3pm, Ithappens and others (including myself) have noticed positive, androgenic like effects by using medication which increases dopamine. But how can that be? At first sight, this doesn’t make sense. The positive effects, that I have experienced, clearly felt androgenic in nature: improved muscle strength, reduced chest/breast pain, fuller penis. Regarding muscle strength, the dopamine receptor is not significantly expressed in human skeletal muscle. So it unlikely that this is a direct effect of dopamine on muscle tissue. On the other hand, dopamine receptors are prominent in the vertebrate central nervous system (CNS). However, this does not sufficiently explain the effect that I got on the muscle side. D1, D2, D4, and D5 receptor subtypes are present in blood vessels (but not significantly in breast tissue). So my substantial reduction in breast pain (gyno) can’t be explained by direct dopamine action either.
Of extremely interesting but unfortunate note, these positive effects started vanishing after about a week. Ithappens also experienced the positive effect of GHB disappearing after a couple of weeks. Three weeks into taking the medicine (Wellbutrin), I started noticing a reversal of the situation. My chest pain was getting increasingly worse, beyond what I was used to in the past 6-12 months. This initially positive but then declining response seemed suspiciously familiar to me. Supplementing DHT had exactly the same effect over time. There has got to be a common denominator here.
So I started taking a closer look at possible links between dopamine and the androgen receptor. Here is what I came up with:
First of all, the androgen receptor (AR) is a member of a large family of transcription factors known as the steroid/thyroid (nuclear) receptor superfamily. This superfamily includes receptors for steroid and thyroid hormones such as glucocorticoid, mineralocorticoid, progesterone, estrogen and vitamin D [1].
Studies have shown that steroid receptors of this superfamily can be activated by neurotransmitters and intracellular signaling systems, through a (poorly understood) process that does not require hormone binding with the receptor.
So what does that tell us? First of all, it is known that dopamine can activate the progesterone and estrogen receptor. Both, as members of the nuclear receptor superfamily, are in many ways similar to the androgen receptor. It is stated that other steroid receptors probably have this property as well. In other words, it is possible that dopamine can also activate the androgen receptor.
This totally makes sense and could very well explain why some of us have experienced an androgenic like response from dopamine raising medication. Since we are getting the same shut down effect, like when supplementing androgens, this further suggests that the same rate limiting mechanism could be involved. The interaction of neurotransmitters with steroid receptors happens roughly midway in the pathway between ligand binding and gene expression[2]. This could indicate that the supposed involved rate limiting mechanism is located even further downstream, that is after dimerization occurs.
I realize this theory is “iffy” and is heavily deduced, but it could well be the bridge that closes the gap between our neurotransmitter and androgen receptor theories.
[1] PETER J. FULLER: The steroid receptor superfamily: mechanisms of diversity
[2] JEFFREY D. BLAUSTEIN: Neuronal Steroid Hormone Receptors
[3] Bhuiyan et. al.: Down-regulation of Androgen Receptor by 3,3’-Diindolylmethane Contributes to Inhibition of Cell Proliferation and Induction of Apoptosis in Both Hormone-Sensitive LNCaP and Insensitive C4-2B Prostate Cancer Cells
