Jan's BloodTest April13/2007

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

    null good starting page


    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.

    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

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  3. 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):
    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):


    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

    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.



    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
    chart on post #41

    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!!

    hCG Monotherapy Success Story -- Staggering Numbers

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

    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  

  5. 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.


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

    Non-Medical e-patient Experts

    Jenny Ruhl Diabetes Update
    Diabetes Update
    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.

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    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.

  7. 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?


    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.

  8. 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?

  9. Example Hair Analysis
    Elemental Analysis, Packed Erythrocytes (RBC's)
    Example Comprehensie Urine Profile
    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

    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.

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

    Quote Originally Posted by cpileri View Post
    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!
    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.

  11. 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.


    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.


    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
    b) psychological stressors

    Ie: we don't get sufficiently repaired because of:
    a) our reduction in metabolic rate (genetic, guaranteed)
    b) our reduction in testosterone (genetic, guaranteed)
    c) our reduction in growth hormone (genetic, guaranteed)
    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 ?

  12. 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
    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

  13. Audio


    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



  14. 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

    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.


  15. Jan.....you looking for me?


  16. http://**************.com/forum/show...51&postcount=1

    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 | Townsend Letter for Doctors and Patients | Find Articles at BNET

    Steroid Hormone Profiles

    24-Hour Comprehensive Steroid Hormone Profile Interpretation

    Estrogens: Estrone (E1), Estradiol (E2) and Estriol (E3)
    Etiocholanolone and Androsterone
    Cortisol and Cortisone
    Tetrahydrocortisone, Tetrahydrocortisol, allo-Tetrahydrocortisol
    Tetrahydrocorticosterone, allo-Tetrahydrocortisosterone

    Estrogens: Estrone (E1), Estradiol (E2) and Estriol (E3)
    (Results fluctuate during the menstrual cycle; results are lower in post-menopausal women.)

    Elevated In Women: Possible Causes


    Hormone replacement therapy (oral E2 dose >0.25 mg/day)
    * Higher transdermal doses may be used without exceeding the normal ranges
    Normal pregnancy in a pregnant woman

    Estrogen hypersecetion (high urinary concentration + low or low normal plasma concentration)
    Ovarian or adrenocortical tumors in a non-pregnant woman
    Adrenocortical hyperplasia in a non-pregnant woman
    Metabolic or hepatic disorder in a non-pregnant woman (i.e. cirrhosis)
    Treatment for infertility

    (Elevated E1 & E2 are associated with a moderate increase in breast cancer risk.)

    Low In Women: Possible Causes


    Menopause or peri-menopause

    Primary ovarian insufficiency, due to Stein-Leventhal syndrome
    Secondary ovarian insufficiency, due to pituitary or adrenal hypofunction
    Ovarian agenesis
    Anorexia nervosa
    Other metabolic disturbances

    Elevated In Men: Possible Causes


    Testosterone supplementation (>75 mg/day)

    Excessive aromatase activity (may be associated with obesity)

    DHEA supplementation
    Testicular, adrenal or hepatic tumors (may be associated with gynecomastia)
    Hepatic cirrhosis


    (Adult testosterone levels decline with aging. Our normal ranges are for young adults.)
    Elevated In Women: Possible Causes


    Testosterone supplementation

    Polycystic Ovary Syndrome (associated with hirsutism)
    Congenital adrenal hyperplasia
    (Pregnanetriol & DHEA may also be elevated)
    Adult-onset adrenal hyperplasia
    (Pregnanetriol & DHEA may also be elevated)
    Ovarian neoplasm
    Pregnenolone supplementation (high dose)

    Elevated In Men: Possible Causes


    Testosterone supplementation (>75 mg/day)

    Pregnenolone supplementation (high dose)
    XYY syndrome

    Low In Men: Possible Causes


    Excessive aromatase activity (testosterone -> estradiol)

    (May be associated with infertility & impotence)
    Klinefelter syndrome

    (Results fluctuate during the menstrual cycle; results are lower in post-menopausal women.)
    Elevated In Women: Possible Causes


    Progesterone supplementation

    Diffuse thecal luteinization
    Luteinized granulosa
    Theca-cell tumors
    Metastatic ovarian cancer
    High-dose pregnenolone supplementation

    Low In Women: Possible Causes



    Uncommon (In non-pregnant women)
    Menstrual abnormalities

    Elevated In Men: Possible Causes


    High-dose pregnenolone supplementation
    Testicular tumors


    (Adult DHEA levels decline with aging. Our normal ranges are for young adults.)
    Elevated In Women: Possible Causes


    DHEA supplementation (androsterone and etiocholanolone may also increase)
    Congenital adrenal hyperplasia (pregnanetriol may also be elevated)
    Adult-onset adrenal hyperplasia (pregnanetriol may also be elevated)
    (May present as anxiety)
    Adrenal neoplasm
    High-dose pregnenolone supplementation

    (Elevated DHEA is associated with hirsutism.)

    Low In Women: Possible Causes


    Age > 40 yr.

    Adrenal insufficiency
    Unipolar depression

    Elevated In Men: Possible Causes


    DHEA supplementation (androsterone and etiocholanolone may also increase)
    Congenital adrenal hyperplasia (pregnanetriol may also be elevated)
    Adult-onset adrenal hyperplasia (pregnanetriol may also be elevated)
    (May present as anxiety)
    Adrenal neoplasm
    High-dose pregnenolone supplementation

    Low In Men: Possible Causes


    Age > 40 yr.

    Adrenal insufficiency
    Unipolar depression


    Etiocholanolone and Androsterone
    (Androsterone and etiocholanolone are in the 17-ketosteroids group of steroid metabolites, which also includes DHEA, pregnanetriol and pregnanediol.)
    Elevated: Possible Causes


    DHEA supplementation (esp. females > 25 mg/day; males > 50 mg/day)

    Androgen producing gonadal tumors
    Congenital adrenal hyperplasia
    Adult-onset adrenal hyperplasia
    Serious illnesses (burns and others)

    Low: Possible Causes


    Age > 40 yr.

    Adrenal insufficiency
    Anorexia nervosa


    Elevated: Possible Causes


    Adrenogenital syndrome (congenital adrenal hyperplasia), which is marked by excessive adrenal androgen secretion and virilization. Women with this condition fail to develop normal secondary sex characteristics and show marked masculinization of external genitalia at birth. Men usually appear normal at birth but later develop signs of somatic and sexual precocity.

    Adult-onset adrenal hyperplasia (may present as anxiety)

    High-dose pregnenolone supplementation


    Cortisol and Cortisone
    Elevated: Possible Causes


    Emotional or physical stress
    Intensive physical exercise

    Cortisol or cortisone administration
    Unipolar depression
    Sleep deprivation

    Cushing's syndrome (hypercortisolism)
    Cushing's disease (hypercortisolism 2 to excess ACTH production by pituitary adenoma)
    Ectopic ACTH production

    Low: Possible Causes


    Adrenal insufficiency
    (follow-up with ACTH challenge test or multi-point serum or saliva cortisol)
    Synthetic corticosteroid administration
    Chronic fatigue syndrome
    Rheumatoid arthritis


    (Aldosterone excretion varies inversely with salt intake.)
    Elevated: Possible Causes


    Low salt diet

    Primary aldosteronism with low renin hypertension
    (associated with polyuria and hypokalemia)
    High-dose pregnenolone supplementation
    May be elevated in patients taking spirinolactone, an aldosterone antagonist

    Low: Possible Causes


    High salt diet

    Adrenal insufficiency
    (In extreme cases may be associated with fatigue, hypotension, dehydration and polyuria)
    Enzyme defects in aldosterone synthesis
    Heparin administration


    Tetrahydrocortisone, Tetrahydrocortisol, allo-Tetrahydrocortisol
    Elevated: Possible Causes


    Medical or surgical stress
    ACTH, cortisone or cortisol therapy

    Cushing's Syndrome
    Adrenocortical adenomas

    Low: Possible Causes


    Synthetic corticosteroid administration

    Adrenal insufficiency
    Congenital adrenal hyperplasia


    Tetrahydrocorticosterone, allo-Tetrahydrocortisosterone
    Elevated: Possible Causes


    18-hydroxylase (Aldosterone synthase I) deficiency
    18-hydroxysteroid dehydrogenase (Aldosterone synthase II) deficiency


  17. http://**************.com/forum/show...6925#post16925

    muscle chat room

    Quote Originally Posted by Chrisgj View Post
    First, before I begin, I will say that I have respect for Dr. Crislers knowledge and I have learned a lot from him. I have to be candid about my thoughts on this thread topic though, as well counter his relentless negative comments about me through the years. That is very rude and ignorant. I appreciate the many of you who support me.

    Dr. Crisler, where have I tried to put myself out as a medical expert? My tag line on RTH and STTM says I'm not. How many times have I said "check with your doctor"? To many to count. I limit myself to a few tests I will give opinions on, I explain when they are doing the HRT wrong (ie using Armour before treating AI) and I usually try to direct people to osteopaths. The people I deal with print out my response and show their doctor. I very rarely mention self treating. I can't remember the last time I mentioned it. Show where I've hurt anyone. I haven't. If I feel someones tests point to them point hypopit, hypothyroid, etc, I say so and help them figure out what to do.

    Dr. Crisler, I should just post links to studies and articles? If I relied on that, most people wouldn't understand what tests to ask for, how the hormone ranges are flawed and virtually everyone falls in them or how to interpret the acth stim test or understand why the doses of dex prescribed for Addison's is messing up everyone or how to properly prepare for and interpret the aldosterone and renin tests or to insist on contrast as well as no contrast for pit MRI...

    Many, many people have told me and that I saved their life from the info I put out. I literally saved the life of a woman who was in a coma and hours from death a couple of years ago. If it wasn't for me, she'd have died. He docs gave her solu-medrol and diagnosed her with Sheehan's syndrome only because of my input. The solu-medrol (the had kept her on solu-cortef) brought her out of the coma within a couple of hours and her recovery was remarkable. The docs with their "great knowledge" would have caused her to die. I also helped her get help with her thyroid.

    You put down my Hypopituitary Faqs earlier this year. People have told me it's great. Are you that threatened by me that you would try keep people from reading good info such as that? There is nothing wrong with it, nothing dangerous about it. It's brilliant. (being arrogant for a moment).

    I wrote an article on the ACTH stimulation test on Wikipedia. Will you put that article down as well because a patient wrote it? It's been read by over 20,000 people since I put it up in Feb. Between STTM and RTH read over 3,000 times. By this time next year at least 100,000 people will have read it. That article is helping a lot of people. I've got nothing but praise for it. Not one doc has criticized it. I've been told by patients their doc thought it was excellent and made sense and now use it to properly diagnose primary or secondary AI. Many of those same docs I'm told have poured over all my info. Doctors have emailed me asking for my opinion. I even have an endo "friend" who learns from me, teaches me and helps me help others.

    It boils down to this, you don't know much about treating adrenals, thyroid and pituitary (I've read many say you aren't good at those) and are jealous and can't stand that the internet gives people like me who didn't go to med school power. I have spent countless hours reading on the net and reading medical books know more than you about how to diagnose and treat all those. Why did I spend all those hours? I know it's not as much as a doctor and I know they overall know more. I had to do this much research because I was trying to help myself where my primary, a gastroenterolist, neurologist and two endos didn't. i got mad and decided I would learn it all (figuratively of course). I started buying endo med books (examples Degroots Endocringoloy, Beckers Endocrinology, Williams Endocrinology). The first two years I read those an average of 2 hours per day in between learning from and helping others. I also read many layperson books on topics such as adrenals and thyroid. Hundreds of hours I spent after spending thousands of doctors on docs who didn't help me while my health went further and further into the tank. I estimate that I'm out at least $100,000 for medical and lost work. I don't want to know what the figure is.

    You would not believe how I suffered. I've you haven't experienced it, you can't know. I finally found a doctor who practices Environmental Medicine in 03. He helped me greatly and doesn't give up on anyone. Seeing him really opened me eyes to how messed up the medical profession really was. My first visit I was there at least 3 hours. Each visit after that is about an hour, sometimes more. Before him, my whole life any doc visit was an average of 15 minutes and they didn't know what was wrong with me (I sufferered for 35 years, before i got so bad I had to find that Environmental doc)

    Dr. Crisler you are part of the problem with health care that I and the public try to counter. That you don't like my posting warning of Anti Aging docs that tells me you consider yourself one. You may not be hurting people, but most of those docs are. Many docs on there have no idea what they are doing and I haven't seen anyone say an anti aging doc did anything besides hurt them. I've seen several people over the years say an anti aging doc prescribed them HGH only. I look at their earlier tests and see the doc should have treated their adrenals, thyroid and hypogonad, but no, HGH cures all. Hormones are not for treating aging, but for treating true hormone deficiencies. Most of those patients aren't even told the therapies will eventually permanently suppress their own natural hormone production and that should always be considered before even treating true adrenal and thyroid disease.

    You just treat a smidge of the body, don't want anyone to know more than you how to treat other areas you don't concentrate on. When people disagree with you, you storm off never to return until you eventually do, just like a spoiled child. I've have books to study hormone behavior and yours suggest a degree of AI, maybe caused by TRT if you're doing that.

    Just treating mens testosterone deficiency isn't good enough. You must be great at treating that as well has adrenals, thyroid, GH deficiency diabetes as well as mineral and vitamin deficiency, allerigies, candida, etc to really help people. I can only recommend osteopaths since as a group they treat the whole body. If doctors were actually helping people, there wouldn't be a need for people like me. Doctors come to me for advice and patients have told that their doc treats them based on my articles and protocols.

    I don't do this because I want to play doctor or seek attention. I do it because there an epidemic of desperate suffering people out there who would have no one to steer them if people like me weren't there for them. Many of those people are told by docs that give them 10 minutes each appointment they have CFS/Fibro and nothing can be done. Most of these people are hypoadrenal and hypothyroid, but those docs aren't trained to look for causes like that.

    Ask people who I've helped where they would be without people like. Go ahead, post a thread on my forum on RTH and ask them. I guarantee you, there will be an avalanche of responses. Look at the comments on my guest book.
    Yahoo! Small Business - Web Hosting

    I could not, in good conscience not help others. I actually got burned out over 2 years ago, but I keep going. Most people like me are an asset and should be regarded by docs in that way. True, i don't know as much as any doctor, but I'm helping my fellow man. If starting tomorrow all doctors were helping people like they should and I wasn't needed anymore, that would be the a very great day for me.


  18. Quote Originally Posted by JanSz View Post
    Some one trying to get attention
    The phrase "bump" works good..

  19. Adrenal fatigue is not a situation where cortisol is continually low, or continually high.

    Adrenal fatigue is a situation where we make insufficient cortisol for a hard day's adventures, and we "run out of cortisol" during the day.

    Since we make the vast majority of our cortisol in our deep sleep, therefore if we get stressed in the morning, even those of us with early onset of adrenal fatigue can pump enough cortisol at that time to get by.

    If a person with early onset of adrenal fatigue has a nice cushy day, then that person's cortisol will read average or lower at all times during the day.

    But when a person with adrenal fatigue (insufficient cortisol) experiences a high stress event towards the end of the day, then that person's cortisol reservoir is inadequate to adequately suppress the free radical damage from the high stress event, and the person's cortisol will not be able to adequately quench the free radical damage from the stressful episode, and the person will experience too many of the effects of the free radical damage. Some obvious symptoms are sweats, nausea, stomach cramp, chest pain, panic attack. But salivary and serum labs are actually very reliable.

    The simplest way to measure adrenal fatigue (insufficient cortisol) is to perform a stress test and see whether you can get a high cortisol response. If you stress yourself at any time of the day, then you should always be able to get a short term high cortisol response.

    A stress test is as simple as a nice hard workout, for say 40 minutes.

    And if you're trying to measure early onset adrenal fatigue (cortisol insufficiency), then you need to do the workout in the evening - eg: after work around 5pm or 6pm is fine. Then as soon as your warm down is finished, collect a salivary cortisol sample and then mail it to the lab. Straight after your workout your cortisol should be high (ie: for a short time only) because a good hard workout creates a lot of free radical damage and cortisol's job is to quench all of the erroneous chemical signaling which arises from that free radical damage.

    But if the cortisol test comes back only average or low, then your body is making insufficient cortisol in the evening for life's nasty little challenges, and you have early onset adrenal fatigue (cortisol insufficiency).

    http://muscle chat room.com/forum/sh...6&postcount=11

    muscle chat room
    The Case Against Saliva Testing
    http://muscle chat room.com/forum/sh...light=salivary

    Salivary cortisol compared to serum cortisol
    http://muscle chat room.com/forum/sh...light=salivary

  20. http://**************.com/forum/show...0&postcount=16
    muscle chat room

    About Estrogen
    TMAGNUM FORUMS - Estradiol: Why You Should Care

    Good thread, read the whole thread, specially

    TMAGNUM FORUMS - Androgel is Useless


    Testosterone Replacement Therapy
    references, short-cuts
    TRT Links

  21. A4M :: Conference Library

    PC02c - Stress & Steroid Synthesis
    $20.00 Purchase Conference: A4M Las Vegas 2007
    Speaker: Patrick Hanaway, M.D.,
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    Length: 01h 50m 32s - 301 Slides

    less DHEA less insuline sensitivity, increase insuline resistance, increased inflamation, problems with cortisol (tends to increase cortisol production)

    DHEAs is a storage, reservuar,

    cortisol, when increased, sugar go up, anti-infalmatory, 2x drop from first morning check (8am 1hr after wake up) to next, increse insulin resistance

    if cortisol up then T3 down

    cortisol steal,


  22. http://muscle chatroom.com/forum/showthread.php?t=1584&page=2
    muscle chat room

    Quote Originally Posted by chilln View Post
    I also looked at your labs from your March thread: "An hard problem".


    The most obvious smoking gun, and its one which you have only partially investigated, is your high level of cortisol.

    You aren't going to be able to get far with your testosterone and estradiol issues whilst your cortisol is maxed out.

    Cortisol and insulin are the most critical hormones in the human body. Cortisol and insulin together interact with most of the hormones in our bodies.

    You really should try hard to convince the medical professionals whom you work with, to help you identify why your cortisol is high in order to get to the bottom of your testosterone/estradiol issues.


    The body's normal mechanism to increase cortisol is like this:
    brain processes several neurological inputs and determines tissue damage (macroscopic and microscopic) has increased, and sends message to hypothalamus ->
    hypothalamus (brain) increases ACTH ->
    puitary (brain) receives ACTH and increases CRH ->
    adrenals (above kidneys) receive CRH and increase cortisol.

    Your adrenals should only pump high cortisol when your brain detects that your body is under abnormal stress (eg: normal immune response, excess free radical damage, trauma injury, etc..)

    So there is a possibility that your body is still under stress - eg: long term damage to a tissue mass which is producing something vital - and the lack of this vital ingredient is causing excess free radical damage - and free radical damage is the usual outcome of a material deficiency.

    Another example of tissue damage is an auto-immune response which may have been triggered by an allergic reaction to finasteride.


    I acknowledge that one of your endos performed the dexamethasone suppression test, and that your cortisol decreased correctly - and yet the cortisol is high.

    The dexamethasone test confirmed a few things:

    It confirmed that your puitary will lower CRH when your ACTH reduces.
    It confirmed that your adrenals will lower cortisol when your ACTH reduces.
    It confirmed that your hypothalamus must therefore be sending excess ACTH to stimulate your pituitary to send excess CRH to stimulate your adrenals to produce excess cortisol.

    But there is still the possibility that your hypothalamus ACTH is "stuck on high" rather than responding normally to some warnings from other parts of your brain about tissue damage.


    So to conclude re the cortisol issue:

    We should be asking ourselves the question: Is you ACTH high (and therefore your cortisol is high) because something in your hypothalamus is broken (?), or is your ACTH high (and therefore your cortisol is high) because your body is responding to an excess of free radical damage somewhere (possibly auto-immune self-harm) ?

    To address this I would be looking at your inflammation markers. They are a very good indicator of microscopic tissue damage.

    If your inflammation markers are at idle, then most likely your ACTH is stuck on high, and you'll need to suppress ACTH - eg: with phosphatidylserine which is over-the-counter but still something which you should only take under the guidance of a medical professional.
    If you do pursue phosphatidylserine, then you and your medical professional should also monitor your cortisol via labs very frequently because as I stated earlier, cortisol and insulin are the most critical hormones in our bodies, so if you mess them in a non-optimal manner, then you're going to get yourself into some serious trouble.

    If your inflammation markers indicate high inflammation, then your previous finasteride use may have triggered an auto-immune response which has damaged some tissues. That's going to take a lot more work to identify which tissues are damaged and what is the workaround, so that discussion is best had after you measure those inflammation markers and confirm whether they indicate high or low inflammation.

    Please take this issue up with your medical professionals. It's non-trivial. Please do not take "no" for an answer. As always, persuasion is better than a direct line of questioning.


    If you identify your cortisol issue, and you reduce cortisol levels to appropriate for health, and even if you still can't boost testosterone via the usual methods, then you will have still done your body a huge favor, and you will have most likely increased your healthy active lifespan.

    On a different and less important tack, you seem to have researched the Fin forum thoroughly to come across the stats you published above, yet you weren't familiar with the difference between an aromatase inhibitor and a SERM, and these are critically different mechanisms to reduce estradiol.

    Perhaps these finasteride users are somehow assuming that all mechanisms to lower estradiol are equal and therefore not worth discussing, and therefore you do not read about comparisons between SERMs and aromatase inhibitors in the Fin forum.

    I'm not yet going to conclude anything about this oversight, but I sense it's going to become critical later on. If you could provide a little insight that would help me understand if there's a link between finasteride use and SERM use ?

  23. http://muscle chatroom.com/forum/showpost.php?p=18638&postcount =28

    muscle chat room

    Quote Originally Posted by Dr. John Crisler View Post
    Nope. I DO NOT want them to get labs drawn the day of the shot, ever.

    The second half of the week is fine. And no HCG then, if that is part of their regimen.
    [table 1 3 0] Weekly T-shots, HCG two days before T shot
    1 | Monday | T-Shot | no blood draw ever
    2 | Tuesday | no shot | no draw because first half of the week
    3 | Wednesday | no shot | no draw because first half of the week
    4 | Thursday | no shot | ambigious, morning no draw, aftenoon yes, (second half of the week)
    5 | Friday | no shot | This is the day to draw blood
    6 | Saturday | HCG | draw blood before HCG, lab available by appointment only,
    7 | Sunday | HCG | had to skip Saturday's HCG, ok to draw blood before HCG, but lab is not available

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

    Quote Originally Posted by Dr. John Crisler View Post
    Oh, I see. IF you are on a twice per week IM schedule, or daily or QOD HCG (as with TD), then go ahead and take your HCG.

    But never labs on IM day. It make sit harder to figure out what is going on.

    I hope this clears things up.
    with this one I am even less sure, but this is my best guess

    [table 1 3 0] 2x weekly T-shots, HCG two days before T shot
    1 | Monday | 0 hrs | T-Shot 7AM | no blood draw ever
    2 | Tuesday | 24+12=36 hrs | HCG 7PM | ok to draw before HCG shot
    3 | Wednesday | 36+24=60 hrs | HCG 7PM | ok to draw before HCG if HCG was skipped the day before
    4 | Thursday | 84 hrs | T-Shot 7PM | no blood draw ever
    5 | Friday | | no shot | ok to draw after 7PM
    6 | Saturday | 84+36=120hrs | HCG 7AM | ok to draw before HCG shot
    7 | Sunday | 168-24=144 hrs | HCG 7AM | ok to draw before HCG if HCG was skipped the day before

    for people doing T shots on other days or hours considered on above tables,
    remember that you are either on 7 or 3.5 day schedule,
    7*24=168 hrs
    3.5*24=84 hrs
    Print the table, write your own days and hours over what I posted.
    ============================== ============
    ============================== ============
    You are not fasting for the test: please make sure it has been a couple of hours since you ate or had sex prior to the draw.

    TAKE ALL MEDICATIONS AS PRESCRIBED. Take all supplements, but no vitamins.

    It is important to always have the labs drawn at the same time each day.


    It does not matter what day of the week you have the draw, except DO NOT HAVE THEM DONE ON TEST CYPIONATE INJECTION DAY, OR FOR TWO DAYS AFTER. For those on a testosterone gel: apply the gel at the same time as always, and make sure it has been about 2-4 hours before you have the draw.

    If you are on my HCG Protocol, with test cypionate, do not take any HCG the week of the labs. If you are on testosterone gel, go ahead and take your HCG as usual. ''

  24. http://**************.com/forum/show...8725#post18725
    muscle chat room
    Post #10
    High Cortisol
    Quote Originally Posted by chilln View Post
    For an AM fasting result, that's really nasty.

    I just want to cover off why you should not eat between dinner and your AM cortisol result. This is because cortisol rises after a meal to suppress the free radicals which eventuate from the digestion process. The free radical eventuate because we cannot provide our digestion machinery with 100% of all of the input micronutrients which our machinery needs to process the vast varieties of foods we eat.

    Thus some of the metabolism processes miss out on a few important molecules, and the break in the production line causes the "hanging" molecules to hit other molecules which are en-route to a different location. Thus causing free radical damage.

    So if you forgot to fast, then please 'fess up. You may need to redo the test.


    Here I've reused some of what I wrote for "way" a few hours ago, but it applies in your case as much as it applies to "way". I've also adapted some salient details to your hypermetabolizer situation.

    When a person is not a hypermetabolizer, then the body's normal mechanism to increase cortisol is like this:

    brain processes several neurological inputs and determines tissue damage levels (macroscopic and microscopic) have increased, and so sends message to hypothalamus ->
    hypothalamus (brain) increases ACTH ->
    puitary (brain) receives ACTH and increases CRH ->
    adrenals (above kidneys) receive CRH and increase cortisol ->
    cortisol quenches erroneous signals from free radical damaged tissues.

    Therefore a non-hypermetabolizer's adrenals should only pump high cortisol when that person's brain detects that their body is subject to an increase in tissue damage (eg: normal immune response, excess free radical damage, trauma injury, etc..)


    If you are a hypermetabolizer, and you have a "hair-trigger" liver, and you have no lingering tissue damage, then your serum cortisol should be low in the mornings, even though your urinary cortisol would be high.

    A hypermetabolizer will produce high volumes of cortisol expecting their liver to metabolize them quickly into metabolites, leaving a residual low level of cortisol.
    A hair-trigger liver is needed to metabolize all the excess cortisol into metabolites as soon as their levels start to rise by even a small amount.

    This is not your situation. I only presented it as supportive info to help explain the next few cases.


    But if you are a hypermetabolizer, and you have a "hair-trigger" liver, and you do have lingering tissue damage, then your serum cortisol will be high in the mornings because your brain will send the message to produce more and more cortisol until it is satisfied that the serum cortisol levels have increased appropriately to address the tissue damage.

    This is the same as a non-hypermetablizer with lingering tissue damage.

    This may be your situation.

    In this case you and your medical professional adviser may want to address the source of the tissue damage as the key to resolving the problem. Suppressing cortisol would only allow the tissue damage to continue to cause problems.


    If you are a hypermetabolizer with a "slow-starting" liver, without any lingering tissue damage, then you would still measure high serum cortisol in the morning, because your liver lets your cortisol get high before it wakes up and starts metabolizing it to metabolites.

    A hypermetabolizer will produce high volumes of cortisol expecting their liver to metabolize them quickly into metabolites, leaving a residual low level of cortisol. But if aging, or wear and tear, have caused your liver to to become a slow-starter, then cortiosl levels will be initially increase until your liver's metabolization rate eventually catches up to your cortisol production rate. At that point your cortisol levels will finally stabilize - but at a high level.

    Your cortisol levels will stay high unnecessarily if your brain doesn't agree to reduce your cortisol production rate (starting by reducing ACTH from the hypothalamus), or if you liver doesn't work a little overtime to catch up the initial lost ground.

    This may be your situation.

    In this case suppressing the high production of cortisol to normal levels may not succeed if the liver allows the cortisol to get high before it starts metabolizing the cortisol into metabolites. But on the other hand, it may work if the liver eventually puts the pedal to the metal and eventually catches up metabolizing the initial excess cortisol.

    Therefore you and your medical professional adviser might want to first eliminate the possibilty of lingering tissue damage via a test for inflammation markers, and provided the inflammation markers are all low, then you may want to work together to consider suppressing the high production of cortisol.


    If you are a hypermetabolizer with a "slow-starting" liver, and you do have lingering tissue damage, then your serum cortisol will be high in the morning, because your liver lets your cortisol get high before it wakes up and starts metabolizing it to metabolites.

    A hypermetabolizer will produce very high volumes of cortisol when only a high level of serum cortisol is required, and the hypermetabolizer expects their liver to metabolize the majority of the cortisol quickly into metabolites, still leaving a residual high level of cortisol.

    But if aging, or wear and tear, have caused your liver to to become a slow-starter, then cortisol levels will initially increase until the liver's metabolization rate eventually catches up to the cortisol production rate. At that point the cortisol levels will finally stabilize - but at a high level.

    This may be your situation.

    Therefore you and your medical professional adviser might want to first determine if you have any lingering tissue damage via a test for inflammation markers, and if any of the inflammation markers are measured to be high, then you may want to work together to find the root cause of your tissue damage, and try to heal that as best as possible to lower your cortisol. You should not necessarily suppress the high production of cortisol unless it's higher than appropriate for the amount of tissue damage (a very difficult calculation in 2008).


    In conclusion:

    So if you are a hypermetabolizer, then it complicates the understanding of your problem, but even for a hypermetabolizer, high cortisol is not an impossible situation to identify and resolve.

    No matter whether you are a hyper metabolizer or not, you and your medical professional adviser should address the possibility of tissue damage via a reasonably rounded investigation of your inflammation markers.

    Then you may want to consider agreeing to suppress cortisol only if inflammation is definitely low.

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    MENTAL ACUITY - Methylcobalamin 12.5 mg
    Methylcobalamin, perhaps the most important and potent of the
    essential cobalamins, plays a vital part in cell growth.
    Particularly important for your central nervous system, it helps
    promote healthy homocysteine levels and helps increase
    the brain's focus and clarity, and the spinal cord's function.

    ENERGY - Dibencozide 12.5 mg
    Dibencozide metabolizes essential fatty acids to produce more energy.
    As a biologically active form of B-12, it reacts with cells to provide
    muscles and nerves with bursts of energy.

    LIVER SUPPORT - Cyanocobalamin 7.5 mg
    Cyanocobalamin, the most common of the cobalamins,
    becomes active in your liver, creating enzymes to help
    the body with blood formation, cell reproduction, iron utilization,
    and tissue synthesis, while aiding the digestion and absorption of foods.

    DETOXIFICATION - Hydroxocobalamin 2.5 mg
    Hydroxocobalamin, one of the three essential cobalamins that
    make up the vitamin B-12 complex, helps remove heavy metals
    from the system and supports overall detoxification.
    It also assists with methylation and energy production.


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