Hi Manue, no worries! Circulating (free) T can most definitely be an issue for men. DHT (Dihydrotestosterone) is simply a more potent form of testosterone used by most of the testosterone sensitive tissues in the body, and synthesized from Testosterone. True, the body converts a small amount of circulating T into E through aromatization, but this is minuscule compared to the total amount of T in most men. For example, the health range of circulating serum Testosterone for men is around 500 ng/ml of blood, while the standard range of circulating serum Estradiol in women is between 100 and 200 pg/ml - a difference of 3 orders of magnitude (1 nanogram == 1000 picograms), and the sub 10 ng/dl amount of T in women is plenty to aromatize into E given the relative difference.
The second important thing to note is that Testosterone acts as an antagonist (inhibitor) in addition to an agonist in certain endocrine and reproductive tissues. Estradiol has a small agonist effect, but in many cases is easily 'drowned out' by the much much stronger antagonistic effect of higher concentrations of circulating T. In the subcutaneous adipose (fat) system, T is a much strong antagonist for fat accumulation generally. So while the gynoid fat regions (and regions in the face) are preferentially active with higher circulating E levels, T has an overwhelming suppressive effect for fat storage across the entire body (and in the gynoid regions specifically) cancelling out any small agonistic effect you might see. The opposite seems to be true in the visceral fat stores, which do show a suppressive effect from E - which is why peri/post menopausal women will gain visceral belly fat and get an 'apple' shape.
The third thing to understand is that phytoestrogens present in plants are estrogen analogs, but not nearly as potent in the human endocrine system as estradiol. Though you will see high (normal) Estradiol levels reduce T production to very low levels over time, phytoestrogens are too weak to have the same effect in male sex and endocrine tissues. Breast tissue, however, is uniquely sensitive to estrogens in the male body. Because the mammary tissue develops early on in gestation (prior to the 8th week when testosterone begins to inhibit development of the female sex organs), both men and women end up with exactly the same set of nascent mammary cells. So when men add in any level of E at all (even weaker phytoestrogens, or through changes to the hypothalamic-pituary axis and aromatization) it can trigger some breast growth. Testosterone doesn't have a clear inhibitory effect on breast tissue itself, since these tissues develop well before T is circulating in the fetal body. Rather decreases or changes in serum T affect how the male body produces Estrogens (lower T can lead to slight increases in circulating E, triggering gynecomastia in older men for example).
There isn’t great research on this, but my theory is that some trans women struggle with advanced breast growth precisely because their T levels are still elevated and inhibit fat deposition which can account for 50% of breast volume in cis women.
Tying it all back together; small breast growth is relatively easy because any amount of elevated E will lead to some amount of growth, and the necessary E concentrations are so small they are achieved either through supplementation (easy) or aromatization of existing T (harder without some sort of pharma or aging, etc). However, other changes in the body that are E dependent (gynoid fat adipogenesis for example) are heavily suppressed by T, so even a relatively large increase in E will have little effect without a dramatic (80-90%) reduction in T (or DHT with a 5a reductase inhibitor like finasteride/dutasteride).
Hope this helps!
--Abbey
The second important thing to note is that Testosterone acts as an antagonist (inhibitor) in addition to an agonist in certain endocrine and reproductive tissues. Estradiol has a small agonist effect, but in many cases is easily 'drowned out' by the much much stronger antagonistic effect of higher concentrations of circulating T. In the subcutaneous adipose (fat) system, T is a much strong antagonist for fat accumulation generally. So while the gynoid fat regions (and regions in the face) are preferentially active with higher circulating E levels, T has an overwhelming suppressive effect for fat storage across the entire body (and in the gynoid regions specifically) cancelling out any small agonistic effect you might see. The opposite seems to be true in the visceral fat stores, which do show a suppressive effect from E - which is why peri/post menopausal women will gain visceral belly fat and get an 'apple' shape.
The third thing to understand is that phytoestrogens present in plants are estrogen analogs, but not nearly as potent in the human endocrine system as estradiol. Though you will see high (normal) Estradiol levels reduce T production to very low levels over time, phytoestrogens are too weak to have the same effect in male sex and endocrine tissues. Breast tissue, however, is uniquely sensitive to estrogens in the male body. Because the mammary tissue develops early on in gestation (prior to the 8th week when testosterone begins to inhibit development of the female sex organs), both men and women end up with exactly the same set of nascent mammary cells. So when men add in any level of E at all (even weaker phytoestrogens, or through changes to the hypothalamic-pituary axis and aromatization) it can trigger some breast growth. Testosterone doesn't have a clear inhibitory effect on breast tissue itself, since these tissues develop well before T is circulating in the fetal body. Rather decreases or changes in serum T affect how the male body produces Estrogens (lower T can lead to slight increases in circulating E, triggering gynecomastia in older men for example).
There isn’t great research on this, but my theory is that some trans women struggle with advanced breast growth precisely because their T levels are still elevated and inhibit fat deposition which can account for 50% of breast volume in cis women.
Tying it all back together; small breast growth is relatively easy because any amount of elevated E will lead to some amount of growth, and the necessary E concentrations are so small they are achieved either through supplementation (easy) or aromatization of existing T (harder without some sort of pharma or aging, etc). However, other changes in the body that are E dependent (gynoid fat adipogenesis for example) are heavily suppressed by T, so even a relatively large increase in E will have little effect without a dramatic (80-90%) reduction in T (or DHT with a 5a reductase inhibitor like finasteride/dutasteride).
Hope this helps!
--Abbey