For as long as I’ve been researching inguinal hernias, the basic message has been pretty simple:

Once you have a hernia, it can’t heal.

The tissue has failed. There’s a hole in the abdominal wall. And the only way to actually fix it is surgery.

If the hernia isn’t bad enough for surgery yet, you may be told to practice “watchful waiting”—basically, keep an eye on it and see what happens.

That’s why a study published in the Journal of Clinical Investigation caught my attention.

Researchers created inguinal hernias in mice and then treated them with a drug called fulvestrant.

The mice already had large, established hernias.

Within about two weeks, the hernias started shrinking.

After four weeks, they were gone.

Not just smaller.

Gone.

And when the researchers examined the tissue, they found something even more interesting: the abnormal fibrosis had reversed and the muscle architecture had returned toward normal.

Read the original study in the Journal of Clinical Investigation.

That raises a pretty big question:

If an established inguinal hernia could be reversed by changing the biology of the tissue, is a hernia really just a mechanical problem?

Why This Study Caught My Attention

If you’ve been following this site for a while, you probably understand why I find this research so interesting.

When I developed my own inguinal hernia, I was told essentially the same thing most people are told: surgery was the solution.

I decided to take a different approach.

I spent years trying to understand what was contributing to my hernia and what I could change. Over time, I became completely asymptomatic and got back to living my life as if I didn’t have a hernia.

Living an active life after becoming asymptomatic from an inguinal hernia.

Living life to the fullest, asymptomatically, without surgery

You can read more about my experience with an inguinal hernia and the approach I took.

My experience obviously isn’t the same thing as a controlled scientific study.

But it caused me to start questioning the idea that the abdominal wall is simply a piece of material that tears and can only be mechanically patched back together.

This study asks a very similar question from a completely different direction.

What If an Inguinal Hernia Is Also a Tissue Problem?

The traditional explanation of an inguinal hernia is pretty easy to understand.

A weak spot develops in the abdominal wall. Pressure from inside the abdomen pushes tissue through that weak area, and you get the familiar bulge.

Mechanically, that makes sense.

But it doesn’t explain why the tissue became weak in the first place.

That’s what makes this research so interesting.

The researchers weren’t only studying the hole.

They were studying what was happening to the muscle and connective tissue before and during hernia formation.

And one of the big things they found was fibrosis.

What Is Fibrosis?

Fibrosis is basically an abnormal buildup of fibrous, scar-like connective tissue.

Normally, collagen is an important part of healthy connective tissue. The problem isn’t simply that collagen exists.

The problem is what happens when normal, functional muscle begins being replaced by excessive fibrous tissue.

Instead of having strong, flexible muscle that can contract and handle load normally, the tissue becomes increasingly fibrotic and dysfunctional.

Earlier work from the same research group identified a population of estrogen-sensitive fibroblasts in lower abdominal muscle that expressed genes associated with inflammation, fibrosis and changes to the extracellular matrix.

Read the earlier fibroblast study in JCI Insight.

In other words, something biological appeared to be driving the tissue toward fibrosis.

Healthy abdominal muscle compared with fibrotic muscle tissue associated with inguinal hernia formation

Healthy abdominal muscle compared with fibrotic muscle tissue

The Estrogen Connection

This is where the study gets really interesting.

The researchers identified estrogen receptor-alpha, or ESR1, as an important driver of this process.

When we hear “estrogen,” we tend to think of it as a female hormone, but men have estrogen too.

The interesting part here wasn’t simply how much estrogen was circulating throughout the body.

It was what estrogen signaling appeared to be doing locally within the lower abdominal muscle.

The researchers found that ESR1 signaling was associated with fibroblast proliferation, extracellular-matrix deposition, fibrosis and ultimately hernia formation.

Think of fibroblasts as some of the body’s construction workers.

They help build and maintain connective tissue.

But if the signals controlling those workers change, they can start remodeling tissue in a completely different way.

That’s essentially what appeared to be happening here.

Estrogen and ESR1 signaling → fibroblast activity → fibrosis → muscle degeneration → hernia

That gave the researchers something they could actually target.

What Is Fulvestrant?

Fulvestrant is a drug that blocks estrogen receptors and causes those receptors to degrade.

The researchers weren’t using it to physically repair the hernia.

They were using it to interrupt the biological signaling that appeared to be driving the deterioration of the tissue.

And that’s an important distinction.

Fulvestrant didn’t patch the hole.

It changed what was happening inside the tissue.

The researchers tested this in two different situations.

Could Fulvestrant Prevent Inguinal Hernias?

First, they treated mice before the hernias had developed.

Some received fulvestrant.

Others received a placebo.

The placebo-treated mice went on to develop progressively larger hernias.

The mice treated with fulvestrant did not develop hernias.

That’s interesting by itself.

But the second part of the experiment is what really got my attention.

Could an Existing Inguinal Hernia Actually Reverse?

The researchers then took mice that already had large, established hernias.

Again, some received fulvestrant and others received the placebo.

Within approximately two weeks, the hernias in the fulvestrant-treated mice had significantly decreased in size.

After four weeks, all of the treated mice showed complete hernia regression.

The placebo group did not.

Inguinal hernia regression after four weeks of fulvestrant treatment in a mouse study

Inguinal hernia regression after four weeks of fulvestrant treatment in a mouse study

This is the part I think is worth slowing down and thinking about.

These weren’t animals that researchers prevented from ever getting a hernia.

They already had hernias.

The researchers changed one biological pathway…

And the hernias regressed.

The Tissue Changed Too

You could look at that result and wonder whether the bulge simply disappeared without the underlying problem really changing.

But the researchers examined the muscle tissue as well.

They found that fulvestrant reversed fibrosis and restored more normal muscle architecture.

So something much more interesting was happening than simply changing the appearance of the hernia.

The underlying tissue was remodeling.

That’s what I find most important about this entire study.

The researchers weren’t mechanically repairing a defect.

They changed the biological environment surrounding that defect, and the structure of the tissue changed with it.

But This Was a Mouse Study

There’s an obvious limitation here.

These results were in mice, not people.

Nobody should read this study and conclude that taking fulvestrant will make a human inguinal hernia disappear.

But the researchers also examined lower abdominal muscle samples from men undergoing inguinal hernia surgery.

They found fibrosis, increased ESR1 expression and fibroblast proliferation associated with the amount of fibrosis in the human tissue.

So although the reversal experiment itself was performed in mice, some of the biological changes being targeted were also found in men with inguinal hernias.

That’s what makes the next step so interesting.

Research update: Since I originally made the video this article is based on, this research has moved into a human clinical trial. Researchers are now testing this hormonal pathway in men with inguinal hernias.

Read the follow-up: Human Trial Begins for a Drug That Reversed Inguinal Hernias in Mice

This Changes How I Think About Watchful Waiting

This research also makes me question the whole idea of watchful waiting even more than I already did.

If your hernia isn’t causing enough problems to justify surgery, you’re often essentially told:

Watch it.

Wait.

And if it gets worse, then we can operate.

I’ve never found that particularly satisfying.

If changes are actively taking place in the muscle and connective tissue, then I want to know what influences those changes.

Doing nothing is still a decision.

I’m much more interested in asking:

What can I do to create the best possible environment for this tissue while I’m living with the hernia?

That’s the approach I took with my own hernia.

For me, that included understanding pressure, posture, movement, mobility, digestion and strengthening rather than simply waiting for things to get worse.

If you’re interested in that side of the discussion, you can also read:

Where a Hernia Belt Fits In

A hernia belt doesn’t change estrogen signaling or reverse fibrosis.

Its job is much simpler.

A properly fitted hernia belt can help keep a reducible inguinal hernia reduced while you’re moving around and living your life.

That was extremely important for me because it allowed me to remain active while I worked on the other things I thought were contributing to my condition.

In fact, my frustration with the bulky hernia belts available at the time eventually led me to design my own.

You can read why I designed the Comfort-Truss hernia belt differently, or view the Comfort-Truss hernia belts.

A belt should only be worn over a hernia that can be fully reduced.

If the hernia cannot be pushed completely back into the abdomen, that’s something I would have evaluated rather than trying to force it in with a belt.

So, Can an Inguinal Hernia Reverse Without Surgery?

We still don’t have evidence showing that this treatment reverses established inguinal hernias in humans.

But I think we can say something we couldn’t say before this research:

An established inguinal hernia was reversed without surgery in an experimental model.

And it happened by changing the biology of the tissue—not by mechanically closing the defect.

That matters.

For decades, the conversation around hernias has largely started and ended with the hole.

This research suggests there may be another conversation worth having:

Why did the tissue weaken enough for the hole to develop in the first place?

And if the biology contributing to that weakness can change…

What else might be possible?

That’s the question I’m interested in.

Where I Went Next

After reading this study, my next question was pretty obvious.

Fulvestrant influenced estrogen signaling and fibrosis.

Are there ways to influence some of those same biological pathways naturally?

That sent me down another rabbit hole involving estrogen metabolism, fibroblasts, TGF-beta, fibrosis, collagen remodeling and several natural supplements.

I’ve now made the follow-up video exploring exactly that question:

Can Natural Supplements Reverse a Hernia? What the Research Shows

And with the human trial now underway, I’ll continue following this research as it develops.

Research Sources

Main study:


Estrogen receptor-α ablation reverses muscle fibrosis and inguinal hernias

Journal of Clinical Investigation

Earlier fibroblast research:


An estrogen-sensitive fibroblast population drives abdominal muscle fibrosis in an inguinal hernia mouse model

JCI Insight