The Pancreas: Our Most Underrated Metabolic Organ & Why Its Health is Vital

Summary

The Metabolic Classroom with Dr. Ben Bikman

Episode Title: The Pancreas: Our Most Underrated Metabolic Organ & Why Its Health is Vital
Date: October 6, 2025
Host: Dr. Ben Bikman
Podcast Host Organization: Insulin IQ

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Overview of the Episode

In this mini-lecture, Dr. Ben Bikman unpacks the remarkably complex and often overlooked role of the pancreas in human metabolism. He explains the dual functionality of the pancreas as both an endocrine and exocrine organ ("the ultimate metabolic multitasker")—responsible for both hormone regulation (notably insulin and glucagon) and digestive enzyme secretion. Through clear, practical explanations, Dr. Bikman lays out why pancreatic health is essential for metabolic balance, digestion, and ultimately, for preventing diseases like type 2 diabetes and malnutrition.

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Key Discussion Points & Insights

1. Pancreas—Anatomy and Structure

(01:52 - 04:30)

• Position & Shape: Tucked behind the stomach, about 20 cm long, consisting of three main sections: head (by the small intestine), body, and wrapped tail (by the spleen).
• Functional Division:
  • Exocrine Pancreas: About 98% of the pancreatic mass; produces digestive enzymes and bicarbonate for the small intestine.
  • Endocrine Pancreas: Only 1–2% of mass; made up of the ‘islets of Langerhans,’ highly vascularized islands of hormone-producing cells.
• Portal-like Blood Arrangement:
  • Blood flows from islets into exocrine tissue, creating rapid, local communication between hormone secretion and digestive activity.
  • “When you have a portal system, you need to send one signal to another part before it runs back throughout the entire body. In other words, you don’t want to wait that long. You want to send the signal much more rapidly.” (Dr. Bikman, 04:18)

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2. Endocrine Pancreas: Hormone Production & Local Interactions

(04:30 - 15:03)

• Islet Cell Types:
  • Beta Cells: ~50% of islet mass; secrete insulin.
  • Alpha Cells: Secrete glucagon.
  • Delta Cells: Secrete somatostatin.
  • PP Cells: Secrete pancreatic polypeptide.
  • Epsilon Cells: Secrete ghrelin (majority from the stomach).
• Paracrine vs. Endocrine Communication:
  • Endocrine: Hormone travels via bloodstream to distant targets.
  • Paracrine: “These small little neighborhoods of cells...one cell releasing a hormone that doesn’t need to get into the blood. It immediately goes right next door.” (Dr. Bikman, 07:03)
• Detailed Hormone Functions:
  • Insulin: Master metabolic hormone, responsible for glucose uptake, fat storage (inhibits lipolysis), protein synthesis.
    • “Insulin is the body's storage manager...problems arise when insulin is chronically high.” (08:38)
  • Glucagon: Counterbalances insulin; raises blood glucose during fasting, promotes fat breakdown (lipolysis).
    • “Glucagon is insulin’s counterbalance. It’s the yang to the yin.” (09:54)
  • Somatostatin: Acts as a metabolic brake—dampens both insulin and glucagon to keep them in check.
    • “You could say that somatostatin acts as kind of a babysitter.” (12:37)
  • Pancreatic Polypeptide: Contributes to satiety, potential future target for weight-loss therapies.
  • Ghrelin: Hunger hormone, stimulates appetite and growth hormone release.
• Dynamic Regulation:
  • Sympathetic nervous system boosts glucagon, inhibits insulin; parasympathetic does the opposite.
• Disease Implications:
  • Disruption of these hormones (especially chronic hyperinsulinemia) can lead to insulin resistance, type 2 diabetes, overeating, and metabolic dysfunction.

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3. Exocrine Pancreas: Digestive Powerhouse

(15:03 - 20:33)

• Secretion Volume:
  • 1–2 liters of alkaline, enzyme-rich fluid into the small intestine daily; critical for digestion.
• Enzymes Produced:
  • Amylase: Breaks down carbohydrates (starch → glucose & fructose).
  • Lipase: Digests fat molecules (triglycerides → fatty acids & glycerol).
  • Proteases (Trypsin, Chymotrypsin, Carboxypeptidase): Digest proteins.
    • Proteases secreted as inactive precursors (‘zymogens’) to prevent auto-digestion of pancreas.
    • “A pretty clever system to make sure that the pancreas isn’t compromising itself.” (18:50)
• Bicarbonate Role:
  • Neutralizes acidic stomach contents entering the small intestine.
• Disorders:
  • Cystic Fibrosis: Thickened pancreatic secretions block enzyme release.
  • Pancreatitis: Inflammation destroys exocrine tissue, causing fat malabsorption; replacement therapy may become essential.

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4. Regulation of Exocrine Secretion

(20:33 - 24:55)

• Three Overlapping Phases:
  • Cephalic Phase: Triggered by sight/smell of food (brain → vagus nerve).
  • Gastric Phase: When food enters the stomach.
  • Intestinal Phase: Most important; as food enters small intestine, stimulates release of CCK and other hormones.
• Endocrine/Exocrine Interplay:
  • Insulin supports growth/synthesis of digestive enzymes.
  • Somatostatin restrains enzyme secretion.
  • Disrupted signaling (e.g., diabetes, pancreatitis) can harm both digestion and glucose regulation.
  • “If one part of the organ is suffering, no surprise that the other follows.” (Dr. Bikman, 25:23)

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5. Pancreatic Disease and Lifestyle Takeaways

(24:55 - 25:48)

• Dual Vulnerability:
  • Damage to exocrine tissue can harm endocrine function and vice versa.
  • Example: Pancreatitis can lead to diabetes. Diabetes (“lack of insulin production”) can cause atrophy in the exocrine pancreas, impairing digestion.
• Diet & Lifestyle:
  • Excess refined carbs and chronic high insulin burden both disrupt endocrine/exocrine harmony.
  • “If you can help keep the endocrine side working well with a proper balance of insulin and glucagon, then you can also help the exocrine side continue to work well…” (25:18)

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Notable Quotes & Memorable Moments

“As much as we often discuss these two aspects of the pancreas—endocrine and exocrine—as being very distinct, they absolutely are connected.”
— Dr. Ben Bikman (03:38)

“Insulin and glucagon create a push-pull system, if you will, that helps maintain metabolic stability… They maintain homeostasis. And one good example of this is just fasting.” — Dr. Ben Bikman (10:28)

“Somatostatin does serve as a modulator… It acts as kind of a babysitter. It helps smooth out what might otherwise be too dramatic of a peak. So it’s kind of like a metabolic brake pedal.” — Dr. Ben Bikman (12:30)

“If one part of the organ is suffering, no surprise that the other follows... by understanding and supporting the balance through diet, exercise, and other just rational, smart lifestyle choices, we protect not only digestion, but also, of course, the entire metabolic function of the body.” — Dr. Ben Bikman (25:23 - 25:48)

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Timestamps for Important Segments

• [01:52] Episode content starts – Introduction to the pancreas and its dual function.
• [04:30] Structure and division into exocrine and endocrine functions.
• [06:17] Types of endocrine cells and hormone interactions.
• [08:38] Detailed roles of insulin and disease implications.
• [09:54] Glucagon function & push-pull dynamic with insulin.
• [12:30] Somatostatin and role as a “brake pedal.”
• [15:03] Transition to exocrine function.
• [17:09] Digestive enzymes and mechanisms protecting the pancreas from self-digestion.
• [20:33] Exocrine disorders (cystic fibrosis, pancreatitis) and their impact.
• [21:00] Regulation phases of exocrine secretion (cephalic, gastric, intestinal phases).
• [24:55] Endocrine-exocrine interplay in disease and lifestyle advice.
• [25:48] Summary and final takeaways.

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Episode Tone and Language

Dr. Bikman speaks in an engaging, accessible tone, breaking down complex biological concepts into straightforward, memorable language. He often uses metaphors (e.g., “metabolic babysitter,” "push-pull system") and addresses listeners as students, reinforcing the classroom format and encouraging practical application of knowledge.

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Summary Takeaway

The pancreas is a critical, underappreciated organ at the crossroads of digestion and metabolism. Its endocrine (hormone-producing) and exocrine (digestive secretion) functions are tightly linked—disruption in one can impact the other. By understanding and protecting pancreatic function through diet, exercise, and lifestyle, we can support both healthy digestion and metabolic balance.

Transcript

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[Ben Bickman]

Welcome to the Metabolic Classroom podcast. I'm Ben Bickman. Thanks for letting me be your guest professor for the next few minutes. Don't worry about any pop quizzes. I'm here to simply make the science of metabolism clear, practical and engaging. Welcome to the Metabolic Classroom. I'm Professor Benjamin Bickman, a biomedical scientist and professor of cell biology. Everyone, thanks for tuning in. Thanks for being my honorary students for another one of these mini lectures where we just consistently unpack the fascinating topic of human metabolism. Today, we're diving deep into a topic that is central to both digestion and metabolism or nutrient control. Nutrient metabolism. And that is the endocrine and the exocrine pancreas. That might be a term you've never heard before, but it is a testament to how remarkable and unique the pancreas is, because this remarkable organ does double duty. It releases hormones into the bloodstream and that these hormones thematically manage nutrient metabolism. But that's the endocrine part. What about the exocrine? Well, that is where this double duty organ also dispatches digestive juices and enzymes into the intestines to help break down our food. In other words, the pancreas works to digest those very nutrients that it then will help regulate as it secretes hormones into the bloodstream. In this episode, we'll explore the key products from each side, endocrine and exocrine, as well as their actions and even how they interact in some pretty interesting ways. As much as we often discuss these two aspects of the pancreas, endocrine and exocrine, as being very distinct, they absolutely are connected. So whether you are a student, a health enthusiast, or you're just curious about how your own body works, I actually think you're going to come away from this mini lecture with a much greater appreciation for the pancreas as a metabolic multitasker. Now, before we get into function, let's just talk about the anatomy and the structure of the pancreas. The pancreas sits within the body, tucked behind the stomach. It's not too big, it stretches to around 20 centimeters in length. And structurally, it has three parts. It has what's commonly called the head, which is near the beginning of the small intestine. Then there's the body of the pancreas. And then there's the tail, this wrapped around tail, which is over near our spleen. But the more important division is between its exocrine and endocrine tissues. It's less of an anatomical distinction in the. In the organ. Now, about 98% of the mass of the pancreas is exocrine. So these are the cells that produce the digestive enzy. Well as bicarbonate. Yes. In fact, the very bicarbonate you may use in your baking. Just 1 to 2% of the pancreas is made up of the endocrine part. And this is made up specifically of these areas called the islets, or these small little islands of cells called the islets of Langerhans, named after the individual who discovered them. And these are heavily vascularized, in other words, lots of blood flow. There are regions with lots of blood flow, which allows a very rapid hormone release into the blood. One fascinating design detail is that blood flows from the islets into the surrounding exocrine tissue. So endocrine hormones like insulin can influence digestion directly. In physiology or anatomy, this is sometimes referred to as a portal, where you have an artery which is coming from the lungs and all of its oxygen and nutrients, it will separate into capillaries to feed some cells and then usually it will then come back to the heart and lungs. So it has one pass through one cell type and then it comes back. But when you have a portal system, you have the blood vessels separating and feeding cells and then going in to feed another set of cells and then coming back to the heart and lungs. So this is a portal. It's a portal like arrangement where we have this elegant managing or of two functions really needing to work, needing to coordinate their efforts together. That's usually what a portal system is going to reveal. It's that you need to send one signal to another part before it runs back throughout the entire body. In other words, you don't want to wait that long. You want to send the signal much more rapidly. Okay, now let's start with, now that you have a general overview of the structure and the anatomy of the pancreas, let's start with the endocrine pancreas. And that is coming back to the islets of Langerhans. The islets contain several types of hormone producing cells. The most famous beta cells, they make up about half of the islet and of course they produce insulin inside. Then you have alpha cells which secrete glucagon. You have delta cells that release a hormone called somatostatin. And then you have pancreatic polypeptide coming from the PP cells. In fact, those cells are named for their product, the pancreatic polypeptide pp. And then you also have ghrelin. Though most ghrelin comes from the stomach, there is some contribution of the epsilon cells in the pancreas. So we have all of these products coming from the endocrine pancreas. Now these hormones of course, do not act in isolation. They communicate constantly, both through local paracrine signaling and through input from the nervous system. Now let me just share some thoughts on the paracrine aspect when we use the term paracrine within the realm of endocrinology, that is distinct from endocrine. Endocrine is when you release a hormone into the blood to then go affect other hormones elsewhere, other cells rather. So one cell type is releasing a Hormone, it flows through the blood to some other faraway cell to tell that cell to do something. That's not what we have happening in the islets, these small little neighborhoods of cells where you can have one cell releasing a hormone that doesn't need to get into the blood. It immediately goes right next door to a different cell, like the beta cell, releasing insulin, going right over to the alpha cell, which would be releasing glucagon. That's paracrine signaling. All right? So that's important to appreciate that there's a lot of signals going back and forth across all of these cells within the islets, never even needing to go into the blood. They're just operating in a paracrine fashion. One of the hormones I just mentioned was somatostatin from the delta cells. Somatostatin can directly dampen insulin from the beta cells and glucagon from the alpha cells. So somatostatin wants to operate as a break on both of those. And then, of course, meanwhile, we have the sympathetic nervous system, the topic of last time's metabolic classroom, which is going to boost glucagon and inhibit insulin, Whereas we have the parasympathetic, which is going to in turn boost insulin. So you also have that direct sympathetic innervation where you have neurons coming right to the eyelets, telling the eyelets that, hey, the brain wants me to tell you to do something, and so I'm going to do it all right? Now, I mentioned the name of the hormone, so let's briefly go through the function, especially of the key ones. So, insulin is the master metabolic hormone. It is the body's storage manager, released in response to typically rising glucose after a meal, insulin will help tissues such as muscle fat, to pull in the glucose. But even in other tissues, like the liver, it helps the liver know what to do with that glucose. And indeed, it promotes glycogen storage in the liver. It will inhibit the breakdown of that glycogen. It will inhibit the production of new glucose gluconeogenesis. And of course, it very, very heavily encourages fat storage, mostly by inhibiting lipolysis. But insulin also supports protein synthesis by helping the muscle cells maintain their muscle protein by inhibiting the breakdown. But problems arise when insulin is chronically high. Of course, something that you've heard me talk about abundantly. Diets that are heavy in refined carbohydrates or constant snacking of those refined carbohydrates keep insulin elevated. And over time, cells stop responding effectively. This insulin resistance forces the pancreas to work harder which can lead to type 2 diabetes as either the insulin production goes down or at the same time, I should say, and or the body continues to just be very resistant to that insulin. Glucagon is insulin's counterbalance. It's the yang to the yin. When blood glucose falls, whether from fasting or prolonged exercise, glucagon signals the liver to release glucose from glycogen and to make new glucose through gluconeogenesis. It will also promote fat breakdown, once again having an opposite effect to insulin, which is then going to be freeing fatty acids from the stored fat cells. What was stored as triglycerides are now getting broken down into free fatty acids. So again, that isn't as much as we focus on how insulin and glucagon are having opposite effects at the liver with regards to either promoting glycogen or breaking it down, respectively, we also see opposing effects at the fat cell. Insulin wanting to inhibit lipolysis, glucagon wanting to stimulate it. Now together they each play a part. Insulin and glucagon create a push pull system, if you will, that helps maintain metabolic stability. It they maintain homeostasis. And one good example of this is just fasting. During fasting, insulin levels drop because blood glucose levels come down and then glucagon rises to make sure that the glucose doesn't go too low. At the same time. This shift insulin down glucagon up increases the mobilization of fat. So lipolysis and, and the fat burning, beta oxidation as well as the production of ketones to help offset the need of the brain in particular for glucose. This natural flexibility is of course diminished in insulin resistance, where insulin stays elevated and glucagon is going not going to be able to do what it wants to do. So we're trapping the body into an energy storage mode. Now I'd mentioned for those of you who are paying attention, you're wondering what about the other hormones? Okay, I'd mentioned somatostatin. Somatostatin does serve as a modulator. It is, it wants to inhibit both insulin and glucagon. It keeps them in check, it prevents them from going too high. So you could say that somatostatin acts as kind of a babysitter. It helps smooth out what might otherwise be too dramatic of a peak. So it's kind of like a metabolic brake pedal. And then pancreatic polypeptide will contribute to satiety signaling. And in fact this is one of the hormones that may be leveraged in future satiety focused drug therapies to help with weight loss. And then ghrelin is a hunger hormone, so it's acting in opposite. It also comes from the epsilon cells. Yes, from the stomach, as I noted earlier, but it wants to stimulate appetite and actually stimulate growth hormone release.

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[Ben Bickman]

Now. These most recently mentioned hormones aren't going to be as famous as insulin, certainly, and not even as famous as glucagon. But disruptions in their signaling can contribute to overeating. Like if you're not making enough pancreatic polypeptide, hunger will be up. If you're making more ghrelin, hunger will be up. It can also affect digestion and just contribute to some of the metabolic mayhem that we see in problems like type 2 diabetes, where the eyelets are just a little disrupted in the population of cells they have. Okay, that is, I think, a sufficient primer on the endocrine pancreas. Let's transition now to discuss the exocrine pancreas that is the digestive powerhouse. Each day, the exocrine pancreas, all of those cells of the pancreas that make these digestive enzymes, it actually secretes up to one to two liters of a very alkaline enzyme rich fluid. All of this what we call digestive juice into the small intestine. Now I say it's alkaline. That means it's basic chemically or its PH is high. That's because of the bicarbonate. It's like that baking soda. The bicarbonate neutralizes stomach acid. So think about how the stomach has this really acidic Mix and it is going to start dripping into the small intestine, which doesn't have that big mucus protective lining that the stomach has. So how do we prevent that acidic mixture from coming into the small intestine and ripping right through it? Well, we negate it. We, we neutralize it with this bicarbonate rich slurry of digestive juices coming from the pancreas. So it helps create the right ph environment for the enzymes to function and just to protect and maintain the anatomy and the function of the small intestine. Now what about the enzymes? So the three, the, these enzymes break down the, the three major macronutrients. For example, the panc is releasing amylase into the small intestine. Well, that's going to help us digest starches, so, you know, carbs into its simple molecules like glucose and fructose. The pancreas also releases lipase. Enzymes, lipases will, you can hear that probably what it does. It will help digest triglycerides. It takes that big three part three fatty acids bound to glycerol molecule and starts pulling off the individual fatty acids and then the glycerol. And that's going to also, of course, do that with the help of bile and another enzyme called CO lipase. So bile is what helps split up all the fats. And then the lipases from the pancreas are going to come in and actually do the kind of individual trimming at the level of the molecule itself. But then we also have protein. And that's where the proteases come in. Proteases like trypsin or chymotrypsin and carboxypeptidase. These are enzymes from the pancreas that digest the proteins. And now interestingly, when it comes to these proteases, they're actually secreted from the pancreas as they get secreted in an inactive form called a precursor. Zymogens, they're referred to in that family of zymogens. And that's just to make sure that the pancreas actually doesn't digest itself. Because imagine if you were releasing an enzyme that could break down proteins. Well, what if you start breaking down the proteins in your own cells, in your, in your cell membranes, so they don't get activated until they actually reach the intestines where there's a particular enzyme called enterokinase which will then start converting trypsinogen, which is what the pancreas actually makes. It converts trypsinogen to trypsin and then trypsin will activate the rest. So it's a pretty clever system to make sure that the pancreas isn't compromising itself.

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[Ben Bickman]

Now. Problems here quickly show up as malnutrition. So if you got a problem in your ability to digest food, you're going to start starving. Even if you're eating like for example, cystic fibrosis that in that instance defective bicarbonate secretion thickens the pancreatic juices and it blocks the enzyme release. But also if you have a chronic inflamed pancreas or pancreatitis, then you can have destruction of the exocrine tissue which causes most commonly fat malabsorption. You can't digest your fat in such cases, of course, what you've got to do is Put those enzymes back in so you have pancreatic enzyme replacement therapy becomes essential just for the person to survive. Now let's talk about the regulation of the exocrine pancreas because there's three overlapping phases here. The first is the cephalic phase. That's a phase that's. It's almost like Pavlov's dog, where it's triggered simply by sight and smell of food, where the signals are traveling from the brain through the vagus nerve. Once again, go revisit the autonomic nervous system mini lecture from last time. But next we have the gastric phase, which is activated when food actually enters the stomach. And then we have the release of the of gastrin, which is a hormone from the stomach. Then finally, and arguably the most important, we have the intestinal phase. That's the most significant because this is where we actually have have the release of other hormones like chistinin, CCK and other responses as the food is coming into the small intestine where a lot of digestion is happening and then all of the absorption. Interestingly, there's an interplay here, as I alluded to earlier, where endocrine hormones influence this process. For example, insulin supports asanar growth and enzyme synthesis. So the asinar are the area that's the part of exocrine pancreas, the production of the digestive enzymes. Well, insulin helps those, those cells maintain their function. Somatostatin actually restrains enzyme secretion. It prevents them from being released when they shouldn't be released. And then pancreatic polypeptide also plays a little role. So we have this really interesting dialogue where we have these three canonical endocrine characters, insulin and the pancreatic polypeptide, somatostatin, each playing a part to regulate the degree to which the exocrine pancreas interacts here. And we do see disrupted communication in disease. For example, I noted pancreatitis. Pancreatitis damages exocrine cells, but it will often lead to diabetes because of collateral damage to islets, the islets of Langerhans, the endocrine part. Conversely, in diabetes, the lack of an insulin production and insulin's effect can lead to exocrine atrophy. Remember how he said how insulin helps keep those exocrine cells functioning? But what if you aren't making insulin or you don't have enough in your pancreas? Then you can start to atrophy those exocrine cells and so you're not going to have enough of those digestive enzymes being produced. So the practical lesson here is that to me, lifestyle habits can directly affect both sides of the pancreas. If you have a diet that is high in refined carbs and you're putting a burden on or less effective production of insulin, disrupted production of insulin, let's say, no surprise that you might start to have disrupted function of the exocrine side. But in in contrast, if you can help keep the endocrine side working well with a proper balance of insulin and glucagon, then you can also help the exocrine side continue to work well, helping you maintain an ideal process of digestion and better gut health and overall better nutrition. So I hope as I wrap up, I've convinced you that the pancreas is in fact a metabolic multitasker. And there's nothing to compare to it. Where when you consider the endocrine hormones, they are regulating nutrient metabolism and energy balance, but you also have the exocrine products that ensure we can actually get those nutrients in the first place, where we digest and absorb those nutrients. The two systems are inseparably linked, of course, not only in function, but in anatomy too, where it's all coming from one single organ. And if one part of the organ is suffering, no surprise that the other follows. Remember, there is direct communication between to as the blood is flowing. By understanding and supporting the balance through diet, exercise and other just rational, smart lifestyle choices, we protect not only digestion, but also of course, the entire metabolic function of the body. Until next time, more knowledge, better health. Big news. Boost Mobile is now sending experts nationwide to deliver and set up customers new phones at home or work. Wait, we're going on tour? Not a tour. We're delivering and setting up customers phones so it's easier to upgrade.

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[Paige Desorbo / Mrs. Claus's Sister]

Mrs. Claus much younger sister and AT T Mobile there's no trade in needed when you switch so you can keep.

[Elf Drew Ski]

Your old phone or give it as a gift.

[Paige Desorbo / Mrs. Claus's Sister]

And the best part? You can make the switch to T Mobile from your phone in just 15 minutes.

[Ben Bickman]

Nice.

[Elf Drew Ski]

My side of the tree is slipping. Kimber the holidays are best better AT.

[Capital One / Mint Mobile / AT&T Mobile Advertiser]

T Mobile switch in just 15 minutes and get iPhone 17 on us with no trade in needed. And now T Mobile is available in US cellular stores with 24 monthly bill credits for well qualified customers plus tax and $35 device connection charge credits and imbalance due if you pay off earlier. Cancel financing agreement. 256 gigs $830 eligible for it in a new line $100 plus a month plan with auto payments, taxes and fees required. Check out in 15 minutes or less per line.

[Ben Bickman]

Visit t mobile.com miccheck12 Are we recording? Hi, I'm Michelle Bernstein, an award winning chef, restaurateur and mom. I have a lot on my plate.

[Paige Desorbo / Mrs. Claus's Sister]

Including my psoriatic arthritis symptoms.

[Ben Bickman]

That's why I was prescribed Cosentyx. It helps me move better.

[Capital One / Mint Mobile / AT&T Mobile Advertiser]

Cosentyx Secukenumab is prescribed for people 2 years of age and older with active psoriatic arthritis. Don't use if you're allergic to Cosentyx. Before starting, get checked for tuberculosis. An increased risk of infections and lowered ability to fight them may occur like tuberculosis or other serious bacterial, fungal or viral infections. Some were fatal. Tell your doctor if you have an infection, infection or symptoms like fevers, sweats, chills, muscle aches or cough. Had a vaccine or plan to or if inflammatory bowel disease symptoms develop or worsen serious allergic reactions and severe eczema like skin reactions may occur. Learn more at 1-844-cosentics or cosentix.com Ask.

[Paige Desorbo / Mrs. Claus's Sister]

Your rheumatologist about Cosentix.