Hi,
I recently decided to give IGF-2 a go in attempt to lower a moderately high prolactin level. I had planned to run it for 2 months, however after 1 month I was forced to stop as I was getting major dizzy spells, blurry vision and was feeling short of breath. After about a week since I finished it, this all cleared up.
Prolactin 367 738 mIU/L (<500)
Testosterone 19.1 14.2 nmol/L (11.0-40.0)
SHBG 35 32 nmol/L (10.0-70.0)
Calculated FTe 393 295 pmol/L (260-740)
As you can see, my prolactin doubled, and my testosterone went DOWN.
I had no strength gains and actually put on fat, despite a clean bulking diet. Pretty disappointing results.
This is interesting- and it does sound like dopaminergic symptoms- under normal circumstances, the product is going to do the exact opposite with prolactin levels, based on most of the literature- one of the studies below is an exception, and it occurred concurrent to prostate issues. We have used this same formula for almost 6 years, along with the same suppliers, so our mucuna source has not changed, and we mfr. and test everything at our own facility, so we can rule out materials and mfg. Are you taking anything else, and have you had any other type of pre-existing condition?
Clin Endocrinol (Oxf). 1980 Dec;13(6):525-33.
Evaluation of two inhibitory tests (nomifensine and L-dopa + carbidopa) for the diagnosis of hyperprolactinaemic states.
Moriondo P,
Travaglini P,
Nissim M,
***lia G.
Abstract
It has been reported that administration of nomifensine (Nom) or of L-dopa + carbidopa (L-dopa + Carb) potentiates central dopaminergic tonus, resulting in decreased prolactin (PRL) secretion. It has been proposed that these drugs would help to discriminate patients with PRL-secreting pituitary tumours from those with so-called 'functional' hyperprolactinaemia. In this study, oral Nom (200 mg) was given to forty-three hyperprolactinaemic patients and L-dopa + Carb (50 mg Carb every 6 h for four doses followed by L-dopa 100 mg and Carb 35 mg) to thirty of them and both treatment to ten normal subjects. The hyperprolactinaemic patients were divided into four clinical groups. Group A, twenty patients with proven PRL-secreting pituitary tumours; Group B, thirteen women with elevated PRL levels (less than 100 ng/ml) without any radiological evidence of a pituitary tumour (hyperprolactinaemia of unknown aetiology or 'functional' hyperprolactinaemia); Group C, four women with polycystic ovarian disease and mildly elevated serum PRL; Group D, six patients with various other disorders associated with hyperprolactinaemia. PRL levels decreased in the normal controls below the basal values by 61.3% +/- 6.2 (SEM) after Nom and 77.6% +/- 4.2 after L-dopa + Carb. Decreases in serum PRL of at least 50% (in three consecutive determinations) were found in group A in 20% of patients after Nom and in 25% after L-dopa + Carb; in group B in 15% and 40% of cases; in most of the hyperprolactinaemic women in group C; and some in group D. In conclusion, these two treatments did not discriminate between tumorous and non-tumorous cases of PRL hypersecretion.
J Clin Endocrinol Metab. 1981 Sep;53(3):594-8.
Calcium and calcium-antagonistic effects on prolactin and growth hormone responses to thyrotropin-releasing hormone and L-dopa in man.
Röjdmark S,
Andersson DE,
Sundblad L.
Abstract
The significance of calcium for the responsiveness of human lactotrophs and somatotrophs to iv TRH and oral L-dopa was investigated in 11 young healthy women. Both TRH and L-dopa were administered on three different background infusions: 1) saline, 2) verapamil, and 3) calcium. Twenty-five micrograms of TRH raised the PRL level from 15.1 +/- 2.3 to 76.9 +/- 8.8 ng/ml in 15 min (P less than 0.001). Calcium infusion blunted this PRL response by 33 +/- 8% (P less than 0.02), whereas verapamil, known for its calcium-antagonistic properties, left in unaffected. Five hundred milligrams of L-dopa increased the GH level from 2.2 +/- 0.7 to 16.7 +/- 2.2 ng/ml in 60 min (P less than 0.002) and reduced the PRL level from 11.6 +/- 2.9 to 3.1 +/- 0.4 ng/ml in 150 min (P less than 0.05). Neither calcium nor verapamil influenced these GH and PRL responses significantly. These findings indicate that human somatotrophs may be less dependent than human lactotrophs on normocalcemia for adequate hormone secretion.
Eur Urol. 2000 May;37(5):569-72.
Paradoxical stimulation of prolactin secretion by L-dopa in metastatic prostate cancer and its possible role in prostate-cancer-related hyperprolactinemia.
Lissoni P,
Mandalà M,
Rovelli F,
Casu M,
Rocco F,
Tancini G,
Scardino E.
Source
Division of Radiation Oncology, San Gerardo Hospital, Monza, Italy.
Abstract
OBJECTIVE:
In addition to sex steroids, prolactin (PRL) may also stimulate prostate cancer growth. Abnormally high blood levels of PRL have been noted in metastatic prostate cancer patients. However, most studies have been limited to the evaluation of basal levels of PRL rather than to investigate its secretion in response to classical endocrine dynamic tests. This study was carried out to analyze PRL secretion in metastatic prostate cancer patients both at basal conditions and in response to L-Dopa and metoclopramide, which represents the most classical inhibitory and stimulatory tests for PRL secretion, respectively.
METHODS:
The study included 12 patients with metastatic prostate cancer. On separate occasions, PRL secretion was evaluated in response to L-Dopa (500 mg orally) and to metoclopramide (10 mg i.v. as a bolus). Serum levels of PRL were measured by RIA.
RESULTS:
Mean PRL concentrations significantly increased after metoclopramide administration, even though no PRL response occurred in 6 of 12 patients. L-Dopa was unable to reduce PRL levels, which, in contrast, paradoxically significantly increased in response to L-Dopa, with mean values comparable to those achieved after metoclopramide injection.
CONCLUSION:
By showing a paradoxical stimulatory effect of L-Dopa on PRL secretion and a lack of response to metoclopramide in some patients, this study would suggest the existence of evident alterations in the neuroendocrine regulation of PRL release in advanced prostate cancer.
