Tracking down libido....

TR90125

New member
I want to start a thread specifically to discuss and learn about the libido aspect of HRT and overall hormonal health.

An obserbavation I have made since starting HRT back in August is that my libido seems to be at its strongest when my body is adjusting to something new. When I very first started my protocol I had a lot of good days and weeks with very strong libido and erections you could hammer nails with. After several weeks on the same dosage levels, libido started to weaken, but was still functional.

As I began adjusting my protocol dosages downward, my libido seemed to come back and again, was very strong for several days.

Recently, I have had very stable test and E2 levels of ~1,000 and ~14 respectively and my libido was average at best. Wood was never really that strong and morning wood was rather rare.

Does your body adapt to stable hormone levels and would this result in loss of libido? Does libido react to a change in levels more than increased but stable levels?

I really would like to figure this out.

My protocol is as follows

75mg test cyp Every 84 hours
600 IU's Human Chorionic Gonadotropin (HCG) Every 84 Hours
.25mg Adex EOD
Armour Thyroid ED (50mg?)

DHEA sub lingual
B Complex sub lingual
Vitamin D 4000 IU's
Fish oil 2000 IU's

I am also in 3J's Modified Carb Cycle Diet, so I'm eating right.

I am about to swtich my Adex dosing to the day after each of my injections, so down to twice a week instead of 3 times a week. The EOD dosing keeps my E2 around 14.
 
I feel like your doing to much adex. That would kill my sex drive. I do .25 mon wed fri. Started with .5 twice a week but feel better with a lil less weekly do switched it.
 
No Increase in Libido on HRT

I have been on HRT for a few months now and my libido, which was poor to begin with, has not improved at all.

I first tried test 50mg E7D, no a-dex, no Human Chorionic Gonadotropin (HCG) for a month - nothing. Blood test showed total T of 600, E at 29.

Next, 150 mg of Test E7D, plus a-dex, and Human Chorionic Gonadotropin (HCG) for a couple months - nothing. Total Test 900, E @ 11.

I am currently on 100mg Test E3D, no a-dex, no Human Chorionic Gonadotropin (HCG) and I have my fingers crossed. Next blood test in 2 weeks.

I am 47, so maybe its the younger guys that get the huge increase in libido.
 
I feel like your doing to much adex. That would kill my sex drive. I do .25 mon wed fri. Started with .5 twice a week but feel better with a lil less weekly do switched it.


Yeah, that much adex would put me in
an embarrassing situation.

Play close att: to you thyroid panel. This is
where I find my problem to be. Be thankful
you can get armor. All I can get is t4 and for me there is a difference.
 
thats a great point, this was originally posted by Dr. Scally

Krassas GE, Poppe K, Glinoer D. Thyroid Function and Human Reproductive Health. Endocrine Reviews 2010;31(5):702-55. http://edrv.endojournals.org/content/31/5/702.full

Via its interaction in several pathways, normal thyroid function is important to maintain normal reproduction. In both genders, changes in SHBG and sex steroids are a consistent feature associated with hyper- and hypothyroidism and were already reported many years ago. Male reproduction is adversely affected by both thyrotoxicosis and hypothyroidism. Erectile abnormalities have been reported. Thyrotoxicosis induces abnormalities in sperm motility, whereas hypothyroidism is associated with abnormalities in sperm morphology; the latter normalize when euthyroidism is reached. In females, thyrotoxicosis and hypothyroidism can cause menstrual disturbances. Thyrotoxicosis is associated mainly with hypomenorrhea and polymenorrhea, whereas hypothyroidism is associated mainly with oligomenorrhea. Thyroid dysfunction has also been linked to reduced fertility. Controlled ovarian hyperstimulation leads to important increases in estradiol, which in turn may have an adverse effect on thyroid hormones and TSH. When autoimmune thyroid disease is present, the impact of controlled ovarian hyperstimulation may become more severe, depending on preexisting thyroid abnormalities. Autoimmune thyroid disease is present in 5-20% of unselected pregnant women. Isolated hypothyroxinemia has been described in approximately 2% of pregnancies, without serum TSH elevation and in the absence of thyroid autoantibodies. Overt hypothyroidism has been associated with increased rates of spontaneous abortion, premature delivery and/or low birth weight, fetal distress in labor, and perhaps gestation-induced hypertension and placental abruption. The links between such obstetrical complications and subclinical hypothyroidism are less evident. Thyrotoxicosis during pregnancy is due to Graves***8217; disease and gestational transient thyrotoxicosis. All antithyroid drugs cross the placenta and may potentially affect fetal thyroid function.


Carani C, Isidori AM, Granata A, et al. Multicenter Study on the Prevalence of Sexual Symptoms in Male Hypo- and Hyperthyroid Patients. Journal of Clinical Endocrinology & Metabolism 2005;90(12):6472-9. Multicenter Study on the Prevalence of Sexual Symptoms in Male Hypo- and Hyperthyroid Patients

Context: Thyroid hormones have a dramatic effect on human behavior. However, their role on sexual behavior and performance has seldom been investigated in men.

Objective: The objective of this study was to evaluate the prevalence of sexual dysfunctions in patients with hyper- and hypothyroidism and their resolution after normalization of thyroid hormone levels.

Design and Setting: We conducted a multicenter prospective study at endocrinology and andrology clinics in university hospitals.

Patients: The study included 48 adult men, 34 with hyperthyroidism and 14 with hypothyroidism.

Main Outcome Measures: Subjects were screened for hypoactive sexual desire (HSD), erectile dysfunction (ED), premature ejaculation (PE), and delayed ejaculation (DE) on presentation and 8***8211;16 wk after recovery from the thyroid hormone disorder.

Results: In hyperthyroid men, HSD, DE, PE, and ED prevalence was 17.6, 2.9, 50, and 14.7%, whereas in hypothyroid men, the prevalence of HSD, DE, and ED was 64.3% and of PE was 7.1%. After thyroid hormone normalization in hyperthyroid subjects, PE prevalence fell from 50 to 15%, whereas DE was improved in half of the treated hypothyroid men. Significant changes were found in the subdomains of the International Index of Erectile Function; ejaculation latency time doubled after treatment of hyperthyroidism (from 2.4 ± 2.1 to 4.0 ± 2.0 min), whereas for hypothyroid men it declined significantly, from 21.8 ± 10.9 to 7.4 ± 7.2 (P < 0.01 for both). TSH and thyroid hormone levels normalized rapidly after treatment, and changes in circulating sex steroids partially reflected the changes in SHBG levels.

Conclusions: In summary, most patients with thyroid hormone disorders experience some sexual dysfunctions, which can be reversed by normalizing thyroid hormone levels. Despite the associated changes in sex hormone levels, the high prevalence of ejaculatory disorders and their prompt reversibility suggest a direct involvement of thyroid hormones in the physiology of ejaculation.


Veronelli A, Masu A, Ranieri R, Rognoni C, Laneri M, Pontiroli AE. Prevalence of erectile dysfunction in thyroid disorders: comparison with control subjects and with obese and diabetic patients. Int J Impot Res 2006;18(1):111-4. http://www.nature.com/ijir/journal/v...f/3901364a.pdf

Diagnosis of erectile dysfunction (ED) requires anamnestic investigation, being rarely spontaneously declared by patients. ED occurs frequently in diabetes mellitus, and anecdotal evidence suggests that ED occurs in obesity and in hypothyroidism. The aim of this study was to evaluate the prevalence of ED in patients affected by thyroid disorders (hypothyroidism and hyperthyroidism), in comparison with control subjects and with patients at risk for ED, such as patients with obesity and with type II diabetes mellitus, and the role of age. Spontaneous deposition and International Index of Erectile Dysfunction (IIEF)-5 questionnaire were considered for control subjects and for all patients. Spontaneous deposition of ED occurred for three diabetic patients, never for obese patients, thyroid patients and controls, confirming the value of IIEF-5 in detecting ED. ED was more frequent in obese subjects (42%), and in patients affected by thyroid diseases (59%), than in controls (30%), although less frequent than in type II diabetes mellitus (81%). Both below and above the age of 50 years, ED score was worse in thyroid patients than in control subjects, while ED was more frequent in obese patients than in control subjects only below the age of 50 years.
 
Over the last week I have skipped 2 Aromatase inhibitor (AI) dosages. I was supposed to be .25mg EOD and I am now thinking about .25 the day after I inject, which is every 84 hours.

My libido is up noticeably, although I did not have morning wood today.

I don't necessarily want to be driving the old lady nuts with a teenage libido, but prior to this week I have had a take it or leave it attitude towards sex. The wife has done all the initiating and even then my erectile quality has been inconsistent.

:wackit:
 
I still have complete loss/failure/destruction of my sex drive.

My E2 was at 15.4 when I got tested in March, I started testosterone replacement therapy (TRT) at the end of March under the direction to take 1MG of Adex every 5 days. Along w/ 200MG of Test-cyp.

Does anyone know if my low level of e2 could be causing my libido to be extinct?

My SHBG levels were 15.3 & Total test @ 119.

Anyone know how I can help get these numbers up if that's the case?
 
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