HCG for Boosting Testosterone

bullmastiff

New Member
I am a 56 year old man with a testosterone that was 360 on my last test.
LH runs low normal. I would like to try a course of HCG as a means of
boosting my T levels. I am 170 punds. What would be a good starting point?
Dosage and how many times a week? Also should HCG be cycled?
 
Why not look into HRT at your age?? ( no offense, young in my book:D) I think hcg would really not benefit you for what you're trying to acheive.


Also, Do you have a bullmastiff? Sweet dog! I have one right now
 
Shippen (Testosterone Syndrome) gave one example of raising test using HCG alone. But it was a short term deal. As I recall, he said it gave the pituitary a shove and the system was rebooted. For some of use the system need more than a little shove. Why not search the board for HRT and TRT, you'll probably find a few protocols recommended by Swale, our HRT/TRT guru.
 
HCG will not do anything but suppress the HPTA. I discussed this with Dr. Shippen a few weeks ago, and he claims to be onto some other meds to boost HP output of LH. I don't know, I think all he was doing was trying to get me to pay to go to one of his seminars. He SHOULD have been recruiting me to teach at it!
 
At your age, you are more likely suffering primary testicular failure, so will not respond to HCG properly.
 
SWALE said:
HCG will not do anything but suppress the HPTA. I discussed this with Dr. Shippen a few weeks ago, and he claims to be onto some other meds to boost HP output of LH. I don't know, I think all he was doing was trying to get me to pay to go to one of his seminars. He SHOULD have been recruiting me to teach at it!


I don't understand the above statement. I understood that HCG would mimic LH and cause the testes to produce Testosterone, this is at least doing something. While HCG will not stimulate the pituary to release LH, and the rise in Testosterone may cause the pituary to release even less endrogenous LH, the testes should keep there part of the bargin and produce more Testosterone, unless they are damaged in some way. What would cause HCG to do nothing?
 
My comment was directed toward the concept that hCG will "jump-start" the HPTA, which it will not.

BTW, primary testicular failure will prevent them from producing T even under the stimulation of HCG.
 
In recap, if the testes are already damaged or have suffered primary failure, then hCG will not cause the testes to produce additional testosterone and will actually hinder Bullmastiff's goal of increasing testosterone levels by futher shutting down the HPTA, is this correct?

Assuming a patient is on a TRT therapy consisting of 100mg of testosterone cyponiate per week and the testes are in primary failure, will the addition of hCG aide in the maintenance of testes' size?
 
Because the testes are in prmary failure does no tmean they cannot prodcue ANY T. it just means they aren't aboe to keep up with the demand of a healthful level. Some HCG can still maintain testicular size in those cases.
 
Per SWALE's comment about Dr. Shippen's mention of new drugs for stimulating the axis there might be something to it. Prior to going on TRT late last year I was being recruited to participate in a clinical trial on a new drug to do just that. As a secondary male, 38, and fit, I was the perfect selection. They just drug their feet and I needed to be treated, not studied.

SWALE, if you want to look into it more, PM me and I will give you my contact and the institution performing this trial/study.

Scotty
 
That is interesting, especially for those men who are infertile due to low sperm motility. I would expect this problem to be more prevalent then in men who are on statin drugs, as same depletes CoQ10.

MitoQ is what?
 
SWALE said:
That is interesting, especially for those men who are infertile due to low sperm motility. I would expect this problem to be more prevalent then in men who are on statin drugs, as same depletes CoQ10.

MitoQ is what?

Dr. Mike Murphy is developing it.

from bdc88,

MitoQ is 2-3 orders of magnitude more potent than
idebenone, for scavenging reactive oxygen species (ROS) in mitochondria.

advantages of MitoQ, may turn out to be that it can do a very good job
protecting mitochondria, w/o disrupting ROS signaling in the cytoplasm.
Additionally, MitoQ looks to be an inhibitor of the mitochondrial
permeability transition pore (MPTP), while idebenone seems capable of
inducing it (as does ALA). The significance of this at concentrations in
vivo is anyone's guess. MPTP opening, is a critical step in apoptosis, but
may also play a role in other forms of Ca2+ signaling.

Now, for exercise.. in response to endurance exercise there is generally an
increase in mitochondria, beyond what is necessary to achieve
circulatory-limited VO2 max. One theory behind this excess in mitochondria,
is that additional mitochondria are needed due to high amounts of ROS
mediated damage done to mitochondria during exercise. If this is a
significant contributor to fatigue, MitoQ might do a nice job extending the
time till fatigue. What I do not know, is how dependent muscle adaptations
are on ROS originating from mitochondria. Determining the best way to use
MitoQ, for enhancing exercise, will probably require some careful
experimentation. I'm excited to hear your observations.

Dose timing doesn't appear to be critical. I suspect that the half life of
MitoQ will be similar to that of the attached cation. This puts the half
life somewhere around 1.5 days, w/ steady state concentrations being reached
after 7-10 days of dosing
 
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