bromocriptine bandwagon
jb1309
that normal prolactin levels are impotant for LH receptor function in
the testes, as well as possibly modulating LH release. Administration
of bromocriptine at pharmacological doses (5 mg) lowers testosterone
in normal men in a number of studies. Here are just a few of the
available medline abstracts stressing the importance of normal
prolactin levels for male testosterone production. Unless you know for
a fact you are hyperprolactinemic, I would avoid bromocriptine.
http://www.ncbi.nlm.nih.gov/entrez/query.f...0&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.f...7&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.f...3&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.f...2&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.f...9&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.f...5&dopt=Abstract
Lyle McDonald
>
> Before jumping onto the bromocriptine bandwagon you should be aware
> that normal prolactin levels are impotant for LH receptor function in
> the testes, as well as possibly modulating LH release. Administration
> of bromocriptine at pharmacological doses (5 mg) lowers testosterone
> in normal men in a number of studies.
And it had no effect in a number of others (#6 below for example). I
suspect dosing, timing and duration as being the major effectors.
Considering that 7.5 mg for 4 months had no effect yet 5 mg for 2 weeks
did, there's something very odd going on. I suspect timing as being the
biggest issue. Research shows that the nighttime increase in PRL may be
a key for testosterone release so if study #2 gave the bromo at night,
that would be a problem.
Lyle
***
1: Life Sci 1993;52(22):1805-7
Bromocriptine effects on plasma luteinizing hormone and its responses to
gonadotropin-releasing hormone in normal men.
Oseko F, Morikawa K, Nakano A, Taniguchi A.
Department of Medicine, Shimane Medical University, Japan.
Secretory changes in plasma pituitary luteinizing hormone (LH) after
administration of a dopaminergic drug were studied in five normal men. Each
subject received orally 5 mg of bromocriptine (Brc) daily for 8 weeks. Each
received gonadotropin-releasing hormone (GnRH) stimulation tests at the
beginning (control), and at 2, 4, 6, and 8 weeks after initiation of Brc
treatment. We referred the basal plasma LH and a ratio of maximally
GnRH-responded plasma LH to its basal level (R-Max) as indicators of secretory
alterations of the LH. Mean basal levels of plasma LH in the five
subjects at
the beginning and those of R-Max were 3.4 +/- 2.3 (SD) mIU/mL and 8.5
+/- 2.9
units, respectively. Statistically, both the mean values of plasma LH
and R-Max
during the control period did not differ significantly from those
obtained after
Brc treatment, although mean basal levels of plasma prolactin during the control
period (15.6 +/- 4.6 ng/mL) decreased significantly (p < 0.05) after initiation
of treatment. A low dose of Brc administered to normal men for 8 weeks
does not
significantly influence pituitary secretion of LH.
PMID: 8492643 [PubMed - indexed for MEDLINE]
2: Fertil Steril 1991 Feb;55(2):355-7
Effects of chronic bromocriptine-induced hypoprolactinemia on plasma
testosterone responses to human chorionic gonadotropin stimulation in normal
men.
Oseko F, Nakano A, Morikawa K, Endo J, Taniguchi A, Usui T.
Department of Medicine, Shimane Medical University, Japan.
To study the role played by normal levels of plasma prolactin (PRL) in the
secretion of testosterone (T) in the testes, we induced
hypoprolactinemia with a
daily dose of 5 mg bromocriptine administered orally in five normal men
20 to 35
years of age for 8 weeks. The basal PRL, T, luteinizing hormone,
follicle-stimulating hormone, and maximum responses of plasma T to human
chorionic gonadotropin (hCG) stimulation were measured every 2 weeks. Basal
levels of plasma T were reduced in the 1st 2-week-long period of
hypoprolactinemia. In the 4-week-long period of hypoprolactinemia, the maximal
response of plasma T to hCG stimulation was significantly reduced. The findings
suggest that normal levels of plasma PRL may play an important role in the
secretion of T in the human testes in vivo.
PMID: 1899397 [PubMed - indexed for MEDLINE]
3: Horm Res 1991;36(1-2):36-40
Restoration of normal gonadotropin responses to naloxone by chronic
bromocriptine treatment in elderly men.
Coiro V, Volpi R, Bertoni P, Marcato A, Vourna S, Bocchi R, Bianconi L, Marchesi
M, Buonanno G, Chiodera P.
Istituto di Clinica Medica Generale e Terapia Medica, Universita di Parma,
Italia.
Naloxone is unable to stimulate FSH and LH secretion in elderly men, suggesting
a reduced endogenous opioid control of gonadotropin secretion in
senescence. In
the present study, we examined whether in elderly men a chronic dopaminergic
stimulation with bromocriptine (5 mg/day for 7 days) modifies the gonadotropin
response to naloxone (4 mg as an i.v. bolus plus 10 mg infused in 2 h). Eleven
younger men (group 1, 22-40 years old) participated as controls. Twenty-two
elderly men were selected from a larger population and were divided into two
groups: subjects with compensated gonadal failure (normal blood
testosterone and
elevated gonadotropin concentrations; group 2, n = 11; 62-80 years old)
and men
with normal gonadal function (normal blood testosterone and gonadotropin levels;
group 3, n = 11; 61-82 years old). Naloxone induced a striking LH and a slight
but significant FSH increase in group 1, but was unable to change serum
gonadotropin concentrations in elderly subjects of both groups 2 and 3. When
experiments were repeated after bromocriptine treatment, no significant
differences in LH and FSH responses to naloxone were observed in the younger
subjects. On the other hand, bromocriptine restored significant gonadotropin
responses to naloxone in elderly men. In fact, after bromocriptine,
naloxone-induced FSH and LH increments in groups 2 and 3 were indistinguishable
from those observed in group 1. These data suggest that in men age-related
dopaminergic alterations may underlie the defective endogenous opioid
control of
gonadotropin secretion.
PMID: 1814799 [PubMed - indexed for MEDLINE]
4: J Endocrinol Invest 1983 Feb;6(1):9-15
Influence of dopaminergic mechanisms on 24-hour secretory patterns of prolactin,
luteinizing hormone and testosterone in recumbent men.
Sowers JR, Viosca SP, Windsor C, Korenman SG.
PMID: 6841919 [PubMed - indexed for MEDLINE]
5: Clin Endocrinol (Oxf) 1982 Oct;17(4):345-52
Relationship of changes in serum concentrations of prolactin and testosterone
during dopaminergic modulation in males.
Nakagawa K, Obara T, Matsubara M, Kubo M.
To evaluate the effect of PRL on the male pituitary-gonadal system, serum
concentrations of PRL, testosterone, LH and FSH were determined in
healthy young
men daily before, during, and after 3-day oral administration of bromocriptine,
metoclopramide or sulpiride. Bromocriptine (2.5 mg as a single dose) caused,
concurrently with a marked suppression of serum PRL, a significant
increase of
serum testosterone and a transient decrease of serum LH. The changes of
PRL and
testosterone were negatively correlated. With metoclopramide (10 mg q.i.d.)
serum PRL was increased and testosterone inversely decreased. There was no
change in LH and FSH. Sulpiride (50 mg q.i.d.) evoked the elevation of
serum PRL
and LH, but no change in testosterone. A significant increase in serum
concentration of testosterone was also observed in a patient with PRL-producing
pituitary tumour and four out of seven patients with acromegaly during
bromocriptine treatment. These results suggest an inhibitory effect of
PRL on
testosterone secretion at the gonadal level, or direct dopaminergic stimulatory
control of testosterone secretion.
PMID: 6814794 [PubMed - indexed for MEDLINE]
6: Clin Endocrinol (Oxf) 1980 Nov;13(5):455-9
Pituitary function in normoprolactinaemic infertile men receiving bromocriptine.
Glatthaar C, Donald RA, Smith R, McRae CU.
A double blind trial of bromocriptine 7.5 mg daily versus placebo was carried
out in ten infertile men. Pretreatment basal plasma prolactin, thyroid
stimulating hormone (TSH) testosterone and luteinizing hormone (LH)
concentrations were normal, but plasma follicle-stimulating-hormone
(FSH) was
raised in four individuals. After 4 months treatment with bromocriptine a
significant fall in plasma prolactin was observed (P less than 0.01),
both under
basal conditions and following thyroid stimulating hormone releasing hormone
(TRH). Basal plasma gonadotrophin, testosterone and thyroid stimulating hormone
(TSH) concentrations did not alter. No change in sperm density, volume or
motility was noted. However an apparent fall in the peak plasma LH (but
not FSH)
response to gonadotrophin releasing hormone (LHRH) was observed in patients
receiving bromocriptine. This reduction in plasma LH responsiveness was
significant when compared with the baseline response (P less than 0.05) but
failed to reach significance when compared with the placebo response. It is
concluded that prolonged bromocriptine therapy in normoprolactinaemic
men does
not suppress FSH secretion, and any reduction in plasma LH
responsiveness to
LHRH is not accompanied by a significant fall in plasma testosterone.
Publication Types:
Clinical Trial
Randomized Controlled Trial
PMID: 6784976 [PubMed - indexed for MEDLINE]
7: Fertil Steril 1980 Aug;34(2):140-3
The effect of prolactin on androgen response to human chorionic
gonadotropin in
normal men.
Lackritz RM, Bartke A.
Testicular androgen responses to human chorionic gonadotropin (hCG) were
compared in normal males before and after suppression of prolactin (PRL)
secretion with bromocriptine. Baseline follicle-stimulating hormone, luteinizing
hormone, and PRL levels were suppressed by bromocriptine, 2.5 mg daily
(P <
0.05). Serum testosterone and dihydrotestosterone (DHT) levels were reliably
increased by one intramuscular injection of hCG (P < 0.05). Although
testosterone responses to hCG were not significantly different in normal
PRL and
suppressed PRL cycles (P > 0.05), the DHT response was significantly increased
in the suppressed cycle (P < 0.05), suggesting a physiologic 5 alpha-reductase
blockage by PRL in men.
PMID: 6773818 [PubMed - indexed for MEDLINE]
8: Arch Androl 1980 Feb;4(1):1-7
Plasma ACTH, cortisol, LH, FSH, testosterone, and dihydrotestosterone responses
to bromocriptine in normal men.
Van Loon GR, Bain J, Ruse JL.
The effects of an initial oral 2.5 mg dose of bromocriptine and of a similar
dose after treatment with 2.5--5 mg daily for one week on plasma concentrations
of ACTH, cortisol, LH, FSH, testosterone, and dihydrotestosterone were studied
in normal men. In addition to its suppressive effects on plasma concentrations
of prolactin and catecholamines which have been reported previously, a single
dose of bromocriptine produced small increases in plasma ACTH and cortisol.
Neither a single dose of bromocriptine nor treatment for one week
altered plasma
concentrations of LH and FSH. Plasma concentrations of testosterone and
dihydrotestosterone were not altered by a single dose of bromocriptine, but
small increases in both were noted in some subjects after treatment for one
week.
PMID: 6243912 [PubMed - indexed for MEDLINE]
joshua....@verizon.com
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=
2654270&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids
=1899397&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids
=8983353&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids
=1133152&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids
=1249179&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids
=3932105&dopt=Abstract
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Lee Michaels
"Lyle McDonald" <lyl...@onr.com> wrote in message
news:3DAEF668...@onr.com...
> jb1309 wrote:
> >
> > Before jumping onto the bromocriptine bandwagon you should be aware
> > that normal prolactin levels are impotant for LH receptor function in
> > the testes, as well as possibly modulating LH release. Administration
> > of bromocriptine at pharmacological doses (5 mg) lowers testosterone
> > in normal men in a number of studies.
>
> And it had no effect in a number of others (#6 below for example). I
> suspect dosing, timing and duration as being the major effectors.
> Considering that 7.5 mg for 4 months had no effect yet 5 mg for 2 weeks
> did, there's something very odd going on. I suspect timing as being the
> biggest issue. Research shows that the nighttime increase in PRL may be
> a key for testosterone release so if study #2 gave the bromo at night,
> that would be a problem.
>
> Lyle
>
OK Lyle, I am going to make a wild guess here. (I am eminently qualified to
make guesses!) And I am not discounting what you said either. Since
hormones are often released in normal precitable cylcles, what you said
makes perfect sense.
I am just wondering if any of this is "fat butt science". I don't know. You
know thw studies. Where EVERYONE associated with the study is sedentary. Is
exercise a factor at all??
It seems that if somebody were to hit the weights hard on a regular basis,
that this would obviously affect their fat loss and muscle retention.
Couldn't the exercise either help with testosterone production or at least
greatly mitigate it??
In other words even if the above statement were true (Bromo eats up test)
would some good old american pumping iron go a long way to counteract that??
If not in fact at least in terms of the fat loss/LBM retention??
Lyle McDonald
>
> "Lyle McDonald" <lyl...@onr.com> wrote in message
> news:3DAEF668...@onr.com...
> > jb1309 wrote:
> > >
> > > Before jumping onto the bromocriptine bandwagon you should be aware
> > > that normal prolactin levels are impotant for LH receptor function in
> > > the testes, as well as possibly modulating LH release. Administration
> > > of bromocriptine at pharmacological doses (5 mg) lowers testosterone
> > > in normal men in a number of studies.
> >
> > And it had no effect in a number of others (#6 below for example). I
> > suspect dosing, timing and duration as being the major effectors.
> > Considering that 7.5 mg for 4 months had no effect yet 5 mg for 2 weeks
> > did, there's something very odd going on. I suspect timing as being the
> > biggest issue. Research shows that the nighttime increase in PRL may be
> > a key for testosterone release so if study #2 gave the bromo at night,
> > that would be a problem.
> >
> > Lyle
> >
>
> OK Lyle, I am going to make a wild guess here. (I am eminently qualified to
> make guesses!) And I am not discounting what you said either. Since
> hormones are often released in normal precitable cylcles, what you said
> makes perfect sense.
>
> I am just wondering if any of this is "fat butt science". I don't know. You
> know thw studies. Where EVERYONE associated with the study is sedentary. Is
> exercise a factor at all??
Not as I can tell.
> It seems that if somebody were to hit the weights hard on a regular basis,
> that this would obviously affect their fat loss and muscle retention.
> Couldn't the exercise either help with testosterone production or at least
> greatly mitigate it??
>
> In other words even if the above statement were true (Bromo eats up test)
> would some good old american pumping iron go a long way to counteract that??
> If not in fact at least in terms of the fat loss/LBM retention??
It really depends on the mechanism involved (I saw the stuff relating
PRL to LH receptors in the testes as well).
Based on some of the stuff I looked at (i.e. a normal nightime increase
in PRL levels appears required for normal testosterone levels), it's got
to be a timing issue. Many of the other effects of bromo are intimately
related to when you
take it and I'd expect this to be the case here. A single morning dose
is going to have a very different effect than dosing once morning and
once evening.
I also can't see any other explanation for why 5 mg for 2-8 weeks did
have an effect but 7.5 mg for 4 months didn't. Since when does a lower
dose have a greater impact than a higher dose on anything? The answer
is since never. But if the first study gave the bromo in such a way as
to block the nightime PRL increase (i.e. dosed it at night which is
commonly suggsted but simply incorrect), that would explain it.
But this is one of the issues I managed to space completely (there were
several others) and I'm pulling all the papers this weekend to see
what in the hell is going on. If it turns out I fucked up and bromo is
a bad idea on a diet because it's whacking testosterone, I'll be the
first one to let
everybody know.
Lyle