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Clonidine - From Grow-er To Show-er?

Discussion in 'Clonidine' started by nullredvector, Feb 2, 2016.

  1. nullredvector

    nullredvector Member

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    I have some clonidine and I have been hesitant to take it because of the possible ED. I have high blood pressure - probably a compensatory mechanism against endotoxemia induced hypotension. Now I was doing some googling and I came across this guy's experience with clonidine (he was also on some other meds that might have had something to do with it).

    I am wondering about other's experience to clonidine as is related to ED - TIA.

    'It's gone from grow to show,' and other odd penis behavior...
    This is the first time I've seen a physiological explanation for the grower/shower phenomena.
     
  2. Dragon

    Dragon Member

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    if it helps....here's some clonidine info I have.

    Over the years, I've collected several thousand copy/pastes of things that struck me as significant about many different pharmas and herbs. These notes are almost all from journal papers and sci. textbooks.

    Here are the notes I have on Clonidine for ya. All these notes/quotes are from papers in sci. journals, not bloggers or 'coaches' or whatever. If something is my own thoughts/words, I'll say so, like 'dragon sez;' or whatever.

    fwiw, I am not a fan of Clonidine at all. I once used it for a time (weeks) and I did not like how my psyche felt to me. 'vague' or 'erased' would be the best words for it maybe.

    I wouldn't use clonidine again, except as a very short-term protocol if a certain healing specifically requires it. Although a few people say it hasn't bothered their sex, it's definitely an anti-sexual compound for the majority of people.

    Bear in mind that virtually all the drugs which are (factually) known to enhance sexuality are alpha-2 receptor ANTagonists...and clonidine is OPPOSITE to that....it's an agonist.

    ps; anxiety/excess-adrenaline is one of the surest killers of sexuality, so if the Clonidine 'cures' that for someone, perhaps it might actually help their sexuality, and thus the few 'contrary' reports we see of "helping libido". But in the medical community, it's commonly thought of as causing sexual dysfunction.

    ps; in re; your high blood pressure, and the matter of erection hardness....
    So long as 'high blood pressure' isn't TOO high...I wouldn't work real hard on lowering it as much as possible.
    Erection hardness/rigidity is directly proportional to your Systolic blood pressure. On top of that pressure, the perineal muscles add additional pressure, but that's proportional to what your systolic BP did for you in the first place. So, for 'rock hard', you want your systolic BP as high as can still be considered 'healthy'. E.g., see....

    Prog Urol. 1992 Feb;2(1):119-27.
    [The physiology of penile rigidity]
    Lavoisier P, Aloui R, Iwaz J, Kokkidis MJ.
    Centre de Recherche sur les Dysfonctions Sexuelles, Clinique Saint-Maurice, Lyon

    pps; note that -many- anti-hypertensives are anti-erectile and/or anti-libido.

    CCB's which cross the BBB are generally anti-erectile....which is a shame, because a few of them (like e.g. Nimodipine) are very healthy for our brain and cerebrovascular health. Conversely, the peripherally-acting Nifedipine is generally sex-neutral.

    Almost all Beta-Blockers are anti-erectile. Nebivolol and Carvedilol might be ok/neutral. Neb. is actually an NO-donor, and Carv. is just plain weird..lol...it seems to work quite differently than other BB's.

    ACE-inhibitors and ARB's are NOT interchangeable, even though the vast majority of 'doctors' will tell you so. They act quite differently and have very different side-effect profiles (arb's essentially have NO sides).

    I much prefer ARB's. They are one of the only classes of drugs which have essentially ZERO side-effects. In fact, an ARB won't even lower your BP if it isn't actually high!
    Losartan, first of the class, also has many healing effects beyond just CV health. Telmisartan is the only sartan that crosses the BBB in useful quantity; and has positive effects on brain health, and cognition/mood. To my knowledge, all the ARB's are sexuality-neutral, or possibly slightly positive (ARBs are effectively anti-inflammatory, and inflammation is an erection-killer)

    In some situations, an ACEi might be preferred....to actually reduce the quantity of AC enzyme, rather than just block its receptors. But most ACEi's give you a dry hacking cough all the time, and other sides. In any case, they're generally sexuality-neutral as well.

    ok, here are the clonidine notes...
    --------------
    --------------
    Clonidine- inhibited sexual activity in rats when administered systemically
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    Intraperitoneal injection of fraction F(3-5) (25 and 50mg/kg) elicited all the three different behavioral responses in a manner similar to yohimbine (2mg/kg, i.p.), a known indole alkaloid. Seventy-five percent of mice treated with yohimbine or F(3-5) showed penile erections, which were completely blocked by clonidine, an alpha-2-adrenoceptor agonist and haloperidol, a dopaminergic antagonist and as well as by l-NAME, a nitric oxide synthase inhibitor."
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    Clonidine can significantly inhibit subjective and physiological sexual arousal in women
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    J Toxicol Sci. 1992 May;17(2):41-50.
    Disturbance or relatively important actions of antihypertensives, antifungal agent and opiate antagonist to the testicular steroidogenesis in rat.
    Masubuchi Y, Akaike M, Kumai T, Tanaka M, Watanabe M, Hirai M.
    ...Then, incubation was made with prazosin (1 micrograms), clonidine (5 micrograms), verapamil (10 micrograms), naloxone (5 micrograms) and ketoconazole (150 micrograms), 37 degrees C for 180 min in fresh KRP-buffer, respectively. Steroids were analysed with RIA, and microfluorometry after purification with quantitative thin layer chromatography.
    Prazosin had a tendency to produce dihydrotestosterone (DHT) indicating a facilitation of 5 alpha-reductase, and
    clonidine showed a significant production of estradiol (E2) with a slight production of DHT indicating a significant facilitation of aromatase.
    Verapamil had a action to produce significantly E2 with a slight production of DHT, and
    naloxone showed a significant production of both DHT and E2. Thus, these two agents showed facilitation of both 5 alpha-reductase and aromatase.
    Ketoconazole had a significant production of both delta 4-androstenedione (delta 4-A) and E2 while it had a significant inhibition of DHT-production, thus this had a significant production of both aromatase and C17,20-lyase while had a significant inhibitory action of 5 alpha-reductase.
    These findings indicates that comparatively large doses of central-nervous system depressants are one of the factors that interfere with sexual function, but it is not necessary to have direct action to testicular function, however present study revealed that some of them can cause gonadal damage and consequently progressive loss of libido.
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    The 5HT antagonists metergoline and methysergide blocked the apomorphine-induced penile erections without affecting the yawning response.
    The alpha 2-adrenoceptor agonist clonidine, the dopamine antagonist sulpiride, the antihistaminic mepyramine and the benzodiazepine chlordiazepoxide inhibited both yawning and penile erections at the same dose level. The alpha 1-adrenoceptor antagonists prazosin and phenoxybenzamine were inactive.

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    good fortune to you,

    Dragon
     
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