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Testosterone replacement therapy (TRT) entails increasing DEFICIENT levels of testosterone to NORMAL or OPTIMAL PHYSIOLOGIC levels per that particular person. A person should be deficient in testosterone in the first place to receive TRT.

Some adverse effects and associated conditions:

1. If only testosterone is used in replacement therapy, a person does run the risk of causing atrophy of the testes and reduction in sperm production. This is because with the higher testosterone levels, the brain does not need to produce luteinizing hormone (LH) and follicle stimulating hormone (FSH) to increase testosterone production. The lower follicle stimulating hormone levels also reduce sperm production. If a person wants to have optimum fertility, while on testosterone replacement therapy, then it is important to supplement testosterone treatment with human chorionic gonadotropin (HCG) treatment. HCG behaves in the human body like LH and FSH. It will keep the testes from atrophy, and maintain sperm production. SWALE has a great protocol to use as a starting point.

2. It is important to monitor for prostate cancer. Testosterone itself does not cause prostate cancer - estrogen is much more of a risk for prostate cancer. However, testosterone, like estrogen, promotes tissue growth. Thus, testosterone needs to be blocked or withdrawn if prostate cancer exists. Some recommend twice a year prostate exams and more frequent prostate specific antigen tests when on testosterone replacement therapy to monitor for prostate cancer.

3. If dihydrotestosterone (DHT) levels become too high (from conversion from testosterone via the alpha-reductase enzyme), then hair loss may accellerate. Excessively high DHT levels may also increase visceral (belly) fat - which then increases the risk of high cholesterol, blood pressure, stroke and heart attacks, cancer, etc. DHT levels are easily monitored via blood tests. An easy way to monitor DHT levels informally is to see if one gets acne - a symptom of perhaps excessive DHT levels. When DHT is increased, one may also notice more body hair or faster hair growth in the DHT-resistant hair follicles (the ones that one does not easily lose when going bald). I, myself, try to aim for testosterone levels between the age of 24-30, not teenage male levels.

4. If estrogen levels become too high (from conversion from testosterone via the aromatase enzyme), then you have a higher risk for weight gain, heart attack, stroke, cancer, etc. A sign of excess estrogens is gynecomastia (breast growth) in men. Estrogen levels are easily monitored and can be treated.

5. If, a person has been deficient in testosterone for a long time, eventually, adrenal fatigue can set in. This means the adrenal glands cannot make enough Cortisol and other hormones when needed to help the mind and body withstand stress. An initial problem with elevating testosterone is that one of testosterone's functions is to suppress the spike in cortisol and other hormones from the adrenal glands. This helps limit the stress response - preventing damage to the body from excessive cortisol and other hormone levels (this includes diabetes, obesity, muscle wasting, etc.). The initial testosterone elevation suppresses cortisol temporarily (until the adrenals can recover from their fatigue from the calming/stress-reducing effects of testosterone). This temporary suppression of cortisol may make a person more susceptible to viral illnesses such as colds. This is not often seen as a problem in people, but is possible, and should be expected to be transient. It is an example of secondary problems that can occur from deficient testosterone levels.

6. Prostatic enlargement (and urinary retention and urinary frequency) from higher DHT and higher Estrogen levels is a possibility with testosterone replacement. Treatment may include taking saw palmetto (which seems to be highly specific for blocking prostate alpha-reductase rather than systemic alpha-reductase - and is thus safer to use than finesteride and other commercial alpha-reductase inhibitors with TRT), and taking arimidex (or other aromatase inhibitor), or taking DIM (to reduce estrogen activity). Testosterone, itself (rather than DHT), over time may reduce prostatic enlargement.

7. Higher red blood cell counts may occur as testosterone levels are increased. This thickens the blood, and if in excess may increase the risk of developing a blood clot. It may also make it more difficult for a person to breath - particularly an elderly person with a lung and cardiovascular system disease. It is important to keep this in mind and check the blood count. One of testosterone's functions is to stimulate the creation of red blood cells - highly useful, but not in excess.

When increasing the testosterone levels, it is important to be aware of other neurotransmitter/hormones that are effected and to be aware if adverse effects can occur, then to take steps to counter those adverse effects.

Most of these adverse effect occur from secondary imbalances in other neurotransmitters and hormones. The watchword is maintaining "balance" - maintaining physiologic levels of all the neurotransmitters and hormones - which minimizes risk and optimizes function. In general, I think when physiologic levels of testosterone and other neurotransmitters and hormones are maintained, the risk of adverse effects is very low with testosterone replacement therapy. Of course, if a person accomplishes testosterone replacement therapy using drugs such as aromatase inhibitors (e.g. arimidex), then the person runs the risk of adverse effects of each individual drug itself.

For each person, it is important to weigh the risks and benefits of treatment. However, the risks of continuing deficient testosterone levels are clear. They include:
1. Heart attacks.
2. Strokes.
3. Prostate cancer, possibly other cancers (from unbalanced estrogens actions).
4. Chronic fatigue and difficulty coping with stress (accompanying adrenal fatigue/insufficiency that secondarily occurs with low testosterone levels)
5. Excessive anxiety, stress, irritability, anger outbursts (the irritable male syndrome)
6. Severe depression.
7. Impaired memory and attention, difficulty learning new material (some to the extent of a dementia-like syndrome).
8. Impaired fertility - if low FSH/LH levels or FSH/LH resistance are the cause of low testosterone levels.
9. Lack of libido, erectile dysfunction - often bandaged with Viagra, but with undiagnosed testosterone deficiency as a direct cause.
10. Obesity - which is difficult to treat with diet alone - which can lead to arthritic conditions.
11. Diabetes
12. Loss of muscle mass.
13. Osteoporosis
14. Impaired immune system.
15. Reduced reaction time, quickness of reaction, mental quickness (from reduced dopamine levels, insulin-resistance associated with testosterone deficiency - among other associated changes)

There is a general progresson of other heretofore "age-associated" changes in one's health and ability to function - which would have been prevented by maintaining optimum testosterone levels.

Ultimately, maintaining testosterone deficiency may significantly reduce the quality of one's life.
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Jakbym czytał o Ginku arta... sog

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jakbys jeszcze przetlumaczyl to bym przeczytal ;)
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ok lużne tlumaczenie :
HTZ uzupełnia niedobór testosteronu do normaklnej czyli fizjologicznej granicy

niektore efekty uboczne HTZ

1.jesli tylko testosteron jest uzywany w HTZ ,u osoby tej zwieksza sie ryzyko atrofii czyli zaniku jader i redukcji produkcji spermy.to dlatego ze wyzszym stezeniem testosteronu we krwi mozg odbiera sygnal ze nie musi juz produkowac LH i FSH zeby podniesc produkcje testosteronu .aby uniknac zmniejszenia sie jader nalezy polaczyc zastrzyki z testosteronu z HCG ktora to nasladujac LH iFSH stymuluje jadra do produkcji testosteronu i spermy:)

2.wazne jest monitorowanie ryzyka raka prostaty.testosteron sam w sobie nie spowoduje raka prostaty-estrogen jest o wiele wiekszzym winowajca na tym polu.
aczkolwiek testosteron tak jak estrogen powoduje rosrost tkanek.aczkowliek testosteron powiniem byc zablokowany jesli rak stercza juz istnieje.zaleca sie badania prostaty 2 razy w roku jak i PSA bedac na HTZ sledzic ewentualny rozwoj raka prostaty.

3,jesli dihydrotestosterone (DHT) bedzie za wysoki(po konwersi z testosteronu poprzez afa reduktaze) wtedy wypadanei wlosow z glowy moze sie przydazyc.wysoki DHT moze rowniez przyczynic sie do gromadzenei tlusczu na brzuchuco zwieksz aryzoko wysokiego cholesterolu,wysokiego ciesnienia,ataku sreca,raka itp,
pozioim DHT mozna łtwo monitorowac za pomoce testow krwi(od tlumacza, gdzei w polsce robia badania DHT!!??-nigdzie).samemu ltwo mozna monitorowac poziom DHT domowymi sposbamI, poprosty zobacz czy masz tradzik ,bujne owłosienie ciala i szybki wzrost owlosieenia,najlepiej jest utrzymywac oziom testosteronu z przedzialu wiekowego 24-30 lat a nie poziomu jak u nastolatków

4.jesli poziom estrogenu jest za wysoki(poprzez konwersje tetosteronu enzymymem aromataza) wtedy wystepuje wieksze ryzyko tycia,ataku serca,zlaman,raka itp, oraz oczywiscie ginekomasti.poziom estrogenow moz ebyc latwo monitorowany i w razie potrzeby zredukowany.

5.CDN, IDE DO KIBLA
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OK TLUMACZIE SOBIE)
Here's an example, where a person has good testosterone levels but still no libido, while on Depo-Testosterone as the only treatment:

To help in understanding the labs, I did some conversions to U.S. units.

Total Cholesterol: 3.19nmol/L (3.57-5.20) = LOW
Trig: 0.8nmol/L (0.0-2.3) = LOW NORMAL

TSH: 1.33uIU/ml (0.27-4.2) = LOW NORMAL
T3: 1.7 nmol/l(1.3-3.1) = LOW NORMAL
T4: 69nmol/l (63-151) = LOW NORMAL

E2: 62pmol/L (26-165) = 16.9 pg/ml = LOW NORMAL

Progesterone: 2.21nmol/l (<0.95) = 0.69 ng/ml = LOW NORMAL
Cortisol: 331nmol/l (221-690) = 12.0 mcg/dl = LOW NORMAL

Total Test: 21.8 (5.2-22) = HIGH NORMAL
Free Test: 175pmol/l (45-149) = HIGH
SHBG: 7.23nmol/l (13-71) = LOW
DHT: 2.58nmol/l (1.13-4.13) = NORMAL


The current lab panel is missing a lot of information, but some thoughts that come to mind include:

SEX HORMONE BINDING GLOBULIN (SHBG) has many functions. A very important function is to bind to its own receptors on cells to transmit signals to the cell depending on whether or not estrogen or testosterone is bound to it. A speculated result of such signals is to increase the production of estrogen or testosterone receptors on the cell - making the cell more sensitive to estrogen or testosterone. Whether or not it is important for libido is speculative, but I would not doubt that it plays a role. A second function is to prolong the life of circulating testosterone, DHT, and estrogens. Testosterone, otherwise, would last only 10-100 minutes. Testosterone bound to SHBG is our body's natural depo-testosterone.

SHBG is produced by the liver in response to estrogen and thyroid hormone. SHBG production is inhibited by testosterone, DHEA, DHT, other androgens, insulin, and growth hormone. When thyroid is low or estrogen is low, SHBG may be low. When free testosterone (and other androgens), DHEA, insulin (such as during insulin resistance or diabetes type 2) or growth hormone is too high, then SHBG may be low. One way of looking at it is that it is a balancing act in the body to prevent excessive levels of anabolic hormones.

THYROID HORMONE when at optimal levels for the person play a role in maintaining libido. Thyroid hormone has mood elevating effects, allows energy production needed for sex, increase sperm production, and increases steroid hormone production (e.g. testosterone) in the testes. There are thyroid hormone receptors in the cells of the testes.

THYROID RELEASING HORMONE: Interestingly, in addition to the hypothalamus of the brain, the testes also release Thyroid Releasing Hormone (TRH). No one has yet explored this idea in the literature, but TRH can go to the pituitary gland and cause it to release Thyroid Stimulating Hormone (TSH), which then causes the thyroid gland to release thyroid hormone.

ADRENAL FATIGUE can stop libido. Lab test findings may include low to low normal progesterone, low to low normal DHEA, low normal cortisol, low testosterone (in perimenopausal women), among other findings discussed in the adrenal thread. Mood swings, irritability, anxiety, lack of energy, feeling burnt out, lack of enthusiasm, lack of libido, etc., are some symptoms. Adrenal fatigue can hide the presence of insulin resistance since low cortisol levels lead to low production of blood glucose, which then lowers blood levels of insulin.

DHEA from the adrenal glands plays a prominent role in reducing SHBG so that more testosterone can be freed to work. When adrenal fatigue is present, SHBG can be high despite normal estrogen, thyroid hormone levels, and testosterone levels because DHEA is low. This can result in low free testosterone and impaired libido.

PROGESTERONE plays a role in libido. It has anxiolytic, mood stabilizing, and antidepressant effects. It allows thyroid hormone to function. It increases neurotransmitter levels in the brain including dopamine. It is the precursor for both cortisol and testosterone. It is generally reduced in level when adrenal fatigue is present. Excessive progesterone, however, can inhibit libido. Excessive progesterone can also overly increase the production of estrogen receptors - resulting in gynecomastia, among other things (such as bleeding in menopausal women). Generally, I prefer at least mid-range values for progesterone in patients.

ESTRADIOL (E2) is the most potent natural estrogen. The value obtained by measuring Estradiol alone (i.e. not obtaining fractionated estrogens) is actually a measure of total estrogens since it varies depending not only on the presence of estradiol but the other estrogens. As such, getting an E2 alone gives some measure of total estrogens.

Estrogen helps determine sexual aggression. To me, this means libido. Thus when estrogen (e.g. estradiol) is too low, there is no libido.

When estrogen is too high, there is also reduced or no libido. One rationale is that estrogen competes with thyroid hormone for thyroid hormone receptors. Progesterone helps prevent this. But if estrogen is too high, estrogen will end up blocking thyroid hormone function - including thyroid hormone's role in promoting libido. Another rationale is that estrogen is a monoamine oxidase inhibitor. It increases primarily serotonin and norepinephrine. At too high a level, these can inhibit libido.

Some clinicians expressed preference for an estradiol of around 32 pg/ml for optimal libido in men. However, this will depend on all the factors that determine libido. Some need more. Some need less.

When estradiol is low, the use of an aromatase enzyme such as Arimidex is not the first thing that I would do to solve the problem of lack of libido.

HOT FLASHES are a symptom of ESTROGEN WITHDRAWAL. When estrogen level is reduced, one gets hot flashes.

AROMATASE ENZYME: Estradiol is produced by the aromatase enzyme from Testosterone.

LUTEINIZING HORMONE (LH): What controls the production of aromatase? Among other things, LUTEINIZING HORMONE increases the production of aromatase enzyme. When Free testosterone and DHT are high enough, the release of Luteinizing Hormone from the brain is reduced. This may lead to reduced production of aromatase and thus estrogen production. LH also helps increase the production of the side cleavage enzyme that starts the first step in converting cholesterol to the steroid hormones.

LOW CHOLESTEROL: indicates that a person may have difficulty in producing steroid hormones.

HUMAN CHORIONIC GONADOTROPIN (HCG) is an analog to LH, FSH, and THYROID HORMONE. Hmmm. Very interesting isn't it as an adjunct to testosterone replacement therapy - so long as the testes are not old enough or damaged enough to respond to it?

BODY FAT: low body fat levels also mean lower levels of aromatase enzyme. This may lead to reduced estrogen production and thus estrogen activity and function.

SHBG: Low SHBG levels can lead to quicker destruction of Estrogen, resulting in lower estrogen levels.

FREE TESTOSTERONE: when low SHBG levels are present, testosterone cannot be stored well, resulting in high free testosterone levels. Excessive free testosterone can cause the reverse of its intended effects. For example, though testosterone usually lowers blood pressure, when high compared to estrogen and progesterone, it can increase blood pressure instead (e.g. by increasing the sensitivity of Angiotensin Receptors). High free testosterone can also increase anxiety rather than reduce anxiety as testosterone usually does. I wonder if such high levels of Free testosterone can inhibit libido rather than promote it.

When SHBG levels are too low, it is better to use Depo-Testosterone or an alcohol-based testosterone than a PLO-based testosterone cream. The reason is that a PLO-based testosterone cream does not allow testosterone to be stored in fat cells - for later dispersal to the body. In the presence of low SHBG, there will be massive peaks free testosterone which can lead to a roller coaster levels of testosterone (as free testosterone is rapidly destroyed), and a shut-down of libido.

LIBIDO is determined by a web of influences from the numerous neurotransmitters from the nervous system, the hormones from the endocrine system, and the cytokines of the immune system - too many to list in this post. But some basic considerations as I have presented, may be useful to think about.

NA KOLANA PRZED POTĘGĄ GINOMANA
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****a za***isty art! Gienek podaj źródło

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sam to napisałem:) mam jeszcze lepszy art w rekawie:) niech ktoś przetłumaczy to bo 90% forumowiczów tego nie przeczyta
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Szacuny 77 Napisanych postów 8068 Wiek 46 lat Na forum 18 lat Przeczytanych tematów 39197
kiedys donkeykong była moja ulubioną grą w salonach gier.
Pewnie nie pamiętacie ale były takie w wozach ala Drzymały ;)

Nie ma postępów? Dodaj węgla a nie koksu !

LeonCountryChopper

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Oj Gienek po co się droczysz, podaj źródło...

Ps. Leon ja pykałem w Punishera notorycznie

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najlepsza gra na 16 bitowe konsole na SUPER NINTENDO SNES byla wlasnie gra donkey kong country 1,2 ,3 ,to było jak na tamte czasy mistrzostwo swata zarowno pod wzgledem grafiki jak i muzyki oraz gamepaly, gral ktos w to?
ej dobra ja wam dałem niezle arty po angielsku to teraz niech ktos to przetlumaczy kto dobrze zna angielski
a tu macie najlepszy,wszystkie arty sa autorstwa endokrynologa-koksiarza


MY CURRENT BEST THOUGHTS ON HOW TO ADMINISTER TRT FOR MEN


-A RECIPE FOR SUCCESS-


--John Crisler, DO



We have already learned a practical bit about the various hormones that make up the metabolic &#8220;symphony&#8221; 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 &#8220;recipe&#8221;, 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&#8212;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&#8212;and to remain compliant in your treatment regimen.

INITIAL LABWORK

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 &#8220;Free and Loosely Bound&#8221;)
Free Testosterone (if Bioavailable T is unavailable)
DHT
Estradiol (specify the Extraction Method, or &#8220;sensitive&#8221; assay for males)
LH
FSH
Prolactin
Cortisol
Thyroid Panel
CBC
Comprehensive Metabolic Panel
Lipid Profile
PSA (if over 40)
IGF-1 (if HGH therapy is being considered)


FOLLOW-UP LABS

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 &#8220;sensitive&#8221; assay for males)
DHT (especially if patient is using a transdermal delivery system)
FSH (3rd Generation&#8212;ultrasensitive assay this time)
CBC
Comprehensive Metabolic Panel
Lipid Profile
PSA (for more senior patients)
IGF-1 (if GH Therapy has been initiated already)


INDIVIDUAL ASSAYS EXPLAINED

TOTAL TESTOSTERONE

This is the assay your patients will most focus on. It&#8217;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:


BIOAVAILABLE TESTOSTERONE

Where we actually get the &#8220;bang&#8221; 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.


DHT

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&#8217;ll explain why later. DHT level may also help indicate cause for ED symptoms.


ESTRADIOL

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&#8217;s individual hormonal system functions, as well as making sure estrogen does not elevate inappropriately secondary to the testosterone supplementation.

I don&#8217;t waste time and money drawing estrone and estriol. E2 is the player of interest here. Unless you specify a &#8216;sensitive&#8217; 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 &#8220;appropriately&#8221; 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.


LH

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.


FSH

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 (&#8220;sensitive&#8221;) 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.


PROLACTIN

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.


CORTISOL

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.


THYROID PANEL

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.


CBC

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.


CMP

Again, just good medicine. Baseline for sodium (which may elevate initially secondary to androgen supplementation) is important. We also want to see LFT&#8217;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&#8217;s, too. Be advised, this will not happen if you choose to elevate their androgens above the top of &#8220;normal&#8221; 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.


PSA

For all patients over 40. Even though prostate CA is rare in men under the age of fifty, we don&#8217;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&#8217;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 &#8220;every six to twelve months&#8221; in their 2002 Guidelines for treating hypogonadotrophic patients with TRT.

IGF-1

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&#8217;s grab a baseline now, before that happens.


THINGS TO LOOK OUT FOR

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.


TESTOSTERONE DELIVERY SYSTEMS

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&#8212;transdermals and injectables. Here are the current options:


TESTOSTERONE GELS AND CREAMS

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&#8217;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 &#8220;freshen up&#8221; 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&#8217;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.


TESTOSTERONE PATCHES

These can be quite effective, but are inconvenient to use. Approaching 2/3&#8217;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&#8217;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&#8212;which can be good or bad, as previously explained.


TESTOSTERONE PELLETS

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&#8212;hemorrhage and infection&#8212;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&#8217;s say you establish a &#8220;usual&#8221; 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&#8217;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&#8217;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&#8217;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.


TESTOSTERONE INJECTION

I&#8217;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.


HCG

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.


OTHER MEDICATIONS

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 &#8220;TRT&#8221;. 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.


THE MEAT AND POTATOES OF TRT

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&#8217;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&#8217;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&#8212;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 &#8220;normal&#8221; 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 &#8220;frontload&#8221; 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&#8217;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 &#8220;right&#8221; (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 &#8220;incredible&#8221; the first couple of weeks (and bursting with libido), but they don&#8217;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&#8217;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 &#8220;normal&#8221; 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 &#8220;normal&#8221; 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 &#8220;tick mark&#8221; 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 systems.

Another risk of jumping the dosage too much is that, should serum androgen levels greatly exceed the top of &#8220;normal&#8221; range, the patient risks becoming &#8220;spoiled&#8221; 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&#8212;and proper&#8212;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&#8212;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 &#8220;nipple issues&#8221; 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 &#8220;nipple issues&#8221; 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 &#8220;nipple issues&#8221;, 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. &#8220;tracers&#8221;), 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&#8217;s say we have the patient in a state where Total Testosterone is in the upper quartile of &#8220;normal&#8221; 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&#8212;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 &#8220;break&#8221; in TRT, much the same way hormonally-supplemented athletes manage the typical anabolic steroid cycle. TRT should not be &#8220;cycled&#8221;. 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.
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no i jeszcze mala ciekawostka która akurat przetłumacze, w skrocie,wg ostatnich badan american jurnal cos tam przeprowadzonych na 4.000 mezczyzn ci którzy jedli najmniej sodu-soli byli o 40 % bardziej narazeni na smierc z powodu chorób układu krazenia!!zbytnie ograniczanie soli moze byc jescze grozniejsze niż jej nadmiar szczegolnie dla intensywnie trenujacych sportowców( smieszne jest to ze we wszystkich poradnich dla kobiet i nie tylko ,kaza ograniczyc podaz soli do minimum hehe)
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