The Official Hard Flaccid Recovery Thread
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Obitoo- did u tell your therapist about your issue? How often do u see your therapist. How much do they charge? Does this help ppl who got this probl from over stretching?
The people who said that were the techs at the vascular lab. They can't write prescriptions for anything.
All Osteos in the US are MDs, they have to be. This rule doesn't exist in all other countries though.
I go to PT once per week. The other six days a week I do it at home, 3 times a day.
Never went into hard flaccid with the PT yet.
No one knows why hard flaccid exists.
It helps people who have pelvic floor problems, hard flaccid or not. For me it does seem to be helping with that though, and others have reported the same.
Came across a case of what very much sounds a hell of a lot like hard flaccid, induced by taking Adderall. Adderall is a stimulant that effects the sympathetic nervous system. It inhibits dopamine and cranks up norepinephrine, which would explain why my doctor thought alpha blockers would help. Worth noting though that some people with hard flaccid have reported improvement with alpha blockers.
Just thought it was interesting and worth looking at.
Adderall and effects on erections and libido - ADD Forums - Attention Deficit Hyperactivity Disorder Support and Information Resources Community
Just thought it was interesting and worth looking at.
Adderall and effects on erections and libido - ADD Forums - Attention Deficit Hyperactivity Disorder Support and Information Resources Community
That is so wierd obitoo. I took adderall, unprescribed (stupid I know), 30 mg, the day hard flaccid occured. First (and last) time I had ever taken it.
Interesting. Found this comment in the thread curious too... "HIgh norepinephrine = soft wood, high sex drive, automatic uncontrolled ejaculation. Even just standing around...."
Adderall is renown for shrinking penises though, and I think that is more what this man is talking about. I remember looking at my penis after taking adderall, but before getting hard flaccid, and I was thinking wow this is like it has no blood in it. I yahoo answered it, and it seems as if there are a million differnt questions about adderall shrinking the penis. So it definitly Shrinks it, but I dont know if it CAUSES hard flaccid. I also noticed that my penis went back to semi normal length after the adderall wore off after I had gotten hard flaccid, when I initially thought that the hard flaccid was causing my penis to be 1 inch long (literally). And theres also something called speed dick, which makes for someones inability to maintain an erection while under the influence of amphetamines, which is the class adderall belongs too.
My first assumption was that aderall caused hard flaccid, and many people said that they have hard flaccid under the influence of adderall, but once it wares off it is gone. Adderall decreases blood flow, so that would make sense. Mine didn't go away. There was still the specific point of injury though, I really do believe it was purely coincidental. While the adderall played a role possibly, I dont believe it caused it directly. Like had I not been masturbating forcefully, I don't think the adderall wouldve given me this permanent hard flaccid. "After one day or so it goes back to normal" says the guy in the link. I do think hes experiencing the same problem of lack of blood flow, just not caused by an actual injury, rather the vascoconstriction of vessels by amphetamines.
My first assumption was that aderall caused hard flaccid, and many people said that they have hard flaccid under the influence of adderall, but once it wares off it is gone. Adderall decreases blood flow, so that would make sense. Mine didn't go away. There was still the specific point of injury though, I really do believe it was purely coincidental. While the adderall played a role possibly, I dont believe it caused it directly. Like had I not been masturbating forcefully, I don't think the adderall wouldve given me this permanent hard flaccid. "After one day or so it goes back to normal" says the guy in the link. I do think hes experiencing the same problem of lack of blood flow, just not caused by an actual injury, rather the vascoconstriction of vessels by amphetamines.
Its my belief that if anything, the adderall does not cause temporary hard flaccid by norepinephrine, but just by the fact that theres extreme constriction of blood vessels when on it. I also noticed my hands and feet became extremely cold. It is terrible for circulation.
Copied and pasted from this thread at Thunder's... Beware, lots of science and big words ahead.
Appendix by Dr. Owens: Physiological cellular events during arousal/erections:
The smooth muscle cells in segments of the penis (corpora cavernosa) can either 1) relax, thereby allowing increased blood flow to the penis, or tumescence, or they can 2) contract, resulting in detumescence, or the flaccid state of the penis. Both events may be initiated in different ways, and it is ultimately the degree of contraction or relaxation of these smooth muscle cells that determines whether the penis is flaccid or erect.
Nerves to the penis release the neurotransmitter noradrenaline (a catecholamine), causing stimulation of alpha-receptors on the surface of adjacent smooth muscle cells. This leads to smooth muscle cell contraction, allowing only limited blood flow into the penis, which is now in the flaccid state, or undergoes detumescence if it was previously erect. Catecholamines can also be released during stressful situations associated with sexual activity such as fear of failure, performance anxiety, anger, shame, or embarrassment (Goldstein, 2000). Or they may be released in painful situations such as genital pain from infection of the prostate, epididymitis, and Peyronie’s disease, or non-genital pain such as headache (Goldstein, 2000). In either case, smooth muscle cells are stimulated to contract, resulting in reduced blood flow to the penis and detumescence.
To complicate matters further, different types of alpha-receptors (alpha-1 and alpha-2-subtypes) are located not only on the smooth muscle cells, but also directly adjacent on the nerve-buds, from where catecholamines and other neurotransmitters are released. From this location alpha-receptors modify how much of the transmitter substance is released from the nerves, and then reaches the smooth muscle cells (Crenshaw and Goldberg, 1996).
By blocking alpha-receptors on the smooth muscle cells with drugs like phentolamine (Regitine, Vasomax, mentioned on page 136), contraction of the smooth muscle cells can be prevented or at least reduced, allowing an erection to persist longer. This is why the drug phentolamine is effective in the treatment of ED and is currently being tested for possible FDA-approval as such a treatment option (Goldstein, 2000). The drug is already used as a blood pressure lowering medication for people with pheochromocytoma, a condition where excess catecholamines are produced in the body.
Alpha-2-receptors are blocked by Yohimbine, an alkaloid obtained from the bark of the African tree, Coryanthe yohimbe (Crenshaw and Goldberg, 1996; Morales, 2000). For over a century Yohimbine has been used as an aphrodisiac, and only recently has it become clear that Yohimbine has central effects (in the brain), increasing sexual arousal, as well as peripheral effects, blocking the catecholamine induced contractility in the smooth muscle of the penis (Bancroft, 2000). Alpha-2 receptors are located throughout the body on blood vessels and in the intestines as well, which explains some of the side effects (indigestion, nausea, dizziness, headache) experienced following the intake of Yohimbine (Crenshaw and Goldberg, 1996).
There are other ways smooth muscle cells in the penis can relax, resulting in an erection: During sexual arousal penile nerves release nitric oxide (NO), which activates the smooth muscle cells to release the messenger cyclic guanosine monophosphate (cGMP) inside the cells. It is this messenger signal which tells the contractile proteins inside the smooth muscle cells to stop contracting and to relax. The more of the messenger cGMP that is available inside the cells, the more they relax, and the more blood is channeled to the penis through widened pass ways, causing tumescence and erection.
Viagra enhances erections by increasing cGMP levels in erectile tissue smooth muscle cells. It increases the amount of intracellular cGMP by inhibiting its breakdown through the enzyme type 5 phosphodiesterase (PDE 5). Viagra only works in men who are sexually aroused (take a Viagra, mow the lawn, and nothing happens) and who produce some cGMP on their own. The drug can enhance a minor erection by making sure that the cGMP produced stays around in the cells for a while longer, instead of being removed by PDE 5. For men taking heart medication such as nitrates, Viagra can fatally potentiate the medicine effect and the cGMP released upon medicine intake may be increased to dangerous levels, causing a potentially deadly drop in blood pressure. It is important to emphasize that this only applies to situations where men take Viagra while simultaneously being on nitrates, and that Viagra otherwise is a safe drug to use. It is of utmost importance that Viagra is prescribed by a doctor and is not shared or taken without a doctor’s consent.
References:
Bancroft, J. (2000) Effects of alpha-2 blockade on sexual response: experimental studies with Delequamine (RS15385); International Journal of Impotence Research; Vol. 12, Suppl. 1, S64-S69
Crenshaw, T. L. & Goldberg, J. P. (1996) Sexual Pharmacology. Drugs That Affect Sexual Function. W. W. Norton & Company. New York. London; ISBN: 0-393-70144-1
Goldstein, I. (2000) Oral phentolamine: an alpha-1, alpha-2 adrenergic antagonist for the treatment of erectile dysfunction; International Journal of Impotence Research; Vol. 12, Suppl. 1, S75-S80
Morales, A. (2000) Yohimbine in erectile dysfunction: the facts; International Journal of Impotence Research; Vol. 12, Suppl. 1, S70-S74
Muller, J.E. et al. (1996) Triggering myocardial infarction by sexual activity. Low absolute risk and prevention by regular physical exertion; Journal of the American Medical Association; 275, 1405-1409
EJHS Book Review
----------------------------------------------------------
Anatomy of the Human Penis: The Relationship of the Architecture Between Skeletal and Smooth Muscles
GENG-LONG HSU*,{dagger}, CHENG-HSING HSIEH*, HSIEN-SHENG WEN*, WEN-LONG HSU*, CHIH-HSIUNG WU*, TSORNG-HARN FONG{ddagger}, SHYH-CHYAN CHEN{dagger} AND GUO-FANG TSENG{dagger}
From the * Microsurgical Potency Reconstruction Center, Taiwan Adventist Hospital, Taipei Medical University Hospital, the {ddagger} Department of Anatomy, College of Medicine, Taipei Medical University, and the {dagger} Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan, Republic of China.
Correspondence to: Dr Geng-Long Hsu, Microsurgical Potency Reconstruction Center, Taiwan Adventist Hospital, 424 Pa-Te Rd, Sec 2, Taipei 10558, Taiwan, Republic of China (e-mail: [email protected]).
To investigate the anatomy of the ischiocavernosus muscle, bulbospongiosus muscle, and tunica albuginea and to determine their relationships to smooth muscle, which is a key element of penile sinusoids, we performed cadaveric dissection and histologic examinations of 35 adult human male cadavers. The tunica of the corpora cavernosa is a bilayered structure that can be divided into an inner circular layer and an outer longitudinal layer. The outer longitudinal layer is an incomplete coat that is absent between the 5-o'clock and 7-o'clock positions where 2 triangular ligamentous structures form. These structures, termed the ventral thickening, are a continuation of the anterior fibers of the left and right bulbospongiosus muscles. On the dorsal aspect, between the 1-o'clock and 11-o'clock positions, is a region called the dorsal thickening, a radiating aspect of the bilateral ischiocavernosus muscles. In the corpora cavernosa, skeletal muscle contains and supports smooth muscle, which is an essential element in the sinusoids. This relationship plays an important part in the blood vessels' ability to supply the blood to meet the requirements for erection, whereas in the corpus spongiosum, skeletal muscle partially entraps the smooth muscle to allow ejaculation when erect. In the glans penis, however, the distal ligament, a continuation of the outer longitudinal layer of the tunica, is arranged centrally and acts as a trunk of the glans penis. Without this strong ligament, the glans would be too weak to bear the buckling pressure generated during coitus. A significant difference exists in the thickness of the dorsal thickening, the ventral thickening, and the distal ligament between the potent and impotent groups (P <= .01). Together, the anatomic relationships between skeletal muscle and smooth muscle within the human penis explain many physiologic phenomena, such as erection, ejaculation, the intracavernous pressure surge during ejaculation, and the pull-back force against the glans penis during anal constriction. This improvement in the modeling of the anatomic-physiologic relationship between these structures has clinical implications for penile surgeries.
Key words: Corpora cavernosa, corpus spongiosum, bulbospongiosus muscle, ischiocavernosus muscle, distal ligament, tunica albuginea
http://www.andrologyjournal.org/cgi...stract/25/3/426
Appendix by Dr. Owens: Physiological cellular events during arousal/erections:
The smooth muscle cells in segments of the penis (corpora cavernosa) can either 1) relax, thereby allowing increased blood flow to the penis, or tumescence, or they can 2) contract, resulting in detumescence, or the flaccid state of the penis. Both events may be initiated in different ways, and it is ultimately the degree of contraction or relaxation of these smooth muscle cells that determines whether the penis is flaccid or erect.
Nerves to the penis release the neurotransmitter noradrenaline (a catecholamine), causing stimulation of alpha-receptors on the surface of adjacent smooth muscle cells. This leads to smooth muscle cell contraction, allowing only limited blood flow into the penis, which is now in the flaccid state, or undergoes detumescence if it was previously erect. Catecholamines can also be released during stressful situations associated with sexual activity such as fear of failure, performance anxiety, anger, shame, or embarrassment (Goldstein, 2000). Or they may be released in painful situations such as genital pain from infection of the prostate, epididymitis, and Peyronie’s disease, or non-genital pain such as headache (Goldstein, 2000). In either case, smooth muscle cells are stimulated to contract, resulting in reduced blood flow to the penis and detumescence.
To complicate matters further, different types of alpha-receptors (alpha-1 and alpha-2-subtypes) are located not only on the smooth muscle cells, but also directly adjacent on the nerve-buds, from where catecholamines and other neurotransmitters are released. From this location alpha-receptors modify how much of the transmitter substance is released from the nerves, and then reaches the smooth muscle cells (Crenshaw and Goldberg, 1996).
By blocking alpha-receptors on the smooth muscle cells with drugs like phentolamine (Regitine, Vasomax, mentioned on page 136), contraction of the smooth muscle cells can be prevented or at least reduced, allowing an erection to persist longer. This is why the drug phentolamine is effective in the treatment of ED and is currently being tested for possible FDA-approval as such a treatment option (Goldstein, 2000). The drug is already used as a blood pressure lowering medication for people with pheochromocytoma, a condition where excess catecholamines are produced in the body.
Alpha-2-receptors are blocked by Yohimbine, an alkaloid obtained from the bark of the African tree, Coryanthe yohimbe (Crenshaw and Goldberg, 1996; Morales, 2000). For over a century Yohimbine has been used as an aphrodisiac, and only recently has it become clear that Yohimbine has central effects (in the brain), increasing sexual arousal, as well as peripheral effects, blocking the catecholamine induced contractility in the smooth muscle of the penis (Bancroft, 2000). Alpha-2 receptors are located throughout the body on blood vessels and in the intestines as well, which explains some of the side effects (indigestion, nausea, dizziness, headache) experienced following the intake of Yohimbine (Crenshaw and Goldberg, 1996).
There are other ways smooth muscle cells in the penis can relax, resulting in an erection: During sexual arousal penile nerves release nitric oxide (NO), which activates the smooth muscle cells to release the messenger cyclic guanosine monophosphate (cGMP) inside the cells. It is this messenger signal which tells the contractile proteins inside the smooth muscle cells to stop contracting and to relax. The more of the messenger cGMP that is available inside the cells, the more they relax, and the more blood is channeled to the penis through widened pass ways, causing tumescence and erection.
Viagra enhances erections by increasing cGMP levels in erectile tissue smooth muscle cells. It increases the amount of intracellular cGMP by inhibiting its breakdown through the enzyme type 5 phosphodiesterase (PDE 5). Viagra only works in men who are sexually aroused (take a Viagra, mow the lawn, and nothing happens) and who produce some cGMP on their own. The drug can enhance a minor erection by making sure that the cGMP produced stays around in the cells for a while longer, instead of being removed by PDE 5. For men taking heart medication such as nitrates, Viagra can fatally potentiate the medicine effect and the cGMP released upon medicine intake may be increased to dangerous levels, causing a potentially deadly drop in blood pressure. It is important to emphasize that this only applies to situations where men take Viagra while simultaneously being on nitrates, and that Viagra otherwise is a safe drug to use. It is of utmost importance that Viagra is prescribed by a doctor and is not shared or taken without a doctor’s consent.
References:
Bancroft, J. (2000) Effects of alpha-2 blockade on sexual response: experimental studies with Delequamine (RS15385); International Journal of Impotence Research; Vol. 12, Suppl. 1, S64-S69
Crenshaw, T. L. & Goldberg, J. P. (1996) Sexual Pharmacology. Drugs That Affect Sexual Function. W. W. Norton & Company. New York. London; ISBN: 0-393-70144-1
Goldstein, I. (2000) Oral phentolamine: an alpha-1, alpha-2 adrenergic antagonist for the treatment of erectile dysfunction; International Journal of Impotence Research; Vol. 12, Suppl. 1, S75-S80
Morales, A. (2000) Yohimbine in erectile dysfunction: the facts; International Journal of Impotence Research; Vol. 12, Suppl. 1, S70-S74
Muller, J.E. et al. (1996) Triggering myocardial infarction by sexual activity. Low absolute risk and prevention by regular physical exertion; Journal of the American Medical Association; 275, 1405-1409
EJHS Book Review
----------------------------------------------------------
Anatomy of the Human Penis: The Relationship of the Architecture Between Skeletal and Smooth Muscles
GENG-LONG HSU*,{dagger}, CHENG-HSING HSIEH*, HSIEN-SHENG WEN*, WEN-LONG HSU*, CHIH-HSIUNG WU*, TSORNG-HARN FONG{ddagger}, SHYH-CHYAN CHEN{dagger} AND GUO-FANG TSENG{dagger}
From the * Microsurgical Potency Reconstruction Center, Taiwan Adventist Hospital, Taipei Medical University Hospital, the {ddagger} Department of Anatomy, College of Medicine, Taipei Medical University, and the {dagger} Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan, Republic of China.
Correspondence to: Dr Geng-Long Hsu, Microsurgical Potency Reconstruction Center, Taiwan Adventist Hospital, 424 Pa-Te Rd, Sec 2, Taipei 10558, Taiwan, Republic of China (e-mail: [email protected]).
To investigate the anatomy of the ischiocavernosus muscle, bulbospongiosus muscle, and tunica albuginea and to determine their relationships to smooth muscle, which is a key element of penile sinusoids, we performed cadaveric dissection and histologic examinations of 35 adult human male cadavers. The tunica of the corpora cavernosa is a bilayered structure that can be divided into an inner circular layer and an outer longitudinal layer. The outer longitudinal layer is an incomplete coat that is absent between the 5-o'clock and 7-o'clock positions where 2 triangular ligamentous structures form. These structures, termed the ventral thickening, are a continuation of the anterior fibers of the left and right bulbospongiosus muscles. On the dorsal aspect, between the 1-o'clock and 11-o'clock positions, is a region called the dorsal thickening, a radiating aspect of the bilateral ischiocavernosus muscles. In the corpora cavernosa, skeletal muscle contains and supports smooth muscle, which is an essential element in the sinusoids. This relationship plays an important part in the blood vessels' ability to supply the blood to meet the requirements for erection, whereas in the corpus spongiosum, skeletal muscle partially entraps the smooth muscle to allow ejaculation when erect. In the glans penis, however, the distal ligament, a continuation of the outer longitudinal layer of the tunica, is arranged centrally and acts as a trunk of the glans penis. Without this strong ligament, the glans would be too weak to bear the buckling pressure generated during coitus. A significant difference exists in the thickness of the dorsal thickening, the ventral thickening, and the distal ligament between the potent and impotent groups (P <= .01). Together, the anatomic relationships between skeletal muscle and smooth muscle within the human penis explain many physiologic phenomena, such as erection, ejaculation, the intracavernous pressure surge during ejaculation, and the pull-back force against the glans penis during anal constriction. This improvement in the modeling of the anatomic-physiologic relationship between these structures has clinical implications for penile surgeries.
Key words: Corpora cavernosa, corpus spongiosum, bulbospongiosus muscle, ischiocavernosus muscle, distal ligament, tunica albuginea
http://www.andrologyjournal.org/cgi...stract/25/3/426
obitoo, when you said you had golfball in the but type pain, was any of that pain around the tailbone. I have pain when I sit now, or do any activity, that feels above my asshole. Like closer to my back. But I am certain its related. Is this where your pain was/is?
Yeah Frenchi found the link of noradrenaline a while ago back on SE forums. Doubt it's a cause to hard flaccid though, increase in anxiety can cause increases in adrenaline which leads to PE/ED issues.
I've noticed though that the biggest issue with me is that whenever I have any sexual stimulation around the glans, a muscle right below the scrotum contracts, it's sort of deeper in and impossible to get at. I feel like it's the sole cause for my hard flaccid, I can make everything else relax except the muscles in behind the scrotum area. It just contracts by itself most of the time, making my glans much more sensitive. It's weird, and I don't know how to release it, after all these months it seems like ive been able to release almost all the muscles down there except for that one clump in behind there, it's too difficult to externally massage as bone sort of blocks it, maybe there's a way to get at it internally, it would be pretty far up though.
I've noticed though that the biggest issue with me is that whenever I have any sexual stimulation around the glans, a muscle right below the scrotum contracts, it's sort of deeper in and impossible to get at. I feel like it's the sole cause for my hard flaccid, I can make everything else relax except the muscles in behind the scrotum area. It just contracts by itself most of the time, making my glans much more sensitive. It's weird, and I don't know how to release it, after all these months it seems like ive been able to release almost all the muscles down there except for that one clump in behind there, it's too difficult to externally massage as bone sort of blocks it, maybe there's a way to get at it internally, it would be pretty far up though.
Yep, my tailbone is where most of the pain in concentrated. Golf ball in the butt was more when the alpha blockers were taking effect. Tailbone just feels incredibly sore and like the muscles around it are just pulling like crazy. Certain stretches help with it but it's time to get the actual bone massaged. Don't try to do it yourself. I've tried and I hurt myself every time. Let a PT do it properly. Requires a finger in the butt of course.
I know what you are referring to. I feel a tightness/burning in it all the time. The PT definitely helps and I can feel it very slowly loosening itself, that's the burning part. Did you experience the "paralyzed" perineum when HF first hit you? Do you have the dent on the underside of the shaft? Not sure that's related at all, but I'm putting together a chart of similar cases.
I occasionally get a subtle burning sensation, deep within my rectum. Definately from the prostate area. I just got one of those ring cushions to take the pressure off while I'm sitting, as being seated for an extended period makes it worse, all the way through the tailbone area as well. I suggest you guys get one of these inflatable cushions also. There only like $6-7 shipped on eBay.
INVALID RING INFLATABLE DONUT CUSHION 17X15 1/Each - eBay (item 280655325549 end time May-05-11 12:21:16 PDT)
INVALID RING INFLATABLE DONUT CUSHION 17X15 1/Each - eBay (item 280655325549 end time May-05-11 12:21:16 PDT)
What caught my attention most is the link to a prolonged build up of it being secreted from epididymitis or prostatitis, of which I had both for a long time. I had a good two months straight of non-stop physical stress (pain) in the testicles and prostate area. If it's not thee cause, it might be keeping it around. I've got no doubt that my stress hormones were through the roof, and I probably depleted myself of a lot of my cortisol. I know that no matter what is going on, I need to undo this stress ASAP, whether it cures HF or not. Yoga Nidra meditation really helps.
For a good laugh, I picked up a self-hypnosis program that is supposed to be designed to reset the HPA axis. It says it's for people with IBS, but it's just targeting the adrenal/cortisol/inflammation system. I don't think it will do anything, but I'm bored.
So, in summary, WHAT techniques/foods etc etc improve the hard flaccid condition?
Im trying to summarize it myself...but going back and forth on nearly a thousand posts, ive found myself lost :/
Maybe its a good new post to post on the hardflaccid.org, saves the new people from havin to go back and read all the posts
Also obitoo, whats the progress of gettin the forum up and running on your site?
Im trying to summarize it myself...but going back and forth on nearly a thousand posts, ive found myself lost :/
Maybe its a good new post to post on the hardflaccid.org, saves the new people from havin to go back and read all the posts
Also obitoo, whats the progress of gettin the forum up and running on your site?
Yeah, I had the paralyzed sensation for sure, when this all first started my pelvic floor was AWFUL, it was ridiculous, one day for an hour I was literally fully clenched and could not unclench the pelvic floor.
I know pelvic floor is responsible, it's just a question of whether or not it's because of lack of blood flow, or if its just the muscles themselves. I'm finding it hard to find a PT, I feel like a pelvic floor PT is the key to getting this fixed for me, or at least getting me a hell of a lot closer.
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