HCG/:LH possible role in prostate growth?

[DragonBits]

There is a lot of positive info about the benefits of HCG, but I don’t think it’s all positive.

IMO higher levels of HCG/LH can contribute to higher PSA levels and BPH, at least in some percentage of men. But as I note, I am not firm in this opinion.

One has to also realize it’s not natural to have a high level of LH along with a high level of testosterone / estrogen. Normally high levels of T suppress LH production.

For me, it’s not a firm conclusion that HCG caused a rise in my PSA level, but it’s strongly suggested that this was the cause. The reason I thought it was likely is because I had been on Nebido for 5 years with no change in my PSA level, but last year I started testosterone undecanoate (Nebido) with HCG / DHEA added in. Then my PSA levels went up from 2.4 > 4.2 in a few months.

Since that time I have not injected HCG, and my PSA level stabilized, then I took LEF ultra prostate formula, and got a decline in PSA levels. (Probably because this supplement caused a decline in FT and DHT).

My intention is to reintroduce DHEA and stop taking the LEF supplement, and retest PSA after a month. I had taken DHEA in the distant past without TRT with no positive or negative effects. (that I knew of). To really get a good idea of HCG's role, at some point in time I would need to restart using HCG, which I am not likely to do.

However, a fair number of men on TRT do inject HCG with no problems, so if this can create a problem it has to be a smaller percentage of men that may react with prostate growth and a higher PSA level. I wanted to see what other forum members thought about this possibility of LH / HCG receptors in the prostate and if this is possible to create prostate growth?
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Growth factors may also play an important role in mediating benign and malignant prostate proliferation. Cetrorelix also has been shown to reduce the amount of epidermal growth factor receptors38 and insulin-like growth factor-II39 in prostate cancer. Cetrorelix may mediate the observed prostate volume reduction by altering levels of growth factors and their receptors. The prostate has been shown to have luteinizing hormone-releasing hormone receptors.40),41 The multifactorial effect of cetrorelix on various hormones and growth factors may explain its durable clinical outcomes despite the normalization of testosterone levels.

The Role of Gonadotropin-Releasing Hormone Antagonists for the Treatment of Benign Prostatic Hyperplasia

For males, animal prostate cells expressed HCG receptor gene upon stimulation, and the authors concluded that luteinizing hormone/hCG receptors are linked to the development of prostatic hyperplasia and prostate carcinomas.9 Carlson et al.10 report that luteinizing hormone/hCG receptor mRNA was found from autopsy archival samples of benign gynecomastia and male breast carcinoma, and suggested that luteinizing hormone and hCG might have a role in the pathogenesis of male breast disorders. At sufficiently high dosage, hCG functions as a growth hormone which modulates the anthropomorphic indicators of older men with partial age-related androgen deficiency.11

An unfortunate resurgence of human chorionic gonadotropin use for weight loss

Expression of luteinizing hormone/human chorionic gonadotropin receptor gene in benign prostatic hyperplasia and in prostate carcinoma in humans.

The findings that normal rat prostates express functional LH/hCG receptors led us to test the hypothesis that benign prostatic hyperplasia (BPH) and prostate carcinomas may also express this receptor gene. The data revealed the presence of LH/hCG receptor transcripts and receptor protein in normal and hyperplastic but not in atrophic glands present in BPH tissue. Smooth muscle and blood vessels in stroma of BPH tissue also contained receptors. Prostate carcinomas contain lower and more heterogeneous receptor levels than BPH tissue. Two human prostate cancer cell lines (LNCaP and DU 145) that were investigated showed the presence of a major 4.5-kilobase transcript and several minor transcripts and also the protein of LH/hCG receptors. However, androgen-sensitive LNCaP cells contained more receptors than androgen-insensitive DU 145 cells. In summary, we demonstrate for the first time that BPH and prostate cancer tissues and cell lines express LH/hCG receptor gene. These findings suggest that higher LH levels in aged men may play a role in BPH and/or prostate carcinomas.

Expression of luteinizing hormone/human chorionic gonadotropin receptor gene in benign prostatic hyperplasia and in prostate carcinoma in humans. - PubMed - NCBI

 

[M.J]

After one month of using HCG I had an increase in psa from 1.4 to 1.53, my 1.4 reading is the highest among a lot of readings. so I can confirm it was an increase because of LH, now did it increase because I had an increase in T or because of other things I am not sure.
After adding testosterone to hcg I further went to 1.56, in two month time I currently 1.69.
An increase of .3 in two month or three month time of using HCG and then both together testosterone and HCG

 

[Vince Carter]

.3 is statistically nothing, it's the same. You're really reaching very hard to make something out of nothing as is @DragonBits

 

[M.J]

.3 is statistically nothing, it's the same. You're really reaching very hard to make something out of nothing as is @DragonBits

Just posting my results, I had maybe 7 test before that never was above 1.4 I was actually near 1.3 that 1.4 reading was the highest, I hope ur right cuz this damn psa keep increasing now I am 1.69 :/

 

[captain]

From John Crisler
A RECIPE FOR SUCCESS-SECOND EDITION

For all patients over 45, and over 40 if Family History of prostate cancer. Even though prostate CA is rare in men under the age of fifty, we don’t want it happening on our watch. At this time, accelerations in PSA above 0.75 are a contraindication to TRT (until follow-up by an Urologist). You may find, at the initiation of TRT in older men, when serum androgen levels are rapidly rising, PSA may, too. This is especially true when transdermal delivery systems are employed, because they more elevate DHT. Once T levels have stabilized PSA drops back down to roughly baseline. New TRT patients need to be cautioned, and reminded, to abstain from sexual relations prior to the draw, as they may now be enjoying greatly elevated amounts of same.
I get a PSA up front on my over 40 patients, at the one month follow-up in my more senior patients, and every six months after that. DRE (Digital Rectal Exam) is recommended twice per year as well, although the American Academy of Clinical Endocrinologists backs “every six to twelve months” in their 2002 Guidelines for treating hypogonadotrophic patients with TRT.

 

[M.J]

From John Crisler
A RECIPE FOR SUCCESS-SECOND EDITION

For all patients over 45, and over 40 if Family History of prostate cancer. Even though prostate CA is rare in men under the age of fifty, we don’t want it happening on our watch. At this time, accelerations in PSA above 0.75 are a contraindication to TRT (until follow-up by an Urologist). You may find, at the initiation of TRT in older men, when serum androgen levels are rapidly rising, PSA may, too. This is especially true when transdermal delivery systems are employed, because they more elevate DHT. Once T levels have stabilized PSA drops back down to roughly baseline. New TRT patients need to be cautioned, and reminded, to abstain from sexual relations prior to the draw, as they may now be enjoying greatly elevated amounts of same.
I get a PSA up front on my over 40 patients, at the one month follow-up in my more senior patients, and every six months after that. DRE (Digital Rectal Exam) is recommended twice per year as well, although the American Academy of Clinical Endocrinologists backs “every six to twelve months” in their 2002 Guidelines for treating hypogonadotrophic patients with TRT.

Thank youuuuuuuuu, I will feel a bit comfortable now knowing this.

 

[DragonBits]

.3 is statistically nothing, it's the same. You're really reaching very hard to make something out of nothing as is @DragonBits

Vince, are you saying my rise in PSA from 2.4 > 4.2 was statistically nothing?

BTW, I agree that I would ignore changes in PSA of 0.3 as it could be anything, even lab variation.

 

[M.J]

Vince, are you saying my rise in PSA from 2.4 > 4.2 was statistically nothing?

BTW, I agree that I would ignore changes in PSA of 0.3 as it could be anything, even lab variation.

I think he meant me, but I can swear that .3 increase is something

 

[DragonBits]

I think he meant me, but I can swear that .3 increase is something

Maybe @Vince Carter is bored, but for some reason he used my alias in his post which sends an alert to me.

I haven't posted here for 5 months in Feb, it's odd he wanted to send me an alert, maybe he just wants to stir the pot, he would have to explain his reasons.

As far as your 0.3 change, my PSA has moved up and down 0.4 several times, I don't consider a 15% change as significant.