What Causes High DHT?
- Thread starter Zooulie12
- Start date
Systemlord
Member
Large infrequent doses of T typically increases estrogen conversion and also increases DHT conversion, both estrogen and DHT are byproducts of testosterone.
As for DHT rage, it sounds made up.
As for DHT rage, it sounds made up.
Vince Carter
Banned
any "rage" associated with hormone use in men is far more likely to be out of control Estrogen.
Progesterone decreases DHT conversion and effects of Estrogen. Supplementing with pregnenolone is the preferred way to boost progesterone.
The Dangers of Progesterone
The Dangers of Progesterone
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Genetics can play a part as well. We know that dht causes hair loss and prostate growth. What we dont know is how much is too much.
That said, those prone to hair loss will see an acceleration of hair loss with higher levels of dht, that we know. As for prostate growth, BPH, dht does cause that condition. Some say estrogen is the cause but i dont buy it. Estrogen can play some roll but dht is the true culprit. Anti dht drugs such as finasteride and avodart crash dht and hence shrink the prostate. Thats proof righ there. Plus, if you dont produce dht, you will never go bald or get an enlarged prostate.
You can completely shut down estrogen with large doses of arimidex and you will still go bald and get an enlarged prostate. Crashing estrogen is more dangerous than crashing dht.
That said, those prone to hair loss will see an acceleration of hair loss with higher levels of dht, that we know. As for prostate growth, BPH, dht does cause that condition. Some say estrogen is the cause but i dont buy it. Estrogen can play some roll but dht is the true culprit. Anti dht drugs such as finasteride and avodart crash dht and hence shrink the prostate. Thats proof righ there. Plus, if you dont produce dht, you will never go bald or get an enlarged prostate.
You can completely shut down estrogen with large doses of arimidex and you will still go bald and get an enlarged prostate. Crashing estrogen is more dangerous than crashing dht.
Diabetics are more than twice as likely to have prostate enlargement compared with men without diabetes. Could be from low SHBG that comes with Diabetes. My DHT is sky high and my prostate is enlarged the same as it was when my DHT was not sky high. If anything the symptoms of enlarged prostate got better with TRT. My hair was thinning before TRT and has not changed much after TRT. In the end you will have a enlarged prostate and your hair will fall out with or without TRT. You can take Anti DHT drugs and make life worse if you like.
madman
Super Moderator
Take arimidex and get your estrogen levels very low and tell me if your prostate shrinks. Lowering dht has shown time amd time again to shrink the prostate.
Again, estrogen may play some part but DHT is the true culprit. If it werent, finasteride would not work since finasteride Lowers DHT and can actually raise estrogen. Think about that.. finasteride and avodart crash DHt and raises estrogen to a certain degree but yet it shrinks the prostate.
Again, estrogen may play some part but DHT is the true culprit. If it werent, finasteride would not work since finasteride Lowers DHT and can actually raise estrogen. Think about that.. finasteride and avodart crash DHt and raises estrogen to a certain degree but yet it shrinks the prostate.
madman
Super Moderator
My post above is related to you stating this..... "You can completely shut down estrogen with large doses of arimidex"
Did you read the thread? Clinical Use of Aromatase Inhibitors in Adult Males
I was being somewhat sarcastic, of course you cant totally shut it down but you can get it to almsot zero. Again, dht is the main culprit. Estrogen can have some impact especially if it is high but all things being equal, dht enlarges the prostate. Estrogen could play a role as i said so i am not completely dismissing that but dht is the prostates enemy as well as the hair follicles.
madman
Super Moderator
Are you still also not understanding this either?
Essential Points
- Circulating levels of DHT in response to testosterone replacement therapy (TRT) do not correlate with those found in androgen sensitive tissue (e.g., prostate, adipose, muscle) due to local regulatory mechanisms that tightly control intracellular androgen homeostasis.
Association of Circulating Levels of DHT and DHT/T Ratio With Prostate Disease
Although androgens support the growth, proliferation, and progression of aggressive prostate cancer, there is no consensus that elevated levels of circulating androgens contribute to the risk of developing prostate cancer. On the contrary, there is strong evidence that circulating levels of DHT are not associated with increased risk of prostate cancer (57,–59). This is because intraprostatic levels of androgens appear to be controlled by an internally regulated system that senses and adapts to circulating levels of T and DHT. So although it is possible (but not proven) that intraprostatic levels of T and DHT (along with estradiol) may play an important role in the development of prostate pathology, cross-sectional and longitudinal data do not demonstrate that elevated levels of circulating DHT increase the risk of prostate disease, even when high DHT levels or DHT/T ratios were sustained for long periods (54, 60).
In eugonadal men, the serum concentration of T probably plays a minor contributory role as a source for intraprostatic T. But in hypogonadal men, intraprostatic T concentrations are dissociated from circulating T concentrations (see Table 2). Marks et al. (66) reported that when hypogonadal men were treated with intramuscular T replacement for 6 months, average serum concentrations of T rose to about 640 ng/dL (22.19 nmol/L), whereas there was no significant effect on the intraprostatic levels of either T or DHT compared with baseline. There also was no effect of T therapy on prostate tissue biomarkers (e.g., AR, Ki-67, or CD34) or gene expression (e.g., AR, PSA, PAPA2, VEGF, NXK3, or clusterin). Lastly, there was no change in prostate histology or the incidence of prostate cancer or severity thereof, although this study was not powered for prostate cancer end points. Thus, at least for serum T, increased circulating levels have essentially no impact on intraprostatic androgen levels.
DHT and DHT/T ratios have been measured (or can be calculated) in a number of TRT clinical trials. The effects of various TRTs on prostate are summarized in Table 3. Although TRT has been associated with adverse prostate events, this table indicates that even striking elevations in DHT and DHT/T ratio for prolonged periods (e.g., up to 24 months) have not been associated with clinically meaningful negative effects on prostate. However, it is important to emphasize that these trials were not designed and powered to detect long-term effects of elevated DHT on prostate tissue.
Key Conclusions and Recommendations for Future Clinical Research
Circulating levels of DHT in response to TRT do not correlate with those found in androgen-sensitive tissue (e.g., prostate, adipose, muscle) due to local regulatory mechanisms that tightly control intracellular androgen homeostasis. 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).
The modest increases observed in serum DHT and in the DHT/T ratio observed after TRT are unlikely to be a cause of clinical concern, particularly when viewed in the context of changes observed in these parameters for currently marketed T replacement products and those under development for which DHT data are available. There is no sound current clinical evidence to indicate that elevated DHT concentrations (either short-lived peaks or sustained supraphysiological levels) are associated with risk beyond that known for androgens (most notably, T), including adverse effects on prostate.
Dihydrotestosterone: Biochemistry, Physiology, and Clinical Implications of Elevated Blood Levels
DragonBits
Well-Known Member
Madman, the problem as I see it here is MANY if not MOST men here aren't doing just testosterone replacement.
Taking HCG increases testicular testosterone and mimics LH causing a high LH level despite having a high testosterone level, I believe the prostate also has LH receptors. DHEA "backfills the pathways", testosterone applied on the scrotum not only increases testosterone but also increases DHT. Many also take pregnenolone.
So IMO one or more of those adjunct hormones we take OVERRIDE the mechanism that androgen-sensitive tissues use to "self-regulate tissue DHT levels by downregulating its synthesis and upregulating metabolism during DHT excess."
I would be especially suspect of HCG, since as noted by many, there are LH receptors in many places in the body.
What tends to be studied, if anything all all is studied, is raising one hormone in isolation.
We know the prostate is small at birth (1.5 g) and remains so until early puberty when it increases in size via an androgen-dependent pubescent growth phase from 10 g to an average of 20 g.
A lot is made about returning our hormone levels to "youthful" levels. Perhaps not all youthful levels are helpful?
I have a reason for thinking this way.
On five years of TRT only, my PSA level remained 2.4.2.8. After 4 months of TRT+HCG+DHEA+NDT my PSA went from 2.4>4.2.
What caused that increase, not sure, but I think for me it's far safer to stay on TRT only. (though I doubt thyroid hormones play any role in the prostate)
A study which won't be done because it's not ethical but would be useful, how does one use all of these hormones to deliberately increase prostate size in adult men? Can we use hormones to restore the prostate to it's youthful growth phase? Not that we want to, but is it possible?
One thing for sure, there aren't studies of what adding all these adjunct hormones to TRT causes, are there negative / positive effects from attempting to achieve an optimal level of many different hormones?
Nelson Vergel
Founder, ExcelMale.com
No proof of high estradiol causing rage. NONE
Nelson Vergel
Founder, ExcelMale.com
Vince Carter
Banned
I was very angry and aggressive when my E was >88
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