DrJMW--It's nice to communicate with a colleague here.
I'm going to simply add a couple of responses to yours, rather than try to paste even more in.
At this time, I see no reason to try to ascertain where any deficiency may be with respect to the cause of hypogonadism, insofar as looking at individual steps downstream. That is to say, beyond whether it is primary or secondary hypogonadism (and the very rare receptor deficiency, of course). When ordering tests, I always ask myself what I am going to do with the results. If DHEA is low, I cannot do anything about it by supplementing DHEA, because all that is going to do is elevate estrogen levels, not raise testosterone. And we cannot (yet!) manipulate individual enzymes within the pathway. So, IMPO, AT THIS TIME (I may change my mind in the future) there is no need to waste the patients' money by ordering tests which provide no useful information. With so many of my patients paying for their testosterone replacement therapy (TRT) out-of-pocket, I jealously protect their wallets.
I think a relience on DHEA is kind of a throw back to when AA'ers were trying to increase T with DHEA. We now know that doesn't work.
While I'm thinking of it, any chance you'll be in Las Vegas at the end of this week for the A4M International Conference? If so, let's hook up.
When you order a Bio T, you also get the Free T and SHBG thrown in. The only way to determine Bio T without specifically ordering it is to use the very rough calculation for it, which gives less accurate results than simply ordering it. Free T and Bio T are well coordinated, by why settle for something less? If you are merely looking for proof that suppleneting androgens, and controlling estrogen, I think that fact is well established.
There is no doubt about it, NO proper testosterone replacement therapy (TRT) workup is complete without Estradiol and Prolactin. Proper administration of testosterone replacement therapy (TRT) absolutley requires management of estrogen. I am now doing some work looking into managing the 2-OH/16-AOHE metabolites of estrogen. In fact, in the first patient I tried this on, a former steroid user now on testosterone replacement therapy (TRT) by me, his years-old hard gyno nodules completely disappered in two weeks! In only one case, to be sure, but that sure opened some eyes wide!
How are you going to monitor and control estrogen without getting labs?
The incidence of elevated PRL is way too high (approaching 5-8%) to ignore it, also. It is a significant cause of hypogonadism. It also signals a possible pituitary tumor when elevated. I've already caught one of these because I was the first to ask for the assay.
My comments regarding IGF-1 and IGFBP-3 were regarding steroid athletes, not an AA workup. I certainly do concur with drawing an IGFBP-3 for AA workups. But if a guy is going to take huge GH dosing for BB'ing anyway, it certainly is not necessary. In any case, there's nothing you can do with the results.
I draw LH up front, but its short half-life and pulsatile production make it almost worthless when only one assay is drawn (as opposed to serial draws). I am really only looking for something really out of whack when I order it. FSH is used on my follow-up labs, as it is a much better indicator of gonadotrophin production as it relates to suppression of the HPTA secondary to TRT.
You really won't see elevated PSA secondary to testosterone replacement therapy (TRT) dosing when administered IM. It may very well accelerate with transdermal delivery systems, because of increased DHT production induced by same, but will stablize to baseline once serum androgen levels have stabilized, too. And this phenomen really only occurs in older men.
If you are drawing a PSA for steroid athletes, what use are the results? You know it is elevated from the AAS, and from the increased sexual activity, but is the guy gong to quit because he has an elevated PSA, when it would be phenomenally rare for a man under the age of forty to get prostate cancer? If you are concerned with elevated DHT levels, then draw that. But again, you can expect that with Anabolic Androgenic Steroids (AAS) use, so the cost of the labwork is unjustified. If he is losing his hair (at a greater pace than he would normally), then switch AAS, or add in some finasteride.
As far as the actual effects of DHT on the prostate, I have learned much through the studies conducted on men with prostate morbidity who engaged in DHT as sole TRT.
As you can see, I am trying to be careful to separate out what we do for testosterone replacement therapy (TRT), and the advice we give steroid athletes.
If you would like to email me at my practice's addy, I would be happy to send you a copy of the report I just wrote for the American Academy of Anti-Aging Medicine. It is a "recipe" for administering testosterone replacement therapy (TRT) for men, and is getting pretty good reviews by the professionals who have seen it thus far.
I'm going to simply add a couple of responses to yours, rather than try to paste even more in.
At this time, I see no reason to try to ascertain where any deficiency may be with respect to the cause of hypogonadism, insofar as looking at individual steps downstream. That is to say, beyond whether it is primary or secondary hypogonadism (and the very rare receptor deficiency, of course). When ordering tests, I always ask myself what I am going to do with the results. If DHEA is low, I cannot do anything about it by supplementing DHEA, because all that is going to do is elevate estrogen levels, not raise testosterone. And we cannot (yet!) manipulate individual enzymes within the pathway. So, IMPO, AT THIS TIME (I may change my mind in the future) there is no need to waste the patients' money by ordering tests which provide no useful information. With so many of my patients paying for their testosterone replacement therapy (TRT) out-of-pocket, I jealously protect their wallets.
I think a relience on DHEA is kind of a throw back to when AA'ers were trying to increase T with DHEA. We now know that doesn't work.
While I'm thinking of it, any chance you'll be in Las Vegas at the end of this week for the A4M International Conference? If so, let's hook up.
When you order a Bio T, you also get the Free T and SHBG thrown in. The only way to determine Bio T without specifically ordering it is to use the very rough calculation for it, which gives less accurate results than simply ordering it. Free T and Bio T are well coordinated, by why settle for something less? If you are merely looking for proof that suppleneting androgens, and controlling estrogen, I think that fact is well established.
There is no doubt about it, NO proper testosterone replacement therapy (TRT) workup is complete without Estradiol and Prolactin. Proper administration of testosterone replacement therapy (TRT) absolutley requires management of estrogen. I am now doing some work looking into managing the 2-OH/16-AOHE metabolites of estrogen. In fact, in the first patient I tried this on, a former steroid user now on testosterone replacement therapy (TRT) by me, his years-old hard gyno nodules completely disappered in two weeks! In only one case, to be sure, but that sure opened some eyes wide!
How are you going to monitor and control estrogen without getting labs?
The incidence of elevated PRL is way too high (approaching 5-8%) to ignore it, also. It is a significant cause of hypogonadism. It also signals a possible pituitary tumor when elevated. I've already caught one of these because I was the first to ask for the assay.
My comments regarding IGF-1 and IGFBP-3 were regarding steroid athletes, not an AA workup. I certainly do concur with drawing an IGFBP-3 for AA workups. But if a guy is going to take huge GH dosing for BB'ing anyway, it certainly is not necessary. In any case, there's nothing you can do with the results.
I draw LH up front, but its short half-life and pulsatile production make it almost worthless when only one assay is drawn (as opposed to serial draws). I am really only looking for something really out of whack when I order it. FSH is used on my follow-up labs, as it is a much better indicator of gonadotrophin production as it relates to suppression of the HPTA secondary to TRT.
You really won't see elevated PSA secondary to testosterone replacement therapy (TRT) dosing when administered IM. It may very well accelerate with transdermal delivery systems, because of increased DHT production induced by same, but will stablize to baseline once serum androgen levels have stabilized, too. And this phenomen really only occurs in older men.
If you are drawing a PSA for steroid athletes, what use are the results? You know it is elevated from the AAS, and from the increased sexual activity, but is the guy gong to quit because he has an elevated PSA, when it would be phenomenally rare for a man under the age of forty to get prostate cancer? If you are concerned with elevated DHT levels, then draw that. But again, you can expect that with Anabolic Androgenic Steroids (AAS) use, so the cost of the labwork is unjustified. If he is losing his hair (at a greater pace than he would normally), then switch AAS, or add in some finasteride.
As far as the actual effects of DHT on the prostate, I have learned much through the studies conducted on men with prostate morbidity who engaged in DHT as sole TRT.
As you can see, I am trying to be careful to separate out what we do for testosterone replacement therapy (TRT), and the advice we give steroid athletes.
If you would like to email me at my practice's addy, I would be happy to send you a copy of the report I just wrote for the American Academy of Anti-Aging Medicine. It is a "recipe" for administering testosterone replacement therapy (TRT) for men, and is getting pretty good reviews by the professionals who have seen it thus far.
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