Still Losing Ground On The Big Three

[Retinoid]

Testosterone binding to the AR and causing male pattern baldness to progress, slower than DHT but still has an effect

This seems to be a theory on the board but I do not think there is a whole lot of proof for this.

I think all people think of is anything that stimulates the ARs in the scalp=bad anything that stimulates the ERs are good.

However it is way more complicated than that. DHT has without a doubt been proven to cause male pattern baldness but not Testosterone.

In fact Testosterone alone has been shown to help females suffering from androgen insufficiency AND hair loss.

Also the pseduohermaphrodites in the DR with no 5AR2 have normal Testosterone levels but have no male pattern baldness.

Estrogen and Testosterone in equally high dosages in vitro stop hair from growing.

It probably has more to do with receptor stimulation as opposed to simple AR==bad. Just like ER==good. Not all types of ER stimulation is good (ERa vs ERb for example, types of estrogen, etc) and not all Androgens will be bad.

 

[el_duterino]

DHT is the main culprit because its more potent than T but T is a male androgen and will bind as well.
This is for regular men not genetically modified people like the infamous pseudo h.

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The actions of androgens such as testosterone and dihydrotestosterone are mediated via the androgen receptor (AR), a ligand-dependent nuclear transcription factor and member of the steroid hormone nuclear receptor family. Given its widespread expression in many cells and tissues, the AR has a diverse range of biological actions including important roles in the development and maintenance of the reproductive, musculoskeletal, cardiovascular, immune, neural and haemopoietic systems. AR signalling may also be involved in the development of tumours in the prostate, bladder, liver, kidney and lung. Androgens can exert their actions via the AR in a DNA binding-dependent manner to regulate target gene transcription, or in a non-DNA binding-dependent manner to initiate rapid, cellular events such as the phosphorylation of 2ndmessenger signalling cascades. More recently, ligand-independent actions of the AR have also been identified. Given the large volume of studies relating to androgens and the AR, this review is not intended as an extensive review of all studies investigating the AR, but rather as an overview of the structure, function, signalling pathways and biology of the AR as well as its important role in clinical medicine, with emphasis on recent developments in this field.


Introduction
Androgens (testosterone and dihydrotestosterone (DHT)) are the male sex hormones required for development of the male reproductive system and secondary sexual characteristics.1Testosterone can be converted to its more biologically active form, DHT, by 5α reductase, and to oestradiol by aromatase. Testosterone and DHT mediate their actions via the AR, a ligand-dependent nuclear transcription factor.2 Other members of the steroid hormone nuclear receptor family include the oestrogen receptor (ER), progesterone receptor (PR), glucocorticoid receptor (GR) and mineralocorticoid receptor (MR). The AR, located on the X chromosome, is expressed in a diverse range of tissues and as such androgens have been documented to have significant biological actions in bone, muscle, prostate, adipose tissue and the reproductive, cardiovascular, immune, neural and haemopoietic systems.3 The AR binds androgens with strong affinity in the low nanomolar range4 with DHT being more biologically active than testosterone, binding to the AR with a 2-fold higher affinity and a decreased dissociation rate of 5-fold compared to testosterone.5

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4810760/

 

[ripple-effect]

Been on rogaine since February and findestrade 1mg March and nirzoal every over day but I’m still losing ground what can do is their anything else help

Which % Nizoral are you using?