Reversing Crohn's and Colitis Naturally

22: Proving Your Bowel Disease is not Genetic, Autoimmune or Unknown, and Proof You Can Heal Yourself

Josh Dech Season 1 Episode 22

Your bowel disease isn't random, and I'm going to prove it to you. This episode is a lecture I did for a medical academy that I want to bring to you.

In this episode I will disprove your doctors and you'll finally have hope that your disease is not random, genetic, or even autoimmune, and that there is much more hope for what comes next!


TOPICS DISCUSSED:

  • Understanding IBD
  • What causes inflammation
  • How it can't be autoimmune, genetic, or idiopathic
  • bowel disease around the world and who has it most
  • Studies to disprove your doctors
  • What is destroying your gut and causing disease
  • The only 2 reasons we get sick
  • The primary drivers of Crohn's and Colitis in my practice
  • Reviewing a colonoscopy report who healed naturally


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[Josh Dech]

You know that your IBD is never random. Whether it's Crohn's or colitis, there's always a root cause. But the question we need to ask is: why does your doctor not understand this? What information do they have that they're telling you this is a lifelong autoimmune genetic condition?

Well, in today's episode, I want to break all of that apart with you so you can really understand what's actually happening beyond this rhetoric or beyond this story that you've been told— that frankly, your doctor's been told— and now they're forced to give to you.

But this episode's a little, a little bit different. Instead of the lives I do on my Facebook that I share here with you, this is actually a lecture that I did for the Priority Health Academy. I do these a couple of times a year, and it's for a group of doctors who are leaving the Western world and saying, “You know what? I don't love that my patients are sick. I don't love that they're just taking medications— that their only options are drugs and surgery. I want to learn more. I want to do better and do right by them by finding the root cause.” Because they know that your body is here to fix itself, and that's why you're sick and inflamed. They want to know what your body is trying to heal you from.

And that's what I'm taking you through today. And so in this episode, you're going to learn why what you've been told is so wrong. We're going to back this up with stats, with studies. We're going to walk through the genetic components and things that are involved and why everything you've been told is wrong. I'm going to show you the primary causes that I see in over 300 cases of bowel disease now reversed. I'm also going to take you through some of the steps we've used and go through a case study— if you remember the episode with Lisa who was diagnosed back in 2013 with severe colitis, almost had her colon removed, said “no thank you,” came off the drugs, and in 16 weeks had a near-perfect colonoscopy report. And of course, there's a Q&A with the doctors in the group at the end of this episode. I'm so excited to share it with you.

Now contrary to what your doctor has told you, Crohn's and Colitis are reversible. I've helped hundreds of people reverse their bowel disease and I'm here to help you do it too. Because inflammation always has a root cause— we just have to find it.

This is the Reversing Crohn’s and Colitis Naturally Podcast. Now I do these live trainings in my Facebook group every single week and put the audios here for you to listen to. If you want to watch the video versions of these episodes, just click the links in the show notes to get access to our Facebook group and YouTube channel. And for weekly updates, information, tips and tricks, you can sign up for our email list by clicking the link in the show notes below.

[Host]
Okay, welcome everyone to October 2024, our Master Class! And we have today a guest speaker, Josh, who many people already know from our previous lectures and also the Q&A. He's kind of a fixture with us— kind of on faculty at the PHA. So I'm going to let Josh Dech kind of introduce himself to some of the folks in the audience, or those listening later who don't know him and his expertise— and then we'll get started on our event tonight.

[Josh Dech]
Thank you so much, JP, appreciate that. Great to be here.

If you don't know me, my name is Josh Dech. I'm a holistic nutritionist, ex-paramedic, and I specialize now in the Crohn's and colitis space. My job, effectively, is to help people figure out why they have IBD, because none of it is random. Ever.

And that’s what I want to go through with you guys today.

I thought I’d take a very chic approach— instead of Breaking Bad, we are Breaking Bowel Disease today. And the whole idea behind this is that everything we've been told— and I want to encourage you to really entertain this thought— everything you've been told about your Crohn's and colitis patients to date is wrong, backwards, misinformed, or lacking a huge piece of information.

And that’s really what this lecture aims to do today.

[Josh Dech]
So the first thing I want to go over is just quickly what we're going to be talking about as a general overview for today.

So, number one: I do want to redefine the way we see IBD. So, our Crohn’s and colitis patients— when we start to look at it, what does it actually mean? Rather than just making assumptions based on what we've been told.

The second one I want to go over is causes and factors, which will be, of course, the things that I see in my practice. We've now helped reverse over 300 different cases of Crohn's and colitis— most of which are fully off the medication now. Many have yet to go, and there's still a fair bit of layers— you know, it's not a simple process— but we will get there.

And of course, I'm going to take you even through some case studies. I got a few that we’ll bring up, but I do have one in particular— I was able to get colonoscopy reports from a 16-week trial, and we're talking with a patient diagnosed back in 2013 with severe UC, who was about to have her colon removed. And so, we’re going to have a chance to go over that.

And then, of course— open to Q&A.

Now, moving on here— let’s look at IBD as it is defined medically speaking. It’s long-term, chronic inflammatory conditions of the tissues in the digestive tract. Now, it’s Crohn’s disease and ulcerative colitis.

We don’t typically know why they happen— genetic, idiopathic, autoimmune, environmental— there’s a lot of assumptions being made. But IBD by its definition is just inflammation of the GI tract in the two umbrellas of Crohn’s and colitis.

And so just to break these down— just to give you guys a bit of a refresher, or if you're listening on another platform— Crohn’s disease is going to be something that’s inflamed mouth to anus, primarily the small intestine.

We do see it to be a little bit different than colitis, which is of course of the colon primarily. Now, in Crohn’s disease, you can get lesions in your mouth, perianal lesions or fissures of some kind, a lot in the small intestine. Instead of going in long strips, it’s patches— known as Peyer’s patches— and they tend to go pretty deep, and they tend to go beyond just the first layer.

So rather than likening it to scuffing your knee on the sidewalk walking outside, instead it does really cut deep.

And some complications: fistulas, strictures, and of course malnutrition. So the fistulas— as infections— tend to burrow into the tissues. Strictures— when we get narrowing. And malnutrition is an absorption issue.

And in colitis— instead of patches of the small intestine— it tends to be large chunks and strips in the large intestine, and it tends to be very surface— like that scuffing of the knee.

And of course, there are the common signs and symptoms across Crohn’s and colitis: blood, mucus, pain, changes of appetite, etc. And we are prone, of course, to things like toxic megacolon, which can be highly emergent, and colon cancer, in ulcerative colitis.

Now, I want to go to the assumption here that we talked about— that it’s this autoimmune condition. We know— or we’re told— IBD is autoimmune, genetic, idiopathic or unknown, and possibly environmental. This is part of the Crohn’s and Colitis Foundation, the Mayo Clinic, and all the big entities who say this is what it is.

So autoimmunity is simply a condition where one’s immune system attacks one’s own tissues. So your body is attacking itself— that's the definition of autoimmunity. And we're going to break this apart here coming up.

Now current treatments, of course, for IBD— you can start off with something very simple: corticosteroids. We see a lot of prednisone, budesonide, or mesalamines, like your 5-ASAs.

And of course, there are immunosuppressants, biologics, and if these don’t work— snip snip, out comes the organs. And this is a major issue that I have with this— kind of as a general whole— and something I want to look at here.

You know— I’ll get to that one in just a minute— let’s move on to the next slide here.
[Josh Dech]
So let’s talk about inflammation.

Inflammation is kind of a funny thing, because again— if we assume that this condition is autoimmune, if we assume it’s genetic, if we assume it’s idiopathic— then we assume across the board that inflammation has no reason.

But inflammation is a natural response to injury or infection.

In the case of Crohn’s and colitis, to define it as idiopathic actually breaks the foundational layer of what inflammation is. And so we want to keep in mind— and this is a thread we’ll pull throughout this lecture— that the body does not make mistakes.

We only get sick for two reasonsever, across the board— and I cannot find any evidence showing otherwise:

Deficiencies or toxicities.

And those deficiencies may be things like nutrients. It may be micros or macros, even water can be a deficiency. But something has to create it.

Or a toxicity, where the body is reacting. We’ll talk about what some of those toxicities look like.

But as an overview, it can be microbes, it can be metals, it can be pesticides and toxins, and you name it— flu virus, COVID— it can be anything.

So I want you to picture this.

You’ve got a patient who comes to you and they’re out for a walk. They stepped on a nail. They come to you and say, “Doc, it’s infected, it’s inflamed, I got this nail in my foot, I need some help, I don’t know what to do.”

Now as a doctor, how crazy would it be if you looked at that patient and went:
 “Oh boy. That nail’s pretty bad, but… it’s just part of your DNA. It’s kind of part of your biology. There’s nothing we can do. Here’s some numbing cream— use this to manage the symptoms for the rest of your life. And if it gets really bad, we’ll cut your foot off.”

You’d lose your license immediately.

But when we look at things like chronic inflammatory conditions like Crohn’s or colitis— what do we do?

“Well, it’s just part of your DNA and biology. There’s nothing we can do about it. It’s inflamed for no reason. Here’s some medications to manage the symptoms for the rest of your life. And if it doesn’t work— snip snip— we’ll cut the colon out.”

It’s the same ideology across a different lens.

And this is where medicine, I believe, gets absolutely crazy— and kind of wrong.

So let’s talk about these a little bit here. The current approach: genetic, idiopathic, autoimmune— therefore we can’t do anything, therefore take the drugs or do surgery.

What we have to look at instead:

Number one: How could it possibly be genetic if 50 to 60% of the global cases reside in North America alone, which is less than 5% of the global population?

When 5% has 50% of the cases, we don’t call it genetic— we call it an epidemic.
And this is why we have to start changing our lens on that.

Number two: If it’s idiopathic— there’s no known cause, it’s kind of just happening— but we can see that cases have risen over 3,000% since the 1950s...

When estimates were about 15 in 100,000, to the 1970s it was about 45, to the 1990s it was 150 to 250 per 100,000, to today where it’s 463 people per 100,000 in North America who have Crohn’s or colitis.

This is massive.

And we’re talking— what, 5% of the population? That’s an insane amount.

On top of this, 70 to 72% depending on the studies we look at, complain of some kind of regular gut issue like constipation, diarrhea, cramping, bloating, pain.

And we know that 17 to 20% of all IBD diagnoses have a previous diagnosis of IBS.

Well, if 70% of the whole population complains of symptoms in line with IBS, and only 17 to 20% have a diagnosis, it makes sense that it can progress.

So we do have a progressive spectrum to consider.

[Josh Dech]
The next one is— if it’s autoimmune, how can it be autoimmune if:

A) We’re not actually testing every patient for antibodies, we’re just making an assumption, and
B) I’m going to show you some information coming up here that shows you that most cases do not have antibodies. And the ones that do? They’re not actually attacking their own tissues.

Now I’m working on a new hypothesis for this— I can’t find any research— but I would love to hear from you if you’ve seen anything in your patients, your clinic, or your contacts so we can research some of this. Because this lines up with the 300+ cases we’ve seen so far. I’m excited to get into that with you here in a moment.

So let’s talk about this: genetics.

We’ve mapped the entire human genome. We know that there is no single gene that causes these diseases.
We know there are genes that are correlated to the disease— where you can say, “Okay, well, if you have this gene, you are more likely to get Crohn’s or colitis.”
But there’s no single gene that causes high blood pressure, liver failure, Crohn’s, or colitis. It doesn’t exist.

And we’re going to go over some of that correlative information, but remember:

Correlation does not equal causation.

We know this as scientists, as clinicians— so we have to dig deeper.

And it’s actually a shockingly low percentage of people who do have any genetic components associated.

We also know that genes don’t operate in isolation— they are strongly influenced by their environment. Certain microbes, toxins, nutrients, stress, infections— all of these things can influence how your genes express.

For better or for worse.

So we have to stop blaming our genes.

Let’s look at this next chart here— now, you won’t be able to find these charts, by the way. I punched a bunch of data into AI and told it to make me some pretty visuals because I don’t know how to use actual charting software.
 But they’re beautiful, so these are mine.

Here’s what we’re looking at: you can see in green the bars representing ulcerative colitis genetics, or the associated links. In blue, it’s Crohn’s disease.

These are your percentage ratios. On the highest end, 25% of ulcerative colitis patients have this HLA gene that’s identified.
At the highest end of Crohn’s, you have your NOD2 and CARD15 genes.

So the most we see in the genetics is 20 to 25%— which means 75 to 80% of these patients do not have any genetic correlation whatsoever.

How can we continue to call it a genetic disease if the correlation is not even there in a strong enough way to make it identifiable or fixable?

We’re not going to edit it with CRISPR, we’re not going to correct it. So what are we doing?

And on the low end, we’ve got 5% correlation— we’re calling this TNFSF15 gene, for example.

Five percent. Why do we even bother looking at it?

And I know that’s kind of a stupid question in a room full of doctors and clinicians— but you get the idea.
 We’re blaming the wrong things.

[Josh Dech]

The next one here— I do want to look at some of these genes and explore them a little bit more in detail so we can understand why this is a thread we’re going to pull on during this talk.

Let’s look at some of these genes here.

You can see these are the associated genes and what they’re designed to do. So your PARK, your PARK7, STAT3, IRGM, IL23R, NOD2— these are the genes we’ve associated or attributed to Crohn’s and colitis.

And we’ve said: “If you have these, it’s a genetic thing. There’s nothing we can really do. This is sort of the assumption.”

However, we have to recognize:

These genes have functional responsibilities.

They actually do things.

And if they’re affected by their environment— microbial or otherwise— the genes are going to express negatively.

So let’s look at how many of these genes— we’ve got in the blue bar here— four of them. These are responsible for microbial interaction and recognition.

Which means they recognize bacteria and things in the gut, and they initiate an immune response.

So their job is to look at this and go: “Wait a minute— that’s a problem. Let’s deal with it. Let’s create an immune response.”

But if your gene is being expressed negatively, the immune response is going to be unhealthy.

Therefore, when it identifies a bacteria, it’s going to go haywire, and now you’ve got a hyperinflammatory response inflaming your entire GI tract.

The math... maths.

Let’s look at your IL23R or STAT3s. These ones here— immunomodulation.
They play a role in regulating the immune responses to ensure that the immune system does not overreact.

Well, if they’re being negatively impacted in their ability to read, interpret, and react, then of course they’re going to overreact.

Because when your body has a problem, it doesn’t downregulate systems— it upregulates them.

It’s on high alert.

Just like if we were outside— you get stuck in traffic, someone breaks your back window, you’re driving, someone’s chasing you through traffic— you’re on high alert.
You get home, what do you do? You shut the door, you lock it, close the blinds, you call the police— you’re on alert.

The Amazon guy knocks at the door? You scream.
Normally, you wouldn’t. Neither would your genes.
But considering the threat they’re under, they’re expressing poorly.

Looking at the HLA gene, for example— now this one is commonly implicated in things like ulcerative colitis, especially.
But this HLA gene is responsible for presenting microbial antigens to the immune system. It brings it forward and says, “Here’s the problem. Do you think we should act on it?”

Again— if it’s negatively influenced? Of course we’re going to have an elevated immune response.

And so the next slide I want to show you here is a chart— and this one shows the things that influence the genes. The ones we just talked about.

Look how much of these genes are influenced by other factors.

Now the reason I put these here: microbial interaction, immune responses, inflammatory responses, environmental factors, cellular stress, diet and nutrient transport— in the cases of inflammation, all these things are going to be a problem.

And in my clinic— in my practice— the primary things we see driving IBD of course are:

  • Toxins
  • Microbes
    (We’ll get into more detail— parasites, Clostridia, E. coli, Candida...)
  • Heavy metals
  • Poor drainage pathways (which create cellular stress and inflammatory response)
  • Microbial interactions

And of course, our genes are reacting poorly.

So the primary drivers I’ve seen in over 300 cases influence our genes negatively.
 And of course, the roles they’re responsible for are going to be poor.
 And the outcomes of our inflammatory or immune pathways are going to be poor.
Because the input does not create a healthy output.

It really is— in my opinion— that simple.

[Josh Dech]
So I want to show you this chart here to back up my claim.

We talked about the distribution. This is from the CDC.

Now, there are estimates saying we have cases anywhere from 6 to 8 million today— it really depends on who you ask— but the CDC, in their own report back in 2019, showed that:

3.1 of the 4.9 million cases of Crohn’s and Colitis around the world were in the USA alone.

That’s 63% of the cases in less than 5% of the global population— it’s about 4.7% of the global population.

This is an epidemic.

And I asked AI once again to put it in a visual chart representation— and you can see the cluster of IBD that we have around here with the numbers and the stats that we were able to pull.

And it’s interesting— this is pretty accurate to my own experience.

I have a fair bit of outreach from India, a little bit from the Middle East, I do have a lot from the UK, Australia, and New Zealand— but primarily the USA.

I bet you 80–90% of our clientele is USA.
The rest would be some in Canada, but UK is a huge resource.

So this is a big problem.

We have to look at the westernization and industrialization of these worlds and how it’s relating to the creation of these pockets of bowel disease.

Ultimately, consider: are genes really to blame?

If you’re telling your client or your patient that it’s just a genetic issue, without maybe knowing— it’s a lie.

We are lying to our patients because we’re blaming something that is more of a bystander effect.

The genes are being manipulated by external factors.

So it’s not just genetic. Things change— microbes, toxins, inflammation, cellular stress, detoxification, drainage pathways, diet, nutrients, environment, whatever it might be— they change your genetic expression.

So the first pillar of genetic, idiopathic, and autoimmunecompletely dismantled.

Can everybody agree with me on that one?
Awesome. Okay. Beautiful. Love that.

[Josh Dech]
Let’s talk about the next one then— autoimmune.
The third leg to the table of IBD.

We want to talk about this.

The definition of autoimmune is:

Your immune system is attacking your own tissues.

But you have to have antibodies for it to be autoimmune. That is the definition of autoimmunity.

There is an antigen, and then an antibody is created, and it attacks.
Bing, bang, boom— problem solved.

However…

If you see a lot of Crohn’s and colitis patients—
 When was the last time you tested their antibodies?

When was the last time someone came to you for help as a functional practitioner with an antibody test that said:
 “Look at all the antibodies I have”?

That’s consideration number one.

Number two, we have to ask ourselves:

If autoimmunity is your body attacking its own tissues...

What if it’s not?

A lot of the antibodies— I’m going to show you some charts here in a minute—
 They don’t just attack “your tissues.” They’re more likely attacking certain proteins, or membranes, or cells within the body.

And again— by bystander effect— your tissues are just caught in the crossfire.

So your Crohn’s and colitis might be inflammation by proximity, not your body attacking itself.

And we’re going to talk about that here in a minute.

So let’s get into this one.

These are the antibody charts that we have for Crohn’s and colitis— this is pulled directly from PubMed, and all over the place.

The most we see here— in red, this is ulcerative colitis. Blue, of course, is your Crohn’s disease, per the legend.

Now, we see a much higher prevalence of antibodies in Crohn’s disease— no doubt about that.

But looking at this chart:
 About 70% of all patients who’ve been tested for antibodies with ulcerative colitis have this P-ANCA antibody.

So this is your perinuclear anti-neutrophil antibody.

That means your body is attacking the neutrophils.

Now— what’s the number one thing we test in patients when we’re looking for the progression or regression of bowel disease?

It’s calprotectin.

Well, calprotectin is simply a byproduct of neutrophil activity.
So if you have an abundance of neutrophils coming in to clean up something— they operate through phagocytosis, meaning they consume and digest— then of course you’re going to have elevated calprotectin.

It’s like having a lot of cars in one parking lot idling.

You’re going to have more exhaust.

So why are we looking at calprotectin rather than going deeper?

Look at these other ones— ASCA, anti-C— all these antibodies? We’re talking 10% or less in ulcerative colitis.

Okay— so we have elevated neutrophils in ulcerative colitis. That’s a gimme.
They’re there for a reason, right?

And then in Crohn’s— we do see a lot more antibody activity.

Let’s take a look at what these antibodies are actually doing.
[Josh Dech]
So we’re assuming— again, the definition of autoimmune is that your body has antibodies attacking your own tissues.

However… this chart shows you what other things these same antibodies can attack.

And many of these are the primary causes of Crohn’s and colitis that we just talked about.

Parasites. Mold. Fungus. Yeast overgrowths. Toxins.

Take a look at this one— P-ANCA, right?
The antibody we see 70% of the time in ulcerative colitis.

Well— antibiotics can elevate it.
IBD drug therapy can elevate it.
I believe— I’ll double check this one, I’ve got a chart somewhere— but mesalamine, Imuran— we see these creating the exact same antibodies.

So if your patient comes in and does have antibodies?

Number one: Are they medicated?
Because if they are, that can create the same antibody response.

Look at Crohn’s disease:

  • Fungi
  • Bacteria
  • IBD drug therapy
  • Parasites
  • Antibiotics
  • Mold

All these things— the things we know your body is trying to react to— can create the same antibodies.

Even the drugs we use can create the antibodies.

So to say it’s autoimmune— like your body just randomly began attacking your own tissues out of the blue because it was bored

It doesn’t make any sense. That is a logical fallacy.

They have to be going after something.

And the antibodies are going to be, more likely in many cases, attacking a foreign pathogen that maybe looks like your own tissues. Or proteins that you produce in response.

So if we’ve got some correlation here, let’s look at this.
 This is sort of my hypothesis I’m working on. And I’d love some help with this, by the way— if you guys want to maybe, you know, win a Nobel Prize with me?

Take a look at this:

Your body is likely inflamed due to the bystander effect.
If your body is attacking something within its own tissues— that would be a problem.

But given the fact that we’ve got 300+ cases we’ve now reversed, and we’ve seen all these commonalities— bacteria, E. coli, Giardia, different parasites like E. histolytica, Blastocystis hominis, Dientamoeba fragilis...

There are 1,400 kinds of parasites that can infect humans out of the million+ we think exist on Earth.

If the body is reacting to them?
The antibodies might be attacking proteins specific to those organisms— or the membranes of the parasites themselves.

So therefore, we must ask:

Are they really attacking your tissues?

Let’s go back— P-ANCA.
70% of all UC patients tested in the study had this antibody.

This is the anti-neutrophil antibody.

So— is it attacking the neutrophil?

Or— since neutrophils operate through phagocytosis— is the antibody attacking the protein inside the neutrophil that it’s trying to clean up?

This would change the entire ideology of autoimmunity.

It would change the landscape if we have this anti-neutrophil antibody— and the assumption is that it’s attacking your neutrophil—

But what if neutrophils are there to clean something up, and the antibodies are actually attacking what the neutrophils consumed?

If that’s the case— and I’m telling you guys, I need help proving this theory—

It would change the entire landscape of how we see autoimmunity, especially in the case of IBD.

And possibly the landscape of autoimmunity across the world.

Now I did run a search for research like this. It sounds like there are some theories ongoing, but nothing conclusive at this time.

So this would be forefront type of stuff.

If you can find any information on it— please do contact me, and I’ll provide as many bodies as we need to get the testing done.
 But that’s my thought currently.

Are we making sense so far on the antibodies and how that’s another logical fallacy?

Perfect.

All right. Let’s move this one on, then.
[Josh Dech]
Next one: idiopathic.
“No known cause.”

Well, we talked about cases rising exponentially3,000% in the last 75 years.
So something has to be causing it.

If idiopathic means there’s no known cause, is it that there truly isn’t a cause
or that we’re not recognizing the causes willingly?

We’re going to talk about some of this as well— what’s going on in the world. But look at the chart we just showed you— the world map.
Look at the concentration:

  • European countries, especially Western Europe
  • The USA
  • Even some in Australia and New Zealand

These are the most Westernized cultures in the world.

They have:

  • Some of the highest food share
  • The highest pesticide use in the world

Look at India— they’ve got something like 8,000 pesticides approved for use across billions of people— and they still have a relatively small concentration of IBD.

Now look at the USA—
 They have 18 to 20,000 pesticides approved for use.

Glyphosate, known to cause cancer, labeled a carcinogen
In fact, Bayer, who bought Monsanto, recently paid out— I believe it was $11 or $14 billion— to settle over 100,000 lawsuits, with another 30,000–40,000 still pending… for glyphosate causing cancer.

Yet it is still approved for use in the USA.
And banned in dozens of other countries.

So if it's idiopathic, but these things are happening— something is driving it.

We have more medication use than ever before.
It’s gone up, calculated for inflation, by 222 times since the 1950s.

We have more processed, refined foods than ever.
More sugar than ever.
We’re talking 101 pounds per year for the average adult in the USA.

That is the size of a panda bear.
You are eating a panda bear worth of sugar every year.

Just… for context. 😅

Seed oils are up exponentially.

There’s another interesting theory we’ll look at soon called generational dysbiosis, from guys like Dr. Justin Sonnenburg and his wife Erica at Stanford.

But first— let me show you this little chart we put together.

It shows you the increase in bowel disease over the last 75 years.

If we don’t know what’s causing this—
 This is a 45-degree line.

If we don’t know what’s causing this exponential growth

We better figure it out pretty freaking fast.

That’s my first thought.

So ultimately, I want to pose the thought:

Is this truly an “unknown cause”?
 Or are we ignoring the cause?

Now, dare I say the C-word (conspiracy)...
But consider this:

The three biggest industries in the USA make up 18% of the entire GDP, worth $4.7 trillion a year.

Those are:

  • Hospital stays and medical care
  • Health insurance
  • Pharmaceuticals

Now— look at how many CEOs bounce around from Big Food, to Big Ag, to Big Pharma, to the FDA.

They just jump around.

Now— is it one big conspiracy to make us all sick?
 Who knows.

But can we say— with confidence— that there are special interest groups approving certain toxins and certain pathogens for whatever elusive profit?

Probably.

Are they doing it intentionally? Or because they’re asked to? Or because they’re lobbied to?

Who knows.

But the reality is— there’s something terrible going on that’s causing these problems.

And it’s being ignored by higher-up authorities.

And this is a big driver of our issues.
[Josh Dech]
So let’s go through this really quick— the primary causes of IBD.

We’ve seen a 3,000% increase from 1950 to today.
Let’s talk about one of the biggest root drivers we see: generational dysbiosis.

Now, generational dysbiosis is this idea that we are inheriting less and less microbial diversity over generations.

Dr. Justin Sonnenburg (Stanford) and his wife Erica Sonnenburg actually did some incredible work here.

They ran studies on mice— over generations— and they slowly changed their diets, introduced them to pesticides, altered their microbial exposure.

And what they found was this cascading effect.

Let me simplify it down to the easiest version:

Let’s say Great Grandma starts with 1,000 microbes.
We introduce toxins, antibiotics, refined foods, sanitization, lack of nature exposure

Now, she gives birth to Grandma, and she only passes on 800 microbes.

Grandma then gives birth to Mom, who gets 600.
Mom gives birth to you— and you only get 400.

You’ve just inherited dysbiosis.

Without even trying, you’ve started life with a massively reduced microbiome.

And where do we get these microbes from?

  • Breastfeeding
  • Vaginal birth
  • Skin-to-skin contact
  • The natural environment
  • Animals, dirt, play, gardens

But in a modern world?
 We’ve cut off most of those pathways.

So if your microbial diversity is lower, what happens?

Well— remember— the only two ways we can get sick are:

Toxicities and deficiencies.

You’ve now inherited a deficiency in gut microbes.

And that matters— a lot— because 70% to 90% of your immune system lives and matures in your gut.

That’s your GALT (gut-associated lymphoid tissue), your MALT, your mucosal layer, your lymphatic tissues— it’s all based in your gut.

So if your defenses are down, your genes are overactive, your inflammatory response is overactive— of course you’re going to have an elevated immune reaction.

Why?

Because you don’t have the microbes to keep things in check.

And that’s why inherited dysbiosis is a major concern.

So now we start to stack all of these issues together.

What does it actually look like?

Well, in my practice, I put together a little Venn diagram for you— to show you the primary causes of IBD I see.

On the outside rings, we’ve got:

  • Toxins
  • Microbial imbalances (which could also be toxic)
  • Deficiencies

What leads to autoimmunity? A trigger.

We’ll get into stress, genetics, and of course leaky gut.

These are the core drivers of bowel disease.

And when they compound, they can create what we call autoimmune cycles.

But then we have to ask again…

Is it really autoimmune? Is it actually genetic? What is the body attacking, and why?

So I want to briefly go over microbiome development with you.
There are four main places we get our microbes.
The first is going to be in utero—when we’re being developed.
Now it’s previously been understood that the fetal gut microbiome is sterile.
But—there’s a concept called fetal microchimerism, where we know that 33% of the metabolites and blood are actually byproducts of bacterium.
So what’s shared between mom and baby?
Blood.
That’s our fetal microchimerism—the sharing of DNA, of cells, of tissues, and even microbes.
Look at what happens in pregnancy, typically:
We see a lot of inflammatory markers elevated.
We see blood sugar issues—insulin sensitivity goes down.
It starts to resemble a kind of type 2 diabetes.
Now—if you’re already sick, of course when you add pregnancy, those issues get worse.
But in a healthy body?
Those shifts are intentional—they shunt food and nutrients to the baby.
Inflammation allows microbes and nutrients to transfer across the gut lining into the blood and over to baby.
We treat pregnancy like a disease, because we see inflammation, blood sugar issues, etc.
But in a healthy body, they wouldn’t be a problem.
They’re only a problem in an already unhealthy body.
So—mom’s gut microbiome changes during pregnancy.
It produces beneficial bacteria that baby will get first through birth and breastfeeding.
A lot of that’s your Bifido and Lactobacillus—super important stuff.
Then of course—birth.
We know vaginal birth is best.
Babies born via C-section have worse outcomes:
  • More prone to eczema
  • Psoriasis
  • Diabetes
  • Other autoimmune conditions
Why?
Because C-section babies miss the exposure to vaginal flora—and often go straight to bottles, antibiotics, sanitized rooms, formula.
And of course—after birth, it’s like seeding a meadow. The microbiome develops.
Best case scenario?
You’re born naturally, you eat organic, grow up on a farm, pesticide-free, playing with animals, in the dirt, picking carrots and licking them before you wash ‘em.
That is how you seed a proper microbiome.
But if we go back to that world map—Westernized countries?
 We do the opposite.
  • 30% of births are C-sections
  • Bottle-feeding is more common than breastfeeding
  • We live in cities, we live indoors, we hyper-sanitize everything
  • And during COVID? We basically cut off all microbial exposure
We did the exact opposite of what we need to do to seed a healthy gut.
And then on top of that?
We add:
  • 100+ pounds of sugar per year
  • Alcohol
  • Antibiotics
  • Fast food—3x/week on average
These are nuclear bombs for the gut.
Medication spending? In 2018, it was almost $1.2 trillion/year—it’s probably closer to $2 trillion now.
Let me show you this interesting chart from Dr. Cate Shanahan.
It’s the introduction of seed oils: canola, corn, sunflower, soy, cottonseed, vegetable oils.
Now— we blame red meat and saturated fat for gut health issues.
But look at the 1950s—fat consumption went down.
Seed oils went up.
Then check this chart— we overlay the rise of IBD from 1950 to now.
Side by side?
The curve is almost identical.
Now—correlation doesn’t equal causation...
 But we know nutrition has a huge role in the health of our guts.
And if our guts are unhealthy, so are our bowels.
[Josh Dech]
So—here’s what I see in my practice as the primary drivers of IBD:
  • Stress is a big one
  • Environmental factors are a big one
  • Microbes—Candida, Clostridia, E. coli
  • Parasites—I’ve seen children as young as 9 years old come in with full-blown bowel disease
And they had no family history. Why?
Because they’ve had loads of antibiotic use from the time they were little.
When you destroy your microbiome, what comes in?
Other invaders.
Other microbes come in and fill the space.
That can lead to (or be compounded by) deficiencies:
  • Macronutrients
  • Micronutrients
  • Short-chain fatty acids
You could even argue dietary fiber—but that’s a whole conversation for another time.
So I want to take you through a quick case study.
This is Lisa.
Lisa is a 43-year-old female who came to see us earlier this year.
She was diagnosed with IBD—moderate to severe. Mayo score of three or four, I believe. We’ll take a look.
She was diagnosed back in 2013.
She had tried every medication—they even moved her onto Uceris, and things got worse.
They told her, “We can remove your colon.”
And she described the pain like having squirrels with razor blades running around her insides.
The bleeding was so severe, in fact—on our first call together, she was actually on the toilet. She couldn’t leave. That’s how bad it was.
I want to show you some of her colonoscopy reports.
The first one—external hemorrhoids, moderate to severe ulcerative colitis, proctosigmoiditis.
They started her on IVs, gave her all the drugs, and put her on Uceris.
So she was moderate to severe, and you can see the lesions inside her colonoscopy report.
It also shows: Mayo score of three, spontaneous bleeding, ulcerations.
That was her exam from September 2023.
This next one is February—even with the drugs, she’s continuing to get worse.
Colonic mucosa, active colitis, erosion, cryptitis, crypt distortion—just, all the things.
They wanted to remove her colon.
So that’s before starting our protocol.
Now what we did with her?
Sixteen weeks.
We focused on:
  • Drainage
  • Detoxing (collecting the trash)
  • Moving it to the curb
We found parasites.
Her follow-up showed:
  • Negative for dysplasia
  • No increase in eosinophils
  • Normal colonic mucosa
  • Normal stomach
  • Normal exam
  • One little spot of mild colitis left, plus a hemorrhoid
That’s after 16 weeks.
Keep in mind—she was diagnosed in 2013 and had been on drugs for 10 years.
Final report:
  • Normal stomach
  • Normal ilium
  • One patch of moderately active Mayo 2 UC
  • Improved since the last examination
Let me show you the side-by-side.
One was drugs, immunosuppressives, and the narrative of genetics, autoimmune, and “nothing we can do”.
The other?
We asked what the immune system is reacting to.
We asked if it’s even autoimmune.
And we addressed the root cause.
And this is what happened in 16 weeks.

[Josh Dech]
So coming towards the end of this thing here, I want to show you guys a few slides—just to brace yourself—of what we actually pulled out of clients this year in the IBD space.
I’d say about 80% of our clients do actively have some kind of parasite activity.
I’d argue 100% have them, but probably 80% are active drivers of disease.
Check this one out:
This one came out of a nurse—15 years of IBD.
Same thing. Full of melanomas, tried the anti-TNF drugs, tried everything—and in 16 weeks, we went after mold, went after parasites—they were gone.
She had multiple rope worms.
This next one? Could have been a roundworm—came out of a 15-year-old boy.
It was his second day on a parasite protocol.
We were supporting drainage, and this came out.
Also from the same nurse, more of these twisting, rope-like structures.
Now, these next ones get a little wild.
These are what’s living inside people’s bodies.
They hide in:
  • The crypts
  • The folds
  • The bile ducts
  • The liver
  • The pancreas
  • Even the appendix
They’re very hard to remove.
Parasites can feed off:
  • Muscle
  • Lung tissue
  • Liver
  • Lymphatic fluid
And you wonder why your patients are chronically anemic, going in for iron infusions constantly…
They love hemoglobin and iron.
And when their levels are low—we have to ask why.
And this is what we’re seeing coming out of our clients.
It’s a little bit unnerving, truthfully—
but this is what can be.
Some might argue this next one could be mucoid plaque—but many are very clearly worms.
Here’s what I want to leave you with.
It is so important in practice to challenge the notion and not just accept the standard of care.
To say it’s “genetic, autoimmune, idiopathic”—and therefore the only treatment is immune-suppressing drugs?
That means we’re saying:
“Your body is broken. It makes mistakes. It’s attacking itself. Let’s suppress it and hope for the best.”
It’s like saying the nail in the foot is just part of your DNA, so all you can do is numb it and eventually cut off the foot.
We cannot accept that.
Inflammation is never random.
Your body is always reacting to something.
It is an innate response to defend you— not to attack you.
There are probably 200+ checks and balances in the immune system before it attacks anything.
If it's attacking?
There’s a reason.
But in the standard of care, you’re told:
“Follow the protocol. Don’t ask questions.”
There’s no critical thinking, no personalization, no innovation—and that means patients are stuck doing what they’re told.
So I believe standard of care is a cancer.
[Josh Dech]
So, let me give you this last wrap-up of where we go from here.
First off:
Medication and surgery are NOT the only answer.
They’re addressing the tissues that are inflamed, not the thing inflaming them.
So even when you get a GI-MAP back from a patient, and it’s messy—gut bacteria all over the place—we still need to ask:
Why?
Is it:
  • Antibiotic use?
  • Environmental exposure?
  • A microbe that entered the system?
  • Pesticide toxicity?
  • Heavy metals?
  • Or an inflammatory response that created a playground for these bacteria?
Even that test doesn’t go deep enough unless we ask what led to it.
Every piece of information has a deeper root of WHY.
And that includes you.
Let me leave you with a few starting places for treatment.
Because we get a lot of questions like,
“Where do you start, where do you end?”
So first:
You can’t evict the tenants from the building if the doors are locked.
Drainage comes first.
Detoxing is collecting the trash.
Drainage is getting it out to the curb.
We look at things like:
  • Grounding, sunlight
  • Turning off the tap—your diet, your stress
  • But also: how is stuff getting out of the body?
Your main drainage pathways are:
  • Skin
  • Sinuses
  • Lungs
  • Lymph
  • Blood
  • Kidneys
  • Bowels
  • Liver + bile ducts
So we support those systems.
If you’re constipated—get things moving:
  • High-dose magnesium citrate or oxide
  • Vitamin C
    (much better than Miralax or other petroleum-based laxatives)
And especially: support liver + bile drainage.
We often use:
  • NAC
  • Milk thistle
  • TUDCA
  • We also like Cellcore products (KL Support, drainage activators)
BUT—go slow.
You can cause someone to Herx (detox reaction) just from biofilm disruption or too much drainage too fast.
Let me give you an example:
Billie Jean, the nurse I showed you—15 years with IBD.
She was totally symptom-free after about 3 months on our mold and parasite protocol.
Off all her drugs.
But when we introduced biofilm disruption, she flared.
Why?
Because her immune system, still hyperactive from years of inflammation and nutrient depletion, finally saw the bad guys hiding under the biofilm, and it reacted.
It was a controlled burn—but it was real.
So: drainage first, then carefully identify what's driving the inflammation.
Parasites? We go by symptomatology, not tests—because tests are 40% accurate at best.
We had one client—she had 8 negative parasite tests over 5 years—and then we pulled out 4-foot-long worms.
Why?
Because parasites hide, bind, bury.
If you’ve got patients with:
  • SIBO
  • Libido issues
  • Early hair loss
  • Dry skin
  • Psoriasis
  • Eczema
  • Teeth grinding
  • Nail biting
  • Trouble digesting fats
That might be parasites or liver toxicity.
So once we know what’s going on?
We remove, replenish, and rebuild.
That’s the arc.
Final thought:
Your body is not broken.
It is brilliant.
It’s not randomly inflamed. It’s not confused. It’s not self-destructive.
It’s trying to save your life.
It’s reacting to things we’ve stopped looking for.
And if we just ask why, we can finally find the root cause—and reverse IBD.
Thank you guys so much for your time, your attention, and your belief in something bigger than the standard of care.
This is how we change medicine.

[Dr. JP]

Great, thank you. That was a wonderful presentation—lots of options to think about and theories.
One question that came up:
Is there mutual exclusivity between the concepts of “idiopathic” and “autoimmune”? And can this theory you just shared be applied to other autoimmune disorders?
[Josh Dech]
Yeah—great question.
I wouldn’t say it’s exclusive to IBD.
I mean, if we consider it—just the very principle of things being idiopathic doesn’t make sense.
Because your body only inflames or gets sick as a result of something.
Number two: in terms of antibodies, I’d love to explore this more.
Like—look at the P-ANCA antibody. Is it really attacking the neutrophil, or something the neutrophil phagocytosed?
If we can understand that—if the body isn’t attacking itself, but rather a microbe, protein, or membrane that’s been consumed—
It would completely change the landscape of how we understand autoimmunity.
And that opens the door to asking the same question about other conditions:
Like MS—is the body really attacking the myelin sheath?
Or is there something in the nervous system that’s triggering that response?
Think about aluminum, mercury, heavy metals, parasites...
Even in cancer—is the tumor a mutation, or is the body intelligently enclosing a toxin or pathogen to protect you?
If this theory holds true for IBD—
Why not for every disease we’ve labeled autoimmune?
[Doctor in Chat]
Can you comment on treatment options? Where do you start? Where do you end?
[Josh Dech]
Totally.
So—first things first:
You can’t evict the tenants from the building if the doors are locked.
That’s why we always start with drainage.
Think:
  • Grounding
  • Sunlight
  • Stress control
  • Cleaning up food
Then support drainage pathways:
  • Skin
  • Sinuses
  • Lungs
  • Lymph
  • Liver
  • Bowels
  • Kidneys
If you’re constipated:
  • High-dose magnesium citrate or oxide
  • Vitamin C
Better than synthetic laxatives.
For liver/bile drainage, we love:
  • NAC
  • Milk thistle
  • TUDCA
  • Cellcore’s KL Support
⚠️ Take it slow.
Biofilm disruption can cause Herxheimer flares.
Example: Billie Jean (the nurse).
After three months, she was off meds and felt great—until we did biofilm work. Boom. Flare.
Why? The immune system finally recognized something hiding under the biofilm. Controlled burn.
So we always:
  1. Drain
  2. Replenish
  3. Remove (gently!)
  4. Rebuild

    [Dr. Gail Makus]
    Hey Josh—quick anecdotal case for you.
    I had a healthy guy in his 50s, worked as a mason, laying limestone. Strong, outdoorsy.
    His doctor kept hounding him because his cholesterol was high. He was on a dud milk diet or something.
    Anyway, he finally agreed to start statins
    And then—bam—acute pancreatitis. So bad he needed TPN (IV nutrition) and got totally shut down for what turned into ulcerative colitis.
    Recovered eventually…
    Years later, his doctor again pushed statins. He tried them again.
    Boom—UC came back, way worse this time. Ended up needing surgery.
    So—have you seen any correlation between statin use and IBD, or colitis specifically?
    [Josh Dech]
    Oof, yeah—great question. First thing I’d say is:
  5. Elevated liver enzymes and high cholesterol can actually be signs of parasites.
  6. So I’d ask: Was his cholesterol truly dietary?
    Or was it influenced by infection, toxins, or biofilm production?
    Remember—biofilms are built using cholesterol.
    So, if statins are lowering cholesterol, they might be disrupting biofilms
    Which could expose hidden microbes, and boom—inflammatory reaction.
    Also consider:
    Statins inhibit the enzyme HMG-CoA reductase, which is crucial for cholesterol synthesis in the liver.
    Could this disrupt bile production, increase toxic recirculation, and trigger a gut-level immune response?
  7. That’s my knee-jerk theory: statins could cause biofilm disruption, and what’s hidden gets exposed.
  8. Which flares the gut.
    We need to look deeper, but it’s a valid hypothesis.
    [Dr. in the Room]
    We had a teenage boy a few years ago—severe Crohn’s, failed everything.
    Surgeons wanted to take out his colon, give him a colostomy bag. Parents freaked out.
    They found a functional medicine doc in Miami, who ran a full root cause workup and found tick-borne pathogens—Lyme disease, and a few co-infections.
    That’s where I got involved—we treated his Lyme. Also gave him LDN (low-dose naltrexone) for symptom control.
    Eventually added peptides, especially Thymosin Alpha 1—2 months of that and he was a different kid.
    When he went back to GI for colonoscopy?
  9. Not a single lesion. Clean.
  10. We published it as a case study on SERMO.
    So we’re definitely seeing root cause stuff—parasites, tick-borne illness, toxins—not just “autoimmune.”
    [Josh Dech]
    I love that story. And yes—LDN is great for modulating the immune system, especially when it’s hyperactive.
    And Thymosin Alpha 1? Huge fan.
    Again—this backs up the hypothesis:
  11. These “autoimmune” flares are triggered by foreign invaders, not by your own tissue being randomly attacked.
  12. If we can identify what's there, and remove it strategically—supporting the immune system and drainage—the body knows how to heal.
    This is what we’re seeing over and over and over.

    [Dr. JP]
    Josh, quick sidebar before we close—
    You’ve mentioned before that you’re not a medical doctor, but clearly you’re getting massive results.
    We’re actually working on a project right now that might be right up your alley...
    We’re trying to create a parallel health care education system.
    One that breaks down all these artificial walls—MD, ND, DC, LAc...
    None of those letters should define who’s allowed to heal.
    We’re building a curriculum and competency-based certification for people who are exemplary healers, regardless of background.
    So that a nurse, or a nutritionist, or a brilliant self-taught person like you, can get recognized.
    Because I’ve got PAs and NPs in this room who are better clinicians than most doctors I know.
    And frankly, some MDs I’m embarrassed to call colleagues.
    [Josh Dech]
    Wow. I love that.
    I’ve said for years—my last name has as many letters as my first, and it still doesn’t get me past the gatekeepers. 😆
    But if we’re being honest?
    Healing doesn’t care about your credentials.
  13. It cares about whether you ask the right questions.
     Whether you see patterns others miss.
     Whether you can look at a person and say:
     “Your body isn’t broken. It’s brilliant. Let’s figure out what it’s reacting to.”


  14. So yeah—count me in.
    Put some letters after my name, sure, why not—
    but I’d rather be known for the bodies we helped heal than the systems we obeyed.
    [Dr. JP]
    Perfect. We’re planning to launch this from the Southeast, so keep your ear to the groun
And maybe you’ll be one of our first graduates—or better yet, one of the faculty.
[Josh Dech]
Heck yes. I’m in.
And thank you again to everyone here—this was one of the biggest turnouts we’ve had in ages, and it shows me how many people are ready for change.
Your body doesn’t make mistakes.
Your symptoms are not random.
And you deserve real answers.

[Josh Dech]
Thanks so much for listening to this episode.

Now—if I can make one quick ask of you...

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