13. Pulling It All Together — A Nightshade Sensitivity Hypothesis


Back to the central question: Can humans suffer from nightshade sensitivity? I began this deep reading project because the evidence from my own family says that we can. Science hasn’t caught up with the question, so I’m here to make the case that it is a valid question for science to be asking.

So far I have presented the history of nightshade sensitivity, explored some of the many compounds present in nightshade vegetables that might influence human health, and compared these issues with drug side effects. Now it’s time to look at how our bodies may be influenced or compromised by these compounds and to think about how such a diverse collection of plants might cause such a range of symptoms. I’ll also look at whether nightshade sensitivity could really go undetected by medical science.

TL;DR Many people label nightshade sensitivity as quackery. In the previous sections I’ve documented how nightshade plants make multiple chemicals that could influence health. In this last essay I demonstrate how these chemicals could affect multiple biological processes entrained in the gut and cause health problems anywhere in the body. The arguments are detailed and nuanced and a TL;DR summary won’t cut it if you want to evaluate them properly.

I can’t prove here how nightshade sensitivity works because science hasn’t actually tackled the problem systematically. That’s partially understandable because the sensitivity itself is probably rare and definitely a challenge to diagnose. And I’ll continue to show that many of the concepts and tools needed to assemble this puzzle are new. Just like doing a jigsaw puzzle, we can begin connecting some edge pieces. We can group like colors and patterns. But we probably don’t even have all of the pieces in the box.

The sections preceding this have extensively documented scientific sources. Here I’m asking questions that medical science hasn’t formally answered yet. I’m looking at the systems and the compounds involved through the filter of medicine and science. Where I’m sharing published facts and interpretations, I’ll keep footnoting. Where I’m making cognitive leaps, I’ll try to make that clear.

This exercise is speculative. Only continued research can prove anything. But I believe that I can show that the question—can humans suffer from nightshade sensitivity?—is legitimate. I hope that medical science eventually solves the puzzle.

Allergy, Sensitivity, Intolerance

Nightshade sensitivity doesn’t easily fit how we understand most food sensitivity. There is, thankfully, no immediate danger of allergic anaphylaxis, the potentially fatal immune response triggered by a single allergen. Nor do the problems associated with nightshade sensitivity appear to be about the inability to digest a particular nightshade component, the way lactose intolerance works.

Nightshades are a large family of plants that include a number of food species. Most people experiencing nightshade sensitivity have problems with one or more of the four most common nightshade vegetables: tomatoes, potatoes, peppers, and eggplant. As members of the same family, these plants produce many of the same or chemically related compounds. Other nightshades are far less common, and reports of sensitivity issues not clear. Our family, for example, has never had a bad experience with goji berries or pepino melon. But we avoid them, and all nightshades, precisely because the sensitivity mechanism is unknown.

The range of reported health impacts seems as diverse as the plants. Some people suffer only neurological side effects, or joint pain, or GI distress. Some suffer a combination of two, or all three.

To pull all of this together, we have to answer three questions:

  • How can such a diverse range of plants cause a diverse range of problems for some people?
  • How can these symptoms be so diverse, affecting different parts of the body?
  • And lastly, are there plausible explanations of how nightshades might, as a family, cause these problems?

The Plants: Solanaceae

As I’ve extensively documented in previous sections, there are a number of compounds in nightshade plants that are bioactive. That means they can influence biology, particularly human biology.

The primary suspect is the glycoalkaloid solanine, most commonly associated with potatoes. Other glykoalkoloids—for example tomatine (in tomatoes) and solamargine (in eggplant) characterize other crops. But solanine is reportedly present across all nightshades, though the publicly available research is not encyclopedic. There are also highly toxic tropane alkaloids. Nicotine, though most common in tobacco, appears across many non-tobacco species (including some non-nightshades) as do apparently less toxic alkaloids such as anatabine. Capsaicin is a membrane irritant. There are also lectins.

There may be other compounds involved that have not been identified in the publicly available scientific literature. Calystigine alkaloids, for example, were not discovered until 1988, and not identified in potatoes until 19931.

Generally speaking, each of these many compounds could act on the body in one or more ways:

  • A single chemical, common across multiple nightshade species—like solanine or anatabine—triggers one or more biological processes.
  • Multiple chemicals, perhaps related, trigger one or more biological processes.
  • Multiple chemicals act synergistically to trigger one or more biological processes. For example, in the glycoalkaloids we know that the ratio of solanine to chaconine in potatoes influences the biological action of the chemicals.2 Could there be similar patterns among other chemically related compounds within the nightshade family?

The Gut is a Complex System

Unless you’re a tobacco smoker, the vast bulk of nightshade exposure takes place in the gut.

While Hippocrates gets credit for first recording that “All disease begins in the gut,” he was probably just repeating the common wisdom of prehistoric human healers. As modern medical science probes the complexity of the gut, it has come to understand that the GI tract is astonishingly intricate. In fact, five different, complex, and interrelated systems come together in our gut. Here they cooperate to influence a startling range of health outcomes.

The tube connecting mouth to anus is more than 5 times the length of a grown human, plumbing trivia that wows most young biologists. But there is yet another dimension: smooth out all the bumps and folds, and the surface area of your intestines runs to very nearly the size of a singles tennis court. That’s 3 to 4 times the surface area of your lungs, and “the largest interface between our body and the outside world.”3

Your GI tract is built around a single layer of cells closely related to skin cells. It’s a permeable barrier, and that’s the point: food and water need to get into your body. Water has an easy time of it, but other substances cross by being passed through cells, and by going between the cells through chemical gateways called tight junctions. In a healthy intestine, it’s not a free for all—your body actually decides what goes through.

Think about that: Your body determines, on a molecule-by-molecule basis, what gets through the gut wall and into the bloodstream. It’s not perfect, but it is highly regulated. What’s allowed through are simple chemicals recognized by your body’s finely tuned metabolism. What’s not allowed are un-digested proteins, other large molecules of foreign origin, and—particularly—microorganisms.

The integrity of this intestinal barrier is critical to maintaining health, and it’s not a job just left to some jacked up skin cells. Woven into the fabric of your intestine are also many different cells from your nervous, endocrine, and immune systems. And these aren’t just making a cameo appearance. There are so many nerve cells in your gut that scientific literature casually calls it a second brain.4 The immune system shows up with even more overwhelming force: an estimated 70 to 80 percent of your body’s immune cells live in the gut.5 And the gut’s endocrine cells, collected together, make up the largest portion of your personal chemistry lab,6 producing some 20 different hormones.7

Each part of this system takes feedback from, and regulates, each other part. Here’s how scientists from one of the more distinguished labs working in the field summarize it: “An important function of the GI tract is to sense and respond to external cues. Diverse cellular interactions are responsible for interpreting them, and these interactions must be amenable to the change and flux in the molecular environment of the GI tract. Thus, countless components necessitate GI function, and equally complex changes can affect it.”8

The Microbiome

It should come as no surprise that all of these components ‘talk’ with each other to support the many functions of the GI tract. Even if we didn’t understand the language, they’re all part of our body, so it’s only natural that they work together. That’s kind of the whole miraculous point of the body, after all.

There is an intriguing fifth voice in this conversation: the intestinal microbiome, your distinctive collection of the trillions of microbes that reside mostly in your large intestine, or colon. You’ll find here at least four kingdoms of life; five if you’re in the “viruses are alive” camp.9 If you follow health or science news, you know that the intestinal microbiome has been under revelatory scrutiny for the last decade.

Bacteria, archaea, fungi, and protists weave together a complex ecosystem. Viruses, particularly the phages that attack bacteria, help balance the ecological scales. Collectively this community weighs about 5 pounds. While generally viewed by biologists as important enough to be considered an organ, its complexity and immense variability make that declaration hard to pin down.10

One goal of microbiome science is to learn the operating instructions for an ideal healthy microbiome. It’s easy insofar as you can take any healthy person, then describe their microbiome. But beyond this kind of list, we’ve figured out few rules that explain healthy microbiomes. None of us have the same combination of microbes—it’s a fingerprint, of sorts, unique to each of us. Indeed we have yet to isolate a single bacterial species present in all healthy microbiomes. (Spoiler alert: there probably isn’t one.)

We don’t just have a lot of bacteria, we play host to many different species and strains of bacteria. Bacteria are tricky to identify, so biologists argue about these numbers a lot. An educated range suggests that each of us hosts between 500 to 1000 species. We don’t know how many species there might be in total. A large 2019 study significantly added to our knowledge, but warned of a “substantial but undetermined degree of unclassified microbial diversity within the gut ecosystem.”11

What do these microbes do for us? Most simply they help us digest the fiber in our diets. Microbes also can play a role in the efficiency of energy harvest. More subtle effects on metabolism arise because hormones that govern insulin sensitivity, glucose tolerance, fat storage, and appetite can all be influenced by gut bacteria.12

Microbes also have a role in keeping out disease. Humans tend to think of bacteria as bad, but relatively few are active bad guys. Because bacteria are everywhere, we can’t help but be exposed to them—especially when eating. You are constantly swallowing stray microbes. A healthy microbial ecosystem in your gut makes it very hard for any bad guys to get established. Those trillions of bacteria range from harmless to helpful—what we call commensal species—that help crowd the bad ones out.

But the relationship with immunity goes far deeper. Microbes actually prime the maturation of our immune systems. Young mammals without microbes simply don’t develop a proper immune response; in humans this happens at around 3 years of age. And microbes continue to influence immunity throughout our lives, even acting to modify genetic risk for chronic inflammatory and immune conditions.13 Microbes are also suspected to play a role in the development of—wait for it—food sensitivities.14

Your microbiota also have an apparent role in the development of the nervous system. Mice raised without microbes develop neurological deficiencies that impair learning, memory, recognition, and emotional behaviors.15 Microbes even manufacture small quantities of key neurotransmitters like GABA, dopamine, and serotonin even as they help regulate the body’s own production of neurotransmitters.16

We are only just beginning to decode these relationships, and there are probably hundreds and perhaps thousands more that we haven’t even imagined yet. Each of these complex chemical tasks is guided by genes. That is the power of the microbiome: your microbes have 100 times more genetic potential than your personal DNA. Scientists are not often given to hyperbole, but they have deep respect for this “overwhelming microbial diversity.”17 As two GI specialists writing in 2015 said: “With this enormous pool of genetic information, the microbiota may influence human life at many levels, far beyond host immunity and metabolic functions.”18

We think of these kinds of relationships as symbiotic—an interaction between two different organisms, usually in close contact, and typically advantageous to both. It’s complicated between humans and microbes because the microbiota is not one organism but an entire ecosystem. There’s a lot of give and take between the microbiome and the human host, and it appears largely beneficial to us. Some bacteria are probably better than others, but it’s hard to delineate because within the microbiome many of the bacteria have their own complex relationship with each other.

As we learn about defining healthy microbiomes, we’re learning more about unhealthy microbiomes. Dysbiosis describes a microbial ecosystem out of balance with its host: the good guys are absent or suppressed and the bad guys have taken over. Some dysbiosis is virulent, like the drug resistant C. difficile infections that kill tens of thousands every year.19 And it’s not a surprise to learn that dysbiosis is observed in GI diseases like ulcerative colitis, Crohn’s disease, and irritable bowel disease. More eye opening is continuing discoveries of dysbiosis in a wide range of maladies, including many diseases with autoimmune components, diabetes, cardiovascular disease, kidney disease, autism, celiac disease, and asthma.20

One surprising disease with possible roots in dysbiosis is multiple sclerosis (MS). In this potentially disabling autoimmune disease of the brain and spinal cord, the immune system attacks the myelin sheath which protects nerve fibers. Communication breaks down between your brain and body. While MS has a suspected genetic component, scientists have also now determined that the commensal microbiota directly effect several types of cells in the central nervous system and “is an essential player in triggering autoimmune demyelination” that leads to MS.21 One lab working with a mouse model of MS was able to show that the right bacteria can protect against this inflammation.22

These kinds of discoveries have the potential to be rewriting the medical playbook for quite some time—particularly with respect to autoimmunity. And while there is clearly some kind of relationship between our microbiome and disease, we still don’t confidently know if gut dysbiosis “is a causal factor or an outcome” of autoimmune diseases.23 Is it the chicken? Is it the egg?

Order in the Gut

Consider the many systems interacting in the gut—five of them, working together to turn food into sustenance and eliminate waste, all while regulating hundreds of other bodily processes.

Imagine the challenge: You eat different things for breakfast, lunch, and dinner. You eat different kinds of foods every day, skip meals, and occasionally overeat. You eat at all hours. Sometimes you’re dehydrated, sometimes you’re drunk. You change it up with travel, by the seasons, and when you discover a new cooking website. But even when you’re hangry, pretty much every time a healthy GI system just rolls with the changes. Even the occasional tummy ache is a feature, a warning to take it easy.

This sublime flexibility is called homeostasis. This is defined as the tendency of a system, especially a physiological system in animals, to maintain its stability. We get homeostasis from a coordinated response of connected systems—a complex web of tweaks here and feedback loops there. From blood sugar to body temperature, our bodies maintain numerous homeostatic arrangements, a continuous harmony of call and response that keeps us alive.

Some of the gut’s homeostatic system is focused on the care, feeding, and restraining of the microbiome. Among the specialized immune cells in your GI tract are goblet cells that secrete two layers of mucus in the large intestine. While we tend to associate mucus with yuck, these are a critical part of the immune system. The inner layer protects the intestinal barrier from being overwhelmed by microbes. Another layer helps facilitate communication between microbes and their host.

So, what’s the relationship between dysbiosis and homeostasis? It’s complicated. One kind of dysbiosis we’re beginning to understand is when there are too many microbes that consume this mucus, leaving the intestinal wall vulnerable. This is the same highly selective barrier that controls what’s allowed to cross the intestinal wall and enter the bloodstream. When barrier function—also called intestinal permeability—breaks down, you’re on a pathway to disease.

Early research in intestinal barrier function dates to the 1970s and following decades when scientists studying inflammatory bowel disease began to realize that an inflamed GI tract compromised the intestinal barrier, and this in turn exacerbated inflammation.24 Ever since, scientists and doctors have been stalking the factors at play in this breakdown and its role in inflammatory disease. It’s again a chicken-and-egg debate: Does the disease cause the loss of permeability, or the loss of permeability cause the disease? And nested within is a similar question: does dysbiosis cause loss of homeostasis, or does loss of homeostasis cause dysbiosis?

Research supports the idea that human systems, particularly the immune system, support and shape the microbial community.25 Research also supports the idea that microbes train and sustain the immune system.26 It’s certainly both, and it probably also varies.27 Whoever is leading the dance, it’s destructive when the two are out of step.

If some of this sounds familiar, that’s because the idea of a leaky gut has infiltrated popular theories of health and diet in a way that drives researchers crazy. Leaky Gut Syndrome is connected to a variety of modern medical complaints—and full disclosure, it looks a lot like the kind of laundry list that’s been composed for nightshade sensitivity. Those who push leaky gut syndrome—often with long videos you click on by mistake—usually have a cookbook and supplements to sell, guaranteed to heal your gut and perhaps raise your IQ in the process.

Researchers argue that this is an oversimplification of a much more complex dynamic that we still don’t completely understand. And oversimplification may provide a false sense of security and also deter a proper search for more serious health problems.

To be clear, intestinal permeability—aka leaky gut—is real and health problems associated with it are real. What’s unknown is the degree to which the leaky gut practitioners are on the right healing track. I tend to side with the research community because what microbiological science is teaching us right now is just how much we don’t know. Quite simply, anyone who claims that they have the cure is lying. In all likelihood there is no single cure. People who claim to have one are either unethical and don’t mind simplifying to make some money. Or they really don’t understand the science.

We don’t need the leaky gut debate solved to talk about nightshades. We need to think about those 5 systems: microbiome, endocrine, nervous, immune, and the intestinal lining itself.

Let’s build a very simple gut model around a relatively simple activity: walking. Strolling is not so complex, just one foot in front of another. Now, imagine that picnic classic, a 3 legged race. Choose a partner, face forward, and bind two legs together. Walking is now more complex, with two brains, each controlling one independent leg and one half of a dependent leg. After a couple of minutes of practice you work it out and start to move.

Now imagine adding two more people, one on each side. You’ve got 5 legs, three of them controlled by 2 brains each. Walking in this configuration is not simple. Just trying to visualize it gives me a headache. And I’m guessing it will take you and your three friends a little while to figure out how to take much more than a step or two.

This is an exceptionally crude model of intestinal homeostasis, with only one goal: to help you imagine the challenge of coordinating five systems to do even one thing. But that is what’s happening in your gut 24/7/365. Five different systems work together to control the digestion and absorption, releasing hormones and enzymes, firing nerve cells, activating tight junctions. All while engaging in a wide range of other regulatory activities with other parts of the body.

Could nightshades stagger any part of these gut systems?

The Nightshade Connection

I’ve shown above some of the evidence that disruptions in the gut can have unexpected, non-allergic consequences in systems far from the gut.

We also know generally that “[d]iet can affect inflammatory processes and the immune system directly, and also through mechanisms involving the microbiota.”28

And I’ve shown specifically that nightshades have the demonstrated capacity to influence the various biological systems that control the gut. Now let’s match a select variety of nightshade chemicals with intestinal systems that they can affect (references can be found above in relevant sections):

Solanine (and to a lesser degree other glycoalkaloids) strip cholesterol from cells lining the intestine. This challenges intestinal permeability.

Solanine, tomatine, and solamargine all affect acetylcholinesterase, the enzyme that breaks down a fundamental neurotransmitter. This has the potential to jam nerve communication in the gut.

Solanine (and to a lesser degree other glycoalkaloids) disrupt cellular membranes. All of that communication we’re talking about in the human gut? Most of it happens across membranes. Microbe to microbe. Microbe to human. Human to microbe. How does this membrane disruption affect the GI tract? Is it like static, drowning out weaker signals but allowing stronger signals through? Or does it distort everything? This certainly could influence immune signaling but may also nerve and endocrine signaling as well.

Membrane disruption may affect some microbes differently from others, with the potential to change the balance of power among different kinds of microbes. Could this shift the proportions of different species of microbes? Might this change set the stage for dysbiosis?

Tomatine is anti fungal. Fungal organisms make up a small part of the gut microbiome but are hypothesized to have control functions in the ecosystem of the microbiome.

Potato and tomato lectins have been shown to elicit immune system IgG activation to sites distant from the gut.

Tomato lectins and glycoalkaloids have both been investigated for their pharmaceutical potential as adjuvants, chemicals that enhance immune reaction. In a GI tract with intestinal permeability issues, could these molecules leach into the blood stream and what impact would they have?

If you think about all of the different bodily processes that we’ve covered so far, it’s simply not difficult to imagine how these compounds might bend, mold, trigger, or break various bits of your gut’s complex signaling. And if intestinal permeability is compromised, presumably any of these molecules could enter the blood stream and get swept to other parts of the body.

Imagine again that five-legged race. Suddenly, one person can’t feel their toes, another has a sore knee, and a third gets distracted by a phone conversation with bad reception. Each one of those bioactive compounds represents a way that nightshades might trip up intestinal homeostasis, and thus human health.

While all of these interactions happen within an individual, there are also larger phenomena at play within populations.

I’ve told the story of three generations of my family, where there seems to be a genetic component to nightshade sensitivity. If it’s genetic, what could be the mechanism? Perhaps we have a receptor that other people don’t, some errant biochemical switch that gets toggled by nightshades? Or perhaps there are nightshade metabolizing bacteria and our genetics do not encourage these to colonize our gut?

Then there is the missing microbes hypothesis. Microbial diversity is dropping in human microbiomes for many reasons. We spend less time out in the dirt. Antibiotics and antiseptics have taken their toll. As our diets become increasingly removed from our hunter-gatherer past, the diversity of plants and animals we eat decreases, starving out some microbes. Even more diversity is squeezed out by industrial ingredients and processing.

Microbiologists are increasingly convinced that losing these microbes has health consequences. Perhaps among the missing are nightshade metabolizing bacteria? Or perhaps a different bacteria is missing, allowing another species to thrive that turns nightshades into something our bodies are not equipped to handle.

The missing microbe hypothesis is also closely related to the hygiene hypothesis —the idea that trapped in our climate controlled homes, away from dirt and chickens, our immune systems are struggling to stay in shape. Many physicians and scientists are increasingly convinced that there is a connection between this and rising rates of food allergies, autoimmune disease, metabolic disease, and functional GI maladies.

Nightshade sensitivity could be a complex subset of one or more of these larger health dynamics. Until it’s studied—or the key is unlocked by accident—we just won’t know.

Parallels with Non-Celiac Gluten Sensitivity

How could medical science have missed nightshade sensitivity?

Science and medicine are both works in progress, imperfect and incomplete. I’ve shown above how most nutritional science is based on population studies, and that the discipline is just now developing powerful tools for the study of individuals. And most of the microbiome science discussed here barely existed just 20 years ago.

But even just 10 years ago, as gluten awareness was sweeping the land, doctors were still puzzled by a small sub-set of patients. These sufferers did not have celiac disease or a wheat allergy, yet they reacted to wheat with both GI and non GI symptoms. Though now called non-celiac gluten sensitivity (NCGS), the condition did not even have a consistent name until 2011.

Research in the biology underlying gluten sensitivity has exploded in the last 10 years. That’s because gluten-free hit the big time, raising awareness, creating markets, and thus the research funding necessary to shine a light. After closer scrutiny, the current view is that NCGS breaks down into multiple sub-groups with “different clinical and pathological manifestations,”according to a 2019 review. Because there are no reliable biomarkers it can best be diagnosed via exclusion diet.29

So has non-celiac gluten sensitivity always existed as a basic incompatibility between a rare few people and this very common food? Or is it an emerging problem, related to the suite of autoimmune and metabolic diseases with complex linkages connecting microbiome, diet, and inflammation?

Either way, nightshade sensitivity could easily be an unpolished facet of the very same stone.


Many people label nightshade sensitivity as quackery. I hope I’ve been able to demonstrate that a close look at the available evidence shows multiple pathways by which the nightshade family—a known and prolific producer of bioactive chemicals–could influence GI function and cause health problems anywhere in the body.

Finding nightshade sensitivity is hard because many of the associated symptoms–creaky joints, anxiety, intestinal discomfort—are generalized symptoms that many people tolerate to some degree on a regular basis. They can be caused by many things, and can be very tricky to diagnose. Removing nightshades from contemporary diets is very difficult.

Nightshade sensitivity is probably rare and hopefully no cause for your concern. If you think you have nightshade sensitivity, at this point the only way to diagnose nightshade sensitivity is by using an elimination diet.

That, joyfully, brings us back to the beginning, and to the ultimate purpose of this site: the food. The No Nightshade Kitchen is here to help you navigate eating in a world dominated by nightshades.

Hopefully you don’t need to eat this way, and you’re here because you’re curious and the recipes look interesting.

My warmest welcome to those who do share this challenge. You’re not alone. Your needs and tastes may be different. Your talents and taste buds are surely welcome. Please stay in touch and tell us about your No Nightshade Kitchen.

  1. page 175, Advances in Potato Chemistry and Technology (Second Edition); “Chapter 7 – Glycoalkaloids and Calystegine Alkaloids in Potatoes” []
  2. “Synergistic interaction between the potato glycoalkaloids alpha-solanine and alpha-chaconine in relation to lysis of phospholipid/sterol liposomes” []
  3. Other calculations put this number both lower and higher; this comes from “All disease begins in the (leaky) gut: role of zonulin-mediated gut permeability in the pathogenesis of some chronic inflammatory diseases” []
  4. “Unexpected Roles for the Second Brain: Enteric Nervous System as Master Regulator of Bowel Function” []
  5. “The Enteric Network: Interactions between the Immune and Nervous Systems of the Gut” []
  6. “Enteroendocrine cells-sensory sentinels of the intestinal environment and orchestrators of mucosal immunity” []
  7. “Function and mechanisms of enteroendocrine cells and gut hormones in metabolism” []
  8. “The Enteric Network: Interactions between the Immune and Nervous Systems of the Gut” []
  9. Clarification of terms: your microbiota is the collection of different microbes that live both on and inside of you. Your microbiome is the sum total of all the genes these microbes carry. The terms are often used interchangeably, and the differences mostly matter in academic discourse. []
  10. “The microbiome as a human organ” []
  11. “A new genomic blueprint of the human gut microbiota” []
  12. “The Influence of the Gut Microbiome on Host Metabolism Through the Regulation of Gut Hormone Release” []
  13. “Impact of the Microbiome on the Human Genome” []
  14. “Mechanisms by which gut microorganisms influence food sensitivities” []
  15. “Impact of microbiota on central nervous system and neurological diseases: the gut-brain axis” []
  16. “Neurotransmitter modulation by the gut microbiota” []
  17. “The human microbiome in health and disease: hype or hope” []
  18. “Food, Immunity, and the Microbiome” []
  19. https://www.cdc.gov/drugresistance/biggest-threats.html#cdiff []
  20. “Defining Dysbiosis for a Cluster of Chronic Diseases” []
  21. “Combined therapies to treat complex diseases: The role of the gut microbiota in multiple sclerosis” []
  22. “Impacts of microbiome metabolites on immune regulation and autoimmunity” []
  23. “Environmental Exposures and Autoimmune Diseases: Contribution of Gut Microbiome” []
  24. “Leaky gut: mechanisms, measurement and clinical implications in humans” []
  25. “How MHCII signaling promotes benign host- microbiota interactions” []
  26. “Microbiota-Nourishing Immunity: A Guide to Understanding Our Microbial Self” []
  27. “Dysbiosis and Its Discontents” []
  28. “Food, Immunity, and the Microbiome” []
  29. “Non-Celiac Gluten Sensitivity: A Systematic Review” []



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