I will seriously consider a third opinion....remember I already went for a "second opinion" from a "well respected" endocrinologist who looked at my initial labs from the internist and the followup labs ordered by Dr. H and said yeah 100mg test IM every week and lose weight....no need to treat thyroid.
The only reason I'm on the fence (and I'm sure you get this as a PhD) is while my understanding of the basics is sound....there are nuances in the presentation and numbers that I just don't get. I experience this as a dentist all the time. Intelligent patients who Google a topic, do some reading and then come in and tell me how to do my job. There's no amount of reading they can do regardless of background that's going to replace my 4 years of dental school, 3 years of residency and 5 years of clinical practice. I'd stop if I absolutely knew it was the wrong decision but even your tone has softened (slightly) after hearing his responses. What if taking the AI boosts testosterone significantly with little or no side effects and it's 1 pill every 3rd day? For all I know he's seen 100's of cases like me and this has worked without issue 99% of the time. He seems very comfortable with the issue of hypogonadism. It's just not a black and white situation to me.
I do as always appreciate your opinion.
If my tone has softened, it's purely in the interest of being respectful to all parties involved. My position is firm that taking an AI is not going to solve your problems.
To better understand whether or not you should be taking anastrozole, let's look at the various kinds of hypogonadism, the various ways to treat hypogonadism (or the symptoms of hypogonadism), and where anastrozole falls in all of this mess.
As you know, hypogonadism is typically classified as either primary or secondary. Primary hypogonadism occurs when the testes fail to respond to gonadotropins. Secondary hypogonadism occurs when the pituitary fails to produce gonadotropins (specifically, LH). Exactly what causes these organs to fail to do their job varies, and can include physical trauma, autoimmune response, anorexia, obesity, neoplasm, genetic mutation, etc. --- too many to list.
The best treatment (as always) is the one that enables the body to resume normal function; primary hypogonadism due to trauma sometimes reverses when the testes heal; secondary hypogonadism caused by rapid weight loss or obesity usually resolves when a normal weight is restored; if a pituitary tumor is causing the problem, and is successfully removed, then that's great too. Sometimes, stimulation with a SERM or hCG (or both), or even GnRH, can restart a suppressed HPT axis. Unfortunately, there are a large number of cases where the hypogonadism cannot be permanently reversed.
For these people, the available treatments primarily differ depending on whether the hypogonadism is primary or secondary in nature. Specifically, methods that stimulate the testes are of no use for treating primary hypogonadism. Thus, the standard treatment for permanent secondary hypogonadism is simply testosterone supplementation. In permanent primary hypogonadism, hCG is sometimes used with testosterone to preserve fertility.
These two protocols, plain old T, or T in conjunction with hCG, are the standard for treatment. As soon as you start deviating from this, you are no longer in the mainstream; the vast majority of doctors will not prescribe outside of this protocol.
As a doctor yourself, I know you appreciate the value of a widely adopted treatment protocol. However, it is one thing to know what the commonly practiced protocol is, and it is another thing to understand why it is the commonly practiced protocol, so let's go into a few of the reasons why. The reasons differ for nonreversible vs reversible hypogonadism.
For nonreversible hypogonadism, an important consideration is sustainability of treatment. If you are going to need treatment for life, how much sense does it make to take a medication that can only be safely used in the short term? There is much literature indicating that while SERMs are a good choice for the short term, particularly as part of a restart protocol, they are not a good choice for long-term treatment because of side effects that eventually occur (this forum has links to many journal articles along these lines). AIs are known to cause major side effects in the long-term as well, such as bone wasting, and thus are also not a good choice even if it were not for the well-known short-term side effect of arthralgia.
Sustainability of treatment is not so much a consideration for reversible hypogonadism. However, dependence is. Most medications to treat hypogonadism, including testosterone, often result in the body's dependence on them, and thus conflict with the goal of reversing the hypogonadism.
Finally, we get to anastrozole. We've already established that it's not a good idea to use an AI for the long-term, which means that no one with a permanent form of hypogonadism should be using it, but what about the short term? And what about those poor bastards that have genetic mutations such as familial hyperestrogenism?
The main reason why anastrozole is not used in the short term is because of the arthralgia that is associated with short-term use; the average time to onset of arthralgia is 4 to 6 weeks. Once the arthralgia is there, the time required for it to go away is 12 to 18 months; about half will recover within a year, and about 90% will recover by 18 months. Many opt for surgery because waiting this long is often not practical. And for an unlucky few, the pain does not go away without surgery.
Furthermore, the short-term cases of hypogonadism are short term because they can be corrected, and there does not exist a form of short-term hypogonadism that requires anastrozole to resolve.
Lastly, there is a class of hypogonadism that is caused by genetic mutation. When anastrozole is used, uniformly inhibits the ability of each aromatase containing cell from being able to convert testosterone into estrogen. In the case of familial hyperestrogenism, the aromatase in every cell of the individual is over-converting testosterone into estrogen. This is not the case in obesity induced hypogonadism; in obesity induced hypogonadism, each cell is producing a normal amount of estrogen, but the cumulative effect is suppressive. In familial hyperestrogenism, every cell is malfunctioning AND the cumulative effect is suppressive. Thus, anastrozole is much less likely to cause side effects when used to treat familial hyperestrogenism, and is thus justified. (Recall that in order for aromatase to reduce the cumulative effect of high estrogen in obesity induced hypogonadism, it must reduce the ability of each and every aromatase containing cell to produce estrogen, causing ALL of them to underproduce; tendon issues arise when aromatase in the tendons can no longer function well enough to maintain tendon health.)
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That pretty much sums it up. I have a feeling you already knew most if not all of this, but are questioning yourself because your doctor is the expert, and you figure you must be missing something. This is why I recommend that you see another endocrinologist, or even two or three more. Unless you go to one of these self-styled anti-aging geniuses, you will not find an endocrinologist that is willing to prescribe anastrozole, because from their perspective,
they can expect to never see a patient where the benefit justifies the risk; not in the short term (for reversible hypogonadism), nor in the long-term (for nonreversible hypogonadism).
The anti-aging endocrinologists out there will happily give you a prescription for every hormone or compound under the sun, regardless of whether or not you need it. But of course, there's a reason why these guys are out on the fringes...
Had I known all of this before I took anastrozole, I would've never done it. Learn from my mistakes...
