6 replies to this topic

[forexworld12]

So I'm a 20 year old guy ...These are my hormones report,what do you think ? - 

 

SHBG -     7.2  nmol/l                                        Normal levels -   15 - 48.4 nmol/l

 

Morning Cortisol -    7.54 ug/dl                          Normal levels -     6.2 - 19.4  ug/dl   

 

Estrodiol (E2) /Oestrogen -    32 pg/ml         Normal level -  (Adult male -  0 - 32 pg/ml)  (I asked the clinic they sad the average for  most men reports  are like 8-10)

 

free testosterone  -   5 pg/ml                         Normal level -  4.30 - 32 pg/ml  (most have 20 above)          

 

Prolactin -        18.56  ng/ml                                Normal level -  2.1 - 17 ng/ml

 

TSH =  0.92 IU/ml                                               Normal = 0.30 - 5.50

 

T3 =     92ng/dl                                                    Normal = 60 - 200

 

T4 =     6.1 ug/dl                                                  Normal =   4.5 - 13.0

 

ACTH -    29.5 pg/ml                                           normal =  7 - 69 pg/ml  

 

Evening Cortisol                                              normal =    8.50    2.3 - 11 ug/dl 

 

symptoms - 

Difficulty Passing Urine + Burning sensation 

Apathy/Ahnedonia

Fatigue/ pain all over

Foggy thinking / Memory loss
Dead libido/numb penis - after post ssri/antipsychotic use
No Muscular Strength

Burning Sensation Urinating

Panic attacks

Hot flashes

Anxiety 

Leg  pain/cramp

Anger / Irritability ( though can't feel real emotions)

Insomnia

heart palpitation 

Feel very hot and burning and depressed after exercise for the next 24 hours !!( though it should be opposite)

 

I went to the endocrinologist yesterday he just prescribed me  caber - said the prolactin needs to come down to 6-8 then the other issues are going to be addressed . 

 

The thing is Caber is a dopamine agonist and I believe my dopamine is down-regulated and that is the cause for ahneonia/lack of emotions,so feeding a dopamine agonist to a down-regulated receptor isn't a good thing

 

 he won't listen 

 

should i consult other doctor ?

Edited by forexworld12, 07 December 2014 - 08:37 PM.

[Area-1255]

As I said, estrogen induces Prolactin, so getting Estro down is First & most important.

Though, dopamine being lowered from SSRI use also doesn'T help, so CABER or APOMORPHINE should be useful!

[forexworld12]

yes i know brother, just getting views from other members

 

Apomorphine looks great because it also acts as an antagonist at serotonin receptors ! 

[Area-1255]

yes i know brother, just getting views from other members

 

Apomorphine looks great because it also acts as an antagonist at serotonin receptors ! 

Yes, and an alphablocker would enhance the effect.

 

 

Br J Pharmacol. 2002 Jul;136(5):701-8.

Enhancement of apomorphine-induced penile erection in the rat by a selective alpha(1D)-adrenoceptor antagonist.

Mizusawa H1, Hedlund P, Sjunnesson J, Brioni JD, Sullivan JP, Andersson KE.

Author information

 

Abstract

1. Effects of A-322312 (alpha(1B)-adrenoceptor (AR) antagonist), A-119637 (alpha(1D)-AR antagonist), prazosin (non-selective alpha(1)-AR antagonist), and yohimbine (alpha(2)-AR antagonist) were studied in rat corpus cavernosum (CC) and cavernous artery (Acc) preparations. Effects of intracavernous (i.c.) or intraperitoneal (i.p.) administration of alpha(1)-AR antagonists on apomorphine-induced erections were investigated. 2. A-119637 attenuated electrically induced contractions in isolated CC (-logIC(50); 8.12+/-0.15), and relaxed noradrenaline (NA)-contracted preparations by more than 90% at 10(-7) M. At the same concentration, the -logEC(50) value for NA in Acc was altered from 6.79+/-0.07 to 4.86+/-0.13. In the CC and Acc, prazosin similarly inhibited contractile responses. 3. Inhibitory effects of A-322312 (10(-7) M) in electrically activated CC were 32.3+/-5.1%, whereas no effect on concentration-response curves for NA was observed in the Acc. Yohimbine (10(-8) M and 10(-7) M), enhanced electrically-induced contractions in isolated CC by 20 to 50%. At 10(-6) M, inhibitory effects of yohimbine were obtained. 4. A-119637 (0.3 micromol kg(-1), i.p.) tripled the number of erections, and produced a 6 fold increase in the duration of apomorphine-induced erectile responses. A-322312, prazosin, or yohimbine did not enhance erections induced by apomorphine. None of the alpha(1)-AR antagonists significantly increased ICP upon i.c. administration. Decreases in blood pressure were seen with A-119637 and prazosin. 5. The present findings show that there is a functional predominance of the alpha(1D)-AR subtype in the rat erectile tissue, and that blockade of this receptor facilitates rat penile erection induced by a suboptimal dose of apomorphine.

PMID:   12086979   [PubMed - indexed for MEDLINE]    PMCID:   PMC1573401          

Now even though this is a rat study, I can say that a single dose of corynanthine , or tumulosin along with apo gave me a stiffy for 5 hours.  

 

Endocrinology. 2007 Mar;148(3):1384-95. Epub 2006 Nov 22.

Estradiol induces expression of 5-hydroxytryptamine (5-HT) 4, 5-HT5, and 5-HT6 receptor messenger ribonucleic acid in rat anterior pituitary cell aggregates and allows prolactin release via the 5-HT4 receptor.

Papageorgiou A1, Denef C.

Author information

 

Abstract

Serotonin [5-hydroxytryptamine (5-HT)] is known to control prolactin (PRL) release at a hypothalamic level, but a pituitary site of action remains poorly studied. The present study explores the acute effect of 5-HT on PRL release in rat anterior pituitary aggregate cell cultures, the influence of steroid and thyroid hormones, and the 5-HT receptor (5-HTR) subtype(s) involved. 5-HT elicited a prompt increase in basal PRL release, an effect strongly potentiated by estradiol (E(2)) in the culture medium (dose response 1-100 nm). In E(2) condition, the PRL response was not affected by the nonselective 5-HTR antagonists methysergide and methiothepin nor by 5-HTR1, 5-HTR2, 5-HTR3, 5-HTR6, and 5-HTR7/5 antagonists, but was fully blocked by the 5-HTR4 antagonist GR 113808. Among various agonist analogs, only the 5-HTR4 agonist cisapride and the 5-HTR2 agonist alpha-methyl-5-HT evoked PRL release. The effect of alpha-methyl-5-HT also required E(2) during culture and was abolished by GR 113808 but not by combined 5-HTR2A, B, and C blockade. In E(2)-treated aggregates, 5-HT caused a 5-fold increase in cAMP levels. The intact anterior pituitary expressed mRNA of all known members of the 5-HTR family. In aggregates, 5-HTR4, 5-HTR5, and 5-HTR6 mRNA expression required E(2) during culture. The effect of 5-HT on PRL release was not affected by blocking the serotonin transporter or the vesicular monoamine transporter. The present data suggest a widespread expression of 5-HTRs in the rat anterior pituitary, several of which are up-regulated by estrogen, and that, in the presence of estrogen, one of these, the 5-HTR4, mediates acute PRL release.

PMID:   17122082   [PubMed - indexed for MEDLINE]

 

Edited by Area-1255, 11 December 2014 - 09:39 PM.

[Nemo888]

Firstly are you coming off a steroid cycle or used them in the last couple of months?
If not have you been in an MVA or received a head injury with loss of consciousness in the last 18 months?
Thirdly what is you blood level of igf1. Growth hormone is too pulsatile to get a good reading from a single test.

[forexworld12]

Firstly are you coming off a steroid cycle or used them in the last couple of months?
If not have you been in an MVA or received a head injury with loss of consciousness in the last 18 months?
Thirdly what is you blood level of igf1. Growth hormone is too pulsatile to get a good reading from a single test.

I haven't taken steroid ever ! I have used SSRI's and an antipsychotic in the past !

No Lol = no head injury 

[Area-1255]

 

Firstly are you coming off a steroid cycle or used them in the last couple of months?
If not have you been in an MVA or received a head injury with loss of consciousness in the last 18 months?
Thirdly what is you blood level of igf1. Growth hormone is too pulsatile to get a good reading from a single test.

I haven't taken steroid ever ! I have used SSRI's and an antipsychotic in the past !

No Lol = no head injury 

 

This is what is going on FOREX.

From a neuro-endocrine standpoint, based on the information you gave me, your neurobiological/hormonal output is being impacted in the following ways.

 

• Your body fat level is increasing aromatase and allowing estrogen to thrive.
• Your type 2A serotonin receptors are either upregulated due to estrogen excess, or downregulated by SSRI use, each resulting in a similar scenario - if they are upregulated - this is causing cortisol and prolactin release, as well as even MORE ESTROGEN RELEASE, if they are downregulated, then serotonin is now moving to 5-HT3, 5-HT4 , 5-HT1A/B which is also inducing cortisol and aldosterone release - in the process, this is lowering your androgen output, which is , with the increased body fat, CREATING EVEN MORE ESTROGEN ISSUES.
• Your pituitary 5-HT4 serotonin receptors are upregulated by the estrogen excess, further raising prolactin, causing a predisposition to anxiety due to calcium channel spiking caused by serotonin - and further stress response at the pituitary level.
• Your pre-synaptic 5-HT1A receptors are de-sensitized and DOWNREGULATED FURTHER BY ESTROGEN DOMINANCE, while the postSYNAPTIC (bad) 5-HT1A is way upregulated, causing cortisol release and estrogen transcription error.
• The above is triggering excessive dynorphin/endorphin/opiate activity which is further blunting your hormonal output, or at the very least, sexual function and dopamine/glutamate levels and transitions.

Edited by Area-1255, 17 December 2014 - 10:45 PM.