Can Stem Cells Reduce Chronic Inflammation? Growth Factors, Cytokines & Systemic Delivery Explained

Inflammation gets blamed for almost everything.

Joint pain.

Fatigue.

Autoimmune disease.

Cardiovascular problems.

Brain fog.

Digestive issues.

Aging.

But inflammation itself is not the enemy.

In fact, without inflammation, your body would have a much harder time responding to injury and infection.

The problem occurs when an inflammatory response that should be temporary becomes persistent or dysregulated.

That is one reason researchers are so interested in the relationship between mesenchymal stromal cells, growth factors, cytokines, and immune signaling.

Rather than functioning simply as replacement cells, MSCs are increasingly studied for the molecules they release and the ways they interact with the immune system.

So can stem cells actually reduce chronic inflammation?

The answer is more complicated than a simple yes or no.

Quick Answer: Can Stem Cells Reduce Inflammation?

Mesenchymal stromal cells, or MSCs, are extensively studied for their ability to modulate immune and inflammatory signaling.

Rather than functioning only by turning into replacement tissue, MSCs can release a collection of biologically active substances that includes:

• Cytokines
• Growth factors
• Chemokines
• Extracellular vesicles
• Lipids
• Other signaling molecules

Researchers commonly refer to this collection as the MSC secretome.

These signals can interact with immune cells such as:

• T cells
• B cells
• Macrophages
• Dendritic cells
• Natural killer cells

Laboratory research has demonstrated that MSC-derived signaling can alter inflammatory pathways and change the behavior of human immune cells.

However, this does not mean that an MSC infusion has been proven to treat every condition associated with inflammation.

Inflammation is involved in hundreds of diseases, and the biology, product, dose, route, and disease being studied all matter.

The more accurate statement is:

MSC-mediated immunomodulation is a legitimate and important area of regenerative medicine research, but clinical effectiveness must be established separately for each product and condition.

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Watch: Dr. John Dame and Dr. Rob Kellar Discuss Chronic Inflammation

Video Transcript

Dr. John Dame:

There’s growth factors, not just inside a joint, but released inside the rest of our body, that actually will help with lots of different conditions.

Dr. Rob Kellar:

There’s nothing unique about these growth factors and cytokines that we’re using in regenerative medicine, meaning they’re found ubiquitously all throughout the body.

They’ll have activity in all sorts of different tissue sites.

So doing systemic delivery, from a science standpoint, it’s not surprising that if you have inflammation that’s out of control in an organ, if the regenerative therapy gets to that organ through the circulation, you’re going to modulate that inflammatory activity.

And a lot of the diseases that we deal with are because of chronic inflammation. Something is chronically out of whack.

Inflammation is not a bad thing. It’s actually a protective mechanism of our body. It’s actually the trigger for the healing process, just like we were talking about before. It’s the domino trigger.

So getting an inflammatory flare is a good thing as long as it’s acute.

The problem in a lot of our patients is the inflammation stays up and it stays elevated. And now it’s chronically inflamed.

So instead of completely shutting it off, you deliver a regenerative fluid that has pro-inflammatory and anti-inflammatory modulators that kind of help balance everything out.

So it’s a little more of a buffer, and that’s how buffers work.

It allows for that inflammation to happen, but it kind of sets guardrails so it can calm things down when they’re out of whack.

Important Context About the Video

There is strong scientific rationale behind several concepts Dr. Kellar describes.

However, there are three areas where the short-form explanation deserves more context.

1. Chronic inflammation contributes to many diseases, but it does not explain every disease.

Persistent inflammatory signaling is involved in many chronic disorders.

That does not mean every chronic disease is simply caused by “too much inflammation.”

Depending on the condition, inflammation may be:

• A cause
• A consequence
• A protective response
• A contributing factor
• Several of those at once

Reducing inflammation is therefore not automatically the same thing as treating the underlying disease.

2. MSCs do not simply “turn inflammation off.”

This is actually one of the strongest parts of Dr. Kellar’s explanation.

MSC biology appears to be context dependent.

Research shows that inflammatory signals can change MSC behavior and influence the molecules they release. Human MSCs exposed to inflammatory cytokines have demonstrated changes in extracellular-vesicle production and immunomodulatory cargo.

So describing MSCs as simple anti-inflammatory drugs misses the complexity.

3. IV MSCs do not automatically travel directly to every inflamed organ.

After intravenous administration, MSCs commonly accumulate initially in the lungs.

A systematic review of MSC biodistribution in animal models and humans found initial pulmonary accumulation following IV delivery, followed by redistribution involving organs such as the liver, spleen, and kidneys.

Researchers are actively investigating how much of an MSC’s systemic effect depends on:

• Where the cells physically travel
• What they release
• How they interact with circulating immune cells
• How the recipient clears the cells

A 2025 expert perspective emphasized that the fate, persistence, clearance, and mechanisms of systemically administered MSCs remain incompletely understood.

So:

“IV stem cells find every inflamed organ” is too simple.

1. What Is Inflammation?

Inflammation is part of the immune system’s response to something it interprets as a threat or injury.

That might include:

• Infection
• Trauma
• Tissue damage
• Toxins
• Foreign material
• Abnormal immune activity

An inflammatory response can involve:

• Blood vessels
• Immune cells
• Cytokines
• Chemokines
• Complement proteins
• Other signaling systems

These mechanisms help recruit cells and resources to an area where something needs attention.

Without inflammation, normal responses to infection and injury would be severely impaired.

2. Acute vs Chronic Inflammation

This distinction is central to Dr. Kellar’s explanation.

Acute Inflammation

Acute inflammation is generally temporary.

Imagine spraining your ankle.

Soon afterward it may become:

• Swollen
• Warm
• Painful
• Tender

Those changes are part of the biological response to injury.

The inflammatory response recruits immune activity and contributes to the sequence of events involved in tissue repair.

Chronic Inflammation

Problems can arise when inflammatory pathways remain active longer than appropriate or become dysregulated.

Chronic inflammatory signaling is involved in many conditions, including some:

• Autoimmune diseases
• Metabolic diseases
• Cardiovascular diseases
• Chronic pulmonary diseases
• Degenerative conditions

But chronic inflammation is not one single biological state.

The cells and cytokines involved in rheumatoid arthritis, for example, are not necessarily identical to those driving inflammatory activity within osteoarthritis or inflammatory bowel disease.

That is why “inflammation” cannot be treated as one diagnosis.

3. What Are Cytokines?

Cytokines are small signaling proteins that cells use to communicate.

Think of them as biological messages.

Different cytokines can tell cells to:

• Become activated
• Move toward an injury
• Increase inflammation
• Decrease inflammation
• Proliferate
• Change their behavior

Examples include:

• Interleukins
• Interferons
• Tumor necrosis factors
• Transforming growth factors

A cytokine is not inherently “good” or “bad.”

Its effect depends on:

• Which cytokine
• Concentration
• Timing
• Tissue
• Receptor
• Other signals occurring simultaneously

This is one reason Dr. Kellar’s concept of balance is more biologically useful than simply saying inflammation needs to be shut down.

4. What Are Growth Factors?

Growth factors are another category of signaling molecules involved in communication between cells.

They may influence processes such as:

• Cell survival
• Proliferation
• Migration
• Blood-vessel biology
• Tissue remodeling

Examples relevant to MSC research include factors from pathways involving:

• Transforming growth factor beta
• Hepatocyte growth factor
• Vascular endothelial growth factor
• Insulin-like growth factors
• Fibroblast growth factors

These molecules already exist throughout the human body.

Regenerative medicine did not invent them.

Researchers are interested in biologic therapies because cells and cell-derived products may influence how these naturally occurring signaling systems behave.

5. What Is the MSC Secretome?

The term secretome describes the collection of substances a cell releases.

The MSC secretome may contain:

• Cytokines
• Growth factors
• Chemokines
• Extracellular vesicles
• Proteins
• Lipids
• Other signaling molecules

This has changed the way scientists think about MSCs.

The older, simplified model was:

Stem cell enters damaged tissue → turns into replacement tissue → repairs the problem.

Modern MSC research increasingly focuses on:

Stem cell enters a biological environment → interacts with host cells → releases signals → alters cellular and immune behavior.

Human laboratory studies have shown that MSC secretomes from different tissue sources contain different cytokine and growth-factor profiles and can influence macrophage behavior.

That is one reason the source and manufacturing of an MSC product matter.

Two products labeled “stem cells” do not necessarily have identical secretomes.

6. How Can MSCs Interact With Inflammation?

One heavily studied mechanism involves the interaction between MSCs and immune cells.

For example, researchers have shown that MSC-derived conditioned media can influence human monocytes and macrophages.

In one human-cell study, adipose-derived MSC conditioned media reduced several inflammatory signals and altered macrophage-associated signaling in laboratory conditions.

Other research has demonstrated MSC interactions involving:

T Cells

MSCs may influence T-cell proliferation and inflammatory behavior.

Macrophages

MSC signaling may shift macrophage behavior toward phenotypes associated with resolution and immune regulation.

Dendritic Cells

MSC signaling can influence antigen presentation and dendritic-cell maturation.

B Cells

MSC interactions may influence B-cell proliferation and antibody-related pathways.

These mechanisms help explain why MSCs have attracted interest well beyond orthopedic medicine.

7. Can MSCs Be Both Pro-Inflammatory and Anti-Inflammatory?

Potentially, yes.

This is one reason calling them simply “anti-inflammatory cells” is incomplete.

MSC behavior can change in response to the inflammatory environment.

Researchers sometimes refer to this as inflammatory priming or licensing.

For example, human adipose-derived MSCs exposed to the inflammatory cytokines interferon-gamma and TNF-alpha increased production of extracellular vesicles containing immunomodulatory cargo. Those vesicles inhibited T-cell proliferation in laboratory testing.

Another study examining MSC secretomes in inflammatory joint models found that inflammatory priming changed the profile of secreted cytokines, chemokines, extracellular vesicles, and microRNAs.

So inflammation does not simply encounter a passive cell.

The inflammatory environment can change what the MSC does.

8. Why the “Buffer” Analogy Makes Sense

Dr. Kellar uses a buffer as his analogy.

That is actually a useful way to think about immunomodulation.

The goal of a buffer is not necessarily to drive something to zero.

It helps prevent excessive movement in either direction.

Similarly, healthy immune function requires balance.

Too little inflammation can impair the body’s ability to respond appropriately to injury or infection.

Too much or prolonged inflammatory signaling may contribute to tissue damage and chronic disease.

MSC research is therefore often described in terms of:

immunomodulation

rather than simply:

immunosuppression.

The distinction matters because the biological objective is not necessarily to turn the immune system off.

It is to influence an abnormal or excessive response.

9. What Happens After an IV MSC Infusion?

This is one of the most fascinating and misunderstood areas of MSC research.

When MSCs are administered intravenously, they enter the venous circulation.

That blood travels directly toward the lungs.

Because MSCs are relatively large compared with many circulating blood cells, a substantial proportion can initially become retained within the pulmonary microvasculature.

This is often called the:

pulmonary first-pass effect.

A systematic review examining biodistribution studies in both animals and humans found that IV MSCs commonly accumulated first within the lungs, followed by later detection involving the liver, spleen, and kidneys.

Another systematic review described limited survival and migration toward some target tissues as an unresolved challenge of systemic MSC delivery.

So the old idea that every IV stem cell simply circulates freely until it finds an injury is not supported by current biodistribution research.

10. Do IV Stem Cells Travel Directly to Inflamed Organs?

Some preclinical research supports the concept that inflammatory signaling can influence MSC migration toward injured tissue.

But that does not establish a universal “homing GPS.”

Different studies have produced different biodistribution patterns.

After IV administration:

• Many MSCs initially reach the lungs
• Many do not permanently engraft
• Some may later redistribute
• Some may be cleared
• Immune interactions can occur during clearance
• Secreted molecules may contribute to systemic effects

Current experts emphasize that the fate and functional persistence of administered MSCs remains incompletely understood.

That means we should be careful with claims such as:

“The cells know where to go.”

or:

“They seek out every damaged organ.”

Those phrases simplify a much more complicated and still evolving field.

11. Can MSCs Affect the Body Without Permanently Reaching an Injured Organ?

Possibly.

This is an especially interesting part of modern research.

Scientists increasingly recognize that long-term engraftment may not be necessary for every MSC-mediated effect.

The cells may influence the recipient through:

• Secreted cytokines
• Growth factors
• Extracellular vesicles
• Immune-cell interactions
• Apoptosis and subsequent clearance by immune cells

A 2025 expert review highlighted MSC apoptosis and interactions between dying MSCs, phagocytes, and blood-vessel barriers as potentially important parts of systemic MSC biology.

So an MSC does not necessarily need to permanently become part of a liver, joint, lung, or other organ to potentially influence biological signaling.

12. What Does Human Research Show About Systemic Inflammation?

Human research provides proof that IV MSCs can influence measurable immune pathways, but clinical outcomes vary considerably by disease.

COPD

In a placebo-controlled randomized trial involving 62 patients with moderate to severe chronic obstructive pulmonary disease, participants received four monthly IV infusions of allogeneic MSCs or placebo.

The treatment was studied partly because COPD involves chronic pulmonary and systemic inflammation.

The trial did not establish broad clinical efficacy, illustrating an important lesson:

Biological rationale does not automatically translate into meaningful clinical improvement.

Follow-up molecular analysis from patients receiving MSC infusions demonstrated a strong but temporary change in circulating immune-cell gene expression, including downregulation of pathways involving IL-8 and IL-1β.

That is a good example of the difference between:

detecting immunological activity

and

proving clinical effectiveness.

Septic Shock

In an early phase human study of allogeneic bone-marrow-derived MSCs in septic shock, researchers measured circulating cytokines before and after IV administration to evaluate biological effects and safety.

The trial was small and designed primarily as a safety and dose-escalation study, not as proof that MSCs cure sepsis.

Again, the research demonstrates why immune markers and patient outcomes must be evaluated separately.

Graft-Versus-Host Disease

One of the most important examples of MSC immunomodulation is acute graft-versus-host disease.

This is no longer only experimental.

In December 2024, the FDA approved Ryoncil, or remestemcel-L-rknd, an allogeneic bone-marrow-derived MSC therapy for steroid-refractory acute graft-versus-host disease in pediatric patients two months of age and older.

It was the first FDA-approved mesenchymal stromal cell therapy in the United States.

This is an important milestone because it shows that an MSC product can successfully move through formal clinical development and FDA review for a specific immune-mediated disease.

But it also demonstrates an equally important principle:

FDA approval belongs to a specific product for a specific indication.

Ryoncil’s approval does not mean other MSC products are approved for unrelated inflammatory or regenerative conditions.

13. Are Stem Cells FDA-Approved for Chronic Inflammation?

There is no general FDA approval for:

“chronic inflammation.”

Ryoncil is FDA-approved specifically for pediatric steroid-refractory acute graft-versus-host disease.

That approval should not be applied to:

• Osteoarthritis
• Chronic pain
• Autoimmune wellness protocols
• General inflammation
• Fatigue
• Anti-aging
• IV wellness
• Other conditions

FDA maintains a current list of licensed cellular and gene-therapy products, including Ryoncil.

A patient’s specific regenerative product, intended use, and regulatory status should therefore be discussed clearly before treatment.

14. Local vs Systemic Regenerative Treatment

Another important distinction is the route of administration.

Local Treatment

A local injection places a regenerative product directly into or around the target structure.

Examples might include:

• Knee
• Shoulder
• Tendon
• Ligament

This approach is designed around a particular anatomical problem.

Systemic Treatment

IV treatment introduces a product into the circulation.

The rationale is therefore different.

Researchers evaluating systemic MSC therapy are interested in:

• Immune modulation
• Paracrine signaling
• Circulating inflammatory pathways
• Cellular interactions
• Biodistribution

A systematic biodistribution review found that administration route strongly influenced where MSCs were detected after treatment. Intra-articular and other local routes did not produce the same systemic distribution pattern as intravenous administration.

Neither route should automatically be considered “better.”

The appropriate route depends on what researchers or clinicians are trying to accomplish.

15. Why Product Quality Matters Here Too

The fact that MSCs release cytokines and growth factors does not mean every MSC product releases the same ones in the same quantities.

Secretome composition can depend on:

• Tissue source
• Donor
• Passage
• Culture environment
• Oxygen concentration
• Inflammatory priming
• Manufacturing
• Cell state

A 2023 study comparing human MSCs from multiple tissue sources found differences in cytokine and growth-factor secretion based on source and culture method.

This connects directly with two questions we have discussed elsewhere:

What cells are actually in the product?

and

How were they manufactured?

If much of MSC biology is mediated through cell signaling, then manufacturing conditions can become biologically important.

16. Does “Anti-Inflammatory” Automatically Mean Better?

No.

This is another misconception worth addressing.

Inflammation is sometimes necessary.

Imagine an infection.

You do not want your immune system completely unable to respond.

Inflammatory signals also participate in:

• Wound response
• Recruitment of immune cells
• Tissue remodeling
• Defense against pathogens

The issue is not simply whether inflammation exists.

It is whether the response is:

• Appropriate
• Proportional
• Properly timed
• Able to resolve

This is why immunomodulation is generally a more accurate term than promising that regenerative therapy will simply eliminate inflammation.

17. What Should Patients Ask About IV Stem Cell Therapy?

If you are considering a systemic regenerative treatment, ask more than:

“How many cells are in the IV?”

Questions may include:

What exact product is being administered?

Ask about:

• Tissue source
• Cell type
• Manufacturing
• Viability
• Passage
• Testing

Why is IV administration being recommended?

What is the treatment goal?

Is it being used for a specific diagnosis or for generalized wellness?

What research applies to my condition?

Research involving one inflammatory disease does not automatically establish effectiveness for another.

What evidence applies to this exact cell product?

A clinical study involving Ryoncil, for example, cannot establish effectiveness for an unrelated umbilical-cord-derived product.

What happens to the cells after IV administration?

A knowledgeable provider should be able to discuss pulmonary first-pass distribution rather than claiming every cell simply migrates directly to an injury.

What clinical outcome are we hoping to improve?

Ask whether the goal is:

• Symptoms
• Function
• Laboratory markers
• Quality of life
• Another measurable outcome

What cannot be promised?

No systemic regenerative treatment should be presented as guaranteed to:

• Eliminate inflammation
• Cure autoimmune disease
• Repair every damaged organ
• Reverse aging
• Treat every chronic condition

Frequently Asked Questions

Can stem cells reduce inflammation?

MSCs can demonstrate immunomodulatory and inflammation-related biological effects in laboratory and human research.

Human studies have documented changes in inflammatory pathways following MSC administration.

That does not mean every MSC product has been proven to improve every inflammatory disease.

How do stem cells affect inflammation?

Researchers are studying several mechanisms, including release of cytokines, growth factors, extracellular vesicles, and other soluble mediators.

MSCs also interact directly and indirectly with numerous immune-cell populations.

What are cytokines?

Cytokines are signaling proteins used by cells to communicate.

Some promote inflammatory responses, while others help regulate or resolve them.

Their effects depend on context.

Are cytokines bad?

No.

Cytokines perform essential functions throughout normal immune biology.

Problems may occur when certain pathways are excessively active, insufficiently regulated, or chronically stimulated.

What are growth factors?

Growth factors are signaling molecules that influence cellular behaviors such as survival, proliferation, migration, and tissue remodeling.

They occur naturally throughout the human body.

What is the stem cell secretome?

The MSC secretome refers to the collection of substances released by MSCs, including cytokines, growth factors, extracellular vesicles, proteins, and other signaling molecules.

Human research demonstrates that secretome composition can vary based on cell source and culture conditions.

Do IV stem cells travel everywhere in the body?

Not exactly.

IV MSCs commonly accumulate initially within the lungs.

Later redistribution to organs such as the liver, spleen, and kidneys has been observed, but biodistribution depends strongly on administration route and other factors.

Do stem cells automatically find inflammation?

Inflammatory signals may influence MSC migration in experimental models, but the concept that every IV cell automatically seeks and reaches every inflamed tissue is an oversimplification.

Systemically administered MSC fate remains an active area of research.

Can MSCs work even if they do not stay in an organ?

Researchers increasingly believe that some MSC effects may occur through temporary signaling, immune interactions, extracellular vesicles, and processes associated with MSC clearance rather than permanent engraftment.

Is inflammation always bad?

Acute inflammation is an essential part of normal immune defense and tissue response.

No.

The concern is often persistent or dysregulated inflammation rather than inflammation itself.

Is there an FDA-approved mesenchymal stem cell therapy?

Yes.

In December 2024, the FDA approved Ryoncil, an allogeneic bone-marrow-derived mesenchymal stromal cell therapy, for steroid-refractory acute graft-versus-host disease in pediatric patients two months of age and older.

It was the first FDA-approved MSC therapy.

Does that mean MSCs are FDA-approved for inflammation generally?

No.

Ryoncil is approved for one specific disease and patient population.

Its approval does not make unrelated MSC products FDA-approved for orthopedic conditions, chronic pain, wellness, fatigue, or generalized inflammation.

Are The Re/ Clinic’s stem cell therapies FDA-approved?

The Re/ Clinic offers stem cell therapies that have not been FDA-approved for the regenerative indications for which the clinic provides them.

Utah law requires an applicable disclosure to patients and in applicable advertising for non-FDA-approved stem cell therapies.

The Goal Isn’t to Turn Inflammation Off

One of the most useful ideas from Dr. Kellar’s explanation is that inflammation should not automatically be treated as the enemy.

Your immune system needs inflammation.

The challenge is regulation.

Researchers are increasingly studying MSCs not simply as replacement cells, but as dynamic signaling cells capable of interacting with inflammatory and immune environments.

Growth factors, cytokines, extracellular vesicles, immune cells, manufacturing conditions, and route of administration all become part of that conversation.

And there is still a great deal we do not know.

At The Re/ Clinic in Sandy, Utah, our regenerative medicine consultations are designed to help patients understand:

• What biologic product is being discussed
• Why a particular route may be considered
• What current research supports
• What remains experimental
• What results can and cannot reasonably be expected

If you are researching regenerative medicine because of a chronic condition, joint problem, or concerns related to inflammation, start with the diagnosis and the science rather than assuming inflammation itself is the disease.

Schedule a consultation with The Re/ Clinic to learn more about regenerative medicine and whether a local or systemic approach may be appropriate to discuss.

Call: 385-240-1000
Location: 9035 S 700 E, Sandy, UT 84070

References

1. Guillén MI, et al. Paracrine Anti-inflammatory Effects of Adipose Tissue-Derived Mesenchymal Stem Cells in Human Monocytes. Frontiers in Physiology. 2018. Human-cell research demonstrating anti-inflammatory paracrine effects of MSC-conditioned media on monocytes and macrophages.
2. Peshkova M, et al. MSCs’ conditioned media cytokine and growth factor profiles and their impact on macrophage polarization. Stem Cell Research & Therapy. 2023. Research showing differences in cytokine and growth-factor profiles among MSCs from several human tissue sources and culture conditions.
3. Mesenchymal stromal cell cytokine-priming study. Human MSC research demonstrating that inflammatory cytokine exposure can alter extracellular-vesicle secretion and immunomodulatory cargo.
4. Inflammatory priming of MSC secretome in joint-disease models. Research demonstrating that inflammatory exposure changes cytokines, chemokines, extracellular vesicles, and microRNA profiles within the MSC secretome.
5. Santos JM, et al. Biodistribution of Mesenchymal Stromal Cells after Administration in Animal Models and Humans: A Systematic Review. 2021. Review showing strong route-dependent biodistribution and initial pulmonary accumulation following IV MSC administration.
6. Fate and function of exogenously administered mesenchymal stromal cells: current insights and future directions. Cytotherapy. 2025. Expert perspective addressing MSC biodistribution, persistence, clearance, apoptosis, and unresolved mechanisms after systemic administration.
7. Transcriptional profiling of circulating mononuclear cells from patients with COPD receiving mesenchymal stromal cell infusions. Human clinical research demonstrating temporary changes in inflammatory gene-expression pathways following IV MSC treatment.
8. Effects of Mesenchymal Stem Cell Treatment on Systemic Cytokine Levels in a Phase 1 Dose Escalation Safety Trial of Septic Shock Patients. Human phase I research evaluating cytokine responses following allogeneic MSC administration.
9. U.S. Food and Drug Administration. FDA Approves First Mesenchymal Stromal Cell Therapy to Treat Steroid-Refractory Acute Graft-Versus-Host Disease. December 18, 2024. Ryoncil became the first FDA-approved MSC therapy.
10. U.S. Food and Drug Administration. RYONCIL. Current indication: steroid-refractory acute graft-versus-host disease in pediatric patients two months of age and older.
11. Utah Code § 58-1-512. Stem Cell Disclosure. Effective May 6, 2026. Requires specified disclosure for applicable non-FDA-approved stem cell therapies, including applicable advertising.

Utah Stem Cell Therapy Notice

THIS NOTICE MUST BE PROVIDED TO YOU UNDER UTAH LAW.

This health care practitioner performs one or more stem cell therapies that have not yet been approved by the United States Food and Drug Administration.

You are encouraged to consult with your primary care provider before undergoing a stem cell therapy.

Utah Code § 58-1-512 requires this notice in applicable stem-cell-therapy advertising.