Jan's BloodTest April13/2007

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  1. I wouldn't sweat the aldosterone reading.

    Unless I see low aldo confirmed by urinary analysis I don't buy much into it.

    Your DHEA and Preg both went down.

    Want to bet that your TT is sky high right now, way above the 4 something range it was before?

    This is common for other androgenic hormones to crash when exogenous T is administered. By knowing that, Im betting 10 -1 your shots are working.

    Im not a fan of oral DHEA.

    Get some Dermacrine JansZ. I think they have a superior delivery system than the usual preg compounded cream you get from a script, plus the added bonus of DHEA transdermal. Start at half dose. Plus added resveratrol and benzoflavone 7,8 in it.

    Where do you get resveratrol( you netioned 200mg a day) LEF is way to expensive. Check my "resveratrol really cheap" post, I like revegentics for pure RSV, the X500, VERY cheap.


  2. Ok, so I have my blood test result from 8/30/07 blood draw.
    They shorted me on
    Testosterone, Free, Bio/Total (LC/MS/MS)
    Dihydrotestosterone, Free, Serum (36168X)
    so next script is on a way and I will have to get poked again.

    There is two Estrodial results, from description I thought that both were ultrasensitive, but I got different results.
    I am going with the one that comes with FreeE2
    My freeE2 is high, (but my pines is working ok).
    I am incresing Liquidex from 0.5 to 0.6cc E3D
    so my weekly dose is now
    0.6*7/3=1.4cc/week
    increase from
    0.5*7/3=1.17cc/week

    my Fibrinogen=424(175-425)
    LEF wants (180-250)
    I asked doc for TRENTAL®
    (pentoxifylline)
    Tablets, 400 mg
    1 or 2 tablets daily
    will see what comes out of this request

    FreeT3 freeT4
    9/16/07 I upped Armour from 3grains to 3.5
    also asked for script for Synthroid 25mcg, I will use 1pill/day.

    9/20/07 Changed back to 3grains plus 2pills Synthroid 25mcg.
    Hopefuly my body can convert some T4-->T3 and I raise both FreeT4 and FreeT3
    will be watching pulse and temps.
    ---------
    Pregnenolone/DHEA

    I upped preg cream from one to 2grams/day
    Started on DHEA, 100mg/day

    ----------------------------
    Genova Diagnostics
    EstroEssence
    and

    Metabolic Analysis Profile and Cellular Energy Profile
    out for testing
    Monday Oct1/2007

    ============================== ============================== ============
    Oct1/2007
    finaly received testosterone results (after second poking), they still omitted DHT.
    .
    68 Testosterone, Free, Bio/Total (LC/MS/MS) Quest Diagnostics: Test Menu
    69 /------------------------------------ 1151 (250-1100) ng/dL Testosterone Total
    70 /------------------------------------ 248.5 (46-224) pg/mL Testosterone Free
    71 /------------------------------------ 456.9 (110-575) ng/dL Testosterone Bioavailable
    72 /------------------------------------ 26 (17-54) nmol/L SHBG
    73 /------------------------------------ 4.0 (3.6-5.1) g/dL Albumin, serum
    74 Dihydrotestosterone, Free, Serum (36168X) --------- Quest Diagnostics: Test Menu
    75 /------------------------------------ 69 (25-75 ) ng/dL Dihydrotestosterone
    76 /------------------------------------ 7.52 (1.00-6.20) pg/mL Dihydrotestosterone, FREE
    77 /------------------------------------ 1.09% (0.62-1.10) % Dihydrotestosterone, FREE %




    ------
    My goal
    FreeT~300, =(248.5-46)/(300-46)=0.7972 (dose is short 20%)
    BAT~575 (top range), =(456.9-110)/(575-110)=0.7460 (dose is short 25%)

    730 740 750 760 770 780 790 800 810 820 830 840 850 860 870 880 890 900 910
    449 454 459 463 468 473 477 482 487 491 496 501 505 510 515 519 524 529 533

    920 930 940 950 960 970 980 990 1000 101 102 103 104 105 106 107 108 109 110
    538 542 547 552 556 561 566 570 575.0 580 584 589 594 598 603 608 612 617 622



    I am still short on both
    The test represents my Depo-Tshots=30units at E3D schedule.
    My new dose should be around
    =30/0.75=40units=186.7mg/week
    =30/0.8=37.5units=175mg/week
    conservatively I make my new dose =38units=177.3mg/week
    ------
    Note1, using dr Shippen chart my FreeT=325pg/mL
    Note2, using (totally unreliable BAT)(but FreeT sort of close)
    Free & Bioavailable Testosterone calculator

    FreeT=343 pg/mL
    BAT=750ng/dL
    .
    Note3, the 31GA 5/16"long leaked out little bit of oil, changed (over month ago) to 30Ga 1/2"Long
    .
    .
    .............................. .............................. .................


    they have Novarel.
    No Novarel
    -----------------------------------------------------------------------
    Note, nov9/07
    For a while I have changed Novarel from 500iu on the day of T shots to 250iu on both days between T shot.
    My testicles are little firmer, scrotum hangs low more often.
    Since now I am doing shots every day, I decided to do T shots E2D and 250iu in beween.
    Testosterone was 38units now 38/3*2=25.33~ 25.5units
    38*7/3=


    my weekly dose is:
    =0.255*200*7/2=178.5mg/week

    my old weekly dose, the one corresponding to current test results was 0.3*7/3*200=140
    I expect that my BAT should raise to 456.9*178.5/140=583
    actually even more because blood was drawn on third day, but now it will be drawn on second day after T shot.

    Liquidex on days of T shot, 0.6/3*2=0.4cc
    Dec6/07
    Started Anastrozole from ChemOne Research it is sweet and do not sting, wonder if will work.
    Dark in color, hard to see numbers on syringe.
    Some morning wood problems, decreasing dose to 0.36=36units
    0.36*7/2=1.295cc/week Arimidex pills/week
    Dec20/07
    EstroEssence from Dec13/07 shows low urine E2
    Change Anastrozole to 0.33*7/2=1.155cc/week

    Feb29/08
    Stopped DualAction, BreastFormula, MiraForte
    Started 2 scoops DIM-Powder
    Change Anastrozole to =0.38*7/2=1.33cc/week
    Piston on my 3/10cc syringe is 6 units high, top of piston is at 38+6=44
    Mar15/08 Anastrozole 45units (45+6=51) .45*7/2=1.575

    --------------------------------------------------------------------------------)



    My E2 story


    See erection weakness.
    Blood drawn 3/19/08, reported 3/31/2008
    DHT=81(25-75)
    E2=4(< or =29)
    E2, Free=.07(< or = 0.45)
    E2,%Free=1.82(1.25 - 1.85)

    Stopped Anastrozole, 3/31/08
    ---
    Pines worked best while in Atlantic City (May 25/08)
    ---
    See erection weakness
    Blood drawn 5/23/08, reported 6/4/08 (instead of 48 hrs, had to draw 24 hrs after T shot, so the TT values are little higher)

    E2D schedule, T=25.5units=178.5mg/week, HCG=500iu
    No Anastrozole since 3/31/08

    TT=1117(250-1100)
    BAT=584.6(46-575)
    FreeT=303.5(46-224)
    SHBG=18
    Albumin=4.2
    DHT=77(25-75)
    E2=39(< or =29)
    E2, Free=1.07(< or = 0.45)
    E2,%Free=2.73(1.25 - 1.85)
    Note:
    See erection weakness, but week ago was still strong.
    Most likely I feel best at E2=29
    June 10/08, restarted Anastrozole
    0.25cc/E2D=0.25*7/2=0.875/week
    about June 15 changed to 0.25cc every day

    June 26/08 first night with strong nightly wood.
    (today is my HCG day, no Anastrozole until second T shot)
    =================

    8/02/08
    Estradiol, Ultrasensitive, LMMSMS=15(<29pg/mL)
    I was using Anastrozole(liquid) before this test, now stopped completely.
    ===============

    1/6/2009
    For no particular reason I decided to change from 25units to 0.22cc=22units each T-shot.
    Mostly because my last SHBG was going down, also I am on 2 ejaculations a week, down from three.

    I plan next blood test end of Feb may be March depending how I feel.
    If I extend to April then will do long test.

    Experiments with glucose/insuline, vegetable juicing, heavy duty probiotics, enzymes, pre-biotics, chlorella,
    result with 1.5 weeks of liquid stool.
    Suspect mostly because of chlorella and change in vitC.
    Previously vitC from NowFoods now changed to LEF brand.
    LEF brand may be the real thing, 3grams/day, 2 morning, 1 evening.
    My list od supplements is now much shorter, very basic, this is in preparation for SpectraCell5000 test.
    Experiments with NutrEval indicate tremendous variations between tests.
    Hopefully will have better luck with following SpectraCell5000.

    (Loose/liquid stool) If not the above, then may be it is a comeback of lactose intolerance, as it was 2005/2006.




    ----------------------------------------------------------------------------------------------------



    Discussion with colkurtz_spf about hcg level.
    HCG not restoring ball size.
    .
    I am going back to 31ga 5/16"long needle 3/10cc
    the dose will fit in that small volume syringe
    Any leaking is small any how, 30ga 1/2"long needle also leaked sometime
    minimizing scar tissue is more important to me.
    .
    -----------------------------------------------------------------
    Located study:
    Low-Dose Human Chorionic Gonadotropin Maintains
    Intratesticular Testosterone in Normal Men with
    Testosterone-Induced Gonadotropin Suppression
    http://calendar.hsl.washington.edu/d...Dose_Human.pdf

    Study shown that:
    125, 250, or 500 IU hCG every other day

    Posttreatment
    ITT was 25% less than baseline in the 125 IU hCG group,
    7% less than baseline in the 250 IU hCG group, and
    26% greater than baseline in the 500 IU hCG group.
    ---------------------------
    I am changing my HCG dose to 110%
    my new dose of HCG=380IU=19units I dissolve hcg in 5mL Bwater.
    today 11/30/2007
    ============================== =================
    Pregnyl® 1500IU - X-PIL
    Pregnyl® 1500 I.U.
    Pregnyl comes as 2 ml ampoules of dry white powder with 1 ml ampoule of solvent.
    ============================== =================
    Pregnyl® 5000IU - X-PIL
    Pregnyl® 5000 I.U.
    Pregnyl comes as 2 ml ampoules of dry white powder with 1 ml ampoule of solvent. That is very little amount of solvent, reason not to buy it.
    ============================== =================
    Low-Dose Human Chorionic Gonadotropin Maintains Intratesticular Testosterone in Normal Men with Testosterone-Induced Gonadotropin Suppression -- Coviello et al. 90 (5): 2595 -- Journal of Clinical Endocrinology & Metabolism
    Low-Dose Human Chorionic Gonadotropin Maintains
    Intratesticular Testosterone in Normal Men with
    Testosterone-Induced Gonadotropin Suppression
    © 2005

    ============================== =========================

    ADDED 10/12/2010

    http://mus clechatroom.com/forum/showpost.php?p=115322&postcoun t=85
    Serum 17-hydroxyprogesterone strongly correlates w... [Fertil Steril. 2008] - PubMed result
    Fertil Steril. 2008 Feb;89(2):380-6. Epub 2007 Apr 26.
    ============================== ==================

    One way to use this report:
    proper levels of
    17-hydroxyprogesterone (17OH-P)
    can be manipulated by use of
    pregnenolone (first)
    and
    HCG injections (second)

    also
    measurements of 17-hydroxyprogesterone
    may tell us if we are using enough HCG.

    ////////////

    RESULT(S): With T administration alone, serum 17OH-P decreased significantly and increased significantly when 500 IU hCG was administered. End-of-treatment ITT strongly correlated with serum 17OH-P. Moreover, serum 17OH-P, but not androstenedione or DHEA, was independently associated with end-of-treatment ITT by multivariate linear regression.

    CONCLUSION(S): Serum 17OH-P is highly correlated with ITT in gonadotropin-suppressed normal men receiving T and stimulated with hCG. Serum 17OH-P is a surrogate biomarker of ITT and may be useful in research and in men receiving gonadotropin therapy for infertility.

    ////

    Group 3 (250iu)
    start-ITT=1239nmol/L
    end-ITT=1037nmol/L
    start-17-hydroxyprogesterone=4.9nmol/L
    end-17-hydroxyprogesterone=4.9nmol/L
    start-Androstenedione=6.4 (nmol/L)
    end-Androstenedione=6.6 (nmol/L)

    Group 4 (500iu)
    start-ITT=1227nmol/L
    end-ITT=1470nmol/L
    start-17-hydroxyprogesterone=4.6nmol/L
    end-17-hydroxyprogesterone=7.8nmol/L
    start-Androstenedione=6.5 (nmol/L)
    end-Androstenedione=9.5 (nmol/L)

    using Group 3 only to raise ITT to original levels requires HCG dose 250*1239/1037=299iu
    using Group 4 only to raise ITT to original levels requires HCG dose 500*1227/1470=417iu
    average(299,417)=358iu

    expect 17-hydroxyprogesterone to be at=6.3+(7.8-6.3)*(358-250)/(500-250)=6.9(nmol/L)=227.72 ng/dL

    expect Androstenedione to be at=8.4+(9.5-8.4)*(358-250)/(500-250)=8.9(nmol/L)=25.50 ng/dL












    3/16/2013


    HCG - 1000IU too much? - Page 2
    ----------------------------

    UPDATE: Very Low-Dose hCG & Intratesticular Testosterone

    UPDATE: Very Low-Dose hCG & Intratesticular Testosterone

    by Michael Scally MD





    ..........




    Serum 17-hydroxyprogesterone strongly correlat... [Fertil Steril. 2008] - PubMed - NCBI

    Serum 17-hydroxyprogesterone strongly correlates with intratesticular testosterone in gonadotropin-suppressed normal men receiving various dosages of human chorionic gonadotropin.
    Attached Images Attached Images  
    •   
       


  3. Quote Originally Posted by JanSz View Post

    my Fibrinogen=424(175-425)
    LEF wants (180-250)
    I asked doc for TRENTAL®
    (pentoxifylline)
    Tablets, 400 mg
    1 or 2 tablets daily
    will see what comes out of this request

    Curcumin is supposed to do a job on fibrinogen. Do you have any experience with it?

  4. Quote Originally Posted by cpeil2 View Post
    Curcumin is supposed to do a job on fibrinogen. Do you have any experience with it?
    I was using Curcumin for a while but then stopped, newer done blood testing.

    LEF recomends Trental. Hopefully my doc will come thru.
    I will see him in an hour. (Good doc, I am able to contact him at will, to ease up on his time, few hour ago I send e-mail with my requests ).

    Inflammation (Chronic) - Print Version : Online Reference For Health Concerns

    Ok, Synthroid 25mcg
    and
    Pentoxifylli 400mg
    are at home.

    I am at 3.5 grains of Armour, that should put my FreeT3 at the top range
    but my freeT4 will lag behind hence 1pill 25mcg/day of Synthroid.
    I newer tried, I may be one of the lucky guys who convert T4-->T3
    Latter may want to get down on Armour and boost up Synthroid.

    Looking for a formula on how to do it.
    Assuming 3.5 Grains of Armour and 25mcg Synthroid keep FreeT3 and FreeT4 on top.
    Assuming that I am able to fully convert T3--->T3 how (without blood testing) figure my theoretical T4 dose that I would need in the basence of Armour.
    ============================== ============================== =========
    Nov9/07 For about 3 weeks I am using 3x25mcg Levothyroxin and 3Grains Armour divided in half.

    Normally I do not use Cortef but if I feel little down, and have dancing or gym ahead, I take one 5mg Cortef 2-3 hours before, sometimes another Cortef before I start dancing and feel much better and have better stamina.

  5. Quote Originally Posted by JanSz View Post

    What is the cheapest injectible fertility drug you can buy in the US?
    Question:
    What is the cheapest injectible fertility drug you can buy in the US? I have heard of quite a few different injectible drugs you can use (i.e., Pergonal, HMG, Humegon, etc) and want to know if there is a drug that is cheaper than the others and also is it effective?
    I recognize most of the drugs listed here as female fertility drugs. Do they also work to increase fertility in males?
    •   
       


  6. HCG works like LH (Luteinizing Hormone). LH in men controls testosterone release.

    HMG works like FSH (Follicular Stimulating Hormone). FSH in men triggers sperm production.

    There's less difference between male and female systems than you might think!

    Mark

  7. Quote Originally Posted by MarkLA View Post
    HCG works like LH (Luteinizing Hormone). LH in men controls testosterone release.

    HMG works like FSH (Follicular Stimulating Hormone). FSH in men triggers sperm production.

    There's less difference between male and female systems than you might think!
    That's very interesting. Which one does Clomid work on, FSH, right? My doctor says that boosting my clomid won't have any effect but I'm not sure about that.

    It sounds like what I need is the hCG, which is an IM injection, correct?

  8. Quote Originally Posted by hardasnails1973 View Post
    Jansz your going taking 3 steps backwards and one forward.
    what is dosage of testosterone you are taking every 3 days?
    The dosages you are doing are crossing the benefit/risk ratio of TRT and are headed into steroid usage which will only put stress on entire endocrine system and will feel good for 2-3 weeks untill your testosterone and estrogen receptors are over loaded and then you will crash. Been there did that done that. Your adrenals are already stress and adjusting your testosterone dosge to 800-900 on blood test on second day after the injection will give you a good average. Your e2 and DHT are going to go out the roof and like Dr Shippen told me using another drug inorder to offset side effects to push above the numbers all the way to high end is fuked up.

    Think of it this way
    bypossible swtiching over to hcg +injections and keeping them in upper 25% of the range you will lower dht and e2 which will reduce the need for finisterde and armidex. More is not better Bro and personally you are going to end up causing major cardiovascaular problems in the future tinkering around with those dosages. Go 42.5 mgs every 3 days with 250 ius retest in 4 weeks then increase if not into target range

    hardasnails

    i was wondering if you are a dr?also wondering where you get the basis for over 800-900 t level is unsafe. not breaking stones...just trying to understand.

    bodybuilders regularly have t levels of double or triple that and when on much higher.

    do you have any links / research that support what you are saying?

    bob

  9. Jan....thanks fo the B12 info

    Hardasnails....bump on the t question

    Bob
  10. rT3 high, how to deal with it


    Use thise three Genova diagnostics tests.

    Comprehensive Thyroid Assesment
    Oxidative Stress Panel (part of NutrEval)
    Elemental Analysis, Packed Erythrocytes (RBC's)(part of NutrEval)


    Read results, follow advice given by those tests.

    So really best would be to use two tests (few extra $$ but lots of informations):
    NutrEval
    Comprehensive Thyroid Assesment
    ---------------------------------------------------------------------------
    -------------------
    -------------------

    High rT3
    5' deiodinase (Se dependent)
    ----------------------------------------------------------
    Selenium also performs other important roles in the body.
    The most important of these is probably as its role as the body's best antioxidant (anti-peroxidant).
    It performs this role as part of glutathione peroxidase (GSHPx or GPX).

    Glutathione Peroxidase (GSH-Px)
    Glutathione peroxidase is a selenium-dependant enzyme found primarily in the cytoplasm (70%) but also in the mitochondria (30%).
    -----------------------------------------------------------------
    Genova Diagnostics' Oxidative Stress Panel
    checks Glutathione Peroxidase
    -----------------------------------------------------------------

    Interactions, (close): (iodine, selenium, zinc, copper)
    ie; at least above four have to be in proper balance
    ---------------------------------------------------------------------------------------------------
    Genova Diagnostics' Elemental Analysis, Packed Erythrocytes (RBC's)
    checks (it is missing iodine):
    TOXICS
    Antimony
    Arsenic
    Cadmium
    Lead
    Mercury
    Thallium
    Tin

    NUTRIENTS
    Chromium
    Copper
    Magnesium
    Manganese
    Potassium
    Selenium
    Vanadium
    Zinc

    ---------------------------------------------------------------------------------------------------
    If the above investigations falls short, further investigations should be made looking into:
    Interactions, (wide range)
    Ag, Co, Cr, Fe, Hg, I,Rb, Sb, Sc, Se, Zn



    -------------------------------------------------------------------------------------------------------------------------------
    http://www.ithyroid.com/iodine.htm
    While I've found research on the interactions of iodine and selenium, there are two other minerals which need to be studied for their interactions with these two: zinc and copper. I found one study which examined the complex interactions of selenium, iodine, and zinc (there are interactions), but none which have looked at all four minerals in a 4 X 4 factorial design. Now that would be an interesting study! Hopefully someone will do that soon.

    I think one lesson from studying the interactions of selenium and iodine is that the interrelationships between minerals are very complicated. Supplementing with one or two can cause further problems. You have to make sure that you correct every deficiency. Health is built from a chain of nutrients and, like a chain, health cannot be accomplished if one nutrient is missing. Sometimes it's complicated putting the chain back together without running into problems (like supplementing with either selenium or iodine, but not both), but every deficiency has to be corrected. John

  11. Blood test at Quest, blood drawn 3/19/2008
    page #1 --Comp metabolic panel
    page #2 --Hepatic function panel
    page #3 --CBC w/Diff , risk factors
    page #4 --
    page #5 -- VAP Cholesterol
    Attached Images Attached Images      

  12. Holy crap your iodine levels are off the chart.

  13. Quote Originally Posted by JanSz View Post
    Blood test at Quest, blood drawn 3/19/2008
    page #1 --Comp metabolic panel
    page #2 --Hepatic function panel
    page #3 --CBC w/Diff , risk factors
    page #4 --
    page #5 -- VAP Cholesterol
    E2 is too low, Jan, as I am sure you realize.
  14. rT3 high, how to deal with it


    rT3 high, how to deal with it


    Use thise three Genova diagnostics tests.

    Comprehensive Thyroid Assesment
    Oxidative Stress Panel (part of NutrEval)
    Elemental Analysis, Packed Erythrocytes (RBC's)(part of NutrEval)


    Read results, follow advice given by those tests.

    So really best would be to use two tests (few extra $$ but lots of informations):
    NutrEval
    Comprehensive Thyroid Assesment
    ---------------------------------------------------------------------------
    -------------------
    -------------------

    High rT3
    5' deiodinase (Se dependent)
    ----------------------------------------------------------
    Selenium also performs other important roles in the body.
    The most important of these is probably as its role as the body's best antioxidant (anti-peroxidant).
    It performs this role as part of glutathione peroxidase (GSHPx or GPX).

    Glutathione Peroxidase (GSH-Px)
    Glutathione peroxidase is a selenium-dependant enzyme found primarily in the cytoplasm (70%) but also in the mitochondria (30%).
    -----------------------------------------------------------------
    Genova Diagnostics' Oxidative Stress Panel
    checks Glutathione Peroxidase
    -----------------------------------------------------------------

    Interactions, (close): (iodine, selenium, zinc, copper)
    ie; at least above four have to be in proper balance
    ---------------------------------------------------------------------------------------------------
    Genova Diagnostics' Elemental Analysis, Packed Erythrocytes (RBC's)
    checks (it is missing iodine):
    TOXICS
    Antimony
    Arsenic
    Cadmium
    Lead
    Mercury
    Thallium
    Tin

    NUTRIENTS
    Chromium
    Copper
    Magnesium
    Manganese
    Potassium
    Selenium
    Vanadium
    Zinc

    ---------------------------------------------------------------------------------------------------
    If the above investigations falls short, further investigations should be made looking into:
    Interactions, (wide range)
    Ag, Co, Cr, Fe, Hg, I,Rb, Sb, Sc, Se, Zn



    -------------------------------------------------------------------------------------------------------------------------------
    http://www.ithyroid.com/iodine.htm
    While I've found research on the interactions of iodine and selenium, there are two other minerals which need to be studied for their interactions with these two: zinc and copper. I found one study which examined the complex interactions of selenium, iodine, and zinc (there are interactions), but none which have looked at all four minerals in a 4 X 4 factorial design. Now that would be an interesting study! Hopefully someone will do that soon.

    I think one lesson from studying the interactions of selenium and iodine is that the interrelationships between minerals are very complicated. Supplementing with one or two can cause further problems. You have to make sure that you correct every deficiency. Health is built from a chain of nutrients and, like a chain, health cannot be accomplished if one nutrient is missing. Sometimes it's complicated putting the chain back together without running into problems (like supplementing with either selenium or iodine, but not both), but every deficiency has to be corrected. John

  15. http://www.muscle_____chat_____room....hread.php?t=18

    null good starting page

    http://www.meta-ehealth.com/site/off...yclopedia&id=6

    Nutritional Influences on Estrogen Metabolism: A Summary


    Nutritional Influences on Estrogen Metabolism: A Summary
    By Douglas C. Hall, M.D.
    Estrogen affects the growth, differentiation, and function of tissues throughout the body?not just those involved in reproduction. It plays an important role in bone health, protects the cardiovascular system, and influences behavior and mood. While appropriate levels of estrogens are essential for good health, several studies conclude that as exposure to estrogen increases, the risk of several cancers, including breast, ovary, prostate, and thyroid, also increases.1-6 Furthermore, excessive estrogen exposure can lead to other health problems such as premenstrual syndrome (PMS), endometriosis, and fibrocystic or painful breasts.

    Various lifestyle and environmental factors can influence estrogen production, metabolism, and balance. These include poor diet, obesity,excess alcohol consumption, high insulin levels, medications such as hormone replacement therapy and birth control pills, overexposure to chemicals found in pesticides and industrial chemicals, and agricultural hormones in animal products consumed by humans.2,7-11 Genetics can also play an important role in determining estrogen levels.

    The Basics of Estrogen Metabolism
    "Estrogen" is a term that is used to collectively describe the female hormones estradiol, estrone, and estriol. The most potent of these is estradiol. Estrogens circulate in the body mainly bound to the sex hormone binding globulin (SHBG) and only unbound estrogens can enter cells and cause biological effects.12,13 Therefore, any change in the concentration of SHBG will alter estrogen activity by changing the availability of estrogen to the target cell.

    The ultimate biologic effect of estrogen in the body depends on how it is metabolized. The metabolism of estrogen takes place primarily in the liver through Phase I (hydroxylation) and Phase II (methylation and glucuronidation) pathways, which allow the estrogen to be detoxified and excreted from the body.

    Hydroxylation ?Hydroxylation yields three metabolites that vary greatly in biological activity: 2-hydroxyestrone (2-OH),16-OH, or 4-OH.14 The 2-OH metabolite is generally termed the "good" estrogen because it generates very weak (and therefore potentially less harmful) estrogenic activity in the body. In contrast, the 16-OH and 4-OH metabolites show persistent estrogenic activity and may promote dangerous tissue growth.14-17 In fact, women who metabolize a larger proportion of their estrogen via the 16-OH metabolite may be at significantly greater risk of developing breast cancer.1,14-16,18,19 Therefore, shifting estrogen balance toward a less estrogenic state through promotion of the 2-OH pathway may prove very beneficial in improving a variety of conditions related to elevated or imbalanced estrogen levels.

    Methylation ?The 2-OH and 4-OH estrogen metabolites are further detoxified via a process called methylation. This is an important pathway, because it renders the harmful 4-OH metabolite significantly less active. Furthermore, if they are not methylated, the 2-OH and 4-OH estrogens can be converted to highly reactive molecules that can damage DNA.16,20,21

    Glucoronidation ?In glucoronidation, a glucuronic acid group combines with an estrogen molecule to facilitate the elimination of excess estrogen from the body.12 These actions make glucoronidation one of the key Phase II liver detoxification pathways for estrogens.

    Nutritional Support of Optimum Estrogen Metabolism
    Many elements of good nutrition and diet play an important part in influencing estrogen metabolism and detoxification. Incorporating dietary changes with the addition of beneficial nutrients and herbs can profoundly affect estrogen balance and potentially reduce the risk of estrogen-dependent cancers and other hormone-related conditions.

    Diet?It has been found that dietary interventions such as increasing consumption of cruciferous vegetables like cabbage and broccoli, and foods such as soy can significantly increase the 2-hydroxylation of estrogen. Dietary fiber intake can promote the excretion of estrogen by binding estrogens in the digestive tract and also increases serum concentrations of SHBG, thus reducing levels of free estradiol.22,23 Complex carbohydrates, such as those found in vegetables and whole grains, are more effective in optimizing estrogen metabolism than simple carbohydrates, which can detrimentally raise blood glucose levels and stimulate insulin release, resulting in secondary adverse influences on sex hormone balance.8

    Phytoestrogens?These plant compounds are similar in shape to the estrogen molecule and can bind to estrogen receptors (ERs). They are much weaker than endogenous estrogens and, through competitive inhibition, have been shown to prevent the receptor binding of "stronger," more stimulating estrogens.7,24,25 Phytoestrogens are currently under extensive investigation as a potential alternative therapy for a range of conditions associated with estrogen imbalance, including menopausal symptoms, PMS, endometriosis, prevention of breast and prostate cancer, and protection against heart disease and osteoporosis.7,25-27

    The two main classes of phytoestrogens are isoflavones and lignans. Soy is perhaps the most common food source of isoflavones, but other excellent sources include legumes, clover, and kudzu root. Higher intakes of soy products and isoflavones, such as consumed in traditional Japanese diets, are associated with low rates of hormone-dependent cancers.28 Lignans are compounds are found in fiber-rich foods such as flaxseed and other oil seeds, whole grains, legumes, and vegetables.29,30 Lignans stimulate the production of SHBG in the liver, and therefore reduce the levels of free estrogen in circulation. They also inhibit aromatase, an enzyme that synthesizes estrogen.

    Vitamin E and Magnesium?Low serum vitamin E is associated with elevated estrogen levels, and may negatively affect estrogen detoxification. Women with PMS have experienced improvements of their symptoms when given supplemental vitamin E.31 Magnesium promotes estrogen detoxification by promoting methylation and glucuronidation, key estrogen detoxification pathways. Ovarian hormones influence magnesium levels, triggering decreases at certain times during the menstrual cycle as well as altering the calcium to magnesium ratio. These cyclical changes can produce many of the well-known symptoms of PMS in women who are deficient in magnesium and/or calcium.32

    Indole-3-Carbinol (I3C)?I3C is a naturally occurring compound derived from cruciferous vegetables such as broccoli, Brussels sprouts, and cabbage that actively promotes the breakdown of estrogen via the beneficial 2-OH pathway.14,33-35 Therefore, I3C is protective to estrogen-sensitive tissues and may be beneficial to those with health issues related to excessive estrogen. Not only does I3C promote healthier estrogen metabolism, but it may also act as a "weak" or anti-estrogen in a similar fashion to isoflavones.36

    B Vitamins?Folate and vitamins B6 and B12 function as important cofactors for enzymes involved in estrogen detoxification; thus, decreased levels of B vitamins can lead to increased levels of circulating estrogens. Certain B vitamins also have the potential to modulate the biological effects of estrogen by decreasing the cell's response when estrogen binds to the ER.37 B vitamins also play a role in the prevention of cancer because they are important for DNA synthesis and repair.

    Calcium D-Glucarate?Calcium D-glucarate is a natural compound found in foods that appears to have some influence on breast cancer by aiding in detoxification and the regulation of estrogen.38,39 It has been found in animal models to lower estradiol levels and inhibit the initiation, promotion, and progression of cancer.38

    Other Beneficial Phytonutrients and Herbs
    Many other naturally occurring compounds derived from a variety of plant sources are available that promote healthy estrogen metabolism. These include curcumin, a compound found in the herb turmeric (Curcuma longa) that increases the phase II detoxification of catechol estrogens;40,41 chrysin, a bioflavonoid that inhibits aromatase activity, thus reducing the synthesis of estrogen activity;42 the herb, rosemary, which promotes the formation of the 2-OH estrogen metabolite;43 and D-limonene from citrus fruits, which promotes the detoxification of estrogen and shows promise in the prevention and treatment of breast and other cancers.44,45 Furthermore, many antioxidant nutrients and phytonutrients can reduce the oxidation of the 2-OH and 4-OH estrogen metabolites. Notable nutrients in this group include vitamin C, N-acetylcysteine, the mineral selenium, and green tea.

    In addition, traditional societies have long relied on a variety of hormone-modulating herbs in treating women's health conditions. These include black cohosh, chasteberry, ginseng, dong quai, and licorice. The mechanism of action of these herbs varies; however, many have been found to contain beneficial phytoestrogens.

    References
    Bolton JL, Pisha E, Zhang F, et al. Role of quinoids in estrogen carcinogenesis. Chem Res Toxicol 1998;11:1113-27.
    Colditz GA. Relationship between estrogen levels, use of hormone replacement therapy, and breast cancer. J Natl Cancer Inst 1998;90(11):814-23.
    Thomas HV, Reeves GK, Key TJ. Endogenous estrogen and postmenopausal breast cancer: a quantitative review. Cancer Causes Control 1997;8(6):922-28.
    Rose PG. Endometrial carcinoma. New Eng J Med 1996;335(9):640-49.
    Hankinson SE, Willett WC, Manson JE, et al. Plasma sex steroid hormone levels and risk of breast cancer in postmenopausal women. J Natl Cancer Inst 1998;90(17):1292-99.
    Zanetta GM, Webb MJ, Li H, et al. Hyperestrogenism: A relevant risk factor for the development of cancer from endometriosis. Gynecol Oncol 2000 Oct;79(1):18-22.
    Kuiper GG, Lemmen JG, Carlsson B, et al. Interaction of estrogenic chemicals and phytoestrogens with estrogen receptor & beta. Endocrinology 1998;139(10):4252-63.
    Kaaks R. Nutrition, hormones, and breast cancer: Is insulin the missing link? Cancer Causes Control 1996;7:605-25.
    Snedeker SM, Diaugustine RP. Hormonal and environmental factors affecting cell proliferation and neoplasia in the mammary gland. Prog Clin Biol Res 1996;394:211-53.
    Fan S, Meng Q, Gao B, et al. Alcohol stimulates estrogen receptor signaling in human breast cancer cell lines. Cancer Res 2000;60(20):5635-39.
    Steingraber S. Living Downstream. Reading (MA): Addison-Wesley; 1997:248-51.
    Murray RK, Granner DK, Mayes PA, et al. Harper's Biochemistry. 24th ed. Stamford (CT): Appleton & Lange; 1996.
    Guyton AC. Textbook of Medical Physiology. 8th ed. Philadelphia: WB Saunders; 1991.
    Bradlow HL, Telang NT, Sepkovic DW, et al. 2-Hydroxyestrone: the 'good' estrogen. J Endocrin 1996;150:S259-S65.
    Muti P, Bradlow HL, Micheli A, et al. Estrogen metabolism and risk of breast cancer: a prospective study of the 2:16-hydroxyestrone ratio in premenopausal and postmenopausal women. Epidemiology 2000;11(6):635-40.
    Yager JD, Liehr JG. Molecular mechanisms of estrogen carcinogenesis. Annu Rev Pharmacol Toxicol 1996;36:203-32.
    Westerlind KC, Gibson KJ, Malone P, et al. Differential effects of estrogen metabolites on bone and reproductive tissues of ovarectomized rats. J Bone Miner Res 1998;13(6):1023-31.
    Meilahn EN, De Stavola B, Allen DS, et al. Do urinary oestrogen metabolites predict breast cancer? Guernsey III cohort follow-up. Br J Cancer 1998;78:1250-55.
    Fishman J, Osborne MP, Telang NT. The role of estrogen in mammary carcinogenesis. Ann N Y Acad Sci 1995;768:91-100.
    Zhu BT, Conney AH. Is 2-methoxyestradiol an endogenous estrogen metabolite that inhibits mammary carcinogenesis? Cancer Res 1998;58:2269-77.
    Butterworth M, Lau SS, Monks TJ. 17-beta-estradiol metabolism by hamster hepatic microsomes. Implications for the catechol-O-methyl transferase-mediated detoxication of catechol estrogens. Drug Metab Dispos 1996;24(5):588-94.
    Shultz TD, Howie BJ. In vitro binding of steroid hormones by natural and purified fibers. Nutr Cancer 1986;8(2):141-47.
    Adlercreutz H, Hockerstedt K, Bannwart C, et al. Effect of dietary components, including lignans and phytoestrogens, on enterohepatic circulation and liver metabolites of estrogens and in sex hormone binding globulin (SHBG). J Steroid Biochem 1987;27(4-6):1135-44.
    Cassidy A. Potential tissue selectivity of dietary phytoestrogens and estrogens. Curr Opin Lipidol 1999;10:47-52.
    Brzezinski A, Debi A. Phytoestrogens: the "natural" selective estrogen receptor modulators? Eur J Obstet Gynecol 1999;85:47-51.
    Lissin LW, Cooke JP. Phytoestrogens and cardiovascular health. J Am Coll Cardiol 2000;35(6):1403-10.
    Knight DC, Eden JA. A review of the clinical effects of phytoestrogens. Obstet Gynecol 1996;87(5):897-904.
    Messina MJ, Persky V, Setchell KD, et al. Soy intake and cancer risk: a review of the in vitro and in vivo data. Nutr Cancer 1994;21:113-31.
    Kirkman LM, Lampe JW, Campbell DR, et al. Urinary lignan and isoflavonoid excretion in men and women consuming vegetable and soy diets. Nutr Cancer 1995;24(1):1-12.
    Thompson LU, Robb P, Serraino M, et al. Mammalian lignan production from various foods. Nutr Cancer 1991;16(1):43-52.
    London RS, Murphy L, Kitlowski KE, et al. Efficacy of alpha-tocopherol in the treatment of the premenstrual syndrome. J Reprod Med 1987;32:400-04.
    Muneyvirci-Delale O, Nacharaju VL, Altura BM, et al. Sex steroid hormones modulate serum ionized magnesium and calcium levels throughout the menstrual cycle in women. Fertil Steril 1998;69(5):958-62.
    Michnovicz JJ, Adlercreutz H, Bradlow HL. Changes in levels of urinary estrogen metabolites after oral indole-3-carbinol treatment in humans. J Natl Cancer Inst 1997;89(10):718-23.
    Tiwari RK, Guo L, Bradlow HL, et al. Selective responsiveness of human breast cancer cells to indole-3-carbinol, a chemopreventive agent. J Natl Cancer Inst 1994;86(2):126-31.
    Michnovicz JJ, Bradlow HL. Altered estrogen metabolism and excretion in humans following consumption of indole-3-carbinol. Nutr Cancer 1991;16(1):59-66.
    Yuan F, Chen DZ, Liu K, et al. Anti-estrogenic activities of indole-3-carbinol in cervical cells: implication for prevention of cervical cancer. Anticancer Res 1999;19(3A):1673-80.
    Tully DB, Allgood VE, Cidlowski JA. Modulation of steroid receptor-mediated gene expression by vitamin B6. FASEB J 1994;8(3):343-49.
    Minton JP, Walaszek Z, Schooley W, et al. Beta-glucuronidase levels in patients with fibrocystic breast disease. Breast Cancer Res Treat 1986;8:217-22.
    Walaszek Z, Szemraj J, Narog M, et al. Metabolism, uptake, and excretion of a D-glucaric acid salt and its potential use in cancer prevention. Cancer Detect Prev 1997;21(2):178-90.
    Goud VK, Polasa K, Krishnaswamy K. Effect of turmeric on xenobiotic metabolising enzymes. Plant Foods Hum Nutr 1993;44(1):87-92.
    Susan M, Rao MN. Induction of glutathione S-transferase activity by curcumin in mice. Arzneimittelforschung 1992;42(7):962-64.
    Jeong HJ, Shin YG, Kim IH, et al. Inhibition of aromatase activity by flavonoids. Arch Pharm Res 1999;22(3):309-12.
    Zhu BT, Loder DP, Cai MX, et al. Dietary administration of an extract from rosemary leaves enhances the liver microsomal metabolism of endogenous estrogens and decreases their uterotropic action in CD-1 mice. Carcinogenesis 1998;19(10):1821-27.
    Maltzman TH, Christou M, Gould MN, et al. Effects of monoterpenoids on in vivo DMBA-DNA adduct formation and on phase I hepatic metabolizing enzymes. Carcinogenesis 1991;12:2081.
    Vigushin DM, Poon GK, Boddy A, et al. Phase I and pharmacokinetic study of D-limonene in patients with advanced cancer. Cancer Chemother Pharmacol 1998;42:111-17.
    Advanced Nutrition Publications ©2002




    --------------------------------------------------------------------------------
    Attached Images Attached Images  
    Attached Images Attached Images

  16. ---------------------------------------------

  17. Quote Originally Posted by JanSz View Post
    rT3 high, how to deal with it


    Use thise three Genova diagnostics tests.

    Comprehensive Thyroid Assesment
    Oxidative Stress Panel (part of NutrEval)
    Elemental Analysis, Packed Erythrocytes (RBC's)(part of NutrEval)


    Read results, follow advice given by those tests.

    So really best would be to use two tests (few extra $$ but lots of informations):
    NutrEval
    Comprehensive Thyroid Assesment
    ---------------------------------------------------------------------------
    -------------------
    -------------------

    High rT3
    5' deiodinase (Se dependent)
    ----------------------------------------------------------
    Selenium also performs other important roles in the body.
    The most important of these is probably as its role as the body's best antioxidant (anti-peroxidant).
    It performs this role as part of glutathione peroxidase (GSHPx or GPX).

    Glutathione Peroxidase (GSH-Px)
    Glutathione peroxidase is a selenium-dependant enzyme found primarily in the cytoplasm (70%) but also in the mitochondria (30%).
    -----------------------------------------------------------------
    Genova Diagnostics' Oxidative Stress Panel
    checks Glutathione Peroxidase
    -----------------------------------------------------------------

    Interactions, (close): (iodine, selenium, zinc, copper)
    ie; at least above four have to be in proper balance
    ---------------------------------------------------------------------------------------------------
    Genova Diagnostics' Elemental Analysis, Packed Erythrocytes (RBC's)
    checks (it is missing iodine):
    TOXICS
    Antimony
    Arsenic
    Cadmium
    Lead
    Mercury
    Thallium
    Tin

    NUTRIENTS
    Chromium
    Copper
    Magnesium
    Manganese
    Potassium
    Selenium
    Vanadium
    Zinc

    ---------------------------------------------------------------------------------------------------
    If the above investigations falls short, further investigations should be made looking into:
    Interactions, (wide range)
    Ag, Co, Cr, Fe, Hg, I,Rb, Sb, Sc, Se, Zn



    -------------------------------------------------------------------------------------------------------------------------------
    http://www.ithyroid.com/iodine.htm
    While I've found research on the interactions of iodine and selenium, there are two other minerals which need to be studied for their interactions with these two: zinc and copper. I found one study which examined the complex interactions of selenium, iodine, and zinc (there are interactions), but none which have looked at all four minerals in a 4 X 4 factorial design. Now that would be an interesting study! Hopefully someone will do that soon.

    I think one lesson from studying the interactions of selenium and iodine is that the interrelationships between minerals are very complicated. Supplementing with one or two can cause further problems. You have to make sure that you correct every deficiency. Health is built from a chain of nutrients and, like a chain, health cannot be accomplished if one nutrient is missing. Sometimes it's complicated putting the chain back together without running into problems (like supplementing with either selenium or iodine, but not both), but every deficiency has to be corrected. John
    Jan, when my RT3 went beyond range, my doc told me it was because I was taking too much Armour. My FT3 was only 330 or so (mid range). I dropped my Armour from 2.5 grains to 1.5 grains. I don't feel differently. I imagine my TSH increased some, and T4 went up as a consequence, thus T3 in turn, balancing the reduction caused by the lesser dose.

    As I recall, you are taking over 3 grains. That's probably too much for you.

    Good luck.

  18. ON FERTILITY

    http://www.medsafe.govt.nz/profs/dat...pregnylinj.pdf

    Data Sheet


    Dosage In The Male
    Hypogonadotropic hypogonadism
    1,000-2,000 I.U. PREGNYL, two to three times per week. If the main complaint is subfertility, additional doses of an FSH-containing preparation (75 I.U. FSH) daily or two to three times per week, may be given. This treatment should be continued for at least three months before any improvement in spermatogenesis can be expected. During this treatment testosterone replacement therapy should be suspended. Once achieved, the improvement may in some cases be maintained by hCG alone.
    ============================== ======

    Cancer News Content: Testosterone replacement therapy: Minimizing its impact on fertility

    Clomid and Armidix
    --------------------------------------------------------------------------------------------------------------------
    MESO-Rx - View Single Post - Bloodwork question? Androgel

    Using HCG as a sole/major way of getting proper testosterone levels the natural way.

    Data Sheet
    Follow a protocol that one would use when attempting to be fertile.
    May skip the HMG part, unless want to make sure and get her actualy pregnant.

    The description there says:
    Dosage In The Male
    Hypogonadotropic hypogonadism
    1,000-2,000 I.U. PREGNYL, two to three times per week.

    That translates to
    minimum 2000iu/week
    maximum 6000iu/week

    Your will have few limits, they have to be found by blood testing:

    The more HCG you use,
    the more Testosterone your testis will produce.
    the more estradiol you will have
    the more Arimidex you will have to use to control Estradiol

    You do not want to get more than FreeT~300 and no ness than 160
    Calculated with:
    Free & Bioavailable Testosterone calculator
    Free & Bioavailable Testosterone calculator
    using TotalT, SHBG and Albumin
    or
    chart on post #41
    http://anabolicminds.com/forum/male-...oodtest-2.html


    You do not want to use more than 2 pills/week Arimidex (divided into halfs or quarters)

    So work within this limitations and see if you can be natural.
    .
    .
    Supposedly there is some evidence that frequency 2x/week or E3D is the best.
    Supposedly E2D is not as good.

    You will find out what works for you by trying and testing your reaction..

    ------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
    MESO-Rx - View Single Post - Dangers of TRT?

    Quote Originally Posted by marianco View Post
    Testosterone replacement therapy increases testosterone levels. This is sensed by the hypothalamus, which then reduces the release of Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH) from the Pituitary. Luteinizing Hormone is needed to increase testosterone production from the testes. Follicle Stimulating Hormone is needed to stimulate sperm production.

    When a person has low testosterone and sperm production because of testicular hypofunction, the FSH and LH levels are very high because the brain is trying its hardest to stimulate testosterone production (which also increases sperm production). Testosterone replacement will reduce FSH and LH, causing a reduction in testosterone and sperm production.

    There is more to the story...

    Sperm production is also dependent on having adequate Estrogen Activity and Oxytocin Activity. Both are linked. Estrogen increases Oxytocin release. Estrogen stimulates sperm production and testicular size - just as FSH/LH and its analog HCG do. Oxytocin, itself, can increase sperm production and ejaculate volume. Ejaculate fluid itself is necessary for normal fertility - the sperm alone would be useless in normal sex.

    High estrogen levels can reduce sex drive and can have other adverse effects - such as heart attacks, strokes, and blood clots.

    Low estrogen levels also can reduce sex drive and can have other adverse effects - such as high cholesterol levels, impaired memory - and low sperm production.

    The use of DIM and I3C to reduce estrogen activity may seriously reduce sperm production just as reducing FSH and LH levels (from increasing testosterone levels) can do. If anything, it is important to maintain physiologic estrogen levels to maintain sperm production.

    If a person has low testosterone levels, which can lead to low estrogen levels, it may be important to increase estrogen to normal physiologic levels to stimulate sperm production.

    It is important to balance estrogen with normal progesterone levels - which helps protect the person from some of the risks of estrogen (blood clots, heart attacks, stroke).

    Oxytocin may be considered to raise sperm production and ejaculate volume. However it is a non-usual and a nonstandard treatment even by TRT standards. It can be compounded into a nasal spray - the dose range is about 10-24 IU a day. It is highly important for this to be monitored by a physician. Oxytocin, at its worse, can raise blood pressure, can result in excessive fluid retention, and other potentially fatal risks (just as estrogen can lead to heart attack, stroke and blood clots). These can be monitored on exam and lab testing.
    colkurtz_spf testicle restoration timeline:
    TRT WORKS, My results have been amazing!!

    jinxie
    hCG Monotherapy Success Story -- Staggering Numbers

    schedule on post #16
    hCG Monotherapy Success Story -- Staggering Numbers


    ==========
    ==========
    ==========
    MERC MANUAL
    http://74.125.47.132/search?q=cache:...ient=firefox-a
    Treatment of infertility due to hypogonadism

    Infertility, which has many possible causes other than hypogonadism, is discussed in full elsewhere (see Infertility). Infertility due to primary hypogonadism does not respond to hormonal therapy. Men with primary hypogonadism occasionally have a few intratesticular sperm that can be harvested with various microsurgical techniques and used to fertilize an egg by an assisted reproductive technique (eg, intracytoplasmic injection).

    Infertility due to secondary hypogonadism usually responds to gonadotropin replacement therapy. Other symptoms of secondary hypogonadism respond well to testosterone replacement therapy alone. If secondary hypogonadism results from pituitary disease, gonadotropin replacement therapy usually is successful. Therapy begins with LH replacement. After all exogenous androgens are stopped, LH replacement is generally initiated using human chorionic gonadotropin (hCG). Doses begin at 375 to 750 IU sc 2 to 3 times/wk and are increased if necessary to 1000 to 2000 IU sc 2 to 3 times/wk. The dose is adjusted after 3 mo to achieve normal serum testosterone levels. Sperm counts are done monthly, but counts are not expected to increase for at least 4 mo. FSH replacement, which is expensive, begins if 6 to 12 mo of LH replacement does not stimulate spermatogenesis. FSH replacement uses human menotropic gonadotropin or human recombinant FSH, beginning with 75 to 150 IU 3 times/wk. The dose may be doubled if conception has not occurred within 6 mo of combination therapy with hCG. Many men become fertile with treatment despite sperm counts that do not usually result in fertility (eg, < 5 million/mL).

    Secondary hypogonadism due to a hypothalamic defect (eg, Kallmann's syndrome) is treated initially with LH and FSH because of their ready availability; if these are ineffective, GnRH replacement therapy (q 2 h sc by a programmable minipump) might be more effective. Most (80 to 90%) of men respond successfully to these regimens.

    Last full review/revision June 2007 by Bradley D. Anawalt, MD
    Attached Images Attached Images  

  19. Cancer


    Risks of Nutrition Therapy
    In an extensive review of the literature, Dr. Adrienne Bendich found the following data on nutrient toxicity59:

    B-6 can be used at up to 500 mg (250 times RDA) for up to 6 years with safety.

    Niacin (as nicotinic acid) has been recommended by the National Institute of Health for lowering cholesterol at doses of 3000-6000 mg/day (150-300 times RDA). Time release niacin is more suspect of causing toxicity as liver damage.

    Vitamin C was tested in eight published studies using double blind placebo controlled design. At 10,000 mg/day for years, vitamin C produced no side effects.

    High doses of vitamin A (500,000 iu daily) can have acute reversible effects. Teratogenecity is the most likely complication of high dose vitamin A intake.

    Vitamin E intake at up to 3000 mg/day for prolonged periods has been shown safe.

    Beta-carotene has been administered for extended periods in humans at doses up to 180 mg (300,000 iu) with no side effects or elevated serum vitamin A levels.


    In a separate review of the literature on nutrient toxicity by John Hathcock, PhD, a Food and Drug Administration toxicologist, the following data was reported60:

    Vitamin A toxicity may start as low as 25,000 iu/day (5 times RDA) in people with impaired liver function via drugs, hepatitis, or protein malnutrition. Otherwise, toxicity for A begins at several hundred thousand iu/day.

    Beta-carotene given at 180 mg/day (300,000 iu or 60 times RDA) for extended periods produced no toxicity, but mild carotenemia (orange pigmentation of skin).

    Vitamin E at 300 iu/day (10 times RDA) can trigger nausea, fatigue, and headaches in sensitive individuals. Otherwise, few side effects are seen at up to 3,200 iu/day.

    B-6 may induce a reversible sensory neuropathy at doses of as low as 300 mg/day in some sensitive individuals. Toxic threshold usually begins at 2000 mg for most individuals.

    Vitamin C may induce mild and transient gastro-intestinal distress in some sensitive individuals at doses of 1000 mg (16 times RDA). Otherwise, toxicity is very rare at even high doses of vitamin C intake.

    Zinc supplements at 300 mg (20 times RDA) have been found to impair immune functions and serum lipid profile.
    Iron intake at 100 mg/day (6 times RDA) will cause iron storage disease in 80% of population. The "window of efficacy" on iron is probably more narrow than with other nutrients.

    Copper can be toxic, though dose is probably related to the ratio with other trace minerals.

    Selenium can be toxic at 1-5 mg/kg body weight intake. This would equate to 65 mg/day for the average adult, which is 812 times the RDA of 80 mcg. Some sensitive individuals may develop toxicity at 1000 mcg/day.

    Manganese can be toxic, though little specific information can be provided for humans.

    .

  20. http://jeffreydach.com/2008/04/28/fu...y-dach-md.aspx

    Non-Medical e-patient Experts

    Jenny Ruhl Diabetes Update
    Diabetes Update
    and
    Blood Sugar 101
    Blood Sugar 101: The Book!

    Jenny is a self taught diabetes expert who has condensed collaborative knowledge from many diabetes message boards into her book Blood Sugar 101.

    Stop the Thyroid Madness Blog and Book.
    Stop The Thyroid Madness » Index Page

    Online resource advocates natural thyroid medication rather than synthetic version. This covers subtleties of treatment of thyroid disorders based on collaborative knowledge of many e-patients.

    Internet Savvy Medical Expert:

    William Davis MD Track Your Plaque,
    Heart Scan Resource Center - Track Your Plaque
    HeartScan Blog
    The Heart Scan Blog
    Dr Davis is a Cardiologist in Wisconsin, and one of a new breed of internet savvy medical experts. He has created an online community which creates new medical knowledge concerning efficacy of various natural treatments to reverse heart disease.

  21. Diabetes Update: The Email I Have Not Received

    I can't imagine why you would consider dropping dairy before dropping the oats, the toast, and the potatoes. Those are all high starch/low nutrient foods whose limited nutritional benefits can be obtained elsewhere from non-starchy foods).

    I can understand dropping milk and substituting cream or half & half to reduce the lactose (milk sugar), but only if dropping the grains and spuds isn't effective enough.

    There's a good chance the missing "puzzle piece" is still too much starch, especially for breakfast, rather than too much dairy. Have you given that any thought or experimentation?

    ruse


    noun
    An indirect, usually cunning means of gaining an end: artifice, deception, device, dodge, feint, gimmick, imposture, jig, maneuver, ploy, sleight, stratagem, subterfuge, trick, wile. Informal: shenanigan, take-in. See honest,

    ---------------
    Your emphasis on “education” is also nothing more than a ruse. All you really do is “educate” diabetics to patronize your corporate sponsors.

    The enclosed letter is only your latest attempt to fraudulently elicit contributions from me. I will consider any further contact by you as harassment and proof that your charitable efforts are akin to fraud/false claims and specifically target vulnerable individuals like myself who has been diabetic for over 50 years.

    What gives you the right to harass me, use my disease as a tool for extortion, and accept money in my behalf from gullible people and corporate sponsors when you have no intention of ever finding a cure.

    ---------------
    ============================== ============================== ===================
    Newly Diagnosed
    Newly Diagnosed.
    Sounds like you're planning a move to take control of your diabetes... good for you.

    There is so much to absorb... you don't have to rush into anything. Begin by using your best weapon in this war, your meter. You won't keel over today, you have time to experiment, test, learn, test and figure out just how your body and this disease are getting along. The most important thing you can do to learn about yourself and diabetes is test test test.

    The single biggest question a diabetic has to answer is: What do I eat?

    Unfortunately, the answer is pretty confusing. What confounds us all is the fact that different diabetics can get great results on wildly different food plans. Some of us here achieve great blood glucose control eating a high complex carbohydrate diet. Others find that anything over 75 - 100g of carbs a day is too much. Still others are somewhere in between.

    At the beginning all of us felt frustrated. We wanted to be handed THE way to eat, to ensure our continued health. But we all learned that there is no one way. Each of us had to find our own path, using the experience of those that went before, but still having to discover for ourselves how OUR bodies and this disease were coexisting. Ask questions, but remember each of us discovered on our own what works best for us. You can use our experiences as jumping off points, but eventually you'll work up a successful plan that is yours alone.

    What you are looking to discover is how different foods affect you. As I'm sure you've read, carbohydrates (sugars, wheat, rice... the things our Grandmas called "starches") raise blood sugars the most rapidly. Protein and fat do raise them, but not as high and much more slowly... so if you're a T2, generally the insulin your body still makes may take care of the rise.

    You might want to try some experiments.

    First: Eat whatever you've been currently eating... but write it all down.

    Test yourself at the following times:

    Upon waking (fasting)

    1 hour after each meal

    2 hours after each meal

    At bedtime


    That means 8 x each day. What you will discover by this is how long after a meal your highest reading comes... and how fast you return to "normal". Also, you may see that a meal that included bread, fruit or other carbs gives you a higher reading.

    Then for the next few days, try to curb your carbs. Eliminate breads, cereals, rice, beans, any wheat products, potato, corn, fruit... get all your carbs from veggies. Test at the same schedule above.

    If you try this for a few days, you may find some pretty good readings. It's worth a few days to discover. Eventually you can slowly add back carbs until you see them affecting your meter. The thing about this disease... though we share much in common and we need to follow certain guidelines... in the end, each of our bodies dictate our treatment and our success.

    The closer we get to non-diabetic numbers, the greater chance we have of avoiding horrible complications. The key here is AIM... I know that everyone is at a different point in their disease... and it is progressive. But, if we aim for the best numbers and do our best, we give ourselves the best shot at heath we've got. That's all we can do.

    Here's my opinion on what numbers to aim for, they are non-diabetic numbers.

    FBG under 110

    One hour after meals under 140

    Two hours after meals under 120

    or for those in the mmol parts of the world:

    Fasting Under 6

    One hour after meals Under 8

    Two hours after meals Under 6.5

    Recent studies have indicated that the most important numbers are your "after meal" numbers. They may be the most indicative of future complications, especially heart problems.

    Listen to your doctor, but you are the leader of your diabetic care team. While his /her advice is learned, it is not absolute. You will end up knowing much more about your body and how it's handling diabetes than your doctor will. Your meter is your best weapon.

    Just remember, we're not in a race or a competition with anyone but ourselves... Play around with your food plan... TEST TEST TEST. Learn what foods cause spikes, what foods cause cravings... Use your body as a science experiment.

    You'll read about a lot of different ways people use to control their diabetes... Many are diametrically opposed. After awhile you'll learn that there is no one size fits all around here. Take some time to experiment and you'll soon discover the plan that works for you.

  22. Diet & Exercise

    What is a whole grain cereal?
    Which whole grains can you manage?
    Can I manage bread?
    Can I manage legumes?
    What fruit can you eat?
    What vegetables can you eat?
    What fats and oils can I eat?
    What alliums can I eat?
    What meat can I eat?
    What nuts can I eat?

  23. Example Hair Analysis
    http://www.gdx.net/home/images/reportpdf/elemental.pdf
    Elemental Analysis, Packed Erythrocytes (RBC's)
    http://www.genovadiagnostics.com/fil...tes_Report.pdf
    Example Comprehensie Urine Profile
    http://www.gdx.net/images/reportpdf/CUEP.pdf
    -------------------------------------
    iTHYROID.com
    http://www.ithyroid.com/
    After going through and recovering from both hyperthyroidism and hypothyroidism, I feel that I have a very good idea what causes these diseases and my theory is at odds with current medical thinking.

    I believe that hyperthyroidism and hypothyroidism, Graves' disease and Hashimoto's Thyroiditis, are caused by a combination of nutritional deficiencies and chemical toxins, usually heavy metals.
    ---------------------------------------
    Table of Contents
    Contents

    Cobalt
    Moreover cobalt deficiency or rather vitamin B12 deficiency was accompanied by a dramatic accumulation of the trace elements iron and nickel in liver. These results indicate that long-term moderate cobalt deficiency may induce a number of physiological changes in cattle,
    ---------------------------------------

    Cobalt deficiency vs. B12 deficiency - The Vegan Forum - a message board for vegans

    Quick fix -- use B12 supplementation
    Long fix -- add cobalt to diet
    Do hair analysis and/or urine analysis to figure out imbalances.

  24. Help with Fertility - Dr. wants off Test and on Clomid or HCG


    Quote Originally Posted by cpileri View Post
    Sir,
    Hi, first post here. Been reading and lurking but i do feel i can help you with this, as we have done this 4 times now successfully.
    Success defined as a live birth.

    "We" defined vaguely (to preserve privacy); suffice it to say that I am either the patient, the doctor, or the patient's wife.

    Bottom Line Up Front: 3 phases. Phase 1: exogenous testosterone and Human Chorionic Gonadotropin until patient's own testosterone is normal. Phase 2: drop the testosterone, stay on hCG, add menotropins (recombinant or purified LH/FSH) until woman is pregnant(*). Phase 3: back to testosterone alone.

    Details: (some accuracy sacrificed for brevity)
    For a hypogonadal male on long-term testosterone therapy, the goals of fertility require sperm numbers, sperm maturation, and sperm quality.
    Phase 3 is where you are now. Injecting T, no T of your own, no Leuteinizing Hormone (LH), no Follicle Stimulating Hormone (FSH), and no sperm.
    Phase 1 leaves you on the T, so you feel OK, and adds hCG to bring your T production back up. You have to get your own body (the Interstitial cells of Leydig in the testes) to make T because the local concentration of T and DHT required for normal sperm maturation is hundreds of times higher than the rest of the circulation- you can't inject that much, believe me! An unenlightened doc might say you are risking 'doubling up' on the testosterone with this combo. Don't worry, it wont go that high. You will notice after 3-4 (or maybe 6) months a bump in your T levels on blood tests from your normal steady state level; and then you will drop the injected T and see that your own T is a meager 300-400. but that's enough for fertility. BTW: if it takes longer than 6 months to see your own T come back, then there is a possibility that this isn't going to work. That is, your testes are shut down permanently. Bummer.

    After your own T comes back, Phase II: you add FSH to get the sperm quality and especially the numbers up. you will get a few normal sperm with just the hCG, but you need to add (not substitute, add) FSH to get both quantity and quality. After another 4-6 months you will get a semenalysis to see if its working. You will stay on the FSH, with either hCG or LH/FSH combo, until pregnancy.

    (*)Some people stay on the lh/fsh for the first trimester if there is a risk of the woman losing the pregnancy.

    What your doctor seems to propose is skipping Phase I. The plan WILL work for fertility (if it is going to work at all). But you will feel like heck. Using the clomiphene to (try to) raise LH and FSH can work if your pituitary gland is ready to come back to production. But it is not usually very successful in pts with long term T use. The clomid effect just isn't that powerful. But heck, its worth a try and would solve all the above problems if it works.

    Another angle you may take with the doc is 'fecundity' which is the ability to copulate. by skipping phase I, you compromise fecundity. Any decent endocrinologist/fertility specialist should be wise to the intertwined concepts of fertility and fecundity as regards to successful reproduction.

    I know I left out a bunch of info for the sake of brevity. So feel free to ask me any questions you want.

    Good Luck!
    C-
    Define "normal testosterone level" for phase #1 and #3.
    Best as BAT (BioAvailableTest) in Quest Diagnostic test
    Testosterone, Free, Bio/Total (LC/MS/MS)

    Should we check and adjust Estradiol level, it may go up on high dose of HCG.

    In phase #3 (after pregnancy), what is the reasonable long term HCG weekly dose to produce maximum endogenous testosterone.
    ------------------
    'fecundity' is a topic discussed often here, mostly outside of intent to impregnate.
    Any helpful pointers you may wish to share on how to maintain ability to copulate.

    .
    .
    Tank you for informative post.
    .

  25. Author: chilln

    --------http://www.matrixnutritionandfitness. com/forum/showpost.php?p=15542&postcount =14
    -----http://www. matrix nutrition and fitness.com/forum/showpost.php?p=15542&postcount =14

    Re: What could be causing near constant fatigue?

    --------------------------------------------------------------------------------

    I haven't found any site which describes this problem simply, so I've summarised it here:

    Constant fatigue, with anxiety, is a dead giveaway for adrenal insufficiency.

    Adrenal insufficiency is another way of saying "insufficient cortisol" plus "insufficient DHEA" (NB: not DHEA-S).
    Note how I didn't say "low cortisol" or "low DHEA". Please pay specific attention to the different terms. Insufficient cortisol or DHEA is not always synonymous with low cortisol or DHEA.

    Adrenal insufficiency is typically either a result of (simplest first):

    1) Tissue damage to your hypothalamus, or pituitary, or adrenals (all are rare). This includes genetic defects and tumors (growths) on these tissues.

    and/or

    2) Lack of deep sleep - because we only make cortisol while we're in deep sleep therefore we need to strive to get normal straight continuous deep sleep to get all of our deep sleep phases each night. May require supps to help ensure continuous sleep, eg: melatonin.

    and/or

    3) An accumulation of free radical damage which is not being adequately repaired each night.

    Ie: we over-stress ourselves from:
    a) too much exercise without rest
    and/or
    b) psychological stressors

    Ie: we don't get sufficiently repaired because of:
    a) our reduction in metabolic rate (genetic, guaranteed)
    and/or
    b) our reduction in testosterone (genetic, guaranteed)
    and/or
    c) our reduction in growth hormone (genetic, guaranteed)
    and/or
    d) poor diet
    ...eg: inadequate iron
    ...........inadequate Omega3
    ...........heavy metal toxins
    ...........too much high glycemic index carbohydrates which create poorly responsive sugar hormones)
    ...........plus many others

    The inadequate repairs use up all our cortisol because the free radical damaged cells are causing many "we're broken" messages which are triggering responses from many sources, and these typically overwhelm the body, so cortisol quenches them to limit the amount of signal to manageable levels. When cortisol runs out, the amount of "we're broken - please fix us" signals overwhelm our central nervous system and create overall fatigue.

    Using up all our cortisol causes a reduction in DHEA because most of the DHEA is quickly converted into downstream metabolites because they are more desperately needed than the DHEA.

    #############

    In your case I'd focus on the sleep and diet issues, since you're working on testosterone. If you already know you're trying to overwork yourself then you should back off.

    From the diet perspective, I always start looking at protein, then sugars, then iron, then oils, then toxins and whatever other interesting results show up from there.

    a) protein

    Please eat lots. Especially the veg proteins from nuts (assuming no allergies) and the whey proteins from milk.

    b) sugar

    Eating high glycemic index carbs (potatoes, rice, pasta, noodles, white bread) degrades our sugar hormones responsiveness over time, especially our insulin responsiveness, and this reduces the availability of sugars for energy, and causes drowsiness at its onset. In your case you should confirm your insulin responsiveness hasn't already started to degrade. All docs know the standard insulin tolerance tests.

    c) iron

    Low iron causes fatigue because iron is required to transport oxygen via the blood, so low iron starves cells of oxygen. Iron levels can be initially assessed from the standard RBC "red blood cell" metric tests including ferritin (iron is stored as ferritin until needed), haemoglobin (ie: red blood cells which transport iron in a usable format), and haematocrit (percentage of blood which is haemoglobin). I'm a fan of lean rare red meat for my iron needs - but I also eat lots of high alkaline vegetables to offset the acidity.

    d) oils

    Oils supply energy over longer periods than high glycemic index carbs, and oils provide simple lubrication functions (eg: tears) just like in cars, and our brains are made from fats which are assembled from oils. Insufficient oils therefore affects energy, joints and our brain. Once you allow your brain repairs to degrade from lack of oils, then you start to affect all your body processes. I typically focus on Omega3 from fish, and saturated oils from coconut oil and some pure butter, and unsaturated oil from virgin olive oil. We need all three types of oils, much to the consternation of the anti-saturated fats fraternity.

    e) toxins

    I typically only start worrying about these once I've squared away the ones above.

    ####

    Regarding your observation about how your fatigue reduces towards the evening, and is maximum in the morning, that suggests that your sleep time waste expulsion is a problem. We process waste mostly during our sleep. It seems as though you have adapted to processing your waste during the day, which is less than optimum.

    Our liver must work efficiently all night to make molecules to bind to the toxins in our blood and belly, and then send them via the urine or faeces.

    Do you have any digestion problems, or do you eat late and then go to sleep with food still in your belly ? Or perhaps you eat too much red meat with no high cellulose vegetables, which may cause a slowdown in the travel of food through the bowel which causes a backup of all of the waste handling processes (there are so many ways to interfere with this mechanism, please be creative here) ?

    If this is an issue for you, then I'm a fan of taking digestive enzymes and probiotics with meals, to improve their digestion, plus the addition of high cellulose vegetables (for fibre content) to ensure reliable waste processing. Eventually you should be able to reduce the enzymes and probiotics to zero, yet still maintain reliable waste processing.

    ###

    Regarding the fact you're on testosterone - it doesn't address the diet and digestion and waste processing issues.

    ####

    So let us know where you stand on these issues, or perhaps you've worked out you have a specific issue you'd like to focus on ?

  26. MESO-Rx - View Single Post - alternatives to HC

    Quote Originally Posted by JanSz View Post
    Hypopituitary Support
    Equivalent maximum doses (do not take pregnenolone
    or any other adrenal supplement that breaks down
    into cortisol with these)

    cortisone acetate 37 1/2 (weak, not recommended)
    hydrocortisone 30 mg
    cortef 30 mg
    prednisone 7 1/2 mg
    prednisolone 7 1/2 mg
    triamcinolone 6 mg
    methylprednisolone 6 mg
    **dexamethasone 1 mg
    betamethasone 0.8 mg

    *Isocort max dose 8 pellets-is said to have 2 1/2 mg of
    cortisol per pellet, so 8 pellets is 20 mg of cortisol.

    **info sources can range from
    1 mg dex = 6 mg medrol = 30 mg Cortef
    to
    1 mg dex =16 mg medrol=80 mg Cortef.
    In my experiance with dex (your experiance may differ),
    I've found the equivalents to be closer to
    1 mg dexamethasone=
    40 mg Prednisone
    32 mg Medrol
    160 mg Cortef/HC.

    ***1 mg medrol =1/32 mg dexamethasone
    ***6 mg medrol = 6/32 mg dexamethsone

    ***Dexamethasone should not be used alone, but in
    combination with Medrol no more than 50% dex/50% medrol.
    ============================== ================

    The relative mineralcorticoid potencies of different steroids

    Human Aldosterone 300
    Fludrocortisone Acetate (Florinef) 150
    Deoxycorticosterone acetate 20
    Cortisol/hydrocortisone 2
    Cortisone 2
    Prednisone 1
    Prednisolone 1
    Methylprednisolone 0.5
    Triamcinolone 0
    Dexamethasone 0
    Betamethasone 0

    These figures are rough estimations
    ============================== ===========================

    Glucocorticoid* Potencies of Different Steroids

    deoxycorticosterone acetate************ 0
    Human Aldosterone *********************** 0.3
    cortisone acetate*********************** ***** 0.8
    hydrocortisone**************** *************** 1.0
    prednisone******************** ***************** 4.0
    prednisolone****************** **************** 4.0
    triamcinolone***************** *************** 5.0

    methylprednisolone************ *********** 6.0
    * Fludrocortisone acetate (florinef) **** 12
    betamethasone***************** ********** 24 - 30
    dexamethasone***************** ************ 32

    *potency is locked up for most people, few actually
    experiance a significant amount.A rare few
    need to lower their cortisol therapy by up to 1/3.

    These figures are rough estimations
    ============================== ================

    Glucocorticoid half lives

    cortisone acetate 30 minutes (weak, not recommended)
    cortisone (oral) 0.8 - 8 hours
    hydrocortisone 1 -8 hours
    cortisone (IM) 1.3 -18 hours
    prednisone 16 -36 hours
    prednisolone 18 - 36 hours
    triamcinolone 18- 36 hours
    methylprednisolone 18- 36 hours
    dexamethasone 36 - 54 hours
    betamethasone 36- 54 hours


    These figures are rough estimations.
    Corticosteroid converterCorticosteroids conversion calculator (hydrocortisone, dexamethasone, prednisone, methylprednisolone, betamethasone

  27. Audio

    http://divcom-house.informz.net/z/cj...MTE/index.html


    Audio: Diana Schwarzbein, MD - Menopause — A Symphony of Hormone Interactions - Women's Health, Women's Health - Integrative Practitioner

    Audio: Menopause - A Symphony of Hormone Interactions
    Diana Schwarzbein, MD explores the connections to insulin, cortisol and thyroid hormones as well as the connections between the sex hormones themselves.

    --------------------------------------------------------------------------------
    My notes:

    fast acting membrane receptors, seconds to minutes
    nuclear receptors, slow acting, hours
    all steroid hormones have membrane and nuclear receptors

    Binding and unbinding is desirable.
    Daily high doses of any hormone may not be apropriate.

    High triglycerides may hog communication and need to be adjusted before thyroid (T3) hormone work properly.

    Not always hormone issue, may be receptor issue (bad fats).

    When at higher levels, most hormones downregulate their own receptors.

    Progesterone and estrodial are closely related.
    Need enough estrodial for progesterone to work.
    Progesterone improves estrodial signals.

    Testosterone & progesterone compete for 5ar, high progesterone may lower DHT.

    She thinks of study to rub progesterone cream on men's scalp to see if it helps in hair loss.

    Cortisol (+), progesterone(-) on aromatase production,
    more cortisol promotes production of aromatase and E2
    more progesterone hinders production of aromatase (less E2)

    Cortisol traping, progesterone increases active cortisol.

    Skipping meals raises cortisol.
    frequent meals lower cortisol

    Stress raises cortisol then raises estrogen (not when AF)

    Progesterone decreases insuline
    Estrogen increases insuline (insuline sensitizing)

    Pogesterone supplementation must not be continouos, must be cycled

    Normal response to low E2 should be that cortisol is high

    T3 --> increases progesterone

    E2 (low) helps T3
    E2 (high) antagonist to T3

    PXR

    B6

  28. http://**************.com/forum/show...6751#post16751
    24 Hour Urine Hormonal Test
    --------------------------------------------------------------------------------
    Someone wanted a thread started on this topic so that we can all learn about the 24 hour urine hormonal evaluation. Here it is. The links below have some useful information on the topic. I hope this leads to a thread useful to everyone. Enjoy!

    Clinical value of 24-hour urine hormone evaluations
    Clinical value of 24-hour urine hormone evaluations | Townsend Letter for Doctors and Patients | Find Articles at BNET

    Steroid Hormone Profiles
    ----------------------------------------------------------------------------------
    Background

    Hormone replacement therapy is the corner stone of anti-aging medicine. It represents a means by which physicians can make a great impact on the health and well being of their patients. Exciting developments in urinary hormone testing have allowed practitioners access to a very sophisticated way of assessing and tracking hormone replacement therapy.

    There are numerous advantages to using the 24-hour urine hormone evaluations. These evaluations indicate the total daily hormone production and utilization. This overcomes a major dilemma of blood evaluations that only provide a snapshot and the assay limitations of saliva. The 24-hour urine provides a stable indicator of output and is not susceptible to minute-by-minute fluctuations seen in serum or salivary measurements. Equally important to knowing hormone levels is knowing how they are metabolized. Some researchers feel that hormone metabolites have as much if not more, biological action than the hormones they were derived from. Determining the levels of metabolites also enables the practitioner to trace a supplemented hormone through its metabolic pathway, which ensures the therapy is having the desired effect from an objective standpoint. No other method is as cost-efficient for the evaluation of hormones and hormone metabolites. To replicate the same number of analytes in serum would triple the cost and metabolites are not measured in saliva. A comprehensive, sophisticated urine hormone panel should consist of the following hormones and metabolites: Cortisol, 17-Hydroxycorticoids, Aldosterone, Dehydroepiandrosterone (DHEA), Testosterone, 17-Ketosteroids, Progesterone metabolites, Estrogens, Estrogen metabolites, Growth Hormone and key minerals.

    Adrenal hormones and their metabolites

    Cortisol is the major stress hormone and should be evaluated in cases of dysglycemia, fatigue, hyper- or hypotension, weight change and immune dysfunction. Additionally, cortisol must be evaluated in those patients who appear hypothyroid yet show no objective signs of thyroid deficiency. Deficiency signs and symptoms manifest as inflammations, hyperpigmentations and pain. Excess cortisol can create swelling as well as hair loss, agitation and weight gain. The urinary evaluation measures the free fraction of cortisol. While levels are commonly thought to rise with aging, it is not unusual to find suboptimal levels in aging populations. Still, clinicians often shy away from treatment due to fears related to pharmacological dosing of synthetic glucocorticoids and associated side effects. In patients deficient in cortisol, judicious use of physiological amounts of hydrocortisone may yield significant improvements. Cortisol has a major impact on many other hormones and it is vital to monitor it by utilizing a comprehensive urine hormone panel.

    The 17-Hydroxycorticoids represent how well the body is dealing with stress. They are primarily metabolites of cortisol and detail cortisol utilization. If the amount of 17-Hydroxycorticoids excreted in the urine is high, then the level of stress on the body is high. Consequently, if cortisol is high and the 17-Hydroxycorticoids are low, then there is poor adaptation to stress. This can also occur with excess hydrocortisone dosing that exceeds the capacity for metabolism. Both alpha- and beta-reduced metabolites of cortisol are measured in the 24-hour urine hormone evaluation, indicating whether the site of metabolic (in)efficiency is peripheral or splanchnic. This can dictate treatment choices when seeking to improve cortisol metabolism.

    Aldosterone, as the main mineralocorticoid, aims to excrete potassium and retain sodium. It is under control of the renin-angiotensin system though many other hormones such as adrenocorticotropic hormone (ACTH) can stimulate release. It is also dependent on water and salt (sodium) intake. Signs and symptoms of aldosterone deficiency include fatigue, dehydration, hypotension and polyuria. An excess of aldosterone may yield water retention and hypertension. Dr. Thierry Hertoghe, an internationally renowned physician experienced in hormone replacement therapy, feels that aldosterone deficiency is more common than previously thought and worthy of treatment. He believes the ideal way to assess aldosterone levels is with the 24-hour urine evaluation. This eliminates the variability seen with serum measurements. This serum variability is probably due to significant influence from many other factors that affect aldosterone release. The 24-hour urine evaluation provides a stable indicator of aldosterone production.

    Dehydroepiandrosterone (DHEA) is the most abundant androgen and has a wide range of physiological effects. Previously thought to exert little or no biological action, DHEA is known to be important for immune function, psychological health, bone mineral density and cardiovascular health. Low levels in aging men have been shown to increase the risk of premature mortality. Common signs and symptoms of DHEA deficiency include loss of pubic and axillary hair, dry skin and mucous membranes, moderate fatigue and anxiety and low resistance to noise. Excess DHEA levels may cause oily skin and hair, acne and in women, androgenic alopecia, hirsutism and menstrual cycle disturbances. The 24-hour urine measurement of DHEA is an ideal way to determine daily production and the simultaneous measurement of 17-Ketosteroids can provide information on DHEA metabolism.
    ============================== ============================== =

    The 17-Ketosteroids are chiefly metabolites of androgens with very minor contributions from glucocorticoids. To accurately measure individual 17-Ketosteroids in the urine, gas chromatography mass spectrometry (GCMS) is the preferred method. These 17-Ketosteroid values help to determine metabolic pathways of androgens. For example, in a comprehensive and advanced 24-hour urine hormone profile, the measurement of androsterone and etiocholanolone details the metabolic fate of testosterone and DHEA. DHEA contributes to the majority of androsterone levels while testosterone contributes to the majority of etiocholanolone results. So with proper utilization of supplemented DHEA, the levels of androsterone should rise proportionally with the amount given and testosterone use should cause a proportional increase in etiocholanolone. Japanese research has found that the 17-Ketosteroids represent a capacity for handling stress and the ability to repair from stress. Low levels of 17-Ketosteroids represent a poor response to stress and in chronic illness indicate an unfavorable prognosis. A sense of the overall capacity regarding stress can be ascertained by comparing the levels of 17-Hydroxysteroids to the 17-Ketosteroids. Ideally, there should be a 1:1 ratio based on the percentile within each respective range. For instance, if the 17-Hydroxysteroids are in the 80th percentile of its range and the 17-Ketosteroids are in the 40th percentile of its particular range, then the person is in a catabolic state sometimes referred to as the adrenal catabolic syndrome. There is too much stress and too little ability to repair from stress. This example highlights the vast amount of information that can be gleaned from a comprehensive, sophisticated 24-hour urine hormone panel.

    Sex hormones and their metabolites

    Andropause is the name given to the decline in testosterone in aging men, but testosterone also plays very critical roles in women. Physiological roles of testosterone include maintenance of mental/emotional health, bone mineral density, libido and cardiovascular health. With normal aging, testosterone levels decline at a slower rate than other hormones, consequently, the signs and symptoms can be harder to detect. To objectively evaluate testosterone levels, serum total testosterone (TT) was first used but these levels remain constant well into advanced age. The more biologically active free testosterone level can be measured but, like many other hormones measured in serum, blood captures only a moment in time. Additionally, weakly bound testosterone has been proposed to be very important in the overall status of biologically active testosterone. The calculation of the free androgen index (FAI) attempts to overcome the absence of knowing the weakly bound testosterone through dividing the TT measurement by the sex hormone binding globulin (SHBG) levels to hopefully reveal the amount of free and weakly bound testosterone together. However, most researchers feel that this calculation is inappropriate for men and only slightly better for women. The 24-hour urinary testosterone evaluation overcomes these problems by measuring the free fraction which is unaffected by circadian rhythms.
    ============================== ============================== ==============

    In young, physically active women, it is quite possible to find enough progesterone in the urine for useful conclusions. This is not the case for those women in the peri- and post-menopausal years. There is very little free progesterone in the urine. The preponderance of progesterone is excreted as metabolites in the urine and there is very little fecal excretion. Quantitatively, the most important progesterone metabolite is pregnanediol. It is easily measured in the urine and provides an accurate, practical marker for progesterone status. Pregnanediol has been used as an indicator for ovulation and correlates very well with serum progesterone status. Urinary pregnanetriol is another important metabolite in the assessment of overall progesterone status. It is largely derived from 17-hydroxyprogesterone and parallels serum levels. The 24-hour urinary measurements of pregnanediol and pregnanetriol to determine progesterone status, is no doubt pertinent to a comprehensive evaluation for an aging population.

    Estrogen supplementation was the first standard hormone replacement therapy employed by physicians specifically for women. The 3 primary estrogens are estradiol, estrone and estriol and their functions and benefits in women are well understood. In men, estrogens are only associated with adverse occurrences such as prostate cancer and gynecomastia. The age related decline in estrogens has been linked to osteoporosis and cardiovascular disease. Conversely, excess estrogens (and perhaps unopposed estrogens) have been implicated as casual factors in breast and endometrial cancers. Menopausal symptoms include many physical and psychological effects that can be very uncomfortable. Like the other sex steroids, estrogens or progesterone and testosterone for that matter, cannot be reliably measured in saliva in the aging population because levels are below the detectable limits of currently available assays and serum is only capturing a moment in time. Therefore the assessment of estrogen status can best be accomplished by a 24-hour urine hormone evaluation. Urinary evaluations also allow the measurement of many estrogen metabolites that are now thought to play a more pivotal role in the positive and negative sequelae related to estrogens. Research into the function of catechol estrogens (metabolites) has recently revealed that some are beneficial, others are detrimental and some need to be in proper ratio with others. For example, 2 and 4 methoxyestrone are beneficial, 4-hydroxyestrone is genotoxic and there is a decreased risk of breast cancer when the ratio of 2-hydroxyestrone to 16-alpha hydroxyestrone is greater than 2.

    Growth Hormone

    Growth Hormone (GH) is arguably the most important anti-aging hormone. The decline in GH production and release is termed somatopause. Signs and symptoms of somatopause include increased body fat, decreased muscle mass, reduced skeletal muscle strength and a host of psychological symptoms. Attempts at measuring GH in serum were futile because of the pulsatile release and relatively short half-life. Physicians turned to assessing more stable biomarkers such as insulin-like growth factor 1 (IGF-1), but these are unreliable in thyroid disease, liver disease, malnutrition and poorly controlled diabetes. Furthermore, obese patients generally have normal to high levels of IGF-1 with very low GH levels. Provocation tests such as the insulin tolerance test (ITT) are accurate but not suited to office-based evaluations and are contraindicated in cardiovascular disease, seizure disorders and diabetes. They also seem to be less effective in obese patients. Urinary GH measurements have been used in research for the last 20 years. Recently, a urinary GH assay has been developed that is commercially viable and affordable for the practicing clinician. It has been clinically proven to reflect the central release of GH. This assay demonstrates sensitivity to dietary manipulations, anaerobic exercise and recombinant GH injections. It may be the best choice to evaluate and monitor GH replacement therapy.
    ============================== ============================== ==============

    Minerals are important cofactors in hormone synthesis and metabolism. Changes in the values of urinary mineral levels usually precede changes in blood. Blood minerals are probably more tightly regulated and urinary excretion may reflect the true clinical picture. Key minerals measured in a comprehensive, advanced 24-hour urine hormone profile include sodium, potassium, calcium, magnesium and phosphorus. Sodium levels help to confirm aldosterone status as increased sodium secretion decreases aldosterone. Potassium, in addition to its relationship with aldosterone, is a very valuable mineral associated with GH status. High calcium and phosphorus in the urine may mean increased bone loss. Magnesium is a key cofactor in the catechol-O-methyltransferase enzyme that renders the estrogen metabolite, 4-hydroxyestrone harmless by converting it to 4-methoxyestrone.

    Urinary hormone measurements are not new and are well-established for the majority of hormones. A comprehensive, sophisticated 24-hour urine hormone panel provides the practitioner with a global view of important hormones and metabolites to both assess the need for and manage, hormone replacement therapy. Additionally, these tests can be valuable for a broad range of endocrine disorders and dysfunctions. This advanced method of endocrine analysis supplies a great deal of clinically useful information that is cost effective to the practicing clinician. The 24-hour urine hormone analysis is rapidly emerging to the forefront of anti-aging diagnostics.

    Bibliography

  29. Jan.....you looking for me?

    Bob
  •   

      
     

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