Hello, Thank You, and (long) Clinical Course Decription

[SecondaryHypo]

Hello Gentlemen.

I am new to this wonderful forum. This is my first post, although I have been staying up late reading your informative posts for just over 2 months now, as I try to deal emotionally with what is going on with me. I am very impressed with the wealth of knowledge you possess, and also with how candid and open you are in expressing the very personal details of your health issues. By your openness, you have created a valuable archive, which the new sufferer can search--looking for posts describing symptoms similar to one's own--in hopes of finding a suitable treatment. Without your brave and honest description of your problems this incredible resource would not exist. Thank you all for that.

I must also acknowledge and thank Dr. Crisler for all of the time, energy, and expense that he clearly puts into this useful forum. I have not met him (yet), but it is evident to me that he is a special physician, advancing the understanding and treatment of these specific health conditions of interest to us all. I have already experienced the frustrating search for a doctor who knows and cares about this subject, with the predictable result. (I'm on the third doctor so far. I've got one more on deck to try locally, and then it's plane ticket time.)

I will now describe my health complaint. It is still unfolding, and there are tests pending, so I will speak of it in general terms, without a lot of numbers. I'm sure that I will eventually post very specific details and lab results, as is the custom here.

I have (secondary) hypogonadotropic hypogonadism (HH). I have never been a body-builder or used AAS. I was first told that I had low testosterone about 4 years ago, by a fertility doctor (an OB/GYN) my wife and I were seeing. I didn't get excited about it then, because I had no obvious symptoms at the time. I was in my early forties, my energy was fine, and my libido and performance had not changed at all since my twenties. Besides, the fertility doctor made it sound like no big deal, "I'll give you some Clomid and it will improve." (I now know that it was no big deal to him, because he had a short-term responsibility: to help me conceive. After that, he would refer me to another doctor anyway for long-term management, so therefore he didn't really feel the need to tell me how serious this was and what unpleasantness I had in store ahead.) The Clomid did raise my T and we did conceive. I soon went off the Clomid out of laziness.

Eventually I decided I didn't like the idea of walking around with low T, (even though I still had no symptoms), so I asked the fertility doctor for another Clomid prescription. He said a man can't be his long-term patient (because he is an OB/GYN), and referred me to a Urologist. The Urologist's labs showed low T with LH and FSH normal (or rather, "inappropriately normal," because they should be high in the setting of low T). Diagnosis: Hypogonadotropic hypogonadism. The Urologist gave me Clomid. My T went up on labs, but my sperm count was still low, so the Urologist changed me from Clomid to Arimidex 1 mg PO QD. I don't know what my T level was on Arimidex (no labs), but I do know that my sperm count doubled and we conceived again, so I assume the T level was decent on Arimidex. I then went off the Arimidex out of laziness. I had moved to a new state (in June 2007), was working crazy hours at a new job, ran out of pills and didn't have the drive to go find a new Urologist in the new state. Again, I still felt fine and had the same libido and performance as in my twenties, so there was no pressure, or so I thought.

Then, one year later, in the summer of 2008, I experienced my first symptoms of hypogonadism. I had decreased libido and diminished performance. I went to a new Urologist in the new state. His labs showed low T with LH and FSH normal (again, "inappropriately normal"). He offered me testosterone gel. I said that this sounded like a drastic step, couldn't we just try the Arimidex again? (I assumed that all Urologists knew about this drug...wrong.) He had never heard of Arimidex, yet offered to write me a script for it! I politely explained that I was really looking for a doctor who deals with this kind of treatment all the time, and could he please refer me to an Endocrinologist.

I saw a private-practice endocrinologist. I showed her my recent labs from the new Urologist. She offered me testosterone gel. (Man, those drug reps are doing a great job!) By now I had been reading a lot about the subject, so I asked her about the possible side effects, such as testicular atrophy and gynecomastia. She very matter-of-factly said that testicular atrophy was likely, and gynecomastia was possible, and then with her silence and her look she implied: "So when do you want to start?" (!) I asked if she had ever treated testicular atrophy with HCG, or prevented gynecomastia using Arimidex. She said "no." I asked if she would be willing to consider these modalities. She said "no." I asked, "Why not?" She gave me a bizarre, other-worldly response which was almost word-for-word, "I only do what I've done, so that's what I'm going to do." (!) After the uncomfortable silence and my shocked expression, I then told her I had been on Arimidex before and it had seemed to help. She said she had never prescribed it before, but she looked it up in her palm pilot on Epocrates and wrote me a script for Arimidex 1 mg PO QD! Then she handed me the lab request slip to bring to the lab, to draw confirmatory labs. I looked at the request, and I had to ask her to add Estradiol. She said ok and added it. She herself hadn't even thought to draw the estradiol, even though we had already discussed my former success with Arimidex, and even though she had already written me a script for Arimidex to raise my testosterone by means of reduced peripheral aromatization to estrogens and diminished negative feedback by same! (Unfortunately, I didn't yet know about the ultrasensitive test.) The estradiol value was normal, 26 pg/mL (Ref Range: less than 54), LabCorp. Prolactin and thyoid studies and IGF-1 were normal.

I told her that I was very interested in the HCG-type management of TRT side effects, and would she kindly refer me to a doctor who has a practice filled with TRT male patients. She referred me to an academic Endocrinologist at the local prestigious medical school. I did not start any Arimidex.

(...this post continued in the first reply, below...)

[SecondaryHypo]

(...continued from the above post...)

While waiting for the appointment with the academic Endocrinologist, a new wrinkle: The first Endo's MRI showed a partially empty sella. As you know, this means that my brain's arachnoid membrane right near the pituitary has a CSF-filled bulge that is putting pressure on my pituitary and squishing it flat against a bony area called the "sella turcica." This is a fairly common incidental finding on brain imaging, which means that lots of people have it and it causes them no problem with their hormones. On the other hand, a small percentage of people with empty sella do indeed experience problems with their pituitary hormones, due to the empty sella. So the differential diagnosis at this point was HH that is either: 1.) Idiopathic, or 2.) Due to empty sella syndrome. I was not thrilled about this. Either one of these means that I will need a lifetime of TRT, yet will have to go to great lengths and expense to find a doctor to properly manage this therapy. Great.

At this same time (October 2008) I was spending huge amounts of time searching the web regarding hypogonadism. Another wrinkle developed: I kept seeing mention of medicines that could potentially cause antiandrogenic effects, and I realized that I was on some. (Yes, I have the references.) You see, for four years I had been taking high-dose antacid meds (H-2 blockers like cimetidine, famotidine, ranitidine) and also a proton-pump inhibitor (omeprazole). Yes, the heavy antacid use had started 4 years ago at about the same time as the initial low T report from the fertility doctor! I also realized that I was eating A LOT of soy, and that my wife was buying laundry detergent and soaps with melaleuca oil ("tea tree" oil). Also, I was a big black licorice fan. I immediately stopped using all this stuff.

Naturally, I am only human and susceptible to wishful thinking, so I was hoping that the antacids (etc.) were the explanation for my hypogonadism. Who wouldn't rather have the cause be something potentially reversible than something chronic? So I stopped all antacids, waited one month, and had my new Endocrinologist draw labs. Result: testosterone went up! That is what I wanted to see, because it implicates the antacids. However, the increase was not dramatic enough to rule out normal inter-test variability. So I had no choice but to wait another month, and test again. (BTW, at this one month point the Estradiol was high-normal at 46 pg/mL (Ref Range: 13 - 54 pg/mL) QuestDiagnostics.)

To my supreme disappointment, the testosterone values at the end of the second month of the antacid-free trial were almost exactly the same low values they had been two months earlier, when I had first D/Ced the antacids! I had hoped the T would go up again--this time definitively--and that I could therefore conclude that the antacids had indeed caused the problem, and that I was going to be OK with normal T and normal libido, yet without any life-long treatment. No such luck. So now I'm left with a differential diagnosis that says I either have Idiopathic HH, or HH caused by empty sella. Neither of these is going to get better, and will require life-long TRT. Alternatively, it is still possible that the HH is antacid-related, but NOT reversible with discontinuation (again, life-long TRT). Or, it might still be reversible, yet it takes longer than 2 months off meds to reverse, or, the antacids may have reset some kind of HPTA "set point," and the reversal may require some kind of hypothalamic/pituitary restart.

(Cortisol AM and PM serum, and also 24-hour urine cortisol were all normal. Vitamin D is pending.)

I eventually saw the new Endocrinologist at the medical school. He was terribly kind and avuncular and patiently spent a very long time with me listening to all my stories and complaints, and I am thankful for that. However, I was disappointed by a few things. He doesn't have any faith that the antacids played any role, even after I showed him the reference articles. I felt him out about any possible future TRT: would he give me HCG, Arimidex, etc.? It is clear that he will not. I asked him about a restart program using Clomid or Tamoxifen for 6 months or so. Negative response. He is very academic and conservative and says things like, "Well, we just don't know for sure that long-term HCG won't cause cancer. Clomid and Tamoxifen can cause visual problems, Arimidex causes bone density loss." I gave him Dr. Crisler's TRT recipe for success, and the HCG update, but it is clear to me that he is not going to follow it. He did offer one hope of a reversable cause, saying that stress and obesity could be playing a role. (I'm 6'1", 240 lbs., flabby and weak, 45 years old.) However, these last blood labs I got included an estadiol, ultrasensitive, from Quest, (which I asked for, having learned it on this forum--Thank You) that came back "less than 2 pg/mL" with a ref range of (< or = 29). So I guess that shoots the obesity/aromatization/elevated E2 theory. (And it also points out the ridiculousness of the two recent doctors willing to throw Arimidex scripts at me with no intention of checking E2!) I guess there is still the possibility of a different estrogen being high (?), or of obesity playing a role by depressing SHBG, which was quite low in my lab reports. But I'm in a catch-22. How am I supposed to lose weight when I have low T?: no energy, decreased lipolysis, and aerobic exercise (stairmaster) exhausts me for days. I also wonder if this recent E2 lab could be wrong. Remember, Arimidex did effectively increase my sperm count in the past, so I was likely high E2 at the time. Wouldn't I still be high E2?

One encouraging thing: the academic Endocrinologist did order a Clomid stimulation test to see if my pituitary is capable of producing gonadotropins. (Draw AM labs, then take Clomid 50mg PO BID times 7 days, then redraw AM labs.) The results are still pending.

I do, of course, want to avoid life-long TRT if possible. So, if this doctor won't guide me through a SERM-type restart, then there is one more local doctor I could try before pulling the trigger and flying to Lansing. This last local doctor is an anti-aging specialist who has published in the medical literature on the subject of treating the HPTA, which is good. Unfortunately, he doesn't take insurance and I will have to pay out-of-network fees, deductible, etc. I suppose I could try a restart by myself, using the liquid research chemicals, but who knows what's really in that stuff?

In conclusion, I assume that in the end I will have one of two outcomes. I will either have a restart that works and I'll be done, or, I will begin lifetime TRT, which I will insist is done in the state-of-the art manner that is represented by the knowledge of Dr. Crisler and of yourselves, dear Gentlemen of this forum.

Alternatively, I suppose I could do TRT for a couple years, lose weight, stay off the antacids longer, and then try a restart at that time, with fingers crossed.

Thanks again to all who have made this forum the great resource that it is.

SecondaryHypo

[BigAk]

Alternatively, I suppose I could do TRT for a couple years, lose weight, stay off the antacids longer, and then try a restart at that time, with fingers crossed.

Amazing.... This is the exact same thing that popped in my head when I read about you weighing 240 at 6'1.... Without a doubt being overweight and out of shape have a very negative impact on Testosterone levels. The idea of going on TRT while employing HCG in an effort to get in shape is a good one.. In the mean time, you can implement a fitness plan that will shuttle you into new healthy body. After that you can easily do a restart given that your testes have been active the whole TRT period. I see a very successful venture here.. Or if not TRT during this period, you can also think about doing cycles of Nolvadex (you have already proved that clomid increased your testosterone). While on these cycles of Nolvadex, you can take advantage of your high testosterone and lose weight and get to your fitness goal. Then, at the end you can taper off the Nolvadex and your Testosterone levels would stay up corresponding to your new good fitness status. I view the fact that you respond well to clomid as very good news.

As far as the empty sella syndrom, I know of one other person on these forums who has the same.. and that is eeso... I'll send him a PM to see if he can come along and chime in... I do know that he also attempted a restart but eventually went back on TRT... But, this is not saying that you will have to follow the same destiny... We all are different... and your empty sella may not have a negative impact.. It's worth talking with him IMO.

Welcome to the board brother.... Let's take a look at the new panel when you get it.


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[eeso]

Hi SH,

As discussed in our PM's and as BigAk mentioned, I also have empty sella.

I've never actually had a doctor explain in depth the implications of this other than potential for diminished HPTA function. My thyroid levels seem to bounce around a bit but after trying HC and Armour I found that I'm much better off without them.

In regards to a restart, Nolva and Clomid got my LH and FSH to the top end of the range, however my testosterone still only went to about 20 on a 11-33 scale so perhaps my nuts don't work very well anyway.

The side effects of the serms were terrible and I had to take painkillers just to walk without huge pain in my knees and shins. Sleep was bad and unrefreshing, and once I came off the SERMS I realised how much better I felt.

Something also else happened - the serms made my TSH (thyroid) reading very high. I went from about 2 up to 5+ which is chronic, so obviously SERMS boost more than just LH and FSH (at least for me).

I found after about 6 months on testosterone I lost my low cortisol/low thyroid symptoms. I also exercise regularly and eat well.

If I were you (but I'm not), I would go on TRT and do the exercise+eating plan and that could give you the best shot of restoring your natural production and health.

I've found that exercise and diet are more important than anything. Lifestyle factors are so important - Hardasnails is an expert in this and a consult with him would be more than worthwhile.

[SecondaryHypo]

Thanks eeso.

I have a question about your experience with the HPTA restart using Nolva & Clomid. You wrote:




In regards to a restart, Nolva and Clomid got my LH and FSH to the top end of the range, however my testosterone still only went to about 20 on a 11-33 scale so perhaps my nuts don't work very well anyway.



Question:

If Nolva and Clomid got your T up to 20 on a scale of 11-33, then that translates (mathematically) in my USA (QuestDiagnostics) scale to a T level of 597.7 ng/dL on a scale of (250 - 1100). So, presuming that your pre-SERM T level was below the low mark (Less than 11 in your scale, or less than 250 in mine), then I would think that 20 (aka 597.7 ng/dL) was a good response to SERMs, no?

Also, I'm interested to know what your T level was a couple of months after stopping the SERMs, when you were "all natural." Did it drop below 20? Or, are you saying that you did a SERM restart, then got off the SERMs and had an "all natural" T level of 20, and yet still decided that 20 wasn't high enough for you so you started TRT?

The reason I ask is that I'm currently at an "all natural" T of 186 (250 - 1100). So, if I did a restart for a few months, then got off all meds and ended up with an "all natural" T of 597.7 (250 - 1100) I would be happy and call it a success. But then I'm 45 years old. Maybe you are much younger and that explains the different viewpoint.

SecondaryHypo

[BigAk]

.
How does empty sella impact the HPTA?? and does it always in every case??

.

[SecondaryHypo]

.
How does empty sella impact the HPTA?? and does it always in every case??

.

No, empty sella does not affect the patient's pituitary hormone functioning in every case. And that is why it was frustrating for me to be diagnosed with empty sella (on MRI) during the course of a hypogonadism work-up. In some patients the empty sella is indeed the cause of their hypogonadism, and in other patients the empty sella is a red herring, or incidental finding. (Which therefore means that the hypogonadism is due to something else, or perhaps it is idiopathic.)

In empty sella there is physical compression and flattening of the pituitary by a bulging, fluid-filled membrane. When it does affect hormone function, empty sella causes hypopituitarism, or, decreased secretion of one or more pituitary hormones. I read somewhere that the order in which the hormones are affected is usually: GH first, then prolactin, FSH, LH, TSH, then ACTH.

There are lots of people walking around with empty sella who don't know it. I have read differing opinions as to what percentage of people with empty sella actually have decreased hormone function. I don't remember the exact number, but it was low (like 5 or 10 %). Then I read another paper that said it is much higher, like 40 to 50 %, but this number represents people with empty sella and with no hormone deficiencies at all in their daily lives, yet subtle deficiencies are revealed using provocative testing. That means the patient is given a drug that releases a certain pituitary hormone, and then labs are drawn to see if secretion of that hormone goes up by the expected amount.

By the way, I had a provocative test recently, a clomid stimulation test. My LH and Testosterone more than doubled, so my Endocrinologist feels that this means that in my case empty sella is not the cause of my hypogonadism. I am very happy about this.

SecondaryHypo

[eeso]

Interesting post SH. My natural testosterone and thyroid levels are on the low end of the range so I figured I just had dimished pituitary output. However the nolva and clomid got my LH and FSH quite high but my test was still below average for my age.

I also have very low SHBG and highish e2. I'm getting a glucose tolerance test soon to investigate the possibility of insulin resistence which is something I've suspect for some time now.

As for the restart - my levels dropped back to my normal low levels after coming off the serms. What's more, the serms made me feel awful and I got severe joint pain and also ended up busitng my ACL and needing a knee reconstruction. I am in no doubt that the serms weekend my joints and ligaments etc and contributed to the injury. They also stop you from sleeping well, and overall you just feel terrible. However, you don't realise how bad you feel until you come off them and you suddenly feel so much better. Put shortly, I felt better with low test than I did on serms with higher test. I felt like I was being poisoned.

As I mentioned in the PM, there's a couple of options for you to try other than drugs at this point.

Primordial Performance Test Recovery stack + genuine Tongkat Ali is well worth a shot. I rate them both VERY highly and have had blood tests to prove that tongkat ali doubled my LH and FSH and raised my testosterone by 50% (unfortunately that still wasn't enough at the time).

I am about to come off TRT and will be using these products and not nolva and clomid as in my experience these are a better and safer option. I have recommended these products to literally dozens of hardcore bodybuilders who did not recover after their usual nolva+clomid PCT and ALL of them have come back to me thanking me for getting them onto it as it fixed them right up.

Primordial Performance Testosterone Recovery Stack: http://www.primordialperformance.com/store/Testosterone_Recovery_Stack.html

Genuine Tongkat Ali:
www.newlifealternatives.com

[BigAk]

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Excellent info eeso... Thank you..

Are you planning on coming off for good again??

.

[BigAk]

By the way, I had a provocative test recently, a clomid stimulation test. My LH and Testosterone more than doubled, so my Endocrinologist feels that this means that in my case empty sella is not the cause of my hypogonadism. I am very happy about this.

SecondaryHypo

This is great news SH.. I would give eeso's recommendations a try followed by bloodwork to confirm results.

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[SecondaryHypo]

Thanks for the advice and encouragement eeso and BigAk.

Actually, I saw my Endocrinologist yesterday and he decided that based on the good result of the Clomid stimulation test he wants me to go on a SERM for a few months. During this time I am to take advantage of the increased T and energy so I can exercise and lose weight. Then we will taper off and see if my T stays up or goes back below 200. So this is similar to a "restart," but without the AAS use preceding it.

He wanted me to go on Clomid. I asked if I could take Nolvadex (tamoxifen) instead, because of what I read in the Belgian study that I pasted below. It says that Clomid desensitizes the pituitary to the effects of GnRH, but tamoxifen actually sensitizes the pituitary to the effects of GnRH. I am hoping that this sensitization will increase my "set point" and therefore the LH will stay elevated once I'm off the tamoxifen. Also, tamoxifen has less intrinsic estrogenic activity than clomid, so I was hoping that it would have less of a chance of giving me emotional side effects.

So yes, he agreed to let me take tamoxifen. He feels that either will have the same chance of working, and he has more experience using clomid, but he is willing to let me take tamoxifen for the reasons stated.

So I started tamoxifen yesterday. The dose is about half of what I have seen others write about taking for HPTA restart. My Endo is extremely cautious and wants to make sure he is giving the "minimum effective dose" and wants to avoid the visual side effects, among others. So I'm happy with the management so far and am starting out on this new drug happily and with high hopes.

I have also pasted below a study which describes a man being cured from "isolated hypogonadotropic hypogonadism" by a SERM (clomid). This demonstrates that it is not just wishful thinking on my part that this set-point might exist. It is, however, still wishful thinking on my part to believe that this is the cause of my problem too, and that I will be cured too. Hopefully, tamoxifen will "turn the thermostat back up" to where it is supposed to be and my pituitary will produce the proper amount of LH, even long after the tamoxifen has been D/Ced. Time will tell...

SecondaryHypo

The Belgian study on sensitization to GnRH:

1: Fertil Steril. 1978 Mar;29(3):320-7.Links
Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.Vermeulen A, Comhaire F.
The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development.

PMID: 640052 [PubMed - indexed for MEDLINE]


The "Set-Point" study:

Volume 86, Issue 5, Pages 1513.e5-1513.e9 (November 2006)

Complete reversal of adult-onset isolated hypogonadotropic hypogonadism with clomiphene citrate
Presented at the 12th International Congress of Endocrinology, Lisbon, Portugal, August 31 to September 2, 2004.

Stella Ioannidou-Kadis, M.D.a, Pat J. Wright, M.B., Ch.B.b, R. Dermot Neely, M.D.c, Richard Quinton, M.D.a

Received 13 December 2005; received in revised form 7 March 2006; accepted 7 March 2006.

Objective
Inhibition of pituitary gonadotropin secretion in men by T is principally mediated by aromatization to estrogen (E), which inhibits hypothalamic secretion of GnRH. We hypothesized that adult-onset isolated hypogonadotropic hypogonadism (IHH) might result from an altered central set-point for E-mediated negative feedback.

Design and Setting
Longitudinal clinical investigation unit-based evaluation of the clinical and biochemical response to E-receptor blockade.

Patient(s)
A 31-year-old man presenting with an 18-month history of sexual dysfunction resulting from severe adult-onset IHH (LH 1.7 U/L, FSH 2.0 U/L, T 3.5 nmol/L).

Intervention(s)
Initial therapy with 50 mg of clomiphene citrate (CC) three times a day for 7 days, with overnight LH pulse profiling and 9 am T levels evaluated at baseline and on completion. A 2-month washout period, followed by low-dose maintenance therapy (25–50 mg/d) for 4 months.

Main Outcome Measure(s)
Baseline and stimulated T levels and LH pulsatility; effect on sexual function.

Result(s)
Clomiphene therapy resulted in complete normalization of pulsatile gonadotropin secretion, serum T level, and sexual function.

Conclusion(s)
Isolated hypogonadotropic hypogonadism may result from an acquired defect of enhanced hypothalamic sensitivity to E-mediated negative feedback. Whereas direct T replacement therapy can further suppress endogenous gonadotropin secretion, treating IHH men with gonadotropins can stimulate endogenous T secretion and enhance fertility potential. On theoretical grounds, reversal of gonadotropin deficiency with CC might be expected to have a similar biological effect.

[RhunDraco]

Hi SecondaryHypo,

I'm very interested in this, as well. How are your results on tamoxifen? What doses and dosing schedule, etc.

[SecondaryHypo]

Thanks for asking, but I got bad news today:

My HPTA restart attempt did not work.

I was on Tamoxifen for 13.5 weeks. The first 2 weeks at 20mg per day, the next two weeks at 10mg per day, and then 9.5 weeks at 5mg per day. My Total T level on Tamoxifen (at about 9 or 10 weeks in) was 406. Then, 4 weeks after stopping the Tamoxifen my Total T is now back down to 172.

So it didn't work.

I guess this means that a needle is in my future. As hard as I wanted to wish that I could avoid lifelong TRT, it is looking like that is my fate.

Good luck to you, RhunDraco, on your efforts. Don't give up hope, there are guys who manage to successfully restart. I am just not one of them. (yet?) Talk to BigAK. He did it.

[SecondaryHypo]

Here's an Update:

I had an appointment with my Endo this week about what to do now that my tamoxifen HPTA restart did not work.

I told him I was dissappointed because I wanted the cure to be something straightforward and mechanistic: I take tamoxifen for a while and I get better and then I am normal without drugs. My theory was that this (supposed) restart would be correcting damage done to me either by my overuse of antacids, or by my being out-of-shape, or by no known reason at all--who knows?--but in my mind the tamoxifen was supposed to fix me with no more effort or discipline (on my part) required than me taking a pill daily.

Well, we have proven that this is not going to be...

I should emphasize that all along my Endo has been humoring me with regard to my proposed etiologies for my problem. His opinion all along has been that my hypogonadism is most likely caused by my obesity, and is a hormonal/metabolic effect acting centrally (meaning in the brain). One can readily envision obesity causing insulin resistance and type 2 diabetes and/or contributing to the cause of the metabolic syndrome. He sees the cause of my hypogonadism as being more like these disease entities than like my other proposed causes for my hypogonadism.

In my past visits with him, I didn't want to believe that my obesity is the cause, for a couple of reasons. Firstly, if this should be the cause, then the cure would require a huge effort on my part. I'd have to live with constant daily discipline and vigilance and to change my eating habits and I'd have to exercise regularly. Who wants that? Secondly, obesity as the etiology has a soft, unsatisfying quality to it (pun intended). I wanted a more mechanical relationship between cause and effect: Antacids changed your pituitary's "set point," and tamoxifen will change it back. This obesity mechanism is quite vague, multifactorial, and mired in "associations" instead of "causes." For example, obesity can cause insulin resistance which can cause low testosterone, yet, low testosterone can cause both obesity and insulin resistance. It goes on and on like this in the literature. Leptin is somehow involved...Growth hormone and DHEA-S levels may play a role...etc.

So, as unsatisfying as it is, I now have to embrace the idea that my next great hope for a cure lies in permanent lifestyle change, meaning weight loss, exercise, stress reduction, and the like.

I asked him directly, "Do you really think that if I lose 50 pounds that I will be walking around with a testosterone of 400 and no meds?" He said "Yes." I asked him, "There are so many American men carrying an extra 50 lbs around, why don't they have it?" He answered in two parts, "Many of them do have lowered androgens, they just don't know it," and, "Well, THIS is the way that the extra weight has effected YOU."

My Endo did recognize that my low T represents a huge barrier to weight loss, and that I am in a "vicious cycle" of low T causing obesity/insulin resistance causing more low T. So he offered me two different ways to boost my T for a few months in order to loose the weight. I could go back on tamoxifen, or I could start HCG monotherapy. Believe me, I was tempted to go with the HCG, because I envision it giving me higher T levels and at the same time making me feel better sexually and strength-wise than the tamoxifen would. But I worry about the Hypothalamic-Pituitary suppression that HCG would cause. I figure that if the ultimate goal is to eventually come off all drugs and use my own functioning HPT-axis, and I am already starting with a poorly-functioning hypothalamus/pituitary system, then why knock it down even further, just to eventually ask it to recover from this new, lower state? My Endo says that he doesn't think that would happen, and gave the an example of some trails he was involved in regarding a male contraceptive. They suppressed the mens' HPTA with testosterone, their LH and FSH went to almost nothing, yet they all recovered after the trial. So his reasoning is I could use HCG if I want to, since the H/P system is resilient. (But theirs were normal and mine is deficient, right? I don't want to push my luck.) I asked him if the H/P suppression from HCG treatment would cause atrophy of the pituitary and allow my partially empty sella to get worse? He answered that again, he does not believe my partially empty sella is playing a role in my hypogonadism. (It was nice to hear that.) I asked him about using Naltrexone. He said it has had spotty efficacy in elevating gonadotropin levels but we could try it for a month if I want, but only by itself--NOT with tamoxifen or HCG. That would delay things...

So in the end I chose to go on tamoxifen again, but this time without a tapering dose. It will be 20mg per day for 4 months, during which time I must use the T generated to get off by butt and lose some weight. (I asked him for 40 mg daily, but he is worried about ocular side effects.) Yes, this is the same medicine as I took before, but conceptually I see this as a very different quest. Before, I was counting on the tamoxifen to cure me by itself. Now, I am using the tamoxifen as a tool to allow me to lose weight, which will hopefully cure me.

I asked my Endo if we should do a glucose tolerance test with insulin sampling? (my fasting glucose was normal but that does not rule out insulin resistance/elevation.) At least if it came back high I would be all the more convinced that the obesity really is the problem and could tackle it with more resolve. He said, "Why do a test when I already know how it will come bacK?...It will be high."

So that's it. I re-started taking tamoxifen and I started a new diet. It is something I found on the web. A company mails me a box of frozen food on Thursday evenings and it lasts a week. So far I have finished the first week and I did a good job sticking to it. I added an apple or banana here or there, but other than that I did not eat inbetween meals. That is a big change from a guy who has eaten dark chocolate nearly every day for years. I lost 3.5 pounds already. Eventually I will get off this plan and back to managing my own meals, but right now it gives me the structure and portion control that I need until I can learn to manage these on my own. It costs $150 week, delivered. (Of course I was already spending above a hundred a week on food, so I save that amount each week since I only eat the diet food now.) Nevertheless, $600 a month for food still seems expensive, but if it works for me, then it will have been worth it. I originally told myself I was going to join the program for one week and see how it goes. I did that. Now I'm thinking about doing it one month and see how it goes.

Well, I hope all this personal revelation (and typing) helps someone out there who is going through the same thing and has found this thread as a result of an anxious midnight web search...

That's exactly how I found this great forum last Fall.

[SecondaryHypo]

Here is an update on my progress trying to cure my hypogonadism:

I did do the mail order diet for about 7 to 8 weeks, and I lost about 22 pounds. I felt optimistic, like this time I was finally going to lose the 50 pounds and solve my problems.

Then I had an unexpected source of stress in my life, went back to my old comfort-eating habits, and gained back the weight I lost. After a couple of months, I tried a self-directed diet focusing on low gylcemic index. This lasted one month. I lost 3 or 4 pounds, and have kept them off. (big deal)

During this time of dieting, I took a small amount of Tamoxifen, like 5 mg per day (just trying to stretch out my supply of pills before the next Rx), and occasional small amounts of Arimidex, like 0.25 mg twice a week or so. My Endo advised me not to take Arimidex due to a study he read showing bone loss, so I stopped it for the most part.

I wasn't interested in seeing my Endo, because he had recommended hCG therapy last time we spoke. I was reluctant to suppress my H&P with hCG, so I asked if we could try Tamoxifen and weight loss first. He said that he believes H&P suppression is not a permanent concern, as evidenced by studies done on using Testosterone as a male contraceptive. All the men in the trials had their HPTA function return to normal after cessation of the T supplementation, so he thinks that my H&P will recover after hCG treatment is withdrawn. (But what about all the HPTA suppression caused by AAS use? How is that different than hCG use? I'm skeptical about my H&P bouncing back from any hCG use, but my Endo is confident.)

During these last few months I have noticed that my belly is getting bigger, more pendulous, yet I am not gaining weight overall. I realized that this is a BAD sign: it means that I am caught in a vicious cycle of increasing fat deposition and concomitant decrease in lean body mass, which leads to more fat deposition, etc. I do notice my arm and leg muscles wasting away.

So a week ago I gave in and agreed to start the hCG monotherapy in order to boost my Testosterone while attempting to lose fat and gain muscle. Then, when (if) I do this, I can come off the hCG and hopefully my H&P will awaken from their suppression (as my Endo believes) and I will be cured.

Another development I will mention is that I now really do believe in my Endo's assertion that my hypogonadism is related to my obesity. He says that the mechanism is unclear, but he believes I will be better if I lose the weight. When he originally told me this, I still clung to my belief that my HH was caused by my antacid abuse, or exposure to tea tree oil and tofu, etc. These causes are comforting, because they don't require me to make any effort to lose weight. But now I have to face facts. Obesity is indeed the likely cause of the hypogonadism that I have, and the insulin resistance/metabolic syndrome that I will likely have if I don't do something.

There are many studies on PubMed that discuss the complicated relationship between Obesity and hypogonadism. Here is the title of just one, for example:

Mechanisms of obesity and related pathologies: Androgen
deficiency and endothelial dysfunction may be the link
between obesity and erectile dysfunction
Abdulmaged M. Traish1, Robert J. Feeley1 and Andre Guay2
1 Department of Biochemistry and Urology, Boston University School of Medicine, MA, USA
2 Department of Endocrinology, Center for Sexual Function, Lahey Clinic, Peabody, MA, USA

So now I am ordering the hCG and trying to get it covered by insurance and ordering vials and syringes and bacteriostatic water, getting ready.

I wrote down my various body measurements and took "before" photos. Getting mentally ready for this next attempt at good health

[Hemochromatosis]

Dear SecondaryHypo:

I have just been informed I have to shorten my 25188 character reply to 10000. So pull up a seat and I will break them into multiple posts. I usually do not post anywhere anymore but you compelled me as follows:

You and I have identical profiles to the extent of age, height and in fact my weight is about 270. A brief background to ensure those who are inevietably going to rage on me for certain assertions I will make in this thread, some objective means of contemplation. Anything that I assert has been a result of first hand experimentation on myself. I come from an athletic background, wrestled for 12 years in Ohio, played football and weight trained. My weight training was not to the point of competition, but I was on the cusp and remember the days it took me 1.5 hour to get through squats. I was the weightroom supervisior at Florida State from 1984-1987 and was a trainer at a few different gyms when I first graduated from college while looking for a better job.

In 1999 while working out at the Pentagon Gym (POAC) I noticed my weight gain to 235 was not being affected by diet or excercise. I tried everything from muscle confusion, antagonistic, flex/extend routines, increased cardio to 1 hour a night (mostly elytpical), counted carbs, increased veggies and still nothing.

WHILE I AM SURE THE VAST MAJORITY WANT TO BELEIVE THEY ARE THEIR MASTER OF THEIR OWN DESTINY YOU CAN ONLY HOPE TO MITIGATE YOUR GENETICS. 70% genetic - 30% environment.

The weight continued to stack and I wrote it off as being attributed to 12hr+ days and tons of stress to include WMD programs. Then it happened in Sep. 2004 I had an ischemic stroke. I was rushed to the ER at Alexandria Hospital, my entire right side was gone, pissed myself, had a siezure on top of it and had clear egg white flem about a cup pouring out of my mouth as I tried to communicate talking with a garbled voice and sensing my synaptic activity getting interupted like a bunch of static in a power storm. While I was being monitored the nurse rushed get authority to adminster a clot buster that carries a significant factor (approximately 30%) of causing a major hemorrage leaving the recepient in a vegetable state/brian dead. I had taken energy work and meditation classes and made a realization while at the same time internally begging God to take me out or put me back, that if I have a blockage maybe if I can stimulate the right side that was turned off that I may be able to force a nureral synaptic surge to move the clot through.

No one was in the room at the time, I focused my energy, raised it from the root, focused everything I had, moved it up through the shakras, it was amazingly intense more intense than any other time in my life. When it was at the point of where I couldn't take it anymore I oepned my eyes sat up as much as I could, took my left hand and started to pull the hair off my right arm and dug in with what little nails I had drawing blood and commanding with a garbled voice "move mother fooker move mother fooker" over and over as directed at my arms and legs. Then out of no where I felt a sonic compression come at me from a 45 degree angle above my head and when it hit me my face came up, voice came back, and right arm and leg fully restored. I yelled for the nurse, now in a regular voice, she came into the room and dropped the clot buster on the floor and said 15 years in DC Metro ER's and she has never seen anything like that happen.

My basil ganglia took a 1cm hit. More importantly the ganglia works in tandum with the cerebelum and controls the excititory function by acting like a govenor on an engine. Needless to say almost any act of kindness from friends would set me off into full on Days of Our Lives, gurly man, cry fest! I spent a few days in the hospital and I still needed to syncopate my walk. Since I had studied music I put a meternome beat in my ear and was able to get my walk back to function within 2 days, it literally felt like I had two distinct halves as if someone drew a line done the center of me. There were some spacial concepts of missing my mouth with a forkfull of peas and my signature was the last to restore fully, which took about three months. The brain has amazing restoration ability and rerouting.

I was told no blockages to my heart or carodial arteries, but that I had Atril Fibrillation (AF) an arrythmia caused by stray electrical discharges within the heart that result in your left atrium not fully contracting, but quivering at 200-300 cycles per minute. The lack of contraction enables clots to form in the left atrial appendage. I was put on coumadin and cardizem (ditalizem generic to control rate) and was sent on my way. There are a series of other interesting events that I will spare the board, but the emphasis here is that I was told the AF caused the stroke.

I was in a position at the time to take 3 years off of life and I commited to researching my problem. I have logged over 35,000 pages of reading on AF and related subjects, to include without limitation, hemochromatosis, secondary hypogonadism, CPPD (calcium pyrophosphate dihydroxide disorder), and have spoken with almost every published Electrophysiologist and Cardiologist, including James Cox of the Cox Maze procedure, Andrea Natale from the Cleveland Clinic and Dr. Kisers group who perform the convergent procedure in NC.

THE MOST IMPORTANT QUESTION IS WHY? Keep asking it and never take "just because" as a valid conclusion or "we are not sure." Why will yield the how. You are in the process of pealing your onion, but self realizations stick and you are making conclusions at certain junctures such as the antacid conclusion that demonstrate the need for a wider array approach. We all want quick answers and the pill that makes it all go away. The reality is, unless you are a government worker, results are the only thing that matter.

I started a process of elimination, and pay attention Secondary Hypo, because I am not providing the story for story’s sake, it is to demonstrate a method and an example of indenture that is required if you expect to survive our modern healthcare system and a government who deems you an unnecessary burden on a system that is about to implode. You have to be in tune, you have to make the self realizations; you have to constantly read, ask and experiment. In many instance I was the exception and had adverse effects where others were fine with certain treatments.


I pressed and pressed and pressed and with the process of elimination started to rule out everything from H-Pylori to vagal toning to Thyroid implications, calcium, potassium, magnesium, sodium and boron balancing to ensure the SA node could have optimum firing ability within the heart and on and on and on. I went on a process of elimination tip that included acupuncture and ultra purified water, anything I could address to remove any possible causation. The options in a maze procedure or pulmonary ablation was not convincing and the efficacy rates of the ablation were eschewed and the cox maze too radical with a full sternum cutting required. (Side note for AF reader – Convergent Procedure is returning note worthy results 4 years out with normal sinus rhythm holding at 2 years and counting by 80% of the patients)

[Hemochromatosis]

I kept getting recurring gout. The frequency when from 3 times a years down 1-2 days to every 12 weeks down a week or more. It was brutal. Classic gout is a persons inability to process the purines that are bound to most every kind of protein (although I need to write the folks at iso-pure to see if purines are still bound even under processed production). The drilling effect on my joints was brutal. I though if this continues, at that time about 3 years of enduring, that soon I will be in a wheel chair and what was the purpose of defying a stroke to be waylaid by some ailment that is often confused by the ignorant as a rich man’s gluttony. Then the event that made it all come to light. I hade a gout event so bad it required me to go to the ER. This time it manifested in both feet. Only problem is gout, the classic, is a unilateral event. The ER doctor explained the other foot that had 90% similar pain symptoms, but notable differences such as Achilles heal attack instead of major ball joint on the side of big toe, etc, as planter facitis.

It just didn’t resonate with me and with uncontrollable over the top pain as my motivator I made it home to research with a search criteria of atril fibrillation and gout, two very unlikely groupings yet the magic question because an AF forum similar to this one contained an FAQ that explained pseudo gout, which manifests identical to classic gout, except it is caused by CPPD as referenced above. CPPD is an expression of Hemochromatosis, an iron overload disorder/disease. The #1 genetic disorder in our country that no one will address and is only $150 dollar test that could result in almost eradicating type II diabetes if our health care professionals would turn back to science instead of insurance billing codes. Hemochromatosis also abbreviated with (HH), be careful how you read or refer to Hypogonad – just be aware and mindful – was on a episode of mystery diagnosis where this triathelete who was turning bronze with over double my max load of iron when I was diagnosed, detailed how he was crippled and laid to waste in a very short period of time.

[Hemochromatosis]

I received friction from my EP when I asked for the bloodtest, but they agreed to run a feretin FE (iron transport protein) test and a few other related to iron leveling, but not the simple $150 HH test to determine if my HFE gene had the c282y and h63d mutations. Always uphill with conventional medicine, although I have an awesome primary now probably due to being a DO doctor of osteopathy, who actually spends usually 30 minutes or whatever it takes when treating me. I have fired over 15 doctors. My Fe was close to 600 and it was obvious to me, but my EP then passed the bong to the hematologist who had some special award and was suppose to be the expert. He argued with me and argued and said the inflammation can cause false increases in Fe levels (all complete bullshit) and then my 73 year old mother walked in and while I was sitting in a full sweat looking like a train wreck the second set of ears and eyes that looked at this doctor and said nice Italian last name my stepfather was a president of a sons of Italy lodge and all of a sudden the evil Mr. Hyde Was back to being a doctor and agreed to perform the test. Lo and behold the dumb patient who is in tune and very intuitive about self, was right. It was the best bad news I ever had because now I was able to set out and kill the beast. As you, I wanted to make the conclusion, but find more often than not that conclusions are usually in hindsight after a reasonable period of time when dealing in solutions of this sort. With a big wow you were right I looked at the doctor and asked if I get my deductible back as he laughed and walked out of the room. A bunch of uber ego demi gods in convention. All important to realize if you want progressive medicine as you are realizing your endo is going to fall short because he is boxed in by big Pharm and the insurance companies. Most every bioidentical specialist worth their salt does not get bound by the overhead and restriction of insurance, which while expensive, should give you an increased hope for the science and not the insurance card being embraced.

So I jumped to the conclusion Hemochromatosis is my end cause. I concluded the heme iron packed the heart wall and as iron would caused an interrupt to the electrical distribution from the SA node via the VA node and bundles messing with the electrochemical firing of the heart. Yes, this is true and you can find MRI’s of thick black sludge packed in around the heart wall, but when do you ever hear this reported? Not their job right? So I began to phlebotomize (give blood) by the pint. Initially 3 pints a week, which diminished in frequency for 35 pints in the first year driving myself into anemia as an objective then allowing the Fe to raise just out of anemic state. My Fe threshold is between 15-20. Then I mobilized the stored iron with 250 grams of vitamin C a day for 30 days and kept giving blood when the Fe would rise to about 30 (again my numbers and not necessarily yours) you have to find your own threshold. I then met with a man who really needs to be recognized as one of the greatest humanitarians on the planet. His name is Dr. John Woods the head of cardiology at Los Angeles Children Hospital. Honestly I am a big grouchy prick mostly, but when I think about this man it humbles me to my knees and makes me take stock. He is the nations, probably one of the worlds, leading experts in T2 Star (T2*) technology. It is a special form of MRI that can read and detect stored iron in the major organs and now he can detect in the pituitary and hypothalamus and I would venture to bet the gonads and adrenals. At the time there were on 6 T2*’s on the country. Woods was responsible for oversight of the other installs and is the man, wow. This guy treat Thalassemia in children. It makes the iron loading of hemochromatosis look like a walk in the park. As I sat my big ass in the childrens waiting area with Disney characters on the wall I had to sit there and endure watching theses kids under 5 years of age pulling their bodies behind them due to having strokes caused by the iron complications of Thalassemia. Dr. Woods met with me for over 3 hours and is all about the science. Putting me in a childrens MRI was like trying to extract a turd through a straw, but after 1.5 hours of scanning I was told not iron in any major organs. I will be going back to get my pituitary, hypothalamus, adrenals and nads scanned soonest.

[Hemochromatosis]

I also had an MRI that concluded no flattening of the pituitary no scares, lesions or tumors, again the process of elimination. Then I found out that it was not just the physical effects of iron on the heart. I had started to read how the iron affects the anterior lobe of the pituitary signally, which Dr. J refers to when discussing the axis elements. Also, as a side note your vagal nerve which starts at the base of the brain transverses the heart an is wrapped as (the wondering nerve – latin) into your intestines, which is why I tested for H-Pylori. It also stands to reason that the hormonal imbalances caused by the iron overload (hemochromatosis) not only caused anterior lobe interrupts, but could have direct impact on the pulsatile action of the pituitary in the region of the vagal nerve.

MORESO, I WAS DIAGNOSED WITH SECONDARY HYPOGONADISM. Although I was still able to catch wood and run a decent batch.

My T level to start was 150, which I was able to elevate with Tribulus Teresteris (Tribuplex 750) to 242, which by QUEST DIAGNOSTICS standards is within range. What a freaking joke! Did you know QUEST age adjusts their ranges? If you want targets you need to understand when does hormonal degradation/decline, which most will put a line in the sand at about 25 years old. So in a perfectly normal/healthy (whatever that means) body your overall hormonal pool is declining at a rate of 2% per annum and I know there is argument for when and the %, but it is a reasonable reference point that most in the bioidentical field use as benchmarking. My goal is the upper 33 percentile of a 25 year old male. I started to notice the blood letting and all of the mineral balancing and everything was starting to positively affect my out of rhythm heart.

Sidenote: you refer to your QUEST testing, which I assume is blood or serum draws. Read Dr. J's sticky on Rhein lab testing and you may want to look into ZRT (salivaand blood spot) http://www.zrtlab.com/. Rhein is a 24 hour urine .

I dropped the Tribulus, although some think it gives better nad protection and semen output than HCG, I have nothing to back up that statement, everything else in this post I do, but I can say that when I was on terestris I had lots of semen output. I went to Testim gel. Huge mistake for me. On this issue I will speak only for me. My nuts shut off at about 2 weeks of using the gel and my body became completely reliant on my external gel, which in a full tube on each arm was not able to elevate me to where I needed to be. Plus it was a pain in the ass I had to be careful who touched me, etc. I went to T cypinate injections and life is good. I am keeping my T not at optimal yet due to adrenal replenishing. I had massive pain for a long period and I thought it was my kidneys. Then I had a bioidentical specialist make the call and put me on an adrenal replenishing program. The T injections, and Dr. J or others should be able to confirm this, increased fight or flight signaling to the adrenals from the pituitary, that burden the adrenals if they are tapped. Keep in mind my background, massive adrenal demands since age 6. She had me on a light cortisol for 90 days, DHEA and nitially Adren-ALL by ortho molecular products. The Adren-ALL has all sorts of other stuff in it to include a good amount of niacin and I had a massive reaction and was throwing heat like crazy although I was also max loading white button mushrooms experimenting to see if I could control E2 via phtotcons. The problem is the WBM (agarigus bisporus) has a ton of purines. SO between the heavy Niacin which will splash uric acid (which functions to preserve your DNA) interesting since I have a genetic consequence, I switch off to Adrenal Rebuilder by Future Formulations which only contained the non hormonal filtered pig gland and had amazing results. I was getting up at 7am back in bad at 9am get up at 11am try to function and was a wreck. The adrenal rebuilder within a few days stood me up, no more ping hurst above the kidneys and has delivered the mail. Looking back and while I know cortisol therapy is documented as a form of adrenal therapy, and even though she dosed me at considerably lower doses as the clinical test used, the application of cortisol to “park” the adrenals can have numerous complications to include permanently turning the adrenals off in sever cases. She did not inform me to ramp off and I had 2-3 weeks of sugar swings and some other issues. Future Formulas offers two other products as a complete replenisher program, which in hindsight I think I would have tried before the cortisol coupled with the adrenal rebuilder and dhea.

WITH EMPHASIS, I NOTE THAT WHEN INTRODUCING A POTENTIAL THERAPY ALWAYS DO IT ONE VARIABLE AT A TIME AND TRY TO LIMIT COMBOS OR FORMULAS THAT ARE LOADED WITH EVERYTHING TO INCLUDE THE KITCHEN SINK. For example if you want to test DIM you do not need the calcium inclusion, get DIM and DIM pure. Isolate the variable and maintain the process of elimination, controlled environment, controlled environment means controlled environment.

Moving on: My heart which after the stroke in 2004 had no identifiable pattern now holds normal sinus rhythm at 2 minutes at a time and is getting stronger and stronger by the day. P wave activity while erratic is now presenting where it was completely quashed or I guess squelched would be the better term. I am back in the gym and my elliptical at 30 minutes no resistance or incline results in a heart rate of 180 and lower where initially it was maxing at 215. Yes, I know it sounds deadly high, you have to understand it is not a true 215, being in Afib the wave variance causes an invalid elevated read. What I use it for is a relativity reference. I am literally training my heart to pace itself.

The big issue now is E2 control and unlike you I almost had a trip to the ER by taking a comparatively low dose of arimidex. After reading all of the female blogs and complications and I know Dr. J sells it and I know many bodybuilders use it like candy, but I am not convinced as applied to myself. I had a massive rash in almost clean looking squares come up the inside of my right calf and felt like I was out of body, freaking bizarre. I researched IC3 and will not try it. I have identified the photocons of the white button mushroom, but need an extractor to remove the purines so I can test it, which then will require me to have access to a GC/MS to be able to get data feedback in a reasonable period. With the amount of proteins with accompanied purines bodybuilders take in pushing the purine level and subsequent uric acid is not a good idea. If I can get the phytocon isolated it may be a winner, too be determined. Recently, I came across the flavone tests and I am sure there are threads on this board that discuss it. However, I recently came across AE-3 (chrysin as derived from nettle root). The argument is that chrysin is not bioavailable and only acts as an AI in a Petri dish. However research in Singapore were able to potentiate chrysin with perine in its process form BioPerine a black pepper extract. I have read blog responses and clinicals and the verdict seems to still be out. Perine has definitely been documented to potentiate and increase valuses such as B6 and many other vitamins and minerals. However, I take coumadin to stay thinned. Coumdin works by suppressing enzymes in the liver. If it over potentiates with perine then I can hemorrhage if it stifles then I have the risk of clotting and stroking. I have been wanting to switch to Dr. Gordons, BC-I, Boluke, Natokinease combo to handle my thinning but even with that, which is not a liver enzyme retardant, what happens if the perine potentiates it to the point of too thin? I need a safe AI bad, real bad and I know I am not fully getting the benefits of my T injections and that my E2 is running high.

[Hemochromatosis]

Onward, reference the red flag, johns Hopkins secondary hypo report/clinical. As with me I went up 30lbs to 303lbs within the first few months of T injections as did the majority of patients in the clinical as documented. No amount of diet or exercise change ups affected the gain. When I started the adrenal rebuilder I lost 30 without any change to anything. If you read the Hopkins report they started the patients on low doses of HGH even without IGF-1 showing low. Without exception the participants in the trial almost all went down to within reasonable rage of their BMI’s, reasonable enough to obtain a good waist measure, etc with diet and exercise regiments. I was scheduled to go to John’s Hopkins and become part of the HGH program, but I wanted, as with everything, to exhaust the other possibilities, which for now has E2 management front and center. I do not want to use a synthetic drug. I want to try AE3 but the perine component scares the hell out of me. I will try to upload the Hopkins report and will post a link if possible.

Updated link to J. Hopkins report: http://www.jhasim.com/files/articlefiles/pdf/journal_p112(V3-2)MC_redflags.pdf

I encourage you to do two things immediately if not sooner.

1) GET TESTED FOR HEMOCHROMATOSIS, GET YOUR FE CHECKED IF IT IS ABOVE 100 DEMAND AND BE A RELENTLESS PITBULL, THAT A HFE (HEMOCHROMATOSIS) TEST IS PERFORMED.

2) ASK FOR A 24 HOUR HOLTER, EKG AND ECHO FOR YOUR HEART IF YOU OR YOUR SPOUSE OR FRIEND CAN DETECT ANY SKIPS IN YOUR HEART BEAT BY LISTENIG AT THE CHEST AND NOT FROM THE WRIST.

If you detect any skips immediately seek an EP, get on some form of thinner and get the test identified in #2 plus a stress test conducted. I suspect, and certainly hope I am wrong, that from what you have indicated, you may be a positive hit for hemochromatosis. Keep pealing the onion back and don’t ever give up. Listen to your body, take time to cool your mind and breath before you go to sleep. I have provided this overly long response to demonstrate many fundamental key saves. Push for causation and never let the bastards grind you down.

Something else to consider and you can thank the FDA for this one. The iron enrichment and fortification programs sponsored, standardized and evaluated by the FDA are actually using nonbioavailable iron shaving in our enriched and fortified foods. Keep in mind the nuclei of every red blood cell is iron. For the nuclie to become satisfied the source needs to be bioavailable, which means under one micron for the cell membrane to be penetrated and for the nuclei to be enriched and of the correct polarity as a process iron form via photosynthesis. What we the people ingest via FDA enrichment and fortification programs is a cost cutter to the mfg’s and is a beta cell killer to us, stifling the utilization of insulin big time, turning us into fatties and creating a type II epidemic. I guess it all can be blamed on an aging society? We should be living to 120-160 years right now. Imagine if only 10% of the population lived over 100 years our already compromised barely surviving by a thread system would implode. You are better off paying the larger fees to see the keepers of science such as Dr. J and his type than thinking you can cut a corner and save because in the long run as with your endo you just get put off and giving obligatory lip service, which often they can’t back up. I am sitting here as living proof.

Go get tested. All the more to be concerned if you are of western European heritage. Since hemochromatosis epicenter is Ireland. Tracked back to the 6 century and the reason why those with high iron were able to handle the dead of the black plague and not be affected. The bacteria could not manage in a high iron host! However, hemochromatosis is not culturally blind and it hits Blacks, Latinos and Asians as well just not in as concentrated numbers. Also, take pictures not just measures.

Be well and keep peddling!

[JanSz]

http://www.convergentprocedure.com/

The Convergent Procedure is a new and innovative treatment option for patients with chronic or difficult to treat atrial fibrillation (AF). The Convergent Procedure is innovative because it is the first AF treatment which truly integrates a surgical and a catheter approach into a single procedure.

During the convergent procedure, the cardiac surgeon and the electrophysiologist work side by side to identify the source of AF and create a pattern of scar on the heart, shown below, to treat these problems. The entire procedure is performed with miniature cameras and instruments and with small catheters and electrodes.

[SecondaryHypo]

Hemochromatosis,

Thanks for all the good info. Man, you have been through a lot.

I got my iron studies done after reading your above posts, and I also looked in my old records and found an iron study from 2006. Here are the values:

Quest Diagnostics
10/21/2006 7:00 AM
13 hours fasting
Iron 153 mcg/dL (40-190)
TIBC 374 mcg/dL (250-400)
Transferrin Saturation 41% (13-48)

LabCorp
01/11/2010 2:20 PM
Only fasting for 4 hours or so.
Iron, serum 84 mcg/dL (40-155)
Iron Bindidng Capacity (TIBC) 431 mcg/dL (250-450)
UIBC 347 mcg/dL (150-375)
Iron Satration 19% (15-55)


So, what do you make of these values? I can tell you that back in 2006 I was eating big bowls of cereal at least once per day, and had been doing so for over 20 years. Also, back in 2006 I had a habit of eating chewable vitamin C tablets, at least 1000 mg per day.

I stopped the cereal sometime in 2009 when I started watching the glycemic index of my food. I stopped the vitamin C 2 years ago, or so...I just dropped the habit.

What do yo think of this theory:

It looks like in 2006 I had high-normal iron levels, and now I have normal to low-normal levels.

To speculate an explanation: Is it possible that I am a carrier for hemochromatosis (I am of mostly Irish ancestry), and therefore under normal circmstances (like now) I don't experience iron overload. But, back when I was eating all that iron-fortified cereal and taking vitamin C, I had a tendency to absorb more iron, and therefore this gave me the high-normal range values in 2006, which is about when my hypogonadism symptoms started? Just a thought. Or, should I just be happy with two tests showing normal values and move on to other possible cases of my problems?

Thanks.

[SecondaryHypo]

Oh yea,

I forgot to mention that on 12/17/2009 I started TRT by injecting hCG (Ovidrel) as monotherapy. My Testosterone went from about 300 before Ovidrel to 700-something after 2 weeks of Ovidrel.

Therefore, the second iron studies were on TRT with high testosterone levels, (high for me, that is). .

[Hemochromatosis]

Oh yea,

I forgot to mention that on 12/17/2010 I started TRT by injecting hCG (Ovidrel) as monotherapy. My Testosterone went from about 300 before Ovidrel to 700-something after 2 weeks of Ovidrel.

Therefore, the second iron studies were on TRT with high testosterone levels, (high for me, that is).

With permission I would like to port your labs to another forum I am a member of and let the peeps have a look for comment. Assuming you are not a man from the future or haven't jacked the way-back machine from Sherman and Peabody and that TRT commenced in 12/17/09 (not 12/17/10) the following:

I can not comment on labcorp, but quest will use each test center as a geographic and at least in part use the cum totals and number of people to find the mean and ranges for many tests. So while I do not totally discount them I always say make it personal. By that to understand your personal baseline would require you to know your anemic threshold and then adjust out of it until optimized "feel." This may sound like leaving the monastery or the Zen Gone Wild, but you have to tune into your body and listen to it.

Your theory is plausible, regarding the Vit-C and food sources/cereals. However, I do not think 1 month of TRT, which you say commenced on 12/17/09, had much affect on the "unproven potentials of cascading and influencing hepcidin (the master iron control hormone). Plus your 2010 labs is that a results date or date the labs were drawn? I know there is a big delay from quest for E2 and other similar labs.

Do you give blood regularly or did you any time since 2004? I would need more on your diet, for example an oversight as small as chamomile tea, an iron upload retardant, can contribute. Eggs, Milk, Spinach, Bagels, etc, your diet needs to be more detailed if you want a comment.

I need to seek additional opinions of your labs and get more from you on lifestyle before I can render any opinion. Also, did you also have an Fe (ferritin) lab ran for both time periods?

Moreso, it is a given that Hemochromatosis can be one of the causes for secondary hypogonadism. How is it that your primary cant write you a script so you can get the HFE gene test covered? My test was paid for by Care First BCBS. I now have a different policy.

The other consideration is that you may be a carrier and you are going to want to know that to pass the info down to any offspring so they and their mates can be tested.

[SecondaryHypo]

Thanks for the reply.
I fixed the date problem.
Yes, please feel free to post my labs elsewhere.
I never give blood.
I ate bagels everyday for my entire life until 2009 when I learned the importance of glycemic index.
I went to 2 Endos re: my hypogonadism, and neither even thought to run iron studies, so I am assuming my Endo will balk at running the genetic test.
I have never tested ferritin. I posted all the iron studies I have.

[Hemochromatosis]

http://www.convergentprocedure.com/

The Convergent Procedure is a new and innovative treatment option for patients with chronic or difficult to treat atrial fibrillation (AF). The Convergent Procedure is innovative because it is the first AF treatment which truly integrates a surgical and a catheter approach into a single procedure.

During the convergent procedure, the cardiac surgeon and the electrophysiologist work side by side to identify the source of AF and create a pattern of scar on the heart, shown below, to treat these problems. The entire procedure is performed with miniature cameras and instruments and with small catheters and electrodes.

The convergent procedure, in my opinion, is the best corrective procedure for AF available. I have been monitoring it for years when it first came out as the exmaze. Incidentally I have spoke to James Cox the founder of the Cox-Maze procedure many times.

Others such as ablations are still experimental and use a 6 month time period to declare success. Interesting that many insurance policies will cover ablations. Also interesting that major cardio centers such as the Cleveland Clinic were allowing potential ablation candidates to be mislead in the absence of clarifying data until I called them out a few years back. There is a significant difference between persistent and paroxysmal (comes and goes) AF and the efficacy values of 85% cure using a flimsy 6 month normal sinus rhythm was at best sadly laughable.

Convergent uses solid metrics and I believe have 80% of chronic Afer's holding NSR for 2 years and counting. I am still patiently watching. These are not procedures you want to be the first person through the door unless you are in a critical way.

More so I believe it is imperative to eliminate any and all obstacles that may prevent a convergent success. I wrote to Dr. Kiser and referenced Dr. Crisler and detailed the positive effects HRT has had for me so far. I strongly believe in getting your hormones, enzymes, vitamins and minerals in order in addition to eliminating other possible obstacle such as h-pylori and iron loading. I have actually seen photos on the web of heme iron packed in around the heart wall. Why is this not reported?

It may take me through 2010, but after 5 years of self modulating I believe I am closing in on being able to self correct my AF. I will also test out with a cardioversion prior, which I have once already. Once I can take a jolt to the heart and get it to NSR for any period then the convergent makes sense. AFer's as a general rule of thumb operate at only 80% of heart output capacity.

[Hemochromatosis]

Thanks for the reply.
I fixed the date problem.
Yes, please feel free to post my labs elsewhere.
I never give blood.
I ate bagels everyday for my entire life until 2009 when I learned the importance of glycemic index.
I went to 2 Endos re: my hypogonadism, and neither even thought to run iron studies, so I am assuming my Endo will balk at running the genetic test.
I have never tested ferritin. I posted all the iron studies I have.

Get an Fe done it is what will help justify the HFE test and it will give me more of a framed picture of your current situation. Insert indemnification clause here, I am not a doctor, I am not asserting you should or should not do anything, anything I post is a matter of opinion that applies to me and only me, not including lab references.

be well......

[SecondaryHypo]

Get an Fe done


Do you mean "get a ferritin done?" Fe is the sybol for iron as you well know. You aren't saying "get an iron done," right?

[Hemochromatosis]

Do you mean "get a ferritin done?" Fe is the sybol for iron as you well know. You aren't saying "get an iron done," right?

Fe is also the reference to a ferritin lab. Yes, get your Fe tested.