We all talk about managing estrogen and it’s importance.
Since starting trt my balls have dissapeared and I miss them. Is hcg a neccesity for overall health or is it more for cosmetics reasons. No man likes buying a smaller cup.
Should I be demanding it from my Doc? And after two years will they come back?
Thanks
sexual self image
sexual image for wife or GF
- these are important
hCG can keep the testes working. The testes are the single largest source of pregnenolone production in the body. This is important for mental health. Pregnenolone is used to make neural steroids in the brain. Most who start hCG report an improvement in mood.
Pregenolone is used in the adrenals to produce DHEA; also important.
Will they respond? The only way to know is to start hCG and see.
[quote]KSman wrote:
sexual self image
sexual image for wife or GF
- these are important
hCG can keep the testes working. The testes are the single largest source of pregnenolone production in the body. This is important for mental health. Pregnenolone is used to make neural steroids in the brain. Most who start hCG report an improvement in mood.
Pregenolone is used in the adrenals to produce DHEA; also important.
Will they respond? The only way to know is to start hCG and see.[/quote]
Okay. I understand that HCG might increase the production of pregnenolone in the testis. But, with respect, can I have a reference for the assertions that it is testicular production that is necessary for other hormone action?
I ask because:
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I can find no such reference. I am not aware that circulating pregnenolone was needed; I think it is made “on site.”
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Prenenolone is produced from cholesterol within the mitochondria of “steroidogenic tissues:” testis, fat, adrenals, etc. Such tissues do not need to import it in order to produce active steroid hormones.
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Apart from a few very rare genetic disorders, there is no such thing as a “pregnenolone deficiency” disorder.
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And there is a natural history experiment: castration of men (surgically or medically) does not cause Addison’s disease, for example. Haven’t seen it yet. (And conversely, only a few people with Addison’s disease also have gonadal failure–but that is an autoimmune disease, and not a failure of gonadal hormone production.)
[quote]KSman wrote:
…
hCG can keep the testes working. The testes are the single largest source of pregnenolone production in the body. This is important for mental health. Pregnenolone is used to make neural steroids in the brain. …[/quote]
A little more on this conjecture.
The Great One, Cy Willson, provides this 2006 reference:
[i]
Injury Elicited Increase in Spinal Cord Neurosteroid Content Analyzed by Gas Chromatography Mass Spectrometry
F. Labombarda, A. Pianos, P. Liere, B, et al.
Address all correspondence and requests for reprints to Dr. R. Guennoun, Institut National de la Santé et de la Recherche Médicale Unité 488, 80 rue du Général Leclerc, 94276 Bicêtre, France. E-mail: guennoun@kb.inserm.fr.
The effects of spinal cord injury (SCI), combined with castration and adrenalectomy, and of progesterone (PROG) treatment on neurosteroid levels and steroidogenic enzyme expression were investigated in the adult male rat spinal cord (SC).
Steroid levels were quantified by gas chromatography/mass spectrometry in SC and plasma, and mRNAs of enzymes by quantitative real-time RT-PCR.
The levels of pregnenolone (PREG), PROG, 5-dihydroprogesterone, 3,5-tetrahydroprogesterone increased in SC 75 h after transection without significant increase in the plasma.
After combined adrenalectomy and gonadectomy, significant levels of PREG and PROG remained in the SC, suggesting their local biosynthesis.
In the SC of adrenalectomized and gonadectomized rats, there was an increase of PREG 24 h after SCI, followed at 75 h by a concomitant increase in its direct metabolite, PROG. These observations are consistent with a sequential increase of PREG biosynthesis and its conversion to PROG within the SC in response to injury.
However, no significant change in P450-side chain cleavage and 3�?-hydroxysteroid dehydrogenase/5-4 isomerase mRNA levels was observed after SCI. Systemic PROG treatment after SCI, resulted in a very large increase in PROG, 5-dihydroprogesterone, and 3,5-tetrahydroprogesterone in both plasma and SC.
Furthermore, high levels of 3�?,5-tetrahydroprogesterone were detected in SC, whereas their plasma levels remained barely detectable. Because the ratio of reduced metabolites to PROG was 65-times higher in SC than in the plasma, it appears likely that reduced metabolites mainly originated from local biosynthesis.
Our results strongly suggest an important role for locally biosynthesized neurosteroids in the response of the SC to injury.[/i]
In short, testes and adrenals are not at all needed for the neurosynthesis of pregnenolone and its neurosteroid metabolites.
Its time to drop this business about HCG being necessary for pregnenolone and sytemic steroid synthesis.
So where does the antidepressant effect of HCG come from? Everyone that uses it experiences it.
[quote]brentf13 wrote:
So where does the antidepressant effect of HCG come from? Everyone that uses it experiences it.[/quote]
Everyone?
This is documented…where?
IF so, is it due to a rise in T?
Placebo effect?
Is there circulating pregnenolone that penetrates some part of the brain and selectively improves mood?
I do not think so.
Well I can tell you it happens and it’s not from the small rise in T from 250IU of HCG. Yes everyone. Ask anyone on this board if a shot of HCG improves their mood.
Per Dr Crisler and this is what we experience:
Patients all report they feel dramatically better once the HCG regimen is initiated (and they were properly tuned up on testosterone before they started it).
HCG, as a LH analog, increases the activity of the P450 SCC enzyme, which converts CHOL to pregnenolone. Thus all three hormonal pathways are stimulated in patients who may be either entirely, or very nearly so, HPTA suppressed.
It is my belief this may be a factor in the heightened sense of well-being my patients report throughout the week�??far in excess of what a minimal dose of HCG would produce by virtue of induced testosterone production.
Do you have any experience with HCG yourself?
[quote]brentf13 wrote:
Well I can tell you it happens and it’s not from the small rise in T from 250IU of HCG. Yes everyone. Ask anyone on this board if a shot of HCG improves their mood.
Per Dr Crisler and this is what we experience:
Patients all report they feel dramatically better once the HCG regimen is initiated (and they were properly tuned up on testosterone before they started it).
HCG, as a LH analog, increases the activity of the P450 SCC enzyme, which converts CHOL to pregnenolone. Thus all three hormonal pathways are stimulated in patients who may be either entirely, or very nearly so, HPTA suppressed.
It is my belief this may be a factor in the heightened sense of well-being my patients report throughout the week�??far in excess of what a minimal dose of HCG would produce by virtue of induced testosterone production.
Do you have any experience with HCG yourself? [/quote]
Fair enough question.
There aref articles on circulating pregnenolone; most of them have to do with the rise of pregnenolone seen with pregnancy (a high HCG state.) But most pregnenolone in this circumstance is converted to progesterone.
I could find no articles in HCG-treated human or animal males indicating an important rise in circulating pregnenolone, and in turn, a change in brain, measured in some way.
What Dr Crisler describes is an event in the mitochondria of steroidogenic tissue and nerves. He then jumps to an assumption. It may be right or it may be wrong, but I can find no proof of it being right. But there is information which indicates that argue against his assumption.
I could as easily conjecture that HCG has a direct effect on mood. Why must there be some testicle-derived pregnenolone as an intermediary? (Remember: nerve tissues makes its own pregnenolone for conversion to neural steroids. Is pregnenolone an undiscovered messenger for an undiscovered prenenolone-receptor in the brain, too? This assumes far too much–but I will search further.)
Proof requires experience, in controlled circumstance, beyond yours, Dr. Crisler’s and mine.
If you are on an HRT regimen, why do you have to decide to get on HCG? To me it’s a no brainer. HRT with no HCG = small nuts. HRT with HCG = normal size ball sack.
Any doctor worth their salt should be putting you on HCG if you are on an HRT program.
Chushin,
Have you seen the research that determined that 250iu was a reasonable low dose replacement for LH?
There is really no sides to replacing your normal testicular activity. [The side effect is a normal state for the testes.]
The costs are trivial. Shortages complicate things.
But if this is of no concern, no problem.
My wife was quite concerned when I had the shrinks.
Most report an improvement in mood with hCG that does not seem to be explained by resulting increases of T. This cannot be explained by increased E as those with estrogen poisoning also report this. I attribute this to increased pregnenolone levels [that the testes produce].
Have you got your luteinizing hormone (LH) levels checked? If they are low I would definitely recommend HCG. I’m taking it myself. And the cost is negligible.
[quote]randman wrote:
If you are on an HRT regimen, why do you have to decide to get on HCG? To me it’s a no brainer. HRT with no HCG = small nuts. HRT with HCG = normal size ball sack.
Any doctor worth their salt should be putting you on HCG if you are on an HRT program.[/quote]
After switching from Androgel to Cyp injections my testicles returned to their normal size and consistency. Nothing about TRT involves black and white answers. While Dr. Crisler is raking in the money, he is in no way the final authority on this subject.
If you returned to normal size after switching to T cyp then something is wrong. Both are suppressive but T cyp tends to be the more suppressive of the two from everything I’ve read. (That would make sense with the constant release of T as opposed to the cyclical nature Agel)
Dr Crisler is not the final authority but the man does do this for a living. Administering TRT every day, I’m sure there isn’t going to be much that takes him by surprise.
What’s the gripe with HCG anyway? Chemically it’s a twin for LH also with the ability to stimulate the receptors for FSH. Why wouldn’t you use it? I prefer to have testicles.
[quote]Chushin wrote:
Edit: Can you point me toward that research?[/quote]
This is really excellent research that directly applys to HRT needs.
http://dspace.hsl.washington.edu/dspace/bitstream/2012/52/1/JCEM_2005_Low_Dose_Human.pdf
[quote]KSman wrote:
Chushin wrote:
Edit: Can you point me toward that research?
This is really excellent research that directly applys to HRT needs.
http://dspace.hsl.washington.edu/dspace/bitstream/2012/52/1/JCEM_2005_Low_Dose_Human.pdf
[/quote]
No quarrel with this article. It is directed at a very different subject: using low dose HCG to assist in spermatogenesis in hypogonadotrophic men.
The men in the study were rendered (presumably) infertile with T. Then HCG was used to increase intratesticular T, a necessary precondition for spermatogenesis. The authors provide a complicated warning regarding the timing of the reported benefit (intratesticular testosterone, not circulating hormones): In short, use HCG early if you are going to use it all for the purposes of infertility treatment.
But nothing in this article says anything about circulating pregnenolone.
I am only being picky. HCG is useful in hypogonadotropic infertile men; I wouldn’t doubt that nut size is preserved. I just don’t see the literature support for the contention that mood is altered by testicular pregnenolone production. This is a “testable hypothesis,” not a fact. Where is the proof ?
This whole field of neurosteroid research is unfamiliar to me. And apparently, it is open to severe technical errors.
(Neurochem Int. 2008 Mar-Apr;52(4-5):522-40. Epub 2007 Oct 9. Pregnenolone sulfate in the brain: a controversial neurosteroid.)
Conjectures are only guesses; I offered one of my own, that HCG itself has brain action. Well whaddya know; seek and ye shall find.
(J Neurochem. 2007 Mar;100(5):1329-39. Epub 2007 Jan 11. Luteinizing hormone receptor mediates neuronal pregnenolone production via up-regulation of steroidogenic acute regulatory protein expression.)
But it still seems that most of the research points to prenenolone and other neurosteroids exerting their effect locally, and not through production from the testis.
(Pharmacol Biochem Behav. 2006 Aug;84(4):555-67. Epub 2006 Oct 4. Sulfated steroids as endogenous neuromodulators. "Central nervous system function is critically dependent upon an exquisitely tuned
balance between excitatory synaptic transmission, mediated primarily by
glutamate, and inhibitory synaptic transmission, mediated primarily by GABA.
… Excessive activation of excitatory glutamate receptors, such as in cerebral ischemia, can result in neuronal damage via excitotoxic mechanisms. The discovery that neuroactive steroids exert rapid, direct effects upon the function of both excitatory and inhibitory neurotransmitter receptors has raised the possibility that endogenous neurosteroids may play a regulatory role in synaptic transmission by modulating the balance between excitatory and inhibitory neurotransmission.)
In short, if you want to use HCG for bigger nuts, ok…If your mood improves, great, but I don’t know why, and it hasn’t been shown to be due to something (pregnenolone) produced from those testicles.
The proposed mechanism of HCG’s effect upon mood in men may not be correct but it is probably genuine. It appears it is the HCG itself as per your speculation. Effects upon mood in women have been documented, men probably respond in some fashion as well.
HCG use is often ideal…one should replace the LH which has been lost due to testosterone administration…otherwise, how is that a true replacement of normal activity? I concur the effects upon mood probably have little to do with any effect upon the testicles but rather, consider all of the unknown functions of LH that lie beyond the testicles (see references). HCG crosses the blood-brain barrier and seems to have direct neurological effects…very interesting.
The exception to this “rule” of HCG use might be men with primary hypogonadism…those that present with elevated LH and low testosterone, indicating their testicles fail to respond to LH or any analog such as HCG. These men will often times be put on testosterone therapy to normalize their high LH to an in range level. In these cases when LH is still within the normal range during testosterone therapy, no HCG is needed. In any other cases, supplement with it in small amounts as suggested.
Semin Reprod Med. 2001;19(1):111-9.
Rat as model for studying behavior effects of hCG.
Lukács H.
The demonstration of receptors for luteinizing hormone (LH)/human chorionic gonadotropin (hCG) in several parts of rat brain suggested their novel functional role. Subsequent studies tested the effect of hCG (intraperitoneally or intracerebroventricularly) on brain arousal and different types of stress situations in an intact female rat model on the day of proestrus. Treatment resulted in changes of activity and several other behavioral patterns associated with sites of brain hCG/LH receptors. hCG given peripherally caused a longer sleeping time and a decreased activity level. Whereas administration of indomethacin alone had no effect, coadministration inhibited the effects of hCG. hCG increased immunoreactive prostaglandin D2 (PGD2) and decreased PGE2 in brain areas controlling activity and sleep. hCG effects were probably mediated via prostaglandin pathways. After central hCG treatment, animals were less active and showed less exploratory behavior in an open-field box than the control animals. Taste and odor neophobias were dramatically decreased following central injection of hCG. hCG-treated rats were less anxious and exhibited a higher level of maternal interest than the controls. hCG treatment also had a beneficial effect against stress ulcer, which was prevented by pretreatment with antisense receptor oligonucleotide, suggesting a direct hCG receptor-mediated effect. In summary, because hCG can cross the blood-brain barrier, both peripheral administration and central administration affect several behavioral patterns. This effect is similar to treatment with anxiolytics and suggests the functional relevance of brain LH/hCG receptors. Some observed behavioral changes have parallels in pregnant women.
Semin Reprod Med. 2001;19(1):103-9.
Neural actions of luteinizing hormone and human chorionic gonadotropin.
Luteinizing hormone (LH) and its homologue, human chorionic gonadotropin (hCG), are able to elicit multiple effects in the central nervous system (CNS) through binding to their receptors. Specific receptors for LH/hCG have been identified in the hippocampus, dentate gyrus, hypothalamus, cortex, brain stem, area postrema, cerebellum, choroid plexus, ependymal cells, glial cells, neural retina, pituitary gland, and neuron processes of the spinal cord. Neurotropic effects of LH and hCG have been demonstrated in fetal rat brain, where the expression of LH/hCG receptors is developmentally regulated. Administration of hCG has been found to be beneficial in restoration of transected spinal cord function in rats. In adult rat brain, LH and hCG are involved in the feedback regulation of synthesis and secretion of gonadotropin-releasing hormone (GnRH) in the hypothalamus and LH in the pituitary gland. LH and hCG also induce several behavioral and other changes that are associated with the hippocampus, which contains the highest density of LH/hCG receptors. Many of the behavioral changes induced by hCG in rats parallel those in pregnant women. Some of these behavioral effects are correlated with changes of eicosanoid metabolism induced by LH and hCG in the brain. The LH/hCG receptors present in the choroid plexus, brain vessels, and perihypophyseal vascular complex may be involved in the modulation of transport of LH, hCG, and GnRH into the CNS. Thus, the CNS is one of the specific target tissues for LH and hCG, by which LH/hCG act as pleiotropic hormones that regulate several reproduction-related as well as reproduction-nonrelated functions in the CNS.