Please Scroll Down to See Forums Below
napsgear
genezapharmateuticals
domestic-supply
puritysourcelabs
UGL OZ
UGFREAK
napsgeargenezapharmateuticals domestic-supplypuritysourcelabsUGL OZUGFREAK

Dostinex, Bromo Resources

GreekGod

New member
Hallo,
is there any profile on the drugs dostinex, bromocriptine, cialis regarding their possible uses in bodybuilding ? Is there any article explaining what prolactin is and how deca relates to it ? I searched Bill Robert's and Big Cat's drug profiles but found nothing. I know these are very new drugs, but many here seem to know a lot about them, so where did you get all that information from ?
 
yes i was actually researching the same thing and fell short.

bump.
 
Interesting read.......BROMO

Bromocriptine is prevelant in the anti-aging scene as it's primary use is the inhibition of Prolactin; this hormone is one of the few that actually appears to increase with age. Prolactin is produced by the pituitary gland and its release is inhibited by Bromocriptine.

Prolactin has been described as a “fat synthesis hormone” because one of its primary functions is to trigger lactation, (milk production...gyno in males) and weight gain in pregnancy. In men it helps to reduce serum Prolactin levels in men (although the precise role of Prolactin in men is unclear).

A further possible need to control age-related Prolactin levels is offered by some researchers who believe that Prolactin is an immune system suppressant.

Bromocriptine also affects the most famous of all pituitary hormones- Growth Hormone (GH). Bromocriptine increases GH secretion in individuals with low or normal GH concentrations, but paradoxically suppresses GH secretion in some patients with acromegaly, (a condition of excessive-production of GH). Studies indicate that Bromocriptine does not affect the release of any other anterior pituitary hormones.

Due to its Dopamine enhancement, Bromocriptine has even been cited as an aphrodisiac, although little effort has been made to study and confirm this action. There have been several reports of “better controlled” orgasms and “almost orgasms” before the real orgasm occurs. If any countries allow for more medical categories such as “weak orgasm syndrome” or perhaps, “clinical sex-drive loss” then Dopamine agonists such as Bromocriptine are going to receive a lot of attention from the pharmaceutical manufacturers, especially in the wake of Viagra (r) sales.

Another interesting clinical study administered a component of tobacco called DMBA to rats at a level where it is known to be very effective in producing breast cancer. However, rats that had been pretreated with Bromocriptine completely avoided any cancer development. Bromocriptine therefore appears to also offer itself as a very potent free radical quencher.

One of the most recent studies indicates that Bromocriptine may be a candidate for the treatment of Type-2 diabetes. This is because Bromocriptine has been shown to suppress lipogenesis and improve glucose tolerance and insulin resistance.

One animal study suggested that a further action of Bromocriptine is to alter CNS (central nervous system), regulating metabolism and as such, has another important use in helping to prevent weight gain, (this would be in addition to its improvement of diabetic conditions).

Bromocriptine has a blood pressure lowering ability.

(sorry-----it wasa copy/paste from awhile back and I do not have a site or reference)
 
BromoFAQ

Most of you have been waiting with bated breath for an update regarding my experiences with the dopaminergic drug, bromocriptine maleate (BM), something I've talked about before here in this column and at the T-Mag forum.

[Editor's note: Bromocriptine's approved use is for treating Parkinson's and other neurologic disorders.]

I've continued to use Parlodel (brand name bromocriptine maleate) as I'm fortunate enough to have an enlightened physician friend who's legally prescribing it for me. While previously I was excited by the theoretical fat loss potential of BM, I have to say that practically, the results surpassed even my expectations.

Currently, I'm 174 pounds at under 6% body fat as measured by calipers. Now I'm sure some of you out there are going to say, "Shit, man, you're tiny!" Well then, this segment of "Useful Stuff" is not for you! If you're interested in becoming a 250-pound monster, my experiences and my opinions are probably of minimal interest and use to you. Lots of luck, fellas. But if you're interested in more of an underwear model type of look (a look that women seem to appreciate a whole lot more than the Conan the Barbarian look), read on.

Are you still with me? Good! BM has helped me lose just over sixteen pounds of adipose tissue in about two months. So how did I do it? I started by taking 2.5mg of BM per day before bed back in the middle of the summer. This was actually a mistake. For starters, the dose was too high for me to start with and taking this before bed was probably not a smart idea. Unfortunately, BM has some CNS stimulatory effects (at least on me) that caused me to have a heck of a time falling a sleep. A few days into this experiment, I opted to switch from taking it before bedtime to taking it around 6 or 7 A.M. in the morning. If you're planning on using BM, I'd strongly suggest that you not take it at night.

However, even switching to the daytime didn't eliminate all the side effects. I still felt "twitchy"… I suppose that's the best way to describe it. Suspecting that the dose might still be too high, I opted to cut back to 1.25mg of BM per day and titrate my way up. I feel this method is the absolute safest and best way to use BM. So I'd also suggest that if you're going to try BM, start at 1.25 mg.

I titrated up as high as 6.25 mg per day which was the threshold of tolerability for me (and then I dropped down to 5.0 mg which is where I am now). The way I titrated up was to increase the dose by 1.25 mg every five days. This seemed to minimize the CNS and psychological side effects that BM can impart.

So how did BM make me feel and what did I use with it? Well, I ended up adding in a small amount of Cytomel around the third week (25 mcg of T3 per day to be exact). I'm not sure how necessary this is for everyone, but I noticed that I was "cold" in the mornings about two weeks after I started the BM. My body temperature was down about 0.4 degrees Fahrenheit and I decided that this could adversely impact my quest to metabolize fat (so hence, I added in enough T3 to get by body temperature back to baseline). I'm not sure if the drop in body temperature was caused by the BM or the change in my diet, but it's surely something you might want to look at and be aware of when you start using BM. Adjust accordingly.

Dopaminergic agonists tend to have a stimulant effect. I actually like the way BM makes me feel; it seems to "up my energy" but not in a speedy, ephedra sort of manner. I'm more alert and less drained when using BM.

It also affected my diet in an unconscious manner. I've always craved carbohydrates — this flaw has always been the demise of any dieting program I've undertaken and made keto dieting (especially Fat Fasting) exceedingly difficult. I noticed that BM tended to blunt my craving for carbs. It also blunted my appetite.

I wouldn't characterize BM as an appetite suppressant in the manner that phenylpropanolamine or phentiramine resins are, but I noticed that instead of eating everything on my plate because it was there, I only ate until I was satiated. So yes, my caloric intake dropped by about 500 calories per day (this is an average and a guesstimate) and I consumed less carbohydrates (this was unintentional).

Upon reflection, my diet looked a lot like the old Isocaloric Diet that Dan Duchaine used to espouse where you eat an almost equal ratio of carbs, fats, and proteins. It's important to add that all of these changes in my diet were unconscious and I never felt hungry or unsatisfied. My tastes just changed quite a bit while using BM.

My results thus far with BM look like this: when I started this experiment, I weighed 196 pounds and held about 13.2% body fat. Yesterday, I weighed in at 174 pounds at approximately 5.5% body fat (it's hard to be exact with the calipers when your skin folds get thinner). This represents just over a sixteen-pound loss in body fat in two months. I realize this may not seem spectacular when compared to keto dieting, after all, this merely represents a two to three-pound weight loss per week. Heck, people do that with Slim Fast. But there are a few things to keep in mind that make this truly interesting, if not downright amazing:

1) My loss of lean body mass was minimal. Of the 22 pounds I dumped, less than six pounds of that was LBM. Had I opted to use a mild anabolic or MAG-10, I'm sure I could've eliminated any and all loss of LBM.

2) I made no conscious effort to change my diet! This is truly huge. Even though my diet did change substantially, it wasn't a conscious effort. All I intended to do was take a few extra pills per day, not suffer through some Draconian dieting scheme. This was very easy!

3) I feel fantastic. When was the last time you heard of anyone feeling truly fantastic while trying to lose weight?

I'm sure I could've lost more fat in this time period had I "known what I was doing" (remember, this was an experiment). I'm going to continue using BM at 5.0mg per day for the next sixty days or so. Expect another, more in-depth update at that time.

I'll leave you with a few final thoughts about using BM for weight loss. I'd suggest not using any ephedra based products (or yohimbine or synephrine) with BM as even the smallest dose of ephedra (8mg) caused the hair on the back of my neck to stand straight up. You'll most likely not enjoy the way you feel with stimulatory alkaloids if you're on BM. I'd also suggest that you consider adding an anabolic with BM (MAG-10 will work fine). If you do choose to use BM, drop us a line here at T-mag and let us know your results.
 
Also I didnt write these but I had them so check them out. Its not fact but its part of learning so enjoy...

By Serge Kreutz
Version 3.0, October 2002


Bromocriptine is a well-established drug for two conditions, increased levels of the hormone prolactin and Parkinson's. The best-known brand name is Parlodel. The standard tablet dosage is 2.5 mg.

Bromocriptine also has a sexuality-enhancing effect, though it is not commonly sold for that purpose. Nevertheless, there is little doubt that in many people, bromocriptine will support sexual response. The reason why the drug is not specifically sold as impotence or frigidity medication: a sufficient number of studies to achieve FDA approval for the purpose of sexual enhancement have not been conducted.

In view of the enormous marketing success of Pfizer's Viagra, many pharmaceutical companies are interested in distributing substances that enhance sexual response. However, for "old" drugs, the patents of which have expired, there is little incentive to invest into the necessary clinical trials.

The sexually enhancing effect of bromocriptine is very different from the effect of Viagra (generic name: sildenafil citrate). Viagra works primarily on the sexual organ, providing chemically for better rigidity, or some rigidity in the first place.

Bromocriptine, on the other hand, works on the brain, making a person more receptive for sexual stimulation and creating a frame of mind for more powerful orgasms. Both effects are a logical consequence of the way, bromocriptine is traditionally used… to lower levels of the hormone prolactin, and to increase levels of the neurotransmitter dopamine.

High levels of prolactin are generally associated with a decreased sex drive. So, by lowering levels of prolactin, especially when they are high, bromocriptine increases the interest in sex.

A similar effect is achieved by bromocriptine through the neurological route. Bromocriptine is used as a medication in Parkinson's because it will cause higher levels of the neurotransmitter dopamine. Parkinson's is a disease caused by dopamine levels that are too low. Low dopamine levels normally also cause a loss of interest in sex, and an increased sex drive is a common "side effect" of many Parkinson's medications. One person's side effect is another person's cure.

While the increase in sex drive caused by bromocriptine may be hard to measure, the effect on orgasms is more obvious. Orgasms become more powerful, ironically because they are better controlled. The pre-orgasm plateau phase can last for minutes on bromocriptine, and orgasm will be accompanied by a pronounced histamine reaction (stuffed nose).

Bromocriptine is a prescription drug most everywhere, though in many countries of the world, prescription drugs can be bought over the counter. In countries where prescription drugs are indeed only sold on prescriptions, it is within a physician's discretion to prescribe a drug for conditions for which it has not originally been approved. To get a prescription for bromocriptine, please proceed to http://online-consultation-prescriptions.com. The site offers a straightforward deal. You subscribe and are referred to a doc who issues prescriptions for sexual enhancement (doc’s fee not included in the subscription price). If, for any reason, you should be denied a prescription, the subscription price will be refunded, and the doc won’t charge either. Prescriptions are issued for men between 25 and 65 years of age.

For a substance to be approved as a medication, an illness has first to be defined for which it is a cure. Nowadays, there are many newly defined illnesses, such as clinical depression, attention deficit disorder, erectile dysfunction … conditions, which have previously not been considered illnesses but just part of the individuality of a particular human being.

Some members of our species are smarter than others, and some are happier, and some of the males are more virile than their neighbors. Not to be as smart as a genius, and not to be as virile as one's neighbor aren't diseases in the classical sense. But new illnesses are constantly defined, because the pharmaceutical industry has on hand a medication to overcome the condition. So, if there will soon be a medical condition named Weak Orgasm Syndrome, or Clinical Sex Drive Loss, bromocriptine is a sure medication candidate.

Bromocriptine belongs to a group of drugs derived from the ergot fungus. A more concentrated dopaminergic drug that is also derived from ergot is Dostinex. Dostinex is a new, patented drug, which is why clinical trials have been financed to look into its application to improve sexual function, especially the enhancement of orgasms.


__________________
 
The use as a prolactin inhibiting drug to increase orgasm sensitivity (like dostinex does, i think) seems interesting. the dieting article is something new to me.

GOOD POST BRO!
 
http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203584.html

http://www.pslgroup.com/dg/f666.htm

http://jcem.endojournals.org/cgi/content/abstract/86/11/5256



Cabergoline vs Bromo.

Comparison of the effects of cabergoline and bromocriptine on prolactin levels in hyperprolactinemic patients.

Sabuncu T, Arikan E, Tasan E, Hatemi H.

Harran University, Medical Faculty, Department of Endocrinology and Metabolism, Sanliurfa, Turkey.

OBJECTIVE: It is well known that bromocriptine has a suppressive effect on the prolactin release in hyperprolactinemic patients. But it also has some adverse effects. The new, long-acting dopaminergic drug, cabergoline, has been reported to be an effective agent in these patients. However, there are relatively few reports comparing the beneficial and adverse effects of these drugs in the treatment of hyperprolactinemic patients. Therefore, here we studied and compared the efficacy and tolerability of cabergoline with bromocriptine in hyperprolactinemic patients. PATIENTS: Seventeen patients (7 with microprolactinoma, 4 with macroprolactinoma, 6 with idiopathic hyperprolactinemia) were given bromocriptine at a dose of 2.5 mg (or 5 mg for macroprolactinomas) twice daily, and 17 patients (8 with microprolactinoma, 4 with macroprolactinoma, 5 with idiopathic hyperprolactinemia) were given cabergoline at a dose of 0.5 mg twice weekly for 12 weeks. RESULTS: At the end of the study, the prolactin reduction was significantly greater in the cabergoline group than in the bromocriptine group (-93 vs. -87.5 %, respectively, p < 0.05). Normalization of prolactin levels was achieved in 10 of 17 patients (59%) in the bromocriptine group, and in 14 of 17 patients (82%) in the cabergoline group (p = 0.13). Two patients (50%) with macroprolactinoma in the bromocriptine group and three patients (75%) with macroprolactinoma in the cabergoline group demonstrated a normalization of their serum prolactin levels. Adverse events were noted in 53% of bromocriptine patients and in 12% of cabergoline patients (p < 0.01). CONCLUSION: These data indicate that cabergoline is a very effective agent for lowering the prolactin levels in hyperprolactinemic patients and that it appears to offer considerable advantage over bromocriptine in terms of efficacy and tolerability.




Yet another...

by Beverly M. K. Biller M.D.
Stephen B. Tatter,M.D., Ph.D., HTML editor

The treatment of choice for prolactinomas is dopamine agonist administration, which results in tumor shrinkage, normalization of prolactin, and restoration of gonadal function in the majority of patients. However, the only dopamine agonist available for this disorder in the United States is bromocriptine. Its use is limited by a high incidence of side effects, a short duration of action, and a lack of effectiveness in some patients. Several other agents have been tested over the last decade in the United States with varying resuIts. However, cabergoline, a long-acting oral doparnine agonist specific for the D2 receptor, has received the most attention recently, and is currenily the only dopainine agonist being pursued for this indication in the U. S.

The most interesting feature of cabergoline in terms of patient comphance is its extremely long half-life. Most patientscan be treated with a single weekly dose, is in contrast to the 1-3 times daily administration required for brornocriptine. Particularly in the population most prone to microprolactinomas, healthy young women without other medical disorders, a once weekly therapy is extremely appealing. What information is available about cabergoline and what is its current status in the United States?

Webster, et al. conducted a European study comparing cabergoline to bromocriptine in the treatment ofhyperprolactinemic amenorrhea. A total of 459 women, the majority of whom had microprolactinomas or idiopathic hyperprolactinernia, were treated with either cabergoline or bromocriptine in a double blind study for 8 weeks, followed by an open label study for 16 weeks during which dose adjustments were made according to response Eighty-three percent of the women treated with cabergoline attained normal prolactin levels in comparison with 59% of women treated with bromocriptine. Seventy-two percent of cabergoline-treated women attained ovulatory cycles or became pregnant during therapy in contrast to only 52% of those treated with bromocriptine. Amenorrhea persisted in 7% of women treated with cabergoline versus 16% of women treated with bromocriptine. Cabergoline was better tolerated than bromocriptine with 3% of women discontinuing cabergoline versus 12% stopping bromocriptine due to intolerance. Gastrointestinal symptoms were significantly less frequent, less severe, and of shorter duration in cabergoline treated patients. The authors concluded that cabergoline is more effective and better tolerated than bromocriptine in women with hyperprolactinemic amenorrhea.

In a United States multicenter study of patients with macroprolactinomas, we have also found cabergoline to he effective and well tolerated. Fifteen patients (8 women, 7 men) ages 18-76 years were followed in an open label, 48-week dose escalation trial of cabergoline administered once weekly. Eleven patients had received prior therapy with other dopamine agonists. The prolactin levels decreased by 93.6% with normal levels obtained in 73% of patients at doses of 0.5-3.0 mg per week. Three of 5 patients who had failed to normalize prolactin on prior dopamine agonists achieved normal levels. Gonadal function was restored in all hypogonadal men and in 75% of premenopausal women with amenorrhea. Tumor size decreased in 11 of 15 patients, but tumor shrinkage may have been compromised by the fact that many patients had achieved substantial decreases in tumor mass on prior dopamine agonists. Side effects were minimal, with no patients discontinuing the medication due to intolerance.

Currently, cabergoline is available under a compassionate use protocol from Pharmacia/Upjohn in Kalamazoo, MI, based on individual requests by each patient's physician. In addition, a new multicenter, international trial is available for patients with macroprolactinonias and serum prolactin levels >200. This study is being conducted in a number of European centers and one United States site, the Neuroendocrine Clinical Center at Massachusetts General Hospital. This one year study is designed to confirm the effectiveness of this therapy in patients with macroprolactinomas. In particular, the focus of the study is to determine whether cabergoline is as effective at tumor shrinkage as bromocriptine. For this reason all patients enrolled are required to have had no prior therapy with any dopamine agonists, in order to avoid studying patients who have already experienced some tumor shrinkage with other agents.

In summary, cabergoline appears to be a more effective and better tolerated dopamine agonist in the therapy of prolactinomas. Patient compliance is high, related to the few mild side effects and once-weekly dosing. Further study is needed to confirm this, and to lead to its availability in the United States.

References
Webster J, et al. 1994. Comparison of cabergoline and bromocriptine in the treatment of hyperprolactinemic amenorrhea. N Engl J Med 31:904-909.

Biller BMK, et al. 1996. Treatment of prolactin secreting macroadenomas with once weekly agonist cabergoline. J Clin Endocrinol Metab 81:2338-43.
 
I still haven't seen any study that associates deca with prolactin. What proves that taking deca will raise one's prolactin levels ?
 
Top Bottom