No, the proteins did not do this. Did you experience any pain in the testes with the dengue?
“”“Dengue virus (DEN) is related to the Hepatitis C virus”“”
What are your lab results for liver enzymes? Liver problems will increase E and lower T.
Low thyroid levels, hypothyroidism leads to weight gain, lower testosterone, low energy, low libido, depression. Most of the symptoms are the same as hypogonadism.
i will ask the doctor to test liver enzymes.
My testes didnt ache at that time.
GOOD DAMNIT i wanna get to the root of the problem. Anastrozole arrived yesterday but maybe i should not take it until im over Meticorten.
Good damnit with my ex i could cum and my dick didnt get down, i cum like 3 times in and didnt get tired, i was skinny like hell but had a good fucking working dick, after she dumped me i had anxiety problems and started smoking like hell and drinking 5 days a week 2 beers per day. That time of my life fucked me up. Now im left with testicles problems and the only aparent way of dealing with it is TRT.
IS THERE ANOTHER FUCKING WAY???
OR SHOULD I STOP TRYING AND JUST TRT???
NO OTHER VALUE THAT COULD BE CAUSING THE PROBLEMS???
MAYBE SITTING 8 HOURS A DAY IN A CHAIR FUCKED MY TESTIS UP???
Your use of adex will be to refine your E levels. Lowering your E to a more favorable “normal” level should not be an issue with prednisone. You need to watch for signs of being an anastrozole over responder.
Remember that one always needs to taper off prednisone. Prednisone also lowers libido. Remember that prednisone destroys bone with long term use and if prednisone must be used long term testosterone is needed to protect the bone. Do not expect many doctors to understand that.
Other long term effects are catabolic muscle loss and weight gain, thin arms and legs and a
round body.
Excelent book the one you recommended me.
I have been reading about use of physiological doses of hcg to upregulate the sensitivity of lh/fsh receptors on leydig cells. So maybe the use of hcg would cure hypogonadism type 1 if the problem is a downregulation on leydig cells.
In 5 days I stop drinking prednisone and will perform another blood test to see if T Goues up.
Another thing i have been reading is that FSH regulates sensitivity of the leydig cells to LH/HCG, and i have good LH but my FSH seems to be a little low, so maybe my leydig cells are downregulated and HCG could still be a good solution. I would like to try that, with the use of anastrozole, and if nothing works for the next 4 months, ill take the final decision on TRT/HCG/DEX
You cannot get FSH or LS as therapeutic agents… if that was what you had in mind.
No, i mean FSH upregulates leydig cells sensitivity to LH, and I have been reading that HCG too upregulates leydig cells sensitivty to LH, SO, maybe i dont need more LH because my body is producing enough, but i could use some HCG to mimic the same as FSH and upregulate sensitivity so my LEYDIG cells respond well to my natural levels of LH. Sorry for my english if you dont understand.
my FSH is in the bottom normal range so maybe leydig cells are downregulated
FSH 2.69 [*__] 0.95-11.95
KSman, since i was 15, no matter how well or how much i sleep i always have a “dark ring under the eyes” or bags, i dont know how you call it, in spanish its called OJERAS. dont know if that is a symptom for something you may know, just wanted to mention it to see if that could help you.
The OJERAS suggest metabolic problems, toxins or free radical damage. Perhaps some dietary issues.
I once did some wood finishing with a water based lacquer that make my eyes dark the next day. The product was meant to be safer by having less organic solvents.
Ok its decided.
Can someone help me with a HCG+PCT CICLE TO FIX REGULATION OF LEYDIG CELLS, TESTICULAR SIZE
I think could be something like this:
HGC 250IU EOD FOR 4 WEEKS
THEN ARIMIDEX 0.25ML EOD FOR 2 WEEKS
No guarantees of anything, but not harmful in any event.
You need adex while taking hCG and then for more than two weeks after moving towards 0.5mg/week in EOD dosing. If your T does not come up, the adex could take your E2 down too far.
Insert standard note re anastrozole over-responders.
5000iu hCG would last 40 days.
Note changes to testes and scrotum.
yes, 5000iu lasts for 20 shots, or 40 days, but you think i should last that long on HCG?
btw finished reading the book Testosterone syndrome.
[quote]KSman wrote:
No guarantees of anything, but not harmful in any event.
You need adex while taking hCG and then for more than two weeks after moving towards 0.5mg/week in EOD dosing. If your T does not come up, the adex could take your E2 down too far.
Insert standard note re anastrozole over-responders.
5000iu hCG would last 40 days.
Note changes to testes and scrotum.[/quote]
How long do you feel aromatase would remain elevated - 2 weeks? Would the taper down be enough to ensure no rebound?
Changes in scrotum and testes? I assume this means that as well as an increase in testes size - scrotum “hanging low”?
When you start hCG with LH/FSH starved testes, there is a time delay as the testes physically change then start to do what they do. They will recover size. Until size recovers, you cannot expect output. That and how they hang are indicators of progress.
As the testes product T, T has its own actions on the testes. Many have a quick improvement in mood with hCG. This might be from restored pregnenolone production. Perhaps hCG has direct effects on the brain.
Aromatase elevated? Did you mean to say that? [Anastrozole has a 36 hour half life.]
Tapering off is all that you can do to reduce chances of rebound [in a normal HPTA].
[quote]KSman wrote:
When you start hCG with LH/FSH starved testes, there is a time delay as the testes physically change then start to do what they do. They will recover size. Until size recovers, you cannot expect output. That and how they hang are indicators of progress.
As the testes product T, T has its own actions on the testes. Many have a quick improvement in mood with hCG. This might be from restored pregnenolone production. Perhaps hCG has direct effects on the brain.
Aromatase elevated? Did you mean to say that? [Anastrozole has a 36 hour half life.]
Tapering off is all that you can do to reduce chances of rebound [in a normal HPTA].[/quote]
Thank you.
Yes I did mean aromatase elevated. When you take HCG or exogenous testosterone I have made the presumption that the body increases the production of aromatase? If this is correct - how long after the administration of HCG or testosterone does aromatase remain elevated?
Thanks again
When hCG increases E production in the testes, aromatase may not be increasing at all. When the testes are pushed to produce high amounts of T [if things work] the IntraTesticular Testosterone [ITT] levels are very high and that increases the T–>E reaction rate with the aromatase enzymes. As ITT can be up to 80 times higher than serum levels, a competitive AI drug is ineffective at controlling T–>E in the testes. This is why hCG mono therapies can fail when docs think that they can simply increase hCG doses to increase TT. hCG should be limited to doses near 250iu EOD and TRT used to achieve therapeutic TT/FT levels.
Why did you assume that the body increased aromatase?
FT and Bio-T react with aromatase. SHBG bound T is not bio-available and does not aromatize. With higher levels of serum FT/bio-T there will be more T–>E in peripheral tissues if aromatase amounts do not change. Competitive AI drugs must be increased in proportion to increasing levels of FT/Bio-T to maintain a particular E2 level.
Aromatase increases with age. I suspect that this increase with age really has to do with increasing body fat. If the amount of body fat did not change, would total aromatase increase at all with age? I have not seen any info that would support that possibility.
Fat old guys with low T typically have more E2 than their post menopausal wives.
[quote]KSman wrote:
When hCG increases E production in the testes, aromatase may not be increasing at all. When the testes are pushed to produce high amounts of T [if things work] the IntraTesticular Testosterone [ITT] levels are very high and that increases the T–>E reaction rate with the aromatase enzymes. As ITT can be up to 80 times higher than serum levels, a competitive AI drug is ineffective at controlling T–>E in the testes. This is why hCG mono therapies can fail when docs think that they can simply increase hCG doses to increase TT. hCG should be limited to doses near 250iu EOD and TRT used to achieve therapeutic TT/FT levels.
Why did you assume that the body increased aromatase?
FT and Bio-T react with aromatase. SHBG bound T is not bio-available and does not aromatize. With higher levels of serum FT/bio-T there will be more T–>E in peripheral tissues if aromatase amounts do not change. Competitive AI drugs must be increased in proportion to increasing levels of FT/Bio-T to maintain a particular E2 level.
Aromatase increases with age. I suspect that this increase with age really has to do with increasing body fat. If the amount of body fat did not change, would total aromatase increase at all with age? I have not seen any info that would support that possibility.
Fat old guys with low T typically have more E2 than their post menopausal wives.[/quote]
Thank you - for your answer. My problem was that I just assumed - I was obviously wrong!! I had not really thought the chemistry through and it seemed obvious to me, at the time, that if you need to increase AI with increasing T - higher T must result in higher aromatase. Your comment has just made me realise that aromatase is not metabolized after a single conversion of T to E and is therefore available to move on to another aromatisation reaction. Correct?
I realize the age related relationship - I agree with you in terms of body fat being the contributing factor. I have recently looked at free testosterone levels and their relationship with both age and body fat in 40 well trained ,males (drug free). A weak but insignificant relationship was present between decreasing FT and increasing age, a strong and significant relationship between increasing body fat and decreasing FT.
Having studied enzyme kinetics in a lab setting… they can catalyze the same reaction up to 40 million times a second! (catalase enzyme). I don’t know about aromitase specifically, but assuming it is relatively efficient, it will be producing thousands if not millions of estradiol molecules per second. And I’m pretty sure that enzymes are not metabolized after every reaction!
The reaction rate is controlled by the concentration of the feedstock, T in a soup of body fluids. T has to wander into the trap.
Exactly. And the higher the T concentration goes, the closer you get to saturation kinetics (what I posted above), and hence why your E2 levels would go out of control with a lot of substrate (T). But come to think of it, normal physiological concentrations of Testosterone would probably be nowhere close to saturation status, but my point is that those enzymes are extremely good at what they do.
I don’t have much time, so I have read only the first post, but I already see one lab result missing for your case. It’s Prolactin. Along libido problems it can also cause gynaecomastia and lactation in men.
If it indeed came out high then you should take something to supress it (I think bromcriptin is used for that). You also MUST find the cause of high prolactinaemia. It usually is one of these things:
Take care!