Jan's BloodTest April13/2007

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  1. 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.

    Internet Savvy Medical Expert:

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

  2. 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.

  3. 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?

  4. 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.

  5. 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.

  6. 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 ?

  7. 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

  8. 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



  9. 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.


  10. Jan.....you looking for me?


  11. 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


  12. 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.


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

  14. 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

  15. 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

  16. A4M :: Conference Library

    PC02c - Stress & Steroid Synthesis
    $20.00 Purchase Conference: A4M Las Vegas 2007
    Speaker: Patrick Hanaway, M.D.,
    Date/Time: December 12, 2007 8:00 am - 5:00 pm
    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,


  17. 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 ?

  18. 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. ''

  19. 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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  23. A4M :: Conference Library

    Thierry Hertoghe, MD

    PC01d - Adult Growth Deficiences Treatments
    $20.00 Purchase Conference: A4M Orlando 2007
    Speaker: Thierry Hertoghe, MD
    Date/Time: April 26, 2007 6:00 pm - 7:00 pm
    Length: 40m 25s - 124 Slides

    PC01d - Cortisone
    $20.00 Purchase Conference: A4M Las Vegas 2006
    Speaker: Thierry Hertoghe, MD
    Date/Time: December 7, 2006 6:00 pm - 7:00 pm
    Length: 55m 31s - 175 Slides

    PC01g - Cortisone
    $20.00 Purchase Conference: A4M Orlando 2007
    Speaker: Thierry Hertoghe, MD
    Date/Time: April 26, 2007 6:00 pm - 7:00 pm
    Length: 48m 58s - 261 Slides

    PC01g - Cortisone
    $20.00 Purchase Conference: A4M Chicago 2007
    Speaker: Thierry Hertoghe, MD
    Date/Time: August 2, 2007 6:00 pm - 5:30 pm
    Length: 57m 20s - 175 Slides

    PC01c - DHEA - The Mother Hormone
    $20.00 Purchase Conference: A4M Chicago 2007
    Speaker: Thierry Hertoghe, MD
    Date/Time: August 2, 2007 6:00 pm - 5:30 pm
    Length: 32m 01s - 87 Slides

    GS02a - Eye Opener: Progesterone Therapy in Men
    $20.00 Purchase Conference: A4M Las Vegas 2006
    Speaker: Thierry Hertoghe, MD
    Date/Time: December 9, 2006 6:00 pm - 4:10 pm
    Length: 38m 22s - 158 Slides

    PC04d - Female Hormones
    $20.00 Purchase Conference: A4M Chicago 2006
    Speaker: Thierry Hertoghe, MD
    Date/Time: July 14, 2006 6:00 pm - 5:30 pm
    Length: 01h 00m 18s - 224 Slides

    PC05Bb - Hormone Balance to Intimacy Health and Quality of Life
    $16.00 Purchase Conference: A4M Las Vegas 2006
    Speaker: Thierry Hertoghe, MD
    Date/Time: December 7, 2006 6:00 pm - 5:30 pm
    Length: 22m 07s - 1 Slide

    GS01c - How Efficient are Melatonin, Growth Hormone, Thyroid, DHEA and Estrogen Corrective Therapies to Prevent or Reverse Coronary Insufficienty: The Data
    $16.00 Purchase Conference: A4M Chicago 2006
    Speaker: Thierry Hertoghe, MD
    Date/Time: July 15, 2006 6:00 pm - 7:30 pm
    Length: 32m 02s - 1 Slide

    GS01h - How to Improve Hormone Levels by Positive Psychological Attitudes: The Scientific Data
    $20.00 Purchase Conference: A4M Chicago 2007
    Speaker: Thierry Hertoghe, MD
    Date/Time: August 3, 2007 6:00 pm - 4:00 pm
    Length: 44m 28s - 184 Slides

    PC01a - Introduction to Treating Adult Hormone Deficiency
    $20.00 Purchase Conference: A4M Chicago 2007
    Speaker: Thierry Hertoghe, MD
    Date/Time: August 2, 2007 6:00 pm - 5:30 pm
    Length: 01h 00m 14s - 308 Slides

    PC01a - Introduction to Treating Adult Hormone Deficiency
    $20.00 Purchase Conference: A4M Las Vegas 2007
    Speaker: Thierry Hertoghe, MD
    Date/Time: December 12, 2007 6:00 pm - 6:00 pm
    Length: 57m 18s - 309 Slides

    PC01a - Introduction to Treating Hormone Deficiency
    $16.00 Purchase Conference: A4M Las Vegas 2006
    Speaker: Thierry Hertoghe, MD
    Date/Time: December 7, 2006 6:00 pm - 7:00 pm
    Length: 01h 07m 51s - 1 Slide

    PC01a - Introduction to Treating Hormone Deficiency
    $20.00 Purchase Conference: A4M Orlando 2007
    Speaker: Thierry Hertoghe, MD
    Date/Time: April 26, 2007 6:00 pm - 7:00 pm
    Length: 01h 04m 24s - 364 Slides

    PC04a - Introduction to Treating Hormone Deficiency: The ABC's with Tips on How to Boost their Safety and Efficacy
    $20.00 Purchase Conference: A4M Chicago 2006
    Speaker: Thierry Hertoghe, MD
    Date/Time: July 14, 2006 6:00 pm - 5:30 pm
    Length: 01h 03m 28s - 469 Slides

    EW03 - Live Consultation
    $20.00 Purchase Conference: A4M Orlando 2007
    Speaker: Thierry Hertoghe, MD
    Date/Time: April 26, 2007 6:00 pm - 8:00 pm
    Length: 02h 08m 16s - 11 Slides

    PC02B - Office Microscopy: Basics in Office Methods of Blood and Saliva Microscopic Diagnostics
    $20.00 Purchase Conference: A4M Chicago 2006
    Speakers: Nick Delgado, PhD , Thierry Hertoghe, MD
    Date/Time: July 14, 2006 6:00 pm - 5:00 pm
    Length: 01h 50m 02s - 66 Slides

    EW05a - Questions & Answers - Hormone Therapy Problems
    $16.00 Purchase Conference: A4M Chicago 2007
    Speaker: Thierry Hertoghe, MD
    Date/Time: August 2, 2007 6:00 pm - 7:00 pm
    Length: 01h 21m 24s - 1 Slide

    PC01k - Questions and Answers
    $20.00 Purchase Conference: A4M Las Vegas 2006
    Speaker: Thierry Hertoghe, MD
    Date/Time: December 7, 2006 6:00 pm - 7:00 pm
    Length: 01h 08m 04s - 11 Slides

    PC01b - Testosterone - Andropause and Sexual Health: DHEA - The Mother Hormone
    $20.00 Purchase Conference: A4M Chicago 2007
    Speaker: Thierry Hertoghe, MD
    Date/Time: August 2, 2007 6:00 pm - 5:30 pm
    Length: 57m 03s - 114 Slides

    PC01b - Testosterone: For Men and Women and Sexual Health
    $20.00 Purchase Conference: A4M Las Vegas 2007
    Speaker: Thierry Hertoghe, MD
    Date/Time: December 12, 2007 6:00 pm - 6:00 pm
    Length: 59m 59s - 195 Slides

    GS03b - The Psychological Attitudes of Centenarians and their Hormonal Roots
    $20.00 Purchase Conference: A4M Las Vegas 2005
    Speaker: Thierry Hertoghe, MD
    Date/Time: December 12, 2005 6:00 pm - 12:00 am
    Length: 55m 16s - 155 Slides

    PC01g - Thyroid Hormone
    $20.00 Purchase Conference: A4M Las Vegas 2006
    Speaker: Thierry Hertoghe, MD
    Date/Time: December 7, 2006 6:00 pm - 7:00 pm
    Length: 35m 41s - 272 Slides

    PC04g - Thyroid Hormones
    $20.00 Purchase Conference: A4M Chicago 2006
    Speaker: Thierry Hertoghe, MD
    Date/Time: July 14, 2006 6:00 pm - 5:30 pm
    Length: 56m 05s - 272 Slides

    PC01i - Weight Loss: The Answer
    $16.00 Purchase Conference: A4M Orlando 2007
    Speakers: Thierry Hertoghe, MD , Pamela Smith, M.D., MPH
    Date/Time: April 26, 2007 6:00 pm - 7:00 pm
    Length: 88 Slides

  24. http://muscle chat room.com/forum/showthread.php?p=21934#post219 34

    My pregnenolone and progesterone levels bother me to no end.
    My lattest known 3/19/08
    Progesterone, LC/MS/MS =0.1(<1.4)ng/mL
    Pregnenolone---------- =11(13-208)ng/dL

    Reading Tierry Herthoge book, he wants Pregnenolone> 100ng/dL
    Now I came across his Dec 2006 speach in Las Vegas.
    I posted below summary of the info included in previev.
    I have also bought the course ($20)
    Will post additional info as I listen to presentation.
    I guess that there is no doubts that dr Herhoge is one of the giants in anti-aging, can't wait to listen to his opinion.

    I know that dr John is against supplying progesterone to men,
    if it is ofensive, I will store my notes elsevere.
    ============================== =======================

    A4M :: Conference Library

    GS02a - Eye Opener: Progesterone Therapy in Men
    Conference: A4M Las Vegas 2006
    Speaker: Thierry Hertoghe, MD
    Date/Time: December 9, 2006 7:00 am - 4:10 pm
    Length: 38m 22s - 158 Slides
    ============================== =====================

    Progesterone theraphy in men.
    By Thierry Herthoge, MD

    About giving progesterone to men.

    Progesterone amount in men is
    7x lower than testosterone
    more than DHT
    more that estrodial and estrone
    10x more than melatonin
    many more times more than FreeT4

    quantity of progesterone than men have is the same as in women during half of their reproductive life (same as during folicular phase, first phase of cycle). During that (folicular phase) progesterone in men and women comes from adrenal glands only. In second part of woman's cycle additional progesterone is made by ovary.
    .............................. .............................. ..........................
    http://www.musc lechatroom.com/forum/showthread.php?4785-What-does-Dr-Thierry-Hertoghe-take-on-a-daily-basis&

    What does Dr Thierry Hertoghe take on a daily basis?
    This is what he takes on a daily basis:

    testosterone gel 10%: 1 dose/day
    pregnenolone: 50 mg/day
    melatonin: 0.5 mg sublingual/day
    thyroid armour: 1.5 grain a day
    hydrocortison: 30 mg/day
    9 alfa fludrocortison: 100 ug/day
    dhea: 40 mg/day
    finasteride: 2.5 mg a day
    progesterone: 100 mg/day
    gh: 0.01 iu/day
    vitamin e: 400 mg/day
    coq10: 100 mg/day
    multivitamin: 1/day
    carnitine: 4g/day
    fish oil: 3/day
    b-complex: 1/day


  25. http://muscle chatroom.com/forum/showpost.php?p=22363&postcount =9
    Quote Originally Posted by OldGator View Post
    Right on.

    But may I add that even with all other things in order I still had high SHBG 57-65 (Quest 18-47) long before I started TRT and even 3-4 months into it. Then Doc Shippen suggested low dose danazol (20mg/day) and my SHBG plummeted to the 22-28 range ever since (almost 12 months now). That pill alone almost doubled my free test (per Shippen's chart).

    Funny thing is, if you Google "danazol" you won't find any mention of SHBG. Must have been a secondary effect thing.
    Quote Originally Posted by chilln View Post
    You're a star.

    After reading your note I found this incredible abstract on Pubmed:

    Changes in the SHBG concentration during danazol t...[Acta Obstet Gynecol Scand Suppl. 1984] - PubMed Result

    This incredible abstract actually spells out all the juicy bits instead of trying to get you to buy the original document (only available on paper)


    Changes in the SHBG concentration during danazol treatment.
    Gershagen S, Döberl A, Rannevik G.

    Serum levels of sex hormone binding globulin (SHBG) were measured by radioelectro-immunoassay before and during administration of danazol in daily doses varying between 200 and 800 mg for a period of 1-6 months. The patients consisted of different groups of regularly menstruating women (n = 76) and of postmenopausal women (n = 12). A rapid proportional decrease in SHBG was seen at all dose levels in both pre- and postmenopausal women, starting within the first 24 hours and reaching statistical significance by 48 hours. The fractional rate of fall appeared to be determined by the metabolic half-life of the protein itself. Plotting log concentrations of SHBG versus time and using the slope of the linear regression for calculations, the half-life of SHBG appeared to be 15 +/- 5.7 (SD) days. After approximately one month of treatment, the SHBG concentrations began to approach a new steady state at a level of approximately 20-30% of the original concentration, depending on the dose of danazol. The proportional suppression of SHBG was significantly greater following 600 or 800 mg of danazol daily than following 200 or 400 mg. However, with all doses the SHBG levels after one month of treatment were well below the levels normally found in healthy males. The mean proportional reduction following a certain dose was almost identical in premenopausal and postmenopausal women. The findings of the present investigation suggest that danazol exerts a direct inhibitory effect on the hepatic synthesis of SHBG, which is dependent of the dose of danazol, independent of estrogen concentration, but possibly accentuated by endogenous androgens.

  26. Page 53 fro dr Hertoghe book.
    Attached Images Attached Images  

  27. edit 12/12/2012

    Dr Hertoghe

    The Hormone Handbook 2Ed 2010

    important, just found looking thru his book

    page 69

    GH Growth Hormone
    Excess, lowers SHBG


    For our friends (man & women)
    with high SHBG

    I have not heard of this connection before today.

    page 58

    IGF-1 men
    220-300 optimal
    0-180 GH probably deficient
    reference (21-30years) (114-492)ug/L

    3000 optimal
    >4000 GH probably deficient
    reference (21-30years) (2000-4000)ug/L


    pppppppppppppppppppppppppppppp pppppppppppppppppppppppppppppp pppppppppppp

    On GH my fasting insulin has gone from 3 to 15.
    I see my doc next week. Hopefully he has a trick up his sleeve.

    I think the usual "trick" is to cut your hGH dose.

    pppppppppppppppppppppppppppppp pppppppppppppppppppppppppppppp pppppppppppp


    ng/mL X 0.035 = nmol/L
    1000 ng/mL = 1 mg/L
    1000 mcg= 1mg
    4mg/L=4000(ng/mL) x 0.035=140(nmol/L)

    Growth Hormone
    per Tierry Hertoghe MD Hormone Solution
    supplementation required when
    dose 0.02 - 0.4mg/day
    1 mg. of powder GH = 3 iu
    Dr Braveman in his presentation shows (0.54, 0.52, 0.48, 0.47, 0.46)mg/day in consecutive years
    There are also values for 10 years study.
    Increasing IGF-1 Levels to the Upper Range of Normal to Fight Disease - A4M Orlando 2009 - American Academy of Anti-Aging Medicine :: PROLibraries.com - Online Professional Education - Online Conferences - Professional Lectures - Conference Education
    Suzan Somers uses 0.08mg=0.24iu/day (because of her breast cancer)(page 66 of her book Breakthru)
    Hertoghe uses 0.02iu/day(page 16) =0.007mg/day

    body produces 0.25 - 0.5mg/day
    body produces 0.75 - 1.5iu/day

    Hertoghe, top p267 (attached) advices HGH at bed time,
    Suzan is takig her's in the morning.

    Signs of overdosage:
    swolen feet, pins and needles in the fingers
    carpral tunnel syndrome
    pain in the joints (real serious)

    Arginine(7-12)g/day at bed time or one hr befor exercise (from table p268), 2-3x/day (text p267), work best in young(20-35) and lean
    Glutamine 2g/day at bed time, works in older adults (32-64)---------4x500mg pills
    Lysine (1-3)g/day at bed time, work in young(15-35) w/arginine
    Ornithine (2.5-5)g/day works in young(20-35) and lean
    Glycine (5-7)g/day-------------------------------------2x1000mg pills
    Tryptophan (5-10)g/day small GH response, best add B6 & C
    GHB(furanone) (0.5-1)g/day
    Niacin (0.2-1)g
    ============================== ============================== =========
    NutrEval June 8/08(uncompleted)


    ONE 11/28/07
    ============================== ===

    DHEA article by James South.

    DHEA --> INSULIN -- glucose
    DHEA --> IGF-1 -- GH
    ============================== ===
    -----http://muscle--------chatroom.com/forum/showpost.php?p=35600&postcount =13

    Quote Originally Posted by chilln View Post
    1 IU per day. 6 days on, 1 day off. 4 weeks on 1 week off. For 3 months, then stop.
    Sleep improved in the "on" weeks, to the point where I didn't need melatonin. But I wasn't stressing at the time because my job had hit a cruisey stage, and I wasn't chasing variety (ie: stress).
    Quote Originally Posted by chilln View Post
    This concept of a "constant" pulse is for body builders and hollywood types who don't know better.

    The smart ones amongst us dose up "just right" (using urinary GH labs and symptoms, not IGF-1 or IGFBP-3) and we get a nice gradual rise and fall overnight - a 12 hour pulse.

    When you actually use recombinant GH, the theories stop and the practical starts.
    Attached Images Attached Images      

  28. Fatty Acid Equivalent Names
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    Saturated Fats

    4:0 butanoic acid butyric acid
    6:0 hexanoic acid caproic acid
    8:0 octanoic acid caprylic acid
    10:0 decanoic acid capric acid
    12:0 dodecanoic acid lauric acid
    13:0 tridecanoic acid
    14:0 tetradecanoic acid myristic acid
    15:0 pentadecanoic acid
    16:0 hexadecanoic acid palmitic acid
    17:0 heptadecanoic acid margaric acid
    18:0 octadecanoic acid stearic acid
    19:0 nonadecanoic acid
    20:0 eicosanoic acid arachidic acid
    22:0 docosanoic acid behenic acid
    24:0 tetracosanoic acid lignoceric acid

    Type Isomer Systematic Name Common Name

    Monounsaturated Fats

    14:1 tetradecenoic acid myristoleic acid
    15:1 pentadecenoic acid
    16:1 undifferentiated hexadecenoic acid palmitoleic acid
    16:1 c
    16:1 t
    17:1 heptadecenoic acid
    18:1 undifferentiated octadecenoic acid oleic acid
    18:1 c
    18:1 t
    20:1 eicosenoic acid gadoleic acid
    22:1 undifferentiated docosenoic acid erucic acid
    22:1 c
    22:1 t
    24:1 c cis-tetracosenoic acid nervonic acid

    Type Isomer Systematic Name Common Name

    Polyunsaturated Fats

    16:2 undifferentiated hexadecadienoic acid
    18:2 undifferentiated octadecadienoic acid linoleic acid
    18:2 n-6 c,c
    18:2 c,t
    18:2 t,c
    18:2 t,t
    18:2 i
    18:2 t not further defined
    18:3 undifferentiated octadecatrienoic acid linolenic acid
    18:3 n-3 c,c,c alpha-linolenic acid
    18:3 n-6 c,c,c gamma-linolenic acid
    18:4 undifferentiated octadecatetraenoic acid parinaric acid
    20:2 n-6 c,c eicosadienoic acid
    20:3 undifferentiated eicosatrienoic acid
    20:3 n-3
    20:3 n-6
    20:4 undifferentiated eicosatetraenoic acid arachidonic acid
    20:4 n-3
    20:4 n-6
    20:5 n-3 eicosapentaenoic acid (EPA) timnodonic acid
    22:2 docosadienoic acid brassic acid
    22:5 n-3 docosapentaenoic acid (DPA) clupanodonic acid
    22:6 n-3 docosahexaenoic acid (DHA)

    Click on any link to see foods highest in that nutrient.

    Fats & Fatty Acids &ndash; NutritionData.com



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


  30. This post is a place maker, please do not respond, thank you.

  31. This post is a place maker, please do not respond, thank you.

  32. Quote Originally Posted by JanSz View Post
    This post is a place maker, please do not respond, thank you.
    has it been 18 months since your last labwork?
  33. Question Question re T-dose chart

    hi JanSz,

    You state below that "in the study endogenous testosterone was blocked, testis were not producing T during study". Does this imply that if one's natural baseline TT is, say 350ng/Dl, then for any given x-y value on the table, one should add 350 to the TT value ( i.e, 200mg TE/wk = ( 1058 + 350 ), or does the 212.23 value represent such a baseline measurement?



    Quote Originally Posted by JanSz View Post
    Using my study above using RoidCalculator, I note that on weekly injection test blood level are half on minimum of what they are at the max.
    Using this study, I know T levels at the minimum. Blood drawn on the day of weekly shot right before the shot.

    AJP - Endocrinology and Metabolism -- Bhasin et al. 281 (6): E1172 Table 2

    Testosterone dose-response relationships in healthy young men -- Bhasin et al. 281 (6): E1172 -- AJP - Endocrinology and Metabolism

    Testosterone dose-response relationships in healthy young men -- Bhasin et al. 281 (6): E1172 -- AJP - Endocrinology and Metabolism

    My analysis is shown on the attached chart, also bottom line results are below. Variation= ±75 should be added when reading the table.
    Also remember that in the study endogenous testosterone was blocked, testis were not producing T during study.

    DepoT TotalT SHBG FreeT SHBG FreeT
    25 353 xxxx 300 xxxx 250
    30 381 xxxx 300 xxxx 250
    35 410 xxxx 300 xxxx 250
    40 438 xxxx 300 xxxx 250
    45 466 xxxx 300 xxxx 250
    50 494 xxxx 300 xxxx 250
    55 522 xxxx 300 xxxx 250
    60 551 xxxx 300 xxxx 250
    65 579 xxxx 300 xxxx 250
    70 607 xxxx 300 xxxx 250
    75 635 xxxx 300 xxxx 250
    80 663 xxxx 300 xxxx 250
    85 692 xxxx 300 xxxx 250
    90 720 xxxx 300 xxxx 250
    95 748 xxxx 300 xxxx 250
    100 776 xx5 300 14.4 250
    105 805 xx7 300 16.5 250
    110 833 xx9 300 18.6 250
    115 861 10.8 300 20.7 250
    120 889 xx13 300 xx23 250
    125 917 xx15 300 xx25 250
    130 946 16.7 300 x27.3 250
    135 974 18.7 300 x29.4 250
    140 1002 xx21 300 x31.5 250
    145 1030 22.6 300 x33.5 250
    150 1058 24.5 300 x35.6 250
    155 1087 26.4 300 xx38 250
    160 1115 28.4 300 xx40 250
    165 1143 30.4 300 x42.2 250
    170 1171 32.3 300 x44.4 250
    175 1199 34.3 300 x46.3 250
    180 1228 36.3 300 x48.5 250
    185 1256 38.2 300 x50.7 250
    190 1284 xx40 300 x52.8 250
    195 1312 xxxx 300 xx55 250
    200 1340 xx44 300 xx57 250
    205 1369 xxxx 300 x59.3 250
    210 1397 xx48 300 x61.5 250
    215 1425 xxxx 300 x63.4 250
    220 1453 51.7 300 xxxx 250
    225 1481 xxxx 300 xxxx 250
    230 1510 55.6 300 xxxx 250
    235 1538 xxxx 300 xxxx 250
    240 1566 xxxx 300 xxxx 250
    245 1594 xxxx 300 xxxx 250
    250 1622 63.5 300 xxxx 250
    255 1651 xxxx 300 xxxx 250
    260 1679 xxxx 300 xxxx 250
    265 1707 xxxx 300 xxxx 250
    270 1735 xxxx 300 xxxx 250
    275 1763 xxxx 300 xxxx 250
    280 1792 xxxx 300 xxxx 250
    285 1820 xxxx 300 xxxx 250
    290 1848 xxxx 300 xxxx 250
    295 1876 xxxx 300 xxxx 250
    300 1904 83.0 300 99.9 250
    Free & Bioavailable Testosterone calculator
    Unit conversion
    Conventional units - SI units

    Chemistry Conversion

    Unit Prefix Conversion Calculator
    Adrenal Labs - How to Interpret them ***
    Stop The Thyroid Madness :: View topic - *** Adrenal Labs - How to Interpret them ***

    Stop The Thyroid Madness » ADRENALS FAQ–the most frequently asked questions

  34. candida Remove Replace Reinoculate Repair

    ============================== ============================
    SCIO - Bio-Energetic Wellness Centre

    Treatment of leaky gut syndrome
    The aim of the treatment protocol is to remove obstructions to metabolic processes, and to encourage the body to self-regulate these vital processes. The four pillars of treatment are: remove, replace, reinoculate and repair.

    1. Remove

    1.1 Parasites, bacteria and fungi: Removal of the latter can be effected with herbal products such as Warburgia,
    Taheebo or Pau D’Arco, Citricidal, Para 90 etc., or an essential oil product such as
    Origanum capsules (Pranarom), or Rife Resonator therapy. Usually about 2 weeks’ treatment is needed.

    1.2 Dietary toxins, additives, chemicals and foods to which the patient may be sensitive can be avoided by placing
    the patient on a diet eliminating foods commonly found to be sensitising, such as wheat, dairy, sugar
    and additives. Occasionally one needs to go further and eliminate soya, gluten and corn as well.

    1.3 Colon Cleansing: Removal of colonic plaque

    2. Replace

    2.1 Insufficient stomach acid and digestive enzymes can be supplemented with products containing Betaine HCl,
    and digestive enzymes such as DigestCo (Mediherb), Digestizyme (Amipro), etc.

    2.2 Nutritional deficiencies, arising from poor digestion, can be corrected with a good functional food (see below).

    3. Re-inoculate

    3.1 Friendly bacteria must be replenished as soon as the parasite cleanse (above) has been completed. This should
    be ongoing for several months. Use a reliable product such as Reuteri, Intestiflora or Probiflora.

    4. Repair

    4.1 Gut lining can be repaired with L-Glutamine, MSM and good-quality, pharmaceutical-grade Omega 3 oils.

    A good-quality functional food forms the cornerstone of the above regimen, by providing a complete range of nutrients, vitamins, minerals, pre-biotics such as FOS (Fructo-Oligo-Saccharide) and insulin to support the bacteria, L-Glutamine and MSM. The locally produced Target Candida is effective and less expensive, but is based on soya, which may disagree with patients if they are intolerant to it. The imported UltraClear Sustain is excellent and rice-based, but more expensive. UltraInflamX is used when there is inflammation in the body, and UltraClear Plus is for promoting Phase 1 and 2 detoxification pathways in the liver. These products are best used under the supervision of a knowledgeable integrative practitioner.

    Liver support and detox
    It is important to support the liver through the above programme with herbal products such as Milk Thistle, LivCo (Mediherb), Livotibb, etc. UltraClear Plus and Chlorella both improve detoxification processes in the liver very effectively.
    ============================== =================
    ============================== ============================== ============================== ==
    ============================== =================
    Intestinal Permeability Assessment

    Consider “4 R” approach to GI health:

    1) Remove mucosal irritants such as allergenic foods, alcohol, gluten (if sensitive), NSAIDS:
    • Consider elimination diet
    • Remove possible pathogens (bacteria, yeast, parasites)
    • Consider Comprehensive Digestive Stool Analysis (CDSA) or Comprehensive Parasitology, Bacterial Overgrowth of the Small Intestine Breath Test
    • Reduce sugar, refined carbohydrates, saturated fat, red meat (meat can induce bacterial enzyme activity)
    • Restore proper transit time
    –Increase dietary fiber (esp. insoluble) and water

    2) Replace agents for digestive support:
    • Consider pancreatic or plant enzymes, bile salts, betaine HCl, digestive herbs, or disaccharidases (e.g. lactase) where needed
    • Consider CDSA, Lactose Intolerance Breath Test (or other disaccharide) to rule out disaccharidase deficiency

    3) Reinoculate with friendly bacteria, if low:
    • Consider CDSA, Microbiology, or Comprehensive Parasitology to rule out gut flora insufficiencies
    • Consider probiotic supplementation, including Lactobacilli and Bifidobacteria
    • Consider fructooligosaccharides and inulin to enhance growth of friendly flora

    4) Repair mucosal lining:
    • Consider L-glutamine, EFAs, zinc, pantothenic acid, vitamins C, E, and A, beta carotene, N-acetyl glucosamine, gamma oryzanol, glycerrhiza, aloe vera
    • Consider antioxidants such as vitamins C, E and A, selenium, carotenoids, glutathione, N-acetyl cysteine, pycnogenol and flavonoids
    • Consider Saccharomyces boulardii, whey globulin concentrate, or bovine colostrum to improve local immunity
    • Consider ginkgo biloba to enhance circulation to intestinal epithelium

  35. Lots of information about hoe to test and how to treat.

    Toronto Naturopathic Clinic - Toronto Naturopath Sushma Shah ND (Yonge & Davisville)

    Medical Laboratory Testing (Blood, Saliva, Urine, Stool) -- Nature's Intentions Naturopathic Clinic

    Thyroid Panel

    Anti Micrsomal Globulin (Thyroid)
    Free T3
    Free T4
    Thyroid stimulating hormone

    Male And Female Hormones

    Bioavailable Testosterone
    Luteinizing hormone
    Follicle stimulating hormone

    Standard Blood Testing


    Lipid Panel

    Cholesterol, HDL / LDL

    Mineral / Vitamin / Nutrient Status In Blood

    Beta Carotene
    Calcium - Phosphatase
    Copper Cyanide
    Copper Serum
    Glucose (Random & Fasting)
    Glycated HGB
    Ionized Calcium
    Iron / Ferritin / Total Iron Binding Capacity
    Plasma Amino Acid
    Serum Folate
    Silver Cyanide
    Vitamin A, B12, E

    Liver And Pancreatic Enzymes

    Gamma glutamyl transferase
    Homocysteine (plasma)

    Food And Environmental Allergy Testing

    93 IgG Food - Antibody Screen
    Cold Agglutins
    Endomysial Abs
    Food Allergy (Ig E) Group sensitivity
    Food Allergy (Ig E) Individual Foods
    Gliadin Igg / Ige (Celiac disease)
    IgE Antibody Screening for foods and environment allergens (list of substances tested available from the clinic)

    Enzymes, Cancer Markers And Other Miscellaneous Tests

    Alkaline Phosphatase isoenzymes (bone specific)
    CA 19-9
    CA 27-29
    CA 15-3 (Breast)
    CA 125 (Ovary)
    Cardiac Enzymes: CK-MB, CK, Total, Myoglobin, CPK
    IGF – 1
    Immunocyte (for bladder CA)
    Prostatic Specific Antigen (PSA Ratio - Free PSA)

    Inflammatory Markers

    Anti-Nuclear Antibody
    C-Peptide (serum)
    C-Reactive Protein
    PT (INR)

    For Infections

    H Pylori Breath Test
    Ova and Parasites (stool)
    Stool Culture
    Stool Parasites
    Swab (General)
    Throat Swab

    Pregnancy & Fertility Tests

    Pregancy - HCG (Serum)
    Pregnancy Test (Urine)
    Sperm Count - Fertility Test
    Blood typing: - ABO - Rh

    Chemical Status Of Urine

    Sodium, Potassium, Creatnine, Uric Acid
    Deoxypyridinoline (urine) "DPD"
    Methylmelonic Acid (random urine)
    Gram Stain
    Urea / BUN
    Urine Culture
    Urine (random)

  36. Hormone Testing / Endocrinology -- Nature's Intentions Naturopathic Clinic

    Women's Hormonal Health Assessment provides a focused overview of hormonal balance in both pre- and post-menopausal women, using a single serum sample to evaluate dynamics of sex steroid metabolism that can profoundly affect a woman's health throughout her lifetime.

    Estrogen Metabolism Assessments, Urine or Serum evaluate how estrogen is being processed in the body. The tests yield clinical insight into many estrogen-dependent conditions and provide important tools for monitoring dietary, lifestyle and hormone therapies.

    Comprehensive Thyroid Assessment is a comprehensive analysis of thyroid hormone secretion and metabolism, including central thyroid regulation and activity, peripheral thyroid function, and thyroid autoimmunity. This serum test allows the practitioner to pinpoint commonly occurring imbalances that underlie a broad spectrum of chronic illness.

    Bone Resorption Assessment is a simple, direct urinary assay of pyridinium crosslinks and deoxypyridinoline, useful in identifying current rate of bone loss, lytic bone disease, and efficacy of bone support therapies.

    Adrenocortex Stress Profile is a salivary assay of cortisol and DHEA, imbalances of which are associated with ailments ranging from obesity and menstrual disorders to immune deficiency and increased risk of cardiovascular disease.

    Male Hormone Profile analyzes four saliva samples over a 24-hour period for levels of testosterone. Elevated levels suggest androgen resistance, while decreased levels can result from such causes as hypogonadism, hepatic cirrhosis, lipid abnormalities and aging. The comprehensive profile includes the Adrenocortex Stress Profile and the Comprehensive Melatonin Profile to reveal how testosterone is influenced by cortisol, DHEA, and melatonin.

    Female Hormone Profile analyzes eleven saliva samples over a 28-day period for the levels of ß-estradiol, progesterone, and testosterone, providing clues about menstrual irregularities, infertility, endometriosis, breast cancer, and osteoporosis. The comprehensive profile includes the Adrenocortex Stress Profile and the Comprehensive Melatonin Profile to reveal how the sex hormones are influenced by cortisol, DHEA, and melatonin.

    Menopause Profile examines three salivary samples over a 5-day period to determine levels of ß-estradiol, estriol, estrone, progesterone, and testosterone for women who are menopausal. The comprehensive profile includes the Adrenocortex Stress Profile and the Comprehensive Melatonin Profile to reveal how the sex hormones are affected by the influences of cortisol, DHEA, and melatonin.

    Comprehensive Melatonin Profile analyzes three saliva samples for the secretion pattern of this important hormone. Melatonin imbalance has been associated with Seasonal Affective Disorder, infertility, sleep disorders, and compromised immune function.


    Hormones Available for Testing (Saliva Collection):
    AM Cortisol (C) is recommended with situational stress and fatigue; indicator of adrenal imbalance.

    AM/PM Cortisol is recommended with excess stress, morning and evening fatigue, difficulty sleeping etc.; indicator of adrenal dysfunction.

    Adrenal Function Test (AFT) is the best comprehensive assessment of adrenal gland function; recommended with excessive stress, chronic fatigue, sleep disorders and allergies; indicator of immune function. Tests; DHEA's and four cortisols: morning, noon, evening and night.

    DHEA-S is recommended with androgen deficiency or excess symptoms; indicator of stress level, mental performance and insulin resistance.

    Estradiol (E2) is the most predominant of the estrogens. Testing is recommended with symptoms of estrogen deficiency or excess; best tested in concert with progesterone, as an imbalance of these two hormones is associated with major symptoms of menopause and disorders of the reproductive system).

    Estriol (E3) it is recommended that Estriol levels be measured when supplementing with a compounded preparation of bioidentical estrogens containing Estriol (e.g. "Biest" preparations contain estriol and estradiol OR "Triest" preparations containing estriol, estradiol and estrone).

    Estrone (E1) it is recommended that Estrone levels be measured when supplementing with a compounded preparation of bioidentical estrogens containing Estrone (e.g. "Triest" preparations contain estrone, estradiol and estriol).

    Hormone Profile I (5 Tests) is a good basic assessment of overall steroid hormone balance or imbalance and association with specific symptoms; indicator of hypothyroidism, bone loss and insulin resistance. Five Tests: Estradiol (E2), Progesterone (Pg), Testosterone (T), DHEA's, and morning Cortisol (C).

    Hormone Profile II + PM Cortisol (6 Tests) is the best value for money; most comprehensive evaluation of overall hormone balance or imbalance; indicator of thyroid and adrenal function; breast cancer profile. Six Tests: Hormone Profile I plus pm Cortisol (C4)

    Hormone Profile III + AFT (8 Tests) tests provides the most complete and in-depth evaluation of hormone balance, imbalance and interrelationship of specific hormone levels as related to symptoms of menopause, andropause and adrenal function. Eight Tests: Estradiol (E2), Progesterone (Pg), Testosterone (T), DHEA's, and 'Diurnal Cortisol' (All four cortisols: morning (C1), noon (C2), evening (C3) and night (C4).

    Progesterone (Pg) is recommended with symptoms of deficiency or excess; best tested in concert with estradiol as an imbalance of these two hormones is associated with major symptoms of menopause and disorders of the reproductive system.

    Testosterone (T) is recommmended with deficiency or excess symptoms; indicator of low sex drive, hair loss/excess, muscle and bone status.

    BloodSpot Test Products
    Fasting Insulin - Fasting Insulin in blood spot for the detection of insulin resistance is collected in the morning after a 12 hour fast and before eating or drinking. The home test kit facilitates optimal collection time for a fasting sample. Process involves a finger prick with lancet, dripping of blood spots and drying on filter paper. Kit is self-contained with step-by-step instructions, filter paper, 2 lancets, antiseptic wipes, etc.

    Fasting Insulin in blood spot is collected in the morning with our home test kit, after a 12 hour fast and before eating or drinking.

    Follicle Stimulating Hormone - (FSH) Marker of Menopause or Andropause onset.

    Free Thyroxine (fT4) - Thyroxine is the main thyroid hormone produced by the thyroid. A well- regulated process causes thyroxine to generate the much more potent thyroid hormone T3 (Triiodothyronine).

    Free Triiodothyronine (fT3) measures the level of active thyroid hormone T3. This level must remain within optimal range to keep the body functioning properly and is crucial for maintaining physical and mental health.

    Lutenizing Hormone (LH) - Marker of Menopause or Andropause onset.

    Male Profile I (T, SHBG, PSA) is an overall assessment of male vitality, performance and prostate health; indicator of prostate enlargement or cancer risk.

    Male Profile II (IGF-1, T, SHBG, PSA) is the best comprehensive assessment of overall male health, vitality, and prostate health; indicator of Adult Growth Hormone deficiency, rapid aging and increased prostate cancer risk.

    Prostate Specific Antigen (PSA) - PSA a protein produced by the prostate gland is an important indicator of prostatic enlargement or increased risk of prostate cancer. High PSA levels are a warning sign of prostate health risks. A normal PSA reading is prerequisite to initiating testosterone therapy.

    Sex Hormone Binding Globulin (SHBG) - SHBG (sex hormone binding globulin) measurement is used as a relative index of overall exposure to all forms of estrogens, as an indirect index of estrogen interaction with the liver and as an indicator of bioavailable testosterone. High levels indicate excess exposure to estrogens and lower bio-availability of testosterone to tissues, It is recommended that SHBG be tested along with testosterone in order to determine an imbalance between testosterone and estrogen. Such an imbalance is an important indicator of Andropause onset and / or premature aging in men.

    Somatomedin C (IGF-1) - IGF-1 is important because it is a reliable indicator of human growth hormone. IGF-1 needs to be within the expected range for this reason: Low IGF-1 levels indicate Adult Growth Hormone Deficiency associated with rapid aging, decreased muscle and bone mass, slowing cognition, low libido and poor quality of life.

    Testosterone (T) is recommended with deficiency or excess symptoms; indicator of low sex drive, hair loss, muscle mass and bone status. It is recommended that Testosterone and SHBG be tested together to determine imbalances of testosterone and estrogen; an important indicator of Andropause onset and/or premature aging in men.

    Thyroid Comprehensive Profile is an in-depth comprehensive assessment of overall thyroid function checking TSH, freeT4, freeT3, and TPO antibodies (Hashimotos). More than 10 million Americans have been diagnosed with thyroid disease, and another 13 million people are estimated to have undiagnosed thyroid problems in the U.S. alone. Women are at greatest risk, developing thyroid problems seven times more often than men.

    Thyroid hormones are transported in the blood "bound" to Thyroid Binding Globulin (TBG), which temporarily holds them inactive. This protein may be manipulated by many illnesses and medications. Therefore, measurement of the "unbound," free levels of T3 and T4 thyroid hormones provides a more accurate interpretation. When TSH, free T3 and T4 are found to be within normal range, a functional thyroid deficiency may be suspected. This can be clarified by testing TPO antibodies (Thyroid Peroxidase Antibody) as part of the comprehensive thyroid panel.

    Thyroid Peroxidase Antibody (TPO) - In 90% of patients with Hashimoto’s (autoimmune thyroiditis) TPO levels are elevated; indicator of other autoimmune disorders and polycystic ovaries.

    Thyroid Stimulating Hormone (TSH) measures the amount of thyroid hormone manufactured by the thyroid gland. General indication of thyroid activity.

  37. Diagnostic Tests for Addison's Disease - WrongDiagnosis.com

    Diagnostic Test list for Addison's Disease:

    The list of diagnostic tests mentioned in various sources as used in the diagnosis of Addison's Disease includes:
    Physical examination - particularly for hyperpigmentation of the skin
    Cortisol levels blood test
    X-ray adrenal glands - detect calcium deposits from TB-related Addison's.
    X-ray pituitary glands
    CT scan pituitary glands
    ACTH level blood test
    ACTH Stimulation Test
    Insulin-Induced Hypoglycemia Test

    ============================== =============
    Diseases Center - WrongDiagnosis.com
    Alzheimer's Disease
    Breast Cancer
    Common Cold
    Eye Disorders
    Heart Disease
    Heart Attack
    Kidney Disease
    Liver disease
    Meningococcal Disease
    Metabolic Syndrome
    Multiple Sclerosis
    Parkinsons Disease
    Thyroid disease

  38. Kimball's Biology Pages

    Kimball's Biology Pages

    ============================== ======================
    Hormones of the Pituitary

    Index to this page
    The Anterior Lobe
    Thyroid Stimulating Hormone (TSH)
    Follicle Stimulating Hormone (FSH)
    FSH in females
    FSH in males
    Luteinizing Hormone (LH)
    LH in females
    LH in males
    Prolactin (PRL)
    Growth Hormone (GH)
    Hormone-replacement therapy
    Alpha Melanocyte-Stimulating Hormone (α-MSH)
    The Posterior Lobe

    Hormones of the Pituitary
    The pituitary gland is pea-sized structure located at the base of the brain. In humans, it consists of two lobes:
    the Anterior Lobe and
    the Posterior Lobe
    Link to graphic showing the location
    of the pituitary and other endocrine
    glands (92K).

    The Anterior Lobe
    The anterior lobe contains six types of secretory cells, all but one of which (#2 above) are specialized to secrete only one of the anterior lobe hormones. All of them secrete their hormone in response to hormones reaching them from the hypothalamus of the brain.
    Thyroid Stimulating Hormone (TSH)
    TSH (also known as thyrotropin) is a glycoprotein consisting of:
    a beta chain of 112 amino acids and
    an alpha chain of 89 amino acids. The alpha chain is identical to that found in two other pituitary hormones, FSH and LH as well as in the hormone chorionic gonadotropin. Thus it is its beta chain that gives TSH its unique properties.
    The secretion of TSH is
    stimulated by the arrival of thyrotropin releasing hormone (TRH) from the hypothalamus.
    inhibited by the arrival of somatostatin from the hypothalamus.
    As its name suggests, TSH stimulates the thyroid gland to secrete its hormone thyroxine (T4). It does this by binding to transmembrane G-protein-coupled receptors (GPCRs) on the surface of the cells of the thyroid.
    Some people develop antibodies against their own TSH receptors. When these bind the receptors, they "fool" the cell into making more T4 causing hyperthyroidism. The condition is called thyrotoxicosis or Graves' disease.

    Hormone deficiencies
    A deficiency of TSH causes hypothyroidism: inadequate levels of T4 (and thus of T3 [Link]). Recombinant human TSH (Thyrogen®) is now available to treat patients with TSH deficiency.

    Some people inherit mutant TSH receptors. This, too, results in hypothyroidism.

    A deficiency of TSH, or mutant TSH receptors, have also been implicated as a cause of osteoporosis. Mice, whose TSH receptors have been knocked out, develop increased numbers of bone-reabsorbing osteoclasts.

    Follicle-Stimulating Hormone (FSH)
    FSH is a heterodimeric glycoprotein consisting of
    the same alpha chain found in TSH (and LH)
    a beta chain of 115 amino acids, which gives it its unique properties.
    Synthesis and release of FSH is triggered by the arrival from the hypothalamus of gonadotropin-releasing hormone (GnRH). The effect of FSH depends on one's sex
    FSH in females
    In sexually-mature females, FSH (assisted by LH) acts on the follicle to stimulate it to release estrogens.

    FSH produced by recombinant DNA technology (Gonal-f®) is available to promote ovulation in women planning to undergo in vitro fertilization (IVF) and other forms of assisted reproductive technology.
    FSH in males
    In sexually-mature males, FSH acts on spermatogonia stimulating (with the aid of testosterone) the production of sperm.
    Luteinizing Hormone (LH)
    LH is synthesized within the same pituitary cells as FSH and under the same stimulus (GnRH). It is also a heterodimeric glycoprotein consisting of
    the same 89-amino acid alpha subunit found in FSH and TSH (as well as in chorionic gonadotropin);
    a beta chain of 115 amino acids that is responsible for its properties.
    The effects of LH also depend on sex.
    LH in females
    In sexually-mature females,
    a surge of LH triggers the completion of meiosis I of the egg and its release (ovulation) in the middle of the cycle;
    stimulates the now-empty follicle to develop into the corpus luteum, which secretes progesterone during the latter half of the menstrual cycle.
    Women with a severe LH deficiency can now be treated with human LH (Luveris®) produced by recombinant DNA technology.
    LH in males
    LH acts on the interstitial cells (also known as Leydig cells) of the testes stimulating them to synthesize and secrete the male sex hormone, testosterone.
    LH in males is also known as interstitial cell stimulating hormone (ICSH).

    Discussion of the negative-feedback loops that control the levels of estrogen, progesterone, and testosterone.

    Prolactin (PRL)
    Prolactin is a protein of 198 amino acids. During pregnancy it helps in the preparation of the breasts for future milk production.
    After birth, prolactin promotes the synthesis of milk.

    Prolactin secretion is
    stimulated by TRH
    repressed by estrogens and dopamine.
    In pregnant mice, prolactin stimulates the growth of new neurons in the olfactory center of the brain.

    Growth Hormone (GH)
    Human growth hormone (HGH; also called somatotropin) is a protein of 191 amino acids. The GH-secreting cells are stimulated to synthesize and release GH by the intermittent arrival of growth hormone releasing hormone (GHRH) from the hypothalamus. GH promotes body growth by:
    binding to receptors on the surface of liver cells
    this stimulates them to release insulin-like growth factor-1 (IGF-1; also known as somatomedin)
    IGF-1 acts directly on the ends of the long bones promoting their growth
    Things that can go wrong.

    In childhood,
    hyposecretion of GH produces the stunted — but normally well-proportioned — growth of a midget.
    Growth retardation can also result from an inability to respond to GH. This can be caused by inheriting two mutant genes encoding the receptors for
    GHRH or
    or homozygosity for a disabling mutation in STAT5b, which is part of the "downstream" signaling process after GH binds its receptor.
    hypersecretion leads to gigantism
    In adults, a hypersecretion of GH or GHRH leads to acromegaly.
    Hormone-replacement therapy
    GH from domestic mammals like cows and pigs does not work in humans. So for many years, the only source of GH for therapy was that extracted from the glands of human cadavers. But this supply was shut off when several patients died from a rare neurological disease attributed to contaminated glands. Now, thanks to recombinant DNA technology, recombinant human GH (rHGH) is available. While a great benefit to patients suffering from GH deficiency, there has also been pressure to use it to stimulate growth in youngsters who have no deficiency but whose parents want them to grow up tall. And so, in the summer of 2003, the U.S. FDA approved the use of human growth hormone (HGH) for
    boys predicted to grow no taller than 5′3″ and
    for girls, 4′11″
    even though otherwise perfectly healthy.
    ACTH — the adrenocorticotropic hormone
    ACTH is a peptide of 39 amino acids. It is cut from a larger precursor proopiomelanocortin (POMC).

    ACTH acts on the cells of the adrenal cortex, stimulating them to produce
    glucocorticoids, like cortisol
    mineralocorticoids, like aldosterone
    androgens (male sex hormones, like testosterone
    in the fetus, ACTH stimulates the adrenal cortex to synthesize a precursor of estrogen called dehydroepiandrosterone sulfate (DHEA-S) which helps prepare the mother for giving birth.
    Production of ACTH depends on the intermittent arrival of corticotropin-releasing hormone (CRH) from the hypothalamus.

    Hypersecretion of ACTH is a frequent cause of Cushing's disease.

    Alpha Melanocyte-Stimulating Hormone (α-MSH)
    Alpha MSH is also a cleavage product of proopiomelanocortin (POMC). In fact, α-MSH is identical to the first 13 amino acids at the amino terminal of ACTH.
    MSH is discussed in a separate page. Link to it.

    The Posterior Lobe
    The posterior lobe of the pituitary releases two hormones, both synthesized in the hypothalamus, into the circulation.

    Vasopressin is a peptide of 9 amino acids (Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly). It is also known as arginine vasopressin (AVP) and the antidiuretic hormone (ADH).
    Vasopressin acts on the collecting ducts of the kidney to facilitate the reabsorption of water into the blood. This it acts to reduce the volume of urine formed (giving it its name of antidiuretic hormone).

    Link to discussion of kidney physiology.

    A deficiency of vasopressin or
    inheritance of mutant genes for its receptor (called V2)
    leads to excessive loss of urine, a condition known as diabetes insipidus. The most severely-afflicted patients may urinate as much as 30 liters (almost 8 gallons!) of urine each day. The disease is accompanied by terrible thirst, and patients must continually drink water to avoid dangerous dehydration.
    Another type of receptor for vasopressin (designated V1a) is found in the brain, e.g., in voles and mice (rodents) and in primates like monkeys and humans.

    Male prairie voles (Microtus pinetorum) and marmoset monkeys
    have high levels of the V1a receptor in their brains,
    tend to be monogamous, and
    help with care of their young.
    Male meadow voles (Microtus montanus) and rhesus monkeys
    have lower levels of the V1a receptor in their brains,
    are promiscuous, and
    give little or no help with the care of their young.
    Meadow voles whose brains have been injected with a vector causing increased expression of the V1a receptor become more like prairie voles in their behavior. (See Lim, M. M. et al., Nature, 17 June 2004.)

    The level of expression of the V1a receptor gene is controlled by a "microsatellite" region upstream (5') of the ORF. This region contains from 178 to 190 copies of a repeated tetranucleotide (e.g., CAGA). Prairie voles have more copies of the repeat than meadow voles, and they express higher levels of the receptor in the parts of the brain associated with these behaviors. A similar microsatellite region is present in the pygmy chimpanzee or bonobo (Pan paniscus) but is much shorter in the less-affectionate common chimpanzee (Pan troglodytes).

    Link to a discussion of some human diseases caused by trinucleotide repeats.

    Changes in the regulatory region of the human gene for the V1a receptor have been linked to autism.

    Oxytocin is a peptide of 9 amino acids (Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-Gly).
    It acts on certain smooth muscles:
    stimulating contractions of the uterus at the time of birth;
    stimulating release of milk when the baby begins to suckle.
    Oxytocin is often given to prospective mothers to hasten birth.

    Oxytocin also acts on the nucleus accumbens and amygdala in the brain where it enhances:
    bonding between males and females after they have mated;
    bonding between a mother and her newborn;
    and, in humans, increases the level of one's trust in other people.
    Welcome&Next Search

    18 November 2008

  39. http://mus clechatroom.com/forum/showpost.php?p=30730&postcount =21

    Quote Originally Posted by Dr. John Crisler View Post
    I will never recommend 5-AR Inhibitors.

    I would instead switch them from TD to IM TRT, in order to reduce androgenic conversion.
    This is a mile stone statement.

    Where do you draw the line? (DHT>??)

    Anything else?



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