What should I do?

ASaxon

New Member
Anyone have any comments on my situation and what I should do. Ive asked this over at H2 with some interesting responses. Some said I had Primary and some said I had Secondary. I dont even know what I have, I dont seem to fit into the standard classifications. Im curious what you think?

Ill let the test results speak for themselves. All I will add is that for the past, roughly, 4 years Ive had marked symptoms of mental fog and difficulty concentrating, considerable anxiety, occasional panic attacks, depression, poor libido (pray for the old days!) and a few others. I also have consistently low Alkaline Phosphatase since I started testing it about 3 years ago. My understanding is that this is often low in osteoporosis patients.

Ive spent the last three years going through 5 specialists (Cardiologist, Pulmonologist, Gastroenterologist, Psychologist and finally an Endocrinologist) not including my PCP all of them trying to figure out why I have all these symptoms. On the very last visit to the Endocrinologist, before giving up and just accepting that I will live with these symptoms for the rest of my life, I asked if a testosterone test would be warranted since Ive had two hydrocele removals, after examining me he agreed and gave me a lab slip without a follow-up appointment. I actually havent gotten his final assessment yet as hes sent me for an MRI which he doesnt think will show anything. His off-the-cuff response was that I might not have a problem.

Well, here are my results and I'll let you decide.

7/15/05
TT: 189 BL (181 - 861 ng/dL)
FT: 40.8 L (47 - 244 pg/mL)

7/27/05
TT: 153 L (400 - 1080 ng/dL :Age Adjusted 20-40yrs)
FT: 41.8 L (47 - 244 pg/mL)
SHBG: 10 L (13 - 71 nmol/L)
FAI: 53.091 (> 70% ???)
%FT: 2.7 (1.6 - 2.9 %)
FSH: 6.3 (0.7 - 11.1 mlU/mL)
LH: 3.1 (0.8 - 7.6 mlU/mL)
Prolac: 15.6 (2.5 - 17 ng/mL)
E2: 26 (0 - 56 pg/mL)

I am also overweight and wonder if these results are just a result of obesity? If it is, should it be treated with TRT? It's so hard to have any get-up-and-go, let alone be able to lose weight, with all these symptoms.

What should I do?

Thanks!
 
hmmm...

I can't believe he:

a)Sent you for an MRI with a prl number within normal range
b)Said nothing could be wrong even though you are clearly deficient in total and free t.

I don't know if you are primary or secondary hypo, but it looks like it could be secondary seeing as how your LH is fairly low. If your doc doesn't treat you with numbers like those, you need a new doctor. Try the A4M website.
 
SPE said:
I can't believe he:

a)Sent you for an MRI with a prl number within normal range
b)Said nothing could be wrong even though you are clearly deficient in total and free t.

I don't know if you are primary or secondary hypo, but it looks like it could be secondary seeing as how your LH is fairly low. If your doc doesn't treat you with numbers like those, you need a new doctor. Try the A4M website.
it might also be primary because his total test is also low, right?
 
I don't think so...

Primary hypo is generally characterized by elevated FSH and LH levels, which he doesn't have.
 
Switch physicians

It would be prudent of you to switch physicians, and if possible give Swale
a try. If you live too far away try to get a pcp to work with him. Swale is my
physician, but it took 2 other physicians to get me there. My question is this:
If you are not getting any answers or results from your current doctor why
would you keep them? They are providing you with their services and their
current level of education. If they have a low level of education and experience
regarding hormone manipulation for men, why would you want them treating you? Swale has experience and knowledge in this area. If anyone could get
to the root of your particular problem, he could.

Michael T, :)
 
Arming myself

Thanks for the responses. I know I have a problem I just dont know how to classify it. Do I treat it as primary with straight TRT or do I treat it like secondary with TRT and hCG? I dont want to loose any fertility I might have left.

In response to your points SPE and Michael T:

> a)Sent you for an MRI with a prl number within normal range

I know non-secreting (NS) adenomas are not common but they do exist. Adenomas sometimes exist when Prl is still normal. I thought he might be checking just to be safe thinking that a NS adenoma could keep my LH and FSH below an expected level given my low T. Of course with mal-practice the way it is he could just be covering his ass too, which I wouldnt blame him.

> b)Said nothing could be wrong even though you are clearly deficient in total and free t.

He hinted at giving me a trial TRT treatment which Im not sure what this means. Does he mean an 8 week treatment and then Im on my own or does he mean well try TRT and see what happens? Ill know more in a few weeks. Arg, a few more week with these symptoms seems like forever but I guess Ill live.

> It would be prudent of you to switch physicians, and if possible give Swale a try.

I wish I could but I live in California and Swale is quite far away. My Endocrinologist is highly recommended in my medical group so I at least want to hear him out in a final analysis of my condition. Im trying to arm myself with information so that I can ask him pertinent questions about my situation. But its kind of hard to come up with a medically supportable opinion when I dont seem to fit into any common category of Hypogonadism, hence, the reason for this post.

If you have any further ideas about my situation please post them so I can arm myself to the teeth (or at least to the testies : P ) before I go see him after the MRI.
 
Ns

I thought it was the high PRL that caused the lowered T? I do believe SWALE recommends T Therapy for both primary and secondary hypo.
 
It's hard to say with absolute certainty whether you are primary or secondary. Based off of the initial labs I would be inclined to say you are secondary since your LH is rather low. If it was primary your LH would be high. (EDIT-there are tests that can be run to see if you are primary or secondary such as a stimulation test....basically stimultaing the testicles to see if they are capable of producing enough T)

As for retaining fertility....you will not become infertile due to TRT! There was a big discussion on the board a while back wbout this and SWALE made a nice post which sums it up quite well. Something like "What do you call a man who uses TRT for birth control? Daddy!"

Relating to this, the use of HcG does increase sperm production. However, there is no doctrine which says it can only be used for secondary hyogonadism. I am primary and I use it. You see, even though my testes aren't working properly they still have a limited capacity to work. So, by using HcG on the two days prior to T injection I am still getting a small boost in T levels. Besides, even if you were a castrated male you could still receive some benefit from Hcg as there are many more HcG receptors which enhance and improve your life.

Your endo's discussion of a trial test would seem to me that he is thinking of trying you out on a low dose of TRT to see if you respond well to it. If you do then he would most likely keep you on it. He's not going to give you 8 weeks worth and send you on your way.

However, I would be concerned with his cavalier attitude towards your health. Your age adjusted T levels show the lowest at 400. Well, to your endo, if you had a T level of 401 you would be within range and not needing TRT. So, he could possibly prescribe you just enough TRT to bring you to barely within range and then call it good (which we know is not the best way to do things). Seeing if he would consider consulting with SWALE would be a good idea. You could play the angle of improving his education so that he becomes one of the most knowledgable in the area increasing his business.

However, don't go off thinking right away that you NEED TRT. Lifestyle can affect T production. Usually it's in men who either have extreme diets such as no-fat diets or anorexics. Stress can also come into play. Consider your life and how you live it. If there is anything that may possibly be contributing to your low T you should bring it up here. We, and SWALE, can look things over and see if you should try some life reorganization first before you take the TRT plunge.

Keep us informed bro!!
 
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SPE said:
I thought it was the high PRL that caused the lowered T? I do believe SWALE recommends T Therapy for both primary and secondary hypo.

High prolactin can be indicative of a pituitary tumor. The tumor would be the cause of reduced LH which, in turn, reduces T.
 
Thanks for your post, I really appreciate it!!!

In response to your statement, Consider your life and how you live it. If there is anything that may possibly be contributing to your low T...

Although I have anxiety I cant figure out why. I dont have any particular stress in my life greater than I had 10 years ago and I am not on a no-fat diet and I definitely dont over train as I have a hard time getting any exercise in because Im tired all the time.

The only thing that I dont know about is how much my weight might be a factor as Im morbidly obese. But out of everything Ive read I could only find one study on obesity and hypogonadism. It was a study out of Brazil which basically said that being overweight can lead to low Total T and SHBG but does not lower Free T except in massive obesity (whatever that is). Looking at their data they had patients in the study with the same BMI as I but the worst Free T they showed was above borderline not as low as mine. I know everyones an individual and I wouldnt not want to go on TRT unless I had to, but my symptoms are severe enough that it affects me every day of my life regardless of the underlying reason HPG Axis, obesity or BOTH. What would you all recommend I do?

One thing I should mention is that I had an extreme hydrocele operation about 5 years ago and the doctor had to take most of my left testicle for fear of cancer (luckily it wasnt). So my left testicle has atrophied and is smaller than a grape. I assume that testicle isnt producing any testosterone. I also had a hydrocele removal on my right side when I was 19 yrs old but its size is normal, maybe larger than normal. So perhaps its a combination of primary along with it being secondary to my obesity!?!? Does this make any sense?

I want to be able to ask my doctor valid questions that, if appropriate, could lead him to doing more tests if needed. Of course, doing all these tests only means something if the results of those tests could change the treatment protocol. If additional tests arent going to change the treatment then I think they just call it a day and start that treatment instead of wasting money. Of course, the only test he hasnt ordered seems to be a stimulation test but is that really necessary?

I mentioned a stimulation test to him but he didnt think that would be necessary.

Thanks again!
 
Frankly, unless there is a concern of testicular cancer or similar, I don't know why many are so concerned about primary vs secondary hypogonadism, unless the testes are capable of producing virtually no testosterone, which I have to assume is extremely rare unless the testes have been removed. If the testes (well, the leydig cells) can produce at least some testosterone, then treatment for primary and secondary is the same. Thus, I do agree that the stimulation test is unnecessary in ASaxon's case.

ASaxon: I'm sure your endocrinologist is very good at treating thyroid disorders but he apparently isn't very good in the TRT department. Maybe he is willing to learn, although his peers haven't set a very good precident. I've been fortunate in that I went to a local general physicican that is willing to listen to me, actually learn from me, and prescribe me appropriate TRT. The general physicians certainly seem to be adopting modern TRT practices more quickly than the bulk of endocrinologists.
 
mranak said:
Frankly, unless there is a concern of testicular cancer or similar, I don't know why many are so concerned about primary vs secondary hypogonadism, unless the testes are capable of producing virtually no testosterone, which I have to assume is extremely rare unless the testes have been removed. If the testes (well, the leydig cells) can produce at least some testosterone, then treatment for primary and secondary is the same. Thus, I do agree that the stimulation test is unnecessary in ASaxon's case.

ASaxon: I'm sure your endocrinologist is very good at treating thyroid disorders but he apparently isn't very good in the TRT department. Maybe he is willing to learn, although his peers haven't set a very good precident. I've been fortunate in that I went to a local general physicican that is willing to listen to me, actually learn from me, and prescribe me appropriate TRT. The general physicians certainly seem to be adopting modern TRT practices more quickly than the bulk of endocrinologists.

what is the local physicians title? and is he your PCP or family doctor?
 
As far as Ive read hCG isn't given usually in Primary Hypogonadism while it is in Secondary. I know some people take both and have primary but from what I can tell many doctors don't do that unless the hypogonadism is secondary. Besides that I really just want to understand why my testosterone is low. If it's weight related and I go on TRT can I lose weight and eventually come off of the meds? Will my system recover? Do I have to do anything special to not cause permanent detestation somewhere in my HPG axis so that this does not occur? From what I can tell if Im primary, or secondary from a Hypothalamus-Pituitary problem, then this isnt likely going to be possible regardless and I'll probably be on TRT for life. I just want to know what my short term and log term options are. I just want to understand why! Maybe its impossible for anyone to know since my situation doesnt seem to be a textbook case.

Thanks!
 
mranak said:
Frankly, unless there is a concern of testicular cancer or similar, I don't know why many are so concerned about primary vs secondary hypogonadism, unless the testes are capable of producing virtually no testosterone, which I have to assume is extremely rare unless the testes have been removed. If the testes (well, the leydig cells) can produce at least some testosterone, then treatment for primary and secondary is the same. Thus, I do agree that the stimulation test is unnecessary in ASaxon's case.
QUOTE]

I bring it up simply because it may be possible in some cases to eliminate a lifestyle hindrance to T production. If that is the case then knowing if the testicles could actually produce in the first place could be a good thing to know. However, like you I agree that for most there is no need to know as the treatment is the same regardless.

ASaxon, I wish I could tell you more but I can't recall any men coming on here with obesity as severe as yours. Usually it's just the opposite...that their eating (or lack thereof) caused the problem. Never heard of weight being a factor. However, I'm sure it's possible as weight plays a factor in many things. Hopefully SWALE can help with this one.

From reading about your surgeries I'd have to hazard a guess that they are the cause of your hypogonadism. One testicle being shrunken that small tells me it's not producing any T. The other having some removed could very well cause the same thing even though it isn't shrunken.

Short term, you could try the trial TRT and see how you feel. You may suddenly feel 1000% better and decide to stick with it. If not you would at least have the option of going off of it and go back to feeling the way you did before.

Long term, you could wait it out for a while and see if there is anything else your doc can come up with before making a decision. I have a feeling though that you may have hypogonadism attributed to your surgeries and not associated with your weight which would mean TRT. But, of course you should also keep searching for any other possible answers.
 
Irrespective of whether you suffer primary or secondary hypogonadism, your treatment is TRT, as your health is further compromised without it.
 
I found this relevant. Note the relevance of the progesterone to testosterone ratio for obese males. This is clearly an example of problematic progesterone levels with declining androgens. Perhaps the prevelence of leptin in obese males (and females?) creates a type of metabolic hypogonadism that shares aspects of primary and secondary types.



1: J Clin Endocrinol Metab. 1999 Oct;84(10):3673-80. Related Articles, Links


Leptin and androgens in male obesity: evidence for leptin contribution to reduced androgen levels.

Isidori AM, Caprio M, Strollo F, Moretti C, Frajese G, Isidori A, Fabbri A.

Cattedra di Andrologia, Dipartimento di Fisiopatologia Medica, Universita La Sapienza, Italy.

Leptin circulates in plasma at concentrations that parallel the amount of fat reserves. In obese males, androgen levels decline in proportion to the degree of obesity. Recently, we have shown that in rodent Leydig cells leptin inhibits hCG-stimulated testosterone (T) production via a functional leptin receptor isoform; others have found that leptin inhibits basal and hCG-induced T secretion by testis from adult rats. In this study, we further investigated the relationship linking leptin and androgens in men. Basal and hCG-stimulated leptin and sex hormone levels were studied in a large group of men ranging from normal weight to very obese (body mass index, 21.8-55.7). Initial cross-sectional studies showed that circulating leptin and fat mass (FM) were inversely related with total and free T (r = -0.51 and r = -0.38, P < 0.01 and P < 0.05, respectively). Multiple regression analysis indicated that the correlation between leptin or FM and T was not lost after controlling for SHBG and/or LH and/or estradiol (E2) levels and that leptin was the best hormonal predictor of the lower androgen levels in obesity. Dynamic studies showed that in obese men the area under the curve of T and free T to LH/hCG stimulation (5000 IU i.m.) was 30-40% lower than in controls and inversely correlated with leptin levels (r = -0.45 and r = -0.40, P < 0.01 and P < 0.05, respectively). Also, LH/hCG-stimulation caused higher increases in 17-OH-progesterone to T ratio in obese men than in controls, whereas no differences were observed between groups either in stimulated E2 levels or in the E2/T ratio. In all subjects, the percentage increases from baseline in the 17-OH-progesterone to T ratio were directly correlated with leptin levels or FM (r = 0.40 and r = 0.45, P < 0.01), but not with E2 or other hormonal variables. In conclusion, our studies, together with previous in vitro findings, indicate that excess of circulating leptin may be an important contributor to the development of reduced androgens in male obesity.

PMID: 10523013 [PubMed - indexed for MEDLINE]
 
Interesting read. So if I'm reading this right, a test for leptin levels could tell us a lot about ASaxon's situation? Is there a test out there for this?

The question then is if his leptin levels are high would lowering his body fat lower the leptin which would then, theoretically, raise his T and Free T? Or, are those researchers missing something and it is actually a high leptin level which is the problem in the first place which contributes to the obesity?
 
the original post has many variables in play: hypogonadism, estrogen levels, morbid obesity, primary vs. secondary hypogonadism. Swale indicated that trt is needed regardless. The presence of morbid obesity changes certain things that make the primary vs. secondary unimportant--which is what the poster was asking. The obesity is associated with declining androgen levels and high leptin levels. Leptins can be measured as the study showed. Manipulating leptin is being pursued by a number of pharm cos. as an intervention of obesity. I am not aware of any success yet. Furthermore, leptin behaves differently in an obese vs. non-obese person. I ran across research pointing that out when I found the study above.
 
Here's another intersting study I found while doing research for another thread.

"de Boer H, Verschoor L, Ruinemans-Koerts J, Jansen M.

Department of Internal Medicine, Ziekenhuis Rijnstate, Wagnerlaan 55, 6800 TA Arnhem, The Netherlands. hdeboer@alysis.nl

BACKGROUND: Morbid obesity is associated with increased estradiol production as a result of aromatase-dependent conversion of testosterone to estradiol. The elevated serum estradiol levels may inhibit pituitary LH secretion to such extent that hypogonadotropic hypogonadism can result. Normalization of the disturbed estradiol-testosterone balance may be beneficial to reverse the adverse effects of hypogonadism. AIM: To examine whether aromatase inhibition with Letrozole can normalize serum testosterone levels in severely obese men with hypogonadotropic hypogonadism. PATIENTS AND METHODS: Ten severely obese men, mean age 48.2 +/- 2.3 (s.e.) years and body mass index 42.1 +/- 2.6 kg/m(2), were treated with Letrozole for 6 weeks in doses ranging from 7.5 to 17.5 mg per week. RESULTS: Six weeks of treatment decreased serum estradiol from 120 +/- 20 to 70 +/- 9 pmol/l (p = 0.006). None of the subjects developed an estradiol level of less than 40 pmol/l. LH increased from 4.5 +/- 0.8 to 14.8 +/- 2.3 U/l (p < 0.001). Total testosterone rose from 7.5 +/- 1.0 to 23.8 +/- 3.0 nmol/l (p < 0.001) without a concomitant change in sex hormone-binding globulin level. Those treated with Letrozole 17.5 mg per week had an excessive LH response. CONCLUSION: Short-term Letrozole treatment normalized serum testosterone levels in all obese men. The clinical significance of this intervention remains to be established in controlled, long-term studies.

Publication Types:
Clinical Trial

PMID: 15811136 [PubMed - indexed for MEDLINE]"

If I'm reading this one right it's stating that excess E2 caused from obesity can inhibit LH thereby causing low T. So, if you can inhibit/lower the E2 to a manageable level you may induce LH production again. Anyone else get that?

I don't think this would apply to ASaxon though as his E2 levels were within the norms. Interesting study though!
 
Good Read!!!

Thanks for those studies, I soak that stuff up like a sponge and its very useful in my analysis although it may not be entirely practical for my treatment.

I did think about E2 and that is why I pushed for that test with my doctor but it came back within an acceptable range so I guess it isnt that. I also had seen a similar study on leptin and androgen levels but thought that since these ideas are still largely experimental I would never be able to get my doctor to test for it. And even if I did get it tested it wouldnt mean anything to my doctor and would not result in any altered treatment path. I also have looked at the levels of androgen decline related to obesity in these studies and I seem to always be below the low data points in those studies so perhaps my condition is a combination of co-morbid conditions.

Regardless of whether its a combination of things or not Im hoping that once my symptoms are gone and I can actually feel normal again I will be able to loose this weight and hopefully my androgen system will normalize and I can come off the TRT. It might be interesting for my own baseline to get leptin tested though, just for future reference.

Thanks for all the great information!!!
 
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