So I'm now four weeks into my HRT regimen and I just had some more bloodwork done. I've been doing 10g of AndroGel daily (I'm currently fighting with the doctor to do IM injections) along with 1/2mg of A-dex per week. My dosing for the A-dex has been four drops EOD, with approx 28 drops equaling 1mg.
E2 levels came back at 68, up from 33 pre-HRT, and for the past week I've been feeling like complete sh*t. I want to up the A-dex to 1mg per week (instead of just 1/2), would I be better to do eight drops EOD or do four drops ED. Does it really matter?
You're better off going 4 drops ED, instead of 8 drops EOD, because one week you get three doses (T,Th,Sat) and the next week you get four doses (M,W,F,Sun) and your b/l's will be all over the place. As I'm sure you've read before, the gels/creams aromitize to E2 much more easily than injections do. This of course will change if you are carrying large amounts of body fat; then injection will be more prone to turn to E2 as well.
..thanks KNB, that's kinda what I figured but was just looking for another experienced opinion. I've been doing the extra 1/2mg, so four drops ED now since Friday and I'm starting to feel much better already. The mental fog is starting to lift, burning in the eyes is now gone (felt like a bad case of allergies?), only problem is that I'm still have the intense mid-afternoon fatigue. I meet with my Urologist in an hour so I'll discuss this with him then. Thank you sir!...hebs
Mid-afternoon fatigue, eh? What are you your thyroid numbers, or do you know? HRT has a habit of screwing up perfectly good operating thyroids, but may especially screw up those that are already compromised. HRT can cause the T4 to not convert to the T3 you so desperately need for energy, therefore causing the "afternoon slump". Just a thought...
...arghh! The appointment with the Urologist got me absolutely no where. He admittedly knows knowing about AI's. He know's even less about HCG and constantly kept confusing it with (and I'm quoting him) "that HGH stuff all the professional athletes down in the states are using".
We talked about doing IM injections, and while I finally got him convinced that it wasn't such a bad idea, he wouldn't script it because he didn't know anything about the dosing......So it's back to the MD to try and get a different referral and keep plugging away at this!
Regarding the thyroid, interesting. Here's some levels from the past year:
December 2007 Free Thyroxine (Free T4) - 15 (reference range of 9-23PMOL/L) Thyrotropin (Sensitive TSH) - 2.46 (reference range of 0.35 - 5.00 MIU/L
May 2007 Thyrotropin (Sensitive TSH) - 2.43 (reference range of 0.35 - 5.00 MIU/L
August 2007 Thyrotropin (Sensitive TSH) - 1.42 (reference range of 0.30 - 4.70 MIU/L
October 2007 Thyrotropin (Sensitive TSH) - 1.88 (reference range of 0.30 - 4.70 MIU/L
March 25/2008 (four weeks into TRT) Thyrotropin (Sensitive TSH) - 2.05 (reference range of 0.35 - 5.00 MIU/L
So my sensitive TSH seems okay. Do you think that it's worthwhile getting my Free Thyroxine (Free T4) checked again?...hebs
ps...and if it matters, I do have a Pituitary Adenoma. Four years ago they classed it as a Macro Adenoma (>10mm). My last MRI/lab report has it as only a Micro Adenoma (4mm)
8 drops EOD is a consistent dosage. The fact that it works out to four doses one week and three the next is a meaningless artifact caused by dividing an odd number by an even number and by switching your frame of reference from days to weeks.
The real question has to do with the half-life of anastrozole, which is 3 days.
Dosing .25mg EOD with a half life of 3 days means that after 3 weeks, you'll be stable and your levels will fluctuate between .51mg and .64mg a day.
Dosing .125mg every day means you'll stabilize after 2 1/2 weeks and stay at about .55mg/day.
I dose anastrozole EOD because I dose testosterone EOD and so I do all my "hormone stuff" on the same day. By dosing both EOD, my anastrozole levels and testosterone levels are highest at the same time.
If I were on gel, I would dose my anastrozole ED just as I was dosing my testosterone ED.
In the final analysis, theoretical numbers really don't mean anything.
What matters is how you feel and everyone involved in a program like this needs to find for himself the dose and dose pattern that works best for him.
! Your thyroid level is fine, but I am having a cramp about something else. One presumes that you have had your prolactin checked? And if not...perhaps your endocrinologist should think about treatment...
Jaffe CA. Division of Metabolism, Endocrinology and Diabetes, The University of Michigan, Michigan, USA, email@example.com. Non-functioning pituitary tumors are relatively common. A large number of these tumors are incidentally found pituitary microadenomas (<1 cm) and are usually of no clinical importance. Those tumors that require treatment are generally macroadenomas and come to medical attention because of mass effect and/or hypopituitarism. Visual field defects are present in roughly 70% of patients with non-functioning macroadenoma at the time of diagnosis and the majority of these patients have at least growth deficiency and hypogonadism. [/i]"
...I haven't had my prolactin levels checked but I do take 300mg Wellbutrin ED. The Wellbutrin (which enhances dopamine) should be helpful in suppressing any high prolactin levels shouldn't it (that's if I was high to begin with)?
With those E2 levels, you need to hit back harder. Go to 10 drops EOD for 1.16mg/wk. [based on my 30 drops per ml count with my dropper]. As the level of the drug builds slowly, you can front load. Take 0.5 mg for the first day. If you do not feel some big changes in two weeks, work up to 2mg/wk in stages. Go by how you feel. Libido is the best and fastest responding barometer for your sense of well-being.
Note for others: Some are over responders to arimidex/anastrozole. 1mg per week, the typical initial dose, will cause a few to have E2 drop very low. That causes brain fog, fast loss of libido, joint pain/stiffness etc. If when you start you feel something good then loose it fast, your E2 levels may have fallen through a past optimal. E2 in the lower 20's [0-53 pg/ml] seems to be optimal. For those who are over responders, they need to stop the AI and let things clear for a week then try 1/4 mg per week and experiment by feel. Some will need 1/8th mg per week. Once you feel like you are in a good dose zone, lab work can provide further refinement. If you do lab work when E2 is too low, it will be below the resolution of the lab test and the the results are not very useful.
Tell your doc that the typical starting dose for injected test cypionate or ethanate is 100mg/wk. The the dose is adjusted if needed after blood work. The goal should be to have total T levels in the high end of the range and free T should be at or slightly above the upper end of the range. If FT will not climb, this can be from E2 levels that are too high which increase SHBG in the liver. T-->E aromatization also consumes FT. The package insert for test cypionate recommends 200mg every two weeks, which is 100mg per week. You will probably be better off injecting more that once a week.
hCG should be 250iu SC EOD, based on this research:
Are you reporting E2 as pg/ml with a range similar to 0-53?
Your high E2 levels are probably caused by the effect of transdermal T on the skin. That can also drive up DHT as well. With injections [perhaps the reason behind your post] E2 levels should drop. Then your dose of anastrozole may be closer to the expected 1 mg/wk.
After 6 to 12 months, sometimes one needs more anastrozole to maintain a given E2 levels. Reasons not known and this may not apply to all. If your E2 levels increase, simply increase your dose. If you want to decrease your E2 from 28 to 21, a 25% change, try increasing the dose by 25% 1mg --> 1.25mg. This may work but may need to be repeated later.
No...not necessarily: [i]J Clin Psychiatry. 1983 May;44(5 Pt 2):209-10.Links Failure of bupropion to affect prolactin or growth hormone in man.
Whiteman PD, Peck AW, Fowle AS, Smith PR. In a double-blind crossover design, 5 male and 5 female volunteers received 5 different oral single-dose bupropion treatments (12.5 mg to 100 mg). Analyses of plasma prolactin and growth hormone levels revealed no significant drug related effects compared to placebo.[/i]
There are other articles which indicate that in the healthy case, buprion may decrease hypophyseal dopamine. But that is the healthy case, not you. The problem with macroadenoma is that the release of prolactin-or macroprolactin, or whatever-is not governed by the typical constraints of the HP axis.
So...start from scratch: Do you know why you are low in T? If it is due to macroadenoma and prolactin, perhaps this should be fixed, and not "covered up." Just perhaps. E is a different issue, and possibly independent of the pituitary tumor, and possibly not. Address the root cause.
...my original blood work (seven years ago) showed low levels of free testosterone and extremely low LH. The follow-up MRI brought up the tumor, which then lead to the diagnosis of secondary hypogonadism. I can only assume that my T is low because of the adenoma.
I had some bloodwork done this afternoon - SHBG, LH, FSH, E2 & Prolactin. The results should be back in a couple days. I'll post them up when they come in...hebs
ps...how do you 'fix' the adenoma? I was told surgical removal wasn't a viable option.
Depending on what other meds you are taking, the lab tests may be screwy.
7 years ago, your options may have been limited. Transphenoidal hypophysectomy? Not everyone's cup of tea. Medicines...well, there is Sandostatin and dopamine analogues (but chronic cabergoline and pergoline may have heart valvular risks) Radiation therapy has changed. Despite the qualifier in the article below, has anyone considered CyberKnife or Gamma-Knife irradiation for you?
[i]1: Minerva Endocrinol. 2004 Dec;29(4):241-75. Links Diagnosis and treatment of pituitary adenomas.
Chanson P, Salenave S. Service of Endocrinology and Reproduction Diseases BicÃªtre University Hospital, Paris, France. firstname.lastname@example.org Pituitary tumors cause symptoms by secreting hormones (prolactin, PRL, responsible for amenorrhea-galactorrhea in women and decreased libido in men; growth hormone, GH, responsible for acromegaly; adrenocorticotropic hormone, ACTH, responsible for Cushing's syndrome; thyroid-stimulating hormone, TSH, responsible for hyperthyroidism), depressing the secretion of hormones (hypopituitarism), or by mass-related effects (headaches, visual field abnormalities...). All patients with pituitary tumors should be evaluated for gonadal, thyroid and adrenal function as well as PRL and GH secretion. Specific stimulation and suppression tests for pituitary hormones are performed in selected situations for detecting the type of hypersecretion or the response to treatment. ... Treatment of pituitary adenomas consists of surgery (performed in more than 99% of cases via a transphenoidal route) and radiotherapy, generally fractionated or, in selected cases, using stereotactic techniques such as gamma-knife. The availability of medical treatment (dopamine, DA, agonists, somatostatin analogs, GH-receptor antagonists...) has profoundly modified the indications of radiotherapy, drugs being now generally used as a second-line treatment, after surgery (or even as first-line treatment). Based on the results of the different treatment modalities for each type of pituitary adenoma, recommendations will be proposed. They may be summarized as follows. For treatment of GH-secreting adenomas, trans-sphenoidal surgery is the first-line therapy except when the macroadenoma is giant or if surgery is contra-indicated; postoperative radiation therapy (fractionated, or by gamma-knife) is performed for partially resected tumors or when GH levels remain elevated (eventually after a trial of somatostatin analog). Somatostatin analogs, now available in slow release form, are proposed when surgery is contra-indicated, or has failed to normalize GH levels, or in waiting for the delayed effects of radiation therapy. If the probability of surgical cure is low (e.g. in patients with very large and/or invasive tumors), then somatostatin analogs may be reasonable primary therapeutic modality provided that the tumor does not threaten vision or neurological function. Pegvisomant, the new GH-receptor antagonist, is indicated in case of resistance to somatostatin analogs. Patients with PRL-secreting microadenomas may be treated either with trans-sphenoidal surgery or medically with DA agonists. In patients with macroadenomas, even in the presence of chiasmatic syndrome, DA agonists are now proposed as primary treatment. Indeed, effects on visual disturbances are often very rapid (within a few hours or days) and tumoral shrinkage is usually very significant. For patients with ACTH-secreting adenomas, primary therapy is generally trans-sphenoidal surgery by a skilled surgeon, whether or not a microadenoma is visible on MRI. Radiotherapy is reserved for patients who are subtotally resected or remain hyper-secretory after surgery. In waiting for the effects of radiotherapy, adrenal steroidogenesis inhibitors (mitotane, ketoconazole) may be indicated. If drugs are not available or not tolerated, bilateral adrenalectomy may be proposed. For patients with clinically non functioning adenomas (generally gonadotropin-secreting adenomas on immunocytochemistry), trans-sphenoidal surgery with or without postoperative radiation therapy is performed for almost all patients whether or not they have visual consequences of their tumor. Selected patients with small, incidentally discovered microadenomas may be carefully followed without immediate therapy. PMID: 15765032 [PubMed - indexed for MEDLINE][/i]
I cannot give advice, but maybe this it's time to review your situation with your endocrinologist.
...you got me thinking with this post and then this one below
...so I pulled old my old labs last night and rechecked a few things.
Nov26/07 (pre-TRT) Estradiol-17 Beta - 123 with a reference range 'up to 206 pmol/L Because most of the info available to me on the net is listed in pg/ml, I did the standard conversion of pmol/L to pg/ml by dividing by 3.67, coming up with 33.5 pg/mL
March25/07 (four-weeks into TRT) Estradiol - 68 with a NEW reference range of 43-151 This time the test came with a note: "Please note change to reference range and methodology, effecetive February 4,2008"
So on this particular lab report I was just given the physician's copy which doesn't list the unit of measurement. Fully expecting to see a large rise in my E2 levels, I based this on the transdermal applications and then the added side effects that I'd been feeling (sore, errect nips, brain fog, etc...), I made the ASSUMPTION (and possibly a very bad one at that!) that they, the lab, had not only changed the reference range but had also changed up the unit of measurement (to match our American cohorts). There's been a lot of talk about standardizing tests lately so this seemed logical.
With this assumption, and not even paying attention to the new ref range (43-151), I didn't do any conversion and just assumed that they were giving me the results in pg/ml now. Seemed logical up until last night. I now had an E2 level of 68pg/mL, up fom 33pg/mL pre-TRT.
What doesn't make sense NOW is the new ref range. It would be illogical to think that they had actually changed the units because a reference range of 43-151pg/mL makes no sense what-so-ever does it?!? It's a whole lot more sensible to think that that's STILL in pmol/L, so it's most likely 43-151pmol/l or 11.7-41pg/mL
So without checking with the doctor, we meet tomorrow, I think that I really f***ed up here and my E2 actually dropped (not increased) by using the .5mg/week of A-dex for the first 3.5 weeks of treatment, and I'm currently sitting at 18.5pg/mL (68pmol/L / 3.67 = 18.5pg/mL), not 68pg/mL. In actuality I must be even lower right now because since that test, thinking that I was way up to 68pg/ml, I've been on an increased dosage of 4drops ED versus EOD, so I've increased from .5mg to 1mg/week. Now that would explain the drop in libido, the fatigue, the fogginess, etc...On the plus side, the nipple sensitivity is gone!
I guess what I should do now is follow the below protocol, stop the AI for a week and then start back up at just .25mg/week, and then retest E2 again a couple weeks after that?
...very good advice, thanks! My Canadian doctors don't use AI's for TRT treatment. The one yesterday actually had to do a Wiki-search just to see what Anastrozole was and what it was used for.
..we meet tomorrow, I'll be better prepared with this!
...according to my Urologist and two pharmacists, hCG is not approved for use and can't be scripted in Canada. Can anyone verify that?
...DHT levels were checked on March25th, the results can take up to two weeks to arrive.
...good info and it definitely won't hurt asking about this. Back when I first met with the surgeon I was classified as having a macroadenoma (>10mm) and he didn't want to touch it. It's since been downgraded to a microadenoma (4mm) so I can't see him being anymore eager to do anything about it. Just the same, I will still inquire about this. Thanks Doc!...hebs
...no bloodwork back yet but surprise, surprise, I actually had a pretty good appt. with my MD today. It turns out that the urologist had sent the MD a letter yesterday giving him, the MD, the 'authority' to take over my current TRT treatment. It's a long story, mostly doctor politics! With that, I now have the go ahead to switch over from Androgel to IM injects and I'm wondering what would be the best option.
I'm currently doing 10g of Androgel ED. I just opened my last box two days ago so I still have a 13 day supply that I would like to use up if I can. Being that he's just a family doctor and admittedly does not know very much about TRT, he's kinda thrown the ball in my court to 'pick a testosterone and an injection schedule'.
I/we decided on doing injects of 50mg at 2xweek (based on literature from you guys that I had brought him). He's offered up his nurse to do the injects at his office. She's available anytime on Mon and Thurs, there's no appt required, I just show up and she'll do the inject. It's free and it's not out of the way so why not right.
The dilemma. Not knowing what would be more cost effective, he wrote me two scripts.