For readers suffering from heart failure, there is a new clinical study from Acorn CorCap looking for participants. The CorCap is a polyester mesh wrapped around the heart to provide support and prevent additional heart enlargement.
There is a section on their website with a survey to identify whether you are a potential candidate.
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.
Good news today at the cardiologist’s office. With six months passing since the placement of my last set of stents, I admit to possessing a certain amount of pessimism concerning my prospects prior to the test. Post test, I was disappointed. Clocking in at 10:40 and comparing that to my record of 15:30 left me a little shell-shocked. Convinced another intervention waited just around the corner, my mood sour with anticipation, one can imagine my surprise at the positive results.
It is possible to explain the angina I feel during heavy exercise, and the poor time performance on the treadmill to my very low testosterone levels (see previous post). Currently, my total-T is around 180 ng/dL (normal is above 250 ng/dL), with my bioavailable testosterone coming in around the low end of normal. This is the first test since stopping testosterone replacement therapy and I have yet to begin the HPTA (hypothalmic, pituitary, testicular axis) normalization protocol.
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:
From the New York Times
For the sake of heart disease research, 809 members of the Old Order Amish community agreed to go to a clinic in Lancaster, Pa., near their homes, and drink a rich milkshake that was made mostly of heavy cream. Over the next six hours, a group of investigators took samples of their blood, determining how much fat was churning through their bloodstreams.
Most of the study participants responded as expected — their levels of triglycerides, a common form of fat in the blood, rose steadily for three to four hours and then declined. But about 5 percent had an extraordinary reaction: their triglyceride levels started out low and hardly budged.
It turns out, the researchers report in the Friday issue of the journal Science, that those individuals who barely responded have a mutation that disables one of their two copies of a gene called apoC-III. The gene codes for a protein, APOC3, that normally slows the breakdown of triglycerides.
With the mutated gene, people break down triglycerides unusually quickly. And, the investigators find, they also have low levels of LDL cholesterol, which at high levels increases heart disease risk. They have high levels of HDL cholesterol, which is associated with a decreased risk of heart disease. And they appear to have arteries relatively clear of plaque.
The article goes on to say that clinical applications are “years away”.