MyRestart

[AndreA]

Hi All-
I'm 58 and have been on test cyp 120/wk split into two doses for one year now and, unfortunately, i am one of those guys whose hair continues to receed, and I have tried all the recommendations I have seen from Nelson, etc. I've even tried a lower dose of 60mg/wk and still each injection takes more hair. (I was also on 0.5/wk arimidex)

Pre-trt my test levels were
Total: 350 ng/dl (264-916)
Free: 5pg/ml (7.2-24)

Last labs 9/21/18
Total: 1049 ng/dl
Free: 42 (pg/ml)
Estradiol sensitive: 24 pg/ml (8-35)
Dhea: 244 ug/do (48-344)
Psa: 0.7 ng/ml (0-4)

Like I said, reduced my dose to 60mg/wk and injected 9/28 and 10/5 which now means I have not injected for nine days.

I do have clomid and arimidex.
I have seen the Defy recommendations to use hcg, tamaxofi, clomid.

Given that I have clomid, is it unreasonable to start a 12.5 mg/day dose starting tomorrow (10 days post last injection). By unreasonable, I mean will it cause me harm? If not start on day 10, what about day 14?

I've read many restart stories on excelmale and realize that everyone is different and opinions vary greatly.

Thanks for your help

 

[fifty]

Were you taking dhea?

You could also try a topical finasteride. Just spitballing here.

 

[Systemlord]

Do you happen to know your SHBG levels? The reason I ask is because your pre-TRT lab indicate high SHBG do to your Total T and Free T numbers and using clomid when SHBG is already elevated will make matters worse.

Low testosterone (low DHT) can protect men's hair who otherwise have the genes for hair loss, so once testosterone is restored, the DHT levels will also rise and hair will recede again, had you never been low testosterone, you would have notice your hair receding years ago.

 

[AndreA]

More info: between the numbers I show pre-trt and trt, I was a clomid mono therapy for 2 years and was able to maintain total test between 600-800 but managing estradiol was always a challenge, same for SHBG, (both elevated) hence switched to injections. Weird how it never affected my hair, go figure.

Fifty: I do not supplement dhea

Systemlord:
SHBG:
Now: 30.9 nmo/L
While on clomid: 42.8
Pre-trt: 33

I have tried finishstride topical and also 1mg tablet (I know bad) with no luck.

 

[Systemlord]

More info: between the numbers I show pre-trt and trt, I was a clomid mono therapy for 2 years and was able to maintain total test between 600-800 but managing estradiol was always a challenge, same for SHBG, (both elevated) hence switched to injections. Weird how it never affected my hair, go figure.

Fifty: I do not supplement dhea

Systemlord:
SHBG:
Now: 30.9 nmo/L
While on clomid: 42.8
Pre-trt: 33

I have tried finishstride topical and also 1mg tablet (I know bad) with no luck.

When I was injecting 50mg twice weekly months ago I started losing hair, then I learned that these large doses of testosterone can produce a lot of DHT which interacts with the gene responsible for hair loss, the larger the dose of testosterone, the higher the DHT for some people.

I can attain the same Total T and Free T numbers using smaller more frequent dosing and not have excess DHT, my hair grew back and ache is gone. Naturally we produce 7-10mg daily, these large infrequent doses are as far from natural as we can get.

 

[madman]

When I was injecting 50mg twice weekly months ago I started losing hair, then I learned that these large doses of testosterone can produce a lot of DHT which interacts with the gene responsible for hair loss, the larger the dose of testosterone, the higher the DHT for some people.

I can attain the same Total T and Free T numbers using smaller more frequent dosing and not have excess DHT, my hair grew back and ache is gone. Naturally we produce 7-10mg daily, these large infrequent doses are as far from natural as we can get.

Regardless of ones dht levels.....it comes down to the sensitivity of ones AR (androgen receptor) to dht as men who are genetically prone to male pattern baldness can still experience balding in the presence of lower dht levels.

 

[madman]

Male human skin and hair express an abundance of SRD5A type I in sebaceous glands, hair follicles, sweat glands, and the epidermis, whereas SRD5A type II is expressed in genital keratinocytes and hair follicles (150). The physiologic role of DHT in the skin is unclear, but it is hypothesized that sex steroids may influence the immune function of skin and locally influence inflammatory processes (143). Androgens clearly play a role in the pathogenesis of acne vulgaris, likely through increased sebum production, and may impact cutaneous wound healing (151); however, a specific role for DHT in many of these processes has not been demonstrated. An exception to this may be DHT-induced upregulation of inflammatory cytokines (e.g., IL-1, IL-6, and tumor necrosis factor-α) in acne (152). Studies of agents that reduce levels of DHT in skin clearly support a role for DHT in the development of male androgenic alopecia (MAA) (male pattern baldness). This is inferred, in part, by the effectiveness of 5AR-Is in suppressing the progression of MAA and the observations that castrated men and men with SRD5A deficiency do not develop baldness (153). However, the effectiveness of SRD5A therapy likely resides at the level of the hair follicle (i.e., lowered follicular concentrations of DHT) and not a reduction of circulating DHT because this has not been shown to correlate with MAA. Support for this conclusion is also found in a study of men exposed to exceptionally high levels of DHT in response to daily application of a DHT gel preparation for 24 months. DHT was not associated with acne, MAA, or other androgen-associated skin pathology (54). Instead, the most important factor in the pathogenesis of MAA is a genetic predisposition for AR polymorphisms [e.g., synonymous nucleotide polymorphism in exon 1 (rs6152) of the AR] (154, 155). In addition, differences in AR concentrations and steroid-converting enzymes in the hair follicle also appear to be play a significant role in MAA (156).



Observations from numerous clinical studies are consistent with current knowledge that androgen-sensitive tissues can self-regulate tissue DHT levels by downregulating its synthesis and upregulating metabolism during DHT excess or, conversely, upregulating synthesis and downregulating metabolism under conditions of T or DHT deprivation. We are reminded of Horton's admonition some 25 years ago when he concluded that blood levels of DHT provide only a hint of tissue levels and that DHT should be regarded as a paracrine hormone formed and acting primarily within target tissues (39).