Read about my battle with heart disease here.
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.
My lipid panel indicated very low total cholesterol and even LDLs were lower than my cardiologist was happy with. At the time my Crestor intake of 20mg a day, coupled with 1 gram of Niaspan, and a strict diet and heavy exercise problem lead to these results.
The high reverse t3 levels (rt3) are a result of a restricted diet with over training. To verify there was no issue the reader will note in the results a lab draw on 10/12 that measured Iodine. The link discusses the relationship between Iodine and the thyroid gland.
Very low cholesterol has been tied to issues with memory loss and dementia, as well as other health issues. While many TRT specialists aim for a total cholesterol of 180 mg/dL I believe the body can function with lower levels. The thinking goes something like this. See the hormone tree below:
Note the cleaving enzyme that cleaves cholesterol into pregnenolone and then on down the steroid pathway. Without enough cholesterol there is not enough fuel for the remaining hormonal system, right? True – to a point.
The reality is everyone is different and that 180 mg/dL is not some magic number or target. For some, 120 may work fine, or even lower. The worry is that patients will remain non-compliant with cholesterol lowering medications without doctor supervision in an effort to “jump-start” their own testosterone or maximize hormone fuel by boosting cholesterol. The warning here is…be careful.
I lowered my dose to 5mg of cholesterol and purchased a cholesterol meter that measures Total Cholesterol, Triglycerides (TG), and HDL. This allows LDL to be calculated using the formula LDL Cholesterol = Total Cholesterol – HDL – (TG / 5). I ensure I am always above 120 and I am doing just fine. If I hit 180, I don’t panic. I get by without any problems with frequent exercise and some sanity in my diet.
Not shown in this lab that did show up on previous labs is an increase in hematocrit and RBC leading to polycythemia – an increase in red blood cell count per unit blood volume. This increases the risk of clot formation. If you have heart disease, watch out for this side effect. More often seen on shot therapy for TRT, it can happen even with gels. Treatment usually involves blood letting, a procedure that can be ordered by your doctor. Also, it helps to cease TRT treatment every 12-18 months for a short period of time.
As far as the testosterone levels go, I was on 1.5 tubes of Testim for this test, applied in the morning, and the blood work done 2 hours after application. My testosterone was screaming high at over 1400ng/dl. This level is a false reading as a future lab would indicate.
WARNING: Never apply Testim or any gel to the area where the blood draw will occur. This can taint the results. This is what happened for this particular test. I had to ignore the results.
This lab was my first check of Estradiol and occurred just before I started the aromatase inhibitor Arimidex to control this strongest estrogen in men. I had just started Testim 5g/day with no HCG. Estradiol is also known as E2 and is blamed often for libido and erection issues. There is a great deal of talk about Estradiol needing to be at a certain “sweet spot” often reported as around 25 pg/mL. In this lab my value is 82 pg/ml, which is high given the lab range reported for men as less than or equal to 29 pg/mL.
Note the really important lesson here is twofold. First, the “sweep spot” theory is just that – a theory, and a bunk one at that. While it may be true in some men, and at the time of this test I thought I found the cause of my own libido issues, later when my levels were steady at a number greater than 82pg/mL functioning and sexual appetite were more than just fine. My sweet spot seems to be a range that is not too high (what that number is I do not know) or too low. Second, the real metric of interest is a stable level that is not bouncing around all over the place.
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.
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.
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.
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.
My decision to create a new section on this site specifically dedicated to Testosterone Replacement Therapy is two-fold. One, TRT has changed my life. With evidence that Testosterone acts very similar to a calcium channel blocker by dilating arteries, my decision to start TRT was not just related to low testosterone levels, but also to the benefits I perceived TRT possesses for heart health in individuals with heart disease. As a sufferer of heart disease and the recipient of 25 stents, I began my TRT with earnest. Secondly, TRT is not always beneficial unless the patient and the doctor understand just what is involved and what systems must be monitored to ensure success. It is my goal to ensure the reader is as educated on cutting edge replacement therapy.
TRT will not magically turn a diminishing libido into a raging storm of sexual passion, nor will it address erectile dysfunction issues in all cases when the only treatment involves measuring testosterone levels, choosing a treatment, and then walking out of the doctor’s office. Too many physicians have very little understanding of TRT, and many have no idea how to handle the tougher cases.