Curving of the penile shaft – fixed?

Curving of the penile shaft - fixed?

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It’s called penile fibrosis and this recent discovery might fix it…

——Important Message—–

“Why is your testosterone so high?”

The doctor crossed out the chemicals I was taking with a big line…

Testosterone injections.

Ron knew why his testosterone got so high…

…and he didn’t have to take any injection or Big Pharma chemicals.

The 29-year-old doctor shrugged. “I’ve never seen a man your age with so much testosterone. Your levels are higher than mine!”

Ron’s testosterone shot higher thanks to a strange natural brew he’s been drinking in the mornings.

Ron wasn’t even in good shape…nope…his newly discovered manliness was all from this strange natural brew…

Ron told his 29-year-old doctor about this brew and warned him:

“It’s a bit bitter, son.”

Here’s what Ron has to say about this strange natural brew:

Here’s the strange brew that sent Ron’s testosterone skyrocketing.

—————–

Curving of the penile shaft – fixed?

Fibrosis is one of the body’s responses to injury.

After trauma, the body produces an excess of connective tissue that leads to scarring.

When fibrotic scar tissue becomes excessive it can invade and destroy organs.

Fibrotic diseases like liver cirrhosis, heart attack, atrial fibrosis, and Crohn’s disease affect hundreds of millions worldwide.

Now scientists have made a major breakthrough in discovering one of the causes of pathological fibrosis.

This groundbreaking study was conducted at Duke University in the United States and recruited experts from around the globe.

Previously, scientists identified a protein known as transforming growth factor beta 12 (TGFB1) as a cause of fibrotic scarring and organ damage.

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Working on the problem, scientists designed drugs to inhibit TGFB1 – in order to prevent the damage caused by pathological fibrosis.

When scientists observed the effect of TGFB1 inhibitors, they found unacceptable side effects from the drugs.

“Transforming growth factor beta 12 (TGFB1) is the principal pro-fibrotic factor – but its inhibition is associated with side effects due to its pleiotropic roles.”

(The side effects were due pleiotropy – a process affecting many genes – the drug or target was not specific enough.)

Looking for another solution, the researchers decided to take a step downstream from TGFB1.

They decided to take a look at some of its metabolites.

The scientists investigated fibroblasts for clues.

Fibroblasts are cells that synthesize collagen and create the structural framework involved in healing – they’re also critical to fibrosis.

That’s when they found it – scientists identified Interleukin 11 (IL-11) as the important fibrotic agent affected by TGFB1.

“Using advanced imaging of primary human fibroblasts, we found that Interleukin 11 (IL11) upregulation is the dominant transcriptional response to transforming growth factor beta 12 exposure and required for its profibrotic effect.”

Transforming growth factor beta 12 is completely dependent on Interleukin 11 to create fibrosis.

Interleukin 11 and its receptor IL11RA (Interleukin 11 receptor subunit alpha) were found to be extremely active in fibrotic tissue and required for the production of fibrotic protein.

“Interleukin 11 and its receptor (IL11RA) are expressed specifically in fibroblasts where they are required for fibrogenic protein synthesis.”

Further investigation showed that injecting mice with Interleukin 11 caused fibrotic diseases and related organ failure.

“In mice, fibroblast-specific Interleukin 11 transgene expression or Interleukin 11 injection causes heart and kidney fibrosis and organ failure.”

Mice who were deficient in the Interleukin 11 receptor were protected from fibrotic diseases.

The Interleukin 11 protein acts on the receptor to create the fibrotic effect (no receptor = no fibrosis).

“In mice, deletion of the Interleukin 11 receptor is protective against fibrotic disease.”

This discovery shows that Interleukin 11 is responsible for the fibrotic response that causes the pathological changes that result in organ failure.

“Thus, inhibition of Interleukin 11 prevents fibroblast activation across organs and species in response to a range of important pro-fibrotic stimuli.”

In the future, scientists will investigate Interleukin 11 inhibitors.

In order to prevent fibrotic disease, we could develop drugs to block Interleukin 11 or its receptor.

“These data reveal a central role of Interleukin 11 in fibrosis and we propose inhibition of Interleukin 11 as a new therapeutic strategy to treat fibrotic diseases.”

Hopefully, this newly identified cause of fibrosis can be selectively and safely inhibited – potentially saving hundreds of millions of lives.

Though it’s still early days in investigating the inhibition of Interleukin 11…

Scientists believe that Interleukin 11 is a much safer drug target than transforming growth factor beta 12 (TGFB1).

Fibrosis is the response to injury that occurs in any tissue – so it can affect every tissue.

Pathological fibrosis is involved in heart disease, liver cirrhosis, and kidney failure, but its effects are much more widespread…

Some of the common diseases caused by pathological fibrosis include:

  • Atrial fibrosis (heart)
  • Endomyocardial fibrosis (heart)
  • Old myocardial infarction (heart)
  • Glial scarring (nervous system)
  • Arterial stiffness
  • Arthrofibrosis (knee, shoulder, other joints)
  • Crohn’s disease (intestine)
  • Pulmonary fibrosis (lungs)
  • Cystic fibrosis (several organs)
  • Idiopathic pulmonary fibrosis (idiopathic meaning the cause is unknown)
  • Radiation-induced lung injury following treatment for cancer
  • Liver cirrhosis
  • Biliary atresia (liver and bile ducts – infants)
  • Dupuytren’s contracture (hands, fingers)
  • Keloid (skin)
  • Mediastinal fibrosis (soft tissue of the mediastinum)
  • Myelofibrosis (bone marrow)
  • Peyronie’s disease (penis)
  • Nephrogenic systemic fibrosis (skin)
  • Progressive massive fibrosis (lungs) – a complication of coal workers’ pneumoconiosis
  • Retroperitoneal fibrosis (soft tissue of the retroperitoneum)
  • Scleroderma/systemic sclerosis (skin, lungs)
  • Some forms of adhesive capsulitis (shoulder)

This exciting discovery about Interleukin 11 could be beneficial to many, many people.

You should see your healthcare professional about any suspected health problems.

—-Keep reading for the fibrosis fix. Important Message—-

Reverse penile fibrosis – here’s how…

The effort can go a very long way, and it’s a simple process.

You can take things like aspirin, caffeine, cyproheptadine antihistamine, and vitamin E.

These can all help reverse fibrosis, most of all penile fibrosis.

And here’s the best treatment – a deep cleansing of the penile chambers with this simple daily shake…

This simple shake reduces fibrosis…it runs through the penile chambers and dissolves any plaque, scarring, and blockage…

As a result, you end up with clean and sensitive nerve endings that feel every touch again.

Even if you haven’t had decent erections in a while, you may be able to restore the health of your penis and make it fatter, bigger…and work better…by ending penile fibrosis.

Here’s a natural and easy way to deep cleanse your penile chambers of fibrosis and restore great erections…even get bigger!

———-

 

 

 


Matt Cook is editor-in-chief of Daily Medical Discoveries. Matt has been a full time health researcher for 26 years. ABC News interviewed Matt on sexual health issues not long ago. Matt is widely quoted on over 1,000,000 websites. He has over 300,000 daily newsletter readers. Daily Medical Discoveries finds hidden, buried or ignored medical studies through the lens of 100 years of proven science. Matt heads up the editorial team of scientists and health researchers. Each discovery is based upon primary studies from peer reviewed science sources following the Daily Medical Discoveries 7 Step Process to ensure accuracy.
IL11 is a crucial determinant of cardiovascular fibrosis https://www.nature.com/articles/nature24676

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