Archive for 'HCG'

Testosterone Restart Failure

Picture of Heart

I just wanted to get everyone up to date on a relatively new way to boost testosterone for hypogonadal males whose cause of low testosterone is not a diagnosed primary (testicular failure) or secondary (issue with hypothalamus or pituitary gland).  In short, medical professionals call such states idiopathic, meaning cause unknown.  For example, some men with low testosterone suffer from insulin resistance, which can lower SHBG to levels low enough that free testosterone increases above the normal range, causing the homeostatic state to finally settle into a low total testosterone state as the body dumps the excess free T.  However, I am not aware of any study which conclusively proves this point.  Therefore, as in my case, decreasing insulin resistance by diet, exercise, and in my case the use of the over-the-counter product Ortho Molecular CM Core.  The later supplement decreased my A1C from 6.8 to 5.1 in about 4 months – an amazing result.

I recently attempted this approach, a therapy which consists of low dose Clomid at 25mg/day for 6 weeks.  In the past, many attempted high dose Clomid of 100mg-150mg/day for a few weeks to a month.  Side effects with dosages this high rarely are well tolerated and include seeing “tracers”, loss of libido, and mood swings.

Clomid is actually a selective estrogen receptor modulator, or SERM.  The drug, available by prescription only, acts on some tissues as an estrogen and in others this SERM will block estrogen. In males estrogen is blocked or inhibited in the hypothalamus resulting in an interesting effect:  the stimulation of Gonadatropin Releasing Hormone (GnRH) which then stimulates the pituitary gland to kick up its production of LH (leutinizing hormone) in the pituitary.  LH then stimulates the Leydig cells in the testicles to pump out testosterone.

One other side effect of Clomid to keep in mind is that over the long term, and especially at higher dosages, the pituitary gland is desensitized to GnRH.  Therefore, a short run of low dose Clomid,if successful in increasing testosterone production, is best looked at as a way to kick start the hypothalamus and pituitary gland into successfully working at full potential.  Upon cessation however, if the cause of low testosterone is still unknown or unaddressed, testosterone levels often drop to pretreatment levels.

One study of 36 men with average total testosterone of 248 ng/dl, placed the subjects on 25 mg/day of Clomid.  After 4-6 weeks the men’s average testosterone was a hefty 610 ng/dl.  This is a nice boost indeed, especially for what is considered a relatively low dose of Clomid.

My recent foray into this treatment ended unsuccessfully.  Prior to treatment, I ceased all TRT for two weeks.  Total T plummeted to 70ng/dL.  After six weeks my levels stood at a paltry 195ng/dL.  However, in my particular case, due in part to the length of time on TRT – over 15 years – the testicular atrophy due to such long use may have been addressed – and in my particular case has successfully been addressed in the past – with high dosages of Human Chorionic Gonadatropin (HCG) injected subcutaneously into the stomach fat using insulin needles.  Doses of 1000-1500IU every other day for 20 days are usually enough to really kick in Leydig cell production of testosterone assuming no issue exists with the function of these cells. At these dosages the need to control the conversion of testosterone to Estradiol or E2 (a potent estrogen) is sometimes necessary.  This conversion process, known as aromatization, typically occurs in the liver and body fat surrounding internal organs – also known as adipose fat.  Small dosages of the aromatase inhibitor Arimidex at .05mg/day usually keeps this process under control, and such dosages can be provided in capsule form by a good compounding pharmacy.  The amount needed varies from person to person, with some requiring more, and many hyper-responders requiring less.

The six week program of Clomid did increase my LH and follicle stimulating hormone to the high end of normal and quite possibly I could have seen an increase in testosterone given more time.  However the concern of desensitizing my pituitary to GnRH lead to the cessation of the Clomid and restarting the Testim for TRT.

Other protocols exist and mileage will vary.  Some add in Tamoxifen, another SERM, to work with the Clomid and also help combat the desensitization of the pituitary gland to GnRH.  I have seen so many protocols out there I can only conclude that the best protocol likely varies depending on the person and the underlying cause of idiopathic hypogonadism.

Testosterone Labs: 5-27-10

The next number of posts will contain information from all of the labs that I still possess copies of starting from 5/27/2010 when I first noted my hypogonadism had returned. This occurred after a failed restart, which initially showed promise, before levels returned to pre-post cycle therapy (PCT). The PCT involved HCG, Clomid, and Tamoxifen. The fact I responded to HCG indicated no issues with the testicles in producing testosterone when stimulated, and my response to both Clomid and Tamoxifen after HCG cessation indicated no issue with the hypothalamus or pituitary gland. Coupled with older MRIs from years ago that indicated no growths or other issues with my adrenals and pituitary gland, as well as a full brain MRI, this strongly pointed to neither primary (testicles) or secondary (hypothalamus and pituitary) hypogonadism, but rather hypogandism that was idiopathic in origin.

It was at this time, years ago after a collapse following treatment with a combination thiazide diuretic and ACE inhibitor for blood pressure, that I first started testosterone replacement therapy (TRT). After the PCT fail, I restarted TRT and began working with my family physician. The initial results that indicated low testosterone follow. However, it should be noted that a body mass index done a couple of months later indicated large adipose fat deposits, and previous labs pointed to insulin resistance. At the time, I did not understand the significance of this finding. My body fat from the hydrostatic chamber test hovered around 27%. With insulin resistance, SHBG tends to be low. Recall the formula: Free T = Total T – SHBG bound T – Albumin bound T. As testosterone is easily ripped off of Albumin, Bioavailable T is basically Free T + Albumin bound T.

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TRT Methods – My Experience

First I must divorce any misconception this is the first flirtation with TRT. About 8 years ago, after taking the blood pressure medication Prinzide – a combination Thiazide diuretic/ACE inhibitor – I had a collapse after four days. Profound in nature, this event changed my life. From a strapping young man capable of 100 push-ups, I could not longer manage even 10. A visit to a local endocrinologist indicated all of my endocrine systems were compromised. Suddenly I was diabetic, I became seriously depressed, and all of my muscles experienced a weakness that was frightening. This included my diaphragm and I required a velcro weight belt to provide support and assist in relieving any weight on the diaphragm just so I could breathe.

I immediately began to treat the depression, and began an exercise program that consisted of 100 deep-knee bends, as many push-ups as I could handle, and walking for short distances. After the depression resolved itself, additional tests which indicated high cortisol and I barely passed a dexamethasone supression test. Failure of this test is indicative of adrenal issues. Measured testosterone was very low at 185 ng/dL. I decided to treat the testosterone only and attempted both Androgel and Testim, finally deciding on the Testim. I saw many specialists including a neurologist, a lung specialist, a neurosurgeon, and a cardiologist. After over fifty thousand dollars worth of tests they found….nothing wrong. MRIs, stress tests, multiple visits to my general practitioner and nothing, nada, zilch. I first suspected rhabdomyolysis, which testing quickly ruled out. MRIs of the pituitary, hypothalamus, and adrenals were negative. The only conclusion offered by one doctor – I suffered from a variant of Guillain-Barre syndrome, an ascending paralysis that in the worse cases becomes complete, with the patient on a ventilator. The disease usually resolves itself after a period of months, weeks, and sometimes years.

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Types of Testosterone Replacement

There are four main types of testosterone replacement that are available.

Transdermal testosterone includes patches (which will not be covered due to their low absorption rates) and gels such as Testim and Androgel, which are both 1% concentrations, and creams from a compounding pharmacy which range from concentrations of 1% to 10% with higher concentration rates equating to lower skin surface area for application. A study indicated Testim absorption to be better than Androgel, however my personal experience is that both are good absorbers. The smell of Testim turns most men off to its use, but I found that women particularly like the odor. However, my insurance does not cover Testim. Androgel efficacy is improved in my case by rubbing it on the flanks as well as the arms. Remember, the more surface area the higher the DHT, which can lead to unwanted side effects such as acne, accelerated hair loss in those prone to male pattern baldness, and hair growth in unwanted areas. However, the boost in libido and improvement in erections is noticeable for me. Shots, mentioned next, worked fine in my case for about 1 month. Two months into the treatment I had profound lack of libido and total erectile dysfunction unresponsive to PDE5 inhibitors such as Viagra and Levitra.

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Testosterone Facts and Education

So just how does the male body produce testosterone? While the number of systems that can impact testosterone production is large in number, the basics are rather simple. Let’s start at the hypothalamus and work our way down.

  • The hypothalamus produces gonadotropin-releasing hormone (GnRH)
  • This hormone triggers the anterior pituitary gland to produce two other hormones
  • These two hormones are luteinizing hormone (LH) and follicle-stimulating hormone (FSH)
  • LH stimulates the Leydig cells in the testicles to produce testosterone while FSH regulates the development, growth, pubertal maturation, and reproductive processes of the body and acts synergistically with LH in male reproductive health.

Simple enough, but what happens is one or more of these systems is compromised in some manner? Defects in the hypothalamus or pituitary gland that compromise the release of GnRH (and subsequently FSH and LH) or adversely affect the release of FSH or LH from the anterior pituitary lead to what is known as secondary hypogonadism. A defect in the testicles that causes a reduction or cessation of gonadal response to LH is characterized as primary hypogonadism. There are many causes of both primary and secondary hypogonadism. The link lists only some of the causes. Also check out this link. Hypogonadism that is present absent any of these conditions or any other known conditions that affect male testosterone production comes under the heading idiopathic hypogonadism. This later label correctly describes my own condition.

Typically a doctor will order a test that measures the total serum testosterone. This is a simple blood test that provides a number, usually in the units of nanograms per deciliter (ng/dl). Normal values vary by the lab performing the test on the blood sample, but typically values are from around 300ng/dL to 1000ng/dl. However, caution should be used in using this raw value as an stark indicator of hypogonadism. For some men presenting with low normal values or even normal values symptoms of low testosterone are often seen. Therefore the entire clinical picture is needed to ensure treatment is provided even in the face of so-called normal results. Also, an entire workup of the thyroid function as well as adrenal function is necessary. Any issue with either of these glands can often lead to hypogonadism or mimic they symptoms of hypogonadism. Also, an understanding of any issues with these glands will guide the treating physician in the selected treatment. As an example, long-standing hypothyroidism will impair the absorption of transdermal testosterone due to build-up of mucin in the skin of people. Mucin causes the skin to thicken impairing absorption of transdermal testosterone.

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Testosterone Renormalization Protocol Day 45

The results are in – my total testosterone is 265ng/dl. This is lower than I would have liked. I get tested again in 1 month. Two weeks of the orals clomiphene citrate and tamoxifen are left and then I take a two week break.

Depending on my next test results, I have a few options according to the Houston doctor who specializes in treating hypogonadism. I could just accept the new number, take another month of clomiphene and tamoxifen once per day as opposed to two and then re-measure after being off the orals for two weeks, or go back on Testim gel for 12-18 months and then repeat the protocol of HCG, clomiphene, and tamoxifen.

What my Houston doctor found amazing is that, when he did this, many of his patients with numbers similar to mine bounced back to 500ng/dl, which is exactly where I would like to be. I think I will be taking this approach if my results are not satisfactory in one month.

The protocol has certainly not been a failure. My original total testosterone was 185ng/dl and now I am sitting at 265ng/dl. I now understand the possible cause of my maximum heart rate drop. My maximum heart rate while on Testim gel (total testosterone around 700ng/dl) was around 182. When my testosterone bottomed out after the Testim cessation it was around 162. Now it is around 166. I believe testosterone to be the main cause of this result. The most testosterone receptor cells can be found in the brain and the heart, so it just makes sense to me. The real test will be if I go back on the Testim and my maximum heart rate increases to 182 bpm.

Testosterone Normalization Day 24

It is now day 24 of my testosterone normalization protocol. The HCG injections stopped at day 19. My total testosterone measured on January 2nd just prior to stopping the HCG injections was measured at 327 ng/dL. The range is about 250-850 ng/dL, so definately an improvement from my pre-protocol result of 187ng/dL. During this time I was also taking the orals clomiphene (50 mg twice a day) and tamoxifen (10 mg twice a day).

Im still on the orals and will get my total testosterone remeasured on January 22nd. My second month or orals has been ordered. The amount taken and dosage will not change. I am not sure what will be done after this.

If my total testosterone is not around 500mg/dL 1 month after stopping the orals, restarting the entire protocol is one option to push my values higher.

During my treatment I expereinced one day of high anxiety and one day of a mild depression. Testicular size, which shrunk after the HCG was stopped, has rebounded on the oral medications to a range of 5-7 cubic centimeters. The average male testicular size is 12 cubic centimeters. When I started the treatment, testicular size was less than 3 cubic centimeters.

I feel great, my confidence levels are boosted, and morning erections have returned. There is also a slow reversal of my erectile dysfunction issues.

I am lucky to have such a good doctor in Houston and here in Austin and a very understanding and supportive wife. I believe I am really making a good comeback. Of course, days will exist when things don’t look so rosy, but for now I am happy at this latest turn of events.

Keep on truking,

Gerald Merits

Testosterone Normalization Day 6

Sorry about the light posting; so much going on right now with holiday shopping, packing to visit relatives, and health related activities.

By the later, I refer to my testosterone normalization protocol. Lucky enough to locate a doctor in Houston and really lucky to find a doctor in Austin willing to work together, by day six I am noticing a difference. Without revealing too much, let’s just say things are a little different in the morning than they were just six days ago. Hopefully, all will go well and I will find myself with normal T-levels and no need for Testim.

Here is the protocol. I take Clomid (50 mg 2x/day), Tamoxifen (10mg 2x/day), and Human Chorionic Gonadatropin (HCG) hormone injections via a small insulin needle into my stomach every other day.

Each injection is around 1cc. Each 10,000IU of HCG powder was mixed by me with 5cc of clean water that comes in its own vial along with the powder in a separate vial. This allows for ten 1cc injections over twenty days. Normally used to aid women with fertility, HCG is similar to luteinizing hormone (LH), a hormone release by the pituatary gland in response to Gonadatropin Releasing Hormone (GnRH) from the hypothalmus. The male testes react to the presence of LH by increasing testosterone. If the testes do not react to LH, this leads to low testosterone levels and primary hypogonadism.

Nolvadex and Clomid act as anti-estogens and stop the negative feedback estrogen has on GnRH release from the hypothalmus. Should failure occur at the pituatary or hypothalmus level and the cause is discernible such as a pitutary growth, the result is secondary hypogandism. Sometimes no reason presents itself for hypogadism, in which case it’s classified as idiopathic.

My only concern is my knowledge of how Nolvadex (Tamoxifen) makes the pituatary gland receptors more sensitive to GnRH, while Clomid desenstizes the pituitary receptors. I just shot off an e-mail to the doctor in Houston asking for a reason behind the dual-therapy. I will keep the reader posted on the response.

Testosterone and Heart Disease

This is a topic dear to my heart. I need to add to my story the fact that I am hypogonadal and my hypogonadism (low testosterone) is addressed with Testim, a gel I rub on my shoulders in the morning. When I stopped using the Testim, my testosterone is slowly recovering.

However, in an effort to “jump start” my testosterone production my primary doctor, in concert with an expert in Houston, is prepared to start me on HCG (human chrorionic hormone), Nolvadex, and Clomid. Not to get too technical, but HCG acts like luteinizing hormone (LH) which stimulates the testicles to generate testosterone. Nolvadex and Clomid are anti-estogens, and Nolvadex’s extra benefit of making the pituitary gland more sensitive to GnRH is an added bonus. GnRH (Gonadotropin Releasing Hormone) is a hormone release by the hypothalamus to the pituitary gland, resulting in the gland releasing LH to the testicles, which in turn create more testosterone.

If all goes well, normalization for me should occur within 1-3 months, instead of 12 months or more. However, in two weeks I will know whether my testicles are capable of producing the needed testosterone from their response to the HCG injections. If normalization does not occur, I will be back on the Testim.

This brings me to the main point of this post. Is heart disease caused by low testosterone, or visa versa? Here is an excellent interview with Hugh Jones, MD on the subject. This is an area just screaming for more study. Also, to my knowledge no study of the effects of testosterone on endothelial coverage of a stent has been done. Some snippets from the article: