JOWS6
I am banned!
Well as some of you know, I decided to give to try the Aromatase inhibitor (AI) solo to increase my testosterone based on a few studies I read. Well, after 6 weeks my Testosterone came in at 638ng/dL, Free Testosterone at 94.9ng/dL and Estradiol from 62pg/dL to 24pg/dL. I was stunned because I did not feel any better!
I decided to contact the guy that ran the study and here is the conversation:
Hello Hans de Boer, I had some questions regarding the long-term efficacy of aromatase inhibition for hypogonadism. I was diagnosed with hypogonadism and it appears to be secondary due to my low levels of gonadotrophins. I was about to commit to a testosterone replacement therapy (TRT) protocol of Testosterone Cypionate, HcG and Anastrazole until I saw a few studies where hypogonadism might be obesity-related. I am 5'9" and at 260 lbs. My Estradiol lab value was recorded at 62 with a range of 20-47. Six weeks on 0.5mg's of Anastrazole every-other-day brought my estradiol number down to 24. Along with this decrease, my testosterone increased to 638 (range 250-1100) up from 316. I am happy with the increase but I feel exactly the same: low mood, low energy, and low libido. Did you observe an increase in mood and libido within the participants in the study? Is this aromatase-inhibition and effective long term solution to hypogonadism? Any input would be greatly appreciated.
Thanks,
-James
Response:
We have just completed a placebo controlled trial with letrozole in men with obesity related hypogonadotropic hypogonadism. Abstract is presented on Endocrine Meeting, Boston, 2011, june 4-6
Despite a marked increase in testosterone we could not detect any clinical benefit => so, aromatase inhibition is not the answer in obesity related hypogonadism.
with regards,
Hans de Boer
Wow pretty funny that they jus' finished a trial testing the very same question I had! Anyways, I looked it up and was only able to view the abstract because it's jus' being published last week:
Letrozole Normalizes Serum Testosterone but Has No Clinical Effects in Men with Obesity-Related Hypogonadotropic Hypogonadism
Sandra Loves, MD2, Jos de Jong2, Adriaan van Sorge, PhD2, Darryl Telting, PhD2, Ad Hermus, PhD, MD1 and Hans de Boer, MD, PhD2
Endocrinology (AH), Radboud University Medical Centre, Nijmegen Netherlands
Internal Medicine (SL,JDJ,AVS,DT,HDB), Rijnstate Hospital, Arnhem Netherlands
Introduction: Hypogonadotropic hypogonadism is frequently observed in morbidly obese men, due to aromatase-dependent conversion of androgens to estrogens in adipocytes. The clinical impact of this sex hormone imbalance is not known.
Aim: To evaluate the clinical effects of aromatase inhibition in obesity-related hypogonadotropic hypogonadism.
Methods: Double-blind, placebo-controlled, 6-month trial in severely obese men (BMI > 35 kg/m2) with obesity-related hypogonadism (serum total testosterone < 10 nmol/l). Predefined drug regimen (letrozole or placebo): Starting dose 1 tablet/week, subsequent dose escalation every month up to a maximum of 7 tablets/week or until a serum total testosterone of 20 nmol/L. The dose was reduced if serum estradiol decreased below 40 pmol/L.Results: 42 patients were included and 39 completed the study according to protocol: 18 on Letrozole and 21 receiving placebo. Mean age 44.6 ± 1.1 years (mean ± SE), BMI 41.1 ± 0.8 kg/m².
At baseline, both groups were well matched for all study parameters. Placebo treatment did not affect serum hormone levels, whereas Letrozole decreased serum estradiol from 119.1 ± 10.1 to 59.2 ± 6.1 pmol/L (P = 0.0001, normal range (NR) 40 - 160 pmol/L), increased serum LH from 3.3 ± 0.3 to 8.8 ± 0.9 U/L (P < 0.0001, NR: 2.0 ***8211; 9.0 U/L) and free testosterone from 244 ± 19 to 691 ± 39 pmol/L (P < 0.0001, NR: 225 - 625 pmol/L). Both groups demonstrated a comparable decrease in body weight of about 5 kg, and a decrease in abdominal circumference of about 4 cm. Changes in fat free mass, fat mass and bone density also did not differ between groups. Glucose metabolism, lipid profiles, physical exercise capacity and psychological characteristics did not change during treatment.
Conclusion: Despite a marked rise in serum free testosterone, low dose aromatase inhibition had no somatic or psychological effects in men with obesity-related hypogonadotropic hypogonadism. We hypothesize that, with respect to non-sexual somatic and psychological parameters, males primarily thrive on oestrogens, not testosterone.
I JUST DON'T GET IT!!!!! Why aren't these people, including me, not feeling any of the increase in testosterone? This is not a small increase, it's a substantial increase.
I decided to contact the guy that ran the study and here is the conversation:
Hello Hans de Boer, I had some questions regarding the long-term efficacy of aromatase inhibition for hypogonadism. I was diagnosed with hypogonadism and it appears to be secondary due to my low levels of gonadotrophins. I was about to commit to a testosterone replacement therapy (TRT) protocol of Testosterone Cypionate, HcG and Anastrazole until I saw a few studies where hypogonadism might be obesity-related. I am 5'9" and at 260 lbs. My Estradiol lab value was recorded at 62 with a range of 20-47. Six weeks on 0.5mg's of Anastrazole every-other-day brought my estradiol number down to 24. Along with this decrease, my testosterone increased to 638 (range 250-1100) up from 316. I am happy with the increase but I feel exactly the same: low mood, low energy, and low libido. Did you observe an increase in mood and libido within the participants in the study? Is this aromatase-inhibition and effective long term solution to hypogonadism? Any input would be greatly appreciated.
Thanks,
-James
Response:
We have just completed a placebo controlled trial with letrozole in men with obesity related hypogonadotropic hypogonadism. Abstract is presented on Endocrine Meeting, Boston, 2011, june 4-6
Despite a marked increase in testosterone we could not detect any clinical benefit => so, aromatase inhibition is not the answer in obesity related hypogonadism.
with regards,
Hans de Boer
Wow pretty funny that they jus' finished a trial testing the very same question I had! Anyways, I looked it up and was only able to view the abstract because it's jus' being published last week:
Letrozole Normalizes Serum Testosterone but Has No Clinical Effects in Men with Obesity-Related Hypogonadotropic Hypogonadism
Sandra Loves, MD2, Jos de Jong2, Adriaan van Sorge, PhD2, Darryl Telting, PhD2, Ad Hermus, PhD, MD1 and Hans de Boer, MD, PhD2
Endocrinology (AH), Radboud University Medical Centre, Nijmegen Netherlands
Internal Medicine (SL,JDJ,AVS,DT,HDB), Rijnstate Hospital, Arnhem Netherlands
Introduction: Hypogonadotropic hypogonadism is frequently observed in morbidly obese men, due to aromatase-dependent conversion of androgens to estrogens in adipocytes. The clinical impact of this sex hormone imbalance is not known.
Aim: To evaluate the clinical effects of aromatase inhibition in obesity-related hypogonadotropic hypogonadism.
Methods: Double-blind, placebo-controlled, 6-month trial in severely obese men (BMI > 35 kg/m2) with obesity-related hypogonadism (serum total testosterone < 10 nmol/l). Predefined drug regimen (letrozole or placebo): Starting dose 1 tablet/week, subsequent dose escalation every month up to a maximum of 7 tablets/week or until a serum total testosterone of 20 nmol/L. The dose was reduced if serum estradiol decreased below 40 pmol/L.Results: 42 patients were included and 39 completed the study according to protocol: 18 on Letrozole and 21 receiving placebo. Mean age 44.6 ± 1.1 years (mean ± SE), BMI 41.1 ± 0.8 kg/m².
At baseline, both groups were well matched for all study parameters. Placebo treatment did not affect serum hormone levels, whereas Letrozole decreased serum estradiol from 119.1 ± 10.1 to 59.2 ± 6.1 pmol/L (P = 0.0001, normal range (NR) 40 - 160 pmol/L), increased serum LH from 3.3 ± 0.3 to 8.8 ± 0.9 U/L (P < 0.0001, NR: 2.0 ***8211; 9.0 U/L) and free testosterone from 244 ± 19 to 691 ± 39 pmol/L (P < 0.0001, NR: 225 - 625 pmol/L). Both groups demonstrated a comparable decrease in body weight of about 5 kg, and a decrease in abdominal circumference of about 4 cm. Changes in fat free mass, fat mass and bone density also did not differ between groups. Glucose metabolism, lipid profiles, physical exercise capacity and psychological characteristics did not change during treatment.
Conclusion: Despite a marked rise in serum free testosterone, low dose aromatase inhibition had no somatic or psychological effects in men with obesity-related hypogonadotropic hypogonadism. We hypothesize that, with respect to non-sexual somatic and psychological parameters, males primarily thrive on oestrogens, not testosterone.
I JUST DON'T GET IT!!!!! Why aren't these people, including me, not feeling any of the increase in testosterone? This is not a small increase, it's a substantial increase.
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