T Nation

KSman is Here


I cannot respond to that, cannot find where that came from for context.

Link me there.


Just a small question , I know i have hypogonadism already but i received new results today with low ggt 7 (15-73) what does it mean ? I can’t seem to find info anywhere ? @KSman


A good place to be. See this:

Can also be lower via different genetics also via enzyme variations.

In summary, genes play a substantial role in explaining differences in plasma levels of GGT, ALT and AST (h2 22–60 %), which are important markers of liver injury and other disease. Genetic influences on liver enzyme levels include additive and non-additive genetic effects. Genotype by sex interactions (for GGT and ALT) and genotype by age interactions (for GGT in males) were present, but there was no evidence that different genes are expressed across sex or age.

Can also be lower via different genetics also via enzyme variations.


Hi KSman, can you take a look at my thread. I think I may be hyperthyroid. I will see my doctor tomorrow to likely do more tests to confirm. Before I see him, I was just wondering if you had advice. Is there any way to treat hyperthyroid without destroying my thyroid?



New lab tests are in on my thread.

Would appreciate your thoughts.




Hey KSman!

Thanks for all the help you’ve been providing for so long. Had a few questions on clarification for some questions you regularly ask people.

I’ve always had sparse and uneven chest hair. Facial hair is a bit more even, but slightly sparse. Even after 1 year of TRT, while my chest and facial hair has filled in more, my chest hair is still pretty uneven, more on the left, asymmetric shape.

I noticed you often ask people if this is the case, but haven’t come across any posts where people confirmed and that led you to discuss a concern related to it. Would you mind going into this for me?

Thanks again!


My sparse beard became dense and even.

I had very little hair on my body and still have very little, but some now. Arms still have little hair, legs are normal below the knees. Below the knees had lost hair as a normal effect of low-T. So hair below the knees was mostly recovery and not new.

Genetics rule and if you were not fully virilized before, TRT will do that but within your genetic envelope.

Do not worry about it. You do not want to be as hairy as a rug. Some areas of hair growth may change over a time window of a few years, not months.

Asymmetric is just the way you are.



Responded to your questions.



Hello @KSman, hello everyone,

my question is somewhat technical. Do you have any information if (and why) adding exogenous testosterone (injections) to clomiphene would hinder its stimulating properties on HPG axis?

My logic is as follows:

1.Clomiphene stimulates hypothalamus, pituitary gland, and gonadal glands. TT and E2 are high, cortisol and SHBG go up as well, IGF-1 and FT go down. Estrogenic properties of zuclomiphene and low FT are the reasons for no subjective rise in quality of life. But hey - at least we are in a process of HPG restart.

2.Adding exemestane lowers E1 and E2 to optimal levels, should lower SHBG and increase FT at least a little.

At this point we stimulate hypothalamus, pituitary gland, and gonadal glands but we don’t stimulate androgen receptors because of low FT (not to mention libido and well-being).

3.We add exogenous testosterone (for example testosterone ethanate) for more FT. E2 receptor in hypothalamus is still “blocked” by clomiphene, so it shouldn’t make any difference if there is more FT or E2 in the system.

That way our testicles and fertility are safe, our axis is working and we are feeling good.

Help me find any holes in my hypothesis.



You are missing some distinctions that make your post a bit fuzzy.

The lower dose SERMs that we use in TRT modulate E2 exposure to the hypothalamus. You cannot be using the term “blocked”.

The bad effects of clomid are only experienced by some guys, not a small fraction. This is showing that some are wired up differently via DNA or DNA expression that probably is via different variations in enzymes. Those who suffer with Clomid are good with Nolvadex.

  1. E2 only gets high if the dose is high enough for LH to be high enough to drive high T–>E2 inside the testes. You missed this distinction and make a bad conclusion. If E2 is high, SHBG can increase, lowering FT %, but this is then a dosing problem, not an absolute fact. I do not see a firm relation to cortisol, please link me to references.

  2. I know that anastrozole does not work to control E2 when testicular T–>E2 is high. Aromasin might work, but I have never seen an lab situation to support that premise. I cannot support your statement as fact. No AI can reduce existing E2 in the blood, only the liver is a major player in that. An AI can only modulate T–>E2 and anastrozole cannot do that inside the testes, aromasin perhaps might, but might not.

“At this point we stimulate hypothalamus, pituitary gland, and gonadal glands but we don’t stimulate androgen receptors because of low FT (not to mention libido and well-being).”

  • I can’t make any sense of that, FT is not low!
  1. yes to some extent, but we are needing to consider modulation not blocking, so T+SERM vs SERM will increase E2.


Thank you for your reply

Yes, you are absolutely right, bad simplification.

I’ve noted a lot of complains on a lot of forums about those side effects and no improvement in anything but lab results.

Yes to the first sentence (again - my simplification). So, according to you, SHBG is dependent on E2 in this case and not on (other) properties of clomiphene? I have doubts. Please read the following (also contains info on cortisol):


So: 1 [AI’s don’t work on aromatase conversion in testicles] or 2 [conversion in testicles happens via different enzyme]?

I meant - a lot of people claim that on Clomid their TT is high, E2 is high but FT is very low (and I know that some medical research papers say different). If FT is low then there is no improvement in for example libido. Also - there are some, that have less sensitive T receptors and for them FT is crucial.

I understand modulation. What did you mean by [T+SERM vs SERM will increase E2]? On T+SERM E2 will be higher than on SERM alone? If that’s the case - yes I think the same.


According to the summary, 3mg/kg/day, 225mg/day for a 75kg male [165 pounds]

This is a study to determine the effects of the drug. This is not a study of a therapeutic dose. This is 9 25mg doses per day.

E2 levels were probably getting insane and E2 would be driving the bus.

You need to learn how to read papers to distinguish between a research paper and clinical paper to not be led astray. Some papers are in-vitro, test tubes for example, and other in-vivo, a living organism. Some are in humans and others in rats etc.

The results are meaningless. They also talk about SHBG but do not report estrogen levels.

Please pretend you never found that article.

“I’ve noted a lot of complains on a lot of forums”

  • they are using stupid high doses for PCT, stacking SERMs and SERMs+hCG. If you do everything wrong, you find things to complain about.

Guys who are typically doing things very wrong do not have labs.
On high dose SERMs with high E2, the liver sees E2 loud and clear and will jack up SHBG.

In the testes, intratesticular testosterone can be 80-100 times higher than serum levels. Anastrozole is a competitive drug that simply is not going to work inside the testes unless you take 80 or 100mg per week which is insane. Aromasin binds to aromatase and might behave differently. But this is hyped so much. If that is so great, why are the doses so high when 1mg/week anastrozole works.

Proper dosing of SERMs does not create high E2. There are always a few/rare guys where things work differently.

Can you apply the above to your thinking. Let me know if you have remaining questions. But I am not hear to edit your summaries, but equipping you with knowledge to think things through.


So, could T + SERM + AI work? I know that it would depend on perfect doses (and frequent lab work), but does it make any sense to you? Do you think it might be better for fertility than T + HCG?

I really don’t want to bore anyone with my story. Docs are clueless in this matter, they know only Clomid monotherapy or T + HCG. I found few instances of T + HCG + Clomid + AI for 3 months before trying to conceive on TRT, but that is overkill in long term.


Hey Brother,
I’m new here and could use some help. Any chance you could take a look at my labs?



I updated my thread.



Just a quick question cause I don’t feel the need for a new topic . I have hypogonadism still untreated and I was wondering if suicidal thoughts was a known symptoms?


Couple of updates on my thread. Appreciate your insight. Thanks!


Updated details on Iodine supplementation.
Big thanks.


Yes, however with TRT lasting the rest of your life, hCG as a natural human hormone is not going to create issues and SERMs are not worry free. I sometimes suggest hCG with SERM holidays occasionally when there is a heightened concern re fertility. LH/FSH needs to be manged to avoid high levels just as high hCG doses need to be avoided.


Tucker, we see lots of guys here treated for depression when the underlying problem is a sex hormone imbalance. Mostly low T, but I need to stress that E2 needs to be in balance. Low thyroid function is a very common problem that robs energy and can create mood-depression problems by itself or compound any other cause/case of depression. In many cases the thyroid issues can be caused by iodine deficiency caused by not using iodized salt.

If your depression has deeper roots, hormone problems still need to be addressed as you peel back the onion.

Some SSRI’s can increase suicidal thoughts as the medication can give one the energy to attempt.

Please open a topic for your case and provide all available labs with lab ranges. I think that we can help a lot. Getting docs to do things right may take some work.