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  1. #1
    Registered User yokingupsick's Avatar
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    dopamine increasing supplements

    I have a few questions regarding usp powerfull product and dopamine increase in general. Any answers would be greatly appreciated

    1. I have read and it came to my understanding that an increase in dopamine will lead to a decrease in serotonin is this true or myth?

    2. Does Mucunine Purienine and p5p - vitamin b6 stack good together or counterproductive? or should one be cycled off of and then cycle onto the other?

    3. If one was to run a cycle of extreme tren would running powerfull alongside it prevent most prolactin issues from arising?
    Last edited by yokingupsick; 09-11-2008 at 10:59 AM.
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  2. #2
    Byronic Hero Catchol's Avatar
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    Originally Posted by yokingupsick View Post
    I have a few questions regarding usp powerfull product and dopamine increase in general. Any answers would be greatly appreciated

    1. I have read and it came to my understanding that an increase in dopamine will lead to a decrease in serotonin is this true or myth?
    It's possible.

    2. Does Mucunine Purienine and p5p - vitamin b6 stack good together or counterproductive? or should one be cycled off of and then cycle onto the other?
    P5P isn't really necessary w/ l-dopa products. P5P is needed as a cofactor for the hydroxylase enzyme that converts tyrosine to dopa. The decarboxylase enzyme is so ubiquitous that it needs no help.

    3. If one was to run a cycle of a prolactin prohormone would running powerfull alongside it prevent most prolactin issues from arising?
    There's no such thing as a prolactin prohormone -- prolactin is a pituitary peptide hormone assembled from individual amino acids.
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    Registered User yokingupsick's Avatar
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    ok there I edit my post. Not a prolactin prohormone but tren kind have prolactin sideffects. Anything I can run with it to prevent it?
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    Byronic Hero Catchol's Avatar
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    Originally Posted by yokingupsick View Post
    ok there I edit my post. Not a prolactin prohormone but tren kind have prolactin sideffects. Anything I can run with it to prevent it?
    Bromocriptine -- if you don't mind the side-effects -- is a POWERFUL prolactin inhibitor. If you choose to take it, start low and go slow. I'd try .625 mg twice daily w/ food for a week, then up the dose gradually. I've taken bromocriptine before, and if you don't like extreme nausea and severe fatigue then I strongly encourage you to work up your dose slowly. The first time I tried it I took 2.5 mg, and I was laid out for 7 hours feeling like I had spent all day eating greasy fair food and riding spinning rides, ugh...

    I learned to start out slowly and the side-effects disappeared.
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    Actual Pharmacist Bane's Avatar
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    Originally Posted by Catchol View Post
    Bromocriptine -- if you don't mind the side-effects -- is a POWERFUL prolactin inhibitor. If you choose to take it, start low and go slow. I'd try .625 mg twice daily w/ food for a week, then up the dose gradually. I've taken bromocriptine before, and if you don't like extreme nausea and severe fatigue then I strongly encourage you to work up your dose slowly. The first time I tried it I took 2.5 mg, and I was laid out for 7 hours feeling like I had spent all day eating greasy fair food and riding spinning rides, ugh...

    I learned to start out slowly and the side-effects disappeared.
    Dihydroergocristine beats the hell out of everything sides/results wise
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    Originally Posted by Bane View Post
    Dihydroergocristine beats the hell out of everything sides/results wise
    Be that as it may, bromocriptine is considerably cheaper and much more widely available. I don't even know of a single NPN/OP that sells this drug...
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    Well recreational drugs such as marijuana increase dopamine but you dont want to that because increasing dopamine will have huge side effect later on such as not being able to laugh or be happy.

    but playing games and other things you consider "fun" will release dopamine in a healthy
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    Dosinex / cabaser is the number one drug for this purpose
    Cabaser can be gotten higher dosages at cheaper prices

    Bromocriptine has too many sides for my use
    Last edited by gjohnson5; 09-11-2008 at 02:09 PM.
    Kickin your azz everytime
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    Registered User yokingupsick's Avatar
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    I am leaning towards more otc supplements/drugs I can buy that will increase dopamine and serotonin
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    Talking

    Originally Posted by Catchol View Post
    Be that as it may, bromocriptine is considerably cheaper and much more widely available. I don't even know of a single NPN/OP that sells this drug...
    Sucks not lining in Greece eh?
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    Originally Posted by Bane View Post
    Sucks not lining in Greece eh?
    In a few years, when the American economy has completely bottomed out and we're all trading in Euros, I'll take some much-needed vacation time, come and visit you, and you can show me some of the many other ways that Europe is economically and pharmacologically superior to the United States.
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    Originally Posted by keven702 View Post
    Well recreational drugs such as marijuana increase dopamine but you dont want to that because increasing dopamine will have huge side effect later on such as not being able to laugh or be happy.

    but playing games and other things you consider "fun" will release dopamine in a healthy
    100% BS. Many compounds raise dopamine levels (cannabis has a very mild effect on dopamine) and do not cause you not to laugh or be happy. Deprenyl is one of the strongest compounds you can take to raise dopamine levels and it is very safe.
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    Originally Posted by yokingupsick View Post
    I am leaning towards more otc supplements/drugs I can buy that will increase dopamine and serotonin
    L-DOPA and 5-HTP.
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    The number of patients who received selegiline in prospectively monitored pre-marketing studies is limited. While other sources of information about the use of selegiline are available (e.g., literature reports, foreign post-marketing reports, etc.) they do not provide the kind of information necessary to estimate the incidence of adverse events. Thus, overall incidence figures for adverse reactions associated with the use of selegiline cannot be provided. Many of the adverse reactions seen have also been reported as symptoms of dopamine excess.

    Moreover, the importance and severity of various reactions reported often cannot be ascertained. One index of relative importance, however, is whether or not a reaction caused treatment discontinuation. In prospective pre-marketing studies, the following events led, in decreasing order of frequency, to discontinuation of treatment with selegiline: nausea, hallucinations, confusion, depression, loss of balance, insomnia, orthostatic hypotension, increased akinetic involuntary movements, agitation, arrhythmia, bradykinesia, chorea, delusions, hypertension, new or increased angina pectoris, and syncope. Events reported only once as a cause of discontinuation are ankle edema, anxiety, burning lips/mouth, constipation, drowsiness/lethargy, dystonia, excess perspiration, increased freezing, gastrointestinal bleeding, hair loss, increased tremor, nervousness, weakness, and weight loss.

    Experience with ELDEPRYL obtained in parallel, placebo controlled, randomized studies provides only a limited basis for estimates of adverse reaction rates. The following reactions that occurred with greater frequency among the 49 patients assigned to selegiline as compared to the 50 patients assigned to placebo in the only parallel, placebo controlled trial performed in patients with Parkinson's disease are shown in the following Table. None of these adverse reactions led to a discontinuation of treatment.

    INCIDENCE OF TREATMENT-EMERGENT ADVERSE EXPERIENCES IN THE PLACEBO-CONTROLLED CLINICAL TRIAL
    Adverse Event Number of Patients Reporting Events
    selegiline hydrochloride
    N=49 placebo
    N=50
    Nausea 10 3
    Dizziness/Lightheaded/Fainting 7 1
    Abdominal Pain 4 2
    Confusion 3 0
    Hallucinations 3 1
    Dry mouth 3 1
    Vivid Dreams 2 0
    Dyskinesias 2 5
    Headache 2 1
    The following events were reported once in either or both groups
    Ache, generalized 1 0
    Anxiety/Tension 1 1
    Anemia 0 1
    Diarrhea 1 0
    Hair Loss 0 1
    Insomnia 1 1
    Lethargy 1 0
    Leg pain 1 0
    Low back pain 1 0
    Malaise 0 1
    Palpitations 1 0
    Urinary Retention 1 0
    Weight Loss 1 0

    In all prospectively monitored clinical investigations, enrolling approximately 920 patients, the following adverse events, classified by body system, were reported.
    Central Nervous System
    Motor/Coordination/Extrapyramidal

    increased tremor, chorea, loss of balance, restlessness, blepharospasm, increased bradykinesia, facial grimace, falling down, heavy leg, muscle twitch*, myoclonic jerks*, stiff neck, tardive dyskinesia, dystonic symptoms, dyskinesia, involuntary movements, freezing, festination, increased apraxia, muscle cramps.
    Mental Status/Behavioral/Psychiatric

    hallucinations, dizziness, confusion, anxiety, depression, drowsiness, behavior/mood change, dreams/nightmares, tiredness, delusions, disorientation, lightheadedness, impaired memory*, increased energy*, transient high*, hollow feeling, lethargy/malaise, apathy, overstimulation, vertigo, personality change, sleep disturbance, restlessness, weakness, transient irritability.
    Pain/Altered Sensation

    headache, back pain, leg pain, tinnitus, migraine, supraorbital pain, throat burning, generalized ache, chills, numbness of toes/fingers, taste disturbance.
    Autonomic Nervous System

    dry mouth, blurred vision, sexual dysfunction.
    Cardiovascular

    orthostatic hypotension, hypertension, arrhythmia, palpitations, new or increased angina pectoris, hypotension, tachycardia, peripheral edema, sinus bradycardia, syncope.
    Gastrointestinal

    nausea/vomiting, constipation, weight loss, anorexia, poor appetite, dys****ia, diarrhea, heartburn, rectal bleeding, bruxism*, gastrointestinal bleeding (exacerbation of preexisting ulcer disease).
    Genitourinary/Gynecologic/Endocrine

    slow urination, transient anorgasmia*, nocturia, prostatic hypertrophy, urinary hesitancy, urinary retention, decreased penile sensation*, urinary frequency.
    Skin and Appendages

    increased sweating, diaphoresis, facial hair, hair loss, hematoma, rash, photosensitivity.
    Miscellaneous

    asthma, diplopia, shortness of breath, speech affected.
    Postmarketing Reports

    The following experiences were described in spontaneous post-marketing reports. These reports do not provide sufficient information to establish a clear causal relationship with the use of ELDEPRYL.
    CNS

    Seizure in dialyzed chronic renal failure patient on concomitant medications.
    The selectivity of selegiline for MAO B may not be absolute even at the recommended daily dose of 10 mg a day. Rare cases of hypertensive reactions associated with ingestion of tyramine-containing foods have been reported in patients taking the recommended daily dose of selegiline. The selectivity is further diminished with increasing daily doses. The precise dose at which selegiline becomes a non-selective inhibitor of all MAO is unknown, but may be in the range of 30 to 40 mg a day.

    Severe CNS toxicity associated with hyperpyrexia and death have been reported with the combination of tricyclic antidepressants and non-selective MAOIs (NARDIL, PARNATE ). A similar reaction has been reported for a patient on amitriptyline and ELDEPRYL. Another patient receiving protriptyline and ELDEPRYL developed tremors, agitation, and restlessness followed by unresponsiveness and death two weeks after ELDEPRYL was added. Related adverse events including hypertension, syncope, asystole, diaphoresis, seizures, changes in behavioral and mental status, and muscular rigidity have also been reported in some patients receiving ELDEPRYL and various tricyclic antidepressants.

    Serious, sometimes fatal, reactions with signs and symptoms that may include hyperthermia, rigidity, myoclonus, autonomic instability with rapid fluctuations of the vital signs, and mental status changes that include extreme agitation progressing to delirium and coma have been reported with patients receiving a combination of fluoxetine hydrochloride (PROZAC) and nonselective MAOIs. Similar signs have been reported in some patients on the combination of ELDEPRYL (10 mg a day) and selective serotonin reuptake inhibitors including fluoxetine, sertraline and paroxetine.

    Since the mechanisms of these reactions are not fully understood, it seems prudent, in general, to avoid this combination of ELDEPRYL and tricyclic antidepressants as well as ELDEPRYL and selective serotonin reuptake inhibitors. At least 14 days should elapse between discontinuation of ELDEPRYL and initiation of treatment with a tricyclic antidepressant or selective serotonin reuptake inhibitors. Because of the long half-lives of fluoxetine and its active metabolite, at least five weeks (perhaps longer, especially if fluoxetine has been prescribed chronically and/or at higher doses) should elapse between discontinuation of fluoxetine and initiation of treatment with ELDEPRYL.
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    Originally Posted by Bane View Post
    The number of patients who received selegiline in prospectively monitored pre-marketing studies is limited. While other sources of information about the use of selegiline are available (e.g., literature reports, foreign post-marketing reports, etc.) they do not provide the kind of information necessary to estimate the incidence of adverse events. Thus, overall incidence figures for adverse reactions associated with the use of selegiline cannot be provided. Many of the adverse reactions seen have also been reported as symptoms of dopamine excess.

    Moreover, the importance and severity of various reactions reported often cannot be ascertained. One index of relative importance, however, is whether or not a reaction caused treatment discontinuation. In prospective pre-marketing studies, the following events led, in decreasing order of frequency, to discontinuation of treatment with selegiline: nausea, hallucinations, confusion, depression, loss of balance, insomnia, orthostatic hypotension, increased akinetic involuntary movements, agitation, arrhythmia, bradykinesia, chorea, delusions, hypertension, new or increased angina pectoris, and syncope. Events reported only once as a cause of discontinuation are ankle edema, anxiety, burning lips/mouth, constipation, drowsiness/lethargy, dystonia, excess perspiration, increased freezing, gastrointestinal bleeding, hair loss, increased tremor, nervousness, weakness, and weight loss.

    Experience with ELDEPRYL obtained in parallel, placebo controlled, randomized studies provides only a limited basis for estimates of adverse reaction rates. The following reactions that occurred with greater frequency among the 49 patients assigned to selegiline as compared to the 50 patients assigned to placebo in the only parallel, placebo controlled trial performed in patients with Parkinson's disease are shown in the following Table. None of these adverse reactions led to a discontinuation of treatment.

    INCIDENCE OF TREATMENT-EMERGENT ADVERSE EXPERIENCES IN THE PLACEBO-CONTROLLED CLINICAL TRIAL
    Adverse Event Number of Patients Reporting Events
    selegiline hydrochloride
    N=49 placebo
    N=50
    Nausea 10 3
    Dizziness/Lightheaded/Fainting 7 1
    Abdominal Pain 4 2
    Confusion 3 0
    Hallucinations 3 1
    Dry mouth 3 1
    Vivid Dreams 2 0
    Dyskinesias 2 5
    Headache 2 1
    The following events were reported once in either or both groups
    Ache, generalized 1 0
    Anxiety/Tension 1 1
    Anemia 0 1
    Diarrhea 1 0
    Hair Loss 0 1
    Insomnia 1 1
    Lethargy 1 0
    Leg pain 1 0
    Low back pain 1 0
    Malaise 0 1
    Palpitations 1 0
    Urinary Retention 1 0
    Weight Loss 1 0

    In all prospectively monitored clinical investigations, enrolling approximately 920 patients, the following adverse events, classified by body system, were reported.
    Central Nervous System
    Motor/Coordination/Extrapyramidal

    increased tremor, chorea, loss of balance, restlessness, blepharospasm, increased bradykinesia, facial grimace, falling down, heavy leg, muscle twitch*, myoclonic jerks*, stiff neck, tardive dyskinesia, dystonic symptoms, dyskinesia, involuntary movements, freezing, festination, increased apraxia, muscle cramps.
    Mental Status/Behavioral/Psychiatric

    hallucinations, dizziness, confusion, anxiety, depression, drowsiness, behavior/mood change, dreams/nightmares, tiredness, delusions, disorientation, lightheadedness, impaired memory*, increased energy*, transient high*, hollow feeling, lethargy/malaise, apathy, overstimulation, vertigo, personality change, sleep disturbance, restlessness, weakness, transient irritability.
    Pain/Altered Sensation

    headache, back pain, leg pain, tinnitus, migraine, supraorbital pain, throat burning, generalized ache, chills, numbness of toes/fingers, taste disturbance.
    Autonomic Nervous System

    dry mouth, blurred vision, sexual dysfunction.
    Cardiovascular

    orthostatic hypotension, hypertension, arrhythmia, palpitations, new or increased angina pectoris, hypotension, tachycardia, peripheral edema, sinus bradycardia, syncope.
    Gastrointestinal

    nausea/vomiting, constipation, weight loss, anorexia, poor appetite, dys****ia, diarrhea, heartburn, rectal bleeding, bruxism*, gastrointestinal bleeding (exacerbation of preexisting ulcer disease).
    Genitourinary/Gynecologic/Endocrine

    slow urination, transient anorgasmia*, nocturia, prostatic hypertrophy, urinary hesitancy, urinary retention, decreased penile sensation*, urinary frequency.
    Skin and Appendages

    increased sweating, diaphoresis, facial hair, hair loss, hematoma, rash, photosensitivity.
    Miscellaneous

    asthma, diplopia, shortness of breath, speech affected.
    Postmarketing Reports

    The following experiences were described in spontaneous post-marketing reports. These reports do not provide sufficient information to establish a clear causal relationship with the use of ELDEPRYL.
    CNS

    Seizure in dialyzed chronic renal failure patient on concomitant medications.
    The selectivity of selegiline for MAO B may not be absolute even at the recommended daily dose of 10 mg a day. Rare cases of hypertensive reactions associated with ingestion of tyramine-containing foods have been reported in patients taking the recommended daily dose of selegiline. The selectivity is further diminished with increasing daily doses. The precise dose at which selegiline becomes a non-selective inhibitor of all MAO is unknown, but may be in the range of 30 to 40 mg a day.

    Severe CNS toxicity associated with hyperpyrexia and death have been reported with the combination of tricyclic antidepressants and non-selective MAOIs (NARDIL, PARNATE ). A similar reaction has been reported for a patient on amitriptyline and ELDEPRYL. Another patient receiving protriptyline and ELDEPRYL developed tremors, agitation, and restlessness followed by unresponsiveness and death two weeks after ELDEPRYL was added. Related adverse events including hypertension, syncope, asystole, diaphoresis, seizures, changes in behavioral and mental status, and muscular rigidity have also been reported in some patients receiving ELDEPRYL and various tricyclic antidepressants.

    Serious, sometimes fatal, reactions with signs and symptoms that may include hyperthermia, rigidity, myoclonus, autonomic instability with rapid fluctuations of the vital signs, and mental status changes that include extreme agitation progressing to delirium and coma have been reported with patients receiving a combination of fluoxetine hydrochloride (PROZAC) and nonselective MAOIs. Similar signs have been reported in some patients on the combination of ELDEPRYL (10 mg a day) and selective serotonin reuptake inhibitors including fluoxetine, sertraline and paroxetine.

    Since the mechanisms of these reactions are not fully understood, it seems prudent, in general, to avoid this combination of ELDEPRYL and tricyclic antidepressants as well as ELDEPRYL and selective serotonin reuptake inhibitors. At least 14 days should elapse between discontinuation of ELDEPRYL and initiation of treatment with a tricyclic antidepressant or selective serotonin reuptake inhibitors. Because of the long half-lives of fluoxetine and its active metabolite, at least five weeks (perhaps longer, especially if fluoxetine has been prescribed chronically and/or at higher doses) should elapse between discontinuation of fluoxetine and initiation of treatment with ELDEPRYL.
    All mostly meaningless for a healthy adult. Those are side effects reported from people with health conditions most if not all also on several other drugs.

    Deprenyl is highly recommended by some of the world's best experts in health namely LEF and A4M.

    You may want to do some reading on it.

    Posting drug interactions information has no bearing on the safety of the drug. As I could post lists for nearly every supplement on BB that could have a drug interaction.

    Also healthy adults do not require the doses used in disorders. It would be unreasonable to expect the same side effects of a drug at lower doses commonly used by healthy adults as an antiaging drug.
    Last edited by CognitiveNutrition; 09-12-2008 at 09:12 AM.
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    When used at "selective MAOI" doses (10 mg /day or less), Deprenyl (selegiline) has an incredibly good safety profile.
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    Registered User Nsaladino's Avatar
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    Originally Posted by Catchol View Post
    When used at "selective MAOI" doses (10 mg /day or less), Deprenyl (selegiline) has an incredibly good safety profile.
    What are the benefits of use in a healthy adult at that dose?
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    Originally Posted by Nsaladino View Post
    What are the benefits of use in a healthy adult at that dose?
    That dose is probably too high for normal, healthy adults.

    I don't feel like writing a novel here, so I'll instead advise you to check out: http://selegiline.com
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    look in to L-tyrosine or L-Dopa for a dopamine boost.

    I like L-Tyro, take it in the morning and pre workout.
    Cant stop, wont stop.
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    is there any supplement out their that is a combination of dopamine and serotonin boosters to help out with brain function?
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    Dorian: Best Mr. O ever SSK1903's Avatar
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    Why is dopamine good for training? To inhibit prolactin relase?


    Should we all just eat a bunch of dark chocolate then?
    Last edited by SSK1903; 09-13-2008 at 02:54 AM.
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    Originally Posted by SSK1903 View Post
    Why is dopamine good for training? To inhibit prolactin relase?


    Should we all just eat a bunch of dark chocolate then?
    Dopamine can raise levels of human growth hormone. If you are taking a supplement such as L-Dopa which is a dopamine precursor, then 500mg-1,000mg at a time will fit your need for raising HGH levels.
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    Originally Posted by Squat2Grow View Post
    Dopamine can raise levels of human growth hormone. If you are taking a supplement such as L-Dopa which is a dopamine precursor, then 500mg-1,000mg at a time will fit your need for raising HGH levels.
    Okkk
    and naturally increasing HGH levels somewhat is beneficially how?
    http://forum.bodybuilding.com/showthread.php?t=6226571
    Last edited by Bane; 09-13-2008 at 09:41 AM.
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    Oh btw


    The effects of vitex agnus castus extract and interaction with bromocriptine on luteinizing hormone and testosterone in male mice



    S.Nasri, PhD 1 Sh.Orian, PhD 2 A.Haeri Rohani, PhD 3 Gh.Amin, PhD 4 M.A.Naghizadeh, MSc 5.

    Assistant professor, Department of Biology, Azad Eslami University Parand branch 1 Full professor, Department of Biology Training & Education University of Tehran 2 Full professor, Department of physiology, Tehran University 3, Assistant professor, Department of pharmacogenozy, Tehran University of Medical Sciences 4, Master of Hematology , Oroomieh Blood Transfusion Organization 5.



    ABSTRACT

    Introduction: Several clinical studies have confirmed the beneficial effect of plants extracts in the treatment of disorders. The purpose of this study was to evaluate the probable effects of vitex agnus?castus (VAC) on the male reproductive physiology, and also the dopaminergic agonist (Bromocriptine) on male mice.

    Methods: In this experimental study, in order to evaluate, the medicinal effects of vitex agnus castus, we used the hydroalcoholic VAC. Extract injection with the following doses: 65, 165, 265,365 and 465 mg/kg; bromocriptine as a dopamine agonist receptor (5,10,20 mg/kg). To study the interaction between VAC. Extract and bromocriptine, we injected the optimum doses of VAC. with bromocriptine at the same time. Intraperitoneal injections were applied in all experiments, once a day for 30 days. The control group remained intact and the sham group received vehicle. After the last injection, we collected the animal blood serums for hormonal assays. For statistical analysis, analysis of variance was used and P<0.05 was considered significant.

    Text Box: Correspondence: S.Nasri, PhD. Department of Biology Azad Eslami University parand branch Tehran, Iran Tel: +98 21 8283777 Email: S_nasri2000@yahoo.com


    Results: LH and testostrone showed significant decrease in bromocriptine group. VAC. Extract decreased significantly the LH and Testosterone levels. The coadministration of VAC. Extract and bromocriptine decreased LH and testosterone.

    Conclusion: These results suggest: Dopamine regulates the gonadotroph ? Leyding cells axis. It appears that VAC. Extract effects through dopaminergic system and other pathways.
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    Originally Posted by SSK1903 View Post
    Why is dopamine good for training? To inhibit prolactin relase?


    Should we all just eat a bunch of dark chocolate then?
    Dopamine is highly expressed in a wide-range of physiological processes: Mood, memory, motor function, libido and so on.

    In terms of memory, Dopa., is the primary neurotransmitter responsible for memory consolidation (at least networked consolidation); this is, theoretically, the consolidation of episodic short-term memory from the hippocampus, to the PFC (specifically, the neocortex). I feel that when dosing L-DOPA containing products, the transmission of compartmentalized sense datum to coherent episodic memory is expedited and less vague, and that recall is increased over chronic administration. Now, increased REM sleep may have an additive effect on memory consolidation, but the Dopaminergic pathway of mTOR and protein synthesis exerts the primary effect on memory consolidation. The effect is not secondary, but rather, primary through the Dopaminergic pathway.

    Further, clinical trials using Dopamine replacement displayed acute increases in both peak torque production, as well as acute increases in EMG amplitude; suggesting that Dopamine agonism exerts direct effects on the contractile strength of striated muscle tissue. In addition, these observations were noted across muscle and movement types.

    Now, this has not as of yet mentioned the prolactin-inhibition mediated increases in Testosterone production via L-DOPA. Obviously, however, the beneficial effects therein are self evident and do not require any extrapolation. More research in normal, healthy patients would need to be conducted to elucidate a strong basis on which to make that claim for the general population.

    In my opinion, if the application is correct, increasing Dopaminergic transmission is a beneficial addition to training and nutrition.
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    taurine

    It's benefits aren't related to merely this but one of the possible effects of taurine is that it may raise dopamine levels in the nucleus accumbens. The part of the brain responsible for pleasure and reward.

    Mostly taurine has an inhibitory effect among other good protective effects.


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