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Dostinex / cabergoline
Old 06-11-2007, 03:40 PM   #1
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Dostinex in context



Version 2.0, December 2004
Dostinex is the drug with the greatest pro-sexual potential since Viagra hit the market in 1998. But it's very different from Viagra.

Viagra is a medication specifically for erectile dysfunction. It will do nothing for other aspects of good sexual function: libido (desire, arousal, excitement), orgasm, and ejaculation. Actually, according to my own experience, taking more Viagra than what would be one's ideal dose will interfere with the strength of orgasm and specifically ejaculation.

My own dose of Viagra is 25 mg. If I go to 50 mg, I will have, off and on for the next few hours, erections that last 15 to 30 minutes, almost without the need for sexual stimulation. They will even persist beyond orgasm. But orgasms in such a condition are rather weak, probably because the parasympathetic nervous system is just too dominant. While during erections, the parasympathetic nervous system is in control, orgasm is a major sympathetic event.

Erections and libido are interconnected, but they are also amazingly independent from each other. Erections are, to some 80 percent, a matter of the vascular system. When the parasympathetic nervous system is in control, blood flow is directed to internal functions such as digestion, as well as to reproductive availability (the facilitation of erections). Partially, this works through the regulation of the adrenergic system (epinephrine and norepinephrine, which, at the same time, work as hormones and neurotransmitters). Adrenergic impact usually causes vascular constriction (making erections impossible). Yohimbine is a peripheral alpha-2-adrenergic receptor blocker, which means that it prevents the adrenergic hormones' effects on alpha-2-adrenergic receptors, which are mainly located in the abdominal and genital areas. If the vasoconstrictive impulse of adrenergic hormones in the abdominal and genital areas is inhibited, erections happen with ease.

However, we have to be aware that in complex biological systems such as the human body, there are usually alternative avenues to achieve a desired effect. The efficacy pathway of sildenafil citrate is very different from that of yohimbine.

Sildenafil citrate (Viagra) works on an enzymatic level. It suppresses the enzyme phosphodiesterase type 5 (PDE5), which naturally occurs in erectile tissue. Phosphodiesterase type 5 (PDE5) breaks down the body chemical known as cyclic GMP. Cyclic GMP is produced during arousal and causes muscular and vascular changes, which lead to an erection. Men who don't produce a sufficient amount of cyclic GMP will have problems achieving an erection, and men with high levels of the enzyme phosphodiesterase type 5 (PDE5) will have problems maintaining one. In both cases, sildenafil citrate provides a solution by keeping phosphodiesterase type 5 in check.

All of this has nothing to do with libido (desire, arousal, and excitement), orgasm, and ejaculation.

Libido is, not totally but to a certain extend, dependent on testosterone, kept in a fine balance with a number of other hormones. When I succeed, for example with tongkat ali extract, to elevate testosterone, my sexual fantasies are more daring, and they occur at a higher frequency. Tongkat ali, and the higher levels testosterone caused by it, also contribute to keeping me focused during intercourse, but I don't think that testosterone alone is the determining factor in libido overall.

The most dramatic effect of elevating testosterone (by tongkat ali or through other means) is seen in men who have clinically low testosterone levels, caused by non-functioning testes or pituitary tumors.

However, in men in whom impotence is caused by problems of the vascular system in the genital area, and not by endocrine insufficiencies, a phosphodiesterase type 5 inhibitor will work much better than testosterone therapy.

However, the diagnosis of impotence in aging men is usually obscured by the fact that there is a parallel decline of a number of bodily functions. For example, men with vascular problems may also have low testosterone levels. While declining testosterone levels may play a role in us becoming less healthy as we age, it is not that low testosterone levels are the direct cause of vascular problems in the male genital area. The two syndromes just tend to emerge at around the same time.

A lack of capability to achieve an erection, or generally weak erections, are the symptoms by which the affected male usually defines impotence. Which is why "erectile dysfunction" is a more precise term for the condition he primarily wants ameliorated.

Viagra can take care of the erectile dysfunction. But then, many men complain that while on Viagra, they, thank you, can have erections all right, but sex still is not the same as it was in their 20's. They become aware of the fact that their libido, too, isn't what it used to be.

Working on one's testosterone levels can have a distinct positive effect on libido, but not all possible methods work equally well. My own experience with direct testosterone replacement therapy (Andriol, Proviron) as well as an indirect approach via the hypothalamus and pituitary glands (clomiphene, anastrozole) is that it is hard indeed to differentiate whether all of this does any good. For me, the only approach that definitely couples a raise in testosterone levels with enhanced libido, has been tongkat ali extract. But then, tongkat ali is a natural compound with hundreds of chemical ingredients, and it is not as completely researched as, for example, sildenafil citrate. It may just be that tongkat ali contains "magic" ingredients that have other, additional effects, not just the one of elevating testosterone.

The connection between testosterone and libido is also not as obvious as the one between Viagra and erections. It's not that one could just apply some testosterone (as gel, patch, or injection) or take a medication that activates testosterone synthesis, and an hour later, one would be ready with heightened libido. If you do take medications to elevate testosterone levels, you can never be quite sure whether and when an effect will kick in. On a regular regimen of testosterone elevation, there may be situations, randomly occurring, when sexual fantasies will, rather suddenly, occupy one's mind. But it cannot be planned when this will happen, and unfortunately, it may not happen during times when one would think that the situation is right for it.

I do not doubt that elevating testosterone has an anabolic effect. Proviron (toxic to the liver) and tongkat ali can make for quicker muscle gains during a weight exercise program, and help with body fat control. And for men grossly deficient in testosterone (hypogonadism), rectifying testosterone supply can be a great help for sexual function. But as a treatment for standard, age-related impotence, or for plain sexual enhancement, just supplying the body directly with testosterone (e.g. with testosterone patches) has practically no value.

Try another approach.

Libido is a mental and neural affair. And while hormones such as testosterone do work on the frame of mind for sex, we have to be aware that evolution has designed humans as an animal species that is primarily guided by sensual input (mainly sights and sounds) and the cognitive processing of this sensual input.

Which is why the right kind of cognitive processing has the greatest potential to positively affect libido. That sounds like a job for a psychologist. But going to the shrink may not be the right move. The function of psychologists in modern society is to make us good members of this society, so that we won't cause any problem, neither to public security, nor to the public health system. It's not their aim to make us ready to pursue the ultimate sexual experience, as this may, when multiplied by hundreds or thousands of men, result in all kinds of social and public health problems. The shrink will condition you to be a monogamous family man, not a wild playboy.

I guess that most of us have clear evidence from own experience on how the right sensual input and the right cognitive processing work wonders on libido. Usually, new sensual signals are more powerful than repeat signals. Which is why our libido usually is stronger when with a new partner. Also, forbidden sensual input, and cognitive awareness that it is forbidden, have a stronger impact on libido than sanctioned or routine sensual input. Which is why, so often, boredom rules conjugal bedrooms.

Need an example for the libido power of cognitive processing? Take jealousy. It's all just perceptions. No medication, no therapy needed.

If your wife loves, or makes love with, another man, your blood will rage, and you will want to establish your rights by sexual penetration. Just imagine how she goes along in bed with her lover, and your ears will feel hot, and your loins ready.

Because jealousy has such a profound effect on libido, and because heightened libido is such a gratifying state of mind, I have been working for years on my own personal strategy of supplying just the right amount of jealousy to my daily love life. This, of course, requires a special kind of relationship. It's not sufficient that my partners give me reason to be jealous by having, or having had, relationships with other men. I must also first perceive a particular partner as my property. Which means that I will have to invest in her, mentally and probably also economically.

But then, I would not want to do so with just any girl with whom I may have casual sexual intercourse. I also have to be free from other close personal relationships. If I do want to harvest the positive effects of well-dosed jealousy, the person who makes me jealous will have to be the main focus of my love life. Which, in turn, is why it is difficult to be made jealous by more than one woman at a particular period of time.

Jealousy is strong medicine. It can raise libido to previously unknown levels. It's great for sexual enhancement. If only we were able to control its supply to our minds in the same way as we can control the supply of Viagra to our bodies.

Close your eyes and imagine your wife loving, and making love with, another man. Don't feel anything? The point is, you can't deceit your cognitive apparatus. Your mind cannot be aware of a perceived unfaithfulness of your wife just because you willfully want to perceive it. It won't work. It will have to be real. And when it's real, then too, it can be out of control.

Isn't there a simpler method? A pill to swallow for better libido.

Sure, there is. Try Dostinex (generic name: cabergoline). Or, in a broader sense: dopamine agonists.

Dostinex is a new drug. But dopamine agonists have been around for many decades, and their pro-libido effect is well established. Apart from cabergoline, the assortment of dopamine agonists includes bromocriptine, pergolide, pramipexole, lisuride, apomorphine, and a few more. Actually, apomorphine (brand name: Uprima) is sold in Europe as a medication for erectile dysfunction.

But it's wrong marketing. Dopamine agonists don't work for erections as reliably as phosphodiesterase inhibitors. They work on libido. Therefore, Uprima typically is a disappointment for men whose problems are primarily vascular. I assume that Uprima is sold as a medication for erectile dysfunction mainly because erectile dysfunction meanwhile is an accepted medical condition, while low libido is not.

I have been using dopamine agonists for sexual enhancement for several years. And not only dopamine agonists.

To summarize my observation: while sildenafil citrate and yohimbine work on erections, and while elevating testosterone levels has an effect only when I do it with tongkat ali extract, dopamine agonists are the agent of choice for enhancing libido and orgasm. (Latest research has indicated that tongkat ali not only elevates testosterone but also works as a dopamine agonist; this explains why it is so much better for sexual enhancement than just plain testosterone.)

Because dopamine agonists (including tongkat ali) suppress the hormone prolactin, which in turn suppresses testosterone, dopamine agonists can, in people with elevated prolactin levels, function in the same way as a testosterone replacement therapy would. This most clearly happens in patients with pituitary cancer, which typically expresses itself in strongly elevated prolactin levels. Those afflicted by the disease have very low testosterone levels. Thus, for them, Dostinex and other dopaminergic agents work as hormonal therapy. The hormonal effects of Dostinex (cabergoline) are less extreme in healthy subjects.

Dopamine agonists not only strongly support libido; they also tend to enhance orgasm and make for a stronger ejaculation (as does tongkat ali extract).

But dopamine agonists have their downsides. All the older ones can cause bad nausea. (The newly discovered fact that tongkat ali has dopaminergic effects also explains the hot-headedness experienced by many tongkat ali users).

I have found a way to counteract the nausea caused by bromocriptine and apomorphine (see the member articles on SexualEnhancement. org - Asiatour. com Love and sex in Asia - Thailand, Philippines, Cambodia, Vietnam, Malaysia, Indonesia, Singapore for details). But only cabergoline and tongkat ali are completely nausea-free for me.
 
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Old 06-11-2007, 03:46 PM   #2
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Dostinex
Indications & Dosage

INDICATIONS
DOSTINEX Tablets are indicated for the treatment of hyperprolactinemic disorders, either idiopathic or due to pituitary adenomas.

DOSAGE AND ADMINISTRATION
The recommended dosage of DOSTINEX Tablets for initiation of therapy is 0.25 mg twice a week. Dosage may be increased by 0.25 mg twice weekly up to a dosage of 1 mg twice a week according to the patient's serum prolactin level.
Dosage increases should not occur more rapidly than every 4 weeks, so that the physician can assess the patient's response to each dosage level. If the patient does not respond adequately, and no additional benefit is observed with higher doses, the lowest dose that achieved maximal response should be used and other therapeutic approaches considered.
After a normal serum prolactin level has been maintained for 6 months, DOSTINEX may be discontinued, with periodic monitoring of the serum prolactin level to determine whether or when treatment with DOSTINEX should be reinstituted. The durability of efficacy beyond 24 months of therapy with DOSTINEX has not been established.

HOW SUPPLIED
DOSTINEX Tablets are white, scored, capsule-shaped tablets containing 0.5 mg cabergoline. Each tablet is scored on one side and has the letter P and the letter U on either side of the breakline. The other side of the tablet is engraved with the number 700.
DOSTINEX is available as follows:
Bottles of 8 tablets NDC 0013-7001-12
STORAGE
Store at controlled room temperature 20° to 25°C (68° to 77°F) [see USP].
LAB-0030-6.0
Revised June 2006
FDA revision date: 12/12/06
 
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Old 06-11-2007, 03:48 PM   #3
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Permax and Dostinex Information
What is Permax? What is Dostinex?
Permax and Dostinex are drugs from a class of medications called ergot-derived dopamine receptor agonists and used in the treatment of Parkinson's, restless leg syndrome, and migraine headaches. Other ergot-derived dopamine receptor drugs include the now banned diet drug Fen-phen, and all are associated with heart valve disease. Permax (pergolide) has been found in studies to make a patient five to seven times more likely to have leaky heart valves than those patients who use other drug therapies for Parkinson's. Dostinex (cabergoline) has only been approved for sale in the United States to treat hyperprolactinemia, a condition in which excessive amounts of the hormone prolactin enter the bloodstream due to benign tumors of the pituitary gland.

It has been shown in two studies that Permax and Dostinex interact with a receptor in the heart valve, causing the valve to overgrow and become floppy and leaky. Of the two, only Permax currently has a black box warning addressing the increased risk of heart valve problems in patients.
 
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Old 06-11-2007, 03:52 PM   #4
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Cabergoline
From Wikipedia, the free encyclopedia

Pregnancy and Lactation
Pregnancy: Approximately 100 female patients became pregnant under therapy with cabergoline for hyperprolactinemic conditions. The incidence of spontaneous abortions and congenital abnormalities was comparable to nontreated patients. Nevertheless, women wishing to become pregnant should wait a period of four weeks after discontinuation of cabergoline. Patients becoming pregnant under therapy should terminate cabergoline immediately, if possible.
Lactation: In rats cabergoline was found in the maternal milk. Since it is not known if this effect also occurs in humans, breastfeeding women should not be treated.


Valvular Heart Disease
In two studies published in the New England Journal of Medicine on January 4, 2007, cabergoline was implicated along with pergolide in causing valvular heart disease.[2][3] Both drugs are ergot-derived dopamine agonists, although their molecular skeletons are different. As a result of this, the FDA removed pergolide from the U.S. market on March 29, 2007.[4] Since cabergoline is not approved in the U.S. for Parkinson's Disease, but for hyperprolactinemia, the drug remains on the market. Treatment for hyperprolactinemia requires lower doses than that for Parkinson's Disease, diminishing the risk of valvular heart disease.



Dosage
Parkinson's disease: Monotherapy: Initial dose should be 0.5 mg daily. The usual maintenance dose is 2 to 4 mg daily. Combination therapy: Usually 2 to 6 mg daily.
Tumors of the pituitary gland and other hyperprolactinemic conditions: Initially 0.5 mg per week, slowly titrated to 4.5 mg per week, if necessary.
Ablactation: According to specific treatment scheme.
 
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Old 06-11-2007, 05:16 PM   #5
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Don't think this qualifies as a supplement. May need to move this to the steroid profile forum.
 
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Old 06-11-2007, 05:50 PM   #6
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nice posts but i agree...although these aren't steroids they do belong in that forum
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