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Old 06-03-2008, 06:26 PM   #91
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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)
Testosterone
Pregnanediol
DHEA
Etiocholanolone and Androsterone
Pregnanetriol
Cortisol and Cortisone
Aldosterone
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

Common

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

Uncommon
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

Common

Menopause or peri-menopause

Uncommon
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

Common

Testosterone supplementation (>75 mg/day)

Intermediate
Excessive aromatase activity (may be associated with obesity)

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


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



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

Common

Testosterone supplementation

Uncommon
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

Common

Testosterone supplementation (>75 mg/day)

Uncommon
Pregnenolone supplementation (high dose)
XYY syndrome

Low In Men: Possible Causes

Intermediate

Excessive aromatase activity (testosterone -> estradiol)

Uncommon
Hypogonadism
(May be associated with infertility & impotence)
Klinefelter syndrome
--------------------------------------------------------------------------------


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

Common

Progesterone supplementation
Pregnancy

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

Low In Women: Possible Causes

Common

Peri-menopause

Uncommon (In non-pregnant women)
Amenorrhea
Anovulation
Menstrual abnormalities

Elevated In Men: Possible Causes

Uncommon

High-dose pregnenolone supplementation
Testicular tumors

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

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

Uncommon

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

Common

Age > 40 yr.

Intermediate
Adrenal insufficiency
Unipolar depression

Elevated In Men: Possible Causes

Uncommon

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

Common

Age > 40 yr.

Intermediate
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

Common

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

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

Low: Possible Causes

Common

Age > 40 yr.

Uncommon
Adrenal insufficiency
Anorexia nervosa
Panhypopituitarism
Aging


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



Pregnanetriol
Elevated: Possible Causes

Uncommon

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

Common

Emotional or physical stress
Intensive physical exercise

Intermediate
Cortisol or cortisone administration
Unipolar depression
Sleep deprivation

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

Low: Possible Causes

Intermediate

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


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



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

Common

Low salt diet

Uncommon
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

Common

High salt diet

Uncommon
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

Intermediate

Medical or surgical stress
ACTH, cortisone or cortisol therapy

Uncommon
Cushing's Syndrome
Hyperthyroidism
Adrenocortical adenomas

Low: Possible Causes

Intermediate

Synthetic corticosteroid administration
Diabetes

Uncommon
Adrenal insufficiency
Congenital adrenal hyperplasia
Hypothyroidism

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



Tetrahydrocorticosterone, allo-Tetrahydrocortisosterone
Elevated: Possible Causes

Uncommon

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

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



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Old 06-03-2008, 06:28 PM   #92
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Quote:
Originally Posted by Chrisgj
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.

Chris
 



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Old 06-03-2008, 07:57 PM   #93
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Quote:
Originally Posted by JanSz
555555555555555555555555555555
Some one trying to get attention
The phrase "bump" works good..
 
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Old 06-10-2008, 10:03 AM   #94
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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).

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



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Old 06-10-2008, 10:04 AM   #95
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About Estrogen
TMAGNUM FORUMS - Estradiol: Why You Should Care

Good thread, read the whole thread, specially
happydog48
KSman

TMAGNUM FORUMS - Androgel is Useless
-------------------------------------------------------------

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Testosterone Replacement Therapy
references, short-cuts
TRT Links
 



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Old 06-10-2008, 10:07 AM   #96
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PC02c - Stress & Steroid Synthesis
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less DHEA less insuline sensitivity, increase insuline resistance, increased inflamation, problems with cortisol (tends to increase cortisol production)

DHEAs is a storage, reservuar,
ubiquitis

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,

insuline
glucose
 



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Old 08-06-2008, 08:00 AM   #97
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post#20

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

http://**************.com/forum/show...58&postcount=1

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 ?
 



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Old 08-06-2008, 08:03 AM   #98
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Quote:
Originally Posted by Dr. John Crisler
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
[/table]

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

Quote:
Originally Posted by Dr. John Crisler
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
[/table]

Note:
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.
 



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Old 08-06-2008, 08:06 AM   #99
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Post #10
High Cortisol
----------------------
Quote:
Originally Posted by chilln
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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Old 08-06-2008, 09:55 PM   #100
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Old 08-10-2008, 09:04 AM   #101
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Old 08-10-2008, 09:51 AM   #102
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