Guest guest Posted May 16, 2006 Report Share Posted May 16, 2006 Hi Sorry to hear of your difficulties. However this is why we say to be at a teaching hospital that states it deals with Pituitary and other important glands other than Diabetes and the pancreas. For example Prolactin and other pituitary hormones are rarely requested by GPs only when a consultant has already tested these hormones and suggested repeat testing. I perhaps should apologise that I am not familiar with your case and so forgive me if you have spend a long time recently saying all of this. As self-help may I suggest we explore which is your nearest Teaching Hospital? I see you have a UK email address. Could you say where about in the UK you are based? I am Dorset based. I am also a Dorset representative for the Pituitary Foundation and can get you some teelphone help and a buddy to speak with as well as helping with getting you to a suitable consultant on the NHS. My Dorset (text based) website is: http://www.communigate.co.uk/dorset/dorsetpituitaryfoundation/index.phtml The National Pituitary Foundation website is at: www.pituitary.org.uk We have guys here from many different areas of the UK with direct experience of hospitals and consultants as well as the National Organisation where there is a National Coordinator and representatives for the counties of England & Wales as well as in Scotland. Perhaps you would you briefly say what your symptoms are and if this is your first referal or are you already diagnosed chronically ill and needing a referal now for some new reason. I feel I should stress that you would NOT EXPECT a GP especially on the NHS where funding is now from your sources to arrange these tests as first time. It is not the job of a GP to do this testing and diagnose a specialist almost rare illness but that of a hospital consultant and their team. At no stage during the last 20 years has a GP when agreeing I needed to be referred to a consultant / hospital previously taken such blood tests. I could understand Testosterone but the GP should be at primary level and testing liver and kidney function and full blood and ruling out more simple illnesses and Diabetes etc. There should be a list of your symptoms that after the GP has taken routine bloods and blood pressure etc diet cannot explain and so feels a consultant is needed to investigate. In referring you to an endocrinologist that means the Gp and you feel the symptoms are explained more on that basis but it may well be that you see a physician first so as to rule out other medical causes. Many on this group even when they have been diagnosed with a pituitary or similar endocrine illness find they have something else wrong as well eg Syndrome X / Metabolic Disorder. Hope this helps and I look forward to your emails. Kind regards from Dorset where it looks as if it is going to rain! On 16 May 2006 at 9:39, paul wey wrote: > well what a crap morning i have had > > took down those tests i have been told about on here > > LH > TESTOSTERONE > ESTRADIOL > PROLACTIN > SHBG > > went to our clinic and gave the nurse the paper the doc had given me > last week,i asked if the aboeve tests that were not already on that > list to be done. > > testosterrone of course was on there,others were not,she had to refuse > as not on the list. > > i got upset and stormed off saying i was going to walk into the path > of a oncoming lorry as i am so pissed off with it all. > > went across road to my doctors surgery,my doc is not in,so nurse there > looked at the piece of paper i had written the above checks. > > she laughed and saif estradoil was a female hormone and could see no > reason why that was on there,i told them i had spoken to people in the > know on a support group,and of course that was met with another > smile!!! > > she went to each doctor and all refused to add on the extra > tsts,saying none were required and that why test a female hormone on a > male its totally irrelevant. > > i then wnet in a panic attack crying and shouting and mumbling to my > self ,and then into meltdown and said i was not leaving the surgery > till the checks were all done and iwas sitting outside the > door,[unless you have seen an aspergerrs/add meltdown its hard to > visualise] > > anyway nurse wnet back to one of the doctors and female nice doctor > called me in. > > she said she was acutally had specialist knowledge in male hormones > etc,and again said the female ones dont need to be looked at,i was > still crying and panicking she calmed me down a bit and said > > SHBG thsats a good one to check,so i will get that one done,but the > others not,but maydo depending on results of the shbg and testosterone > and also ask my doctior to refer me to a specialist at hospital. > > anyway i sat waiting for the tests but i was still panciking/tense and > crying > > i have always had problems with them getting blood from me and today > was no expcetion > > both arms and one hand tried to get enough blood but she gave up . > > so i know have go to hospital and try there when i get time that > is,and have to starve mysefl for 12 hours so it wont be today,maybe > wednesday or thursday and hope they manage to get blood > > one time even in hosptial it took two nurse and two doctros trying > various thingss before blood came out and even then it was a bout 75 > per cent slower than expected and the procedure i had took much longer > !!! > > typical me that is > > anyway i did ask why is my blood like this,it happend so often since i > was little and once turned a lovely shade of green puking up on doctor > when about 10 i think. > > one reason is if one is tense/anxious etc,so i told this nurse > differant from the one who had seen me when i arrived i have had a > panic attack/meltdown etc and am usually nervous most times so that > might expalin all the problems they have. > > anyway rather upset at momnet but will ty and relax before i try again > at hospital > > regards paul > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 16, 2006 Report Share Posted May 16, 2006 hi peter i am in baldock north hertfordshire regards paul Re: my tests muck up tpday Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 16, 2006 Report Share Posted May 16, 2006 This kind of heavy handed ignorance makes me VERY angry! I wish I had of been there with you as I would used that anger in the most articulate manner and gave them a lesson in endocrinology and the absolute necessity of testing estradiol in men. If you get a copy of Eugene Shippen's book The Testosterone Syndrome and take that to the female doctor and tell her to read the chapter on estrogen, you might be able to educate her on this matter. As an alternative perhaps one of the guys here can provide you with details that you can print off regarding the importance of testing estradiol. I hope you can get treated for your low testosterone, irrespective of your other medical situations, you might find that your emotions are on more of an even keel if you are treated with TRT. I wish you the best. > > well what a crap morning i have had > > took down those tests i have been told about on here > > LH > TESTOSTERONE > ESTRADIOL > PROLACTIN > SHBG > > went to our clinic and gave the nurse the paper the doc had given me last week,i asked if the aboeve tests that were not already on that list to be done. > > testosterrone of course was on there,others were not,she had to refuse as not on the list. > > i got upset and stormed off saying i was going to walk into the path of a oncoming lorry as i am so pissed off with it all. > > went across road to my doctors surgery,my doc is not in,so nurse there looked at the piece of paper i had written the above checks. > > she laughed and saif estradoil was a female hormone and could see no reason why that was on there,i told them i had spoken to people in the know on a support group,and of course that was met with another smile!!! > > she went to each doctor and all refused to add on the extra tsts,saying none were required and that why test a female hormone on a male its totally irrelevant. > > i then wnet in a panic attack crying and shouting and mumbling to my self ,and then into meltdown and said i was not leaving the surgery till the checks were all done and iwas sitting outside the door,[unless you have seen an aspergerrs/add meltdown its hard to visualise] > > anyway nurse wnet back to one of the doctors and female nice doctor called me in. > > she said she was acutally had specialist knowledge in male hormones etc,and again said the female ones dont need to be looked at,i was still crying and panicking she calmed me down a bit and said > > SHBG thsats a good one to check,so i will get that one done,but the others not,but maydo depending on results of the shbg and testosterone and also ask my doctior to refer me to a specialist at hospital. > > anyway i sat waiting for the tests but i was still panciking/tense and crying > > i have always had problems with them getting blood from me and today was no expcetion > > both arms and one hand tried to get enough blood but she gave up . > > so i know have go to hospital and try there when i get time that is,and have to starve mysefl for 12 hours so it wont be today,maybe wednesday or thursday and hope they manage to get blood > > one time even in hosptial it took two nurse and two doctros trying various thingss before blood came out and even then it was a bout 75 per cent slower than expected and the procedure i had took much longer !!! > > typical me that is > > anyway i did ask why is my blood like this,it happend so often since i was little and once turned a lovely shade of green puking up on doctor when about 10 i think. > > one reason is if one is tense/anxious etc,so i told this nurse differant from the one who had seen me when i arrived i have had a panic attack/meltdown etc and am usually nervous most times so that might expalin all the problems they have. > > anyway rather upset at momnet but will ty and relax before i try again at hospital > > regards paul > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 16, 2006 Report Share Posted May 16, 2006 Hi Right, Baldock. One of those towns I have passed through more than once when crossing the country such as from M11 to M1. I quickly looked on the map as you have various possibilities. you are also near enough to London to be considered for NHS treatment at a London teaching hospital if you and your GP felt this would be advisable. If you wish I can ask the National coordinator at Pituitary Foundation for advice as to nearby hospitals specialising in Pituitary and related illness? We have contacts who are patients at most of the major hospitals and so can always verify situations. Within London Barts and Royal London have 2 Endocrinology Departments and several professors of endocrinology. St s Hospital (Paddington) also has a good endocrinology department. What I would like to know is a more detailed background to your medical history so we can see if you need add-on services such as genetics etc etc. Can you repeat what your medical history is including age range and main symptoms? What tests have you already had and what does your GP say so far? Best wishes, On 16 May 2006 at 14:58, paul wey wrote: > hi peter i am in baldock north hertfordshire > > > regards paul > > Re: my > tests muck up tpday > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 16, 2006 Report Share Posted May 16, 2006 Gee , Sorry to see you have so much of a problem with this testing. And yes you need to be calm when doing a blood test. It's good you did not do it feeling that upset. In the UK things are different then here in the States. Is this your first test or a follow up test. I have felt like your feeling and 20 yrs. ago started doing this to calm down and it works read the link and try this it takes time to get good at it but even trying it helps you feel better. I do this 2 times a day first thing in the morning and about 8 pm at nigh. http://www.ucop.edu/humres/eap/relaxationrespone.html You can't get the test we can get so you need to work on your Dr. showing him studies and info on this from the net. http://www.smart-drugs.com/ias-estrogen.htm http://www.medibolics.com/ArimidexBoostsTestosterone.htm Phil paul wey <promachief@...> wrote: well what a crap morning i have had took down those tests i have been told about on here LH TESTOSTERONE ESTRADIOL PROLACTIN SHBG went to our clinic and gave the nurse the paper the doc had given me last week,i asked if the aboeve tests that were not already on that list to be done. testosterrone of course was on there,others were not,she had to refuse as not on the list. i got upset and stormed off saying i was going to walk into the path of a oncoming lorry as i am so pissed off with it all. went across road to my doctors surgery,my doc is not in,so nurse there looked at the piece of paper i had written the above checks. she laughed and saif estradoil was a female hormone and could see no reason why that was on there,i told them i had spoken to people in the know on a support group,and of course that was met with another smile!!! she went to each doctor and all refused to add on the extra tsts,saying none were required and that why test a female hormone on a male its totally irrelevant. i then wnet in a panic attack crying and shouting and mumbling to my self ,and then into meltdown and said i was not leaving the surgery till the checks were all done and iwas sitting outside the door,[unless you have seen an aspergerrs/add meltdown its hard to visualise] anyway nurse wnet back to one of the doctors and female nice doctor called me in. she said she was acutally had specialist knowledge in male hormones etc,and again said the female ones dont need to be looked at,i was still crying and panicking she calmed me down a bit and said SHBG thsats a good one to check,so i will get that one done,but the others not,but maydo depending on results of the shbg and testosterone and also ask my doctior to refer me to a specialist at hospital. anyway i sat waiting for the tests but i was still panciking/tense and crying i have always had problems with them getting blood from me and today was no expcetion both arms and one hand tried to get enough blood but she gave up . so i know have go to hospital and try there when i get time that is,and have to starve mysefl for 12 hours so it wont be today,maybe wednesday or thursday and hope they manage to get blood one time even in hosptial it took two nurse and two doctros trying various thingss before blood came out and even then it was a bout 75 per cent slower than expected and the procedure i had took much longer !!! typical me that is anyway i did ask why is my blood like this,it happend so often since i was little and once turned a lovely shade of green puking up on doctor when about 10 i think. one reason is if one is tense/anxious etc,so i told this nurse differant from the one who had seen me when i arrived i have had a panic attack/meltdown etc and am usually nervous most times so that might expalin all the problems they have. anyway rather upset at momnet but will ty and relax before i try again at hospital regards paul Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 16, 2006 Report Share Posted May 16, 2006 i had tests done two years ago previously and that was 10.5 nmo/l that was takne earrly morning so again that was at i guess peak time,so in reality i may be under. i decided to get tests done again and on advice from here of course asked for the extra tests,anyway as said in end no blood of any worth was drawn so,i will go to hospital on thursday and get tested there,again providing the staff can get blood out of me. regards paul Re: my tests muck up tpday Gee , Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 16, 2006 Report Share Posted May 16, 2006 Hi Thanks for this information. Now I can remember reading some parts recently. OK, as Chis has said and repeated recently even higher than 10.5nmol/L one should be investigated and treated. When I attended Barts and the Royal London ca 1993 and my level repeatedly returned ca 8nmol/L (previously it had been below 5nmol/L0 the medics there said " We take 10nmol/L as some arbitrary lower limit but we are treating patients even now who have a totally testosterone level higher than 10nmol/L. So you have confirmed Total Testosterone level of 10.5nmol/L Although I would hope you have been treated what is also important is that you are not treated before having other blood tests as the pituitary hormones and Hypothalmus ones are investigated and a diagnosis taken at that time - prior to treatment if possible. Others will have told you it is important to find out why you have low testosterone and if this is primary or secondary. However so as to ensure the best way forward this is for a specialist teaching hospital and not really for GPs. This is especially so with NHS. In the USA and some other countries it is possible for medicines to be issued by GPs but here in the UK some medicines CANNOT be prescribed by GPs unless a hospital consultant has first decided. Originally this was true for Testosterone although I think that has been eased. Besides blood tests you might need scans as well. Now I am stressing my previous question: What are your symptoms? Are you able to work? Why did you go to a doctor in the first place? What symptoms do you have at the moment? One way in the UK with the NHS that works well if you wish is for you to have just 1 private consultation with a specialist who is also NHS. This means you can see a consultant within a week and at least have an examination and for your GP to be informed by a consultant that you might need specialist investigations. That might costs ca £100 but gives you an expert letter for you to quote to GP etc. However, you say your GP IS going to refer you to an endocrinologist, yes? So again we are back to ensuring the GP refers you to a good endocrinologist and not a Diabetologist etc. May I also ask: Age range Weight and height Have you have usual blood tests such as glucose, lipids, cholesterol, liver and kidney function? Kind regards, On 16 May 2006 at 17:45, paul wey wrote: > i had tests done two years ago previously and that was 10.5 nmo/l > > that was takne earrly morning so again that was at i guess peak > time,so in reality i may be under. > > i decided to get tests done again and on advice from here of course > asked for the extra tests,anyway as said in end no blood of any worth > was drawn so,i will go to hospital on thursday and get tested > there,again providing the staff can get blood out of me. > > > regards paul > > Re: my tests muck up tpday > > Gee , > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 16, 2006 Report Share Posted May 16, 2006 Wow , sorry to hear about your lousy day. First off I have a history of panic attacks too so I know what you're going through. You really should be taking something for them as my life literally changed when I started taking Zoloft for my panic attacks. I haven't had one since and when I do get those weird feelings they only last for a few mins and then are gone. I really recommend you try to get some treatment for your anxiety as there is no need for you to have to live with it. Secondly, I don't recall if these are your first tests but it is not uncommon for the first tests to only include Total Testosterone, that's all they tested on my first test. After that they ordered the full battery. Here's the deal. If your Total T is good then it's highly unlikely that your Free T or Bio-T will be low (although it is not impossible.) Usually only after a low Total T is shown with a test will doctors order the LH, Prolactin, SHBG, Free T/Bio T, etc. And Estradiol isn't hardly ever tested for unless you have signs of high E2 (i.e. gynocomastia, sensitive nipples, or if successful TRT isn't working on symptoms.) So it's not surprising for your doctors not to run those tests at this time so don't get stressed about it. If this is your first round of screening tests then they're ordering the right tests for the first time. I'd prefer that they do a Bio-T or Free-T test as well but like I said it's not critical and SHBG would give a decent look at what free-T and Bio-T are likely to be. Those other tests (LH, FSH, Prolactin) are good for helping to determine what the cause of hypogonadism is not necessarily that it exists. A total T test should be fine for this initial test. Finally, I want to reiterate that you get some treatment for your anxiety and panic attacks. It could be that if you have hypogonadism then this disorder is contributing, possibly significantly, to your anxiety and panic disorder. But with that said you should be in treatment for anxiety immediately as even if you do have hypogonadism it can take many, many months to get it under control and eventually change your anxiety profile. And even then there's no guarantee that it treating low T will actually cure the anxiety disorder. So what I'm saying is get treatment now, there's no need to live with that crap. I did for years and it's simply not worth it. In time it might be that you can eliminate anxiety medications but only after time has healed the underlying heath condition be it hypogonadism or anything else. ASaxon > > well what a crap morning i have had > > took down those tests i have been told about on here > > LH > TESTOSTERONE > ESTRADIOL > PROLACTIN > SHBG > > went to our clinic and gave the nurse the paper the doc had given me last week,i asked if the aboeve tests that were not already on that list to be done. > > testosterrone of course was on there,others were not,she had to refuse as not on the list. > > i got upset and stormed off saying i was going to walk into the path of a oncoming lorry as i am so pissed off with it all. > > went across road to my doctors surgery,my doc is not in,so nurse there looked at the piece of paper i had written the above checks. > > she laughed and saif estradoil was a female hormone and could see no reason why that was on there,i told them i had spoken to people in the know on a support group,and of course that was met with another smile!!! > > she went to each doctor and all refused to add on the extra tsts,saying none were required and that why test a female hormone on a male its totally irrelevant. > > i then wnet in a panic attack crying and shouting and mumbling to my self ,and then into meltdown and said i was not leaving the surgery till the checks were all done and iwas sitting outside the door,[unless you have seen an aspergerrs/add meltdown its hard to visualise] > > anyway nurse wnet back to one of the doctors and female nice doctor called me in. > > she said she was acutally had specialist knowledge in male hormones etc,and again said the female ones dont need to be looked at,i was still crying and panicking she calmed me down a bit and said > > SHBG thsats a good one to check,so i will get that one done,but the others not,but maydo depending on results of the shbg and testosterone and also ask my doctior to refer me to a specialist at hospital. > > anyway i sat waiting for the tests but i was still panciking/tense and crying > > i have always had problems with them getting blood from me and today was no expcetion > > both arms and one hand tried to get enough blood but she gave up . > > so i know have go to hospital and try there when i get time that is,and have to starve mysefl for 12 hours so it wont be today,maybe wednesday or thursday and hope they manage to get blood > > one time even in hosptial it took two nurse and two doctros trying various thingss before blood came out and even then it was a bout 75 per cent slower than expected and the procedure i had took much longer !!! > > typical me that is > > anyway i did ask why is my blood like this,it happend so often since i was little and once turned a lovely shade of green puking up on doctor when about 10 i think. > > one reason is if one is tense/anxious etc,so i told this nurse differant from the one who had seen me when i arrived i have had a panic attack/meltdown etc and am usually nervous most times so that might expalin all the problems they have. > > anyway rather upset at momnet but will ty and relax before i try again at hospital > > regards paul > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 16, 2006 Report Share Posted May 16, 2006 Another thing, if you are anxious your blood pressure is probably high, which is probably possibly caused by blood vessel constriction (a common reaction when under stressful conditions). This may be partially why they are having a hard time finding a blood vessel. Perhaps if you were more relaxed they'd have an easier time at it. If you are deathly afraid of needles then that probably doesn't help either. ASaxon > > i had tests done two years ago previously and that was 10.5 nmo/l > > that was takne earrly morning so again that was at i guess peak time,so in reality i may be under. > > i decided to get tests done again and on advice from here of course asked for the extra tests,anyway as said in end no blood of any worth was drawn so,i will go to hospital on thursday and get tested there,again providing the staff can get blood out of me. > > > regards paul > > Re: my tests muck up tpday > > Gee , > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 16, 2006 Report Share Posted May 16, 2006 my first testosterone test was 2 years ago taken 9 am and was 10.5 nmo/l and was told this was low side of normal and perefectly fine. since i was a toddler i was not like my siblings or peers i nver like climbing trees or doing anything that exhausting most of the time,though at times i was hpyeractive and still can be today but more like manically doing mental cartwheels being overloaded by loads of thoughts and not being able to concetrate . at 6 i had a reptuation at school already being disruptive/argumentative but not nasty i could do and say bad things,but i never did them out of spite. was throwing chairs at teachers at 7/7/9 etc and had quite a reputation. anyway at 11 things changed as time for big school in showers at my early abysmal sporting attempts i and others could see something was wrong,ie no visible testicles. a long story but cut very short boys told girls i got then bullied by both,physically and mentally, and i never really could tell anyone as i thought i was not a full male. again all my co ordination/temper problems and inablity to concetrate,lack of co ordination so bad at 11 my form tutor told my parents " i wont let pull hold knives/scissors etc he is a danger to himsel and others,especially if he has a rage as well " always told i was lethargic,alwayts told lazy,clever but not learning 22 i broke down while working as a chef,still plagued by all the problems i had at school. 18-22 i was actually perfect weight and size yet lethargy and all other problems still same. diagnosed when i told people about how i felt ,with both testicles confirmed undescended,NHS in uk said as it eas not an important op i prob would have to wait 3 years,not important!!!! i was by know working in warehosing and private medical cover meant i had orchidepxy in 3 weeks ,one check up 6 months later but no after care,no thought to my mental health problems caused by the lack of testicles[so i had thought as a confused teenager] several years of working losing jobs for temper/illness and always making way too many errors. flash to 2002 lost job yet again this time temper again had always felt differant,trying to do just 35 hours weeks was impossible and as well as sick days i used most holidays up once a week as trying to work 5 days was near impossible how i felt and indeed feel,doing 5 hours at college now,i have had to cut down to 3 as i cant cope. so again temper/low energy[not laziness i can assure you,thats whats so upsetting] diagnosed aspergers syndrome in 2003,then dyspraxia/mild dyslexia in 2004 and now in middle of my ADD diagnosis,and many of the those prroblems are both prresent in those conditions but also low testosterone,i believe 10.5 nmo/l is too low for my needs especially when adding hthe lethargy problems already associated with my other problems,and the executive functioning and attention problmes,my tics i have also use a lot of energy up,,my metdowns and panic attacks allso drain me of precious energy. never have slept well in block of 2 hours or so on a good night 2 hours sleep,2 awake or similar,dozing durign day,if i go out i like to find a place to sit and doze rather than do anytihng energetic. of course over years lack of energy leads to getting larger,also eating ,depression and so on so its a vicious circle. i have no ambition [apart from finding out how i can overcome my problems and failing] very low self esteem,i want perfection from me and others ,and not getting either as is most of time then i get more anxious/stressed. so no work,on disabled living allowance and incapacity beneifts,college 3 hours in english and maths i have stopped ,all at a level i should of been able to do at school,and all now getting to a level where i just cant do much more. i will get the testosterone checked in the hospital,again only the testosteerone and sbhg or whatever its called but my guess is it wont be much higher than 10.5 again i will come back on here when i get the figures and see what you think then. so even if with help on the testosterone i may still feel more letharigc than many,and will still have my executive functioning/organisational/short term visual/audio and also long term memory problems,at least i will hoepfully be just a bit more alert, i am not expecting miracles just a little bbost to get me going a bit. i fall asleep with gf when we are together,and sometimes in the street,my sexual intercourse abiltites are nil,but as said before i can give her so many orgasms in other ways she does not lose out thats for sure. but i cant do anytyhing more becauae i dont have the energy orr the abilities as for referal NO my gp is not ,well not based on figures 2 years ago,hoefully if still about same or worse then maybe i can persuade him,the doc i saw today said to ask him,well i did last week and no go so far,hoepfully the results of these tests when i get them done will spur him on to refer me. all those other blood tests on bottom of this mail are yes part of the tests i will be getting,last itme my blood sugar was also too high but again thats all he said. so 2 years since last blood tests,so i will get them done and see what they are this time i will get gp to put it all down on papeer for me and try and expalin to me,as normally he just reels off figures and expects me to know what he is on about,and even with them on paper i still get very lost,as memory problems are a real pain,people get pissed off i keep asking same questions all the itime,they say " i told you that loads of times " and expect me to remember,well i dont and its damend annoying to say the least thanks for yourr pateince ps age 40 and now 21 stone i bleeive,at 18-22 11.5 stone [ideal weight] 22-38 15-18 stone or so,but now as aid about 21 stone. but i know many large people with so much more energy than me ,holding down jobs ,relatiosnships and even sporting abilties etc regards paul Re: my tests muck up tpday > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 16, 2006 Report Share Posted May 16, 2006 its not so much being afraid of needles but in fsct being touched to have my tight foreskin looked at last year by surgeon i had to be given a full anaesthetic and 2 nights in hospital,that was just to be examained as when being examined awake i was kicking/shouting and screaming i have lots of sensory issues again due to my aspergers/dyspraxia etc. that also goes for stress meds,anti depressants and sleeping tabs i have tried in past,some dont do anytihng,some make me worse and some have had bad side affects i am not kiding its bloody diffiucult,agin sensory issues dont help when trying sexual stuff with gf either!! and yes dont know what it is at moment was takne yesterday but doc did not tell me what it was,but yes its usually ihgh nowadatys,i spend 99 per cent of any day stressed and thats witohut working,you can imagine what i was like when working and travelling every day. i am very difficult some day i think the doctors will just give up on me,i am too hard to deal with regards paul Re: my tests muck up tpday Another thing, if you are anxious your blood pressure is probably high, which is probably possibly caused by blood vessel constriction (a common reaction when under stressful conditions). This may be partially why they are having a hard time finding a blood vessel. Perhaps if you were more relaxed they'd have an easier time at it. If you are deathly afraid of needles then that probably doesn't help either. ASaxon Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 16, 2006 Report Share Posted May 16, 2006 if you had two undecended testies and you had them fixed post puberty I think it is pretty darn obvious why you are likely to have a low testosterone level. I would also guarentee that your testicles would appear much smaller if tested with an orchidometer. You need to cut through the veil of bullshit. Go to your gp and demand a referral to an endocrinologist and don't take no for an answer. If they ultimately refuse you need help in registering with another practice and a gp who will act on your behalf. The gps simply do not know what they are doing and likely never will. If you get to see a reasonable endocrinologist and tell them that you had two undecended testies, brought down post puberty you have a far better chance of getting somewhere with this. If you don't get to see a reasonable endocrinologist for this I just see you going around in circles. > > my first testosterone test was 2 years ago taken 9 am and was 10.5 nmo/l and was told this was low side of normal and perefectly fine. > > since i was a toddler i was not like my siblings or peers i nver like climbing trees or doing anything that exhausting most of the time,though at times i was hpyeractive and still can be today but more like manically doing mental cartwheels being overloaded by loads of thoughts and not being able to concetrate . > > at 6 i had a reptuation at school already being disruptive/argumentative but not nasty i could do and say bad things,but i never did them out of spite. > > was throwing chairs at teachers at 7/7/9 etc and had quite a reputation. > > > anyway at 11 things changed as time for big school > in showers at my early abysmal sporting attempts i and others could see something was wrong,ie no visible testicles. > > a long story but cut very short > > boys told girls i got then bullied by both,physically and mentally, and i never really could tell anyone as i thought i was not a full male. > > again all my co ordination/temper problems and inablity to concetrate,lack of co ordination so bad at 11 my form tutor told my parents " i wont let pull hold knives/scissors etc he is a danger to himsel and others,especially if he has a rage as well " > > always told i was lethargic,alwayts told lazy,clever but not learning > > > 22 i broke down while working as a chef,still plagued by all the problems i had at school. > > 18-22 i was actually perfect weight and size yet lethargy and all other problems still same. > > diagnosed when i told people about how i felt ,with both testicles confirmed undescended,NHS in uk said as it eas not an important op i prob would have to wait 3 years,not important!!!! > > i was by know working in warehosing and private medical cover meant i had orchidepxy in 3 weeks ,one check up 6 months later but no after care,no thought to my mental health problems caused by the lack of testicles[so i had thought as a confused teenager] > > several years of working losing jobs for temper/illness and always making way too many errors. > > > flash to 2002 > > lost job yet again this time temper again > > had always felt differant,trying to do just 35 hours weeks was impossible and as well as sick days i used most holidays up once a week as trying to work 5 days was near impossible how i felt and indeed feel,doing 5 hours at college now,i have had to cut down to 3 as i cant cope. > > > so again temper/low energy[not laziness i can assure you,thats whats so upsetting] > > diagnosed aspergers syndrome in 2003,then dyspraxia/mild dyslexia in 2004 and now in middle of my ADD diagnosis,and many of the those prroblems are both prresent in those conditions but also low testosterone,i believe 10.5 nmo/l is too low for my needs especially when adding hthe lethargy problems already associated with my other problems,and the executive functioning and attention problmes,my tics i have also use a lot of energy up,,my metdowns and panic attacks allso drain me of precious energy. > > never have slept well > > in block of 2 hours or so on a good night 2 hours sleep,2 awake or similar,dozing durign day,if i go out i like to find a place to sit and doze rather than do anytihng energetic. > > of course over years lack of energy leads to getting larger,also eating ,depression and so on so its a vicious circle. > > i have no ambition [apart from finding out how i can overcome my problems and failing] > > very low self esteem,i want perfection from me and others ,and not getting either as is most of time then i get more anxious/stressed. > > so no work,on disabled living allowance and incapacity beneifts,college 3 hours in english and maths i have stopped ,all at a level i should of been able to do at school,and all now getting to a level where i just cant do much more. > > i will get the testosterone checked in the hospital,again only the testosteerone and sbhg or whatever its called but my guess is it wont be much higher than 10.5 again > > i will come back on here when i get the figures and see what you think then. > > > so even if with help on the testosterone i may still feel more letharigc than many,and will still have my executive functioning/organisational/short term visual/audio and also long term memory problems,at least i will hoepfully be just a bit more alert, i am not expecting miracles just a little bbost to get me going a bit. > > i fall asleep with gf when we are together,and sometimes in the street,my sexual intercourse abiltites are nil,but as said before i can give her so many orgasms in other ways she does not lose out thats for sure. > > but i cant do anytyhing more becauae i dont have the energy orr the abilities > > as for referal NO my gp is not ,well not based on figures 2 years ago,hoefully if still about same or worse then maybe i can persuade him,the doc i saw today said to ask him,well i did last week and no go so far,hoepfully the results of these tests when i get them done will spur him on to refer me. > > all those other blood tests on bottom of this mail are yes part of the tests i will be getting,last itme my blood sugar was also too high but again thats all he said. > > so 2 years since last blood tests,so i will get them done and see what they are this time i will get gp to put it all down on papeer for me and try and expalin to me,as normally he just reels off figures and expects me to know what he is on about,and even with them on paper i still get very lost,as memory problems are a real pain,people get pissed off i keep asking same questions all the itime,they say " i told you that loads of times " and expect me to remember,well i dont and its damend annoying to say the least > > thanks for yourr pateince > > > ps age 40 and now 21 stone i bleeive,at 18-22 11.5 stone [ideal weight] 22-38 15-18 stone or so,but now as aid about 21 stone. > > but i know many large people with so much more energy than me ,holding down jobs ,relatiosnships and even sporting abilties etc > > > regards paul > > > > Re: my tests muck up tpday > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 16, 2006 Report Share Posted May 16, 2006 Hi Now 3AM and so a new day dawning and I hope for you too! Now as the emails arrived I read Chis' email first and so was eager to get to your email to see what you had read. Wow - Yes, now we understand better. Where to start: I don't think your main problem is testosterone deficiency but the testosterone deficiency is present and your medical history shows that someone has been mis-treating you. I agree with Chis but I want to try and get you to analyse the situation more so you might get more help more quickly. As to some of your symptoms there is a lot of work showing you can be helped - medically - with disruptive behaviour as child or adult. I will get you the contact details but if you wish to search look for Oxford university clinical Physiology and Dyspraxia as an example. Clinical trials have confirmed " brain foods " such as Omega 3, 6 and 9 at the right concentrations and frequency can help within 3 - 6 months. Last year a UK TV Documentary gave a full life story and clinical history of a guy who was so ill and depressed he was suicidal and all the worse of symptoms that he consented to his consultant to stop his medication and use just Omega 3,6,9 mix. A very high dose. He was given an MRi prior to starting treatment and at a stage where he was responding to treatment. To the consultant's surprise this patient's brain size had increased! Where he was almost certainly going to succeed at taking his own life just with these oils his life changed. Now this is rare but children given these special mixes have been shown in double blind trials to respond. Oxford will arrange a full test and will frequently arrange payment for treatment or find help if it is not available from your local authorities. Now to the undecended testicles. This is a condition which is not rare and which needs to be treated. When one is treated one would expect a caring and proficient hospital to test the patient for any other abnormalities. As said - Go immediately to your GP. Try not to get emotional as this will not help. Write on a card so you do not have to remember in front of your GP and whilst perhaps upset what you want to ask. Say I am 40 and realize I have problems and know my Total Testosterone at 10.5nmol/L is low and too low for my age. I wish to see a specialist who is experienced in this field not just any endocrinologist and I would like to attend a teaching hospital where they have experience of treating males with undecended testicles and hypogonadism. THEN " BTW: whilst I am here I would like some routine blood tests as I have continued to feel fatigued and know my blood glucose levels were raised in the past " Am I Diabetic or do I have glucose intolerance as just one example? Would you arrange a fasting blood glucose test plus fasting lipids and routine liver / kidney function plus full blood count prior to my going to the endocrinologist? As soon as I read some of your symptoms I thought of Diabetes and if you look back to my earlier email Syndrome X / Metabolic Disorder. You weight, and symptoms imply further testing and should include: Blood pressure and pulse Fasting blood glucose Serum Insulin measurement of waist BMI Your GP should eagerly do this when you visit. If they have signed the NHS contract then they get paid by doing these tests for Diabetes etc! [[[[[ If for any reason your GP fails to order the tests - Go straight to your local pharmacy such as Boots or Lloyds and ask them for Fasting blood glucose and lipids. This might be free of £5 per test. Do not accept treatment such as Statins as you need to see a hospital consultant for your other conditions but get a report so you can submit it to your new GP and hospital consultant! Then measure you waist and get your height recorded - Somewhere like Boots might also do this for you.The BMI is important and Boots will frequently take your blood pressure or know where this can be done if your GP needs to be changed. This information in itself would should possible risk of CVD. Well that's it for now. Keep in touch and keep smiling even though it feels impossible. I will not speak here of the hypersensitivity but this can be neurological and can be caused by untreated illness such as Diabetes if nerve damage or neuropathy has occurred. Take care On 16 May 2006 at 22:47, paul wey wrote: > my first testosterone test was 2 years ago taken 9 am and was 10.5 > nmo/l and was told this was low side of normal and perefectly fine. > > since i was a toddler i was not like my siblings or peers i nver like > climbing trees or doing anything that exhausting most of the > time,though at times i was hpyeractive and still can be today but more > like manically doing mental cartwheels being overloaded by loads of > thoughts and not being able to concetrate . > > at 6 i had a reptuation at school already being > disruptive/argumentative but not nasty i could do and say bad > things,but i never did them out of spite. > > was throwing chairs at teachers at 7/7/9 etc and had quite a > reputation. > > > anyway at 11 things changed as time for big school > in showers at my early abysmal sporting attempts i and others could > see something was wrong,ie no visible testicles. > > a long story but cut very short > > boys told girls i got then bullied by both,physically and mentally, > and i never really could tell anyone as i thought i was not a full > male. > > again all my co ordination/temper problems and inablity to > concetrate,lack of co ordination so bad at 11 my form tutor told my > parents " i wont let pull hold knives/scissors etc he is a danger to > himsel and others,especially if he has a rage as well " > > always told i was lethargic,alwayts told lazy,clever but not learning > > > 22 i broke down while working as a chef,still plagued by all the > problems i had at school. > > 18-22 i was actually perfect weight and size yet lethargy and all > other problems still same. > > diagnosed when i told people about how i felt ,with both testicles > confirmed undescended,NHS in uk said as it eas not an important op i > prob would have to wait 3 years,not important!!!! > > i was by know working in warehosing and private medical cover meant i > had orchidepxy in 3 weeks ,one check up 6 months later but no after > care,no thought to my mental health problems caused by the lack of > testicles[so i had thought as a confused teenager] > > several years of working losing jobs for temper/illness and always > making way too many errors. > > > flash to 2002 > > lost job yet again this time temper again > > had always felt differant,trying to do just 35 hours weeks was > impossible and as well as sick days i used most holidays up once a > week as trying to work 5 days was near impossible how i felt and > indeed feel,doing 5 hours at college now,i have had to cut down to 3 > as i cant cope. > > > so again temper/low energy[not laziness i can assure you,thats whats > so upsetting] > > diagnosed aspergers syndrome in 2003,then dyspraxia/mild dyslexia in > 2004 and now in middle of my ADD diagnosis,and many of the those > prroblems are both prresent in those conditions but also low > testosterone,i believe 10.5 nmo/l is too low for my needs especially > when adding hthe lethargy problems already associated with my other > problems,and the executive functioning and attention problmes,my tics > i have also use a lot of energy up,,my metdowns and panic attacks > allso drain me of precious energy. > > never have slept well > > in block of 2 hours or so on a good night 2 hours sleep,2 awake or > similar,dozing durign day,if i go out i like to find a place to sit > and doze rather than do anytihng energetic. > > of course over years lack of energy leads to getting larger,also > eating ,depression and so on so its a vicious circle. > > i have no ambition [apart from finding out how i can overcome my > problems and failing] > > very low self esteem,i want perfection from me and others ,and not > getting either as is most of time then i get more anxious/stressed. > > so no work,on disabled living allowance and incapacity > beneifts,college 3 hours in english and maths i have stopped ,all at a > level i should of been able to do at school,and all now getting to a > level where i just cant do much more. > > i will get the testosterone checked in the hospital,again only the > testosteerone and sbhg or whatever its called but my guess is it wont > be much higher than 10.5 again > > i will come back on here when i get the figures and see what you think > then. > > > so even if with help on the testosterone i may still feel more > letharigc than many,and will still have my executive > functioning/organisational/short term visual/audio and also long term > memory problems,at least i will hoepfully be just a bit more alert, i > am not expecting miracles just a little bbost to get me going a bit. > > i fall asleep with gf when we are together,and sometimes in the > street,my sexual intercourse abiltites are nil,but as said before i > can give her so many orgasms in other ways she does not lose out thats > for sure. > > but i cant do anytyhing more becauae i dont have the energy orr the > abilities > > as for referal NO my gp is not ,well not based on figures 2 years > ago,hoefully if still about same or worse then maybe i can persuade > him,the doc i saw today said to ask him,well i did last week and no go > so far,hoepfully the results of these tests when i get them done will > spur him on to refer me. > > all those other blood tests on bottom of this mail are yes part of the > tests i will be getting,last itme my blood sugar was also too high but > again thats all he said. > > so 2 years since last blood tests,so i will get them done and see what > they are this time i will get gp to put it all down on papeer for me > and try and expalin to me,as normally he just reels off figures and > expects me to know what he is on about,and even with them on paper i > still get very lost,as memory problems are a real pain,people get > pissed off i keep asking same questions all the itime,they say " i told > you that loads of times " and expect me to remember,well i dont and its > damend annoying to say the least > > thanks for yourr pateince > > > ps age 40 and now 21 stone i bleeive,at 18-22 11.5 stone [ideal > weight] 22-38 15-18 stone or so,but now as aid about 21 stone. > > but i know many large people with so much more energy than me ,holding > down jobs ,relatiosnships and even sporting abilties etc > > > regards paul > > > > Re: my tests muck up tpday > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 27, 2006 Report Share Posted June 27, 2006 On Tue, 16 May 2006 09:39:57 +0000 (GMT), you wrote: >she went to each doctor and all refused to add on the extra tsts,saying none were required and that why test a female hormone on a male its totally irrelevant. > >i then wnet in a panic attack crying and shouting and mumbling to my self ,and then into meltdown and said i was not leaving the surgery till the checks were all done and iwas sitting outside the door,[unless you have seen an aspergerrs/add meltdown its hard to visualise] > >anyway nurse wnet back to one of the doctors and female nice doctor called me in. > >she said she was acutally had specialist knowledge in male hormones etc,and again said the female ones dont need to be looked at,i was still crying and panicking she calmed me down a bit and said Gawd but I had ignorant " specialists " and doctors. But you have to deal with them. They hold the control of your treatment, unfortunate as that may be. So steel yourself, calm your self and go to them with calmness and open mind and present them with these things in their language. (also make sure you are talking to them about estradiol not estrogen) Inform them that you understand T converts to estradiol through aromotization. And that T levels can actually decrease in people not getting treatment because of high aromotase levels - particularly if the person is at all over weight. (Aromotase is created and " lives " in fat. I've given you some related studies. there is one I cannot lay my hands on today that is actually the best of the bunch. It is a case study that showed in some older men T levels could be raised by 200 to 300 points simply by controlling estradiol and aromitization - without any T supplementing. Maybe someone has a copy at hand? Could you post the link? But these are some I have found that might nudge them a bit: (Also know that estradiol levels much beyond 50 pg/ml lead to ED, emotionalism, gynomastia, severley dimished sex drive, etc. It wouldn't hurt to tell them this as well. But studies on high E2 levels are hard to find.) The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 3 1174-1180 Copyright © 2004 by The Endocrine Society Effects of Aromatase Inhibition in Elderly Men with Low or Borderline-Low Serum Testosterone Levels Z. Leder, L. Rohrer, D. Rubin, Gallo and Longcope Endocrine Unit (B.Z.L., J.L.R.), Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; Departments of Medicine and Obstetrics and Gynecology (C.L.), University of Massachusetts Medical School, Worcester, Massachusetts 01655; and AstraZeneca Pharmaceuticals (S.D.R., J.G.), Wilmington, Delaware 19850 Address all correspondence and requests for reprints to: Z. Leder, Endocrine Unit, Massachusetts General Hospital, Bulfinch 327, Fruit Street, Boston, Massachusetts 02114. As men age, serum testosterone levels decrease, a factor that may contribute to some aspects of age-related physiological deterioration. Although androgen replacement has been shown to have beneficial effects in frankly hypogonadal men, its use in elderly men with borderline hypogonadism is controversial. Furthermore, current testosterone replacement methods have important limitations. We investigated the ability of the orally administered aromatase inhibitor, anastrozole, to increase endogenous testosterone production in 37 elderly men (aged 62–74 yr) with screening serum testosterone levels less than 350 ng/dl. Subjects were randomized in a double-blind fashion to the following 12-wk oral regimens: group 1: anastrozole 1 mg daily (n = 12); group 2: anastrozole 1 mg twice weekly (n = 11); and group 3: placebo daily (n = 14). Hormone levels, quality of life (MOS Short-Form Health Survey), sexual function (International Index of Erectile Function), benign prostate hyperplasia severity (American Urological Association Symptom Index Score), prostate-specific antigen, and measures of safety were compared among groups. Mean ± SD bioavailable testosterone increased from 99 ± 31 to 207 ± 65 ng/dl in group 1 and from 115 ± 37 to 178 ± 55 ng/dl in group 2 (P < 0.001 vs. placebo for both groups and P = 0.054 group 1 vs. group 2). Total testosterone levels increased from 343 ± 61 to 572 ± 139 ng/dl in group 1 and from 397 ± 106 to 520 ± 91 ng/dl in group 2 (P < 0.001 vs. placebo for both groups and P = 0.012 group 1 vs. group 2). Serum estradiol levels decreased from 26 ± 8 to 17 ± 6 pg/ml in group 1 and from 27 ± 8 to 17 ± 5 pg/ml in group 2 (P < 0.001 vs. placebo for both groups and P = NS group 1 vs. group 2). Serum LH levels increased from 5.1 ± 4.8 to 7.9 ± 6.5 U/liter and from 4.1 ± 1.6 to 7.2 ± 2.8 U/liter in groups 1 and 2, respectively (P = 0.007 group 1 vs. placebo, P = 0.003 group 2 vs. placebo, and P = NS group 1 vs. group 2). Scores for hematocrit, MOS Short-Form Health Survey, International Index of Erectile Function, and American Urological Association Symptom Index Score did not change. Serum prostate-specific antigen levels increased in group 2 only (1.7 ± 1.0 to 2.2 ± 1.5 ng/ml, P = 0.031, compared with placebo). These data demonstrate that aromatase inhibition increases serum bioavailable and total testosterone levels to the youthful normal range in older men with mild hypogonadism. Serum estradiol levels decrease modestly but remain within the normal male range. The physiological consequences of these changes remain to be determined. This work was supported by National Institutes of Health Grant K23-RR16310 (to B.Z.L.), the Massachusetts General Hospital Clinical Research Center grant (RR-1066), and AstraZeneca Pharmaceuticals. Current address for S.D.R.: Glaxo Kline Pharmaceuticals, Collegeville, Pennsylvania. Current address for J.G.: Eximias Pharmaceuticals, Berwyn, Pennsylvania. Abbreviations: DHT, Dihydrotestosterone; PSA, prostate-specific antigen. 1: J Urol. 2002 Feb;167(2 Pt 1):624-9. Related Articles, Links Comment in: * J Urol. 2002 Oct;168(4 Pt 1):1509. Aromatase inhibitors for male infertility. Raman JD, Schlegel PN. Department of Urology, Buchanan Brady Urology Foundation, Center for Male Reproductive Medicine and Microsurgery, New York Presbyterian Hospital, Weill Medical College of Cornell University, New York, New York, USA. PURPOSE: Testosterone-to-estradiol ratio levels in infertile men improve during treatment with the aromatase inhibitor, testolactone, and resulting changes in semen parameters. We evaluated the effect of anastrozole, a more selective aromatase inhibitor, on the hormonal and semen profiles of infertile men with abnormal baseline testosterone-to-estradiol ratios. MATERIALS AND METHODS: A total of 140 subfertile men with abnormal testosterone-to-estradiol ratios were treated with 100 to 200 mg. testolactone daily or 1 mg. anastrozole daily. Changes in testosterone, estradiol, testosterone-to-estradiol ratios and semen parameters were evaluated during therapy. The effect of obesity, diagnosis of the Klinefelter syndrome, and presence of varicocele and/or history of varicocele repair on treatment results was studied. RESULTS: Men treated with testolactone had an increase in testosterone-to-estradiol ratios during therapy (mean plus or minus standard error of the mean 5.3 +/- 0.2 versus 12.4 +/- 1.1, p <0.001). This change was confirmed in subgroups of men with the Klinefelter syndrome, a history of varicocele repair and those with varicocele. A total of 12 oligospermic men had semen analysis before and during testolactone treatment with an increase in sperm concentration (5.5 versus 11.2 million sperm per ml., p <0.01), motility (14.7% versus 21.0%, p <0.05), morphology (6.5% versus 12.8%, p = 0.05), and motility index (606.3 versus 1685.2 million motile sperm per ejaculate, respectively, p <0.05) appreciated. During anastrozole treatment, similar changes in the testosterone-to-estradiol ratios were seen (7.2 +/- 0.3 versus 18.1 +/- 1.0, respectively, p <0.001). This improvement of hormonal parameters was noted for all subgroups except those patients with the Klinefelter syndrome. A total of 25 oligospermic men with semen analysis before and during anastrozole treatment had an increase in semen volume (2.9 versus 3.5 ml., p <0.05), sperm concentration (5.5 versus 15.6 million sperm per ml., p <0.001) and motility index (832.8 versus 2930.8 million motile sperm per ejaculate, respectively, p <0.005). These changes were similar to those observed in men treated with testolactone. No significant difference in serum testosterone levels during treatment with testolactone and anastrozole was observed. However, the anastrozole treatment group did have a statistically better improvement of serum estradiol concentration and testosterone-to-estradiol ratios (p <0.001). CONCLUSIONS: Men who are infertile with a low serum testosterone-to-estradiol ratio can be treated with an aromatase inhibitor. With treatment, an increase in testosterone-to-estradiol ratio occurred in association with increased semen parameters. Anastrozole and testolactone have similar effects on hormonal profiles and semen analysis. Anastrazole appears to be at least as effective as testolactone for treating men with abnormal testosterone-to-estradiol ratios, except for the subset with the Klinefelter syndrome, who appeared to be more effectively treated with testolactone. PMID: 11792932 [PubMed - indexed for MEDLINE] The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 9 3027-3035 Copyright © 2000 by The Endocrine Society From the Clinical Research Centers Aromatase Inhibition in the Human Male Reveals a Hypothalamic Site of Estrogen Feedback1 Frances J. , B. Seminara, Suzzunne DeCruz, A. Boepple and F. Crowley, Jr. Reproductive Endocrine Unit of the Department of Medicine and National Center for Infertility Research, Massachusetts General Hospital, Boston, Massachusetts 02114 Address correspondence and requests for reprints to: Frances , MB, MRCPI, Reproductive Endocrine Unit and National Center for Infertility Research, Massachusetts General Hospital, Fruit Street, Boston, Massachusetts 02114. E-mail: hayes.frances@.... Abstract The preponderance of evidence states that, in adult men, estradiol (E2) inhibits LH secretion by decreasing pulse amplitude and responsiveness to GnRH consistent with a pituitary site of action. However, this conclusion is based on studies that employed pharmacologic doses of sex steroids, used nonselective aromatase inhibitors, and/or were performed in normal (NL) men, a model in which endogenous counterregulatory adaptations to physiologic perturbations confound interpretation of the results. In addition, studies in which estrogen antagonists were administered to NL men demonstrated an increase in LH pulse frequency, suggesting a potential additional hypothalamic site of E2 feedback. To reconcile these conflicting data, we used a selective aromatase inhibitor, anastrozole, to examine the impact of E2 suppression on the hypothalamic-pituitary axis in the male. Parallel studies of NL men and men with idiopathic hypogonadotropic hypogonadism (IHH), whose pituitary-gonadal axis had been normalized with long-term GnRH therapy, were performed to permit precise localization of the site of E2 feedback. In this so-called tandem model, a hypothalamic site of action of sex steroids can thus be inferred whenever there is a difference in the gonadotropin responses of NL and IHH men to alterations in their sex steroid milieu. A selective GnRH antagonist was also used to provide a semiquantitative estimate of endogenous GnRH secretion before and after E2 suppression. Fourteen NL men and seven IHH men were studied. In Exp 1, nine NL and seven IHH men received anastrozole (10 mg/day po x 7 days). Blood samples were drawn daily between 0800 and 1000 h in the NL men and immediately before a GnRH bolus dose in the IHH men. In Exp 2, blood was drawn (every 10 min x 12 h) from nine NL men at baseline and on day 7 of anastrozole. In a subset of five NL men, 5 µg/kg of the Nal-Glu GnRH antagonist was administered on completion of frequent blood sampling, then sampling continued every 20 min for a further 8 h. Anastrozole suppressed E2 equivalently in the NL (136 ± 10 to 52 ± 2 pmol/L, P < 0.005) and IHH men (118 ± 23 to 60 ± 5 pmol/L, P < 0.005). Testosterone levels rose significantly (P < 0.005), with a mean increase of 53 ± 6% in NL vs. 56 ± 7% in IHH men. Despite these similar changes in sex steroids, the increase in gonadotropins was greater in NL than in IHH men (100 ± 9 vs. 58 ± 6% for LH, P = 0.07; and 85 ± 6 vs. 41 ± 4% for FSH, P < 0.002). Frequent sampling studies in the NL men demonstrated that this rise in mean LH levels, after aromatase blockade, reflected an increase in both LH pulse frequency (10.2 ± 0.9 to 14.0 ± 1.0 pulses/24 h, P < 0.05) and pulse amplitude (5.7 ± 0.7 to 8.4 ± 0.7 IU/L, P < 0.001). Percent LH inhibition after acute GnRH receptor blockade was similar at baseline and after E2 suppression (69.2 ± 2.4 vs. 70 ± 1.9%), suggesting that there was no change in the quantity of endogenous GnRH secreted. From these data, we conclude that in the human male, estrogen has dual sites of negative feedback, acting at the hypothalamus to decrease GnRH pulse frequency and at the pituitary to decrease responsiveness to GnRH. Published online ahead of print October 13, 2004, 10.1210/jc.2004-0834 This Article Full Text Full Text (PDF) All Versions of this Article: 90/1/211 most recent jc.2004-0834v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission PubMed PubMed Citation Articles by Veldhuis, J. D. Articles by Iranmanesh, A. Related Collections Male Endocrinology The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 1 211-218 Copyright © 2005 by The Endocrine Society Short-Term Aromatase-Enzyme Blockade Unmasks Impaired Feedback Adaptations in Luteinizing Hormone and Testosterone Secretion in Older Men Johannes D. Veldhuis and Ali Iranmanesh Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Medical and Graduate Schools of Medicine, General Clinical Research Center, Mayo Clinic, Rochester, Minnesota 55905; and Endocrine Section, Medical Service, Salem Veterans Affairs Medical Center, Salem, Virginia 24153 Address all correspondence and requests for reprints to: Johannes D. Veldhuis, Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Medical and Graduate Schools of Medicine, General Clinical Research Center, Mayo Clinic, Rochester, Minnesota 55905. E-mail: veldhuis.johannes@.... The mechanisms subserving hypoandrogenemia and relative hypogonadotropism in older men are not known. The present study tests the clinical hypothesis that aging impairs hypothalamopituitary adaptations to feedback withdrawal induced by antagonism of estrogen biosynthesis. To this end, we appraised gonadal axis responses to estrogen depletion induced by anastrozole (a potent and selective aromatase inhibitor) in nine older and 11 young men vs. placebo in 17 other older and eight young men. The study design comprised a prospectively randomized, double-blind, parallel-cohort intervention. To monitor LH release, blood was sampled every 10 min for 24 h; LH concentrations were assayed by two-site monoclonal immunoradiometric assay; pulsatile LH release quantitated by a model-free discrete peak-detection technique (Cluster); feedback-dependent orderliness of LH secretion via the approximate entropy statistic; and 24-h rhythmicity of LH concentrations by cosine analysis. At baseline, older men had comparable estradiol and testosterone but lower LH concentrations than young controls. Exposure to anastrozole reduced (24-h pooled) serum estradiol concentrations by 50% (P < 0.001) and elevated mean LH concentrations by 2.1-fold (P < 0.001) in both the young and older cohorts. However, older men failed to achieve young adult augmentation of the following: 1) total testosterone concentrations (P < 0.01) or molar testosterone to SHBG ratios (P < 0.01); 2) incremental LH pulse amplitude (P < 0.001) and LH peak area (P < 0.01); 3) mean LH pulse frequency (P = 0.0044); and 4) quantifiable irregularity (approximate entropy) of LH release patterns (P < 0.001). FSH concentrations became comparable in the two age cohorts. In summary, administration of a potent and selective aromatase antagonist reduces estradiol and elevates mean LH concentrations equivalently in young and older men. The low estrogen-feedback state in elderly men unmasks diminished incremental LH pulse amplitude and area; absence of further acceleration of LH pulse frequency; impaired regulation of the orderliness of LH release; and reduced testosterone to SHBG ratios. Thus, aging alters expected hypothalamopituitary-gonadal adaptations to short-term partial estrogen depletion in healthy men. ________________ I am human; nothing in humanity is alien to me. Terence Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 27, 2006 Report Share Posted June 27, 2006 Hey bro, good information and don't let all the b-s get to you again. I know the feeling of just wanting to run a mock, in which you did lol. I think I will have to beg for my new ( hot russian with nice legs but Im sure a scary ) Endo doc to put me on HCG and see if my well being can very much improve. I posted some new tests I took earlier this month, and it concluded my E2 is up there around the normal-high range. That sucks and now I know why the older males in here continue to emphasize E2, but still have no idea how high E2 makes me feel. Yet, another medication I must take now. Groovy...... Just be calm and just be patient and use the force of passive but affirm when dealing with doctors, etc that simply dont care what we have been thru and still do thru just to try and get healthy. retrogrouch@... wrote: On Tue, 16 May 2006 09:39:57 +0000 (GMT), you wrote: >she went to each doctor and all refused to add on the extra tsts,saying none were required and that why test a female hormone on a male its totally irrelevant. > >i then wnet in a panic attack crying and shouting and mumbling to my self ,and then into meltdown and said i was not leaving the surgery till the checks were all done and iwas sitting outside the door,[unless you have seen an aspergerrs/add meltdown its hard to visualise] > >anyway nurse wnet back to one of the doctors and female nice doctor called me in. > >she said she was acutally had specialist knowledge in male hormones etc,and again said the female ones dont need to be looked at,i was still crying and panicking she calmed me down a bit and said Gawd but I had ignorant " specialists " and doctors. But you have to deal with them. They hold the control of your treatment, unfortunate as that may be. So steel yourself, calm your self and go to them with calmness and open mind and present them with these things in their language. (also make sure you are talking to them about estradiol not estrogen) Inform them that you understand T converts to estradiol through aromotization. And that T levels can actually decrease in people not getting treatment because of high aromotase levels - particularly if the person is at all over weight. (Aromotase is created and " lives " in fat. I've given you some related studies. there is one I cannot lay my hands on today that is actually the best of the bunch. It is a case study that showed in some older men T levels could be raised by 200 to 300 points simply by controlling estradiol and aromitization - without any T supplementing. Maybe someone has a copy at hand? Could you post the link? But these are some I have found that might nudge them a bit: (Also know that estradiol levels much beyond 50 pg/ml lead to ED, emotionalism, gynomastia, severley dimished drive, etc. It wouldn't hurt to tell them this as well. But studies on high E2 levels are hard to find.) The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 3 1174-1180 Copyright � 2004 by The Endocrine Society Effects of Aromatase Inhibition in Elderly Men with Low or Borderline-Low Serum Testosterone Levels Z. Leder, L. Rohrer, D. Rubin, Gallo and Longcope Endocrine Unit (B.Z.L., J.L.R.), Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; Departments of Medicine and Obstetrics and Gynecology (C.L.), University of Massachusetts Medical School, Worcester, Massachusetts 01655; and AstraZeneca Pharmaceuticals (S.D.R., J.G.), Wilmington, Delaware 19850 Address all correspondence and requests for reprints to: Z. Leder, Endocrine Unit, Massachusetts General Hospital, Bulfinch 327, Fruit Street, Boston, Massachusetts 02114. As men age, serum testosterone levels decrease, a factor that may contribute to some aspects of age-related physiological deterioration. Although androgen replacement has been shown to have beneficial effects in frankly hypogonadal men, its use in elderly men with borderline hypogonadism is controversial. Furthermore, current testosterone replacement methods have important limitations. We investigated the ability of the orally administered aromatase inhibitor, anastrozole, to increase endogenous testosterone production in 37 elderly men (aged 62�74 yr) with screening serum testosterone levels less than 350 ng/dl. Subjects were randomized in a double-blind fashion to the following 12-wk oral regimens: group 1: anastrozole 1 mg daily (n = 12); group 2: anastrozole 1 mg twice weekly (n = 11); and group 3: placebo daily (n = 14). Hormone levels, quality of life (MOS Short-Form Health Survey), ual function (International Index of Erectile Function), benign prostate hyperplasia severity (American Urological Association Symptom Index Score), prostate-specific antigen, and measures of safety were compared among groups. Mean � SD bioavailable testosterone increased from 99 � 31 to 207 � 65 ng/dl in group 1 and from 115 � 37 to 178 � 55 ng/dl in group 2 (P < 0.001 vs. placebo for both groups and P = 0.054 group 1 vs. group 2). Total testosterone levels increased from 343 � 61 to 572 � 139 ng/dl in group 1 and from 397 � 106 to 520 � 91 ng/dl in group 2 (P < 0.001 vs. placebo for both groups and P = 0.012 group 1 vs. group 2). Serum estradiol levels decreased from 26 � 8 to 17 � 6 pg/ml in group 1 and from 27 � 8 to 17 � 5 pg/ml in group 2 (P < 0.001 vs. placebo for both groups and P = NS group 1 vs. group 2). Serum LH levels increased from 5.1 � 4.8 to 7.9 � 6.5 U/liter and from 4.1 � 1.6 to 7.2 � 2.8 U/liter in groups 1 and 2, respectively (P = 0.007 group 1 vs. placebo, P = 0.003 group 2 vs. placebo, and P = NS group 1 vs. group 2). Scores for hematocrit, MOS Short-Form Health Survey, International Index of Erectile Function, and American Urological Association Symptom Index Score did not change. Serum prostate-specific antigen levels increased in group 2 only (1.7 � 1.0 to 2.2 � 1.5 ng/ml, P = 0.031, compared with placebo). These data strate that aromatase inhibition increases serum bioavailable and total testosterone levels to the youthful normal range in older men with mild hypogonadism. Serum estradiol levels decrease modestly but remain within the normal male range. The physiological consequences of these changes remain to be determined. This work was supported by National Institutes of Health Grant K23-RR16310 (to B.Z.L.), the Massachusetts General Hospital Clinical Research Center grant (RR-1066), and AstraZeneca Pharmaceuticals. Current address for S.D.R.: Glaxo Kline Pharmaceuticals, Collegeville, Pennsylvania. Current address for J.G.: Eximias Pharmaceuticals, Berwyn, Pennsylvania. Abbreviations: DHT, Dihydrotestosterone; PSA, prostate-specific antigen. 1: J Urol. 2002 Feb;167(2 Pt 1):624-9. Related Articles, Links Comment in: * J Urol. 2002 Oct;168(4 Pt 1):1509. Aromatase inhibitors for male infertility. Raman JD, Schlegel PN. Department of Urology, Buchanan Brady Urology Foundation, Center for Male Reproductive Medicine and Microsurgery, New York Presbyterian Hospital, Weill Medical College of Cornell University, New York, New York, USA. PURPOSE: Testosterone-to-estradiol ratio levels in infertile men improve during treatment with the aromatase inhibitor, testolactone, and resulting changes in semen parameters. We evaluated the effect of anastrozole, a more selective aromatase inhibitor, on the hormonal and semen profiles of infertile men with abnormal baseline testosterone-to-estradiol ratios. MATERIALS AND METHODS: A total of 140 subfertile men with abnormal testosterone-to-estradiol ratios were treated with 100 to 200 mg. testolactone daily or 1 mg. anastrozole daily. Changes in testosterone, estradiol, testosterone-to-estradiol ratios and semen parameters were evaluated during therapy. The effect of obesity, diagnosis of the Klinefelter syndrome, and presence of varicocele and/or history of varicocele repair on treatment results was studied. RESULTS: Men treated with testolactone had an increase in testosterone-to-estradiol ratios during therapy (mean plus or minus standard error of the mean 5.3 +/- 0.2 versus 12.4 +/- 1.1, p <0.001). This change was confirmed in subgroups of men with the Klinefelter syndrome, a history of varicocele repair and those with varicocele. A total of 12 oligospermic men had semen analysis before and during testolactone treatment with an increase in sperm concentration (5.5 versus 11.2 million sperm per ml., p <0.01), motility (14.7% versus 21.0%, p <0.05), morphology (6.5% versus 12.8%, p = 0.05), and motility index (606.3 versus 1685.2 million motile sperm per ejaculate, respectively, p <0.05) appreciated. During anastrozole treatment, similar changes in the testosterone-to-estradiol ratios were seen (7.2 +/- 0.3 versus 18.1 +/- 1.0, respectively, p <0.001). This improvement of hormonal parameters was noted for all subgroups except those patients with the Klinefelter syndrome. A total of 25 oligospermic men with semen analysis before and during anastrozole treatment had an increase in semen volume (2.9 versus 3.5 ml., p <0.05), sperm concentration (5.5 versus 15.6 million sperm per ml., p <0.001) and motility index (832.8 versus 2930.8 million motile sperm per ejaculate, respectively, p <0.005). These changes were similar to those observed in men treated with testolactone. No significant difference in serum testosterone levels during treatment with testolactone and anastrozole was observed. However, the anastrozole treatment group did have a statistically better improvement of serum estradiol concentration and testosterone-to-estradiol ratios (p <0.001). CONCLUSIONS: Men who are infertile with a low serum testosterone-to-estradiol ratio can be treated with an aromatase inhibitor. With treatment, an increase in testosterone-to-estradiol ratio occurred in association with increased semen parameters. Anastrozole and testolactone have similar effects on hormonal profiles and semen analysis. Anastrazole appears to be at least as effective as testolactone for treating men with abnormal testosterone-to-estradiol ratios, except for the subset with the Klinefelter syndrome, who appeared to be more effectively treated with testolactone. PMID: 11792932 [PubMed - indexed for MEDLINE] The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 9 3027-3035 Copyright � 2000 by The Endocrine Society From the Clinical Research Centers Aromatase Inhibition in the Human Male Reveals a Hypothalamic Site of Estrogen Feedback1 Frances J. , B. Seminara, Suzzunne DeCruz, A. Boepple and F. Crowley, Jr. Reproductive Endocrine Unit of the Department of Medicine and National Center for Infertility Research, Massachusetts General Hospital, Boston, Massachusetts 02114 Address correspondence and requests for reprints to: Frances , MB, MRCPI, Reproductive Endocrine Unit and National Center for Infertility Research, Massachusetts General Hospital, Fruit Street, Boston, Massachusetts 02114. E-mail: hayes.frances@.... Abstract The preponderance of evidence states that, in men, estradiol (E2) inhibits LH secretion by decreasing pulse amplitude and responsiveness to GnRH consistent with a pituitary site of action. However, this conclusion is based on studies that employed pharmacologic doses of steroids, used nonselective aromatase inhibitors, and/or were performed in normal (NL) men, a in which endogenous counterregulatory adaptations to physiologic perturbations confound interpretation of the results. In addition, studies in which estrogen antagonists were administered to NL men strated an increase in LH pulse frequency, suggesting a potential additional hypothalamic site of E2 feedback. To reconcile these conflicting data, we used a selective aromatase inhibitor, anastrozole, to examine the impact of E2 suppression on the hypothalamic-pituitary axis in the male. Parallel studies of NL men and men with idiopathic hypogonadotropic hypogonadism (IHH), whose pituitary-gonadal axis had been normalized with long-term GnRH therapy, were performed to permit precise localization of the site of E2 feedback. In this so-called tandem , a hypothalamic site of action of steroids can thus be inferred whenever there is a difference in the gonadotropin responses of NL and IHH men to alterations in their steroid milieu. A selective GnRH antagonist was also used to provide a semiquantitative estimate of endogenous GnRH secretion before and after E2 suppression. Fourteen NL men and seven IHH men were studied. In Exp 1, nine NL and seven IHH men received anastrozole (10 mg/day po x 7 days). samples were drawn daily between 0800 and 1000 h in the NL men and immediately before a GnRH bolus dose in the IHH men. In Exp 2, was drawn (every 10 min x 12 h) from nine NL men at baseline and on day 7 of anastrozole. In a subset of five NL men, 5 �g/kg of the Nal-Glu GnRH antagonist was administered on completion of frequent sampling, then sampling continued every 20 min for a further 8 h. Anastrozole suppressed E2 equivalently in the NL (136 � 10 to 52 � 2 pmol/L, P < 0.005) and IHH men (118 � 23 to 60 � 5 pmol/L, P < 0.005). Testosterone levels rose significantly (P < 0.005), with a mean increase of 53 � 6% in NL vs. 56 � 7% in IHH men. Despite these similar changes in steroids, the increase in gonadotropins was greater in NL than in IHH men (100 � 9 vs. 58 � 6% for LH, P = 0.07; and 85 � 6 vs. 41 � 4% for FSH, P < 0.002). Frequent sampling studies in the NL men strated that this rise in mean LH levels, after aromatase blockade, reflected an increase in both LH pulse frequency (10.2 � 0.9 to 14.0 � 1.0 pulses/24 h, P < 0.05) and pulse amplitude (5.7 � 0.7 to 8.4 � 0.7 IU/L, P < 0.001). Percent LH inhibition after acute GnRH receptor blockade was similar at baseline and after E2 suppression (69.2 � 2.4 vs. 70 � 1.9%), suggesting that there was no change in the quantity of endogenous GnRH secreted. From these data, we conclude that in the human male, estrogen has dual sites of negative feedback, acting at the hypothalamus to decrease GnRH pulse frequency and at the pituitary to decrease responsiveness to GnRH. Published online ahead of print October 13, 2004, 10.1210/jc.2004-0834 This Article Full Text Full Text (PDF) All Versions of this Article: 90/1/211 most recent jc.2004-0834v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission PubMed PubMed Citation Articles by Veldhuis, J. D. Articles by Iranmanesh, A. Related Collections Male Endocrinology The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 1 211-218 Copyright � 2005 by The Endocrine Society Short-Term Aromatase-Enzyme Blockade Unmasks Impaired Feedback Adaptations in Luteinizing Hormone and Testosterone Secretion in Older Men Johannes D. Veldhuis and Ali Iranmanesh Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Medical and Graduate Schools of Medicine, General Clinical Research Center, Mayo Clinic, Rochester, Minnesota 55905; and Endocrine Section, Medical Service, Salem Veterans Affairs Medical Center, Salem, Virginia 24153 Address all correspondence and requests for reprints to: Johannes D. Veldhuis, Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Medical and Graduate Schools of Medicine, General Clinical Research Center, Mayo Clinic, Rochester, Minnesota 55905. E-mail: veldhuis.johannes@.... The mechanisms subserving hypoandrogenemia and relative hypogonadotropism in older men are not known. The present study tests the clinical hypothesis that aging impairs hypothalamopituitary adaptations to feedback withdrawal induced by antagonism of estrogen biosynthesis. To this end, we appraised gonadal axis responses to estrogen depletion induced by anastrozole (a potent and selective aromatase inhibitor) in nine older and 11 young men vs. placebo in 17 other older and eight young men. The study design comprised a prospectively randomized, double-blind, parallel-cohort intervention. To monitor LH release, was sampled every 10 min for 24 h; LH concentrations were assayed by two-site monoclonal immunoradiometric assay; pulsatile LH release quantitated by a -free discrete peak-detection technique (Cluster); feedback-dependent orderliness of LH secretion via the approximate entropy statistic; and 24-h rhythmicity of LH concentrations by cosine analysis. At baseline, older men had comparable estradiol and testosterone but lower LH concentrations than young controls. Exposure to anastrozole reduced (24-h pooled) serum estradiol concentrations by 50% (P < 0.001) and elevated mean LH concentrations by 2.1-fold (P < 0.001) in both the young and older cohorts. However, older men failed to achieve young augmentation of the following: 1) total testosterone concentrations (P < 0.01) or molar testosterone to SHBG ratios (P < 0.01); 2) incremental LH pulse amplitude (P < 0.001) and LH peak area (P < 0.01); 3) mean LH pulse frequency (P = 0.0044); and 4) quantifiable irregularity (approximate entropy) of LH release patterns (P < 0.001). FSH concentrations became comparable in the two age cohorts. In summary, administration of a potent and selective aromatase antagonist reduces estradiol and elevates mean LH concentrations equivalently in young and older men. The low estrogen-feedback state in elderly men unmasks diminished incremental LH pulse amplitude and area; absence of further acceleration of LH pulse frequency; impaired regulation of the orderliness of LH release; and reduced testosterone to SHBG ratios. Thus, aging alters expected hypothalamopituitary-gonadal adaptations to short-term partial estrogen depletion in healthy men. ________________ I am human; nothing in humanity is alien to me. Terence --------------------------------- Sports Fantasy Football ’06 - Go with the leader. Start your league today! Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 27, 2006 Report Share Posted June 27, 2006 Wow Retro you out did you self on this one were have you been. Thanks hell this info helped me. Phil retrogrouch@... wrote: On Tue, 16 May 2006 09:39:57 +0000 (GMT), you wrote: >she went to each doctor and all refused to add on the extra tsts,saying none were required and that why test a female hormone on a male its totally irrelevant. > >i then wnet in a panic attack crying and shouting and mumbling to my self ,and then into meltdown and said i was not leaving the surgery till the checks were all done and iwas sitting outside the door,[unless you have seen an aspergerrs/add meltdown its hard to visualise] > >anyway nurse wnet back to one of the doctors and female nice doctor called me in. > >she said she was acutally had specialist knowledge in male hormones etc,and again said the female ones dont need to be looked at,i was still crying and panicking she calmed me down a bit and said Gawd but I had ignorant " specialists " and doctors. But you have to deal with them. They hold the control of your treatment, unfortunate as that may be. So steel yourself, calm your self and go to them with calmness and open mind and present them with these things in their language. (also make sure you are talking to them about estradiol not estrogen) Inform them that you understand T converts to estradiol through aromotization. And that T levels can actually decrease in people not getting treatment because of high aromotase levels - particularly if the person is at all over weight. (Aromotase is created and " lives " in fat. I've given you some related studies. there is one I cannot lay my hands on today that is actually the best of the bunch. It is a case study that showed in some older men T levels could be raised by 200 to 300 points simply by controlling estradiol and aromitization - without any T supplementing. Maybe someone has a copy at hand? Could you post the link? But these are some I have found that might nudge them a bit: (Also know that estradiol levels much beyond 50 pg/ml lead to ED, emotionalism, gynomastia, severley dimished sex drive, etc. It wouldn't hurt to tell them this as well. But studies on high E2 levels are hard to find.) The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 3 1174-1180 Copyright © 2004 by The Endocrine Society Effects of Aromatase Inhibition in Elderly Men with Low or Borderline-Low Serum Testosterone Levels Z. Leder, L. Rohrer, D. Rubin, Gallo and Longcope Endocrine Unit (B.Z.L., J.L.R.), Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; Departments of Medicine and Obstetrics and Gynecology (C.L.), University of Massachusetts Medical School, Worcester, Massachusetts 01655; and AstraZeneca Pharmaceuticals (S.D.R., J.G.), Wilmington, Delaware 19850 Address all correspondence and requests for reprints to: Z. Leder, Endocrine Unit, Massachusetts General Hospital, Bulfinch 327, Fruit Street, Boston, Massachusetts 02114. As men age, serum testosterone levels decrease, a factor that may contribute to some aspects of age-related physiological deterioration. Although androgen replacement has been shown to have beneficial effects in frankly hypogonadal men, its use in elderly men with borderline hypogonadism is controversial. Furthermore, current testosterone replacement methods have important limitations. We investigated the ability of the orally administered aromatase inhibitor, anastrozole, to increase endogenous testosterone production in 37 elderly men (aged 62–74 yr) with screening serum testosterone levels less than 350 ng/dl. Subjects were randomized in a double-blind fashion to the following 12-wk oral regimens: group 1: anastrozole 1 mg daily (n = 12); group 2: anastrozole 1 mg twice weekly (n = 11); and group 3: placebo daily (n = 14). Hormone levels, quality of life (MOS Short-Form Health Survey), sexual function (International Index of Erectile Function), benign prostate hyperplasia severity (American Urological Association Symptom Index Score), prostate-specific antigen, and measures of safety were compared among groups. Mean ± SD bioavailable testosterone increased from 99 ± 31 to 207 ± 65 ng/dl in group 1 and from 115 ± 37 to 178 ± 55 ng/dl in group 2 (P < 0.001 vs. placebo for both groups and P = 0.054 group 1 vs. group 2). Total testosterone levels increased from 343 ± 61 to 572 ± 139 ng/dl in group 1 and from 397 ± 106 to 520 ± 91 ng/dl in group 2 (P < 0.001 vs. placebo for both groups and P = 0.012 group 1 vs. group 2). Serum estradiol levels decreased from 26 ± 8 to 17 ± 6 pg/ml in group 1 and from 27 ± 8 to 17 ± 5 pg/ml in group 2 (P < 0.001 vs. placebo for both groups and P = NS group 1 vs. group 2). Serum LH levels increased from 5.1 ± 4.8 to 7.9 ± 6.5 U/liter and from 4.1 ± 1.6 to 7.2 ± 2.8 U/liter in groups 1 and 2, respectively (P = 0.007 group 1 vs. placebo, P = 0.003 group 2 vs. placebo, and P = NS group 1 vs. group 2). Scores for hematocrit, MOS Short-Form Health Survey, International Index of Erectile Function, and American Urological Association Symptom Index Score did not change. Serum prostate-specific antigen levels increased in group 2 only (1.7 ± 1.0 to 2.2 ± 1.5 ng/ml, P = 0.031, compared with placebo). These data demonstrate that aromatase inhibition increases serum bioavailable and total testosterone levels to the youthful normal range in older men with mild hypogonadism. Serum estradiol levels decrease modestly but remain within the normal male range. The physiological consequences of these changes remain to be determined. This work was supported by National Institutes of Health Grant K23-RR16310 (to B.Z.L.), the Massachusetts General Hospital Clinical Research Center grant (RR-1066), and AstraZeneca Pharmaceuticals. Current address for S.D.R.: Glaxo Kline Pharmaceuticals, Collegeville, Pennsylvania. Current address for J.G.: Eximias Pharmaceuticals, Berwyn, Pennsylvania. Abbreviations: DHT, Dihydrotestosterone; PSA, prostate-specific antigen. 1: J Urol. 2002 Feb;167(2 Pt 1):624-9. Related Articles, Links Comment in: * J Urol. 2002 Oct;168(4 Pt 1):1509. Aromatase inhibitors for male infertility. Raman JD, Schlegel PN. Department of Urology, Buchanan Brady Urology Foundation, Center for Male Reproductive Medicine and Microsurgery, New York Presbyterian Hospital, Weill Medical College of Cornell University, New York, New York, USA. PURPOSE: Testosterone-to-estradiol ratio levels in infertile men improve during treatment with the aromatase inhibitor, testolactone, and resulting changes in semen parameters. We evaluated the effect of anastrozole, a more selective aromatase inhibitor, on the hormonal and semen profiles of infertile men with abnormal baseline testosterone-to-estradiol ratios. MATERIALS AND METHODS: A total of 140 subfertile men with abnormal testosterone-to-estradiol ratios were treated with 100 to 200 mg. testolactone daily or 1 mg. anastrozole daily. Changes in testosterone, estradiol, testosterone-to-estradiol ratios and semen parameters were evaluated during therapy. The effect of obesity, diagnosis of the Klinefelter syndrome, and presence of varicocele and/or history of varicocele repair on treatment results was studied. RESULTS: Men treated with testolactone had an increase in testosterone-to-estradiol ratios during therapy (mean plus or minus standard error of the mean 5.3 +/- 0.2 versus 12.4 +/- 1.1, p <0.001). This change was confirmed in subgroups of men with the Klinefelter syndrome, a history of varicocele repair and those with varicocele. A total of 12 oligospermic men had semen analysis before and during testolactone treatment with an increase in sperm concentration (5.5 versus 11.2 million sperm per ml., p <0.01), motility (14.7% versus 21.0%, p <0.05), morphology (6.5% versus 12.8%, p = 0.05), and motility index (606.3 versus 1685.2 million motile sperm per ejaculate, respectively, p <0.05) appreciated. During anastrozole treatment, similar changes in the testosterone-to-estradiol ratios were seen (7.2 +/- 0.3 versus 18.1 +/- 1.0, respectively, p <0.001). This improvement of hormonal parameters was noted for all subgroups except those patients with the Klinefelter syndrome. A total of 25 oligospermic men with semen analysis before and during anastrozole treatment had an increase in semen volume (2.9 versus 3.5 ml., p <0.05), sperm concentration (5.5 versus 15.6 million sperm per ml., p <0.001) and motility index (832.8 versus 2930.8 million motile sperm per ejaculate, respectively, p <0.005). These changes were similar to those observed in men treated with testolactone. No significant difference in serum testosterone levels during treatment with testolactone and anastrozole was observed. However, the anastrozole treatment group did have a statistically better improvement of serum estradiol concentration and testosterone-to-estradiol ratios (p <0.001). CONCLUSIONS: Men who are infertile with a low serum testosterone-to-estradiol ratio can be treated with an aromatase inhibitor. With treatment, an increase in testosterone-to-estradiol ratio occurred in association with increased semen parameters. Anastrozole and testolactone have similar effects on hormonal profiles and semen analysis. Anastrazole appears to be at least as effective as testolactone for treating men with abnormal testosterone-to-estradiol ratios, except for the subset with the Klinefelter syndrome, who appeared to be more effectively treated with testolactone. PMID: 11792932 [PubMed - indexed for MEDLINE] The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 9 3027-3035 Copyright © 2000 by The Endocrine Society From the Clinical Research Centers Aromatase Inhibition in the Human Male Reveals a Hypothalamic Site of Estrogen Feedback1 Frances J. , B. Seminara, Suzzunne DeCruz, A. Boepple and F. Crowley, Jr. Reproductive Endocrine Unit of the Department of Medicine and National Center for Infertility Research, Massachusetts General Hospital, Boston, Massachusetts 02114 Address correspondence and requests for reprints to: Frances , MB, MRCPI, Reproductive Endocrine Unit and National Center for Infertility Research, Massachusetts General Hospital, Fruit Street, Boston, Massachusetts 02114. E-mail: hayes.frances@.... Abstract The preponderance of evidence states that, in adult men, estradiol (E2) inhibits LH secretion by decreasing pulse amplitude and responsiveness to GnRH consistent with a pituitary site of action. However, this conclusion is based on studies that employed pharmacologic doses of sex steroids, used nonselective aromatase inhibitors, and/or were performed in normal (NL) men, a model in which endogenous counterregulatory adaptations to physiologic perturbations confound interpretation of the results. In addition, studies in which estrogen antagonists were administered to NL men demonstrated an increase in LH pulse frequency, suggesting a potential additional hypothalamic site of E2 feedback. To reconcile these conflicting data, we used a selective aromatase inhibitor, anastrozole, to examine the impact of E2 suppression on the hypothalamic-pituitary axis in the male. Parallel studies of NL men and men with idiopathic hypogonadotropic hypogonadism (IHH), whose pituitary-gonadal axis had been normalized with long-term GnRH therapy, were performed to permit precise localization of the site of E2 feedback. In this so-called tandem model, a hypothalamic site of action of sex steroids can thus be inferred whenever there is a difference in the gonadotropin responses of NL and IHH men to alterations in their sex steroid milieu. A selective GnRH antagonist was also used to provide a semiquantitative estimate of endogenous GnRH secretion before and after E2 suppression. Fourteen NL men and seven IHH men were studied. In Exp 1, nine NL and seven IHH men received anastrozole (10 mg/day po x 7 days). Blood samples were drawn daily between 0800 and 1000 h in the NL men and immediately before a GnRH bolus dose in the IHH men. In Exp 2, blood was drawn (every 10 min x 12 h) from nine NL men at baseline and on day 7 of anastrozole. In a subset of five NL men, 5 µg/kg of the Nal-Glu GnRH antagonist was administered on completion of frequent blood sampling, then sampling continued every 20 min for a further 8 h. Anastrozole suppressed E2 equivalently in the NL (136 ± 10 to 52 ± 2 pmol/L, P < 0.005) and IHH men (118 ± 23 to 60 ± 5 pmol/L, P < 0.005). Testosterone levels rose significantly (P < 0.005), with a mean increase of 53 ± 6% in NL vs. 56 ± 7% in IHH men. Despite these similar changes in sex steroids, the increase in gonadotropins was greater in NL than in IHH men (100 ± 9 vs. 58 ± 6% for LH, P = 0.07; and 85 ± 6 vs. 41 ± 4% for FSH, P < 0.002). Frequent sampling studies in the NL men demonstrated that this rise in mean LH levels, after aromatase blockade, reflected an increase in both LH pulse frequency (10.2 ± 0.9 to 14.0 ± 1.0 pulses/24 h, P < 0.05) and pulse amplitude (5.7 ± 0.7 to 8.4 ± 0.7 IU/L, P < 0.001). Percent LH inhibition after acute GnRH receptor blockade was similar at baseline and after E2 suppression (69.2 ± 2.4 vs. 70 ± 1.9%), suggesting that there was no change in the quantity of endogenous GnRH secreted. From these data, we conclude that in the human male, estrogen has dual sites of negative feedback, acting at the hypothalamus to decrease GnRH pulse frequency and at the pituitary to decrease responsiveness to GnRH. Published online ahead of print October 13, 2004, 10.1210/jc.2004-0834 This Article Full Text Full Text (PDF) All Versions of this Article: 90/1/211 most recent jc.2004-0834v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission PubMed PubMed Citation Articles by Veldhuis, J. D. Articles by Iranmanesh, A. Related Collections Male Endocrinology The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 1 211-218 Copyright © 2005 by The Endocrine Society Short-Term Aromatase-Enzyme Blockade Unmasks Impaired Feedback Adaptations in Luteinizing Hormone and Testosterone Secretion in Older Men Johannes D. Veldhuis and Ali Iranmanesh Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Medical and Graduate Schools of Medicine, General Clinical Research Center, Mayo Clinic, Rochester, Minnesota 55905; and Endocrine Section, Medical Service, Salem Veterans Affairs Medical Center, Salem, Virginia 24153 Address all correspondence and requests for reprints to: Johannes D. Veldhuis, Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Medical and Graduate Schools of Medicine, General Clinical Research Center, Mayo Clinic, Rochester, Minnesota 55905. E-mail: veldhuis.johannes@.... The mechanisms subserving hypoandrogenemia and relative hypogonadotropism in older men are not known. The present study tests the clinical hypothesis that aging impairs hypothalamopituitary adaptations to feedback withdrawal induced by antagonism of estrogen biosynthesis. To this end, we appraised gonadal axis responses to estrogen depletion induced by anastrozole (a potent and selective aromatase inhibitor) in nine older and 11 young men vs. placebo in 17 other older and eight young men. The study design comprised a prospectively randomized, double-blind, parallel-cohort intervention. To monitor LH release, blood was sampled every 10 min for 24 h; LH concentrations were assayed by two-site monoclonal immunoradiometric assay; pulsatile LH release quantitated by a model-free discrete peak-detection technique (Cluster); feedback-dependent orderliness of LH secretion via the approximate entropy statistic; and 24-h rhythmicity of LH concentrations by cosine analysis. At baseline, older men had comparable estradiol and testosterone but lower LH concentrations than young controls. Exposure to anastrozole reduced (24-h pooled) serum estradiol concentrations by 50% (P < 0.001) and elevated mean LH concentrations by 2.1-fold (P < 0.001) in both the young and older cohorts. However, older men failed to achieve young adult augmentation of the following: 1) total testosterone concentrations (P < 0.01) or molar testosterone to SHBG ratios (P < 0.01); 2) incremental LH pulse amplitude (P < 0.001) and LH peak area (P < 0.01); 3) mean LH pulse frequency (P = 0.0044); and 4) quantifiable irregularity (approximate entropy) of LH release patterns (P < 0.001). FSH concentrations became comparable in the two age cohorts. In summary, administration of a potent and selective aromatase antagonist reduces estradiol and elevates mean LH concentrations equivalently in young and older men. The low estrogen-feedback state in elderly men unmasks diminished incremental LH pulse amplitude and area; absence of further acceleration of LH pulse frequency; impaired regulation of the orderliness of LH release; and reduced testosterone to SHBG ratios. Thus, aging alters expected hypothalamopituitary-gonadal adaptations to short-term partial estrogen depletion in healthy men. ________________ I am human; nothing in humanity is alien to me. Terence Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 27, 2006 Report Share Posted June 27, 2006 Here is the link. http://www.medibolics.com/ArimidexBoostsTestosterone.htm Phil retrogrouch@... wrote: On Tue, 16 May 2006 09:39:57 +0000 (GMT), you wrote: >she went to each doctor and all refused to add on the extra tsts,saying none were required and that why test a female hormone on a male its totally irrelevant. > >i then wnet in a panic attack crying and shouting and mumbling to my self ,and then into meltdown and said i was not leaving the surgery till the checks were all done and iwas sitting outside the door,[unless you have seen an aspergerrs/add meltdown its hard to visualise] > >anyway nurse wnet back to one of the doctors and female nice doctor called me in. > >she said she was acutally had specialist knowledge in male hormones etc,and again said the female ones dont need to be looked at,i was still crying and panicking she calmed me down a bit and said Gawd but I had ignorant " specialists " and doctors. But you have to deal with them. They hold the control of your treatment, unfortunate as that may be. So steel yourself, calm your self and go to them with calmness and open mind and present them with these things in their language. (also make sure you are talking to them about estradiol not estrogen) Inform them that you understand T converts to estradiol through aromotization. And that T levels can actually decrease in people not getting treatment because of high aromotase levels - particularly if the person is at all over weight. (Aromotase is created and " lives " in fat. I've given you some related studies. there is one I cannot lay my hands on today that is actually the best of the bunch. It is a case study that showed in some older men T levels could be raised by 200 to 300 points simply by controlling estradiol and aromitization - without any T supplementing. Maybe someone has a copy at hand? Could you post the link? But these are some I have found that might nudge them a bit: (Also know that estradiol levels much beyond 50 pg/ml lead to ED, emotionalism, gynomastia, severley dimished sex drive, etc. It wouldn't hurt to tell them this as well. But studies on high E2 levels are hard to find.) The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 3 1174-1180 Copyright © 2004 by The Endocrine Society Effects of Aromatase Inhibition in Elderly Men with Low or Borderline-Low Serum Testosterone Levels Z. Leder, L. Rohrer, D. Rubin, Gallo and Longcope Endocrine Unit (B.Z.L., J.L.R.), Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; Departments of Medicine and Obstetrics and Gynecology (C.L.), University of Massachusetts Medical School, Worcester, Massachusetts 01655; and AstraZeneca Pharmaceuticals (S.D.R., J.G.), Wilmington, Delaware 19850 Address all correspondence and requests for reprints to: Z. Leder, Endocrine Unit, Massachusetts General Hospital, Bulfinch 327, Fruit Street, Boston, Massachusetts 02114. As men age, serum testosterone levels decrease, a factor that may contribute to some aspects of age-related physiological deterioration. Although androgen replacement has been shown to have beneficial effects in frankly hypogonadal men, its use in elderly men with borderline hypogonadism is controversial. Furthermore, current testosterone replacement methods have important limitations. We investigated the ability of the orally administered aromatase inhibitor, anastrozole, to increase endogenous testosterone production in 37 elderly men (aged 62–74 yr) with screening serum testosterone levels less than 350 ng/dl. Subjects were randomized in a double-blind fashion to the following 12-wk oral regimens: group 1: anastrozole 1 mg daily (n = 12); group 2: anastrozole 1 mg twice weekly (n = 11); and group 3: placebo daily (n = 14). Hormone levels, quality of life (MOS Short-Form Health Survey), sexual function (International Index of Erectile Function), benign prostate hyperplasia severity (American Urological Association Symptom Index Score), prostate-specific antigen, and measures of safety were compared among groups. Mean ± SD bioavailable testosterone increased from 99 ± 31 to 207 ± 65 ng/dl in group 1 and from 115 ± 37 to 178 ± 55 ng/dl in group 2 (P < 0.001 vs. placebo for both groups and P = 0.054 group 1 vs. group 2). Total testosterone levels increased from 343 ± 61 to 572 ± 139 ng/dl in group 1 and from 397 ± 106 to 520 ± 91 ng/dl in group 2 (P < 0.001 vs. placebo for both groups and P = 0.012 group 1 vs. group 2). Serum estradiol levels decreased from 26 ± 8 to 17 ± 6 pg/ml in group 1 and from 27 ± 8 to 17 ± 5 pg/ml in group 2 (P < 0.001 vs. placebo for both groups and P = NS group 1 vs. group 2). Serum LH levels increased from 5.1 ± 4.8 to 7.9 ± 6.5 U/liter and from 4.1 ± 1.6 to 7.2 ± 2.8 U/liter in groups 1 and 2, respectively (P = 0.007 group 1 vs. placebo, P = 0.003 group 2 vs. placebo, and P = NS group 1 vs. group 2). Scores for hematocrit, MOS Short-Form Health Survey, International Index of Erectile Function, and American Urological Association Symptom Index Score did not change. Serum prostate-specific antigen levels increased in group 2 only (1.7 ± 1.0 to 2.2 ± 1.5 ng/ml, P = 0.031, compared with placebo). These data demonstrate that aromatase inhibition increases serum bioavailable and total testosterone levels to the youthful normal range in older men with mild hypogonadism. Serum estradiol levels decrease modestly but remain within the normal male range. The physiological consequences of these changes remain to be determined. This work was supported by National Institutes of Health Grant K23-RR16310 (to B.Z.L.), the Massachusetts General Hospital Clinical Research Center grant (RR-1066), and AstraZeneca Pharmaceuticals. Current address for S.D.R.: Glaxo Kline Pharmaceuticals, Collegeville, Pennsylvania. Current address for J.G.: Eximias Pharmaceuticals, Berwyn, Pennsylvania. Abbreviations: DHT, Dihydrotestosterone; PSA, prostate-specific antigen. 1: J Urol. 2002 Feb;167(2 Pt 1):624-9. Related Articles, Links Comment in: * J Urol. 2002 Oct;168(4 Pt 1):1509. Aromatase inhibitors for male infertility. Raman JD, Schlegel PN. Department of Urology, Buchanan Brady Urology Foundation, Center for Male Reproductive Medicine and Microsurgery, New York Presbyterian Hospital, Weill Medical College of Cornell University, New York, New York, USA. PURPOSE: Testosterone-to-estradiol ratio levels in infertile men improve during treatment with the aromatase inhibitor, testolactone, and resulting changes in semen parameters. We evaluated the effect of anastrozole, a more selective aromatase inhibitor, on the hormonal and semen profiles of infertile men with abnormal baseline testosterone-to-estradiol ratios. MATERIALS AND METHODS: A total of 140 subfertile men with abnormal testosterone-to-estradiol ratios were treated with 100 to 200 mg. testolactone daily or 1 mg. anastrozole daily. Changes in testosterone, estradiol, testosterone-to-estradiol ratios and semen parameters were evaluated during therapy. The effect of obesity, diagnosis of the Klinefelter syndrome, and presence of varicocele and/or history of varicocele repair on treatment results was studied. RESULTS: Men treated with testolactone had an increase in testosterone-to-estradiol ratios during therapy (mean plus or minus standard error of the mean 5.3 +/- 0.2 versus 12.4 +/- 1.1, p <0.001). This change was confirmed in subgroups of men with the Klinefelter syndrome, a history of varicocele repair and those with varicocele. A total of 12 oligospermic men had semen analysis before and during testolactone treatment with an increase in sperm concentration (5.5 versus 11.2 million sperm per ml., p <0.01), motility (14.7% versus 21.0%, p <0.05), morphology (6.5% versus 12.8%, p = 0.05), and motility index (606.3 versus 1685.2 million motile sperm per ejaculate, respectively, p <0.05) appreciated. During anastrozole treatment, similar changes in the testosterone-to-estradiol ratios were seen (7.2 +/- 0.3 versus 18.1 +/- 1.0, respectively, p <0.001). This improvement of hormonal parameters was noted for all subgroups except those patients with the Klinefelter syndrome. A total of 25 oligospermic men with semen analysis before and during anastrozole treatment had an increase in semen volume (2.9 versus 3.5 ml., p <0.05), sperm concentration (5.5 versus 15.6 million sperm per ml., p <0.001) and motility index (832.8 versus 2930.8 million motile sperm per ejaculate, respectively, p <0.005). These changes were similar to those observed in men treated with testolactone. No significant difference in serum testosterone levels during treatment with testolactone and anastrozole was observed. However, the anastrozole treatment group did have a statistically better improvement of serum estradiol concentration and testosterone-to-estradiol ratios (p <0.001). CONCLUSIONS: Men who are infertile with a low serum testosterone-to-estradiol ratio can be treated with an aromatase inhibitor. With treatment, an increase in testosterone-to-estradiol ratio occurred in association with increased semen parameters. Anastrozole and testolactone have similar effects on hormonal profiles and semen analysis. Anastrazole appears to be at least as effective as testolactone for treating men with abnormal testosterone-to-estradiol ratios, except for the subset with the Klinefelter syndrome, who appeared to be more effectively treated with testolactone. PMID: 11792932 [PubMed - indexed for MEDLINE] The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 9 3027-3035 Copyright © 2000 by The Endocrine Society From the Clinical Research Centers Aromatase Inhibition in the Human Male Reveals a Hypothalamic Site of Estrogen Feedback1 Frances J. , B. Seminara, Suzzunne DeCruz, A. Boepple and F. Crowley, Jr. Reproductive Endocrine Unit of the Department of Medicine and National Center for Infertility Research, Massachusetts General Hospital, Boston, Massachusetts 02114 Address correspondence and requests for reprints to: Frances , MB, MRCPI, Reproductive Endocrine Unit and National Center for Infertility Research, Massachusetts General Hospital, Fruit Street, Boston, Massachusetts 02114. E-mail: hayes.frances@.... Abstract The preponderance of evidence states that, in adult men, estradiol (E2) inhibits LH secretion by decreasing pulse amplitude and responsiveness to GnRH consistent with a pituitary site of action. However, this conclusion is based on studies that employed pharmacologic doses of sex steroids, used nonselective aromatase inhibitors, and/or were performed in normal (NL) men, a model in which endogenous counterregulatory adaptations to physiologic perturbations confound interpretation of the results. In addition, studies in which estrogen antagonists were administered to NL men demonstrated an increase in LH pulse frequency, suggesting a potential additional hypothalamic site of E2 feedback. To reconcile these conflicting data, we used a selective aromatase inhibitor, anastrozole, to examine the impact of E2 suppression on the hypothalamic-pituitary axis in the male. Parallel studies of NL men and men with idiopathic hypogonadotropic hypogonadism (IHH), whose pituitary-gonadal axis had been normalized with long-term GnRH therapy, were performed to permit precise localization of the site of E2 feedback. In this so-called tandem model, a hypothalamic site of action of sex steroids can thus be inferred whenever there is a difference in the gonadotropin responses of NL and IHH men to alterations in their sex steroid milieu. A selective GnRH antagonist was also used to provide a semiquantitative estimate of endogenous GnRH secretion before and after E2 suppression. Fourteen NL men and seven IHH men were studied. In Exp 1, nine NL and seven IHH men received anastrozole (10 mg/day po x 7 days). Blood samples were drawn daily between 0800 and 1000 h in the NL men and immediately before a GnRH bolus dose in the IHH men. In Exp 2, blood was drawn (every 10 min x 12 h) from nine NL men at baseline and on day 7 of anastrozole. In a subset of five NL men, 5 µg/kg of the Nal-Glu GnRH antagonist was administered on completion of frequent blood sampling, then sampling continued every 20 min for a further 8 h. Anastrozole suppressed E2 equivalently in the NL (136 ± 10 to 52 ± 2 pmol/L, P < 0.005) and IHH men (118 ± 23 to 60 ± 5 pmol/L, P < 0.005). Testosterone levels rose significantly (P < 0.005), with a mean increase of 53 ± 6% in NL vs. 56 ± 7% in IHH men. Despite these similar changes in sex steroids, the increase in gonadotropins was greater in NL than in IHH men (100 ± 9 vs. 58 ± 6% for LH, P = 0.07; and 85 ± 6 vs. 41 ± 4% for FSH, P < 0.002). Frequent sampling studies in the NL men demonstrated that this rise in mean LH levels, after aromatase blockade, reflected an increase in both LH pulse frequency (10.2 ± 0.9 to 14.0 ± 1.0 pulses/24 h, P < 0.05) and pulse amplitude (5.7 ± 0.7 to 8.4 ± 0.7 IU/L, P < 0.001). Percent LH inhibition after acute GnRH receptor blockade was similar at baseline and after E2 suppression (69.2 ± 2.4 vs. 70 ± 1.9%), suggesting that there was no change in the quantity of endogenous GnRH secreted. From these data, we conclude that in the human male, estrogen has dual sites of negative feedback, acting at the hypothalamus to decrease GnRH pulse frequency and at the pituitary to decrease responsiveness to GnRH. Published online ahead of print October 13, 2004, 10.1210/jc.2004-0834 This Article Full Text Full Text (PDF) All Versions of this Article: 90/1/211 most recent jc.2004-0834v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission PubMed PubMed Citation Articles by Veldhuis, J. D. Articles by Iranmanesh, A. Related Collections Male Endocrinology The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 1 211-218 Copyright © 2005 by The Endocrine Society Short-Term Aromatase-Enzyme Blockade Unmasks Impaired Feedback Adaptations in Luteinizing Hormone and Testosterone Secretion in Older Men Johannes D. Veldhuis and Ali Iranmanesh Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Medical and Graduate Schools of Medicine, General Clinical Research Center, Mayo Clinic, Rochester, Minnesota 55905; and Endocrine Section, Medical Service, Salem Veterans Affairs Medical Center, Salem, Virginia 24153 Address all correspondence and requests for reprints to: Johannes D. Veldhuis, Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Medical and Graduate Schools of Medicine, General Clinical Research Center, Mayo Clinic, Rochester, Minnesota 55905. E-mail: veldhuis.johannes@.... The mechanisms subserving hypoandrogenemia and relative hypogonadotropism in older men are not known. The present study tests the clinical hypothesis that aging impairs hypothalamopituitary adaptations to feedback withdrawal induced by antagonism of estrogen biosynthesis. To this end, we appraised gonadal axis responses to estrogen depletion induced by anastrozole (a potent and selective aromatase inhibitor) in nine older and 11 young men vs. placebo in 17 other older and eight young men. The study design comprised a prospectively randomized, double-blind, parallel-cohort intervention. To monitor LH release, blood was sampled every 10 min for 24 h; LH concentrations were assayed by two-site monoclonal immunoradiometric assay; pulsatile LH release quantitated by a model-free discrete peak-detection technique (Cluster); feedback-dependent orderliness of LH secretion via the approximate entropy statistic; and 24-h rhythmicity of LH concentrations by cosine analysis. At baseline, older men had comparable estradiol and testosterone but lower LH concentrations than young controls. Exposure to anastrozole reduced (24-h pooled) serum estradiol concentrations by 50% (P < 0.001) and elevated mean LH concentrations by 2.1-fold (P < 0.001) in both the young and older cohorts. However, older men failed to achieve young adult augmentation of the following: 1) total testosterone concentrations (P < 0.01) or molar testosterone to SHBG ratios (P < 0.01); 2) incremental LH pulse amplitude (P < 0.001) and LH peak area (P < 0.01); 3) mean LH pulse frequency (P = 0.0044); and 4) quantifiable irregularity (approximate entropy) of LH release patterns (P < 0.001). FSH concentrations became comparable in the two age cohorts. In summary, administration of a potent and selective aromatase antagonist reduces estradiol and elevates mean LH concentrations equivalently in young and older men. The low estrogen-feedback state in elderly men unmasks diminished incremental LH pulse amplitude and area; absence of further acceleration of LH pulse frequency; impaired regulation of the orderliness of LH release; and reduced testosterone to SHBG ratios. Thus, aging alters expected hypothalamopituitary-gonadal adaptations to short-term partial estrogen depletion in healthy men. ________________ I am human; nothing in humanity is alien to me. Terence Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 27, 2006 Report Share Posted June 27, 2006 On Tue, 27 Jun 2006 11:06:43 -0700 (PDT), you wrote: > >Wow Retro you out did you self on this one were have you been. > Thanks hell this info helped me. > Phil Thanks. I've been doing well, and I've been busy so not reading or posting much. But these sort of things catch my eye. I'm struggling a bit with E2 myself but for good reasons. I did my 50 year checkup and saw some metabolic syndrome results and that set me about loosing weight, exercising etc. A bit of pre-diabetic stuff made me look at how much sugar I eat. I found even the " healthy " things I ate were packed with sugar. my yogurt had 5 teaspoons of sugar in a cup!. I cut out all the cookies, cereals and sugar foods and went sort of Atkin on cheese, salami, etc, and dropped over 10 pounds with no real restrictions on how much I eat. ( I had seen some program with an interview of a diet doctor and he was urging cutting sugars, and the interviewer said 'and fats too right? " He said someone who eats a tablespoon of olive oil or margarine is not going to be hungry any time soon, so he didn't worry about fats as long as they weren't transfats. Boy it worked for me. But with the continuing weight loss I have very little fat, so I'm suspecting very little aromotase. So readjusting is a bit of a challenge. It takes weeks for the e2 to climb and it comes down quickly with very little arimidex. But I'm getting there. ________________ I am human; nothing in humanity is alien to me. Terence Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 27, 2006 Report Share Posted June 27, 2006 Thats great sounds like all is going well E2 will always be a problem I just stopped use my Arimidex for a week was going to low yet I have been down as low as 13 and still felt good. My E2 is best at 20 as for the post about the rebound effect never have seen anything yet that states this. And I feel if there is anything on this it is not about men on TRT. Stay Well Phil retrogrouch@... wrote: On Tue, 27 Jun 2006 11:06:43 -0700 (PDT), you wrote: > >Wow Retro you out did you self on this one were have you been. > Thanks hell this info helped me. > Phil Thanks. I've been doing well, and I've been busy so not reading or posting much. But these sort of things catch my eye. I'm struggling a bit with E2 myself but for good reasons. I did my 50 year checkup and saw some metabolic syndrome results and that set me about loosing weight, exercising etc. A bit of pre-diabetic stuff made me look at how much sugar I eat. I found even the " healthy " things I ate were packed with sugar. my yogurt had 5 teaspoons of sugar in a cup!. I cut out all the cookies, cereals and sugar foods and went sort of Atkin on cheese, salami, etc, and dropped over 10 pounds with no real restrictions on how much I eat. ( I had seen some program with an interview of a diet doctor and he was urging cutting sugars, and the interviewer said 'and fats too right? " He said someone who eats a tablespoon of olive oil or margarine is not going to be hungry any time soon, so he didn't worry about fats as long as they weren't transfats. Boy it worked for me. But with the continuing weight loss I have very little fat, so I'm suspecting very little aromotase. So readjusting is a bit of a challenge. It takes weeks for the e2 to climb and it comes down quickly with very little arimidex. But I'm getting there. ________________ I am human; nothing in humanity is alien to me. Terence Quote Link to comment Share on other sites More sharing options...
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