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Megalophallus Hypoxia Growth Key.

Originally Posted by RomeoPlus
Ummm, Gomez is a hardcore pumper and Shorty Mac has silicone or something surgically inserted into his dick.

Do you know this for a fact? I don’t understand how both of them resemble the shape of priapism megalophallus exactly (huge bloated MSEG and small normal sized glans). Also they never have fluid buildup. How would Gomez even fit in any pump, his penis hangs down to his knee and is as thick as his arm. Pumping to add a few temporary inches makes since. But you can’t pump any normal penis twice it’s length and 7+ girth with zero signs of fluid.

And there are actually many people who believe shorty mac has sickle cell and has had priapisms. His penis doesn’t look anything like silicone implants. The shape of it is not uniform in the slightest, and the way it widens out at the upper girth and the has a tiny glans wouldn’t make sense. But it’s the exact priapism shape seen in other sickle cell studies.

Originally Posted by Xxxi
Do you know this for a fact? I don’t understand how both of them resemble the shape of priapism megalophallus exactly (huge bloated MSEG and small normal sized glans). Also they never have fluid buildup. How would Gomez even fit in any pump, his penis hangs down to his knee and is as thick as his arm. Pumping to add a few temporary inches makes since. But you can’t pump any normal penis twice it’s length and 7+ girth with zero signs of fluid.

And there are actually many people who believe shorty mac has sickle cell and has had priapisms. His penis doesn’t look anything like silicone implants. The shape of it is not uniform in the slightest, and the way it widens out at the upper girth and the has a tiny glans wouldn’t make sense. But it’s the exact priapism shape seen in other sickle cell studies.

Or he may just have had the fairly common PMMA injections.

are you crazy mate


Then- 5.7 x 4.7 (bpel x mseg)

Now- 7.1 x 5.1 (beg 5.5) // Goal-> 8 x 5.5+

Extender Log 2017

Not sure on the validity, but I’ve heard rumors that Gomez had whatever surgery is involved with cutting the suspensory ligament. On the note of “how would he even pump” all you need is a big enough glass tube and some way to create pressure.

As far as Shorty, if he has sickle cell I’d buy your theory. That said, trying to replicate that seems rather hazardous.

With complete occlusion of blood flow, cell necrosis begins around 18 minutes and progresses exponentially from there. The cells run out of energy and die. If blood flow is not completely deprived, then longer times are possible before necrosis occurs.

In medicine, tourniquets can be used up to 90-120 minutes on lower extremities, and 60-90 minutes on upper extremities. If it’s necessary to go beyond that time frame, they reperfuse the limb (i.e. remove the tourniquet) for 5 minutes out of every 30, or 10 minutes out of every 60. They’ll do these reperfusions starting from the beginning of the surgery if they anticipate the need for a longer tourniquet duration.

But tourniquets allow some blood flow whereas clamping (of the kind that would replicate a megalophallus event) allows almost zero. And even with the standard tourniquet reperfusion procedures, there’s probably some degree of necrosis happening.

The risk of complications goes up the longer the ischemia continues, and some of them are nasty. Nerve cells are particularly susceptible to ischemic injury, and that makes them further susceptible to compression injury from the clamp. Risk of thrombosis (forming blood clots) goes way up over time and can have potentially life threatening side effects if they embolize. Reperfusion injury is another component, when the buildup of metabolites and dead cells becomes so great that oxidation injury happens when fresh blood gets back. Neutrophils infiltrate the entire area in response to the necrotic tissue and kill additional cells that were not yet necrotic from the ischemia alone.

So yes, it’s possible to clamp for 1 to 2 hours without complete loss of your penis. But there will be significant cellular death and high risk of complications from it. There could be a risk of losing it, or permanently compromising functionality even after 30 minutes. There are just so many factors involved, and we’re not doing this in a hospital being monitored by a 5 man surgical team that can respond to complications and monitor the post-ischemic recovery period.

The safest way to pursue the type of growth you’re talking about is clamping for 18 minutes sets with 4 minute breaks.

Maybe the mechanism of priapism induced megalophallus is related to the cellular complications of the ischemic event. Some part of the clean up process in the wake of the ischemic / reperfusion injury allows for greater growth. Or maybe the ischemia potentiates damage to the PE target tissues while the priapism (or clamping) simultaneously provides a very long duration and high intensity stress. But is taking the chance that prolonged ischemia promotes gains really worth the extreme health risks and undeniable cellular damage to the erectile tissues? Our dicks still have to be healthy and working after our gains.

I have to admit I’m interested. In my own clamping regimen, I never go close to 18 minute sets with complete occlusion. Usually the tighter I clamp, the shorter I make the set and fully clamped off sets are no more than 5 minutes. But now i may push the limits a bit. I won’t be guinea-pigging anything beyond 18 minutes though.


Before 5.5" x 4.1" ///////// Now 7.4" x 4.9"

Originally Posted by Xxxi
Hi guys, this is my first post here. I’ve read a lot of deep thinking on this forum as a non-member though, and I’d like to post now and share some thoughts.

So, I’ve been experimenting for a while with the idea of replicating a megalophallus. I know this subject has been talked about many times, but not quite in the way I’m thinking about it. I’ve read every study on priapism and it’s resulting functional megalophallus. While not every priapism produces an incredibly over-grown phallus, it is very possible. And I feel like we can eventually replicate it.

Now, there are two schools of thought regarding megalophallus. Extreme pressure, and hypoxia (blood oxygen deprivation). I firmly believe that pressure is not the true cause of megalophallus because in several studies, the patients extreme growth came in a relatively short time following episodes of hypoxic priapism, there was recorded new healthy bleeding fibrous tissue synthesis, and I think the amount of force you would need to stretch to the extent of the massive gains seen in megalopgallus priapism cases would rupture and tear apart the tunica before it would stretch to that point.

In one study, a penis reduction case actually, the 17 year old developed 10inch girth after only 3 priapisms and the growth was the result of tons of new healthy bleeding tissue formation. The case report even said that this was most likely hypoxia induced growth as hypoxia is known to cause cellular proliferation.

I’ve been basically clamping an erection insanely tight and just letting it sit for a while until it’s purple. This usually takes about 40 minutes. I feel that if I can induce a low oxygen environment in the tissue over and over for short periods of time, I can stimulate tissue growth. However, I’m not sure exactly how long penile tissue can live without oxygen. Obviously I don’t want to kill cells. I just want to deprive them enough to stimulate a little bit of tissue growth at the cellular level. Not tunica stretching force, but rather brand new healthy fibrous tissue growth in the CC like in the case of the 10in girth case.

Any thoughts or input is welcome. Thanks!

I think you have it completely backwards. All case reports on megalophallus that I have read have stipulated very specifically that they were high flow priaptic events, ie there was no hypoxia, there was pressure with a constant stream of highly oxygenated blood.

Could you post the case report you are talking about as this line ‘hypoxia is known to cause cellular proliferation’ is completely opposite to the vast majority of information available. In the majority of cell types, hypoxia shuts down cell proliferation.

ie - Regulation of cell proliferation by hypoxia-inducible factors

For most cell types, hypoxia induces decreased cell proliferation, since an increased number of cells, with a consequent increase in O2 demand, would only exacerbate hypoxic stress. However, certain cell populations maintain cell proliferation in the face of hypoxia. This is a common pathological hallmark of cancers, but can also serve a physiological function, as in the maintenance of stem cell populations that reside in a hypoxic niche.


Starting Stats - 5.5 BPEL x 5.6 EG

Current Stats - 5.7 BPEL x 6.5 EG

Goal - 7 x 6 (with hopefully a large flaccid hang)

Originally Posted by Xxxi
Do you know this for a fact? I don’t understand how both of them resemble the shape of priapism megalophallus exactly (huge bloated MSEG and small normal sized glans). Also they never have fluid buildup. How would Gomez even fit in any pump, his penis hangs down to his knee and is as thick as his arm. Pumping to add a few temporary inches makes since. But you can’t pump any normal penis twice it’s length and 7+ girth with zero signs of fluid.

And there are actually many people who believe shorty mac has sickle cell and has had priapisms. His penis doesn’t look anything like silicone implants. The shape of it is not uniform in the slightest, and the way it widens out at the upper girth and the has a tiny glans wouldn’t make sense. But it’s the exact priapism shape seen in other sickle cell studies.

I can’t state it for a fact, but Gomez has all the signs of hardcore pumping, shape size etc. And I’m sure he pumps before filming because he has that just-pumped look and can’t get real hard. He’s about 9x6.5, maybe 9.5x6.5 based on the few vids i’ve seen. Shorty Mac has a very weird shape with thick opaque shaft skin and a much smaller glans. He looks like pictures I’ve seen of guys with hard inserts like a silicone sleeve.

Sorry to take away from the last 2 good posts re safety etc. My thoughts are that ANY form of restricting oxygen to the penis is a VERY BAD IDEA.

Originally Posted by boner7484
I think you have it completely backwards. All case reports on megalophallus that I have read have stipulated very specifically that they were high flow priaptic events, ie there was no hypoxia, there was pressure with a constant stream of highly oxygenated blood.

Could you post the case report you are talking about as this line ‘hypoxia is known to cause cellular proliferation’ is completely opposite to the vast majority of information available. In the majority of cell types, hypoxia shuts down cell proliferation.

Ie - Regulation of cell proliferation by hypoxia-inducible factors

For most cell types, hypoxia induces decreased cell proliferation, since an increased number of cells, with a consequent increase in O2 demand, would only exacerbate hypoxic stress. However, certain cell populations maintain cell proliferation in the face of hypoxia. This is a common pathological hallmark of cancers, but can also serve a physiological function, as in the maintenance of stem cell populations that reside in a hypoxic niche.

"In this boy’s case, each instance of prolonged reduction in blood circulation caused a serious lack of oxygenation in the surrounding penile tissues, called the corpus cavernosum. His penis began to progressively grow fibrous tissue in response to these episodes, with substantial enlargement and deformity."

—Quote from this article regarding the boy I mentioned with the 10in girth.
https://www.goo gle.com/amp/s/w … ry-grow-up/amp/

"Blood oxygen level-dependent magneticresonance imaging revealed enlarged, hypoxic corpora cavernosa."

—-Quote from megalophallus case
(PDF) Megalophallus as a sequela of priapism in sickle cell anemia: use of blood oxygen level-dependent magnetic resonance imaging | H. Umans - Academia.edu

That’s just two mentions of hypoxia being related to the growth. But sickle cell is known to cause megalophallus as a side effect, and a sickle cell priapism is not high flow. The cells clot and block outflow in the veins, the priapisms are ischemic, painful, and low oxygen.

Originally Posted by Xxxi
"In this boy’s case, each instance of prolonged reduction in blood circulation caused a serious lack of oxygenation in the surrounding penile tissues, called the corpus cavernosum. His penis began to progressively grow fibrous tissue in response to these episodes, with substantial enlargement and deformity."

—Quote from this article regarding the boy I mentioned with the 10in girth.
https://www.goo gle.com/amp/s/w … ry-grow-up/amp/

Fibrous tissue? Deformity? Is that your goal?

Wouldn’t it make more sense (and be safer?) to figure out which chemicals the cells release when they suffer from (mild) hypoxia to cause this potential explosive growth and then inject a bit of that into the CCs?


February '16: 173 mm BPEL (6.81") 132 mm MEG (5.20")

November '18: 190 mm BPEL (7.48") 137 mm MEG (5.39")

Goal: A sustained 7.7" by 5.8" during intercourse

Originally Posted by CrusherBrooks
Wouldn’t it make more sense (and be safer?) to figure out which chemicals the cells release when they suffer from (mild) hypoxia to cause this potential explosive growth and then inject a bit of that into the CCs?

Yes that does make a lot more sense. It would most likely be VEGF. Vascular Endothelial Growth Factor. That is the hormone released that signals to make new blood vessels. TGF-1 would help too. Transforming Growth Factor. But we don’t have access to these injectibles. The androgen receptors in the penis are shut off after puberty so any dht/testosterone steroid wouldn’t work. The closest thing we have access too would be HGH which releases IGF-1. The IGF-1 can stimulate cell proliferation but we have no way of directing it to the penis. HGH releases igf1 from the liver and it is then sent to whatever tissue needs the growth factor. It is systemic. So isolating a high enough concentration in the penis would be incredibly difficult. And all the injectable forms of IGF1 on the market (non-pharma) are junk. So that leaves us with really no good drugs to use to directly grow. Unfortunately. I agree though if we could have access to inject an array of tissue growth factors, PE would be easy, quick, and widely available as a medical service.

Originally Posted by sta-kool
Fibrous tissue? Deformity? Is that your goal?

Well, yes. The priapisms that result in “healthy bleeding fibrous tissue” sound great. And the case said that the penis worked fine. Was just too big to fit in a vagina lol. But yea I would be fine with some extra healthy tissue in there.

And yea deformity means changing the shape. We’re all here trying to deform cells by either lengthening them or stressing them to the point of proliferating them. I mean.. I thought that’s our goal. I don’t know of another growth mechanism other than new tissue growth or cellular changes.

Originally Posted by Xxxi
Yes that does make a lot more sense. It would most likely be VEGF. Vascular Endothelial Growth Factor. That is the hormone released that signals to make new blood vessels. TGF-1 would help too. Transforming Growth Factor. But we don’t have access to these injectibles. The androgen receptors in the penis are shut off after puberty so any dht/testosterone steroid wouldn’t work. The closest thing we have access too would be HGH which releases IGF-1. The IGF-1 can stimulate cell proliferation but we have no way of directing it to the penis. HGH releases igf1 from the liver and it is then sent to whatever tissue needs the growth factor. It is systemic. So isolating a high enough concentration in the penis would be incredibly difficult. And all the injectable forms of IGF1 on the market (non-pharma) are junk. So that leaves us with really no good drugs to use to directly grow. Unfortunately. I agree though if we could have access to inject an array of tissue growth factors, PE would be easy, quick, and widely available as a medical service.

I know this is rather off topic but on the note of HGH, don’t some studies raise the possibility of arginine releasing growth hormone?

Growth hormone, arginine and exercise

http://www.nejm .org/doi/full/1 … 196702232760803

This isn’t along the lines of instant growth from the result of a single event, but if it produces growth hormone could that be a reason why people say it’s a good supp for PE?

The next line of that quote is important.
"Blood oxygen level-dependent magnetic resonance imaging revealed enlarged, hypoxic corpora cavernosa. Megalophallus probably resulted from permanent loss of elasticity of the tunica albuginea due to severe engorgement during the episode of priapism."
- "Megalophallus as a sequela of priapism in sickle cell anemia:" Urology 2000

While I think the main mechanism for priapism gains is indeed the prolonged physical stress on the tunica of the CC’s, there is some merit to the idea that hypoxia promotes hypertrophy.

Here’s one example.
"Hypoxia increases muscle hypertrophy induced by resistance training."
Hypoxia increases muscle hypertrophy induced by resistance training

There are also many articles on the relationship between hypoxia and cardiac hypertrophy.

Here’s a link to a case study on a sickle cell disease patient who developed a functional megalophallus over the course of 7 years of priapisms. From what I understand, it is very likely for patients to get permanent erectile dysfunction in priapisms lasting beyond 2 days, but this guy did not lose any erectile function.

"AN UNUSUAL CASE OF PRIAPISM"
https://www.ncb i.nlm.nih.gov/p … a00281-0075.pdf

" On the one
end of the spectrum [of sickle-cell] is total venous occlusion
resulting in priapism, cavernous ischemia and subsequent
fibrosis, and impotence, and on the other end is
the minimal venous occlusion with no priapism and no
ischemic changes. In the middle of the spectrum, there
appears to be various degrees of partial venous
obstruction, resulting in priapism associated with
adequate oxygenation of the cavernous tissue because
of continued circulation in the presence of incomplete
venous occlusion. Our patient represents such an
example. Furthermore, repeated episodes of mild
hypoxia resulting from the transient partial venous
obstruction in our patient might have been a stimulus
for the hypertrophy of corpora cavernosa, because
hypoxia is known to result in hypertrophy of tissues.4 It
is interesting to note that the penile hypertrophy was
confined to the corpora cavernosa and that the glans and
the corpus spongiosum were of normal size. It is well
known that the latter structures are not involved in
priapism5-7 and hence they are not subjected to hypoxic
stimulus to under hypertrophy."

In other words, he had a moderate ADC style clamp effect going on, or something like a 7/10 erection as opposed to a 10/10. This guy was an exception.

Priapism patients do routinely get permanent erectile dysfunction when the episodes last too long. Here’s the drill for a priapism at the ER - most of these are sickle cell related, or drug use related (erectile enhancement drugs - usually injectibles)

<4 hour - pain relief, hydration, urination, ejaculation, etc is recommended - also recommended to hear toward an ER if getting close to 4 hours.

4-12 hours - drain the blood from the penis with needles and attempt to chemically stop the erection if it was drug induced, repeat over and over again, blood transfusions as necessary

12+ hours - surgery, if they can’t get the CC’s to stop filling, surgical shunt installed to bypass the venous occlusion mechanism (the way we get erections), permanent ED possible

Priapisms lasting 12-48 hours have a high chance of causing permanent ED - and those lasting 48+ hours have a near certainty of causing permanent ED.

It’s not worth the risks in my opinion. But reading about all this does make me feel better about clamping sets up to 18 minutes, and the benefits of wearing a moderate ADC device for several hours at a time.


Before 5.5" x 4.1" ///////// Now 7.4" x 4.9"

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