Archive for May, 2011

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 I appear to have lost was 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. More discussion can be found here. 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. Note the high total testosterone level. 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.

10-6-10.pdf

The following 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. As the reader can see mine was 82 pg/ml, which is high given the lab range for men of 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.

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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.

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