Gynaecomastia and Finasteride, The Science and Biochemistry
It seems paradoxical at first: finasteride lowers DHT, which is an androgen, so why would the breasts grow? The answer is that DHT is only one part of the hormonal balance controlling male breast tissue.
The key is the testosterone–DHT–oestrogen balance
Finasteride inhibits 5-alpha-reductase, the enzyme that converts testosterone into dihydrotestosterone (DHT).
Finasteride → ↓ DHT
But the testosterone that would otherwise have been converted to DHT remains available. Some of that testosterone can be converted by aromatase into oestradiol:
Testosterone → aromatase → oestradiol
Finasteride doesn't directly increase aromatase, and it doesn't usually produce a dramatic increase in oestradiol. However, the combination of less DHT's anti-oestrogenic/androgenic influence and a relative shift in the androgen–oestrogen balance can favour breast-tissue stimulation in susceptible men.
Why does DHT matter to breast tissue:
DHT is a particularly potent androgen. It acts through the androgen receptor and tends to oppose the effects of oestrogen on breast tissue.
Oestrogen, meanwhile, stimulates: 1)growth of the breast ducts 2)connective tissue surrounding them 3) blood supply 4) fluid and tissue remodelling.
So you can think of breast development as being a balance between stimulation by oestrogens and inhibition by androgens.
Finasteride can shifts that balance towards the oestrogenic side in a proportion of men.
But there's an important misconception because it isn't correct to say that "Finasteride increases oestrogen, therefore breasts grow."
The actual hormonal changes are much more subtle. Studies of men taking finasteride generally find only a modest increase in testosterone and sometimes oestradiol, but both remain in the normal male range. Most men therefore don't develop gynaecomastia.
The susceptibility of the individual breast tissue seems to matter enormously.
Which is why I developed it, but most men don't
Two men can take exactly the same dose of finasteride and have very different responses because of differences in:
- androgen and oestrogen receptor sensitivity
- aromatase activity
- baseline testosterone/oestradiol balance
- breast-tissue susceptibility
- age-related hormonal changes
- the amount of pre-existing breast tissue.
At 71, there seems to be a naturally greater tendency toward gynaecomastia because testosterone levels generally decline with age while at the same time oestrogen levels doesn't necessarily fall to the same degree.
So finasteride was probably the additional factor that shifted my particular breast tissue across the threshold for growth.
And this explains other things I've noticed:
Once glandular tissue has started growing, it isn't just extra fat. It is real, hormonally responsive breast tissue. During the active growth phase it can be surprisingly tender.
This is a plausible connection between my finasteride-associated gynaecomastia and nipple sensitivity and aching I've noticed. The tenderness doesn't necessarily mean that the breast is continuing to enlarge rapidly - although it may be slowly growing. The sensitivity reflects on the newly developed, and developing, glandular tissue.
In short:
Finasteride ↓ DHT → changes the androgen/oestrogen balance → susceptible breast tissue can respond to oestrogenic stimulation → glandular breast tissue grows → tenderness/sensitivity can occur.
And importantly, this can happen without testosterone becoming abnormally low or oestrogen becoming abnormally high.