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PostPosted: Wed Nov 01, 2006 7:23 am 

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TRT: A Recipe for Success

Following is a copy of the report I wrote, included in the American
Academy of Anti-Aging Medicine 2004/5 Anti-Aging Clinical Protocols
manual. Of note, some of the editing integrity has been compromised
via transferal to this medium. Readers please take note of the
restrictions imposed by my copy right at the end.



--John Crisler, DO

We have already learned a practical bit about the various hormones
that make up the metabolic "symphony" which comprises our hormonal
milieu. We know where these hormones are produced, what modulates
their production, and the target tissues of their various and varied
actions. But we still need to integrate this knowledge into a
practical "recipe", if you will, so the clinician may return to
his/her practice, and immediately begin screening for, and
successfully treating, male hypogonadism. In other words, how do you
actually administer Testosterone Replacement Therapy for men?

Should EVERY adult male patient who presents at your office be
automatically screened for hypogonadism? About half of all men over
the age of fifty are in fact hypogonadal (when tested for Bioavailable
testosterone—more on that later). Certainly the answers to Medical
History will lead the way toward suspicion of same, yet the complaints
related to this insidious condition are sensitive without being
specific. Clinical suspicion is further clouded because there is no
way to correlate either the number of individual complaints, or the
relative magnitude of each, to the severity of the hypogonadotrophic
state on laboratory assay. The number one complaint which should hoist
the proverbial red flag is Erectile Dysfunction. This is also the
symptom of hypogonadism which, aside from all the seriously
deleterious effects of same (coronary artery disease, diabetes,
osteoporosis, increased risk of cancer, depression, dementia, etc.),
is most likely to bring the patient to actively seek TRT—and to remain
compliant in your treatment regimen.


Following a good Medical History, which laboratory assays should be
run as part of your initial hypogonadism workup? Following is my list,
but certainly other specialists in this area run expanded or
attenuated panels, per their experience and expertise. Of note, there
are several other tests which should be included to complete the true
comprehensive Anti-Aging Medicine workup (i.e. homocysteine, fasting
insulin, comprehensive thyroid study, etc.), as this chapter is
concerned solely with administering TRT. And as always, the panel is
tailored to the individual patient. Here they are:

• Total Testosterone
• Bioavailable Testosterone (AKA "Free and Loosely Bound")
• Free Testosterone (if Bioavailable T is unavailable)
• Estradiol (specify the Extraction Method, or "sensitive" assay for
• LH
• Prolactin
• Cortisol
• Thyroid Panel
• Comprehensive Metabolic Panel
• Lipid Profile
• PSA (if over 40)
• IGF-1 (if HGH therapy is being considered)


Two weeks after initiating a transdermal, or five weeks after the
first IM injection:

• Total Testosterone
• Bioavailable Testosterone
• Free Testosterone (if Bioavailable T is still unavailable)
• Estradiol (specify the Extraction Method, or "sensitive" assay for
• DHT (especially if patient is using a transdermal delivery system)
• FSH (3rd Generation—ultrasensitive assay this time)
• Comprehensive Metabolic Panel
• Lipid Profile
• PSA (for more senior patients)
• IGF-1 (if GH Therapy has been initiated already)



This is the assay your patients will most focus on. It's also the one
physicians who do not understand TRT will use to deny patients the
testosterone supplementation they want, and need, when Total T is at
low-normal levels. Total T is important for titration of dosing, but
its relevance is reduced in older men (by virtue of their increased
serum concentrations of SHBG), in favor of:


Where we actually get the "bang" for the hormonal buck, so to speak.
This is the actual amount the body has available for use, as the
concentration of hormone available within the capillary beds
approximates the sum of the Free Testosterone plus that which is
loosely bound to carrier proteins, primarily albumin. If Bio T is not
readily available, Free T may be a second choice substitute, as Bio T
and Free T serum concentrations are well correlated.


This assay is especially important to draw, up-front and at follow-up,
if a transdermal testosterone delivery system is preferred by the
patient. I'll explain why later. DHT level may also help indicate
cause for ED symptoms.


There are several reasons why this assay is VERY important, and should
not be ignored in ANY hypogonadism work-up (or subsequent regimen).
First, you definitely need to draw a baseline. Next, elevated estrogen
can, in and of itself, explain hypogonadal symptoms. If E is elevated,
controlling serum concentrations (usually with an aromatase inhibitor,
which prevents conversion of T into E) may suffice in clearing the
symptoms of hypogonadism. And finally, rechecking it after beginning
the initial dose of testosterone will give the astute physician
valuable information as to how the patient's individual hormonal
system functions, as well as making sure estrogen does not elevate
inappropriately secondary to the testosterone supplementation.

I don't waste time and money drawing estrone and estriol. E2 is the
player of interest here. Unless you specify a `sensitive' assay for
male patients, the lab will run the Rapid Estradiol for fertility
studies in females, which is useless for our purpose here. Quest
Diagnostics calls this their Estradiol by Extraction Method.

Some practitioners believe that it is only the T/E ratio which is
significant, and therefore, as long as E "appropriately" rises with
elevations in T, all is well. However, the absolute concentration of E
is of concern, too, especially in light of new information pointing to
elevated estrogen as cause, or adjunctively encouraging, several
serious disease processes, including prostate and colon cancer.


As everyone knows, it is LH which stimulates the Leydig cells of the
testes to produce testosterone. A caveat, however: LH has a half-life
of only about 30 minutes. When you combine this fact with the absolute
pulsatile nature of its pituitary release, care must be taken to not
place too much weight upon a single draw. A luxury would be to acquire
serial draws, say, twenty minutes apart. However, such would be both
inconvenient and probably prohibitively expensive for the patient. The
most important reason to assay the gonadotrophins is to differentiate
between primary and secondary (hypogonadotrophic) hypogonadism.


The eight hour half-life of this hormone makes it a better marker for
gonadotrophin production. It is also less an acute phase reactant to
varying serum androgen and estrogen levels than LH. Greatly elevated
FSH levels could signal a gonadotrophin-secreting pituitary tumor.

Of note, I run FSH (but not LH) on the follow-up labs, the new third
generation ("sensitive") assay, to determine the magnitude of HPTA
suppression secondary to androgen therapy. It also provides valuable
information for those patients undergoing TRT who are interested in
the state of their fertility.


A very important hormone, and must not be overlooked on initial
work-up. Approaching five percent of hypogonadotrophic hypogonadism is
associated with hyperprolactinemia, due to inhibition of hypothalamic
release of LHRH. Its serum concentration must be maintained within
physiological range (meaning neither too high nor too low). Greatly
elevated hyperprolactinemia, or hyperprolactinemia plus a Total
Testosterone less than 150ng/dL, equals a trip to an Endocrinologist
for an MRI of the sella turcica.


True Anti-Aging medicine must be well-familiarized with the ins and
outs of this hormone, the only one our bodies cannot live without.
Elevated levels can cause secondary (hypogonadotrophic) hypogonadism.
I try controlling elevated cortisol with Phosphatidylserine, 300mg QD,
with good results. It is just as important to watch for depressed
cortisol levels, as well. The assay of choice for that condition is a
24-hour urine.


I have, for my own convenience, omitted the specifics of the
obligatory thyroid function panel you certainly will want to run.
Hypothyroidism mimics hypogonadism in several of its effects.


This is just good medicine. Ruling out anemia is important, of course,
as it may be a cause for the fatigue which brought the patient into
your office. You also want to establish baseline H&H, for those rare
cases where polycythemia becomes a problem (and we are reminded
smokers are at increased risk for polycythemia). Above 18.0/55.0 TRT
is withheld, and therapeutic phlebotomy recommended.


Again, just good medicine. Baseline for sodium (which may elevate
initially secondary to androgen supplementation) is important. We also
want to see LFT's, as elevations in same secondary to androgen
supplementation are listed as a possible side effect in the product
literature (although I have yet to see this actually happen). I like
the BUN/creatinine ratio as a marker for hormonal hemo-concentration,
and also it gives me a hint of how compliant the patient will be
(because I always tell them to make sure to drink plenty of water
while fasting for the test).

Lipid Panel

This is drawn to provide your bragging rights when you drop the CHOL
30 points, thanks to your own good administration of TRT. You should
expect to see lowered TRIG and LDL's, too. Be advised, this will not
happen if you choose to elevate their androgens above the top of
"normal" range, i.e. providing what amounts to an anabolic steroid
cycle. Of course, this would no longer constitute TRT, as the
practitioner would then be choosing to damage the health and
well-being of the patient.

HDL does frequently drop a bit, but that is believed to be due to
increased REVERSE cholesterol transport; so much of the plaque is,
after being scavenged from the lining of the CV system by HDL, now
being chewed up by the liver. Androgens also elevate hepatic lipase,
and this may have an effect. The important thing to keep in mind is
that TRT inhibits foam cell formation.


For all patients over 40. Even though prostate CA is rare in men under
the age of fifty, we don't want it happening on our watch, do we? At
this time, rises in PSA above 0.75 are a contraindication to TRT
(until follow-up by a Urologist). You may find that, at the initiation
of TRT in older men, when serum androgen levels are accelerating, PSA
may, too. This is especially true when transdermal delivery systems
are employed, because they more greatly elevate DHT. Once T levels
have stabilized, PSA drops back down to roughly baseline. You won't
really see gross elevations in PSA secondary to TRT administration in
younger patients. New TRT patients need to be cautioned, and reminded,
to abstain from sexual relations prior to the draw, as they may now be
enjoying greatly elevated amounts of same.

I get a PSA up front on my over 40 patients, at the one month
follow-up in my more senior patients, and every six months after that.
DRE (Digital Rectal Exam) is recommended twice per year as well,
although the American Academy of Clinical Endocrinologists backs
"every six to twelve months" in their 2002 Guidelines for treating
hypogonadotrophic patients with TRT.


For those who are considering the addition of GH to their Anti-Aging
regimen. IGF-1 will rise from testosterone supplementation, and vice
versa. Let's grab a baseline now, before that happens.


CO-MORBIDITIES. Currently, only breast and active prostate cancer are
absolute contraindications for TRT. Patients with serious cardiac,
hepatic or renal disease must be monitored carefully due to possible
edema secondary to sodium retention. Also, TRT may potentiate sleep
apnea in some chronic pulmonary disease patients, although studies
have also shown it can actually ameliorate the symptoms of sleep apnea.

DRUG INTERACTIONS. TRT decreases insulin or oral diabetic medication
requirements in diabetic patients. It also increases clearance of
propranolol, and decreases clearance of oxyphenbutazone in those
receiving such medications. TRT may increase coagulation times as well.


Now we have to decide, TOGETHER with our patient, what form of
testosterone delivery system we will START with. There are two basic
subsets of same—transdermals and injectables. Here are the current


The only way to go, in my professional opinion, if physician and
patient prefer a transdermal delivery system. They are easy to apply,
well absorbed, and rapidly establish stable serum androgen levels
(usually by the end of the second day). I recommend all practitioners
first try a testosterone gel for their TRT patients.

Much is made of the risk posed by accidental transferal of
testosterone to others, such as children or sexual partners. Simply
covering with a T-shirt has been shown to block transfer of the
hormone. The testosterone sinks into the skin within an hour, which
acts as the actual reservoir for the hormone's delivery. One may then
shower, or even swim, without worry. I remind my patients that most of
us have neither the time, nor the opportunity, for romance until
evening (given the recommended early morning application), and a quick
shower is always nice to "freshen up" then anyway.

Gels and creams, like all transdermal delivery systems, provide a
bigger boost in DHT levels, compared to injectable testosterone
preparations. This can be a double-edged sword. As DHT is responsible
for all the things of manhood, the transdermals are better at treating
ED than the injectables. However, issues of hair loss and possible
prostate morbidity (a contentiously debatable point, to be sure) then
come into play. Either way, please make sure to monitor DHT with the
transdermals. I'm just not comfortable with gross elevations in DHT,
and prefer to avoid adding finasteride whenever possible.

Some have reported an increase in hair growth over the application
area(s). All physicians who administer TRT must be prepared to
disappoint their patients at this time by pointing out, sadly, this
same effect cannot be achieved on the scalp.


These can be quite effective, but are inconvenient to use. Approaching
2/3's of your patients will develop a contact dermatitis from them at
some point. Another drawback is that some patients report they are
constantly aware of their placement, and the patches are
embarrassingly obvious to other gentlemen in certain public places,
such as in the locker room.

The scrotal application variety is the most inconvenient. To see what
I would be putting my patients through, I tried them. After just a
couple days, I'd had more than enough. Men do not generally enjoy
shaving their scrotum, and the patches just do not stay on well
anyway. Applying a hair dryer to the patch, as they must be warmed
first, is also an annoyance. If you go to the gym during the day, they
look strange affixed to the genitals, and must be removed, then
reapplied, to shower. They do not stick well in the first place, and
even less so once they have been reapplied. Of the two options, I
found only the type with the extra adhesive had any chance of
remaining in place. The scrotal variety causes the largest increases
in DHT—which can be good or bad, as previously explained.


In my opinion, their use is absolutely Stone Age. Sure, they can
provide extra revenue by virtue of a billable office based procedure.
However, needlessly exposing patients to the risks ALL surgeries
pose—hemorrhage and infection—is unwarranted. And the area of
insertion will be much tenderer than that following a mere IM
injection. But the real issue which selects against pellet
implantation is concerned with dosing. Let's say you establish a
"usual" initial dose for the pellets. As will be described in the next
section, there is absolutely no way to predict, up front, how a
patient will react to a given dose of testosterone, regardless of the
delivery system. So you bury these pellets in your patient's backside,
and (hopefully) draw follow-up labs in a month or so. What are you to
do if the total testosterone ends up greatly exceeding the top of
normal range (meaning the patient hyper-responded to the treatment)?
Now you must make a much wider incision to remove them, or a portion
of them (and who knows how many to take out?). With their very long
half-life, SOMETHING must be done, lest you risk actually damaging the
health of the patient by elevating testosterone levels into what might
be considered a bodybuilding steroid cycle. And what if the pellets do
not elevate T enough? You must bring them back in to implant more, and
it's difficult to sell them on this idea, since they probably are not
yet feeling the advantages of TRT enough yet to motivate them into
undergoing another surgical procedure. It just doesn't make sense, to
my way of thinking.
Testosterone pellets do have some benefit in that selected patients
may believe it more convenient to come in every month or six weeks,
and then be done with it for a while. Also, because they release T in
a slow, steady rate, the pellets are less likely to induce increases
in aromatase activity.


I'll start out by describing the drawbacks of IM testosterone. They
are inconvenient for patients who do not wish to give themselves their
own injections, as they must then make weekly trips to your office for
same. Why IM test MUST be dosed weekly will be described in detail in
another section. Some patients, as you well know, just hate shots
(although I have noticed several who had initially claimed this, but
admitted, once they had come to enjoy the benefits of TRT, actually
came to look forward to their weekly injection). And no doubt, an
invasive delivery system brings more risk than, for instance, a
testosterone gel or cream (the other best choice for TRT).

When considering dosing of testosterone cypionate, it is important to
remember that, due to the weight of the cypionate ester, a 100mg
injection delivers, at best, 70mg of testosterone. This is important
to keep in mind when comparing the effects of a 100mg weekly injection
of test cyp to the 35mg total dose provided by Androgel 5gms QD over
the same period.


Many practitioners consider this incredible hormone treatment of
choice for hypogonadotrophic (secondary) hypogonadism. Such certainly
makes sense, as supplementing with a LH analog indeed increases
testosterone production in patients who do not concurrently suffer
primary hypogonadism. But often, upwards of 1000IU per day must be
given to achieve the desired serum T level. Even then, for some
unexplained reason, while serum T levels may be adequately elevated,
the patients simply do not report realization of the benefits of TRT,
when HCG is administered as sole TRT. You also run the risk of
inducing LH insensitivity at that dosage, and therefore may actually
cause primary hypogonadism while attempting to treat secondary
hypogonadism. HCG, especially at higher doses, also dramatically
increases aromatase activity, thus inappropriately elevating
estrogens. Personally, I recommend never giving more than 500IU of HCG
at a time.

A real benefit of HCG is that it will prevent testicular atrophy. I do
not think we should ignore the aesthetics of that consideration. Your
patients will feel the same way.


I occasionally hear of physicians trying to use a SERM (Selective
Estrogen Receptor Modulator) such as Clomid or Nolvadex, or even an
Aromatase Inhibitor (AI), such as Arimidex, as sole "TRT". All have
been shown to elevate LH, and therefore Total Testosterone levels.
However, patients report no long-term subjective benefits from these
strategies, and the studies thus far reported no long-term changes in
lean body mass, fatigue levels, libido, etc. An added risk of using an
AI is of driving estrogen levels too low, with deleterious
consequences for the lipid profile, calcium deposition, libido, etc.

Finally, Deca-Durabolin (Nandrolone) has no place in TRT. It has a
nasty side effect profile, including uncontrollable progesterone-like
effects (including gynocomastia) and risk of long-term impotence.


Now we will delve into the general strategy for administering TRT.

The decision is made, TOGETHER with the patient, which of the various
testosterone delivery systems is to be tried first. Be prepared to
make adjustments, and try other application methods. You just don't
know which will be best for each particular patient until you try.
Besides the simple fact the patient may have a personal preference, or
a logistical consideration (i.e. inability/unwillingness to
self-inject) for a given application, every-body reacts differently to
hormonal manipulation. Some hyper-respond to a given initial dose,
others show hardly any bump in serum T levels on same. Yet when you
switch to a different delivery system, on initial dosing, they may
convert to supraphysiological androgen levels. The same is true of the
subjective benefits from TRT. I have patients who love testosterone
gel because it successfully treated their ED (the expected outcome
because of dramatically increased DHT production), others get more
from IM testosterone cypionate. My experience thus far has taught me
two lessons: (1) You don't know how a patient will react to a given
dose/system until you try and (2) NOTHING surprises me anymore.

There simply is no way to predict how a particular patient will
respond—not Medical History (i.e. number or severity of symptoms),
body weight, baseline hormone levels, even anabolic steroid history. I
have had very slight gentlemen barely elevate on 100mg of test cyp per
week, and massively muscled former steroid athletes who went to nearly
two times the top of "normal" range on the same dosage (they had
similar baselines). Likewise, one man may see only a modest increase
in DHT on 5gms of Androgel, another may become quite
supraphysiological on same.

I start my guys out on either testosterone cream/gel 5mgs QD or
testosterone cypionate 100mg per week. The IM test cyp must be
administered in weekly injections, as opposed to taking twice the
dosage every other week. Some physicians even dose every third or
fourth week, producing wide swings in serum androgen levels. This puts
the patient on an emotional roller coaster, increases the risk of
developing polycythemia, greatly accentuates aromatase activity, and
actually leaves them lower than they were when they started for the
last half of the cycle. In order to get the serum androgen
concentration to a stable level more quickly, I "frontload" 200mg the
first injection (unless converting over from a gel/cream).

No other medications which manipulate hormone levels are provided
until follow-up labs are returned. For IM test cyp patients, the
second panel is run following the fifth injection. I also keep in mind
the coordination of the injection with the lab draw, as peak serum
levels are attained at about the 48 hour point, then fall to about 35%
at the one week point. However, by the end of the fifth week, the
pharmacodynamics of testosterone cypionate (half life is 5-8 days) are
such that relatively stable serum levels are now being produced via
weekly injections.

Transdermals can be rechecked in two weeks. They produce stable serum
levels, as previously mentioned, for most by the end of the second or
third day. Logistically, it makes sense to send the patient for
follow-up labs after a fortnight, as there is then time to get the
labs back, and bring the patient in, before the initial 30-day supply
of the medication runs out. This is better if an adjustment in dosage
is mandated by the follow-up labs, or to convert to IM dosing should
the patient produce too much DHT. It would be a shame to have the
patient refill a script for 5gms of Androgel, when they, by their
labs, are going to have their dosage reduced to 2.5gms per day because
they hyper-responded to the initial dose, or waste money when what
they reallyneed is to be converted to test cyp.

The question of which testosterone delivery system is to be tried
first (IM or transdermal) is one which brings much confusion amongst
beginning practitioners of TRT. I would, when possible, always start
out a patient on a testosterone cream or gel. Ease of application,
avoidance of intrusion by injection, and increased probability of
successful ED treatment make this so. Also, stable serum levels are
attained quickly, determination of successful treatment is more
forthcoming (although the manufacturer of this product recommends at
least a couple months as adequate trial of therapy). If the labs AND
patient's answers to follow-up subjective report lead to a change to
IM testosterone, the conversion is an easy one to make. Simply apply
the gel, give the shot, then D/C the gel. However, if a patient is
started out on IM test cyp, for instance, yet the patient still does
not feel "right" (and thus you may want to try a transdermal delivery
system to better raise DHT levels), how are you, given the
pharmacodynamics of the testosterone ester, going to safely and
successfully dose the conversion to a transdermal?

Dosing changes are made, TOGETHER with the patient, once follow-up
labwork is back AND the patient is interviewed regarding their
subjective reports of changes in libido, sexual performance, fatigue,
strength, mental outlook, etc. Often they will tell you they felt
"incredible" the first couple of weeks (and bursting with libido), but
they don't feel quite as good now, but still much better than before
they started the TRT. This is because subjective findings are the best
while serum androgen levels are accelerating. Adjunctive to this
phenomenon is the fact their HPTA was not yet being suppressed, so
their endogenous production was higher then than it would be by the
end of the month. TRT patients are always HPTA suppressed to greater
or lesser degree.

Much weight is placed upon the patient's subjective findings, as they
are not likely to remain compliant in the TRT program unless they feel
noticeably better, irrespective of the less obvious long term
improvements in CV health, bone density, decreased risk of dementia
and cancer, etc. Certainly, if the patient reports they are quite
happy at a Total Testosterone level of 600ng/dL, I feel there is
little reason to increase their dosage. As an Osteopath, I am loath to
provide ANY medication, or increase in dosage, without proven need. As
a practical limit, the top of "normal" range for Total Testosterone
provides a ceiling, more or less, above which we can expect to find
the benefits of TRT beginning to reverse themselves. Actions following
androgen receptor binding dramatically improve health and happiness as
we go from the hypogonadal state to the top of "normal" range, but
beyond that the Lipid Profile and level of insulin sensitivity, for
instance, are damaged.
Changes in IM dosing are made in small increments, as response to same
is not linear. It is convenient and practical to increase, or decrease
IM dosing by 20mg at a time, as this is one "tick mark" on the side of
the syringe (for the 200mg/mL concentration). For Androgel patients,
we are more limited by their provided dosing whereas we can only
either drop down to 2.5gms, or add an extra pack each day (at which
time BID dosing may be considered) to reach the 7.5gm, or even 10gm,
per day dose. More flexibility is provided through compounded products
for those committed to employment of transdermal testosterone delivery

Another risk of jumping the dosage too much is that, should serum
androgen levels greatly exceed the top of "normal" range, the patient
risks becoming "spoiled" at that level. They would then feel the
subjective benefits steroid athletes report, and it would be difficult
to get the patient then to be happy at a more moderate—and
proper—dose. It is likely you would also therefore produce elevated
estrogen activity as well, and further muddy the waters with respect
to how the patient feels—and looks (due to emotional changes and even
water retention issues from the elevated estrogen). It is far better
to make changes in dosing conservatively.

Once the method and dosing is set, by laboratory assay AND subjective
report from the patient, then you may address any side effects due to
elevated estrogen levels which have occurred. I do not use an AI
initially, even when E2 is elevated, because some patients will
actually see a drop in estrogen over baseline on follow-up. We would
have otherwise added an unnecessary (and relatively expensive)
medication. Should the patient develop any "nipple issues" secondary
to accelerating serum androgen levels and/or elevated estrogen, you
cannot start them on a SERM right away because doing so will
invalidate your estradiol assay at follow-up. Of note, males can
experience said "nipple issues" even while estrogen levels are within
physiological range, due to changes in hormone levels. A drug of the
class SERM is treatment of choice in this case, until symptoms subside.

If a patient has "nipple issues", even while estrogen is within normal
range, I add a SERM, emergently. I prefer Nolvadex over Clomid, and
Evista is probably best of all for antagonizing estrogen (although
much more expensive). Clomid often induces untoward visual effects
(i.e. "tracers"), and can cause emotional lability by virtue of its
estrogen agonistic effects at the more peripheral (emotion) brain
sites. I do like my patients to keep some Nolvadex on hand, should
they experience nipple swelling or sensitivity, so they may begin 40mg
per day until the symptoms abate, and then taper to 20 mg QD for a few
days, then 10mg for a few more, then finally 5mg QD to taper off.

My TRT male patients who suffer E2 elevations above the top of normal
range are placed on 0.25mg of Arimidex every third day. If that is not
enough, I use the same dose EOD. It is possible to cut the tiny 1mg
tabs into quarters, but here a gel or cream preparation, compounded to
convenient dosing, makes a lot of sense. A month later I recheck E2,
and make further adjustment if necessary. It is important to not lower
estrogen too far, which is easy to do with an AI, as doing so has
disastrous effects on the Lipid Profile, bone deposition, etc. I
prefer to maintain E in mid-range.

So now let's say we have the patient in a state where Total
Testosterone is in the upper quartile of "normal" range, Bioavailable
Testosterone is nicely elevated, with E2 safely in check. At this
point I offer the patient my HCG protocol. I add in 250-500IU of HCG,
on day five, and day six of the week, for those who use the IM
injection. In other words, the two days prior to their shot. For those
using a transdermal delivery system, every third day. For the IM
patients, this compensates for the drop off in serum androgen levels
by the half-life of the test cyp. But the main reason is to stave off
atrophy of the testicles, by directly stimulating them with the LH analog.

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, 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.

Many TRT practitioners add in HCG for a short course every few months,
to re-stimulate the testes. My opinion is that it is far better to
keep them up to form and function all along the way. The physicians
who intermittently use HCG also use it as a "break" in TRT, much the
same way hormonally-supplemented athletes manage the typical anabolic
steroid cycle. TRT should not be "cycled". Once I get my patients
properly tuned up, I want them to stay that way. They also erroneously
believe this allows the HPTA to recover, when it clearly does not. The
HCG-induced testosterone production is every bit as suppressive of the
HPTA as the TRT, and the supplemented testosterone is still at
suppressive serum levels during that time, anyway.

Once the patient is all set, I like to run follow-up labs every six
months. It is important to monitor the general health and well-being
of the patient, but also insure compliance with treatment protocols
and continued effectiveness of same.

My hope is that the preceding diatribe will gainfully assist the
practitioner in implementing Testosterone Replacement Therapy regimens
for their qualifying patients. Be prepared, however, to blush as they
shower you with accolades following their vast improvements in health
and happiness. You may even receive thank you notes from their wives!

Please watch for coming articles and books by John Crisler, DO on
this, and other, continuing subjects related to anti-aging.

Copyright John Crisler, DO 2004. This article may, in its entirety or
in part, be reprinted and republished without permission, provided
that credit be given to its author, with copyright notice and clearly displayed as source. Written permission
from Dr. Crisler is required for all other uses.

Dr. John Crisler may be reached at:


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