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Category: Paleo Diet

  • BEET CARROT APPLE SALAD: low carb + paleo

  • Instant Pot Zucchini Bolognese

    Post From https://nomnompaleo.com/instant-pot-zucchini-bolognese

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    Have you heard of Meghan Markle’s genius zucchini bolognese recipe? The one that takes OVER FOUR HOURS to make? Of course you have—that’s why a bunch of you have asked me to make a speedier Instant Pot version! At the request of those persistent Nomsters, I’ve created this simple and delicious Whole30-friendly Instant Pot Zucchini Bolognese recipe that takes just a fraction of the time, and is a whole lot meatier. (Because PALEO.) So if you’ve got a bumper crop of zucchini in your garden and you want to eat like a royal, this recipe is perfect for you!

    Before she became a fairytale princess, Meghan Markle wasn’t just a Hollywood actress—she had a side gig as a food and lifestyle blogger. One of her recipes that went viral after her wedding was a simple pasta sauce that she made with zucchini (or courgettes, for you proper Brits), onions, olive oil, water, and a bouillon cube. According to Meghan, the trick for a creamy, dreamy sauce was just to cook everything low and slow for 4 hours.

    But who has 4 hours to babysit a pot on the stove? (Certainly not Meghan Markle—at least not these days.) When one of my readers asked me if I knew of an Instant Pot hack for Meghan’s recipe, I started brainstorming ways to make this recipe Whole30-friendly and significantly cut down the cooking time. Plus, to add some protein to this dish and make it a complete meal, I wanted to beef up the sauce (pun intended).

    After numerous attempts, I finally arrived at this simple and delicious Instant Pot Zucchini Bolognese recipe. I replaced the chemical-laden bouillon with my umami-packed Magic Mushroom Powder, and tossed in a pound of bulk Italian sausage for extra protein. Best of all, this recipe can be made from start to finish in an hour in an Instant Pot. I’m super chuffed!

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    You can serve this meaty sauce on your favorite veggie noodles, gluten-free noodles, or even regular old pasta (I won’t tell anyone of your Paleo heresy), and you’ll be amazed at how tasty and simple it is. Thanks for the inspiration, Duchess of Sussex!

    Serves 4




    Grab your Instant Pot or pressure cooker and turn on the Sauté function. When the metal insert is hot, pour in the olive oil.

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    Toss in the diced onions…

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    …and cook, stirring frequently, for 2 to 3 minutes or until slightly softened.

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    Add the Italian sausage and break it up with a silicone spatula.

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    Cook the sausage until it’s no longer pink.

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    Dump in the zucchini, minced garlic…

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    …and 1 teaspoon of Magic Mushroom Powder or Diamond Crystal brand kosher salt. (The salt won’t add extra umami, so you may want to add a few drops of fish sauce or a couple of dried mushrooms to the pot for extra savoriness.)

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    Stir well.

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    You don’t need to add any extra liquid. Trust me—the zucchini will release enough liquid for the contents to reach high pressure. Lock the lid and program the Instant Pot to cook for 35 minutes under high pressure.

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    When the sauce is done cooking, you can wait for the pressure to release naturally or you can manually vent it if you’re impatient.

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    The zucchini and onions should be fork-tender and easily mashed with a spatula…

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    …to form a chunky sauce.

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    Taste the sauce and adjust the seasoning with additional Magic Mushroom Powder, salt, or freshly ground pepper. Stir in the juice from half a lemon and taste it again. (Always, always, ALWAYS taste your food and season accordingly!)

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    When the sauce is ready, grab a spiralizer to prepare some zucchini noodles (or grab some ready-to-go spiralized veggies at the store).

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    If I’m serving this sauce on zoodles, I drop the raw spiralized zucchini straight into the pot and toss ’em around until the hot sauce softens the zoodles to my liking.

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    Top with your favorite herbs and dig in!

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    This sauce freezes really well so make a batch whenever your vegetable crisper is overflowing with zucchini!

    Instant Pot Zucchini Bolognese by Michelle Tam https://nomnompaleo.com

    Want more Instant Pot recipes? Check out my ever-growing roundup of Instant Pot recipes here.

    Also, you can watch the replay of me and the boys making this dish live from my kitchen on my Facebook page on August 15, 2018 below:

    Looking for more recipe ideas? Head on over to my Recipe Index. You’ll also find exclusive recipes on my iPhone and iPad app, and in my cookbooks, Nom Nom Paleo: Food for Humans (Andrews McMeel Publishing 2013) and Ready or Not! (Andrews McMeel Publishing 2017)!

    Recipe IndexNom Nom Paleo CookbooksNom Nom Paleo App


    Instant Pot Zucchini Bolognese

    Prep 10 mins

    Cook 50 mins

    Total 60 mins

    Author Michelle Tam

    Yield 4 servings

    This simple and quick Whole30-friendly Instant Pot Zucchini Bolognese recipe is a riff on Meghan Markle’s original version, but a whole lot meatier!



    1. Grab your Instant Pot or pressure cooker and turn on the Sauté function. When the metal insert is hot, pour in the olive oil.
    2. Toss in the diced onions and cook, stirring frequently, for 2 to 3 minutes or until slightly softened.
    3. Add the Italian sausage and break it up with a silicone spatula. Cook the sausage until it’s no longer pink.
    4. Dump in the zucchini, minced garlic, and 1 teaspoon of Magic Mushroom Powder or Diamond Crystal brand kosher salt. (The salt won’t add extra umami, so you may want to add a few drops of fish sauce or a couple of dried mushrooms to the pot for extra savoriness.) Stir well.
    5. You don’t need to add any extra liquid. Trust me—the zucchini will release enough liquid for the contents to reach high pressure. Lock the lid and program the Instant Pot to cook for 35 minutes under high pressure.
    6. When the sauce is done cooking, you can wait for the pressure to release naturally or you can manually vent it if you’re impatient. 
    7. The zucchini and onions should be fork-tender and easily mashed with a spatula to form a chunky sauce.
    8. Taste the sauce and adjust the seasoning with additional Magic Mushroom Powder, salt, or freshly ground pepper. Stir in the juice from half a lemon and taste it again. (Always, always, ALWAYS taste your food and season accordingly!)
    9. When the sauce is ready, grab a spiralizer to prepare some zucchini noodles (or grab some ready-to-go spiralized veggies at the store). If I’m serving this sauce on zoodles, I drop the raw spiralized zucchini straight into the pot and toss ’em around until the hot sauce softens the zoodles to my liking.
    10. Top with your favorite herbs and dig in! This sauce freezes really well so make a batch whenever your vegetable crisper is overflowing with zucchini!

    Courses Dinner

    Cuisine Italian, Whole30, Paleo, Primal, Gluten-free, Keto,

    The post Instant Pot Zucchini Bolognese appeared first on Nom Nom Paleo®.

  • Carrot Halwa – Guest Post by Bethany Darwin

    Post From https://www.thepaleomom.com/carrot-halwa-bethany-darwin/

    Bethany Darwin is the blogger behind Adventures in Partaking and the author of AIP Safari: Fast, Friendly Foods for Any Adventure (an AIP travel cookbook full of tips for AIP travel based on 40 years of international travel) and My Paleo AIP Indian Adventure (a fully AIP elimination phase compliant Indian cookbook full of authentic flavor). Bethany lives in Abu Dhabi, UAE with her hubby (who happens to be Indian and her Indian food inspiration) where she spends her days creating fun and flavorful recipes and exploring the world around her. After years of undiagnosed lower back pain, sudden eye pain in 2013 led to a diagnosis of uveitis, which led to a rheumatologist appointment and finally a diagnosis of spondyloarthritis. In an attempt to avoid immunosuppressants, she searched online and found the Autoimmune Protocol (via The Paleo Mom). Now, four years later she is living well and managing her pain through the AIP diet and lifestyle. Bethany shares many of her meals on instagram and posts several AIP friendly recipes or articles on Facebook every day.

    The night before I jumped into the AIP world with both feet, I ate a homemade vegetarian thai green curry. I believed this was a healthy choice to make. For a few years I had been gluten free, dairy free and sugar free as well as limited meats (mainly only eating seafood). So,  I made this beautiful curry with homemade green curry paste and eggplant and tomatoes and potatoes and you’re starting to see the problem, right? I ate dinner then went for my evening walk.
    A few blocks into the walk I noticed my left knee was hurting and thought I must have been sitting funny at work. A few minutes later my left ankle was hurting and I contributed it to a run earlier in the week. Then it was my right knee. Then it was my neck and my fingers started getting stiff and sore. What was happening to me? Why did every joint in my body hurt? I was even taking anti-inflammatory drugs. This didn’t make any sense.
    As I walked I started thinking back to some reading I had done earlier in the day here on THE PALEO MOM’s site. I remembered reading something about nightshades and how they caused inflammation in a lot of people. You see, I had been searching a mere 6 hours earlier with the keywords ‘autoimmune disease diet’ and I had found the AIP. I had read it with a grain of salt because I was already eating so well. I didn’t need this diet. I was doing ok.
    But, by the time I got home I was in worse pain than I had experienced in years. I pulled out the computer and came back to the Paleo Mom and began my AIP journey. I woke up the net morning and had leftovers for breakfast instead of eggs. I cleaned out my pantry. I got rid of all of my nightshades. I jumped in with two feet and I haven’t looked back.
    Almost 4 years later and I’ve added a few things back into my diet, but 90% of the time I’m still in the AIP elimination phase and I’m loving the life this diet has given back to me. BUT, I was still missing my curries. And this love of curry and feeling of deprivation over spicy foods was magnified as a little over a year ago I met and married a wonderful Indian man. I wanted to cook his favorites, but how could I? I spent hours chatting with him and his mom and researching ideas and recipes and after a few successful recreations he said, ‘why don’t you write a cookbook?’ And that my friends, was the start of  My Paleo AIP Indian Adventure.
    Over the next few months, my hubby and I worked together to create the recipes for this cookbook and he was my taste tester and quality control, expert. Nothing was added to the cookbook without his (and sometimes my in-laws) stamp of approval. Each and every dish we recreated is full authentic Indian flavor without a hint of grains, dairy, sugar, eggs or nightshades.
    paleo indian adventureWe managed to create for you more than 60 authentic Indian recipes that will allow anyone and everyone to enjoy Indian food again. All of the recipes are written fully AIP compliant and many also include reintroduction notes for those of you who may have been able to reintroduce seed-based spices or nuts. But the whole cookbook remains completely free of nightshades (those pesky little veggies). This cookbook is now available as both an ebook and a paperback.
    Along with all these recipes I’ve also included information about the food culture of India, spice and substitution guides, a glossary of Indian ingredients, substitutions for coconut sensitivity, as well as a discussion about the stages of grief when losing chili spices (or other foods) on the AIP.
    To help you get a taste of the recipes in this cookbook, I want to share one of the recipes. I asked my hubby what I should share and he quickly rattled off several of his favorites… Lamb Rogan Josh, Chicken Reshmi Kebabs, Plantain Bajis. And then he stopped, smiled and said, ‘you have to give them the recipe for carrot halwa.’ Carrot Halwa was his favorite recipe growing up in India and a special treat that his mom would always make in the fall. But, it’s pretty much just ghee and sugar (with some carrots), so he didn’t think it would be possible, but when I served this dish to him his face lit up and I knew we had a winner. This carrot halwa is dairy free, processed sugar-free (it has AIP compliant sugars & dried fruit…. so still needs to be consumed in moderation), and according to my hubby and my mother-in-law, tastes just like the real thing. And I love being able to serve my hubby one of his faves without worrying about all the yucky ingredients.
    Hope you enjoy!!!

    Carrot Halwa

    Serves 4 – Time- 50 minutes


    • 3 cloves
    • 1/8 tsp cinnamon powder
    • 1/8 tsp ginger powder
    • 2 TBSP coconut oil
    • 2 1/2 cups grated carrots (about 4 large)
    • 1 1/2 cups coconut milk
    • 1/4 cup shredded coconut
    • 3 TBSP coconut sugar
    • 1/4 tsp pink salt
    • 1/4 cup raisins
    • OPTIONAL – nuts for garnish (AIP reintroduction)


    • wash, peel and grate the carrots – this is best done by hand to maintain texture 
    • heat a medium saucepan over a low to medium flame and add the spices to the dry pan – cloves, cinnamon & ginger and allow to dry roast until fragrant – about 90 seconds
    • add coconut oil to pan and mix into spices and continue cooking about 30 seconds
    • add grated carrots and stir well to incorporate oil and spices through the carrots
    • let cook and start to soften for about 5 minutes
    • add coconut milk and stir regularly until milk is more than half absorbed. This will take 15-20 minutes
    • add coconut sugar, shredded coconut and salt and stir regularly until liquid is almost completely absorbed – no need to stir continually, just every 1-2 minutes. You may need to turn the heat down if the mixture starts to stick to the pan.
    • add raisins and continue cooking and stirring continually until all liquid is absorbed.
    • remove from heat and try to find the cloves and remove
    • serve warm or cold – optionally you can garnish with nuts (if you have reintroduced them).

    In Bethany Darwin e-cookbook, My Paleo AIP Indian Adventure, you will find:

    • breads – chapatis, roti, dosa, paratha
    • basics – curry powder, coconut milk, ‘rice’, etc.
    • snacks – chat, samosas, bajis, etc.
    • chutneys -coconut, tamarind, mango, etc.
    • curries, kebabs and biryani – meat, chicken, seafood
    • veg dishes – cabbage, cassava, okra, pumpkin, bitter gourd, etc.
    • drinks – kahwa, chai, etc.
    • desserts – halwa, burfi, kulfi, gulab jamun, etc.
    • and more!!!

    Download your copy of My Paleo AIP Indian Adventure or grab a paperback. copy and have fun adding some spice to your AIP meals.

    paleo indian adventure

    The post Carrot Halwa – Guest Post by Bethany Darwin appeared first on The Paleo Mom.

  • Cooking Jill’s low-carb moussaka

  • How Gluten (and other Prolamins) Damage the Gut

    Post From https://www.thepaleomom.com/how-gluten-and-other-prolamins-damage-the-gut/

    One of the core principles of a Paleo diet is avoiding foods that contain compounds called toxic lectins. The term toxic lectin originates from the fact that lectins are a class of carbohydrate-binding proteins found in all foods (and indeed all forms of life, including humans!), but that only a subset of these are an issue for human health via food consumption (hence lectins versus toxic lectins). The lectins that are of concern have a few important properties: they are relatively stable through food preparation; they are difficult for humans to digest; they are known to interact strongly with the brush border of the intestine (which may impact cell viability and/or barrier function in addition to allowing protected transport of the toxic lectin into the body); and they are biologically active once they enter the body. There are two main classes of these toxic lectins: prolamins and agglutinins. Agglutinins will be discussed in another post.


    What are Prolamins?

    Prolamins are a toxic lectin that are abundant in grains, legumes, and pseudo-grains (more specifically, in the seed of the plant, which includes wheat, oats, barley, quinoa, rice, peanuts, and soy).

    Gluten is the best-known example of a prolamin, the most thoroughly studied, and is also the most dangerous. Most recently, the term glutenoid has been coined to emphasize the connection between other members of this glycoprotein family and the effects of gluten. Much of the current understanding of the effect that prolamins have on the gut barrier, but also on the overall immune system, comes from studies of gluten (and more specifically, the protein component of gluten, which is called gliadin), often conducted in the context of celiac disease. Although glutenoid has yet to catch on, when it does it may be easier for people to understand that there are similar proteins in nongluten-containing grains as well as pseudo-grains and legumes that are similarly problematic for health.

    Prolamins function as storage proteins in plants and are the major source of important proteins for seed germination. In fact, prolamins account for approximately half the total protein in all grains. There are many different prolamins, all characterized by their high content of the amino acid proline. Examples of prolamins are gliadin in wheat (gliadin is the protein fraction of gluten), hordein in barley, secalin in rye, zein in corn, kafirin in sorghum, orzenin in rice, and avenin in oats.

    Usually food proteins are degraded into very small peptides or individual amino acids by digestive enzymes (called peptidases or proteases) before they are transported across the gut epithelium. However, prolamins are not completely broken down in the normal digestive process, both because the structure of these proteins is not compatible with our digestive enzymes (which are not good at breaking apart proline-rich proteins into individual amino acids) but also because the seeds that contain prolamins also contain protease inhibitors (compounds that stop our enzymes from breaking down proteins, a part of the seed’s natural defense mechanisms, discussed more in Wheat and Innate Immunity and How Do Grains, Legumes and Dairy Cause a Leaky Gut? Part 2: Saponins and Protease Inhibitors). Therefore, many prolamin fragments travel though the digestive tract but are also able to cross the gut barrier largely intact, and in doing so, damage the barrier and cause a leaky gut.


    How Do Prolamins (like Gluten) Cross the Gut Barrier?

    Most of the current understanding of how prolamins cross and damage the gut barrier comes from studies of various gliadin fragments (which are commonly formed when gluten is partly digested by our proteases). Several fragments of gliadin have been well-characterized in terms of their effect on the gut barrier and their ability to activate both the innate and the adaptive immune systems. Gliadin fragments can cross the gut barrier through one of two pathways:

    1. paracellular—in between the cells that line the gut
    2. transcellular—through the cells that line the gut (which encompasses multiple routes)

    In some people, one route or the other will dominate (probably dependent on genetic factors). For others, both pathways are important contributors to a leaky gut. And while it doesn’t really matter which way prolamins are causing your gut to be leaky, understanding these pathways is important for grasping the necessity of avoiding grains, pseudo-grains, and legumes. See also Grains: What Are They?Are Pseudograins Pseudobad?3 Myths About Legumes — Busted!The Green Bean Controversy and Pea-GateWhat Is A Leaky Gut? (And How Can It Cause So Many Health Issues?)What Should You Eat To Heal a Leaky Gut?, and 8 Nutrients for Leaky Gut.


    Quick Review of Gut Cell Biology

    The gut is a barrier between the inside of your body and the outside world. Yes, as unintuitive as it may be, the stuff inside your digestive tract is actually outside your body. But, the gut is a very unique barrier. Its job is to let important nutrients inside the body while keeping everything else out. This makes it a highly selective semi-permeable barrier. Nutrients enter the body through a variety of tightly controlled mechanisms.

    What forms this highly selective semi-permeable barrier is a single layer of highly specialized cells called gut epithelial cells, or enterocytes.

    Epithelial cells are amazing (I happen to be very fond of them in large part because the last two years of medical research I did before having my first daughter was studying these guys!). They are one of a few types of cells within the human body that have a top and a bottom. The structure of the cell membrane is different at the top of the cell compared to the sides and bottom. At the top (also called the apical side of the cell), the outer cell membrane is shaped into thousands of fingerlike projections called microvili which act to increase the surface area of the top of the cell. The membrane that forms the sides and bottom of the cell (also called the basolateral membrane) is smooth. These two membranes have different jobs to do. The apical membrane faces inside the gut, and has the very important job of engulfing nutrients to transport through the cell, across the basolateral membrane, and then into the body.

    What separates the apical and basolateral sides of the epithelial cell is a phenomenally complex and essential structure called a tight junction. Tight junctions are formed by the interweaving of dozens of different proteins, including several that cross the cell membrane (so part of the protein is inside the cell, part is embedded in the membrane, and part is outside the cell). These proteins tangle together in complex and dynamic ways to form a bond to the adjacent cells. Not only are tight junctions how the epithelial cell differentiates between its top and bottom, but it’s also part of the glue that holds this ever important sheet of cells together!

    Tight junctions are dynamic structures and the epithelial cell can control just how open or closed the junction is. The junction can be rapidly opened and closed to allow some larger nutrients across the cell. But, when something happens to damage the tight junction, or impact the cell’s ability to control how open or closed it is, that’s when a variety of bad things happen.

    There are two ways that a gut can become “leaky”. If something damages the gut epithelial cell and the cell dies, that leaves a small hole (at least until the gut can repair itself). If something triggers the opening of the tight junctions, that also leaves small holes that substances inside the gut can leak through into the body.  Not only does this create a pathway for things to leak into the body, but it’s also a tremendous stress on the cell. It can kill the cell (creating an even bigger hole), or worse: the loss of tight junction assembly is one of the steps for an epithelial cell to become a cancer cell.

    A leaky gut, or more technically “increased intestinal permeability”, means things can get across the gut barrier that aren’t supposed to. This happens when either the epithelial cells or the tight junctions are damaged. And right on the other side of that barrier is 80% of our body’s immune systems, acting as a sentinel, ready to attack anything that might try to cross the barrier. So, when you have a leaky gut, you also have an activated immune system. Read more in What Is A Leaky Gut? (And How Can It Cause So Many Health Issues?)What Should You Eat To Heal a Leaky Gut?, and 8 Nutrients for Leaky Gut.

    Okay, now on to the how prolamins interact with our enterocytes…


    Paracellular Pathway – Zonulin

    The best-understood way that gluten increases intestinal permeability is by stimulating the release of a protein called zonulin. Zonulin (also identified as haptoglobin 2 precursor) used to be thought of simply as a precursor protein, without a distinct function. However, now it is recognized as the only (so far, anyway) extracellular protein that impacts tight junction assembly. (As an aside, zonulin is a precursor for hatoblogin 2, which circulates in the blood and binds with free plasma hemoglobin to facilitate degradation and iron recycling while avoiding kidney damage from free hemoglobin.)

    Zonulin is released by enterocytes into the gut lumen (inside the gut), where it travels downstream and then binds to at least two different types of receptors in the enterocyte apical membrane, PAR2 and EGFr, which creates intracellular signaling cascades that displace important tight junction proteins (decreasing the protein-protein interactions that form the tight junction) thereby causing tight junctions to open and intestinal permeability to increase.

    Zonulin may play a normal role in digestion, by opening up the tight junctions to facilitate the absorption of some nutrients into the body. For example, even though glucose is actively transported into enterocytes (via the insulin-dependent GLUT4 transporter), the major portion of glucose is absorbed paracellularly, via increased tight junction permeability.

    Zonulin may have a normal role in protecting us from gut pathogens. Zonulin secretion is also stimulated by the presence of enteroinfectious bacteria, which has two effects. First, when the tight junctions open due to zonulin secretion, the hydrostatic pressure gradient flips so that water is secreted into the intestinal lumen (as opposed to being absorbed into the body), which helps to flush bacteria out of the body (in fact, this may explain the high frequency of loose stools and/or diarrhea as a symptom of enteropathogens).  Second the increased intestinal permeability exposes the invading pathogen to the immune system, allowing for a more efficient immune response.  Interestingly, this might be why gut pathogens are common triggering events for autoimmune disease.  And, here’s another way that an unhealthy or unbalanced gut microbiome may be linked to chronic disease: even nonpathogenic strains of E. coli (a Gram-negative normal resident of the human gut, at least in small quantities), causes an increase in intestinal permeability via increased zonulin release. This may represent another important link between leaky gut and the microbiome, see What Is the Gut Microbiome? And Why Should We Care About It?.

    The problem is when there’s too much zonulin.

    Too much zonulin causes increased intestinal permeability–yes, leaky gut. And, as you know, leaky gut is linked to every chronic illness in which a potential link has been investigated, hypothesized to be a necessary precursor to autoimmune disease and other conditions. Read more in What Is A Leaky Gut? (And How Can It Cause So Many Health Issues?)What Should You Eat To Heal a Leaky Gut?, and 8 Nutrients for Leaky Gut.

    When we consume gluten, it is partially digested (because of its incompatibility with our digestive enzymes) and predictable gliadin fragments are produced. These gliadin fragments bind with a specific receptor in the apical cell membrane of enterocytes, called the chemokine receptor 3 (CXCR3) , which stimulates the release of zonulin into the gut lumen (inside the gut).  This happens in everyone, but people with celiac disease are known to have an exaggerated zonulin response to gluten consumption, and this may be a key driver of the disease.  Interestingly, even people without celiac disease but who still have celiac risk genes (HLA-DQ2 and HLA-DQ8, which impacts an estimated 40% to 55% of the population, see Genes to Know About: Celiac Genes) have an exaggerated zonulin response when they consume gluten. This may be the cause of Irritable Bowel Syndrome, but also increases risk of a variety of other chronic health problems. See also Why Grains Are Bad – Part 1, Lectins and the Gut, and Gluten Cross-Reactivity: How your body can still think you’re eating gluten even after giving it up.

    In fact, increased zonulin levels are also linked to a variety of diseases, including:

    • Celiac Disease
    • Type-1-Diabetes
    • Inflammatory Bowel Disease/Colitis
    • Multiple sclerosis / EAE
    • Obesity/Insulin resistance
    • Type-2-Diabetes
    • Polycystic ovary syndrome
    • Acute Lung Injury
    • Asthma
    • Coronary artery disease
    • Glioma
    • Septicemia
    • HIV
    • Irritable Bowel Syndrome
    • Non-Celiac gluten sensitivity
    • Environmental Enteropathy
    • Necrotizing Enterocolitis

    A recent paper even linked low zonulin and endotoxin levels to longevity–centenarians have much lower zonulin levels than people aged less than 40 who had suffered acute myocardial infection and even lower than healthy young controls! Given that endotoxin is a toxic bacterial protein from the cell membranes of Gram-negative bacteria (which as discussed above, at least some of which stimulate zonulin release), it’s a reasonable assumption that being gluten-free and taking care of our gut microbiomes may be key to extending lifespan and lowering risk of chronic disease!

    And that’s just one mechanisms by which gluten and other prolamins increase intestinal permeability!


    Transcellular Pathways

    There are two transcellular pathways—retrotranscytosis and lysosomal. Retrotranscytosis of gliadin has only recently been identified, and thus far has been studied only in the context of celiac disease. The mechanisms of retrotrancytosis are not necessarily limited to celiac disease, however, and could occur in anyone with gluten intolerance and iron deficiency. Lysosomal pathways are also not limited to those with gluten antibodies or genetic susceptibilities.



    IgA antibodies produced by B cells in gut-associated lymphoid tissue are normally transported from the basolateral side of the gut enterocytes (the side facing inside the body) to the apical side of the gut enterocytes (the side facing inside the gut) and into the gut lumen (the space inside the gut). This is called transcytosis (which basically means transportation across a cell). IgA antibodies perform a variety of functions in the brush border and lumen of the intestine, including what is called immune exclusion, which is the interference with the ability of antigens (including viruses, bacteria, bacterial toxins, and enzymes) to adhere to and penetrate the gut barrier. IgA antibodies are then recycled by a mechanism called retrotranscytosis; that is, they are transported from the apical to the basolateral side of the cell, or from inside the gut back into the body. In addition to allowing for the recycling of these IgA antibodies, retrotranscytosis allows for antigen presentation from inside the gut to the immune system in a very controlled way. Importantly, retrotranscytosis may protect the gut enterocytes from viral and bacterial infection (by binding to antigens inside the cells) and thereby preserve the integrity of the gut barrier. Also, IgA retrotranscytosis is a form of protected transport across the cell, meaning that the IgA antibodies are not degraded or modified as they cross the cell (which occurs with many other forms of transport across the cell).

    IgA antibodies produced against gliadin bind to specific gliadin fragments in the intestinal lumen and form a stable complex. This IgA-gliadin complex fits into a specific receptor (called the transferrin receptor, which is normally used for the absorption of iron) in the apical membrane of the gut enterocytes. The complex is retrotranscytosed, and this causes intact gliadin fragments to be delivered to the basolateral side of the cell, where they can activate the immune system. This retrotranscytosis of gliadin has been well-characterized in the context of celiac disease. Once across the cell, the gliadin fragments are delivered to the gut-associated lymphoid tissue to stimulate the innate and adaptive immune systems. Again, the resulting production of cytokines and stimulation of inflammation can cause damage to gut enterocytes, thereby causing a leaky gut.

    Where do these IgA antibodies against gliadin come from? No one knows, but high levels of these gliadin-specific serum IgA antibodies in the intestinal lumen are found not only in individuals with active celiac disease, but also in healthy individuals. Importantly, there are an abnormally high number of transferrin receptors, which transport the IgA-gliadin complex into the cell, in the gut enterocytes of celiac disease patients. The increase in transferrin receptors may be caused by iron deficiency (iron-deficiency anemia is extremely common in celiac disease), forming yet another link to micronutrient deficiency.

    When gliadin crosses the gut barrier by retrotranscytosis, it is basically exploiting a normal recycling pathway and mechanism meant to protect the cells of the gut barrier from being damaged by infectious organisms.


    Lysosomal Pathway

    Even in healthy individuals, gliadin fragments are taken up by enterocytes through a process called endocytosis. Endocytosis is a normal function of all cells in the body by which they absorb molecules (such as long proteins that cannot enter the cells through the cell membrane or through specific transporters embedded in the cell membrane) by engulfing them (and other compounds) in a membranous structure (sort of like a bubble where the bubble surface is made of membrane that was part of the outer cell membrane before endocytosis). These “bubbles”are called endosomes, and they allow the cell to sort and recycle proteins in a targeted way (protein recycling is a very important function for every cell since it allows proteins to be reused, which is more efficient that building new proteins).

    Within the enterocyte, endocytosed proteins are held within a type of endosome called a lysosome. Lysosomes contain enzymes (called lysosomal-acid proteases) that can break proteins apart into individual amino acids. Lysosomes then travel to the basolateral membrane (the side of the cell facing inside the body, rather than inside the gut), where the contents of the lysosome can be exocytosed (which is the opposite of endocytosis, in which the contents are secreted out of the cell and the lysosome membrane can integrate back into the outer cell membrane). Even though the proteins are traveling from the apical side of the cell to the basolateral side of the cell, this is transcytosis (because this is the normal direction of transport across the cell for these proteins). In many healthy individuals, gliadin peptides can be fully digested within the lysosomes, but this is not the case for those with celiac disease. It is unknown what percentage of gliadin peptides may remain undigested through this process in those with autoimmune disease.

    There is also evidence that lysosomal damage may occur in response to gliadin fragments. (Interestingly, casein, a milk protein, does the same thing.) If a lysosome is damaged, not only do the still-intact gliadin fragments enter the cell cytoplasm, but so do the enzymes within the lysosome, which can then attack proteins within the cell, damaging and probably killing the cell. Basically, if a lysosome is damaged while digesting and transporting proteins across the cell, the release of the contents of the lysosome within the cell causes the cell to die. A damaged or dead cell opens up a hole through which other components of the gut can leak into the body and activate the immune system. This is one mechanism by which gliadin (and casein) can cause a leaky gut, even in healthy individuals who have no gluten sensitivity or intolerance. It is unknown if a dietary threshold exists for this lysosomal damage to occur or whether such a threshold could vary depending on genetic or other factors.

    An additional effect of the lysosomal pathway is the stimulation of inflammation through the production of oxidants. The accumulation of specific gliadin fragments within the lysosomes causes an increase in the production of reactive oxygen species (oxidants) without causing damage to the lysosome. Although not all the details of this process are understood, some of the signaling pathways have been uncovered, and it appears that some gliadin fragments stimulate signals known to drive inflammation. The production of oxidants can also cause damage to the cell, which may result in alterations in cell morphology (that is, cell shape, which also affects cell function) and cell division (proliferation), and may affect cell viability and cause apoptosis (programmed cell suicide). And, again, damage or enterocyte cell death leaves a hole in the gut barrier.

    Another damaging effect of lysosomal transport of gliadin fragments is the mobilization of intracellular calcium-ion stores, which causes endoplasmic-reticulum stress (because the endoplasmic reticulum contains the highest concentration of calcium ions within the cell, and the cell cannot function properly if it loses them). The endoplasmic reticulum is the organelle within every cell responsible for protein synthesis, lipid metabolism, carbohydrate metabolism, and detoxification. When it is stressed, it can’t do its job efficiently. Calcium ions are mobilized in response to gliadin fragments in the intact lysosome, although we don’t yet know quite how. In the context of celiac disease, this production of oxidants and the mobilization of calcium ions drive the initial increase in tissue transglutaminase (see Why Grains Are Bad-Part 1, Lectins and the Gut). And importantly, when endoplasmic-reticulum stress is severe or prolonged, cell death (via apoptosis) occurs. Again, this causes a hole in the gut barrier. As in the case of lysosomal damage, it is unknown whether dietary thresholds or genetic predisposition are factors; however, both of these mechanisms appear to apply generally. The generation of reactive oxygen species and calcium-ion mobilization may also be the result of specific gliadin fragments entering the cell via retrotranscytosis.

    What Is the Role of Genetics?

    What’s the takeaway here? There are many ways the prolamin gliadin (the protein fraction of gluten) can cross and damage the gut barrier, even in people without a genetic susceptibility to a leaky gut and even in people without diagnosed gluten sensitivity. Whether by paracellular or transcellular pathways, once outside the gut, these protein fragments interact with the gut-associated lymphoid tissue, stimulating the release of inflammatory cytokines and activating cells of both the innate and adaptive immune systems.

    There are a variety of ways gliadin can cause damage and death of gut enterocytes, all of which result in holes in the gut barrier through which various contents of the gut can leak out. Inflammation is triggered by gliadin fragments that cross the gut barrier, as well as by other partly digested food proteins, gut bacteria, bacterial fragments, and waste products or toxins likewise crossing over. This further activates the immune system, causing a vicious cycle of inflammation and gut-barrier damage.

    How important is genetic susceptibility? Certainly it is involved in the zonulin response to gliadin (it is unknown if HLA-DQ2 and HLA-DQ8 are the only genes that impact zonulin secretion). Although the role that genetic factors play in enterocyte damage caused by transport through the gut enterocytes remains unstudied, genetic predisposition may explain the variability in the severity of the damage caused by wheat consumption. It is likely that some damage is caused to the gut barrier of everyone who consumes wheat, but genes might explain why some people suffer from a severely leaky gut or autoimmune disease in response to wheat consumption while others seem to tolerate wheat without experiencing any overt health issues.

    It is important to emphasize that studies do confirm that gliadin fragments enter the human body intact, and bind with receptors in human cells, indicating biological activity. This is particularly implicated in obesity, see The Link Between Gluten and Obesity


    Prolamins and Gut Bacteria

    Prolamins also contribute to gut dysbiosis, which, as discussed What Is the Gut Microbiome? And Why Should We Care About It?, can cause a leaky gut all by itself. Not only are prolamins inherently difficult for our bodies to digest, but they interfere with important digestive enzymes in the brush border of the intestine. In particular, gliadin is known to inhibit the activity of three important enzymes: lactase, sucrase, and dipeptidyl peptidase 4. These are important for breaking sugars down into monosaccharides and proteins into amino acids for transport across the enterocyte barrier (lactase breaks apart lactose; sucrase breaks apart sucrose; dipeptidyl peptidase 4 has diverse functions related to digestion, metabolism, and immune regulation). This may have a profound effect on the gut microbiome because the inhibition of these enzymes alters what’s available for gut bacteria farther down the digestive tract (see Modifying Paleo for Small Intestinal Bacterial Overgrowth (SIBO))

    A recent study in gluten-sensitive primates demonstrated that gluten consumption causes a substantial and undesirable shift in the microbiome. In particular, gluten consumption significantly decreased alpha-diversity of the microbiome (recall that diversity is the single most important train of a healthy microbiome) with certain bacterial families being enriched (e.g., Streptococcaceae and Lactobacillaceae)..  A recent human study evaluating the microbiome shift caused by adopting a gluten-free diet showed decreases in several bacteria species, the strongest effect being a substantial reduction in Veillonellaceae, a Gram-negative, pro-inflammatory bacterium linked to Crohn’s disease and other gut pathologies.


    Is This Just about Gluten?

    So, if most of what is known about prolamins comes from the study of gluten and celiac disease, how do we know this applies to all prolamins?

    There is much similarity in structure and function (due to homology, or similarity in amino acid sequences) between the prolamins of different grains and legumes. While there have been no comprehensive studies evaluating the detrimental health effects of all food sources of prolamins, there is enough convincing evidence of similar proteins in nongluten-containing grains and pseudo-grains to support their complete removal from our diets. For example, studies show that prolamins in quinoa, corn, and oats can cause damage to the gut and stimulate the immune system in celiac sufferers in a manner completely analogous to gliadin. Clearly, this means that those with celiac disease should never consume these other grains or pseudo-grains. But also, because of the understanding that gluten increases intestinal permeability, which is strongly linked with all chronic illness, anyone struggling with a diagnosis should probably avoid the consumption of grains, pseudo-grains, and legumes.



    Alaedini, A. & Latov, N., Transglutaminase-independent binding of gliadin to intestinal brush border membrane and GM1 ganglioside, J Neuroimmunol. 2006 Aug;177(1-2):167-72

    Ballard ST, et al. Regulation of tight-junction permeability during nutrient absorption across the intestinal epithelium. Annu Rev Nutr. 1995;15:35-55.

    Bonder MJ, et al. The influence of a short-term gluten-free diet on the human gut microbiome. Genome Med. 2016 Apr 21;8(1):45. doi: 10.1186/s13073-016-0295-y.

    Cabrera-Chávez, F., et al., Maize prolamins resistant to peptic-tryptic digestion maintain immune-recognition by IgA from some celiac disease patients, Plant Foods Hum Nutr. 2012 Mar;67(1):24, 30

    Caputo, I., et al., Gliadin peptides induce tissue transglutaminase activation and ER-stress through Ca2+ mobilization in Caco-2 cells, PLoS One. 2012;7(9):e45209

    Carrera-Bastos, P, et al. Serum Zonulin and Endotoxin Levels in Exceptional Longevity versus Precocious Myocardial Infarction. Aging Dis. 2018 Apr; 9(2): 317–321.

    Clemente MG, et al. Early effects of gliadin on enterocyte intracellular signalling involved in intestinal barrier function. Gut. 2003;52:218–23.

    de Rooij, F.W., et al., Lysosomal damage by gliadin and gliadin peptides; an activity not related to coeliac disease, Clin Chim Acta. 1979 Jan 15;91(2):127-31.

    El Asmar R, et al. Host-dependent zonulin secretion causes the impairment of the small intestine barrier function after bacterial exposure. Gastroenterology. 2002;123:1607–15.

    Fasano A. Leaky gut and autoimmune diseases. Clin Rev Allergy Immunol. 2012 Feb;42(1):71-8.

    Fasano A. Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiol Rev. 2011 Jan;91(1):151-75.

    Fasano A., Physiological, pathological, and therapeutic implications of zonulin-mediated intestinal barrier modulation: living life on the edge of the wall. Am J Pathol. 2008; 173:1243–1252

    Fasano A., Surprises from celiac disease. Sci Am 2009; 301:54–61

    Fasano, A., Zonulin, regulation of tight junctions, and autoimmune diseases, Ann N Y Acad Sci. 2012 Jul;1258:25-33

    Friis, S., et al., Gliadin uptake in human enterocytes. Differences between coeliac patients in remission and control individuals, Gut. 1992 November; 33(11): 1487–1492

    Heyman, M. & Menard, S., Pathways of gliadin transport in celiac disease, Ann N Y Acad Sci. 2009 May;1165:274-8

    Holding, D. & Messing, J., Evolution, Structure, and Function of Prolamin Storage Proteins, in Seed Genomics (ed P. W. Becraft), 2013, Wiley-Blackwell, Oxford, UK.

    Kozáková, H., et al., Brush border enzyme activities in the small intestine after long-term gliadin feeding in animal models of human coeliac disease, Folia Microbiol (Praha). 1998;43(5):497-500

    Lebreton, C., et al., Interactions among secretory immunoglobulin A, CD71, and transglutaminase-2 affect permeability of intestinal epithelial cells to gliadin peptides, Gastroenterology. 2012 Sep;143(3):698-707.e1-4

    Luciani, A., et al.,  Lysosomal accumulation of gliadin p31-43 peptide induces oxidative stress and tissue transglutaminase-mediated PPARgamma downregulation in intestinal epithelial cells and coeliac mucosa, Gut. 2010 Mar;59(3):311-9

    Mamone, G., et al., Identification of a peptide from alpha-gliadin resistant to digestive enzymes: implications for celiac disease, J Chromatogr B Analyt Technol Biomed Life Sci. 2007 Aug 15;855(2):236-41

    Matysiak-Budnik, T., et al., Alterations of the intestinal transport and processing of gliadin peptides in celiac disease, Gastroenterology. 2003 Sep;125(3):696-707

    Matysiak-Budnik, T., et al., Secretory IgA mediates retrotranscytosis of intact gliadin peptides via the transferrin receptor in celiac disease, J Exp Med. 2008 January 21; 205(1): 143–154

    Mazumdar, K., et al., Visualization of transepithelial passage of the immunogenic 33-residue peptide from alpha-2 gliadin in gluten-sensitive macaques, PLoS One. 2010 Apr 19;5(4):e10228

    Ménard S., et al., Paracellular versus transcellular intestinal permeability to gliadin peptides in active celiac disease, Am J Pathol. 2012 Feb;180(2):608-15

    Reichelt KL, Jensen D. IgA antibodies against gliadin and gluten in multiple sclerosis. Acta Neurol Scand. 2004 Oct;110(4):239-241.

    Mohan M, et al. Dietary Gluten-Induced Gut Dysbiosis Is Accompanied by Selective Upregulation of microRNAs with Intestinal Tight Junction and Bacteria-Binding Motifs in Rhesus Macaque Model of Celiac Disease.Nutrients. 2016 Oct 28;8(11). pii: E684.

    Sturgeon C, Fasano A. Zonulin, a regulator of epithelial and endothelial barrier functions, and its involvement in chronic inflammatory diseases. Tissue Barriers. 2016 Oct 21;4(4):e1251384.

    Uibo, O., et al., Serum IgA anti-gliadin antibodies in an adult population sample. High prevalence without celiac disease, Dig. Dis. Sci. 1993; 38:2034–2037

    van de Wal, Y., et al., Selective deamidation by tissue transglutaminase strongly enhances gliadin-specific T cell reactivity, J Immunol. 1998 Aug 15;161(4):1585-8

    Vanuytsel T, et al, The role of Haptoglobin and its related protein, Zonulin, in inflammatory bowel disease. Tissue Barriers. 2013 Dec 1;1(5):e27321.

    Vojdani, A. & Tarash, I., CrossReaction between Gliadin and Different Food and Tissue Antigens,Food and Nutrition Sciences 2013; 4 (1): 20-32

    Zevallos, V.F., et al., Variable activation of immune response by quinoa (Chenopodium quinoa Willd.) prolamins in celiac disease, Am J Clin Nutr. 2012 Aug;96(2):337-44

    The post How Gluten (and other Prolamins) Damage the Gut appeared first on The Paleo Mom.

  • Keto Kafta Burgers

  • TPV Podcast, Episode 312: 6 Year Podversary Show

    Post From https://www.thepaleomom.com/podcast-favorite-episodes/

    In this episode, we’re 6 years old! Let’s celebrate by talking favorite episodes!


    Click here to listen in iTunes

    or download and listen by clicking the PodBean Player below

    If you enjoy the show, please review it in iTunes!

    The Paleo View (TPV), Episode 312: 6 Year Podversary Show

    favorite episodes

    The post TPV Podcast, Episode 312: 6 Year Podversary Show appeared first on The Paleo Mom.

  • Spicy Mango Cabbage Slaw

    Post From https://nomnompaleo.com/spicy-mango-cabbage-slaw

    Spicy Mango Cabbage Slaw by Michelle Tam https://nomnompaleo.com

    During the summer, I love nothing better than pairing grilled meats with a refreshing fruity and spicy slaw. One of my favorite Whole30-friendly salads is my Spicy Mango Cabbage Slaw from our latest cookbook, Ready or Not!

    Cabbage slaw may sound boring to you, but once you taste this combination of sweet mango, tongue-tingling jalapeño, tangy lime, and fresh mint, you’ll be turning to this fab slaw as your go-to side dish every time you break out the barbecue!

    Watch this quick cooking video to see how simple it is:

    .embed-container { position: relative; padding-bottom: 56.25%; height: 0; overflow: hidden; max-width: 100%; } .embed-container iframe, .embed-container object, .embed-container embed { position: absolute; top: 0; left: 0; width: 100%; height: 100%; }


    Don’t want to cook? If you happen to live in Northern California or Reno, you can wander into your neighborhood Whole Foods Market store and find this dish ready-to-eat and for sale behind the chef’s case until the end of September 2018!

    Spicy Mango Cabbage Slaw by Michelle Tam / Nom Nom Paleo https://nomnompaleo.com

    You can learn all the deets here!

    Serves 4


    • ¼ cup thinly sliced shallots or red onion
    • Juice from 2 limes
    • 2 mangoes, peeled pitted, and thinly sliced (I prefer Ataulfo mangos ’cause they’re the best.)
    • ½ small cabbage, cored and thinly sliced
    • ¼ cup fresh mint leaves, thinly sliced
    • 1 jalapeño pepper, thinly sliced (optional)
    • Diamond Crystal brand kosher salt
    • Freshly ground black pepper



    In a small bowl, soak the thinly sliced shallots in the lime juice with a cube of ice for at least 10 minutes.

    Spicy Mango Cabbage Slaw by Michelle Tam https://nomnompaleo.com

    Prep the other ingredients as the shallots chill out in lime juice.

    Spicy Mango Cabbage Slaw by Michelle Tam https://nomnompaleo.com

    My favorite type of mangos are the Ataulfo (a.k.a. honey or champagne) mangos because they are sweeter and less fibrous than Kent and Tommy Atkins varieties.

    Spicy Mango Cabbage Slaw by Michelle Tam https://nomnompaleo.com

    When you’re ready to assemble the salad, toss the mango and sliced cabbage into a large bowl. Add the soaked shallots, sliced mint, and jalapeño pepper.

    Spicy Mango Cabbage Slaw by Michelle Tam https://nomnompaleo.com

    Season to taste with salt and pepper. Pour in the lime juice/shallot soaking liquid for the dressing.

    Spicy Mango Cabbage Slaw by Michelle Tam https://nomnompaleo.com

    Toss well, taste, and adjust seasoning if necessary.

    Spicy Mango Cabbage Slaw by Michelle Tam https://nomnompaleo.com

    Plate it up and serve it with something meaty!

    Spicy Mango Cabbage Slaw by Michelle Tam https://nomnompaleo.com

    The slaw will keep for up to two days in a sealed container in the fridge.

    Looking for more recipe ideas? Head on over to my Recipe Index. You’ll also find exclusive recipes on my iPhone and iPad app, and in my cookbooks, Nom Nom Paleo: Food for Humans (Andrews McMeel Publishing 2013) and Ready or Not! (Andrews McMeel Publishing 2017)!

    Recipe IndexNom Nom Paleo CookbooksNom Nom Paleo App


    Spicy Mango Cabbage Slaw

    Prep 10 mins

    Cook 15 mins

    Total 25 mins

    Author Michelle Tam

    Yield 4 servings

    This simple Spicy Mango Cabbage Slaw is the perfect Whole30-friendly side dish for all of your favorite grilled proteins!


    • ¼ cup thinly sliced shallots or red onion
    • Juice from 2 limes
    • 2 mangoes, peeled pitted, and thinly sliced (I prefer Ataulfo mangos ’cause they’re the best.)
    • ½ small cabbage, cored and thinly sliced
    • ¼ cup fresh mint leaves, thinly sliced
    • 1 jalapeño pepper, thinly sliced (optional)
    • Diamond Crystal brand kosher salt
    • Freshly ground black pepper


    1. In a small bowl, soak the thinly sliced shallots in the lime juice with a cube of ice for at least 10 minutes. Prep the other ingredients as the shallots chill out in lime juice.
    2. When you’re ready to assemble the salad, toss the mango and sliced cabbage into a large bowl. Add the soaked shallots, sliced mint, and jalapeño pepper. Season to taste with salt and pepper. Pour in the lime juice/shallot soaking liquid for the dressing and toss well. Taste the slaw and adjust seasoning if necessary.
    3. Plate it up and serve it with something meaty! The cabbage will keep for up to two days in a sealed container in the fridge.


    My favorite type of mangos are the Ataulfo (a.k.a. honey or champagne) mangos because they are sweeter and less fibrous than Kent and Tommy Atkins varieties.

    Courses Salad

    Cuisine Whole30, Paleo, Gluten-free, Vegetarian, Vegan

    The post Spicy Mango Cabbage Slaw appeared first on Nom Nom Paleo®.

  • Steal My Best Food Prop Tips

  • RHR: The Shift from Treatment to Prevention, with Vipul Vyas, Laura Conley, & Pat Charmel

    Post From https://chriskresser.com/the-shift-from-treatment-to-prevention-with-vipul-vyas-laura-conley-pat-charmel/

    revolution health radio

    In this episode, we discuss:

    • What the U.S. healthcare system focuses on
    • The cost of maintaining this system
    • How conventional medicine got to this point
    • How the healthcare landscape is changing
    • The shift from “sickcare” to true healthcare
    • How employers can help employees manage their health
    • The social factors that impact health

    Show notes:

    [smart_track_player url=”http://traffic.libsyn.com/thehealthyskeptic/RHR_-_Shift_from_Treatment_to_Prevention.mp3″ title=”RHR – The Shift from Treatment to Prevention, with Vipul Vyas, Pat Charmel, and Laura Conley” artist=”Chris Kresser” ]

    Chris Kresser:  Vipul, Pat, and Laura, thank you so much for being with me today.

    Vipul Vyas:  It’s a pleasure.

    Pat Charmel:  Appreciate the opportunity.

    Laura Conley:  Thanks, Chris.

    Chris Kresser:  So, I’m really looking forward to this conversation. Most of the discussion that I’ve had around this topic has been with people who are working outside of the conventional medical system. And certainly those perspectives are valuable, and I think we all agree that we need to make significant changes to the current system. But what I’ve certainly come to realize over the past several years is that while Functional Medicine on its own can make an impact and people working in private practice and using that model can make a difference to really scale this and have the impact that we need to have on a population health scale, we need to change the system from the inside out. And that’s why I’m so excited to have this conversation today.

    So let’s start with the first question. Where has healthcare historically focused and what have the traditional economic drivers of healthcare been in the U.S.? Pat, if you could get us started, that would be great, and Vipul and Laura, if you want to jump in, feel free.

    What the U.S. healthcare system focuses on

    Pat Charmel:  Well, thanks, Chris. Obviously, the U.S. healthcare system has been focused on, or at least the bulk of the resource allocation has been focused on, for the delivery of acute care. Let me just sort of talk about it more generally. Most of the focus is, when we talk about spending in healthcare, and the costs compared to, say, other industrialized countries, it’s been looking at the more expensive inputs. Things like hospitalization, for instance, or high-cost pharmaceutical treatment. And if you look at the U.S., our model has been focused essentially on taking care of sick people. And the incentives in the system pay higher for those more complex interventions.

     Has conventional medicine finally seen the light? Find out how some progressive leaders in hospitals, primary care groups, and corporations are driving the shift from treatment to prevention. 

    So, whether it’s high-cost diagnostics, or whether it’s complex surgery, or it’s the treatment of acutely ill patients with higher complexity … And so our system has actually focused on that and built capabilities around that following those incentives. And we do that pretty well, although some would say it may not be as efficient as it should be and it’s not as consistent as it should be because there’s still a lot of variation around how we take care of sick people. And because of that variation, there are some differences in terms of cost and quality in terms of outcomes between organizations. But generally speaking, we do that pretty well.

    Chris Kresser:  Right.

    Pat Charmel:  And again, I’m sure we’ll talk about the fact whether that model is viable long term because most of the focus has been on raising questions about whether that’s sustainable or not.

    Chris Kresser:  Right. So our system’s been primarily, it sounds like, focused on acute care, acute interventions. If we look at disease on the spectrum where you have perfect health on the left and death on the right, it’s a system that really, it does a pretty good job at intervening at the far right end of that spectrum. People already have disease and they’re already at the point where they need that kind of acute care.

    Pat Charmel:  Right.

    Chris Kresser:  So let’s actually talk about how sustainable that is and how the these economic drivers are changing. Where are we at here in 2018 with the system that we have?

    The cost of maintaining this system

    Pat Charmel:  Well, let’s talk about how the system gets paid for in the U.S., and we can get into the specifics in terms of our ability to treat disease because that’s where most of the innovation has been, whether it’s been in terms of devices or pharmaceuticals, and we can talk about the cost of those inputs here versus elsewhere. But the question of sustainability, the cost of providing that kind of care, has been growing faster than the capacity of the individuals that pay for it to actually pay for it. So who is that, right?

    So we’re talking about government if it’s the care of the elderly, the Medicare program. And if it’s the care of the indigent, it’s states and the federal government, right? So, through the Medicaid program. And then the rest is essentially employer-provided healthcare through those who work for employers who provide health insurance coverage. And our system has been one of cross-subsidies. And it’s not something that gets talked about a lot, but generally speaking, when the government buys healthcare from providers, doctors, and hospitals, it essentially pays less than the actual cost of providing that care.

    Now you may say that the cost is higher than it should be, but the cost is the cost and they pay less. So the employer-provided insurance is through commercial insurance companies, and generally speaking, they pay more than the cost. And it’s not insignificant. It’s 30, 40, 50 percent more than the actual cost of that care. So the cost of delivering that care by the provider, the commercial insurance pays much more than that because they’re subsidizing the cost based on the shortfall by government payers who pay less.

    Chris Kresser:  Right.

    Pat Charmel:  And that was kind of something that everybody knew about and everybody agreed to. But costs have continued to grow, and the gap between what government pays and the actual cost is growing, which means the subsidy for commercial payers is getting larger. So the only way that the commercial payer can sort of shoulder that burden is to push that cost onto employers. And employers have complained about it for the last 20 years but have accepted it. But in the last four or five years, they have said, “Look,” especially after the economic crisis in 2007, 2008, they really started to say, “We literally do not have the capacity to pay this. Our profits have shrunk. We can’t afford this. We’re not competitive compared to foreigners who don’t have to shoulder this burden.”

    So what did they do in response? They could’ve said to the health insurers, “We are just not going to pay this and you’ve got to figure out another way to buy care less expensive than what we’re buying now.” But no, they didn’t. In the short term, they pushed more of the cost onto their employee in the form of higher deductibles or higher share of premium, right? So, the average employer in the U.S. is asking its employees to pay 30 percent of the premium. In addition to that—and that premium for a family policy, by the way, could be as much as $20,000 and sometimes more—and then after you pay your 30 percent of $20,000, or $6,000 in payroll deduction, in an environment where wages are not growing, you’re actually seeing an increase of what you’re paying out of your weekly pay toward your share of the premium. That’s a problem. Then once you pay that, you get the privilege of having a $3,000 or $5,000, or even more, deductible, which means that your insurance coverage that you paid for through your payroll deduction doesn’t kick in until you’ve paid $5,000 out of pocket.

    Chris Kresser:  Yeah, and then depending on your plan, sometimes you still have a copay after that.

    Pat Charmel:  On top of that. So now the average employee that has employer-provided health insurance is paying $0.42 of every dollar out of their own pocket. So the question is, is that sustainable? That’s what’s really changed is that employers couldn’t afford it, so they pushed it onto the employee. The employee is saying literally, “I cannot afford this. I don’t want your health insurance.” And the penalty for not taking insurance is not that large. So now it’s backing up. So they’ve gone back to the employer and said, “I can’t afford this anymore. So you’re going to have to shoulder this burden, Mr. Employer.” And they’re saying, “We can’t afford it,” and they’re finally going back to the health insurers, who by the way, were part of this conspiracy because they never really wanted premiums to go down.

    Chris Kresser:  Sure.

    Pat Charmel:  Right? Why would they want it? If you get 15 percent of the premium for overhead and profit, why would you want the premium to go down? As long as somebody’s willing to pay that premium, you want the premium to go up. That was kind of the dirty little secret. So the insurers, when they sat down with my hospital as an employer, and we have 1,600 employees and spend a lot of money on health insurance, they were always very sympathetic. They always had a sympathetic demeanor when we talked about the costs going up, and kind of … it’s interesting when you’re a provider and an employer of healthcare. But at the same time, you say, “Hey, it is what it is.” Now it’s at the point where those that are actually paying are saying, “We cannot afford it anymore.” And you have state governments, especially after Medicaid expansion, pushing back and saying, “We’ve got to change the incentive.” Employers who are now becoming somewhat enlightened and saying, “There’s got to be a way if we can no longer just push the cost onto our employees, we’ve got to figure out a way to actually make care less expensive.” In my view, that’s what’s sort of fueling kind of the innovation around a different approach.

    Chris Kresser:  Right.

    Pat Charmel:  And providers who were part of the conspiracy as well because they knew that the insurer was going to continue to raise the premium, and if they’re getting a fixed share of that premium themselves, they were sympathetic, but didn’t change. Now we’re forced to change because the current model is not sustainable. And as much as we’d like to continue to get fee-for-service and take care of sick people, which covers the overhead, we’re realizing that we actually have to be partners with the employer and the insurer and the employee or the member or the consumer to basically work together to say, “Folks, we could wait for people to get sick and then try and do a whole bunch of stuff here, but nobody can afford to pay for that. So let’s get in on the front end now.” And now the problem with that is that disrupts your business model and it’s pretty scary.

    If you’re a provider with a lot of fixed costs, how do you shoulder that burden during the transition period? How do you reduce your operating costs so you can live with the low utilization that results from actually keeping people healthy?

    How conventional medicine got to this point

    Chris Kresser:  So, let me see if I can summarize this briefly. So, historically, there’s been a misalignment of incentives where you have these various players—the providers, the payers and companies—who weren’t necessarily aligned in terms of their best interests. And so that led to a lot of inefficiencies and excess costs, and it got us to this point where we have a system that’s inherently unsustainable. And what’s happening now, it sounds like, is there’s a shift towards more aligned incentives and maybe even opportunities where providers and payers and employers can work together, or at least where their incentives are now aligned and there can be more efficiencies created there.

    Pat Charmel:  Yeah, Chris, I think you have it. I don’t know that the incentives are quite aligned yet, but I think they have to be if we’re going to get through this. Because that’s really the only way that it’ll work. If we’re … each of the stakeholders is trying to maximize their position at somebody else’s expense, we’ll basically come up with another unsustainable solution. I think it is that question, and then the question also is what is the role, the historical role, the traditional role of each of these individuals and if that needs to change. What’s the payer’s role?

    Chris Kresser:  Right.

    Pat Charmel:  The payer used to be, I’m a health maintenance organization. Inherent in that name was we actually manage care. And they really didn’t because there really wasn’t an incentive to do that. And by the way, even if there was, how effective are they at doing that truly? And what’s the relationship between a health plan and a consumer? And do you trust your health plan to manage your care?

    How the healthcare landscape is changing

    Chris Kresser:  Most people would say no, for sure. I want to talk more about that. Vipul, you’ve been really instrumental in educating me about this landscape, which I appreciate. Let’s talk a little bit more about incentives because, of course, in most industries, there is an incentive to perform better and more efficiently, and you’re rewarded for that. That hasn’t really always traditionally been the case in many areas of healthcare. So, what kind of changes are we seeing now in healthcare to move more towards this more of an incentive-based system of value-based care? I’ve talked about companies like Iora Health with my audience that are using capitated payments for diabetes prevention. So, can you give us a kind of overview of some of the broader changes that are happening here?

    Vipul Vyas: I think Pat can obviously weigh in, in a much more deeper level as well. But I think what you’re seeing, Pat just shared it, is that as a risk has sort of cascaded from the insurance company—and I would actually argue to Pat’s point around the insurance company taking a 15 percent cut off the top, the insurance company really isn’t much of an insurance company. More they’re a transaction agent, similar to Visa. They own the network, they collect the premiums, they make the payments, they handle the claims. But in the end they’re not really assuming risk like they historically have. That’s been largely pushed to employers.

    And many people may not realize, though I’m sure many do, that the employer typically, especially large employers, self-insure. Meaning they’re the ones taking the risk, and the insurance company is simply a transaction facilitator. And so to Pat’s previous point, there’s a significant interest on the part of the employer to reduce these costs. So in the end, it’s the employee, and then by extension, the employer, who’s probably the prime economic driver saying, “I can’t afford this anymore.” I’m sure the federal and state governments are, to Pat’s point, saying the same thing, saying, “I can’t afford this anymore.” Therefore there’s a competitive market emerging in terms of value-based care that says, “If someone comes along with a plan that says they’re going to be cheaper because their cost of production is lower,” and again, kind of referring back to Pat’s point about changing your cost structure, if you’re a provider or health system, if you can change your cost structure and create a competitive advantage by way of being able to price lower and going to an employer and saying, “Look, I can deliver the same set of services as my local large competitor at a lower price in partnership with an insurance plan. And then I can actively manage your employee population to be healthy as a sweetener to keep those costs down or at least keep the growth of those costs in check or at a manageable level,” then that becomes an economically attractive option for the employer.

    And so creating those bundles and making that programmatic and scalable is sort of the key evolution that we’re going to see. When it comes to the general market and what the ACA did, it really fosters some innovations I think the market was going to kind of fall to anyway, just given the premiums rising and healthcare costs rising, and there’s just economic pressure to do something. Because the paying entities, the government, employers, employees just didn’t have any more money in their pocket to pick, has driven this sort of capitated payments. And capitated payments is where eventually the risk is taken by the entity that can probably manage it the best, and that’s the providers.

    So instead of paying $1,000 to Aetna and them keeping it, it basically flows to the provider to, say, Aetna takes their 15 percent off the top, and there’s $850 that goes to the provider. And the provider’s then told for $850 a month keep this person healthy. If they spend more than $850 a month on average, then you lose. If they spend less, then that’s your margin. And that’s where things are headed. Pat can comment on that much more intelligently, but that’s the gist of I think some of the drivers that are emerging.

    Chris Kresser:  I think a lot of people who are listening to this might be surprised that that’s the way it hasn’t worked all along. Because that’s the way it works in most other fields. You have a certain performance target and if you meet it, you’re rewarded and if you don’t meet it, there’s some consequence. But that actually is not how it’s been going so far. Laura, I just wanted to touch base with you because I know the Heritage LifeFit Program that you’re working on is maybe a good example of this. I think some of my listeners are less familiar with the terminology we’ve been using. This might kind of help people to understand what this looks like in practice.

    Laura Conley:  Yeah, so I’m actually kind of on the ground level working with people, and Heritage started this way ahead of their time, just kind of as an experiment. And I think it grew beyond what they even imagined because it started out as fitness classes at the healthcare facility. And over time it grew into a community of, “Okay, so you’re not just going to see your doctor, you’re actually going to take some fitness classes as well.” And then it grew into a community of really deep bonds and friendships where these people were changing their lives together. And so we really saw that this could be so much bigger than just “how do we get these people healthy and reduce their cost?”, but how do we actually change their lives forever in multiple areas. Not just in maybe chronic diseases like heart disease or diabetes, but also in their wellness scores of anxiety, depression, just how they were feeling about themselves and their happiness.

    So it really hit across all levels and it’s been fun to watch this evolution happen. But yeah, it’s kind of what we’ve been doing.

    Chris Kresser:  That’s a great example. Yeah, that’s an amazing shift that’s happening. And Pat, you’re CEO of a hospital and so I think some people might not expect that a CEO of a hospital would be someone who’s actually looking at how the practice of medicine itself has to change and how we have to shift away from acute care towards more preventative, integrated type of care. So tell us a little bit about how you came to that realization and what you’re thinking of in terms of the future.

    Pat Charmel:  Yeah, so, we have a pretty long history, and again, as Laura said, she was a little ahead of our time. And I think Griffin, my organization, was as well. We actually made a decision in the early 1990s to start our own health plan. Not because we saw having a health plan as a wonderful business opportunity; we just kind of came to realize the perversity and the currency for a service system.

    Now you have to understand, Griffin is a relatively small hospital. So in the fee-for-service environment, we don’t have the leverage that, say, a large academic medical center has or a large system of possibles when it comes to negotiating with, say, commercial payers who if you have that leverage, you get paid more. We didn’t have that, so we get paid less, significantly less, and many of your listeners don’t realize that the rate that a commercial insurance company contracts with a hospital for a specific service varies by hospital pretty dramatically. So in a single market, what most of it is is case rates, and the case rates are paid by diagnoses. So what a health plan or a commercial insurance company pays a hospital in a market for, say, a pneumonia admission may vary from, say, $7,000 per case for the lowest-paid hospital in the market by that insurer to $14,000. Twice as much.

    Chris Kresser:  Wow.

    Pat Charmel:  With essentially the care of the exact same condition. And often times the lower-cost hospital is the independent community hospital, less complex, but they produce a better patient experience and a better outcome.

    So we were one of those:

    • Higher performing
    • Better patient experience
    • Better outcome
    • Fewer complications
    • Lower infection rates, and
    • Getting paid half of what the highest-cost hospital in the state was.

    And because we lack that leverage, the margin on our business is razor thin. And we recognized also that there’s perversity in the system. We were paid to wait for people to get sick, the sicker the better. And then when they showed up being sent to us to (audio cuts out 23:48), I like to say whether they need it or not. But I don’t want to be righteous about this. If I was that large academic medical center CEO who had the leverage to get high rates, that I would have been so enlightened about the perversity of the system.

    Chris Kresser:  Right.

    Pat Charmel:  But I was, so our team decided to … the way to address this is to actually go upstream and control the premium dollar, own your own health plan, and then once you have that premium, decide how you want to spend it. And frankly, if you spend it on prevention and wellness and good primary care, as a health plan you could win, right? Because you’re collecting the money up front. So that’s what we did. Now what we didn’t realize is how difficult it is to run a health plan. And I won’t get into that. So it was a great idea poorly executed, and it didn’t work financially for us. But it put us on a different path, and it was really because of our underlying philosophy about we really should be engaging patients and make them partners in their care. And this is what you’re hearing form Laura, she’s actually doing this.

    Chris Kresser:  Right.

    Pat Charmel:  And a partnership to keep them healthy or if they’ve already got an underlying chronic condition, how to manage that condition effectively to improve the quality of their life. So we began to do that and we built all kinds of infrastructure around it. We’re a teaching hospital. Most teaching hospitals who teach graduate medical students usually treat them in traditional internal medicine. And most of that training happens in an acute care setting, and a lot of it in an ICU. So their mindset is wait for people to get sick, the sicker the better, and then take really good care of them. And we did that.

    But we decided in addition to internal medicine, which we changed the focus to community-oriented primary care training within internal medicine, we took it one step further and said, “Why don’t we actually train graduate medical students in preventive medicine?” And we did that 15 years ago. We started a preventive medicine training program, and they were fairly rare, and still today they’re fairly rare because when … why would a physician who’s looking at the current incentives in the healthcare system want to be trained in preventive medicine? Nobody was rewarding that. In fact, you might be the medical director or the director of a local health department, or maybe you would get into occupational medicine and work in an employer health clinic. But for the most part, there were no jobs for these people.

    Chris Kresser:  Right.

    Pat Charmel:  So we did it anyway, and we developed a prevention research center that CBC funded, and we’ve developed lots of capabilities. Well, I like to say now that our preventive medicine residents are the rock stars of the healthcare industry. As our industry’s beginning to change with a focus on prevention and wellness, and there’s move to value, all of our residents have agents representing them.

    Chris Kresser:  Right, in the highest demand. Getting recruited.

    Pat Charmel:  Right, so the food chain is being reordered. The people who were at the top used to be the proceduralists, who were really good at taking care of sick people. And now it’s people who have this capability. So we’ve had to move here before the incentives were there, and partly because who we are, what we believed in philosophically, the disadvantage where because of our size … And so we are one of those organizations because we have these capabilities, we have the cost structure, we’re trying to move the market in that direction because it’s the right thing to do and it would advance us as well.

    And I’m trying to bring a lot of other more traditional providers along with us. And they also know it’s the right thing to do, but they’re having a struggle with the economics. Because if you’re successful in the short term and you aren’t in one of these risk arrangements like Vipul described where you’re actually taking premium dollars up front, you’re acting more as much like an insurance company as a provider. And there’s an inherent financial risk in that. If you’re mostly a fee-for-service organization, you build this capability and keep people healthy, you’re actually cannibalizing your business.

    Chris Kresser:  Right, right. Yeah, you’d better have a new model for that.

    Pat Charmel:  And if you don’t have large reserves, how do you do that, and why would you do that? Most of these arrangements, and I have these conversations with colleagues all the time, the federal government is trying to create incentives through the Medicare program to push providers along this continuum more toward value-based care. And we’re doing some things here in Connecticut where we’re getting out to employers who are mostly self-insured, who didn’t realize, by the way, that their health plan that’s administering their self-insured program pays between $7,000 and $14,000 for the exact same care. That was kind of a mystery to them. And now they’re saying, “Maybe I can change my plan design. Maybe I can look for those enlightened providers who will partner with me and my employees to keep them healthy.” But again, we’re in the early days of this.

    The shift from “sick care” to true healthcare

    Chris Kresser:  Now that’s just a really big sea change that I want to highlight right here. In my book, I shared a statistic: it costs about $14,000 a year, from a few studies I found, to treat a patient with type 2 diabetes. So it becomes clear that even if you have to spend a little bit more up front in preventive care and intervening earlier on that spectrum when the patient has high normal blood sugar or even prediabetes, and you can reverse that so that they never develop type 2 diabetes, you can save an enormous amount of money over the lifetime of that patient. But what that requires is not waiting until the patient develops type 2 diabetes and ends up in your hospital or in the doctor’s office. It’s actually going out and making contact and being proactive in engaging, creating new programs where these preventive efforts can become effective.

    So anyone, Vipul, Laura, Pat, let’s talk a little bit about this shift. Because it seems to me that that’s, from a 30,000-foot view, one of the biggest shifts that is happening and needs to happen. Because historically in this country, I think we have had a, like you said in the start Pat, we have had a “sickcare” system where people just think of the doctor as a place to go only when they’re sick, not as a place to go to get healthy or to prevent getting sick in the first place. So what’s happening now, and what do we need to continue to do to drive this forward?

    Pat Charmel:  Let me just give a little additional context, because I think it’ll enrich the conversation. So we do a lot of comparison between the U.S. and other industrialized countries, and it is true that we are spending a much larger percentage of our GDP. And on a per capita basis, spending twice as much as the average of other industrialized countries.

    Chris Kresser:  Yes.

    Pat Charmel:  But what we don’t talk about is that the U.S. spends a whole lot less on social service support per capita than other industrialized countries who have better health outcomes. And so if you look at the combination between medical spending and social spending for us and the other industrialized countries, we look pretty good. Because we have this huge spending on medical and a little bit on social services. You combine them and we’re good, and we’re obviously better than the average. But if you look at social service spending as a percentage of total healthcare spending, that’s the combination of health and social service spending, we’re last of any industrialized country.

    Chris Kresser:  Wow.

    Pat Charmel:  And most of what you were just talking about, what can we do differently to manage somebody or prevent the progression of disease or help people develop healthy lifestyles so they don’t even get the precursors for something like diabetes, we’re going to have to spend much more money on social determinants.

    Chris Kresser:  Right.

    Pat Charmel:  Here’s the rub. Where does that money come from when, as a nation, we’re already spending too much money on traditional medical care? There has to be a resource reallocation. Now the people who are doing this wonderful work like Laura and local social service providers, when I say “resource reallocation” to them, they love it. When you say that to a bunch of hospitals and traditional medical providers, they’re thinking, “Oh, my gosh, you’re saying taking my resources and giving them to someone else.” That is a huge … that’s one of the huge challenges. So are we willing to build that social service infrastructure? In my community, we’re beginning to invest in that, basically looking at who’s got the capabilities. We’ve been doing this work in obscurity with under-resourced social service providers, who in partnership with medical providers can actually begin to make a difference. And that is something that we, from a policy standpoint, are going to have to really focus on. But a lot of people don’t want to have that conversation.

    Chris Kresser:  I get it. I can see why. Vipul and Laura?

    Vipul Vyas:  I was just going to suggest to reinforce Pat’s point, when it’s New Year’s Eve or New Year’s Day, when people are doing their resolutions, very few people think about the healthcare system when it comes to, “I want to change. I want to transform. I want to improve my health.” It doesn’t really exist for the provider today and that’s what’s got to change in terms of engagements. So that people perceive the provider as engaged in their health. And that shift happens, I mean if you look at other industries, can you imagine, like, FedEx used to just be about shipping packages, but surely transformed beyond that to being a logistics provider. It’s more ingrained in your day-to-day life for a small business. Banks used to just be where you put your money. But now they try to take an active role in managing your whole financial life.

    So these transformations have happened in other industries and can happen here. But it’s going to be an evolution. There’ll be a lot of experimentation. I think what you see happening with Laura’s program, and I’ll let her comment on it a bit more, is that the Victor Valley system is actually viewing their patents not as just patients, which as a word has a horrible connotation, but as a member, and members work for additional privileges beyond the traditional care. They also get access to these resources, all the services are free, the fitness passes are free, the engagement is free, the education is free in terms of how to be healthier, and how to transform yourself, and that comes along as a perk. And that is a first step conceptually, just like FedEx went from just shipping packages to giving people pick and pack, shipping software, and logistic software, so that they’re your logistics company. Or Amazon has gone from being just a place where you buy books to kind of where you get everything and anything for your household, the same way Victor Valley and what Laura’s doing sort of represent the start of that transformation as well.

    Chris Kresser:  Yeah, Laura, what did you see there of the transition from when it started when it was just a fitness program to where it is now? I mean, was there resistance along the way? How was that in your organization?

    Laura Conley:  Oh, yeah, definitely. So in the beginning, it was purely just fitness classes, and we grew with time. But one of the things that really built it was we told our members, bring somebody with you. Drag a friend in here with you. Literally, they sometimes had to drag. And the resistance in the beginning was really high, but then over time that touchpoint kept increasing, and okay, they would bring a friend, they’d bring a family member, and they would eventually start working out with us. And what happened that we all know is, you start to get results. And results actually build motivation.

    So the more results they started seeing, the more motivated they became. And then other people within the community started noticing, and then the question became, “What are you doing? How did you change so much?” And the answer shocked people. Well, going to my healthcare facility. And in the beginning, the first two years, it was completely open to the community. So you didn’t even have to be a member of that healthcare facility. You could just be a member of the community and come take any fitness class for free. And then eventually we built it into, okay, now let’s have you switch over and become your primary care doctor as well. But really, it just took the community slowly building on itself of one person would bring in one friend, and maybe they’d bring in a friend.

    And then the relationships grew and the camaraderie of doing these workouts together—I’m sure we all know, misery loves company—and you’re going through a hard workout, but you have these people next to you that are all pushing through together, and you build a relationship that’s really strong. And I think that that just organically grew on its own in addition to providing really good educational resources like free cooking classes and women’s seminars. And just the more we offered those and opened those up to the whole community, that’s what really brought everybody in and brought them together.

    How employers can help employees manage their health

    Chris Kresser:  That’s interesting. I can’t help thinking that the solution, we need a multi-prong solution here, and I’m a small employer myself, about 35 employees across a couple different companies. And what I’ve noticed, I’ve been thinking about this just in my own small scale for a long time, we’ve taken a lot of steps to create a culture of health within the company, and ways that we support employee health and wellness, everything from offering health coaching and mindfulness to having an environment where we do challenges, start to do challenges where people are getting together and accomplishing their health goals and cheering each other on and using that social support. And I know, the whole corporate wellness conversation is another big one, and there’s a problem with adoption, but I think that for a lot of people, they spend most of their time at work. Their employer is their payer, especially if they work at a big self-insured company. So it seems to me that that’s got to be, employers, especially large employers, getting smart about this is going to be one of the big drivers of change, or should be, at least.

    Vipul Vyas:  And I think, Chris, to that, Pat can comment on this further, but I think it is a three-part solution in terms of the payer, the employer, and the provider all have to be rowing in the same direction to create transformative change in society. Because if you think about modern life, it’s really geared to incenting you to be quite unhealthy. In terms of stay up late and binge-watch TV, binge-eat food, be socially isolated by just focusing on your phone all day long, all the construct of modern life is really pushing against you. So we need all those other entities to be rowing in unison and aligned to push back against those forces. And it’s going to be a challenge. I mean it can be an amalgamation of lots of small things, where the provider works with the employer to figure out how to make a healthier environment in terms of stand-up desks. Little things that just sort of in aggregate, add up and cumulatively make an impact.

    Chris Kresser:  Yeah.

    Vipul Vyas:  I think that’s probably the path that’s most realistic. And to your point, work is where people spend most of their day, so that’s where things likely have to start.

    Chris Kresser:  So I know all three of you have been engaged in some interesting examples of this. Pat, I’d love for you to share a little bit about new partnerships between healthcare systems, employers, and payers that you’ve been experimenting with. I think you and Vipul and maybe Laura have been working on something together.

    Pat Charmel:  Yes, yes. And just to comment on sort of employee wellness programs in the workplace, they were, they are sort of enjoying a bit of a resurgence because I think that comes with the understanding. It’s a little bit more comprehensive this time and connected. So before you had employers who were aligned who understand what you understand, but were doing what they did sort of in isolation. It really wasn’t a partnership with the provider community or the payer. So if you had something at work, for instance, that employee’s primary care physician really wasn’t aware of what was happening at work, wasn’t necessarily encouraging participation. Certainly the payer wasn’t aware. Most of the approaches now that are real successful are where all of those are working together.

    So I know that we’re working with area employers on everything from an occupational health program. So everything from pre-employment physicals to actually treating injuries where they occur, but:

    • Looking at biomechanics in the workplace
    • Looking at physical activity in the workplace
    • Looking at the food that served in the cafeterias in the workplace
    • Looking at exercise throughout the day

    And we actually have programs where we can help employers incorporate physical activity throughout the day into the workplace. We’re also helping them identify who their employees are that have underlying chronic problems that need to be managed more effectively. And as you say, most people, their waking hours are spent at work. The effectiveness of the interventions are tied to what’s happening at work as well as at home. So that wasn’t happening before. You were doing what you were doing and it was successful. The level of engagement varied by employer. But we all need to be working together to do that.

    So, for instance, Vipul has been helping us build the information infrastructure to be able to … everybody who’s doing this work together knows what’s been done throughout the system and knows everything that we need to know about that individual to keep them on that path, to either more effective disease management, or to help them move to healthier practices, a healthier lifestyle. So the integration of this workplace wellness into the overall approach of health management, or disease management, if you want to call it that, is critical. And it starts, it starts early on. We are actually bringing a large employer into our sphere as we speak and we’re starting to do so to baseline engagement with the employer and the employees. Everything from biometric screening to workplace assessment to developing a platform for education and coaching. Again, it’s a much broader approach, where all of the pieces are connected and we can monitor progress. And then the employer can build in the right incentives to motivate the kind of behaviors that are going to bring about success.

    Chris Kresser:  So in that case, Pat, is the employer also the payer? Is it a self-insured company? Or is there also an insurance company involved?

    Pat Charmel:  There is an insurance company involved. It happens to be one that we are partnering with with in sort of an accountable care relationship. But this is a self-insured employer with that payer as the administrator of their health insurance program.

    Chris Kresser:  So that’s an interesting example of how this, all of the various players are realigning in a way that I would imagine serves everybody’s interests. I mean, what, is everybody happy in that arrangement? Is the payer, I don’t know as much about this, but I wonder if a payer is happy to be … “relegated” might not be the right word … but to the role of just serving as the administrator rather than taking or playing a bigger role.

    Pat Charmel:  Well, I think Vipul said earlier, and I’ll let him address it again, the payer doesn’t necessarily mind being the administrator of the self-insured program role, because they’re not taking financial risk taking, they’re not taking insurance risk. As long as they’re getting enough margin on playing that role of administrator. But they see what I just described as the ability to develop a comprehensive program as they’re differentiated. Now they were moving toward sort of a health-promotion, keep-people-healthy model. There are folks who could process claims a lot cheaper. If you were just serving that administrative function, you’re going to get marginalized or commoditized.

    So what they’re saying is the way we differentiate ourselves or add value is to be that integrator. Not that we’re going to provide the care delivery piece of it ourselves or the health promotion. They tried that before. And the problem with that is, consumers don’t want to engage with their health plan. They don’t trust and they don’t have a relationship with their health plan. But the enlightened payers are now partnering with providers and say, “Look, we’re going to admit that we’re not really good at that. But we’re going to find the people who are really good at that, and we’re going to build the infrastructure and the glue to sort of make that really effective.” So there are a couple of payers that have really stepped up to look for providers like us in true partnerships.

    And we’re still finding our way, but … and then also stepping forward together with the employer and their employees in ways that have never been done before, where you have both the employer and the provider, excuse me, the insurer and the provider talking to the employer and their employees. And so they’re trying to get their engagement and build their trust, and provide them with the information that they need to make intelligent decisions, which also has never taken place before. As a self-insured employer who used to pay a lot of administrative fees through the health plans to administer our program, who told us they were managing our patients with serious underlying disease, the fact of the matter is we never got actionable information, and frankly we didn’t get, we never got the information that we need. So even though we knew that we might’ve had, out of 1,200 employees at the time, 300 that had serious chronic problems, what we heard from the health plan is, “Well, we have disease management programs,” but when you really push them and say how many of our employees and their spouses are actually engaged in those programs, and we would find that it was maybe less than 10.

    Chris Kresser:  Right.

    Pat Charmel:  Now we’re saying to the provider and more so the physicians, especially primary care physicians who have a relationship with those employees or those consumers, we need to build capabilities around them because they’re the ones that are going to bring about that engagement. And if we have things happening in the workplace and we have the right incentives so employees actually participate, they’re actually engaged, we’re going to get the kind of results that we’re looking for.

    The social factors that impact health

    Chris Kresser:  This is so fascinating. I wish we could keep going. We only have a couple minutes left here. You touched on the social determinants of health earlier, Pat. And I just wondered if you could say a few more words about that because so often, at least within the functional integrative medicine discussion and for now, since it’s not really integrated into our conventional health system, it’s really limited to people who are middle class, upper middle class and above. It’s quite expensive and yet if we, as we said in the beginning of the show, if we want to have an impact on the population health scale and really bring everyone along in this movement, we need to be thinking about things in a different way in terms of just the shocking number of people in this country that don’t even have access to fresh food. And just even the basic things that are required for health. So can we talk just about this for a couple minutes as we close?

    Pat Charmel:  Yeah. So we’re in a suburban community that most people look at the community and say this is a middle-class community, a working-class community. But when we did a study recently, we found that about 40 percent of the households in our community don’t generate enough income as a household to meet essentially the basic needs of that household. So when you look at poverty, those numbers may be 5, between 5 and 10 percent. But when you’re looking at almost 40 percent can’t meet the basic needs of the household, so what suffers? So food, the quality of their housing, their ability to pay for traditional medical care now that we know that folks are paying $0.42 out of every dollar. They may not have adequate transportation, and it sort of goes on and on.

    So what we recognize, if we really are serious about keeping populations healthy, we have to address the needs that come as a result of the fact that 40 percent don’t have the resources. So we’re looking at housing insecurity, we’re looking at folks that have … the quality of their housing too. It’s not folks that, we’re not looking just at, obviously, at the homeless, so we have a huge problem with pediatric asthma in this community. And we truly believe that it’s tied to the quality of housing. So we have problems with homes that aren’t air conditioned, we have lots of homes that have mold problems, and folks can’t afford to do mold remediation. They could be in rental properties where we have landlords who are not addressing those problems. So they have code violations that are not being addressed by local governments.

    So do we have to intervene there? How are we dealing with the issue of people who can’t afford food, or nutritious food? We’re dealing with that as well. We’re addressing issues of transportation. We’re trying to get at the underlying causes of that, which are the inadequate household income and looking at things like job training. And how can we get people to sort of progress and build the skills they need to increase household income? Now you’re talking about a traditional healthcare provider looking at all of those issues.

    Chris Kresser:  Yes.

    Pat Charmel:  As I said before, that’s going to reach … we’re actually beginning to screen individuals in our community for those needs. And there are traditional providers of those kinds of services. Meal assistance, transportation, fuel assistance, housing assistance, they exist. But they’re under-resourced. So we’re out in the community now screening, and now we’re referring to them and building a system to track individuals who are referred to make sure that they follow through. But what are we doing? We’re burdening these agencies who don’t have adequate resources. And they said, “It’s great that you’re doing this, but we have to now build additional capacity to meet the needs of the individuals that you’re sending us because they weren’t finding us before.”

    Chris Kresser:  Right, right.

    Pat Charmel:  So we’re actually now beginning to actually say, “Hey, what is it going to take for those organizations to create the capacity to meet the needs that we’re screening for and referring?” And it’s a little daunting because the economics of our business model don’t necessarily support that yet. But that’s the reality. And in many parts of the country, there are providers who do not want to go here. They know intellectually that it has to be done if we’re  really serious about managing the health of populations, but do they want to take on the social support burden that comes along with it?

    Chris Kresser:  The full scope and complexity, and everything that … yeah. I mean, what occurs to me as you were talking is in holistic medicine or integrative medicine, we recognize that you can’t just treat one part of the body without treating, addressing the rest of the body. Everything’s connected. Well, it’s exactly the same with this healthcare situation. As you’ve pointed out, we can’t just address how care is being delivered, and providers and payers, we actually have to think about the social determinants of health and really pay attention to those. Because if we leave that part out, no matter what changes are made elsewhere, they aren’t going to be effective because if someone can’t afford to buy the healthy food or they’re living in a house with terrible indoor air quality, then we’re going to be starting from 10 steps behind.

    So it’s really illuminating and it’s just a, to me, an invitation or a reminder that we really have to be approaching this and thinking about it systemically. And I just want to say kudos to you, Pat, for providing an example of how this can be done. I think it’s incredible what you’ve accomplished at Griffin and the way you’ve been thinking about this for several decades now. And I’m really grateful for your time and willingness to come on and share your vision with us. And Vipul and Laura, thank you so much as well for being here and for all the work you’ve done in this area. I’m excited. I mean it is a little daunting and overwhelming on the one hand, and on the other hand, it’s exciting to know that these changes are taking place and that everyone has a role to play. There are a lot of different ways that people can contribute to this effort.

    Pat Charmel:  Absolutely.

    Laura Conley:  Absolutely.

    Chris Kresser:  Okay, everybody, thanks for listening. Hope you got a lot out of this show. Remember to keep sending in your questions to ChrisKresser.com/podcastquestions, and we’ll see you next time.

    Vipul Vyas:  Thank you, Chris.

    Chris Kresser:  Okay, thanks everybody.

    Vipul Vyas:  Bye-bye.

    Chris Kresser:  Bye.

    Laura Conley:  Thanks, bye.

    The post RHR: The Shift from Treatment to Prevention, with Vipul Vyas, Laura Conley, & Pat Charmel appeared first on Chris Kresser.

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