Dostinex is a medication based on ergot alkaloids. Ergot, of course, is the fungal disease of rye and other grasses, and a potent neurotoxin. Ergot alkaloids heavily interfere with neurotransmitter activity. Probably the best known ergot derivate is LSD, which strongly messes with the neurotransmitter serotonin.
There are a good number of ergot alkaloids that are used in conventional medicine. Usually, these medications are developed for their dopaminergic capabilities. Such medications are needed to treat the severe deficiency of the neurotransmitter dopamine that leads to Parkinson's.
The ergot alkaloid bromocriptine (Parlodel) can be used for its sexuality enhancing properties. Actuality, of all substances I have tested on myself for their sexuality-enhancing properties, bromocriptine, as well as Dostinex, are among the few for which I can attest effectiveness. However, bromocriptine has to be taken in a specific manner to avoid the nausea that otherwise would overshadow its sexuality-enhancing properties. Please see the bromocriptine articles on apomorphine.org for details. Dostinex is largely free of negative side effects, at least in me.
Of all dopaminergic medications used for the treatment of Parkinson's, Dostinex and Parlodel are the most similar to each other, with their double action of enhancing dopamine levels and inhibiting the secretion of the hormone prolactin from the anterior pituitary gland.
I am convinced that this dual action is crucial to sexual enhancement. Prolactin, the hormone, which has been named for its function of inducing lactation in women, directly interferes with sex drive in both women and men. It controls to a certain extent the secretion of gonadotropin, the hormone, which, one step further down the chain, controls the secretion of testosterone in both men and women. Regardless of which hormonal constellation in this sequence is responsible for a lowered sex drive, the reversal of the sequence through drugs like Dostinex and Parlodel clearly supports sexual desire.
As sexuality is the main source of happiness for practically all forms of higher living, including man, and as utmost sexual satisfaction can only be experienced as a sequence to sexual desire, it is a logical quest to provide ourselves with a better long-term hormonal profile than intended by our genetic blueprints. Anti-sexual changes of our hormonal levels as a consequence of the aging process is an unacceptable provision, which nature, our enemy, has designed in order to install the specific generation turnover rate of humans (20 to 30 years).
Increasing prolactin levels and, at the same time, decreasing testosterone levels are two inter-linked causes why aging men don't have as much sex drive as younger men, why they don't have orgasms as powerful as they used to have, and why they don't get as much pleasure out of their sex lives as they did when they were in their 20's.
To interfere with this chain of events isn't easy. Testosterone supplementation often doesn't do the trick. Each person's body has its own genetically set ideas what the person's age-appropriate testosterone levels ought to be. Supplying additional testosterone will, in healthy subjects, just provoke the body to down-regulate its own testosterone production, as well as to initiate other measures by which the testosterone balance returns to the aforementioned genetically set levels.
Willfully oversupplying testosterone, or supplementing with synthetic steroids is usually useless, at least for men. Women, if they don't mind the androgenic side effects (increased muscle buildup), may be able to increase desire and orgasmic capacity through both testosterone and synthetic steroid supplementation.
But for men, forcing testosterone levels beyond the genetic set points, mainly through the supplementation with synthetic steroids, has some very counterproductive side effects. It will, for example, result in shrinkage of the male organ, and problems achieving an erection.
The prolactin reduction pathway doesn't seem to be bedeviled in the same manner. I can attest from my own experience that Dostinex and bromocriptine enhance sexual functionality as well as the intensity of orgasm. (Please see my articles on bromocriptine for the finer points on how to dose bromocriptine for sexual enhancement, and how to avoid the nausea.) On the other hand, my own experimentation with the supplementation of testosterone (Andriol capsules) had no measurable effect on sexual desire at all, not immediate and not long-term.
There are an enormous number of compounds, both herbal and synthetic, which can kill sex drive and interfere with sexual performance. There are also a good number of products, both herbal and synthetic, which are sold with the promise that they help to overcome a lack of sexual desire or so-called erectile dysfunction.
I have been writing about pharmacological sexual enhancement for years, and I take the matter seriously. I have tried almost everything that is available under the sun, whether from below (ginseng) or above (ginkgo) the grass line, and both natural and synthetic (such as Viagra).
While Viagra definitely works for erections, I feel that Viagra alone does not provide any kick in the desire or orgasm departments. A combination with other drugs, especially Dostinex, can bring out the best in Viagra.
Are yohimbe
and/or yohimbine MAO inhibitors? There seems to be a fair bit of confusion. The
confusion is caused by the fact that while yohimbe and yohimbine are not MAO
inhibiting in the same manner as drugs used expressively as MAO inhibitors (see
list at the end of this article), there indeed seems to be some influence on
MAO activity.
Ellen
Coleman, RD, MA, MPH, claims on the Health Care Reality Check web site (quoted
August 19, 1999):
"Yohimbine
is a monoamine oxidase inhibitor which means that tyramine containing foods
(red wine, liver, cheese) and nasal decongestants or diet aids containing
phenylpropaanolamine should be rigorously avoided if it is used to prevent a
hypertensive crisis."
While the
Health Care Reality Check web site is dedicated to the noble task (as are we)
of protecting consumers from quacks who will sell anything as remedy against
any condition as long as it earns them a buck, they exaggerated their reporting
on yohimbe and yohimbine:
"According
to the FDA, documented health hazards include low blood pressure, weakness, and
nervous stimulation, followed by paralysis, fatigue, stomach disorders, kidney
failure, seizures and death. The FDA has declared yohimbine unsafe and
ineffective for over the counter sale."
This is
simply wrong. Yohimbine may not be an over-the-counter medication. But
yohimbine is a FDA-approved prescription drug. If it were inappropriate, the
FDA approval would be withdrawn. And as far as "documented health
hazards" are concerned, well, death, and a variety of diseases leading to
it, are documented health hazards for many antibiotics. And like antibiotics,
yohimbine is useful in spite of documented health hazards associated with it.
But the topic
of this article is neither the Health Care Reality Check web site nor the
documented health hazards of yohimbe and yohimbine in general. The topic is
yohimbe / yohimbine and MAO inhibition.
Monoamine
oxidase (MAO) inhibition is a profound physiological event, definitely not
something to be overlooked in the description of any medication. Chairman MAO
is an enzyme present in various parts of the body, primarily in the digestive
system and the central nervous system. Its function is the deamination of foods
and neurotransmitters.
The crucial
impact of monoamine oxidase (MAO) inhibitors is related to this parallel
occurrence of monoamines in food and catecholamine neurotransmitters such as
dopamine, epinephrine (adrenaline), and norepinephrine (noradrenaline). If the
action of the MAO enzyme is interrupted, the breakdown of these catecholamine
neurotransmitters is hindered. This is, to a certain degree, wished for in the
treatment of Parkinson’s, a disease characterized by a depletion of dopamine.
MAO inhibitors
are "dangerous" medications because they not only inhibit the
breaking down of monoamine neurotransmitters but also can interfere with the
deamination of monoamines in the digestive tract. If then, monoamines make
their way past the digestive tract they can start acting in the same manner as
neurotransmitters, primarily norepinephrine, on a number of physiological
functions, especially blood pressure. A combination of MAO inhibiting drugs
with many ordinary foods that contain tyramines is a sure recipe for
hypertensive shock and death.
Usually,
red wine, chocolate, and cheeses are given as examples of foods containing
tyramines, but tyramines can occur in many other foods as well. Also, the
tyramine content of foods is difficult to predict. The content of tyramines in
many foods tends to increase with storage. In a fresher state, many different
kinds of food have a lower (or insignificant) content of tyramines, while after
having been stored for some time, the contents of tyramines are higher. There
are very long and explicit lists on tyramine contents in specific foods,
compiled for patients who have to take MAO inhibitors to control Parkinson’s.
Obviously,
the above is not a complete characterization of chairman MAO and MAO
inhibitors. For example, we have not discussed the difference between MAO-A and
MAO-B, as well as the effects of MAO on behavior (low levels of MAO are
associated with criminal behavior as well as with a polygamous lifestyle).
Nevertheless, the above may already give the reader an idea why it is very
unlikely that with a prescription medication such as yohimbine, there wouldn't
be an explicit warning if it were a MAO inhibitor.
Yohimex is
one of several brands of yohimbine tablets sold in the US. Yohimex is a prescription drug with 5.4 milligram of yohimbine hydrochloride as active
ingredient, manufactured by Jones Medical Industries in Canton, OH 44702, and distributed by Kramer Laboratories in Miami FL 33174. As Yohimex is a
prescription drug, it had to be reviewed by the FDA. It's hard to believe that
if yohimbine were indeed a definite MAO inhibitor, a specific note on the
subject matter would be missing from the brochure accompanying every bottle of
Yohimex.
Alas, the
package literature contains no reference claiming that yohimbine would be a MAO
inhibitor. The package literature has the following to say about the clinical
pharmacology of yohimbine hydrochloride:
"Yohimbine
blocks presynaptic alpha-2 adrenergic receptors. Its action on peripheral blood
vessels resembles that of reserpine, though it is weaker and of short duration.
Yohimbine's peripheral autonomic nervous system effect is to increase
parasympathetic (cholinergic) and decrease sympathetic (adrenergic) activity.
It is to be noted that in male sexual performance, erection is linked to
cholinergic activity and to alpha-2 adrenergic blockade which may theoretically
result in increased penile inflow, decreased penile outflow or both. Yohimbine
exerts a stimulating action upon the mood and may increase anxiety. Such
actions have not been adequately studied or related to dosage although they
appear to require higher doses of the drug…."
No word on
MAO inhibition. The Mosby RxList website also does not mention yohimbine as MAO
inhibitor.
(Reserpine
is a white to yellowish powder isolated from the roots of certain species of
Rauwolfia and used as a sedative and an antihypertensive.)
Well,
yohimbine and yohimbe are not exactly the same. Yohimbe is the raw tree bark,
and yohimbine is just one of its active ingredients that has been extracted.
Even if yohimbine is not a MAO inhibitor, it may still be the case that yohimbe
is.
We have
seen a number of web sites that claim that either yohimbine or yohimbe is a MAO
inhibitor, or that yohimbine isn't but yohimbe is.
However, we
haven't seen any conclusive study on yohimbe and MAO inhibition. If yohimbe
were a strong and definite MAO inhibitor, one would have to expect fatalities
if the usual precautions against tyramine-containing foods were not heeded. Any
herb that functioned as a definite MAO inhibitor would long ago have been
classified as a poison. But yohimbe has been sold as a supplement for years. If
incidences of death would have occurred after ingesting yohimbe because of
yohimbe being a MAO inhibitor, it's unlikely this fact would not be reported
widely. Alas, there are no widely circulating reports of yohimbe causing deaths
because of its effects as MAO inhibitor.
Sure,
yohimbe and yohimbine cause side effects, which could be interpreted as an
effect of MAO inhibition, mainly nervousness. But yohimbe usually does not
cause an increase in blood pressure.
A safe
assessment is that even if both yohimbine and yohimbe are not definite MAO
inhibitors, they shouldn't be taken together with MAO inhibitors. I would add
that people who are on MAO inhibition medication are anyway not physically well
enough to take an additional leisure medication as strong as yohimbe or
yohimbine.
Now, while
yohimbe and yohimbine are not MAO inhibitors to the extent in which the term
"MAO inhibitor" is pharmacologically understood, there is
nevertheless some correlation between yohimbine and MAO activity.
It has been
documented that yohimbine is an anxiogenic agent, a substance that can induce
anxiety in humans and other higher animals. The Yohimex package literature
states: "Yohimbine exerts a stimulating action upon the mood and may
increase anxiety. Such actions have not been adequately studied or related to
dosage although they appear to require higher doses of the drug…."
Anxiety is
the missing link between yohimbine / yohimbe and MAO inhibition, and it points
to a possible explanation why yohimbine / yohimbe act as aphrodisiacs, apart
from facilitating erections.
In 1996, a
study on the effects of some anxiogenic agents on brain monoamine oxidase
inhibitory activity was conducted at the Department of Pharmacology, Banaras Hindu University, Varanasi, India (Bhattacharya SK; Chakrabarti A; Sandler M; Glover
V). The study was done on rats, not on humans, as it involved dosages of
yohimbine far too high to be used for sexual stimulation. The study came to the
conclusion that in a state of anxiety induced by a sufficiently high dosage of
yohimbine, there has been a noticeable increase of MAO-inhibitory activity
without specific MAO-inhibitory pharmaceutical agents having been added.
This is of
course not surprising as in any stress situation, there will likely be
increased epinephrine (adrenaline) activity in any higher animal. Epinephrine
activity in the body is regulated twofold: as secretion and as deactivation
through chairman MAO. Additional secretion and inhibition of deamination by
chairman MAO have comparative effects: an increased epinephrine level, with the
typical stress-related symptoms.
A
reasonable hypothesis regarding the aphrodisiac properties of yohimbe and
yohimbine would probably have to consider the effect of the bark and its active
ingredient on the neurotransmitter dopamine. While the usual aim of any
treatment with MAO inhibitors is to raise levels of dopamine to control
Parkinson’s disease, it has been noted that raised dopamine levels normally
also bring about sexual agitation.
The link
between dopamine and sexual urge is so strong that scientific studies have been
undertaken to check to what extent measurable dopamine levels correlate to
sexual perversion (paraphilic disorder).
A 1995
research on "Dopamine and sexual behavior" at the Bernard B. Brodie
Department of Neuroscience, University of Cagliari, Italy, came to the
following result: "Despite some differences, most studies show that
treatments that increase or decrease, respectively, brain dopaminergic activity
improve or worsen, respectively, several parameters of copulatory activity,
supporting a facilitatory role of dopamine in male sexual behavior."
And a 1997
study at the Harvard Medical School in Boston on "A monoamine hypothesis
for the pathophysiology of paraphilic disorders" drew the following
conclusion:
"A
monoamine pathophysiological hypothesis for paraphilias in males is based on
the following data: (i) the monoamines norepinephrine, dopamine, and serotonin
are involved in the appetitive dimension of male sexual behavior in laboratory
animals; (ii) data gathered from studying the side effect profiles of
antidepressant psychostimulant, and neuroleptic drugs in humans suggest that
alteration of central monoamine neurotransmission can have substantial effects
on human sexual functioning, including sexual appetite; (iii) monoamine
neurotransmitters appear to modulate dimensions of human and animal
psychopathology including impulsivity, anxiety, depression, compulsivity, and
pro/antisocial behavior, dimensions disturbed in many paraphiliacs; (iv)
pharmacological agents that ameliorate psychiatric disorders characterized by
the aforementioned characteristics, especially central serotonin enhancing
drugs, can ameliorate paraphilic sexual arousal and behavior."
The study
refers to the well-known fact that many medications for Parkinson’s disease,
which all aim to increase levels of dopamine, have an increased sexual appetite
as a common side effect. Many, but not all Parkinson’s medications are MAO
inhibitors. If scientific studies were to be undertaken on any aphrodisiac
effect of yohimbine or yohimbe (apart from their well-documented effect of
making better erections), they would have to check on what effect yohimbine and
yohimbe have on dopamine levels, either through MAO modulation or via any
alternative pathway.
MAO
inhibitors, generic names and brand names:
benmoxin - Nerusil, Neuralex
echinopsidine iodide - Adepren
etryptamine - Monase
iproclozide - Sinderesin, Sursum
iproniazid - Iprozid, Ipronid, Marsilid, Rivivol, Propilniazida
isocarboxazid - Enerzer, Marplan, Marplon
mebanazine - Actamol
metfendrazine - H.M.-11
moclobamide - Aurorix, Manerix (reversible inhibitor)
nialamide - Espril, Isalazina, Mygal, Niamid, Niaquitil, Nuredal, Psicomidina,
Surgex
pargyline - Eudatine, Eutonyl, Tenalin
phenelzine - Nardil, Stinerval, Monofen, Fenelzin, Kalgan, Nardelzine
pheniprazine - Catron, Catroniazide, Cavodil, Fenizin
phenoxypropazine - Drazine
pivhydrazine - Neomarsilid, Tersavid
safrazine - Safra
selegiline, l-deprenyl - Eldeprine, Eldepryl, Jumex, Jumexal, Lesotal, Movergan
(selective MAO-B inhibitor)
toloxatone - Hymoryl, Perenum (selective MAO-A inhibitor)
tranylcypromine - Parnate, Sicoton, Transamin, Transapin, Tylciprine
