37 replies to this topic

[factsmachine]

I've been reading for days on this stuff. What I thought before was cortisol could be NE. Cortisol is said to give consistent energy to get things accomplished, its supposed to feel less jumpy than NE. Here's a few points:

-I feel jumpy, extremely stimulated all the time

-Erection quality is suffering, and flaccid my body wants to bring my penis into my body instead of the relaxed normal position people normally get

-Social anxiety, sleeplessness, irritability, feels like im on a perpetual adrenaline rush.


This describes what I'm talking about in detail: 
http://forums.phoeni...ne.22518/page-2

My social life, sex life, mental, physical and emotional health are suffering from feeling like i'm on a perpetual adrenaline rush. 
Benzos work, of course. But they can't be sustained. 
I'm depressed, anxious, feel stressed, irritable, angry, and just terrible. 
Thoughts?
 

[Metagene]

You should see a endocrinologist.

[Area-1255]

You should see a endocrinologist.

He's correct, high norepinephrine is usually caused by hormonal imbalance, particularly high estrogen levels - or copper dominance leading to both high DHT and estrogen - which both can increase adrenaline - but primarily estrogen, as it causes dopamine to convert into norepinephrine by means of increasing dopamine beta hydroxylase (DBH).

In addition , estrogen triggers the increase in the stimulatory serotonin receptor family of 5-HT2A/2C complexes, this causes calcium channels to be overactivated thus leading to double the increase in norepinephrine and especially, glutamate.

 

~CONSIDER THE FOLLOWING~

• Take Vitamin C supplements; which can help to reduce copper and norepinephrine-induced vasoconstriction.
• Take ZINC AND MAGNESIUM @ night, which can help tone down the sympathetic nervous system.
• Pursue an endocrinologist, and get a complete hormone panel done, including thyroid hormones.
• TSH,T4,T3,Free Thyroxine and all comprehensive metabolic parameter's should be checked.
• Get a urine test for the metanephrine and serotonin metabolites; (5-H1AA).
• Total Testosterone,Estrogen,FREE T, Prolactin, DHT,SHBG(SexHormoneBindingHormone) should all be checked.
• If your estrogen turns out HIGH; Go on an anti-estrogen diet, including plenty of broccoli, cabbage, drinking pomegranate juice and mangosteen.
• You may also need arimidex. 
• If your hormones turn out NORMAL; then my next concern would be either a pheochromocytoma or adrenaline secreting tumor, or just high copper levels and adrenaline due to heavy metals, not to scare you, these two things are pretty rare, other than high copper........
• Thus get hair copper and zinc levels checked as well.

[factsmachine]

I have normal thyroid hormones, low testosterone. and now I'm on TRT with axiron 120mg a day. been on it for 2 weeks. Ijust ttook ambien and im still feeling extremely stimulated.
my E2 seems to be in check, I take AIs.
still need to get them tested. also what else?
also I'm 19 years old. can't exdit post on mobile
also I'm 19 years old. can't exdit post on mobile

[Area-1255]

I have normal thyroid hormones, low testosterone. and now I'm on TRT with axiron 120mg a day. been on it for 2 weeks. Ijust ttook ambien and im still feeling extremely stimulated.
my E2 seems to be in check, I take AIs.
still need to get them tested. also what else?
also I'm 19 years old. can't exdit post on mobile

Copper, zinc, test for all kinds of heavy metals....get blood histamine checked, it's an important regulator of GABA..

 

do you take any GABA antagonists? do you eat soy? eating soy based foods, ginkgo biloba, kudzu, pea protein excess...can all cause high norepinephrine!

[StevesPetRat]

Good info. I want to be like Area-1255 when I grow up.

[factsmachine]

excellent info. thank you very much. what about callousness and aggression towards other people? like a self-protective sociopath. if I feel like anybody is trying to belittle me I will get aggressive fast.
here's some new info I just found out. my mom never once breastfed me and rarely held me as a baby.
theoretically.... Mom had too little oxytocin (sociopathic trait) and thus production of breast milk was not possible. never felt bonded to me.
as a kid actually I was alone most of the time. I really raised myself. even at a young age (like 8) my mom would say something mean to me and I'd grab a knife. never did anything to harm her, but its just a little insight. I've always been like that, but normally I'm very friendly, never aggressive. when I'm low, I lose all self control and will drive fast, thought of doing plenty of illegal immoral things.
also heard this type of shit is impossible to treat. it really makes me wonder if I'm doing society a favor if I ended it all. but then again I'm intelligent, I want to be a research scientist. I have good intentions but when people cross me, morals go out the window..

[BlueCloud]

 

You should see a endocrinologist.

He's correct, high norepinephrine is usually caused by hormonal imbalance, particularly high estrogen levels - or copper dominance leading to both high DHT and estrogen - which both can increase adrenaline - but primarily estrogen, as it causes dopamine to convert into norepinephrine by means of increasing dopamine beta hydroxylase (DBH).

In addition , estrogen triggers the increase in the stimulatory serotonin receptor family of 5-HT2A/2C complexes, this causes calcium channels to be overactivated thus leading to double the increase in norepinephrine and especially, glutamate.

 

~CONSIDER THE FOLLOWING~

• Take Vitamin C supplements; which can help to reduce copper and norepinephrine-induced vasoconstriction.
• Take ZINC AND MAGNESIUM @ night, which can help tone down the sympathetic nervous system.
• Pursue an endocrinologist, and get a complete hormone panel done, including thyroid hormones.
• TSH,T4,T3,Free Thyroxine and all comprehensive metabolic parameter's should be checked.
• Get a urine test for the metanephrine and serotonin metabolites; (5-H1AA).
• Total Testosterone,Estrogen,FREE T, Prolactin, DHT,SHBG(SexHormoneBindingHormone) should all be checked.
• If your estrogen turns out HIGH; Go on an anti-estrogen diet, including plenty of broccoli, cabbage, drinking pomegranate juice and mangosteen.
• You may also need arimidex. 
• If your hormones turn out NORMAL; then my next concern would be either a pheochromocytoma or adrenaline secreting tumor, or just high copper levels and adrenaline due to heavy metals, not to scare you, these two things are pretty rare, other than high copper........
• Thus get hair copper and zinc levels checked as well.

 

 

mmm...  it's the complete  opposite. Vitamin C actually enhances conversion of Dopamine to Norepinephrine, and Estrogen inhibits Norepinephrine responsiveness.

 

See for Estrogen/Norepinephrine  :

http://www.ncbi.nlm....pubmed/17592033

http://www.medscape....rticle/406718_2

http://www.ncbi.nlm....pubmed/10404954

 

for Vitamin C / Norepinephrine :

http://www.jbc.org/c...nt/260/29/15598

"Ascorbic acid efficiently enhances neuronal synthesis of norepinephrine from dopamine."  http://www.ncbi.nlm....pubmed/23022576

 

I agree however that  Copper does contribute strongly to raising Norepinephrine levels.

 

Edited by BlueCloud, 01 December 2014 - 01:31 PM.

[Area-1255]

 

 

You should see a endocrinologist.

He's correct, high norepinephrine is usually caused by hormonal imbalance, particularly high estrogen levels - or copper dominance leading to both high DHT and estrogen - which both can increase adrenaline - but primarily estrogen, as it causes dopamine to convert into norepinephrine by means of increasing dopamine beta hydroxylase (DBH).

In addition , estrogen triggers the increase in the stimulatory serotonin receptor family of 5-HT2A/2C complexes, this causes calcium channels to be overactivated thus leading to double the increase in norepinephrine and especially, glutamate.

 

~CONSIDER THE FOLLOWING~

• Take Vitamin C supplements; which can help to reduce copper and norepinephrine-induced vasoconstriction.
• Take ZINC AND MAGNESIUM @ night, which can help tone down the sympathetic nervous system.
• Pursue an endocrinologist, and get a complete hormone panel done, including thyroid hormones.
• TSH,T4,T3,Free Thyroxine and all comprehensive metabolic parameter's should be checked.
• Get a urine test for the metanephrine and serotonin metabolites; (5-H1AA).
• Total Testosterone,Estrogen,FREE T, Prolactin, DHT,SHBG(SexHormoneBindingHormone) should all be checked.
• If your estrogen turns out HIGH; Go on an anti-estrogen diet, including plenty of broccoli, cabbage, drinking pomegranate juice and mangosteen.
• You may also need arimidex. 
• If your hormones turn out NORMAL; then my next concern would be either a pheochromocytoma or adrenaline secreting tumor, or just high copper levels and adrenaline due to heavy metals, not to scare you, these two things are pretty rare, other than high copper........
• Thus get hair copper and zinc levels checked as well.

 

 

mmm...  it's the complete  opposite. Vitamin C actually enhances conversion of Dopamine to Norepinephrine, and Estrogen inhibits Norepinephrine responsiveness.

 

See for Estrogen/Norepinephrine  :

http://www.ncbi.nlm....pubmed/17592033

http://www.medscape....rticle/406718_2

http://www.ncbi.nlm....pubmed/10404954

 

for Vitamin C / Norepinephrine :

http://www.jbc.org/c...nt/260/29/15598

"Ascorbic acid efficiently enhances neuronal synthesis of norepinephrine from dopamine."  http://www.ncbi.nlm....pubmed/23022576

 

I agree however that  Copper does contribute strongly to raising Norepinephrine levels.

 

Vitamin C stimulates norepinephrine, but it also chelates and removes excess copper when used with Zinc, thus, the net effect is still sympathetic balance...now on your ABSURD comment on estrogen - if that were the case, then everyone with high estrogen would not have any anxiety , is that the case? No , and anybody who knows what high E2 feels like would understand that!

 

Now I will crush the rest of your statement with the following. 

 

 

Neuroendocrinology. 2002 Mar;75(3):193-200.

Estradiol stimulates gene expression of norepinephrine biosynthetic enzymes in rat locus coeruleus.

Serova L1, Rivkin M, Nakashima A, Sabban EL.

Author information

 

Abstract

Gender-specific differences in susceptibility to a number of disorders related to catecholaminergic systems, including depression and hypertension, have been postulated to be mediated, at least in part, by estrogens. In this study, we examined if estrogens may regulate gene expression of norepinephrine biosynthetic enzymes. Administration of five injections of 15 or 40 microg/kg estradiol benzoate to ovariectomized (OVX) female rats elicited a dose-dependent elevation in mRNA levels of tyrosine hydroxylase (TH) in locus coeruleus, to as great as 3-fold over control. Dopamine beta-hydroxylase (DBH) mRNA levels were also similarly increased. To examine the mechanism, PC12 cells were cotransfected with luciferase reporter constructs under control of DBH or TH promoters [pDBH/Luc(-2,236/+21) or pTH/Luc(-272/+27 or -773/+27)] with an expression vector for estradiol receptor alpha. The cells were treated with 17beta-estradiol (E(2)) for 12-36 h. E(2) triggered a several fold increase in luciferase activity under control of the DBH promoter in a dose-dependent fashion. Omission of estrogen receptor alpha or addition of the estrogen receptor antagonist ICI 182,780 prevented the DBH promoter-driven increase in luciferase. When E(2) was given with 0.2 mM CPT-cAMP, reporter activity with pDBH/Luc(-2,236/+21) was increased greater than with either treatment alone. In contrast, addition of E(2) to cells transfected with pTH/Luc(-272/+27) elicited no change in basal luciferase activity nor in the response to 0.2 mM CPT-cAMP. These findings are the first to reveal that estrogen can stimulate DBH gene expression. Differing mechanisms may underlie the regulation of TH and DBH gene expression by estrogens.

Copyright 2002 S. Karger AG, Basel

PMID:   11914591   [PubMed - indexed for MEDLINE]

[Area-1255]

excellent info. thank you very much. what about callousness and aggression towards other people? like a self-protective sociopath. if I feel like anybody is trying to belittle me I will get aggressive fast.
here's some new info I just found out. my mom never once breastfed me and rarely held me as a baby.
theoretically.... Mom had too little oxytocin (sociopathic trait) and thus production of breast milk was not possible. never felt bonded to me.
as a kid actually I was alone most of the time. I really raised myself. even at a young age (like 8) my mom would say something mean to me and I'd grab a knife. never did anything to harm her, but its just a little insight. I've always been like that, but normally I'm very friendly, never aggressive. when I'm low, I lose all self control and will drive fast, thought of doing plenty of illegal immoral things.
also heard this type of shit is impossible to treat. it really makes me wonder if I'm doing society a favor if I ended it all. but then again I'm intelligent, I want to be a research scientist. I have good intentions but when people cross me, morals go out the window..

Adrenaline does this - it makes you very serious and territorial, if you have low dopamine, and high norepinephrine, as well as low serotonin, then you already have the recipe for being either paranoid and having some subset of antisocial personality, or BOTH - from a physiological standpoint at the least, of course, sociopathy/psychopathy is stronger from the psychology, and physiology is influenced more so by the mindset the person in question decides to internalize as their truth.

People who are truth sociopaths and psychopaths are so because they choose to be, and even though genetics play a role, the bottom line is if someone doesn't want to change, it doesn't matter how many times their biochemistry changes, they will not change. 

That being said, I firmly believe that a deficiency in any of the following oxytocin signaling hormones can predispose one to a more natural psychopathy or just a lack of trust and connection to humanity.

 

 

-Dopamine

-Histamine

-Glutamate

 

 

 

Serotonin kind of but not really, because the thing is, serotonin being elevated can also destroy oxytocin and create a similar dissociated state or can cause lack of empathy in some individuals who also lack the above, but it can play a positive role - depending on the person, and their genetics. 

Edited by Area-1255, 01 December 2014 - 03:26 PM.

[factsmachine]

good job guys. this is the kind of stuff I like to read and learn.

I used to believe my problem was high cortisol so I took about 5,000mg of Vit C a day. I thought it would help my anxiety. it never really did
There's a study out there that had people do a public speaking task. the ones that took 1,000mg vit C beforehand had less cortisol and less anxiety.
however I just learned that Glucocorticoids (think its cortisol, may be CRH) cause a feedback thatdecreases norepinephrine.

so I'm going to the doctor in 2 days. probably switching from axiron testosterone gel to testosterone cyp injections. my E2 was so high, I was gonna wait it out till bloodwork but started to grow lumps under my nipples that hurt. most doctors say "oh youre low bodyfat percentage! no way youll get gyno silly!" well shiiit I said fuck that and got formestane to use as an AI.

I've had this adrenaline rush problem for what seems like my whole life, I have a lot of tests I need to convince my doc to do now. I am ready to just go on some benzos. they work every time.

[factsmachine]

Arena, that's DEFINITELY it. i feel very territorial, like im fighting for my life when really its just my neural chemistry.
I'm also very manic. I'm quiet and my mind races. but when I talk about something I care about I just get diarrhea of the mouth.
I wouldn't mind being a sociopath at all. I'd be better off without my emotions. if I could be calmer then logic would do wonders for me.
I had a concussion when I was 15, I got hit on the top right of my hairline on the front and almost went unconscious. never went back to the Dr. they said that I was fine because I didn't go unconscious. the rock was bigger than my head, some kid threw it and it hit me. that could play some significace..

[factsmachine]

in the book by James Fallon (highly reccomended) he says that those born with the warrior gene (mao-a) have too much serotonin during development, and the brain adjusts accordingly by therefore decreasing the effect that serotonin will have. where is serotonin most highly concentrated in the brain? I hypothesise limbic, and orbitofrontal

[BlueCloud]

Vitamin C stimulates norepinephrine, but it also chelates and removes excess copper when used with Zinc, thus, the net effect is still sympathetic balance...now on your ABSURD comment on estrogen - if that were the case, then everyone with high estrogen would not have any anxiety , is that the case? No , and anybody who knows what high E2 feels like would understand that!

 

 

Now I will crush the rest of your statement with the following. 

 

 

 

 

 

 

 

It's not "my" statement, it's just what the science indicates, and it's not as clear cut as you say :

 

 

 

Estrogen inhibition of norepinephrine responsiveness is initiated at the plasma membrane of GnRH-producing GT1-7 cells.

Morales A1, Gonzalez M, Marin R, Diaz M, Alonso R.

Author information

 

Abstract

The modulatory action of estradiol (E2) on the GnRH network can be exerted indirectly on presynaptic neurons or directly on estrogen receptors (ERs) located within GnRH hypothalamic neurons. Using the GnRH-producing GT1-7 cell line, we have investigated whether E2 is able to modify the response of these cells to norepinephrine (NE) stimulation. A 48-h exposure of GT1-7 cells to 10 nM E2 reduced NE-induced cAMP accumulation. However, 15-min exposure was enough to induce this inhibitory action, provided that a hormone-free period of 48 h after steroid treatment was allowed. Furthermore, this effect was mimicked by E2 coupled to (E-BSA), indicating that it may be exerted through a membrane-mediated mechanism. In addition, competition experiments using E-BSA coupled to fluorescein isothiocyanate (FITC) revealed the presence of cell membrane-binding sites for E2. Binding of E-BSA coupled to FITC was blocked by preincubation of cells with either E2, antiestrogen ICI 182 780, or tamoxifen. Moreover, fluorescence staining of non-permeabilized cells with antibodies against receptors alpha and beta confirmed the presence of both receptor subtypes at the cell membrane. To determine the nature of the ER involved in this response, specific agonists for ERalpha 4,4',4''-(4-propyl-[1H]pyrazole-1,3,5-triyl)tris-phenol (PPT) and ERbeta 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN) were used. Since PPT, but not DPN, reproduced the effect of E2, it is suggested that estrogen-induced modulatory action on NE responsiveness was mediated by the ERalpha isoform. Taken together, these results indicate that E2 modulates the adrenergic sensitivity of GT1-7 cells by a mechanism compatible with the activation of membrane-associated ERs.

 

 

 

 

Estrogen supplementation decreases norepinephrine-induced vasoconstriction and total body norepinephrine spillover in perimenopausal women.

Sudhir K1, Elser MD, Jennings GL, Komesaroff PA.

Author information

 

Abstract

Estrogens are reported to provide protection against the development of cardiovascular disease in women, but the mechanisms underlying these effects are not well defined. We hypothesized that estrogen might reduce neural cardiovascular tone. We therefore studied responses to exogenous norepinephrine and norepinephrine spillover in 12 perimenopausal women randomized to 8 weeks of estrogen supplementation (estradiol valerate, 2 mg daily, n=7) or placebo (n=5). Forearm blood flow was measured by venous occlusion plethysmography, and vasoactive agents were infused through a brachial artery cannula in doses that did not influence blood pressure or heart rate. Total body and forearm norepinephrine spillover were measured by radiotracer methodology. Forearm vasoconstrictor responses to norepinephrine (25, 50, and 100 ng/min) were attenuated after estrogen supplementation (P=.002). Vasoconstrictor responses to angiotensin II (8, 16, and 32 ng/min) were unchanged postestrogen. There was a significant reduction in total body spillover of norepinephrine after estrogen supplementation (pre-estrogen, 700+/-152; postestrogen, 439+/-150 ng/min; P<.05), but there was no change after placebo. Total body clearance and forearm spillover of norepinephrine were unchanged by either estrogen or placebo. Estrogen supplementation also significantly decreased both systolic and diastolic blood pressures. Therefore, estrogen supplementation in perimenopausal women selectively attenuates vasoconstrictor responses to norepinephrine and reduces total body norepinephrine spillover, which is an index of sympathetic neural activity.

 

 

Estrogen depletion increases blood pressure and hypothalamic norepinephrine in middle-aged spontaneously hypertensive rats.

Hypertension

Hypertension 2003 May 24;41(5):1164-7. Epub 2003 Mar 24.

Ning Peng, John T Clark, Chi-Chang Wei, J Michael Wyss

•  
• In male spontaneously hypertensive rats (SHR) a high NaCl diet increases arterial pressure via a reduction in anterior hypothalamic nucleus norepinephrine release. Young female SHR are relatively well protected from this NaCl-sensitive hypertension, but depletion of both endogenous and dietary estrogens greatly exacerbates NaCl-sensitive hypertension. This study tests the hypothesis that estrogen also protects late middle-aged female SHR from NaCl-sensitive hypertension and that this effect is mediated by an estrogen-related effect on hypothalamic norepinephrine release. Ten-month-old female SHR were ovariectomized and placed on a phytoestrogen-free diet containing either basal or high NaCl. Each rat was implanted with a silastic tube containing 17beta estradiol or vehicle. Three months later, arterial pressure and hypothalamic norepinephrine metabolite levels (MOPEG) were measured. On the basal NaCl diet, estrogen-depleted rats displayed increased arterial pressure (12 mm Hg) and decreased anterior hypothalamic nucleus MOPEG (20%). Both effects were reversed by estrogen treatment. In all groups, the high NaCl diet increased arterial pressure by over 35 mm Hg and reduced anterior hypothalamic nucleus MOPEG by >60%. Across all groups, there was a significant inverse correlation between arterial pressure and anterior hypothalamic nucleus MOPEG. These data suggest that both dietary NaCl excess and estrogen depletion raise arterial pressure in middle-aged female SHR by a decreasing hypothalamic norepinephrine.

Affiliation

Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Ala 35294-0006, USA.

 

[Area-1255]

 

Vitamin C stimulates norepinephrine, but it also chelates and removes excess copper when used with Zinc, thus, the net effect is still sympathetic balance...now on your ABSURD comment on estrogen - if that were the case, then everyone with high estrogen would not have any anxiety , is that the case? No , and anybody who knows what high E2 feels like would understand that!

 

 

Now I will crush the rest of your statement with the following. 

 

 

 

 

 

 

 

It's not "my" statement, it's just what the science indicates, and it's not as clear cut as you say :

 

 

THIS IS IRRELEVANT - AS IT STATES GTI-7 CELLS, IT IS TALKING ABOUT THE HYPOTHALAMIC NETWORKS DIRECTLY RELATING TO GONADOTROPIN FEEDBACK - NOT NEURAL NETWORKS OR OTHER BRAIN REGIONS INVOLVED WITH ANXIETY !

Estrogen inhibition of norepinephrine responsiveness is initiated at the plasma membrane of GnRH-producing GT1-7 cells.

Morales A1, Gonzalez M, Marin R, Diaz M, Alonso R.

Author information

 

Abstract

The modulatory action of estradiol (E2) on the GnRH network can be exerted indirectly on presynaptic neurons or directly on estrogen receptors (ERs) located within GnRH hypothalamic neurons. Using the GnRH-producing GT1-7 cell line, we have investigated whether E2 is able to modify the response of these cells to norepinephrine (NE) stimulation. A 48-h exposure of GT1-7 cells to 10 nM E2 reduced NE-induced cAMP accumulation. However, 15-min exposure was enough to induce this inhibitory action, provided that a hormone-free period of 48 h after steroid treatment was allowed. Furthermore, this effect was mimicked by E2 coupled to (E-BSA), indicating that it may be exerted through a membrane-mediated mechanism. In addition, competition experiments using E-BSA coupled to fluorescein isothiocyanate (FITC) revealed the presence of cell membrane-binding sites for E2. Binding of E-BSA coupled to FITC was blocked by preincubation of cells with either E2, antiestrogen ICI 182 780, or tamoxifen. Moreover, fluorescence staining of non-permeabilized cells with antibodies against receptors alpha and beta confirmed the presence of both receptor subtypes at the cell membrane. To determine the nature of the ER involved in this response, specific agonists for ERalpha 4,4',4''-(4-propyl-[1H]pyrazole-1,3,5-triyl)tris-phenol (PPT) and ERbeta 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN) were used. Since PPT, but not DPN, reproduced the effect of E2, it is suggested that estrogen-induced modulatory action on NE responsiveness was mediated by the ERalpha isoform. Taken together, these results indicate that E2 modulates the adrenergic sensitivity of GT1-7 cells by a mechanism compatible with the activation of membrane-associated ERs.

 

 

LOL, IN PERIMENOPAUSAL WOMEN?  THAT'S NOT GOING TO APPLY TO A MALE WHO HAS CONFIRMED ADRENALINE ISSUES ----ALSO , IF YOU ARE SO CORRECT, THEN WHY DOES OP (facts machine) have CONFIRMED HIGH ESTROGEN AND ALSO HAS HIGH ADRENALINE? EVEN IF YOU ARE GOING TO STATE YOUR PROVIDED STUDIES ARE CORRECT, EVERYTHING IN THIS THREAD, WITH PEOPLE'S PERSONAL EXPERIENCES, ASIDE FROM TAKING SHIT OUT OF CONTEXT, EVEN FROM YOUR STUDIES, IMMEDIATELY THROWS YOUR CREDIBILITY OUT THE WINDOW!

 

Estrogen supplementation decreases norepinephrine-induced vasoconstriction and total body norepinephrine spillover in perimenopausal women.

Sudhir K1, Elser MD, Jennings GL, Komesaroff PA.

Author information

 

Abstract

Estrogens are reported to provide protection against the development of cardiovascular disease in women, but the mechanisms underlying these effects are not well defined. We hypothesized that estrogen might reduce neural cardiovascular tone. We therefore studied responses to exogenous norepinephrine and norepinephrine spillover in 12 perimenopausal women randomized to 8 weeks of estrogen supplementation (estradiol valerate, 2 mg daily, n=7) or placebo (n=5). Forearm blood flow was measured by venous occlusion plethysmography, and vasoactive agents were infused through a brachial artery cannula in doses that did not influence blood pressure or heart rate. Total body and forearm norepinephrine spillover were measured by radiotracer methodology. Forearm vasoconstrictor responses to norepinephrine (25, 50, and 100 ng/min) were attenuated after estrogen supplementation (P=.002). Vasoconstrictor responses to angiotensin II (8, 16, and 32 ng/min) were unchanged postestrogen. There was a significant reduction in total body spillover of norepinephrine after estrogen supplementation (pre-estrogen, 700+/-152; postestrogen, 439+/-150 ng/min; P<.05), but there was no change after placebo. Total body clearance and forearm spillover of norepinephrine were unchanged by either estrogen or placebo. Estrogen supplementation also significantly decreased both systolic and diastolic blood pressures. Therefore, estrogen supplementation in perimenopausal women selectively attenuates vasoconstrictor responses to norepinephrine and reduces total body norepinephrine spillover, which is an index of sympathetic neural activity.

 

Now you are trying to cite a study indicating middle aged spontaneously hypertensive rats, I need not even say anything to do this, it's absurd. lmao

Estrogen depletion increases blood pressure and hypothalamic norepinephrine in middle-aged spontaneously hypertensive rats.

Hypertension

Hypertension 2003 May 24;41(5):1164-7. Epub 2003 Mar 24.

Ning Peng, John T Clark, Chi-Chang Wei, J Michael Wyss

•  
• In male spontaneously hypertensive rats (SHR) a high NaCl diet increases arterial pressure via a reduction in anterior hypothalamic nucleus norepinephrine release. Young female SHR are relatively well protected from this NaCl-sensitive hypertension, but depletion of both endogenous and dietary estrogens greatly exacerbates NaCl-sensitive hypertension. This study tests the hypothesis that estrogen also protects late middle-aged female SHR from NaCl-sensitive hypertension and that this effect is mediated by an estrogen-related effect on hypothalamic norepinephrine release. Ten-month-old female SHR were ovariectomized and placed on a phytoestrogen-free diet containing either basal or high NaCl. Each rat was implanted with a silastic tube containing 17beta estradiol or vehicle. Three months later, arterial pressure and hypothalamic norepinephrine metabolite levels (MOPEG) were measured. On the basal NaCl diet, estrogen-depleted rats displayed increased arterial pressure (12 mm Hg) and decreased anterior hypothalamic nucleus MOPEG (20%). Both effects were reversed by estrogen treatment. In all groups, the high NaCl diet increased arterial pressure by over 35 mm Hg and reduced anterior hypothalamic nucleus MOPEG by >60%. Across all groups, there was a significant inverse correlation between arterial pressure and anterior hypothalamic nucleus MOPEG. These data suggest that both dietary NaCl excess and estrogen depletion raise arterial pressure in middle-aged female SHR by a decreasing hypothalamic norepinephrine.

Affiliation

Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Ala 35294-0006, USA.

 

 

Looks ridiculous, I've done you the favor and OP of dis-assembling your nonsense..as you seem to only have an interest in proving your own distorted views correct ----- for the safety of OP and the sanity of ANYONE reading this, it had to be done.

 

OP, please ignore this guy, he is trying to prove something, whereas I am obviously encouraging the stable use of common sense in combination with available evidence, do not trust studies that are used in the wrong context. 

 

 

Edited by Area-1255, 01 December 2014 - 04:11 PM.

[BlueCloud]

 

 

LOL, IN PERIMENOPAUSAL WOMEN?  THAT'S NOT GOING TO APPLY TO A MALE WHO HAS CONFIRMED ADRENALINEISSUES ----ALSO , IF YOU ARE SO CORRECT, THEN WHY DOES OP (facts machine) have CONFIRMED HIGH ESTROGEN AND ALSO HAS HIGH ADRENALINE? EVEN IF YOU ARE GOING TO STATE YOUR PROVIDED STUDIES ARE CORRECT, EVERYTHING IN THIS THREAD, WITH PEOPLE'S PERSONAL EXPERIENCES, ASIDE FROM TAKING SHIT OUT OF CONTEXT, EVEN FROM YOUR STUDIES, IMMEDIATELY THROWS YOUR CREDIBILITY OUT THE WINDOW!

 

Looks like your norepinephrine is shooting through the roof. Suit yourself. 

 

 

 

 

OP, please ignore this guy, he is trying to prove something, whereas I am obviously encouraging the stable use of common sense in combination with available evidence, do not trust studies that are used in the wrong context. 

 

Unlike you, Im' not trying to "prove" anything ( this is not a war or an olympic competition). I'm simply observing that when it comes to estrogens, one can't simply say : "Lower your estrogen and it will lower your norepinephrine". It 's more complex than that and we can't deduct simple statements at this time.

Also note that the study you mentioned is done on Ovariectomized Female Rats...

Edited by BlueCloud, 01 December 2014 - 05:08 PM.

[Area-1255]

in the book by James Fallon (highly reccomended) he says that those born with the warrior gene (mao-a) have too much serotonin during development, and the brain adjusts accordingly by therefore decreasing the effect that serotonin will have. where is serotonin most highly concentrated in the brain? I hypothesise limbic, and orbitofrontal

Well, I have the warrior gene as well, and I used to higher serum levels of serotonin and norepinephrine in blood work/urine tests, it's still probably a bit above average, but I have adjusted my diet to create a positive shift.......namely a histamine boosting diet. 

I believe the warrior gene is very similar to someone who takes phenylzine or another MAO inhibitor, you will have more serotonin, dopamine and norepinephrine, but , eventually because the cortisol level rises from the later two - you will have a wearout of serotonin receptors .

People with the warrior gene tend to have de-sensitized or chronically increased 5-HT1A serotonin receptor expression, this is noted as a secondary effect , whereas for some reason, 5-hT1D receptors are downregulated, especially in those who also have obsessive-compulsive-disorder.

 

 

 

LOL, IN PERIMENOPAUSAL WOMEN?  THAT'S NOT GOING TO APPLY TO A MALE WHO HAS CONFIRMED ADRENALINEISSUES ----ALSO , IF YOU ARE SO CORRECT, THEN WHY DOES OP (facts machine) have CONFIRMED HIGH ESTROGEN AND ALSO HAS HIGH ADRENALINE? EVEN IF YOU ARE GOING TO STATE YOUR PROVIDED STUDIES ARE CORRECT, EVERYTHING IN THIS THREAD, WITH PEOPLE'S PERSONAL EXPERIENCES, ASIDE FROM TAKING SHIT OUT OF CONTEXT, EVEN FROM YOUR STUDIES, IMMEDIATELY THROWS YOUR CREDIBILITY OUT THE WINDOW!

 

 

 

 

 

 

Looks like your norepinephrine is shooting through the roof. Suit yourself. 

 

More adhominems, shows you can't defend yourself very well - sit it down little fella.

[BlueCloud]

More adhominems, shows you can't defend yourself very well - sit it down little fella.

 

 

 

well, your advice is clearly not working, because I just pointed out that the litterature is not clear-cut ( wich means we can't say for sure one way or the other at this time) when it comes to estrogen ( you "crush" it by saying that they're done on perimenopausal women or middle aged rats,  but you want to prove it by a study done on 5 ovariectomized female rats ???)  and you start screaming like I just killed your cat and made sushi with it !

 

This is NOT a personal attack on you or a popularity competition and there's no reason to react like this, this is debate, that's how knowledge advances, we debate and we try together to get closer to the truth. 

Edited by BlueCloud, 01 December 2014 - 05:25 PM.

[Area-1255]

 

More adhominems, shows you can't defend yourself very well - sit it down little fella.

 

 

 

well, your advice is clearly not working, because I just pointed out that the litterature is not clear-cut ( wich means we can't say for sure one way or the other at this time) when it comes to estrogen ( you "crush" it by saying that they're done on perimenopausal women or middle aged rats,  but you want to prove it by a study done on 5 ovariectomized female rats ???)  and you start screaming like I just killed your cat and made sushi with it !

 

This is NOT a personal attack on you or a popularity competition and there's no reason to react like this, this is debate, that's how knowledge advances, we debate and we try together to get closer to the truth. 

 

Lol, since when is typing in caps screaming? 

Again, my quotes stand for themselves, looks like you have your adam's apple a little too high up in your throat again bub.

 

And to say my advice is not working, when clearly, I was addressed and thanked foremost, not that I care, I just don't want OP to get the wrong idea from someone who clearly doesn't have his best interests at hand.

Area, that's DEFINITELY it. i feel very territorial, like im fighting for my life when really its just my neural chemistry.
I'm also very manic. I'm quiet and my mind races. but when I talk about something I care about I just get diarrhea of the mouth.
I wouldn't mind being a sociopath at all. I'd be better off without my emotions. if I could be calmer then logic would do wonders for me.
I had a concussion when I was 15, I got hit on the top right of my hairline on the front and almost went unconscious. never went back to the Dr. they said that I was fine because I didn't go unconscious. the rock was bigger than my head, some kid threw it and it hit me. that could play some significace..

 

Edited by Area-1255, 01 December 2014 - 05:28 PM.

[factsmachine]

Well, that escalated quickly.
remember guys, we are in pursuit of knowledge, not powerful egos. discussions need not be against one another. I can see from both sides because I can see how each side has a point to an extent. for the sake of my health and your guys' knowledge, we should look for other possibilities that could be causing this Adrenaline problem. estrogen is less of my worries, that can be controlled easily through arimidex.

I've dropped my estrogen real low before to see if I'd feel better. oh boy, that was a mistake. feel like sleeping, can't sleep, body feels too warm, feels like you have no motivation, no drive, no sex drive either.

here's some symptoms I have: Depressed, anxious, aggressive, pissed off, no motivation, stressed out, thought loops, terrible muscle tension, jaw clenching, social avoidance

I started raking tianeptine and it did a few things for me. didn't fix everything but. less aggressive (could also be the TRT, haven't lost my temper much since), feel hope, not direct happiness. it doesn't affect my adrenaline problem much. does make it harder to sleep. and weird dreams. (took it to stay awake today for an appointment, ended up falling asleep. had VIVID dreams of performing surgery and then defibrillation. lost the patient and woke up)
when I take klonopin, I feel less anxious but still get myself into these depressive thought loops. just like I normally do.

this is a damn puzzel. I wish opiates were sustainable. low dose of anything hitting opiate receptors gets me out of my depression short term.
might add that the low estrogen didn't fx my anxiety and depression, just made me feel terrible. high estrogen seems to change the "flavor" of the anxiety.

[Area-1255]

Well, that escalated quickly.
remember guys, we are in pursuit of knowledge, not powerful egos. discussions need not be against one another. I can see from both sides because I can see how each side has a point to an extent. for the sake of my health and your guys' knowledge, we should look for other possibilities that could be causing this Adrenaline problem. estrogen is less of my worries, that can be controlled easily through arimidex.

I've dropped my estrogen real low before to see if I'd feel better. oh boy, that was a mistake. feel like sleeping, can't sleep, body feels too warm, feels like you have no motivation, no drive, no sex drive either.

here's some symptoms I have: Depressed, anxious, aggressive, pissed off, no motivation, stressed out, thought loops, terrible muscle tension, jaw clenching, social avoidance

I started raking tianeptine and it did a few things for me. didn't fix everything but. less aggressive (could also be the TRT, haven't lost my temper much since), feel hope, not direct happiness. it doesn't affect my adrenaline problem much. does make it harder to sleep. and weird dreams. (took it to stay awake today for an appointment, ended up falling asleep. had VIVID dreams of performing surgery and then defibrillation. lost the patient and woke up)
when I take klonopin, I feel less anxious but still get myself into these depressive thought loops. just like I normally do.

this is a damn puzzel. I wish opiates were sustainable. low dose of anything hitting opiate receptors gets me out of my depression short term.
might add that the low estrogen didn't fx my anxiety and depression, just made me feel terrible. high estrogen seems to change the "flavor" of the anxiety.

Yet ironically, there are many males with undetectable estrogen levels who feel fine, which brings it back to individuality and personal preference and genetics; one person's anxiety is another persons sanity. 
For the most part, it seems like androgen's , especially DHT and 3-a-diol play the largest roles in male anxiety and depression, and the decrease of them, ESPECIALLY 3-a-diol, can account for depression and anxiety symptoms. 

The Role of the Androgen Receptor in Anxiety-related Behaviors, the ... - Damian G. Zuloaga - Google Books

 

 

Pharmacol Biochem Behav. 2004 Jul;78(3):473-81.

Testosterone's metabolism in the hippocampus may mediate its anti-anxiety effects in male rats.

Frye CA1, Edinger KL.

Author information

 

Abstract

Androgens may mediate anxiety behaviors; however, these effects and mechanisms of androgens are not well understood. The following experiments investigated whether testosterone (T)'s effects on anxiety behavior are mediated by its 5alpha-reduced, nonaromatizable metabolite dihydrotestosterone (DHT) and/or its 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD) reduced metabolite 3alpha-androstanediol (3alpha-diol). In Experiment 1, gonadally-intact adult male rats and gonadectomized (GDX), DHT-replaced rats had similar low levels of anxiety behavior in the open field and elevated plus maze and fear behavior in the defensive freezing task compared with GDX control rats. In Experiment 2, intact or DHT-replaced rats that received blank inserts to the hippocampus demonstrated less anxiety behavior than did rats administered an implant of indomethacin, a 3alpha-HSD inhibitor, to the dorsal hippocampus. These data indicate that T's 5alpha-reduced metabolite, DHT, can reduce anxiety behavior and that blocking metabolism to 3alpha-diol in the hippocampus can attenuate these effects.

PMID:   15251256   [PubMed - indexed for MEDLINE]

 

Horm Behav. 2008 Nov;54(5):726-34. doi: 10.1016/j.yhbeh.2008.07.013. Epub 2008 Aug 8.

Androgens with activity at estrogen receptor beta have anxiolytic and cognitive-enhancing effects in male rats and mice.

Frye CA1, Koonce CJ, Edinger KL, Osborne DM, Walf AA.

Author information

 

Abstract

Testosterone (T) and its metabolites may underlie some beneficial effects for anxiety and cognition, but the mechanisms for these effects are unclear. T is reduced to dihydrotestosterone (DHT), which can be converted to 5alpha-androstane,3alpha,17beta-diol (3alpha-diol) and/or 5alpha-androstane-3beta,17beta-diol (3beta-diol). Additionally, T can be converted to androstenedione, and then to androsterone. These metabolites bind with varying affinity to androgen receptors (ARs; T and DHT), estrogen receptors (ERbeta; 3alpha-diol, 3beta-diol), or GABA(A)/benzodiazepine receptors (GBRs; 3alpha-diol, androsterone). Three experiments were performed to investigate the hypothesis that reduced anxiety-like and enhanced cognitive performance may be due in part to actions of T metabolites at ERbeta. Experiment 1: Gonadectomized (GDX) wildtype and ERbeta knockout mice (betaERKO) were subcutaneously (SC) administered 3alpha-diol, 3beta-diol, androsterone, or oil vehicle at weekly intervals, and tested in anxiety tasks (open field, elevated plus maze, light-dark transition) or for cognitive performance in the object recognition task. Experiment 2: GDX rats were administered SC 3alpha-diol, 3beta-diol, androsterone, or oil vehicle, and tested in the same tasks. Experiment 3: GDX rats were androsterone- or vehicle-primed and administered an antagonist of ARs (flutamide), ERs (tamoxifen), or GBRs (flumazenil), or vehicle and then tested in the elevated plus maze. Both rats and wildtype mice, but not betaERKO mice, consistently had reduced anxiety and improved performance in the object recognition task. Androsterone was only effective at reducing anxiety-like behavior in the elevated plus maze and this effect was modestly reduced by flumazenil administration. Thus, actions at ERbeta may be required for T's anxiety-reducing and cognitive-enhancing effects.

PMID:   18775724   [PubMed - indexed for MEDLINE]    PMCID:   PMC3623974    

 

Front Aging Neurosci. 2010 Apr 8;2:15. doi: 10.3389/fnagi.2010.00015. eCollection 2010.

3alpha-androstanediol, but not testosterone, attenuates age-related decrements in cognitive, anxiety, and depressive behavior of male rats.

Frye CA1, Edinger KL, Lephart ED, Walf AA.

Author information

 

Abstract

Some hippocampally-influenced affective and/or cognitive processes decline with aging. The role of androgens in this process is of interest. Testosterone (T) is aromatized to estrogen, and reduced to dihydrotestosterone (DHT), which is converted to 5alpha-androstane, 3alpha, 17alpha-diol (3alpha-diol). To determine the extent to which some age-related decline in hippocampally-influenced behaviors may be due to androgens, we examined the effects of variation in androgen levels due to age, gonadectomy, and androgen replacement on cognitive (inhibitory avoidance, Morris water maze) and affective (defensive freezing, forced swim) behavior among young (4 months), middle-aged (13 months), and aged (24 months) male rats. Plasma and hippocampal levels of androgens were determined. In experiment 1, comparisons were made between 4-, 13-, and 24-month-old rats that were intact or gonadectomized (GDX) and administered a T-filled or empty silastic capsule. There was age-related decline in performance of the inhibitory avoidance, water maze, defensive freezing, and forced swim tasks, and hippocampal 3alpha-diol levels. Chronic, long-term (1-4 weeks) T-replacement reversed the effects of GDX in 4- and 13-month-old, but not 24-month-old, rats in the inhibitory avoidance task. Experiments 2 and 3 assessed whether acute subcutaneous T or 3alpha-diol, respectively, could reverse age-associated decline in performance. 3alpha-diol, but not T, compared to vehicle, improved performance in the inhibitory avoidance, water maze, forced swim, and defensive freezing tasks, irrespective of age. Thus, age is associated with a decrease in 3alpha-diol production and 3alpha-diol administration reinstates cognitive and affective performance of aged male rats.

KEYWORDS:

3α-diol; affect; aging; androgens; cognition; depression; testosterone

PMID:   20552051   [PubMed]    PMCID:   PMC2874398    

 

Edited by Area-1255, 02 December 2014 - 08:17 PM.

[factsmachine]

interesting as my anxiety got bad and better (probably doesn't make much sense, you'd have to feel it yourself) when I went on axiron (testosterone gel) the gel causes high increases of both DHT and estrogen. shots have less effect on both. I'm convincing my doctor to give me home shots from now on. also some HCG. its been 2 weeks and my nuts shrank and ache constantly. any male can understand how bad this sucks.

today I asked a gay dude if I was ugly because I honestly have no confidence and I'm very insecure. he told me that I took his breath away and I said I have no interest in me and there's no reason to lie to me.
so I felt a lot better about myself, I took a small dose of klonopin and went to taco bell. I felt calm and confident. met these 2 girls, talked to a few other people and we told stories. (never seen these people before, EXTREMELY unusual for me). Then this girl gave me her number, I didn't ask. the other girl really liked me too. I finnaly feel not depressed! temporary most likely, but this gives me hope!

[factsmachine]

Dr appointment today.
switching from axiron to test injections at home wooooo! also got a low dose script of klonopin, 30 .5 mg, 3 refills.
had to persuade him for DHT and estrogen labs. won't give me HCG. my nuts are shrinking and aching. hate to say this because I respect forum rules.. but I need an online hcg source so I won't permanently damage my hpta.
today I felt great with the klonopin, and met 2 really hot girls. didn't try too hard like I normally do. just felt chill. one gave me her number, didn't have to ask for it. sweeeet. can't wait to get some action (; I've got confidence again, can't wait to drown in that poon honestly. I've missed being a teenager.
THANKS EVERYBODY! let's gain knowledge and help each other, every research article, every tangent of information I thank all of you for. thank you.
doctor said I'm worrying too much and trying too hard for my health. wouldn't give me a copper test...

[factsmachine]

I am in opiate withdrawal. one low dose of tramadol gives me withdrawal. also took phenbut, 3rd time in the last 4 days probably get withdrawal. I screwed up definitely... any way tomanage this? iI have access to baclofen also may do taper with it .

[Area-1255]

Dr appointment today.
switching from axiron to test injections at home wooooo! also got a low dose script of klonopin, 30 .5 mg, 3 refills.
had to persuade him for DHT and estrogen labs. won't give me HCG. my nuts are shrinking and aching. hate to say this because I respect forum rules.. but I need an online hcg source so I won't permanently damage my hpta.
today I felt great with the klonopin, and met 2 really hot girls. didn't try too hard like I normally do. just felt chill. one gave me her number, didn't have to ask for it. sweeeet. can't wait to get some action (; I've got confidence again, can't wait to drown in that poon honestly. I've missed being a teenager.
THANKS EVERYBODY! let's gain knowledge and help each other, every research article, every tangent of information I thank all of you for. thank you.
doctor said I'm worrying too much and trying too hard for my health. wouldn't give me a copper test...

Congrats to you brotha! I'll see to hCG, not sure of any sources off hand. I'll do some research for ya. 

Edited by Area-1255, 03 December 2014 - 03:27 AM.

[factsmachine]

Hey guys! 
I was prescribed 200mg testosterone cypionate injections, 200mg every 2 weeks. This will cause huge peaks and troughs! I'd feel amazing for 3 days and be in supraphysiological levels. Then it would level down by day 5-7. Then the next week would be HELL. 
So after doing some research I am doing 50mg 2x week split evenly. I already feel a little better, it feels like my testosterone levels are higher and my DHT is lower. Probably a very arbitrary statement as feelings are subjective. But I do believe my DHT levels have decreased a bit. Also my estradiol was 37 (most people on trt say that the sweet spot is 15-25. Given that I was using AI's before the test and they still came out slightly high I am displeased with Axiron testosterone gel. 
I am getting DHT and Free and Total Testosterone level results within the next few days. I'll post em up. 
My WBC count was on the lower end, what could this mean? Also Glycohemoglobulin A1C was almost pre diabetic. My doctor told me that sugar attatches to the platelets and reflects the history of my diet for the last 3 months. So I'm eating more fruits and veggies, less crap. Back in the gym and feeling great! 
High cholesterol as well. Although Low T plays a factor in cholesterol as it has an impact on reverse transport and makes HDL "do its job". The reverse transport mechanism brings cholesterol back to the liver to be metabolised, thus lowering cholesterol. 

"These data indicate that T's 5alpha-reduced metabolite, DHT, can reduce anxiety behavior and that blocking metabolism to 3alpha-diol in the hippocampus can attenuate these effects."
How can I increase the metabolite, 3alpha-diol? It says DHT is made from T through 5 alpha reductase. And converted to 3-alpha-diol via 3bHSD enzyme.
"Olive oil and coconut oil increase the activity of the 3beta-HSD and 17beta-HSD enzymes. These are involved in the manufacture of testosterone. Olive oil and coconut oil also raise the concentration of the body’s own antioxidants in the Leydig cells," The last part with the leydig cells in the testis aren't relevant for me as mine are shut down. But the first part with the enzymes are interesting. Also, Oleuroptin (in olives) was researched to lower Cortisol and increase T production. I'll try to find that one. Here's the study that showed the enzymatic effects of these agents, as well as the Testosterone effects. study:http://www.ergo-log....-anabolism.html

Edited by factsmachine, 06 December 2014 - 07:47 AM.

[Area-1255]

Hey guys! 
I was prescribed 200mg testosterone cypionate injections, 200mg every 2 weeks. This will cause huge peaks and troughs! I'd feel amazing for 3 days and be in supraphysiological levels. Then it would level down by day 5-7. Then the next week would be HELL. 
So after doing some research I am doing 50mg 2x week split evenly. I already feel a little better, it feels like my testosterone levels are higher and my DHT is lower. Probably a very arbitrary statement as feelings are subjective. But I do believe my DHT levels have decreased a bit. Also my estradiol was 37 (most people on trt say that the sweet spot is 15-25. Given that I was using AI's before the test and they still came out slightly high I am displeased with Axiron testosterone gel. 
I am getting DHT and Free and Total Testosterone level results within the next few days. I'll post em up. 
My WBC count was on the lower end, what could this mean? Also Glycohemoglobulin A1C was almost pre diabetic. My doctor told me that sugar attatches to the platelets and reflects the history of my diet for the last 3 months. So I'm eating more fruits and veggies, less crap. Back in the gym and feeling great! 
High cholesterol as well. Although Low T plays a factor in cholesterol as it has an impact on reverse transport and makes HDL "do its job". The reverse transport mechanism brings cholesterol back to the liver to be metabolised, thus lowering cholesterol. 

"These data indicate that T's 5alpha-reduced metabolite, DHT, can reduce anxiety behavior and that blocking metabolism to 3alpha-diol in the hippocampus can attenuate these effects."
How can I increase the metabolite, 3alpha-diol? It says DHT is made from T through 5 alpha reductase. And converted to 3-alpha-diol via 3bHSD enzyme.
"Olive oil and coconut oil increase the activity of the 3beta-HSD and 17beta-HSD enzymes. These are involved in the manufacture of testosterone. Olive oil and coconut oil also raise the concentration of the body’s own antioxidants in the Leydig cells," The last part with the leydig cells in the testis aren't relevant for me as mine are shut down. But the first part with the enzymes are interesting. Also, Oleuroptin (in olives) was researched to lower Cortisol and increase T production. I'll try to find that one. Here's the study that showed the enzymatic effects of these agents, as well as the Testosterone effects. study:http://www.ergo-log....-anabolism.html

Lowering cortisol shifting the T:E ratio, reducing SHBG; using protodioscin , sorghum oil, and doing heavy resistance training / weight lifts will also raise DHT and neurosteroid production.

 

 

Unless you know for sure you have low conversion of DHT to 3-alpha-diol, you should focusing on raising its precursor; DHT !

 

• Resistance Training, heavy weight training, strength training.
• Decrease cortisol.
• Use SHBG blockers / free test boosters such as divanil extract.
• Protodioscin from tribulus stimulates 5-alpha-reductase.
• Sorghum oil can promote 5-alpha-reductase.
• Increasing androgen receptor expression and sTAR will help, a beta agonist like higenamine (noroclaurine) would do this.
• Decrease estrogen receptor expression, use something like Triazole and work on decreasing body fat if it is an issue!

Edited by Area-1255, 12 December 2014 - 10:38 PM.

[Flex]

If You think that Glucocortids are implicated, try vitamin D

 

The authors suggest that vitamin D can help restore glucocorticoid responsiveness

Nicotinic Acid-Mediated Activation of Both Membrane and Nuclear Receptors towards Therapeutic Glucocorticoid Mimetics for Treating Multiple Sclerosis

http://www.hindawi.c...ar/2009/853707/

 

Nicotinamide seems to be somewhat implicated but its too hard to investigate for me:

 

Human kidney 11 beta-hydroxysteroid dehydrogenase is a high affinity nicotinamide adenine dinucleotide-dependent enzyme and differs from the cloned type I isoform.

http://www.ncbi.nlm..../pubmed/8045966

 

Mutations in NNT encoding nicotinamide nucleotide transhydrogenase cause familial glucocorticoid deficiency.

http://www.ncbi.nlm....pubmed/22634753

 

and this ??

Role of nicotinamide adenine dinucleotide and adenosine triphosphate in glucocorticoid-induced cytotoxicity in susceptible lymphoid cells.

http://www.ncbi.nlm..../pubmed/3108318

[factsmachine]

Turns out DHT was a huge factor.
Total testosterone 557 (250-1100)
Free Testosterone 144 (13-155)
DHT 97 (17-62)
E2 27 (I had used AIs)
I took 1 pump of axiron 6 hours prior to the test.

Now I'm on 50mg testosterone Cypionate 2x week. I need an AI, my nipples are swollen, itchy, painful, and the lumps are getting bigger.

Edited by factsmachine, 14 December 2014 - 05:46 AM.

[factsmachine]

So we must assume that my DHT will slowly decline now that I'm not taking transdermal anymore. My acne is really really bad right now.
If I reduce cortisol, won't I be up regulating NE because of the feedback loop that exists for that?
Klonopin works amazing for my anxiety. I'll be on it at least 3 months. So inevitable benzo withdrawl and hopefully not regression to previous patterns.

I guess I could talk to my Dr about clonidine, an alpha 2 agonist. That could help but the side effects would be bad.