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Goering
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Después de leer los posts de William Llewellyn (w_llewellyn) y macrophage69alpha acerca del Nolvadex y el HCG, e investigar un poco en el MedLine, he cambiado mi opinión acerca del mejor stack para restaurar el eje HPTA. Antes pensaba que el HCG no tenía aplicación práctica post ciclo, pero ahora me doy cuenta que la tiene si es usada en el momento preciso. Y ese momento preciso es entre la últimas inyecciones y antes de tomar las ayudas necesarias para restaurar la LH (más adelante hablaremos de estas ayudas). La idea es que, aunque restauremos la LH, el tamaño reducido de los testículos como consecuencia de la atrofia de los mismos causada por el ciclo, hará que produzcan menos testosterona y se tardará más en restaurar los niveles normales de testosterona. Ahi es donde es útil la HCG, para aumentar previamente durante dos semana el tamaño de los testículos (no más de 3 semanas, para los que se quieran extender, la sobreestimulación por períodos de tiempo más largos producirá insensibilidad de los testículos a la LH).
Cómo usar la HCG para este propósito ? Digamos que voy a estimular los testículos aproximadamente dos semanas. La primera inyección de HCG será de 5000 UI, y cada 4 días 2000 UI, esto nos dá:
Día 0 -> 5000 UI
Día 4 -> 2000 UI
Día 8 -> 2000 UI
Día 12 -> 2000 UI
Día 16 -> 2000 UI
Día 20 ------> Se empieza el uso de las ayudas para restaurar la LH
El día 20 debe coincidir con el momento en que el nivel de los esteroides post-ciclo es ya lo suficientemente bajo, que para la mayoría de los esteres yo estimaría en menos de 100 mg de esteroide en la sangre. Se puede estimar con la vida media de los esteres. Evidentemente, si ya conocemos el momento del "día 20", podemos retroceder en el tiempo para saber cuando se comienza el tratamiento con la HCG ("día 0").
Ahora, sobre las ayudas para restaurar la LH, también he cambiado la opinión con respecto al clomifeno (por ahora, es una teoría que comprobaré con examenes de laboratorio, pero los estudios parecen indicar lo que voy a exponer). William Llewellyn trajo a colación la idea de que Nolvadex es más efectivo restaurando la LH que el clomifeno, basado en el siguiente estudio:
1: Fertil Steril 1978 Mar;29(3):320-7 Related Articles, Books, LinkOut
Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.
Vermeulen A, Comhaire F.
The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development.
PMID: 640052 [PubMed - indexed for MEDLINE]
Ok, aqui hay varias cosas que concluir de este estudio:
1. El tamoxifeno a 20 mg es comparable a tomar 150 mg de clomifeno en cuanto a la estimulación de la LH en el hipotálamo.
2. El tamoxifeno es superior que el clomifeno estimulando la LHRH en la pituitaria. El clomifeno reduce la LHRH (relativamente poco, pero la reduce) producida por la pituitaria para estimular el hipotálamo a producir más LH.
3. El tamoxifeno no es eficaz en los casos de oligospermia idiopatica. Esto no tiene ninguna importancia para nuestro caso, nuestro problema no tiene que ver con esta patología, sino con el aumento de la testosterona natural como fín último para no perder la masa muscular ganada en el ciclo. Otros estudios que encontré contradicen este último aspecto, pero la mayoría muestra que el tamoxifeno no juega un rol importante en este punto.
Si se buscan estudios en contra, como ha argumentado macrophage69alpha, solo se encontrará en animales (principalmente en ratas), y en pacientes oligospermicos idiopáticos. Confío más en los estudios sobre personas normales. Investigando un poco más, encontré otros estudios que apoyan la idea del tamoxifeno en la estimulación de la LH (hechos en personas, particularmente en hombres y no en mujeres con cáncer de mama):
1: Hum Reprod 1995 Jul;10(7):1740-4
Inhibin and steroid responses to testicular stimulation in normal men.
Comhaire FH, Rombauts L, Vereecken A, Verhoeven G.
Leuven Institute for Fertility Technologies, Belgium.
Static measurements of immunoreactive inhibin have proved to be of little relevance in the diagnosis of testicular disorders. To explore whether a dynamic evaluation of inhibin secretion might yield a more useful parameter of testicular function we compared the responses of inhibin with steroids to i.v. injections of pure follicle-stimulating hormone (FSH; 300 IU) or human chorionic gonadotrophin (HCG; 1500 IU) and oral administration of the anti-oestrogen Tamoxifen (20 mg/day for 7 days) in four normal fertile men. Blood was aspirated between 1 and 72 h after the injections and daily during Tamoxifen intake. Four controls were injected with physiological saline solution. An additional four men were injected with pure FSH, and blood was taken after 24, 48 and 72 h. Injection of FSH was accompanied by nycthemeral variations of testosterone comparable with those observed in the controls. The concentration of inhibin showed similar nycthemeral variations but a significant increase was observed in all eight cases at 12 noon on days 2 and 3 after FSH injection. HCG injection resulted in the expected biphasic response of testosterone. Inhibin displayed a pronounced increase 18 h after injection but the delayed response after 48 and 72 h was not observed. Tamoxifen intake increased testosterone but not inhibin, and caused a moderate and temporary increase of luteinizing hormone and FSH. It was concluded that primary stimulation both of Leydig cells by HCG and Sertoli cells by FSH increase circulating inhibin.(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 8582972 [PubMed - indexed for MEDLINE]
-----------------------------------------------------------------------
1: J Clin Endocrinol Metab 1988 Feb;66(2):355-60
Divergent effects of the antiestrogen tamoxifen and of estrogens on luteinizing hormone (LH) pulse frequency, but not on basal LH levels and LH pulse amplitude in men.
Spijkstra JJ, Spinder T, Gooren L, van Kessel H.
Department of Internal Medicine, Free University Hospital, Amsterdam, The Netherlands.
We studied the role of estrogens on LH pulse modulation in men in two ways. Firstly, we compared LH pulse frequency and amplitude in 13 normal men before and after 6 weeks administration of the antiestrogen tamoxifen (10 mg twice daily). Secondly, we compared LH pulse frequency and amplitude between a group of 10 agonadal men not receiving sex steroid treatment and a group of 9 agonadal men (male to female transsexuals) continuously treated with 50 micrograms ethinyl estradiol/day. Tamoxifen administration to normal men resulted in a significant rise in the mean serum LH level from 5.7 +/- 1.3 (+/- SD) to 10.1 +/- 2.4 U/L, which was associated with significant increases in LH pulse frequency (from 4.2 +/- 1.5 to 5.8 +/- 1.7/7 h) and LH pulse amplitude (from 3.8 +/- 0.9 to 4.6 +/- 0.7 U/L). In the group of agonadal men the mean LH pulse frequency was 6.8 +/- 1.5/7 h, while it was 5.9 +/- 1.7/7 h in the estrogen-treated agonadal group (P = NS). The mean serum LH level and LH pulse amplitude were, however, significantly lower in the estrogen-treated agonadal men than in the agonadal men (14.7 +/- 7.0 vs. 34.3 +/- 8.6 and 4.1 +/- 1.8 vs. 7.4 +/- 1.8 U/L, respectively). We conclude that estrogens reduce basal LH levels and LH pulse amplitude. With regard to the modulation of LH pulse frequency our data provide contradictory results. While an antiestrogen increased LH pulse frequency in normal men, estrogen alone produced no change in LH pulse frequency in agonadal men. The study design in the agonadal men ignores the possible interaction of the two major testicular hormones (estradiol and testosterone) on gonadotropin secretion. Therefore, a possible explanation for this discrepancy in the effects of antiestrogen and estrogen could be an interaction between estrogens and androgens on gonadotropin secretion at the level of the LHRH pulse generator.
PMID: 3339109 [PubMed - indexed for MEDLINE]
------------------------------------------------------------------
La otra ayuda que usaría sería el arimidex (anastrozole) o femara (letrozole), por las razones expuestas por mí en este post:
http://boards.elitefitness.com/forum/showthread.php?s=&threadid=27223
Otra cosa es que se puede argumentar que el nolvadex reduce los niveles de IGF-1 producidos por el hígado, pero esto ocurre porque se necesita estimulación del estrógeno para la producción de la IGF-1 (un escenario de elevación del estrógeno es no deseable en un post-ciclo), como lo demuestra este estudio (seleccione a propósito uno hecho en hombres, descarté todos los que apuntaban a mujeres con cáncer de mama o de útero, o en personas acromegálicas, o en animales, o en vitro, por ser controversial su aplicación en la discusión):
1: J Clin Endocrinol Metab 1993 Jun;76(6):1407-12 Related Articles, Books, LinkOut
Activation of the somatotropic axis by testosterone in adult males: evidence for the role of aromatization.
Weissberger AJ, Ho KK.
Garvan Institute of Medical Research, St. Vincent's Hospital, Sydney, NSW, Australia.
To determine whether testosterone modulates the somatotropic axis in adult males, we compared 24-h GH secretion (from 20-min sampling, using Cluster analysis) and insulin-like growth factor-I (IGF-I) levels of five hypogonadal men (aged 20-32 yr) with those of six normal men (aged 21-27 yr), and examined the effects of testosterone replacement (testosterone enanthate 250 mg im monthly). To elucidate whether the action of testosterone on the somatotropic axis is direct, or requires the aromatization of testosterone to estradiol, we also examined the effects of the nonsteroidal antiestrogen, tamoxifen (20 mg/day for 3 weeks), on 24-h GH secretion and IGF-I levels in the normal men and in four of the hypogonadal men during concurrent testosterone treatment. Compared to the normal men, the hypogonadal men had significantly reduced mean GH pulse amplitude (3.1 +/- 0.6 vs. 8.4 +/- 1.7 micrograms/L, P < 0.05), but not pulse frequency. Testosterone treatment resulted in a significant increase in 24-h mean serum GH (0.7 +/- 0.2 to 1.4 +/- 0.2 micrograms/L, P < 0.05), mean GH pulse amplitude (3.1 +/- 0.6 to 5.2 +/- 0.8 micrograms/L, P < 0.01) and serum IGF-I (0.9 +/- 0.1 to 1.1 +/- 0.1 U/mL, P < 0.05). In the normal men, tamoxifen significantly reduced 24-h mean serum GH (1.1 +/- 0.3 to 0.5 +/- 0.1 micrograms/L, P < 0.05), mean GH pulse amplitude (8.4 +/- 1.7 to 4.7 +/- 0.4 micrograms/L, P < 0.05), and serum IGF-I (1.0 +/- 0.1 to 0.7 +/- 0.1 U/mL, P < 0.001). In the hypogonadal men on testosterone replacement, tamoxifen lowered 24-h mean serum GH (1.3 +/- 0.2 to 0.6 +/- 0.2 micrograms/L, P < 0.01), mean GH pulse amplitude (5.5 +/- 1.0 to 2.4 +/- 0.8 micrograms/L, P < 0.01), and serum IGF-I (1.2 +/- 0.1 to 0.8 +/- 0.1 U/mL, P < 0.05). We conclude that testosterone plays an important role in the modulation of the male somatotropic axis in adulthood, as appears to be the case in puberty, and that this effect is partly dependent on the aromatization of testosterone to estradiol.
PMID: 8501143 [PubMed - indexed for MEDLINE]
------------------------------------
Un beneficio adicional del tamoxifeno es que incrementa los niveles de HDL (colesterol "bueno").
También por las razones expuestas por mí en este post, no usaría la bromocriptina (por su efecto supresor de la GH):
http://boards.elitefitness.com/forum/showthread.php?s=&threadid=78968
Opiniones u otros hechos / estudios que quiera exponer ? Bienvenidos, la discusión se abre
Saludos.
Cómo usar la HCG para este propósito ? Digamos que voy a estimular los testículos aproximadamente dos semanas. La primera inyección de HCG será de 5000 UI, y cada 4 días 2000 UI, esto nos dá:
Día 0 -> 5000 UI
Día 4 -> 2000 UI
Día 8 -> 2000 UI
Día 12 -> 2000 UI
Día 16 -> 2000 UI
Día 20 ------> Se empieza el uso de las ayudas para restaurar la LH
El día 20 debe coincidir con el momento en que el nivel de los esteroides post-ciclo es ya lo suficientemente bajo, que para la mayoría de los esteres yo estimaría en menos de 100 mg de esteroide en la sangre. Se puede estimar con la vida media de los esteres. Evidentemente, si ya conocemos el momento del "día 20", podemos retroceder en el tiempo para saber cuando se comienza el tratamiento con la HCG ("día 0").
Ahora, sobre las ayudas para restaurar la LH, también he cambiado la opinión con respecto al clomifeno (por ahora, es una teoría que comprobaré con examenes de laboratorio, pero los estudios parecen indicar lo que voy a exponer). William Llewellyn trajo a colación la idea de que Nolvadex es más efectivo restaurando la LH que el clomifeno, basado en el siguiente estudio:
1: Fertil Steril 1978 Mar;29(3):320-7 Related Articles, Books, LinkOut
Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.
Vermeulen A, Comhaire F.
The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development.
PMID: 640052 [PubMed - indexed for MEDLINE]
Ok, aqui hay varias cosas que concluir de este estudio:
1. El tamoxifeno a 20 mg es comparable a tomar 150 mg de clomifeno en cuanto a la estimulación de la LH en el hipotálamo.
2. El tamoxifeno es superior que el clomifeno estimulando la LHRH en la pituitaria. El clomifeno reduce la LHRH (relativamente poco, pero la reduce) producida por la pituitaria para estimular el hipotálamo a producir más LH.
3. El tamoxifeno no es eficaz en los casos de oligospermia idiopatica. Esto no tiene ninguna importancia para nuestro caso, nuestro problema no tiene que ver con esta patología, sino con el aumento de la testosterona natural como fín último para no perder la masa muscular ganada en el ciclo. Otros estudios que encontré contradicen este último aspecto, pero la mayoría muestra que el tamoxifeno no juega un rol importante en este punto.
Si se buscan estudios en contra, como ha argumentado macrophage69alpha, solo se encontrará en animales (principalmente en ratas), y en pacientes oligospermicos idiopáticos. Confío más en los estudios sobre personas normales. Investigando un poco más, encontré otros estudios que apoyan la idea del tamoxifeno en la estimulación de la LH (hechos en personas, particularmente en hombres y no en mujeres con cáncer de mama):
1: Hum Reprod 1995 Jul;10(7):1740-4
Inhibin and steroid responses to testicular stimulation in normal men.
Comhaire FH, Rombauts L, Vereecken A, Verhoeven G.
Leuven Institute for Fertility Technologies, Belgium.
Static measurements of immunoreactive inhibin have proved to be of little relevance in the diagnosis of testicular disorders. To explore whether a dynamic evaluation of inhibin secretion might yield a more useful parameter of testicular function we compared the responses of inhibin with steroids to i.v. injections of pure follicle-stimulating hormone (FSH; 300 IU) or human chorionic gonadotrophin (HCG; 1500 IU) and oral administration of the anti-oestrogen Tamoxifen (20 mg/day for 7 days) in four normal fertile men. Blood was aspirated between 1 and 72 h after the injections and daily during Tamoxifen intake. Four controls were injected with physiological saline solution. An additional four men were injected with pure FSH, and blood was taken after 24, 48 and 72 h. Injection of FSH was accompanied by nycthemeral variations of testosterone comparable with those observed in the controls. The concentration of inhibin showed similar nycthemeral variations but a significant increase was observed in all eight cases at 12 noon on days 2 and 3 after FSH injection. HCG injection resulted in the expected biphasic response of testosterone. Inhibin displayed a pronounced increase 18 h after injection but the delayed response after 48 and 72 h was not observed. Tamoxifen intake increased testosterone but not inhibin, and caused a moderate and temporary increase of luteinizing hormone and FSH. It was concluded that primary stimulation both of Leydig cells by HCG and Sertoli cells by FSH increase circulating inhibin.(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 8582972 [PubMed - indexed for MEDLINE]
-----------------------------------------------------------------------
1: J Clin Endocrinol Metab 1988 Feb;66(2):355-60
Divergent effects of the antiestrogen tamoxifen and of estrogens on luteinizing hormone (LH) pulse frequency, but not on basal LH levels and LH pulse amplitude in men.
Spijkstra JJ, Spinder T, Gooren L, van Kessel H.
Department of Internal Medicine, Free University Hospital, Amsterdam, The Netherlands.
We studied the role of estrogens on LH pulse modulation in men in two ways. Firstly, we compared LH pulse frequency and amplitude in 13 normal men before and after 6 weeks administration of the antiestrogen tamoxifen (10 mg twice daily). Secondly, we compared LH pulse frequency and amplitude between a group of 10 agonadal men not receiving sex steroid treatment and a group of 9 agonadal men (male to female transsexuals) continuously treated with 50 micrograms ethinyl estradiol/day. Tamoxifen administration to normal men resulted in a significant rise in the mean serum LH level from 5.7 +/- 1.3 (+/- SD) to 10.1 +/- 2.4 U/L, which was associated with significant increases in LH pulse frequency (from 4.2 +/- 1.5 to 5.8 +/- 1.7/7 h) and LH pulse amplitude (from 3.8 +/- 0.9 to 4.6 +/- 0.7 U/L). In the group of agonadal men the mean LH pulse frequency was 6.8 +/- 1.5/7 h, while it was 5.9 +/- 1.7/7 h in the estrogen-treated agonadal group (P = NS). The mean serum LH level and LH pulse amplitude were, however, significantly lower in the estrogen-treated agonadal men than in the agonadal men (14.7 +/- 7.0 vs. 34.3 +/- 8.6 and 4.1 +/- 1.8 vs. 7.4 +/- 1.8 U/L, respectively). We conclude that estrogens reduce basal LH levels and LH pulse amplitude. With regard to the modulation of LH pulse frequency our data provide contradictory results. While an antiestrogen increased LH pulse frequency in normal men, estrogen alone produced no change in LH pulse frequency in agonadal men. The study design in the agonadal men ignores the possible interaction of the two major testicular hormones (estradiol and testosterone) on gonadotropin secretion. Therefore, a possible explanation for this discrepancy in the effects of antiestrogen and estrogen could be an interaction between estrogens and androgens on gonadotropin secretion at the level of the LHRH pulse generator.
PMID: 3339109 [PubMed - indexed for MEDLINE]
------------------------------------------------------------------
La otra ayuda que usaría sería el arimidex (anastrozole) o femara (letrozole), por las razones expuestas por mí en este post:
http://boards.elitefitness.com/forum/showthread.php?s=&threadid=27223
Otra cosa es que se puede argumentar que el nolvadex reduce los niveles de IGF-1 producidos por el hígado, pero esto ocurre porque se necesita estimulación del estrógeno para la producción de la IGF-1 (un escenario de elevación del estrógeno es no deseable en un post-ciclo), como lo demuestra este estudio (seleccione a propósito uno hecho en hombres, descarté todos los que apuntaban a mujeres con cáncer de mama o de útero, o en personas acromegálicas, o en animales, o en vitro, por ser controversial su aplicación en la discusión):
1: J Clin Endocrinol Metab 1993 Jun;76(6):1407-12 Related Articles, Books, LinkOut
Activation of the somatotropic axis by testosterone in adult males: evidence for the role of aromatization.
Weissberger AJ, Ho KK.
Garvan Institute of Medical Research, St. Vincent's Hospital, Sydney, NSW, Australia.
To determine whether testosterone modulates the somatotropic axis in adult males, we compared 24-h GH secretion (from 20-min sampling, using Cluster analysis) and insulin-like growth factor-I (IGF-I) levels of five hypogonadal men (aged 20-32 yr) with those of six normal men (aged 21-27 yr), and examined the effects of testosterone replacement (testosterone enanthate 250 mg im monthly). To elucidate whether the action of testosterone on the somatotropic axis is direct, or requires the aromatization of testosterone to estradiol, we also examined the effects of the nonsteroidal antiestrogen, tamoxifen (20 mg/day for 3 weeks), on 24-h GH secretion and IGF-I levels in the normal men and in four of the hypogonadal men during concurrent testosterone treatment. Compared to the normal men, the hypogonadal men had significantly reduced mean GH pulse amplitude (3.1 +/- 0.6 vs. 8.4 +/- 1.7 micrograms/L, P < 0.05), but not pulse frequency. Testosterone treatment resulted in a significant increase in 24-h mean serum GH (0.7 +/- 0.2 to 1.4 +/- 0.2 micrograms/L, P < 0.05), mean GH pulse amplitude (3.1 +/- 0.6 to 5.2 +/- 0.8 micrograms/L, P < 0.01) and serum IGF-I (0.9 +/- 0.1 to 1.1 +/- 0.1 U/mL, P < 0.05). In the normal men, tamoxifen significantly reduced 24-h mean serum GH (1.1 +/- 0.3 to 0.5 +/- 0.1 micrograms/L, P < 0.05), mean GH pulse amplitude (8.4 +/- 1.7 to 4.7 +/- 0.4 micrograms/L, P < 0.05), and serum IGF-I (1.0 +/- 0.1 to 0.7 +/- 0.1 U/mL, P < 0.001). In the hypogonadal men on testosterone replacement, tamoxifen lowered 24-h mean serum GH (1.3 +/- 0.2 to 0.6 +/- 0.2 micrograms/L, P < 0.01), mean GH pulse amplitude (5.5 +/- 1.0 to 2.4 +/- 0.8 micrograms/L, P < 0.01), and serum IGF-I (1.2 +/- 0.1 to 0.8 +/- 0.1 U/mL, P < 0.05). We conclude that testosterone plays an important role in the modulation of the male somatotropic axis in adulthood, as appears to be the case in puberty, and that this effect is partly dependent on the aromatization of testosterone to estradiol.
PMID: 8501143 [PubMed - indexed for MEDLINE]
------------------------------------
Un beneficio adicional del tamoxifeno es que incrementa los niveles de HDL (colesterol "bueno").
También por las razones expuestas por mí en este post, no usaría la bromocriptina (por su efecto supresor de la GH):
http://boards.elitefitness.com/forum/showthread.php?s=&threadid=78968
Opiniones u otros hechos / estudios que quiera exponer ? Bienvenidos, la discusión se abre
Saludos.
