The next number of posts will contain 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.

If SHBG is low, this will drive Free T (and Bioavailable T) high. The body will attempt to dump excess high Free T in numerous ways, one of which, for those of us with larger deposits of adipose fat (fat surrounding internal organs) is conversion to estrogen via the aromatization process. This occurs in various areas of the body, including adipose fat and the liver, as well as other locations. One can have normal to high normal or even high Free T and low Total T. That is why a total T measurement by itself is not the best of tools to diagnose what is really happening. Subjective reports are also important. Although in this case my Free-T was normal, my %Free-T was high. Subjectively I had low libido, low energy, and poor erection quality. I also found it difficult to think. In this case, Total T was probably a good measurement when coupled with my subjective report to diagnose hypogonadism. However, an SHBG measurement when coupled with an A1C would have indicated insulin resistance.

Treatment of insulin resistance may have been the best approach in my case. The result would be increased SHBG bound T. This would have, over time, caused my Total T to raise. The bodies attempt to dump free-T, including conversion to estrogens, which would lower total-T, is mitigated with less adipose fat. By reducing adipose fat, one way to control or reverse insulin resistance, this conversion would not have taken place and a balance would have been struck with normal Free T and normal total T, with much less estrogens. Instead, after the results below came back I started on Testosterone Cypionate 100mg/week intramuscular injection (IM). Levels after five weeks were around 500 Total T. A bump up to 125mg brought my levels higher (see the other set of labs from my new doctor (8-31-10).

The issue with the shots? At first the dopergenic effect created a raging libido and strong erections. Strength skyrocketed and I started building muscle. However, after a short period of time – about 4-6 weeks, the libido and erection effects wore off profoundly. My doctor did not know what to do and recommended I seek out a specialist. As I had a wedding anniversary cruise in two weeks I needed help fast. I knew that many who used T shots also used an aromatase inhibitor (Arimidex is popular) to bring down the strongest of the estrogens (E2 or Estradiol). I also knew the shots would do little to increase DHT (a testosterone byproduct responsible for all things male) and that gels converted on the skin via the 5-AR enzyme into DHT in the body. DHT increase libido and erections. My thought was to start Testim immediately 5g/day, with .25mg Arimidex every three days, and HCG 250IU every three days. More on those last two medications in a later post, but needless to say in a very short period of time I came raging back just in time for the cruise. Dr. Dan Freeland worked with me and we would continue to work together. It would be later that Shawn Bean would enter into my treatment program in consultation with the doctor. The ride was just beginning, but at least for now I was good to go.

Here are the two labs referenced above:

• 5-27-10.pdf
• 8-31-10.pdf