Confused e2 to e1 ?

hardasnails1973

Registered User
I'm curious to why blood estrones could be higher then e2 if one was on armidex. I thought e2 goes into e1 so therefore e1 should be suppressed from the armidex, hower ever if one is taking hcg could this swing the ratio the other way? Would it be advisiable to get the estrone metabolism fixed before implimenting HCG possible due to the fact that it could over flood the estrogen metabolism if it has not been stabilized first. Information about DIm is intersting, thing is that we know that it affects androgen receptors in the prostate which is a good thing, but can it affect receptors any where else? One of my freinds mentioned about taking DIM to control e2 to Shippen and had mixed reviews about it. Again when one hand talks to the other information does get altered, but from what he understood that DIm works in the prostrate to cause androgen receptor down grades which is a good thing, but mentioned about new studies coming out saying it may affect other areas as well..other then just prostate. I just want to clarify the truth is all. Or could it before the fact people are taking it you do not need it and causing more damage to receptors. Now that could be a plausible reason..Time will tell..
 
hardasnails1973 said:
I'm curious to why blood estrones could be higher then e2 if one was on armidex. I thought e2 goes into e1 so therefore e1 should be suppressed from the armidex, hower ever if one is taking hcg could this swing the ratio the other way? Would it be advisiable to get the estrone metabolism fixed before implimenting HCG possible due to the fact that it could over flood the estrogen metabolism if it has not been stabilized first. Information about DIm is intersting, thing is that we know that it affects androgen receptors in the prostate which is a good thing, but can it affect receptors any where else? One of my freinds mentioned about taking DIM to control e2 to Shippen and had mixed reviews about it. Again when one hand talks to the other information does get altered, but from what he understood that DIm works in the prostrate to cause androgen receptor down grades which is a good thing, but mentioned about new studies coming out saying it may affect other areas as well..other then just prostate. I just want to clarify the truth is all. Or could it before the fact people are taking it you do not need it and causing more damage to receptors. Now that could be a plausible reason..Time will tell..
Click to expand...

Read up on theory but do the testing.

Test any and all estrogen you can.

Trust but verify.
 
JanSz said:
Read up on theory but do the testing.

Test any and all estrogen you can.

Trust but verify.
Click to expand...

Getting 24 hour estrogen urine test done which also tests all estrogens and methyated metabolites identifying proper methylation in the liver (which mine plainly sucks !!) which rheins does not test for..but will in the future

All dim stopped 4 weeks prior before test.
 
hardasnails1973 said:
I'm curious to why blood estrones could be higher then e2 if one was on armidex. I thought e2 goes into e1 so therefore e1 should be suppressed from the armidex, hower ever if one is taking hcg could this swing the ratio the other way? Would it be advisiable to get the estrone metabolism fixed before implimenting HCG possible due to the fact that it could over flood the estrogen metabolism if it has not been stabilized first. Information about DIm is intersting, thing is that we know that it affects androgen receptors in the prostate which is a good thing, but can it affect receptors any where else? One of my freinds mentioned about taking DIM to control e2 to Shippen and had mixed reviews about it. Again when one hand talks to the other information does get altered, but from what he understood that DIm works in the prostrate to cause androgen receptor down grades which is a good thing, but mentioned about new studies coming out saying it may affect other areas as well..other then just prostate. I just want to clarify the truth is all. Or could it before the fact people are taking it you do not need it and causing more damage to receptors. Now that could be a plausible reason..Time will tell..
Click to expand...

E2 does not go into E1.

E2 is primarily from Testosterone but also E1.

E1 comes from 4 - androstenedione.

4 andro comes from 5 andro, which comes from DHEA and progesterone(17 hydroxy).

I do not know of arimidex effect on other estrogens. I do know it lowers E2. But for the rest Im not sure.

DIM seems to control E2 within the prostate. It may be specific to the region, as are alot of drugs are able to do(saw palmetto/5 alpha blockers/lycopean/nettle/etc.
 
plymouth city said:
E2 does not go into E1.

E2 is primarily from Testosterone but also E1.

E1 comes from 4 - androstenedione.

4 andro comes from 5 andro, which comes from DHEA and progesterone(17 hydroxy).

I do not know of arimidex effect on other estrogens. I do know it lowers E2. But for the rest Im not sure.

DIM seems to control E2 within the prostate. It may be specific to the region, as are alot of drugs are able to do(saw palmetto/5 alpha blockers/lycopean/nettle/etc.
Click to expand...

taking HCG increases progesterone which would explain the increased ratio of e1:e2
Could put exta strain on already over loaded estrogen pathway causing alteration which could effect the prostrate gland,in the brain and other elevated estrogen symptoms..

Now if these estrogen metabolites are not disposed of properly could they be reciruclated around in the liver possible bind to other e2 receptors sites resulting in increased Shbg since estrogens do raise them?
Reasoing behind DIm is to use it if one is using hcg, dhea to keep the pathways flowing in the proper direction..
If one is already undermethyltated then this pathway has probably been previous dysrupted
 
Plymouth,
E1 and E2 can convert back and forth to each other, and are generally kept roughly in equilibrium by that mechanism. The conversion can go BOTH ways. That is the reason for the original question, because you would expect a corresponding decrease in E1 due to lowering E2 (even when E2 is not the primary source for E1 the ratio would usually be in balance). But, Arimidex blocks the conversion of estrone to estradiol, so I guess it is possible to cause the ratio to be out of balance, though I thought aromatase catalyzed the andro to E1 conversion also. Of course in men the main aromatase reaction we want blocked is Test to E2. Have to do some extra study.
 
RPHMark said:
Plymouth,
E1 and E2 can convert back and forth to each other, and are generally kept roughly in equilibrium by that mechanism. The conversion can go BOTH ways. That is the reason for the original question, because you would expect a corresponding decrease in E1 due to lowering E2 (even when E2 is not the primary source for E1 the ratio would usually be in balance). But, Arimidex blocks the conversion of estrone to estradiol, so I guess it is possible to cause the ratio to be out of balance, though I thought aromatase catalyzed the andro to E1 conversion also. Of course in men the main aromatase reaction we want blocked is Test to E2. Have to do some extra study.
Click to expand...

E1 and E2 for the most part are seperate of eachother. E2 comes primarily from T. Arimidex main ability is NOT to block E1 to E2, but to block T - E.

It is very common to have elevated E2 but normal E1. And vice versa. Over active aromatase comes to mind. This is all seperate of E1.

The main proof we all have is the action of plant based herbs like resveratrol and DIM. They do an exceptional job at blocking E1, yet E2 remains unnaffected. This has been proven time and time again. People on Dim and/or resveratrol always see a lowered E1 level, yet E2 remians unchanged. If E1 gets converted into E2 at any significant amount, we would see a lowered E2. But we never see that.

This pretty much in itself disproves E1 going into E2 in noted amounts. That may occur in VERY small amounts, but nothing to be noted. If E1 did convert to E2 in any tangible amounts, most would never need arimidex, and would instead rely on a much safer(and healthier AI) like resveratrol or DIM. Yet pretty much most have resorted to arimidex to control E2.
 
"But, Arimidex blocks the conversion of estrone to estradiol, so I guess it is possible to cause the ratio to be out of balance"

In the very small amount that E1 goes into E2, probably, but it is mostly irrelevant. Its the T into E2 were arimidex works its majic.
 
plymouth city said:
"But, Arimidex blocks the conversion of estrone to estradiol, so I guess it is possible to cause the ratio to be out of balance"

In the very small amount that E1 goes into E2, probably, but it is mostly irrelevant. Its the T into E2 were arimidex works its majic.
Click to expand...

So if one is using preg creame, dhea, hcg we would be more concerned with E1 and there for DIM and reservatrol would be in need to control these pathways.

Using testosterone we be more concerned with e2 which armidex or chrysin, or natural AI be..

This brings up a good point even though breast cancer take AI daily. Conversion to estrone is totally over looked which could also pose just an important threat if not more to other areas of the body..Reason I bring this up is my moms dhea is off the charts and she is taking armidex, but with high dhea she be more prone to altered e1 pathways. Could altering e1 pathways to more benefical estrogens reduce patience with cancer having it spread to other areas of the body?
 
hardasnails1973 said:
So if one is using preg creame, dhea, hcg we would be more concerned with E1 and there for DIM and reservatrol would be in need to control these pathways.

Using testosterone we be more concerned with e2 which armidex or chrysin, or natural AI be..

This brings up a good point even though breast cancer take AI daily. Conversion to estrone is totally over looked which could also pose just an important threat if not more to other areas of the body..Reason I bring this up is my moms dhea is off the charts and she is taking armidex, but with high dhea she be more prone to altered e1 pathways. Could altering e1 pathways to more benefical estrogens reduce patience with cancer having it spread to other areas of the body?
Click to expand...

Estrogen: estrone (E1), estradiol (E2), estriol (E3) and estetrol (4)

Estetrol
Estra-1,3,5(10)-triene-3,15 alpha,16 alpha,17 beta-tetrol. A metabolite of estradiol in man, with estrogenic properties.

I just found this on internet, should I be concerned about this one??
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===============================================

Your Mother is already taking Arimidex.
Possibly have her do the urine test by RheinLabs

if waranted by the 2/16 ratio
possibly she could benefit from LEF supplements

DualAction
TMG
calcium glutharate
Resveratol

she could also do the Quest estrogen tests, the lattest discussed, just use ranges as for females:


60 Estradiol, Free, LC/MS/MS (36169X) Invalid Link Removed
61 /------------------------------------ Estradiol, Free (Males (Adult): < or = 0.45 pg/mL )
62 /------------------------------------ Estradiol (Males (Adult): < or = 29 pg/mL)
63 Estrogens, Fractionated, LC/MS/MS (36742X) Invalid Link Removed
64 /------------------------------------ 968-1**Estrone, LC/MS/MS
65 /------------------------------------ 968-2**Estradiol, Ultrasensitive, LC/MS/MS
66 /------------------------------------ 968-3**Estriol
67 Estrogen, Total, Serum (439X)
 
JanSz said:
Estrogen: estrone (E1), estradiol (E2), estriol (E3) and estetrol (4)

Estetrol
Estra-1,3,5(10)-triene-3,15 alpha,16 alpha,17 beta-tetrol. A metabolite of estradiol in man, with estrogenic properties.

I just found this on internet, should I be concerned about this one??
Invalid Link Removed
===============================================

Your Mother is already taking Arimidex.
Possibly have her do the urine test by RheinLabs

if waranted by the 2/16 ratio
possibly she could benefit from LEF supplements

DualAction
TMG
calcium glutharate
Resveratol

she could also do the Quest estrogen tests, the lattest discussed, just use ranges as for females:


60 Estradiol, Free, LC/MS/MS (36169X) Invalid Link Removed
61 /------------------------------------ Estradiol, Free (Males (Adult): < or = 0.45 pg/mL )
62 /------------------------------------ Estradiol (Males (Adult): < or = 29 pg/mL)
63 Estrogens, Fractionated, LC/MS/MS (36742X) Invalid Link Removed
64 /------------------------------------ 968-1**Estrone, LC/MS/MS
65 /------------------------------------ 968-2**Estradiol, Ultrasensitive, LC/MS/MS
66 /------------------------------------ 968-3**Estriol
67 Estrogen, Total, Serum (439X)
Click to expand...


Already got her on calcoum d, DIm, adding TMG might be next step. I am getting her urine testing through great smokies it measures the methyated metabolites as well, Having her do the iodinne loading test very soon as well too.. I be she is really really low !!
 
hardasnails1973 said:
Already got her on calcoum d, DIm, adding TMG might be next step. I am getting her urine testing through great smokies it measures the methyated metabolites as well, Having her do the iodinne loading test very soon as well too.. I be she is really really low !!
Click to expand...

You do know that not all DIM's are equal.
 
hardasnails1973 said:
shes taking indoplex Biorepsonse from VRP
Why we are going to get her tested For validation
Click to expand...

Probably this:
Invalid Link Removed

This works for somebody who believe that DIM is an answer to most of 2/16 and E2 problems.

When I treat my self I use
DualAction from LEF
it does have only small amount of DIM
but instead have other ingredients.
 
JanSz said:
Probably this:
Invalid Link Removed

This works for somebody who believe that DIM is an answer to most of 2/16 and E2 problems.

When I treat my self I use
DualAction from LEF
it does have only small amount of DIM
but instead have other ingredients.
Click to expand...

I'm getting urine tested
tueday for evasive estrogen testing ..
 
I knew you would back me up on this Dr. John. The E1 to E2 and back conversion happens readily and constantly in order to keep the ratio in balance normally. Dr. John answered what I could not remember about andro to E1 also being an aromatase conversion. Obviously our main concern on Testosterone therapy is the T to E2 conversion. When you read prescribing info on arimidex (keeping in mind it is targeted at women) their main contention is its ability block E1 to E2 in peripheral tissue (fat mainly), though clearly it also blocks the andro to E1 also.
HAN- this is interesting because most researchers seem to think estrone has more proliferative effect on breast tissue than estradiol so it seems something targeted at E1 may also be warranted if the ratio is out of balance in a breast CA pt
 
RPHMark said:
.
HAN- this is interesting because most researchers seem to think estrone has more proliferative effect on breast tissue than estradiol so it seems something targeted at E1 may also be warranted if the ratio is out of balance in a breast CA pt
Click to expand...

Yes this makes me wonder about my moms double higher then normal dhea levels that concern me. She having breast cancer and having high dhea levels makes me wonder if your pathways are all messed up causing alot of her mental fog, joint pains, and tiredness. I have a suspcion that she is severly iodine defieint because she has not responded to armour like she should have. I am going to ask dr to run estrogen metabolism test and I have iodine test here for her to see if cancer patience have lower then normal iodine saturation plus altered e1:e2:E3 ratios..If one is low in iodine then estrones are not converted to e3 which are the protectivee estrogens and there for these could cause breasts cancerPROSTATE enlargment may as well result from altered good:bad ratios
 
HAN- You might look into some of the research on estriol in breast CA pts as a preventative and/or therapy. I know it was and/or is done in Europe to some extent as a sort of partial agonist on estrogen receptors (think Evista). If her Dr. thought it would not be harmful, it certainly might help her brain fog, joint pain, etc. I am also certain that in some types of tumors there is simply no way it would be appropriate in a risk:benefit ratio.
 
RPHMark said:
HAN- You might look into some of the research on estriol in breast CA pts as a preventative and/or therapy. I know it was and/or is done in Europe to some extent as a sort of partial agonist on estrogen receptors (think Evista). If her Dr. thought it would not be harmful, it certainly might help her brain fog, joint pain, etc. I am also certain that in some types of tumors there is simply no way it would be appropriate in a risk:benefit ratio.
Click to expand...

I concur if her e3 is down that could explain alot since it is the protective one and Estrone goes into e3 via metabolic pathways which DIM does help..My theory is find the bottleneck and correct it ..
 
Dr. John said:
DIM hinders 16-OHE formation. 16-OHE is prohormone for Estriol.

This is a BIG question when considering use of I-3-C/DIM, along with issues of possible androgen receptor antagonism (anyone seen anythng more about that?).

But, as you have pointed out, iodine favors conversion of 16-OHE to E3. Hey, wait a minute! I wonder if low iodine--DEFINITELY linked to cancers--is what induces elevated 16-OHE (also linked to cancers), since it then does not flow downstream to protective Estriol???
Click to expand...

HELLO!!!
Thats what I have been trying to say in round way !!
helps favor estrone into estriol. I spotted this 2 consecuitive times on rhein urine test from people
estrones be high and estriol would be low and This may be a red flag for iodine deficeincy..
Invalid Link Removed

Excellent read about iodine..
KUJ:Invalid Link Removed
 
Dr. John said:
DIM hinders 16-OHE formation. 16-OHE is prohormone for Estriol.

This is a BIG question when considering use of I-3-C/DIM, along with issues of possible androgen receptor antagonism (anyone seen anythng more about that?).

But, as you have pointed out, iodine favors conversion of 16-OHE to E3. Hey, wait a minute! I wonder if low iodine--DEFINITELY linked to cancers--is what induces elevated 16-OHE (also linked to cancers), since it then does not flow downstream to protective Estriol???
Click to expand...
15th ANNUAL WORLD CONGRESS ON ANTI-AGING MEDICINE & REGENERATIVE BIOMEDICAL TECHNOLOGIES
July 31- August 4, 2007

Invalid Link Removed

4:00 PM

Estrogen Metabolism
Patrick Hanaway, MD
====================================================================================
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GS02m - Estrogen Metabolism: Modifying Risk in Clinical Practice
$20.00 Speaker: Patrick Hanaway, MD
April 9, 2006 5:00 pm - 5:40 pm

There is a 7 articles available, cost mostly $20 ea

Any idea which ones may be on 2/16 , E3 topic, if any ??
 
Invalid Link Removed

You can listen to Dr Shippen or Dr Crisler

not much information in a preview part
but you can hear the voice of THE men.

Preview part of his speaches is available free.
============================================
 
Dr. Hanaway spoke at a conference I atttended, and let me say, the dude can go DEEP into estrogen metabolism and genetic polymorphisms leading to cancer. I am virtually certain I remember him making that low iodine to increased 16OHE connection. So Dr. John, does it make sense to use DIM/I3C to block some 16OHE conversion and supply exogenous Estriol for a protective effect (in addition to the previously mentioned arimidex)?
 
Estrogen Metabolism
Patrick Hanaway, MD
====================================================================================
Invalid Link Removed

GS02m - Estrogen Metabolism: Modifying Risk in Clinical Practice
$20.00 Speaker: Patrick Hanaway, MD
April 9, 2006 5:00 pm - 5:40 pm

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

My take home (due to many discussions):
Brassica, I3C and DIM are important, in this order, I3C should not be missed.
I am staying with DualAction.

rosemary, turmeric, kudzu (Dr Delgado supplement contains kudzu)
======================================
RPHMark
please refresh your memory, you are probably well qualified to provide executive summary of:

testing, what to test, how blood urine, how read report
corrective actions, list of supplemets, doses, details
____________________________________________



DIM hinders 16-OHE formation. 16-OHE is prohormone for Estriol.

This is a BIG question when considering use of I-3-C/DIM, along with issues of possible androgen receptor antagonism (anyone seen anythng more about that?).

But, as you have pointed out,

iodine favors conversion of 16-OHE to E3.

Hey, wait a minute! I wonder if low iodine--DEFINITELY linked to cancers--is what induces elevated 16-OHE (also linked to cancers), since it then does not flow downstream to protective Estriol???
=====================================================================
=====================================================================
Dr. Hanaway spoke at a conference I atttended, and let me say, the dude can go DEEP into estrogen metabolism and genetic polymorphisms leading to cancer. I am virtually certain I remember him making that low iodine to increased 16OHE connection. So Dr. John, does it make sense to use DIM/I3C to block some 16OHE conversion and supply exogenous Estriol for a protective effect (in addition to the previously mentioned arimidex)?
========================================================================

2/16 Estrogen Metabolism:
Modifying Risk
in Clinical Practice
Patrick Hanaway, MD
-----------------------------------------------------------------------------------
page 10
Estrone(E1) -->2-hydroxyestrone (protective page12)
promote-Indole 3C, excercise, flax, ligams, soy, EPA
inhibit-Pesticide, ETOH (what is that)
---
Estrone(E1) ---> 16-alpha-Hydroxyestrone (carcinogenic page 12)
inhibit-obesity, hypothyroidism, pesticide, cimetidine (Taganent)

Estrone---> 4-OHE1

4-OHE1---- can be neutralized (good) or convert to Quinones (carcinogenic)
-----------------------------------------------------------------------------------
Modification of 2:16 OHE1 Ratio
16 OH-estrone (confers risk)
increased by:
• pesticides
• obesity
• cimetidine
• hypothyroidism
Generally, it is the
2OH-Estrone
that is more modifiable
----------------------------

Modification of 2:16 OHE1 Ratio
2 OH-estrone (protective)
increased by:
• flaxseed
• omega-3 fatty acids
• soy isoflavones
• indole 3-carbinol (I3C)
• diindolylmethane (DIM)
• rosemary, turmeric, kudzu (Dr Delgado supplement contains kudzu)
• strenuous exercise
• weight loss
-------------------------------------------------------------------------
Testing Considerations
• Measure in serum or urine; and stay
with same specimen type for followup
monitoring of risk!
• For women on Hormone Therapy
collect specimen 8-10 hrs after last
dose
• 2-OHE1 clears more rapidly in urine
than the 16α-OHE1
• First morning urine for greater
concentration
-----------------------------------------------------------------------------
page 50
The apparent induction of CYP1A1 was mirrored by a
66% increase in the urinary 2-hydroxyestrone/ 16α-
hydroxyestrone ratio in response to I3C. The maximal
increase was observed with the 400 mg daily dose of I3C,
with no further increase found at 800 mg daily.
----------------------------------------------------------------------------
page 49
Cytochrome P-450
1A1 & 1B1
Intervention:
• Red wine extract (resveratrol)
• DHEA: Inhibits induced expression of
CYP1B1 (in vitro study)
• Increase 2-hydroxylation of estrogen
• I3C and DIM inhibit CYP1B1
• Antioxidants
• Minimize exposure to xenoestrogens
------------------------------------------------------------------------------
page 58
COMT– Intervention
• Limit alcohol intake
• Support methionine metabolism (+/+
women with breast CA have higher Hcy)
with SAMe supplementation; B-Vitamins
• Anti-oxidants (reduce quinones)
• Avoid excess weight, stress
• Avoid oral HRT (E2 levels higher in
supplemented women with SNP; which
is associated with increased breast
density on ERT)
--------------------------------------------------------------------------------
page 60
GST – Intervention
• Glutathione precursors and cofactors (NAC, Lglutamine,
glycine, Mg, methionine or SAMe)
• Minimize GSH depletion (e.g., alpha lipoic acid,
silymarin, ginkgo biloba, whey protein)
• Anti-oxidants
• Brassica based diets (stimulates GSTs and
provides chemoprotective isothiocyanates to
GSTM1-nulls)
• Allium diet increases GST activity, even in
GSTM1-null individuals
--------------------------------------------------------------------------------
In Summary. . .
Support Healthy metabolic pathways:
• Increase Production of 2-OH Estrone (E1)
• CYP450 1A1
• Decrease Production of 4- and 16-OH E1
• CYP450 1B1
• Increase Production of 2-Me Estrone (E1)
• COMT
• Decrease Production of 4- Quinones
• GST
---------------------------------------------------------------------------------
In Summary. . .
Women using Hormone Therapy should
be offered Genomic testing:
CYP450 1A1
CYP450 1B
COMT
GST
-----------------------------------------------------------------------------------



• Estrone Sulfate (E1S)
• Estrone (E1)
• Estradiol (E2)
• Estriol (E3)
 
This is an EXCELLENT thread. Should be "stickied." Also, if you don't take care of your prostate, you may become prostrate. (Sorry, I haven't had my coffee yet this morning.):p
 
JanSz,
My notes from Dr. Hanaway mirror much of your post, but I am going back to review them again, and see if I missed something that is relevent here. I wish more people (drs and patients) were willing to pay attention to these types of "details". Side note- Premarin is metabolized primarily into 4OHE and other quinones, topic for another discussion.

Dr. John- I buried a question in my other post, curious about your opinion. If we use DIM/I3C to alter E1 metablism and arimidex to alter E2 should we provide exogenous estriol for its protective effects? This seems like a best of all worlds scenerio, what am I missing?
 
Summary for daily use/guidance:
do not copy this post in references, the post is under construction

I was just trying to get a chart.
Forgetting that hi is pushing DIM alone, just looking at the chart, or better replace DIM with (Brassica+I3C+DIM):
Invalid Link Removed

Estradiol (E2) if too high can be controlled with Arimidex
To get desirable E2 level:
Use Quest blood test and aim for E2 and FreeE2 at top range
Estradiol, Free, LC/MS/MS (36169X)
Estradiol, Free (Males (Adult): < or = 0.45 pg/mL ) ie. 0.44 is best
Estradiol (Males (Adult): < or = 29 pg/mL) ie. 28 is best
Invalid Link Removed

------------------------------------------------------------
To get desirable E1 & E2
Use Quest blood test and aim for top range
Estrogens, Fractionated, LC/MS/MS (36742X)
968-1**Estrone, LC/MS/MS (note it is high quality test)
968-3**Estriol (note old fashion, possibly unreliable)
Invalid Link Removed

Please help with a list of applicable supplements
I start with
Dual-Action Cruciferous Vegetable Extract With Resveratrol & Cat's Claw
It contains the best goodies, but I gauge dose by desired minimum of I3C=400mg
So I need 5pills daily, then retest in 2 months.
TMG
Resveratol
.
.
to be continued/edited/updated here

.
.
Urine test at RheinLab
desirable (2/16)>2
• Ratio as marker of breast cancer survival (ratio > 2.0
>10 yr survivial; ratio < 2.0 mean survival < 5 yrs
------------------------------------------------------------
• Estrone Sulfate (E1S)
• Estrone (E1)
• Estradiol (E2)
• Estriol (E3)
--------------------------------------------------------------
 
Could also support estrogen metabolism
methylation- SAMe, Bvits and Folic Acid (especially methyl forms)

Glucuronidation- NAC, SAMe, antioxidants
 
RPHMark said:
Could also support estrogen metabolism
methylation- SAMe, Bvits and Folic Acid (especially methyl forms)

Glucuronidation- NAC, SAMe, antioxidants
Click to expand...

On them !! Like i said I got all basis covered..ITs e2 imbalance is killing me low e2 = hypomethyation as well as possible elevated 16 and 4 hydroxyestrone ...

Could the pregenonlone creame be lowering e2 as well since it is progesterone or is the preg and dhea causing too much bottle necking in estrogen metabolism.
 
The preg/dhea angle is interesting. Could they feed the E1 side while arimidex is blocking E2 conversion? Seems like that is at least possible.
 
Dr. John said:
I just read through the Arimidex PI and could not find that.
Click to expand...

so in breast cancer armidex only blocks conversion to e2, but literature I have found that estrone can cause just enough havoc on the same receptor sites with in the breast tissue. My moms dhea was off the charts making me think that the AI is doing its job on the e2 but the estrone metabolism is probably running rampant as well as the 16 and 4 hyrdroxy-estrones most likelyl. Going to see if i can get her to do a rheine hormone profile and see if compunded estriol would help reduce the symptoms of joint pains and other estrogen defeincy symtpoms as well as identifying iodine defieincy and link all of this stuff together and come up with some kind of protocol for her to enjoy rest of her life with out pain..
 
Dr. John said:
You are making some generalizations here which are not supported by my clinical experience. Or medical text.
Click to expand...

TRue I was on DIM, TMG, calcium D, reservatrol and AI and e1 was elevated and e2 was in the ground. blood test to back that one up :twisted:

Some one with a COMT defeiincy? How is that corrected ? by sam-e
Will AN AI will stop conversion from estrone back to e2 ?
 
hardasnails1973 said:
TRue I was on DIM, TMG, calcium D, reservatrol and AI and e1 was elevated and e2 was in the ground. blood test to back that one up :twisted:

Some one with a COMT defeiincy? How is that corrected ? by sam-e
Will AN AI will stop conversion from estrone back to e2 ?
Click to expand...

This could have been from lack of T. Androgens are the major contributor of E2, and then TO A LESSOR DEGREE E1

You can block E1 all day and that won't keep E2 at bay. This has been proven time and time again. Im not saying NO E1 goes into E2But E2 is primarily an act of androgen aromatase. And guess where the E1 is coming from anyways? 4 - Andro. Blaming E1 for elevated E2 just doesn't make sense.

If blocking E1 stopped E2, we wouldn't need arimidex. Plant based AI's all have a terrific ability to act on E1 - Yet most fail to live up to the hype for E2. This is because they don't block androgenic hormones from converting to E2 strong enough.
 
Dr. John said:
I know of no way to "block E2".

I have to say that you have gotten off into some ideas which really don't follow.
Click to expand...

Via 17b-HSD enzyme

Estrone is less potent, but all this means is that one needs more of it to accomplish the same job.

Thats a good thing, given use of an AI lowers all estrogens
 
Quote:
Originally Posted by JanSz
Probably this:
Invalid Link Removed

This works for somebody who believe that DIM is an answer to most of 2/16 and E2 problems.

When I treat my self I use
DualAction from LEF
it does have only small amount of DIM
but instead have other ingredients.


Dr. John said:
Be aware that many of the claims made by Dr. Zeligs do not stand up to rigorous evaluation, IMPO.
Click to expand...

That statement should be repeated many times.

Right on this board we have a people that use Indolplex (pure DIM) exclusively because they believe in dr Zelig's claims.
 
Dr. John said:
I just read through the Arimidex PI and could not find that.
Click to expand...

Actually I don't know what I intended to say, but what I said did not make sense, for the life of me I can't figure out how that statement should have read.:wtf:

HAN, I think that statement mislead you also. I guess I had brain lock, but armidex won't block E1 to E2 (which is basically what I wrote). It will block andro to E1 or testosterone to E2. The question to me is if there is simply much more "raw material" on one side (like DHEA feeding into andro) then wouldn't it be possible to have some aromatization leading to more E1 than E2? I'm not sure how to find out if that is even a real possibility.
 
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Dr. John said:
I didn't know that, I always thought it acted as 16-OHE.

Of note, the good 2-OHE is a quinone, too.
Click to expand...

It is of course largely estrone sulfate, and at least 2 of its components metabolize primarily to 4OHE. Premarin also inhibits COMT activity, leading estrone to 4OHE

I went off subject without saying so on the estriol post earlier, I was talking about HAN's mother/breast cancer pts. Though we could make some case in men it would be a tough sell.
 
RPHMark said:
HAN, I think that statement mislead you also. I guess I had brain lock, but armidex won't block E1 to E2 (which is basically what I wrote). This is no biggie given both DIM and Resveratrol block E1 fantastically well

It will block andro to E1 or testosterone to E2. The question to me is if there is simply much more "raw material" on one side (like DHEA feeding into andro) then wouldn't it be possible to have some aromatization leading to more E1 than E2? I buy this, especially considering DHEA metabolism varies GREATLY from one person to the next. Some have a fantastic ability to convert DHEA to specific androgens and others do not. This may be the reason behind the disparity. I'm not sure how to find out if that is even a real possibility.
Click to expand...

Answers in bold
 
Plymouth,
That's where that idea is headed. There are clearly large disparities in how people metbolize DHEA. I've seen this several times with similar doses producing vastly different effects in pts (almost as if they were on completely different drugs).
 
Dr. John,
Is there a reason you know of that supplementing DHEA would lead to a high E1 level with a normal/low E2 (in a pt on an AI). I can't find anything to back me up, but it makes sense to me that supplying exogenous DHEA could supply more "raw material" for E1 production while peripheral aromatase is blocked by the AI thus limiting E2 production. I guess the real questions HAN brought up that I can't answer are 2 fold:
1. Do the AI drugs block both aromatase reactions equally? (andro to E1 and Test to E2) I can't find this answer
2. What would disrupt the E1-E2 interconversion to favor E1 leading to high levels despite low/normal E2?
 
RPHMark said:
Dr. John,
Is there a reason you know of that supplementing DHEA would lead to a high E1 level with a normal/low E2 (in a pt on an AI). I can't find anything to back me up, but it makes sense to me that supplying exogenous DHEA could supply more "raw material" for E1 production while peripheral aromatase is blocked by the AI thus limiting E2 production. I guess the real questions HAN brought up that I can't answer are 2 fold:
1. Do the AI drugs block both aromatase reactions equally? (andro to E1 and Test to E2) I can't find this answer
2. What would disrupt the E1-E2 interconversion to favor E1 leading to high levels despite low/normal E2?
Click to expand...

On possiblility may be that DHEA may some how convert to progesterone then E1 is increased and e2 is un changed. I know hcg when given has more likely hood of having a higher estrone : e2 ratio. I found infomration supporting this ..
So again on an AI and a person taking dhea or hcg, preg creame there will be more e1 then e2 due to the fact that the aromatase does not interfer with specific conversions of e1 to e2. therefore people with upper levels progesterone, taking hcg, dhea, preg cream may want to furher explore where the e1 is going to make sure it would lead down the wrong metabolitic pathway..an in there is a metabolic block or bottle neck using DIM or other natural alternatives would be key to rebalanced pathways to positive estrogens..
 
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