TRT: A Recipe for Success. CAUTIONARY ADVICE.

[asih.net]

A read of the file, TRT: A Recipe for Success, is incorrect for a number of reasons. There are many inaccuracies in this opus but one strikes me as possibly causing the greatest harm. In this file a special note is given to monitoring FSH as the best indicator of HPTA suppression. This could not be farther from the truth. More troubling is the person who would look to the FSH level to determine HPTA functionality. Under no conditions except for fertility should one look to the FSH level as a measure of HPTA suppression or likewise HPTA functionality. Clinically, FSH has returned with minimal or absent LH return after AAS cessation. One only has to look at the literature where after AAS cessation a study has investigated the return of spermatogenesis. In fact, a very simple look at the HPTA feedback for LH and FSH explains this quite easily. It appears as if the author of this article has either forgotten or neglected this fact.

After AAS cessation the negative feedback inhibition of the hypothalamo-pituitary area by testosterone and estradiol would be gone or at the minimum dissipating. If these were the only factors inhibiting the gonadotropins their return in approximately the same timeline is expected. However, the feedback of FSH by Inhibin and its delay in returning after AAS cessation will often have a return of FSH prior to LH. The bottom line is one should not depend upon the FSH as a measure of HPTA functionality or for that matter HPTA suppression. I hope this fully explains the reasons why FSH is not to be used for HPTA normalization or functionality.

Studies of sex steroid regulation of gonadotropin secretion in the human male have focused primarily on the respective site(s) of negative feedback of testosterone (T) and estradiol (E2). Studies provide evidence of differential regulation of gonadotropin secretion by T in the human male. T exerts both direct and indirect feedback on LH secretion, whereas its effects on FSH appear to be mediated largely by aromatization to E2.

Because androgens can undergo aromatization to estrogens in a variety of tissues, including adipose tissue, brain, and testis, it is important to be able to distinguish T effects that are mediated directly by the androgen receptor as opposed to those indirect effects that only occur after aromatization to E2. If the hypothesis is correct that T has no direct negative feedback effects on FSH, it follows that administration of T in conjunction with an aromatase inhibitor or administration of nonaromatizable androgens should not inhibit FSH secretion.

Comparing the gonadotropin responses to selective E2 inhibition vs. complete castration demonstrates that T has both direct negative feedback effects on LH presumably mediated by the androgen receptor as well as indirect effects mediated by aromatization to E2. In contrast, T’s effects on FSH appear to be mediated exclusively by aromatization to E2.

Selective suppression of E2 secretion with an aromatase inhibitor results in a significant increase in both gonadotropins.
Administration of nonaromatizable androgens, such as DHT or fluoxymesterone, has been shown to have no impact on FSH secretion except at very high doses. It is possible that given the high affinity of DHT for sex hormone-binding globulin, such high doses of DHT may displace E2 and T from sex hormone-binding globulin, increasing free levels of these sex steroids and thus confounding the impact of what was presumed to be a pure DHT effect.

Studies that E2 is the major sex steroid negative feedback regulator of FSH are supported by experiments of nature that have resulted in models of unopposed T action (congenital estrogen deficiency) and unopposed E2 action (androgen insensitivity syndrome). Men with E2 receptor mutations and congenital aromatase deficiency have a 2- to 3-fold increase in FSH despite elevated T levels. Patients with congenital androgen insensitivity syndrome (AIS) provide further evidence for the differential regulation of gonadotropin secretion by T in men, with the demonstration of normal or minimally elevated FSH despite markedly elevated LH levels.


Mike

[lou123]

Did Swale write the TRT recipe ? If so this thread should get VERY interesting, lol

[asih.net]

Another inaccuracy noted. This will result in unnecessary lab work only.


INITIAL LAB WORK: CORTISOL
Nowhere within the literature is there a correlation or association of hypercortisolemia and hypogonadotropic hypogonadism. Literature exists for the association between the critically ill and HH.


Interestingly, the effect of chronic administration of phosphatidylserine, 800 mg/d for 10 days, significantly blunted the ACTH and cortisol responses to physical exercise. In another study the effects of 750 mg of soybean-derived phosphatidylserine, administered daily for 10 d, on exercise capacity, oxygen uptake kinetic response, neuroendocrine function, and feeling states during exhaustive intermittent exercise showed improved exercise capacity.

Mike

[lou123]

Dr Mike,

What do you think of E2 blood tests while taking Clomid ? Are they accurate or as others have led us to believe do the SERMS cause an innacurate test result ?

Thanks

[mranak]

Have you emailed "the author" Dr. John Crisler to discuss your concerns?

[DLMCBBB]

Mike,

I don't see anythign that swale wrote, that would cause you to LABLE his post as "CAUTIONARY."

Swale wrote to me a while back:

There isn't much value in testing LH as a marker for HP function. It's production is so variable, and the half-life so short (30 min.) that you would have to run frequent serials draws to get a true picture. I get it initially, with a FSH, mostly to make sure it isn't too high (which could mean something else). I also want to see the relationship between the LH and FSH. At the one-month check-up, I just get a FSH, because its half-life is 8 times longer, so is a better marker for comparison of suppression.

I remember I attended a conference back in 99 with the president of cenergenics, and he stated the same thing, that he too checks FSH, but mainly to rule out a Pit Tumor.

Dustin

[hackskii]

WOW!


Respect.

[DLMCBBB]

Originally Posted by asih.net

Interestingly, the effect of chronic administration of phosphatidylserine, 800 mg/d for 10 days, significantly blunted the ACTH and cortisol responses to physical exercise. In another study the effects of 750 mg of soybean-derived phosphatidylserine, administered daily for 10 d, on exercise capacity, oxygen uptake kinetic response, neuroendocrine function, and feeling states during exhaustive intermittent exercise showed improved exercise capacity.

Mike

Interesting, you have the citations for those studies?

I can't argue for his clinical obervations in his patients, but I remember reading once that it might result in a feedback increase in CRH; I'm not sure about that, or whether it acts ultimately at the hypothalamic level to lower CRH release.

What are your thoughts?

Dustin

[HeadDoc]

It's unclear to me if the comments made about the Recipe are warranted relative to context the the Recipe was written. The comments are prefaced on observation of hypogonadal male post AAS. The Recipe refers to post 50 year old males who are showing declines. If FSH is very high, could it not be an indicator of pituitary tumor? Would a damaged pituitary not reflect impaired functionality? There is concurrance between Mike's comments and the Recipe relative to fertility. Are males who are aging and experiencing hypogonadism the same biologically as those coming off AAS?

Concerning cortisol assay, does it not make sense to get some initial look at the adrenals---and the thyroid for that matter on initial evaluation? We haven't, yet, heard much from Mike on adrenal or thyroid assays of post AAS males. However, for 50 year-old guys, who have never been on AAS the tests would seem appropriate. Many of the guys seeking such complain of fatique, interrupted sleep, sometimes labile moods, erratic eating, and sexual dysfunction or libido problems.

So is the conclusion of causing ......harm overstated?

[DLMCBBB]

Perhaps marianco would like to chime in?

Dustin

[marianco]

ASIH.net's critique of the use of FSH alone is notable and useful.

I would give SWALE leeway, despite the inaccuracies.

SWALE comes from the point of view of anti-aging medicine - where hormone replacement therapy involving all endocrine organs are central to the practice. As a D.O., his focus is on a more holistic point of view of health.

His TRT protocol was not designed for those with ASIH. It was developed for men in the general population with age-related health issues. He does acknowledge culling the list of labs from a much large list for doing a comprehensive anti-aging workup. The lab list thus has to be further customized for the patient because it may not apply for everyone and every case.

Despite the inaccuracies in the rationale in the lab orders, the initial lab list he specified has usefulness - a starting point for those who have had no prior experience with hormone replacement, who don't have a mentor to tap for their wisdom.

There are many other practitioners with similar though different lists depending on their focus - each with their own quirks.

Regarding Cortisol, I would not do testosterone replacement without first checking at least for adrenal function (e.g. with at least a cortisol, progesterone, DHEA-s, fasting comprehensive metabolic panel, hemoglobin A1c.).

I have too often seen where patients with significant mental health components to their illness (stress, depression, anxiety, mood swings, concentration problems, etc - where there is often significant influence on Hypothalamic-Pituitary-Adrenal axis - both in increased and decreased HPA activity) deteriorate (some unfortunately resulting in psychosis and hospitalization) or have no significant improvement when testosterone replacement is started before addressing functioning along the HPA axis. Since testosterone and its metabolites have variable effects on nervous system functioning dependent on the status of the HPA axis, it is important to evaluate functioning in this area.

As each practitioner who starts from this TRT protocol gains experience, knowledge, and wisdom, no doubt each will create his or her own more optimized and accurate version of this protocol for their own focus in medical practice. Its a starting point with educational utility.

[DLMCBBB]

Originally Posted by marianco

His TRT protocol was not designed for those with ASIH.

Noted Marianco, good post, im so glad to have you here at Meso. I have learned so much from you.

The only "thing" we do have for SWALE treating AAS individuals was his tailored PCT protocol, I think we all remember this one.

I advise my AAS patients to use small amounts of HCG (250IU to 500IU) two days each week, right from the beginning of the cycle. This serves to maintain testicular form and function. It makes more sense to me to keep the horse in the barn, so to speak, then to have to chase it across three counties later on. I am also a big fan of maintaining estrogen within physiological ranges. Both therapies have been shown to hasten recovery.

Any more than 500IU of HCG per day causes too much aromatase activity. Some feel aromatase is actually toxic to the Leydig cells of the testes. You are then inducing primary hypogonadism (which is permanent) while treating steroid-induced secondary (hypogonadotrophic) hypogonadism (which is temporary--hopefully).

If 250IU or 500IU on two days each week isnt enough to stave off testicular atrophy, then I recommend using it more days each week (as opposed to taking larger doses). In fact, I wouldnt mind having a guy use 250IU per day ALL THROUGH the cycle. Those that have tell me they thus avoid that edgy, burned-out feeling they usually get. They also say they simply feel better each day. Subjective reports, to be sure, but they are hard not to appreciate. Especially when HCG is so inexpensive.

The testes are then ready, willing and able to again produce testosterone at the end of the cycle. LH levels rise fairly rapidly, but endogenous testosterone production is limited by lack of use. I also want to make sure a SERM, such as Clomid or Nolvadex, is at effective serum dosage (around 100mg QD for Clomid, 20-40mg QD for Nolvadex) when serum androgen levels drop to a concentration roughly equal to 200mg of testosterone per week. That is when androgenic inhibition at the HP no longer dominates over estrogenic antagonism with respect to inducing LH production. Of course, if the fellow has been doing Clomid or Nolvadex all along the way (and I now prefer Nolvadex over Clomid, due to the possibility of negative sides from the Clomid), he is all set to simply continue it at the end (no need to switch from one to the other). BTW, I see no evidence of any benefit in using BOTH SERMs at the same time. I used to think a couple of weeks of the SERM was enough; now I like to see an entire month after the last shot of AAS (and migration of long to short esters as the cycle matures). Tapering the SERM is probably a good idea during the last week, as well.

I want my patients to stop taking HCG within a week after the end of the cycle. The testosterone production it induces will further inhibit recovery, as will using Androgel, or any other testosterone preparation, while in recovery. There is no escaping this, as there is no such thing as a bridge. Just because you are not inhibiting the HPTA for the entire 24 hours does not mean you are not suppressing it at all. IOW, you cant foolthe body it is smarter than you are.

I like Arimidex during the cycle (in fact, consider use of an AI while taking aromatisables a necessity) but it ABSOLUTELY should not be used post cycle (even though it has been shown to increase LH production) because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground and we dont want that, do we?).

All this is meant to get my guys through recovery as fast as possible (the real goal, yes?). So far, all of them who have tried it have reported they are recovering faster than when they have tried other protocols.

Dustin

[Cryptochid]

Confused about this comment
Patients with congenital androgen insensitivity syndrome (AIS) provide further evidence for the differential regulation of gonadotropin secretion by T in men, with the demonstration of normal or minimally elevated FSH despite markedly elevated LH levels.

Does this mean a male with elevated t levels that also elevates fsh and Lh is actually AIS? or PAIS? or CAH? od CAIS?....may give me some answers from the past

[pmgamer18]

As you can see, the author (I assume that it is is Scally?) repeatedly refers to a hypogonadal state that exists AFTER one has been using anabolic steroids... Just look at the examples... Every time he refers to AAS he is talkingabout Anabolic Androgenic Steroids (which are chemically different animals than natural testosterone like you and I use... the Board has become nothing more than a large PCT - Post Cycle Therapy - forum for the steroid users. It has nothing to do with Men's Health anymore.

Here's some examples:

Clinically, FSH has returned with minimal or absent LH return after AAS cessation. One only has to look at the literature where after AAS cessation a study has investigated the return of spermatogenesis. In fact, a very simple look at the HPTA feedback for LH and FSH explains this quite easily. It appears as if the author of this article has either forgotten or neglected this fact.

And:

After AAS cessation the negative feedback inhibition of the hypothalamo-pituitary area by testosterone and estradiol would be gone or at the minimum dissipating. If these were the only factors inhibiting the gonadotropins their return in approximately the same timeline is expected. However, the feedback of FSH by Inhibin and its delay in returning after AAS cessation will often have a return of FSH prior to LH.

I don't have much respect for a person or find it very Professional to Post Cautionary Advice on this with out first confronting the man that wrote it. Looks very unprofessional to me. In all the yrs. that I worked as an Engineer when we seen this happen the guy that did was Full of It.

It has come to my attention that David Z , Larry and Scott have been kicked off this Forum for specking there minds on what is now going on. So now I am specking my mind.

[Axl]

I'm sorry, but I have to agree with Phil and mranak. I would have preferred that the author of this thread had consulted SWALE on his writings. There is no use in discussion misinterpreted lines of text.

From one doctor (Asih.net) to another (SWALE), I find this post disturbingly unprofessional... Maybe it was not intended that way by Asih.net?

On the other hand, I do like the fact that everybody strives to improve TRT-protocols. Open discussions have always been the way to do this here on this forum. Respect for everybody's opinion has always been the second value that distinguishes this forum from the average other ones. The words CAUTIONARY ADVICE on top of this thread are, in my humble opnion, exaggerated.

Respect for ourselves guides our morals; respect for others guides our manners.