testosterone declines and before you say you knew that - we are talking strictly endogenous testosterone - ONLY the testosterone produced by your shrunken testis.

The Shrunken testis are smaller because roughly 20-25% of the "mass" of this great organ is due to full and normal sized Leydig Cells. These are the cells that most of us know shrink up like a broken 18 inch arm in a cast. The rest is FSH/Sertoli mass- but lets stay on track.

Ok - so everyone is on the same page and ready for some of the oldest most boring information that is probably the most on... 2. Prolactin - lets kill debate from all self-proclaimed experts (whether you are one of them, think they are right, whatever man!) Lets agree that we are interested in this topic for one reason - a SOLUTION. So stop judging consider this rule of BASIC PHYSIOLOGY: Testosterone Goes Down due to elevated estradiol, LH goes down too. The Leydig cells have DECREASED stimulation for testo production. Dopamine, being sustained by healthy testosterone and yet 'normal' (not high not low) E2 levels also declines. PHYSIOLOGY RULE:

Dopamine goes down when E2 goes up out of the reference ranges. Where? Not enough studies to know - any large men with abnormally small marbles and big soft boobies wanting to volunteer for a University Double-Blind Study on man boobs? Didn't think so. For now lets just define high as "out of the lab reference range for E2 - say an average ceiling of 70pg/ml. When this happens something else has already BEEN HAPPENING - declining levels of dopamine (DA) allow Prolactin to rise because the primary physiological function of DA is to keep Prolactin in check (at least in the male body).

Once you have prolactin joining the keg party things start to get rowdy - in a bad way. Now before all the "ANTI-Prolactin" gyno experts cut me off consider this: Prolactin's sole job in the female body is to promote "ductal growth and differentiation" of the mammary glands in the human breast. For this to happen you need to have a somewhat elevated Prolactin level and just a wee bit of progesterone (see factor #3 below) standing by to synergistically allow "ductal growth". What is "ductal growth" - Tit Growth!!! 3. Progesterone (P4) - needs to be present and available but does not need to be "HIGH". Elevated P4 definitely won't help GYNO at this point - but you don't need a ton of it - it is what Endocrinologists and Physiologists call "PERMISSIVE". Prolactin needs P4 before Prolactin becomes evil and the bosoms start blossoming.

Lastly, is a culprit you probably would never guess and may not even accept in about three seconds when you read it - -



Insulin-LIKe-Growth-Factor-I (IGF-I). Yup. UH-huh. Remember how I like to throw out facts and not opinions (well only when backed by facts and experience) - well -all humans without genetic defect have IGF-I receptors in the breast glands. We also have E2, Prolactin, and Progesterone receptors located in the breasts. All we need to do is put in the right hormone cocktail and make it enough like a teenage girl and whallah! Boobies!!

What does IGF-I do at the breast? Probably the worst thing of all in this specific scenario. IGF-I causes epithelial cell proliferation. Huh? Cellular breast growth by way of replication. Why do you think IGF-I is always found in metastatic cancer growths? Ah - ha! Something else to consider: in Estrogen dependent (ER-alpha) breast cancer in females IGF-I is the lighter fluid under one condition - sufficient E2 levels to allow 'synergy' of effects and stimulation of epidermal cell proliferation (breast tissue growth).

This is good news for bodybuilders - it works the same way in our chest/breast. Obviously it is not IGF-I by itself that causes the breast growth - if it did everyone who ever did a single kit of Serostim would probably need a small training bra. Only when accompanied by sufficient E2 (which normally is extremely high for a healthy man when compared to a healthy woman) levels will the result be breast growth.

If it goes on long enough and the 'anabolic state' in the breast is sustained P4 jumps in with Prolactin and decides to tell the ductal cells that milk is needed. Ever hear the horror stories of male gynecomastia with ummmm....MILK LET-DOWN. Yikes!

In summary this situation described above has the following components or RECIPE FOR GYNO:

1. Elevated E2 (allowing for decreased Testo which leads to less DA activity in the higher brain centers)

2. Elevated Prolactin (due to the removal of the 'normal state' negative feedback of sufficient DA levels)

3. Progesterone - P4 - only its presence is required and not much is known about the quantity needed. Suffice to say though, all men have a little floating around the blood stream (serum) with a few molecules making it to the breast tissue to 'hibernate'.

4. IGF-I - from endogenous or exogenous sources - needs to reach a minimum threshold level. This is going to be HIGHER THAN IT WAS BEFORE GYNO SYMPTOMS yet not necessarily HIGH by lab readings or general definition.

And - LASTLY - WARNING: OPINION COMING UP... The GYNO cases I have worked with privately and in a medical setting have not manifested with an IGF-I under 200 ng/dL. I am not saying keep it low, and I am not saying that 200 is magic threshold, simply my experience based on somewhere between 8-10 otherwise healthy and symptom free male patients/client-consults.

If you've never done substantial growth during your cycles and are at all sensitive in the breast tissue from past experience, either don't start the GH or don't increase it beyond a level that you have already done in the past without nipple/breast sensitivity.

If you do start/up the GH dose while sensitivity is present, - Get more protection via proper AIs and or low dose SERM as described in my ebook manual "Underground Guide to the Use of Antiestrogenic Drugs for Optimal Male Form and Function".