I came across one of the papers I'd been looking for recently on gynecomastia (and found it had recently been updated to 2015).
One of the issues we constantly face on bodybuilding boards is about the role of oestrogen in gyno. Many, many, many people still believe that gyno is almost entirely the result of oestrogen, and that if you can (somehow, miraculously) abolish all oestrogen, you'll not develop gyno.
Obviously, part of the problem with that theory, even if it were (partially) true is that you almost certainly can't (and wouldn't want to) suppress oestrogen entirely while using AAS, even non-aromatising ones, as I've discussed before. And not least because even the adrenals produce testosterone and oestrogen independently of the HPG axis.
But as this fairly basic review should help you to understand, even in the absence of an oestrogen receptor you can develop gyno. Two of the key players in gyno are actually GH and IGF-1; to quote: "neither estrogen alone, nor estrogen plus progesterone can sustain breast development without other mediators, such as GH and IGF-1."
While both progesterone and oestrogen can initiate gyno (with GH & IGF-1, in a synergistic cycle), prolactin "stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobulo-alveolar differentiation only with concomitant progesterone."
Probably the easiest way to understand the gyno cascade is diagrammatically:
Anyway, the purpose of my posting this is not to say everything we know about treating gyno is wrong. It's not: you should always try to tackle oestrogen first and foremost, and not over-medicate attempting to treat eg prolactin without first having tried to reduce oestrogen levels.
I simply want to point out that a complex issue like gynecomastia cannot be simplified to just oestrogen, and that in unresponsive cases treating it may require thinking outside the box.
I'll let you read the rest of the paper yourselves (it's free, fairly short and easy to read, but let me know if you need some clarification). There are plenty of links from the paper if you want to swot up some more on the subject.
http://www.ncbi.nlm.nih.gov/books/NBK279105/?report=classic
One of the issues we constantly face on bodybuilding boards is about the role of oestrogen in gyno. Many, many, many people still believe that gyno is almost entirely the result of oestrogen, and that if you can (somehow, miraculously) abolish all oestrogen, you'll not develop gyno.
Obviously, part of the problem with that theory, even if it were (partially) true is that you almost certainly can't (and wouldn't want to) suppress oestrogen entirely while using AAS, even non-aromatising ones, as I've discussed before. And not least because even the adrenals produce testosterone and oestrogen independently of the HPG axis.
But as this fairly basic review should help you to understand, even in the absence of an oestrogen receptor you can develop gyno. Two of the key players in gyno are actually GH and IGF-1; to quote: "neither estrogen alone, nor estrogen plus progesterone can sustain breast development without other mediators, such as GH and IGF-1."
While both progesterone and oestrogen can initiate gyno (with GH & IGF-1, in a synergistic cycle), prolactin "stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobulo-alveolar differentiation only with concomitant progesterone."
Probably the easiest way to understand the gyno cascade is diagrammatically:
Anyway, the purpose of my posting this is not to say everything we know about treating gyno is wrong. It's not: you should always try to tackle oestrogen first and foremost, and not over-medicate attempting to treat eg prolactin without first having tried to reduce oestrogen levels.
I simply want to point out that a complex issue like gynecomastia cannot be simplified to just oestrogen, and that in unresponsive cases treating it may require thinking outside the box.
I'll let you read the rest of the paper yourselves (it's free, fairly short and easy to read, but let me know if you need some clarification). There are plenty of links from the paper if you want to swot up some more on the subject.
http://www.ncbi.nlm.nih.gov/books/NBK279105/?report=classic
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