rodge zei:
nee eigenlijk omdat letro als enige helpt tegen progesterone sides van 19nor varianten in dit geval de tren.
-rodge
hmm ..het enige wat letro doet is je estro zwaar onderdrukken zodat je geen last krijgt van prog sides...als je echt iets aan prog sides wilt doen moet je aan bromo of carbo gaan...
T3 schijnt trouwens tijdens tren gebruik zeer nuttig te zijn (in lage dosis 25-50mcg)...kan misschien prog gyno voorkomen (van ander board gepikt):
Gynecomastia with risperidone-fluoxetine combination.
Benazzi F.
Department of Psychiatry Public Hospital Morgagni Forli, Italy.
Gynecomastia (breast enlargement) is a side effect of neuroleptic antipsychotic drugs, related to prolactin elevation caused by dopamine D2 receptor blockade (Richelson, 1996). The atypical antipsychotic risperidone is less likely to cause gynecomastia at low doses (Casey, 1996). It can cause a dose-dependent increase in serum prolactin concentration (Peuskens, 1995), by blocking dopamine D2 receptors (Richelson, 1996). I would like to describe a patient who did not have gynecomastia with risperidone at a dose of 3 mg/day, but had it when risperidone, at a dose of 0.5 mg/day, was combined with fluoxetine. A MEDLINE search failed to find any reports about such an interaction.
It has been established that in humans TRH is also capable of stimulating the release of prolactin (2). In hypothyroid patients there is often an elevation of TRH and prolactin due to diminished levels of T4. (3) Galactorrhea often presents as a symptom of hypothyroidism.
In sheep, administration of trenbolone acetate results in 45% decrease in thyroxine levels (4). This should exert a stimulatory effect on TRH. ( Interestingly, the same study shows that unlike in humans prolactin levels in the sheep remained unchanged. This is due to the fact that in sheep, unlike in humans, TRH and prolactin are secreted independently of each other (5).)
If it assumed that trenbolone acetate also lowers thyroxine levels in humans, the resulting rise in TRH would stimulate prolactin release, leading to galactorrhea and gynecomastia.
Due to the lack of human studies involving tren, we are all forced to speculate, and try to extrapolate from animal studies.
Feedback regulation of thyrotropin-releasing hormone gene expression by thyroid hormone in the caudal raphe nuclei in rats.
Yang H, Yuan P, Wu V, Tache Y.
CURE
igestive Diseases Research Center, West Los Angeles VA Medical Center, Department of Medicine and Brain Research Institute, UCLA, California 90073, USA.
hoyang@ucla.edu
Medullary TRH regulates autonomic activity, and altered thyroid status is associated with autonomic disorders. We investigated whether thyroid hormone exerts a negative feedback regulation on TRH gene expression in the medullary caudal raphe nuclei. Medullary pro-TRH messenger RNAs (mRNAs) were mainly located in the raphe pallidus and raphe obscurus neurons as shown by in situ hybridization and were significantly increased by 70% and 160-230% by Northern blot analyses in 24 h fasted rats at 1 and 3-5 weeks after thyroidectomy, respectively, when serum T4 levels were reduced by 75-87%. The increased pro-TRH mRNA on the 30th day after thyroidectomy was reversed to euthyroid levels by T4 replacement (2 or 4 microg/100 g x day). T4 injections (10 or 100 microg/100 g x day for 30 days) did not significantly influence medullary pro-TRH mRNA levels in sham-operated rats. Thyroidectomized rats fed normally showed a 500% increase in pro-TRH mRNA levels 30 days after the surgery, while those fasted for 24 h showed only a 180% increase. These data indicate that medullary TRH gene expression is enhanced during hypothyroidism due to the lack of negative feedback regulation by thyroid hormone, and this response is modulated by feeding state. These findings may have important relevance to understanding autonomic-related visceral alterations induced by hypothyroidism.
Incidence of hyperprolactinemia in patients with Hashimoto's thyroiditis.
Notsu K, Ito Y, Furuya H, Ohguni S, Kato Y.
Department of Medicine, Shimane Prefectural Central Hospital, Izumo, Japan.
The causes of hyperprolactinemia, the correlation between serum levels of PRL and thyroid function and magnetic resonance imaging (MRI) of the pituitary were studied in patients with chronic thyroiditis. Seventy-four female patients and 15 normal control women participated in this clinical survey. Fourteen of 74 patients with various thyroid conditions had increased serum PRL. The incidence of hyperprolactinemia in the overt primary hypothyroid group was 42.4% and was significantly higher than in any other group with normal serum thyroxine. There was a close association between the increment in serum PRL and of free triiodothyronine above the basal level after TRH administration.There were 14 patients with hyperprolactinemia in three of which serum PRL was over 60 micrograms/L. PRL producing tumor, severe primary hypothyroidism and liver cirrhosis were detected in these three patients, respectively. These results indicate that the pathogenesis of increased serum PRL was not uniform in patients with Hashimoto's thyroiditis, although there was a correlation between hyperprolactinemia and impaired thyroid function. It is proposed, therefore, to measure and follow serum levels of PRL and MRI of the pituitary in patients with chronic thyroiditis, especially with impaired thyroid function.
Growth hormone, insulin, prolactin and total thyroxine in the plasma of sheep implanted with the anabolic steroid trenbolone acetate alone or with oestradiol.
Donaldson IA, Hart IC, Heitzman RJ.
(5) Endocrinol 1988 Apr;117(1):115-22
Release of prolactin is independent of the secretion of thyrotrophin-releasing hormone into hypophysial portal blood of sheep.
Thomas GB, Cummins JT, Yao B, Gordon K, Clarke IJ.
Medical Research Centre, Prince Henry's Hospital, Melbourne, Australia.
In order to determine whether pituitary prolactin release was directly related to the secretion of TRH into hypophysial portal blood, serial portal and jugular venous blood samples were collected from seven lactating and three non-lactating ewes. In another experiment, samples were collected from five ovariectomized ewes while being exposed to an audio-visual stress and then later administered with chlorpromazine. Secretion of TRH was pulsatile in all ewes and independent of prolactin secretion; TRH pulses coincided with significant increases in prolactin secretion in only 15% of cases and only 29% of prolactin pulses were associated with TRH pulses. Sixty-seven per cent of suckling bouts were associated with increases in prolactin secretion, but only 22% of these were associated with significant increases in TRH secretion. Chlorpromazine increased prolactin levels fourfold but did not affect portal concentrations of TRH. Audio-visual stress was not a reliable method of causing prolactin release in this model. Mean portal concentrations of TRH and jugular concentrations of prolactin were not significantly correlated. These results show that hypothalamic TRH and pituitary prolactin are secreted independently in the sheep, implying that increases in prolactin release caused by suckling or chlorpromazine are not the direct result of increased TRH secretion.
