Daniel sent us this one — he wants to talk about leaky gut and intestinal permeability. He says it seems like one of those conditions wedged in the uneasy space between real health concerns and things the internet overstretches to fit any problem. But in the real and clinical sense — what is it, how is it detected, how does it manifest? There's a lot to unpack here, because this is genuinely one of those terms that means something very specific in gastroenterology and something very different on wellness blogs.
The gap between those two things is where most of the confusion lives. I want to start with the actual biology, because once you understand the structure, you immediately see why the pop-culture version of leaky gut is both onto something and wildly off base.
Walk me through the wall. What are we actually talking about when we say intestinal permeability?
You've got a single layer of epithelial cells lining your small intestine — these are called enterocytes — and they're packed together with what are essentially protein zippers between them. Those zippers are tight junction proteins. Claudins, occludins, zonula occludens proteins. They form these selectively permeable seals. The space between cells is called the paracellular pathway, and in a healthy gut, those tight junctions regulate what slips through that pathway with extraordinary precision.
It's not a solid wall. It's more like a gated checkpoint.
And it has to be. Your small intestine isn't supposed to be impermeable — it's supposed to be selectively permeable. You need to absorb nutrients, water, electrolytes. The villi and microvilli give you this enormous surface area — roughly the size of a tennis court, if you flattened it all out — and across that surface, things are constantly crossing. The question is what crosses, and through which route.
When people say leaky gut, they're talking about the checkpoint getting sloppy.
In clinical terms, increased intestinal permeability means those tight junctions have loosened. The protein zippers are unzipping when they shouldn't be. And the paracellular pathway opens up enough that larger molecules — things that should never cross intact — start slipping through. Partially digested food proteins, bacterial fragments like lipopolysaccharides, microbial metabolites. These things end up on the wrong side of the epithelium, in the lamina propria, where your immune system is heavily concentrated.
Your immune system does what immune systems do when they encounter things where they shouldn't be.
It mounts a response. The gut-associated lymphoid tissue — GALT — represents something like seventy percent of your entire immune system. It's there precisely because the intestinal lining is the largest interface between your internal environment and the outside world. When the barrier gets leaky, that immune tissue gets activated in ways that can become chronic and systemic.
This is the mechanism people point to when they blame leaky gut for everything from eczema to brain fog to autoimmune disease.
This is where we need to separate the wheat from the chaff. The mechanism is real. The question is what clinical conditions it's actually implicated in, how reliably we can measure it, and whether treating permeability treats the underlying problem or just a symptom.
Okay, so let's start with what's firmly established. Where does the evidence actually land?
The strongest evidence is in inflammatory bowel disease — Crohn's and ulcerative colitis. Increased intestinal permeability is well documented in both, and in Crohn's specifically, it often precedes clinical relapse. There was a landmark study back in the nineties — Hilary Steinhart and colleagues, I think — showing that asymptomatic first-degree relatives of Crohn's patients had elevated permeability. And those who later developed Crohn's, the permeability spike came before the inflammation.
It's not just a consequence of an already inflamed gut. It might be part of the ignition.
That's the chicken-and-egg problem that still isn't fully resolved. But the temporal sequence in some of those studies is suggestive. Permeability rises, then inflammation follows. The other well-established connection is celiac disease. Gliadin — a component of gluten — triggers the release of zonulin, which is a protein that directly regulates tight junction opening. Alessio Fasano's group at Harvard discovered this. Zonulin signals those tight junctions to loosen, and in people with celiac, this response is amplified.
Gluten literally tells the gate to open.
The zonulin pathway is normal physiology — it's one way the gut regulates permeability. But in celiac patients, the response is exaggerated, and combined with the autoimmune reaction to gliadin, you get a vicious cycle. More permeability means more gliadin crossing, which means more immune activation, which means more inflammation, which means more permeability.
Outside of celiac and IBD? What about the broader claims — the ones that show up in the comments section of every health forum?
This is where the evidence gets thinner. There's emerging research connecting increased permeability to type one diabetes, to non-alcoholic fatty liver disease, to certain aspects of metabolic syndrome. The gut-liver axis is particularly interesting — when the intestinal barrier is compromised, bacterial products reach the liver via the portal vein, and the liver's immune cells, Kupffer cells, react. That can drive hepatic inflammation.
The mechanism is plausible across multiple conditions. The question is whether it's causal or just along for the ride.
And that question is much harder to answer than wellness influencers make it sound. The gut barrier doesn't exist in isolation. It's influenced by the microbiome, by diet, by stress, by circadian rhythms, by medications. When someone has a chronic condition and also has increased permeability, untangling what's cause and what's effect is difficult.
This is where I think the internet version of leaky gut goes off the rails. It takes a real physiological phenomenon and turns it into a universal explanation.
The all-purpose villain. You're tired? Your sourdough didn't rise?
The gluten intolerance of explanations for gluten intolerance.
What makes it particularly tricky is that some of those connections might eventually prove out. The gut-brain axis is real. There are pathways by which systemic inflammation from gut-derived triggers could affect mood, cognition, energy levels. But the evidence for treating leaky gut as a primary diagnosis — as something you walk into a clinic and get tested for and treated directly — is not there for most of the claims being made.
Which brings us to detection. How do you actually measure this?
This is one of the most misunderstood aspects of the whole topic. The gold standard in research is the lactulose-mannitol test. You drink a solution containing two sugar molecules — lactulose, which is a disaccharide that's too large to cross a healthy intestinal barrier through the paracellular route, and mannitol, which is a monosaccharide that crosses freely. Then you collect urine for several hours and measure how much of each shows up.
If the barrier is intact, you see lots of mannitol and very little lactulose.
The lactulose-to-mannitol ratio tells you how permeable the small intestine is. High ratio means more of the large molecule crossed, which means the tight junctions are loose. It's a well-validated test that's been used in research for decades.
This is what you get when you order a leaky gut test from one of those direct-to-consumer labs?
Sometimes yes, sometimes no. There are commercial labs offering lactulose-mannitol testing, but the standardization is inconsistent. Collection protocols vary, dietary prep varies, reference ranges vary. And even when the test is done properly, it tells you about small intestinal permeability at one point in time. It doesn't tell you why it's elevated, or whether it's clinically significant for your particular symptoms.
What about other methods? I've seen people talk about zonulin levels in blood, or IgG food sensitivity panels.
Serum zonulin is controversial. There are commercial assays, but the specificity has been questioned — some researchers argue the available tests are measuring something else that cross-reacts, or that serum zonulin doesn't reliably reflect intestinal zonulin activity. It's not a settled biomarker. And IgG food sensitivity testing — I want to be careful here, because this is a hill I've seen people die on.
I can hear you choosing your words.
IgG antibodies to foods are a normal immunological phenomenon. They're essentially a memory response — they indicate exposure, not intolerance. Elevated IgG to a food often just means you eat that food regularly. Using IgG panels to diagnose leaky gut or to prescribe elimination diets is not supported by the major allergy and immunology organizations. The American Academy of Allergy, Asthma and Immunology has been pretty clear about this.
What you're saying is a lot of the testing people are paying for out of pocket is built on shaky foundations.
Some of it is useful in research contexts. Some of it is premature commercialization of incompletely validated biomarkers. And some of it is — I'll just say it — actively misleading. When a test tells you that you're intolerant to thirty-seven foods based on IgG, and you weren't having symptoms from those foods, the test might be creating a problem rather than solving one.
Like adopting a feral cat to deal with a mouse.
Except the cat now needs specialized veterinary care and a raw diet and you're reading feline nutrition blogs at two in the morning.
Let's talk about what actually causes increased permeability in the first place. What loosens those tight junctions?
A bunch of things, and this is where the clinical picture gets complicated. Non-steroidal anti-inflammatory drugs — ibuprofen, naproxen, aspirin — are well-documented to increase intestinal permeability, and the effect can happen within hours of ingestion. Alcohol does it. Intense exercise can do it temporarily — marathon runners often show elevated permeability markers post-race, which is thought to be related to splanchnic hypoperfusion, reduced blood flow to the gut during exertion.
The gut barrier gets less blood flow during intense exercise, and that compromises the tight junctions?
Part of the mechanism. There's also thermal stress — core temperature rising — and oxidative stress. The interesting thing is that this exercise-induced permeability is usually transient and may actually be part of a hormetic response. A short period of increased permeability that stimulates adaptive repair mechanisms.
Not all permeability is pathological.
That's a crucial point. The gut barrier is dynamic. It opens and closes in response to various signals. The problem is when it's chronically open, or when it opens in response to inappropriate triggers, or when the repair mechanisms can't keep up.
What about diet? This is where the wellness industry has a lot to say.
Gluten is the big one, and we already talked about zonulin. But it's worth emphasizing that the zonulin response to gliadin happens in everyone — it's just more pronounced in celiac patients and possibly in non-celiac gluten sensitivity, though that's a separate and also contentious topic. Beyond gluten, there's evidence that certain food additives — emulsifiers like carboxymethylcellulose and polysorbate eighty — can increase permeability in animal models. There was a study from Benoit Chassaing's group at Georgia State that got a lot of attention. High-fat diets also seem to increase permeability, possibly through changes in bile acid metabolism and microbiome composition.
On the protective side?
Short-chain fatty acids, especially butyrate, are critical for maintaining barrier integrity. Butyrate is produced when gut bacteria ferment dietary fiber — it's the primary energy source for colonocytes, the cells lining the colon, and it directly strengthens tight junction expression. This is one reason fiber intake correlates with gut barrier health. Zinc is important for tight junction function. Vitamin D plays a role in regulating tight junction protein expression. Glutamine is a major fuel for enterocytes.
The standard advice — eat fiber, get enough vitamin D, don't live on ibuprofen and vodka — is basically leaky gut prevention.
It's almost disappointing how unsexy the evidence-based recommendations are. The things that support overall gut health also support barrier integrity. The problem is that "eat more vegetables and don't drink excessively" doesn't sell supplement protocols.
Speaking of supplements — this is where the market really blooms. L-glutamine, collagen peptides, colostrum, various proprietary blends. What actually has evidence?
L-glutamine has the strongest mechanistic rationale. It's the preferred fuel for enterocytes and it's been shown to reduce permeability in some clinical contexts — particularly in critically ill patients receiving total parenteral nutrition, where the gut is atrophic from disuse. Whether oral glutamine supplements meaningfully affect permeability in otherwise healthy people with normal diets is less clear. The doses used in clinical studies are often much higher than what's in commercial supplements.
The theory is that collagen provides glycine and proline, which are amino acids used in connective tissue synthesis. The gut lining has connective tissue components. But the leap from "these amino acids are building blocks" to "ingesting collagen powder repairs tight junctions" is — let's say the bridge has a few missing spans.
The supplement industry's favorite engineering technique: building bridges with missing spans.
Bone broth is in a similar category. It's not harmful — it's basically a source of amino acids and minerals — but the specific claims about sealing the gut lining are extrapolated well beyond the evidence. Colostrum is interesting because it contains growth factors and immunoglobulins that do support gut barrier development in neonates. Whether adult guts respond similarly, and whether commercially available bovine colostrum supplements deliver those factors in bioactive form, is not well established.
We have a real physiological phenomenon, some validated measurement techniques, a handful of well-established clinical associations, and then a vast wellness ecosystem built on top of it that's mostly scaffolding.
That's a fair summary. And the scaffolding is profitable. The global digestive health supplements market is — I want to say north of forty billion dollars now. Leaky gut has become a marketing term as much as a medical one.
Which is a problem, because it muddies the water for people who actually have barrier dysfunction contributing to their condition. If leaky gut means everything, it means nothing.
It creates this dynamic where skeptical clinicians dismiss the entire concept, while alternative practitioners overdiagnose it based on dubious testing. The people in the middle — the patients with real symptoms and unclear etiology — get caught between those two extremes.
If someone's listening and thinking, okay, I have digestive issues, maybe some systemic symptoms, and I'm wondering if intestinal permeability is part of the picture — what should they actually do?
I'd start by saying: treat the known before chasing the speculative. If you have IBS symptoms, get evaluated for celiac disease, for IBD, for SIBO. These are conditions with established diagnostic criteria and treatment pathways. If those are ruled out, and you're still symptomatic, the conversation gets more nuanced.
At that point, what does a legitimate clinical approach look like?
You'd look at the things known to increase permeability and address them systematically. Are you taking NSAIDs regularly? That's a direct, reversible cause. Is your alcohol intake significant? Is your diet extremely low in fiber? Do you have uncontrolled stress — because cortisol and catecholamines do affect barrier function through mast cell activation and altered gut motility.
The stress connection is underappreciated.
It really is. The brain-gut axis isn't metaphorical. Corticotropin-releasing hormone, which is released during stress, directly increases intestinal permeability in animal models. Mast cells in the gut degranulate in response to stress signals and release mediators that affect tight junctions. This is one reason people with IBS often flare during stressful periods — and IBS itself is associated with increased permeability in a subset of patients.
We've got NSAIDs, alcohol, low fiber, stress. What about the microbiome?
Dysbiosis — an imbalanced gut microbial community — can both cause and be caused by increased permeability. It's a bidirectional relationship. When the barrier is leaky, bacterial products cross and trigger inflammation, which alters the luminal environment, which shifts the microbial composition. And certain microbial profiles — reduced diversity, loss of butyrate-producing species like Faecalibacterium prausnitzii — are associated with reduced barrier integrity.
Which brings us to probiotics. Another multi-billion-dollar category. Do they help with permeability?
Certain strains show promise. Lactobacillus rhamnosus GG has the most evidence — it's been shown to reduce permeability in children with atopic dermatitis, in patients with IBS, in some post-infectious settings. Bifidobacterium infantis has some data. But the effect is strain-specific and context-dependent. You can't just grab any probiotic off the shelf and assume it'll tighten your tight junctions.
The specificity problem again. Probiotics aren't interchangeable, but they're marketed as if they are.
It's like saying "medication" as a category. Technically true that they're all medications, but you wouldn't swap your blood pressure pill for an antibiotic and expect the same result.
Let's zoom out and talk about the broader clinical picture. Where is the research heading? What's the frontier?
A few directions. One is the role of permeability in metabolic disease. There's growing evidence that endotoxemia — low levels of bacterial lipopolysaccharide in the bloodstream, originating from a leaky gut — contributes to the chronic low-grade inflammation that drives insulin resistance and atherosclerosis. This is sometimes called metabolic endotoxemia. It was first really characterized by Patrice Cani's group in Belgium about fifteen years ago.
The gut barrier might be a player in type two diabetes and cardiovascular disease.
The data in animal models is strong. In humans, it's more associative than causal so far. But it's a plausible pathway. Another frontier is the gut-brain axis in neurodegenerative disease. There's some evidence that increased intestinal permeability is more common in Parkinson's disease, and that it might precede the motor symptoms — which is interesting because alpha-synuclein aggregates, the pathological hallmark of Parkinson's, have been found in the gut before they appear in the brain.
That's a wild idea. Parkinson's starting in the gut.
The Braak hypothesis. Heiko Braak, a German neuroanatomist, proposed that Parkinson's pathology might begin in the gut and spread to the brain via the vagus nerve. It's still debated, but there's enough evidence that it's being taken seriously. And if the gut barrier is compromised, that could be part of how environmental triggers gain access to the enteric nervous system.
Leaky gut, in the serious research context, is less about bloating and food sensitivities and more about being a possible early mechanism in major chronic diseases.
That's where the real stakes are. And it's why the wellness co-opting of the term is frustrating — because it trivializes something that might actually be medically important in ways we're only beginning to understand.
It also creates a weird paradox, right? The wellness industry has been talking about leaky gut for twenty years. Mainstream medicine dismissed it. Now the research is catching up to some version of the concept, but the terminology is so tainted that serious researchers sometimes avoid the phrase entirely.
They prefer "intestinal permeability" or "barrier dysfunction" precisely to avoid the baggage. "Leaky gut syndrome" is not a recognized medical diagnosis. It doesn't appear in the ICD. But increased intestinal permeability is a measurable, documented phenomenon implicated in multiple diseases. The language matters because it signals whether you're in the evidence-based conversation or the alternative medicine one.
Which is a shame, because they're describing the same biology.
From different directions with different standards of evidence. The wellness version takes the mechanism and extrapolates it to explain essentially any symptom, then sells you the solution. The medical version says: here's a physiological process, here's where we've demonstrated it matters, here's where we're still uncertain, and here's what we can actually do about it.
The humility gap.
That's exactly what it is. And the humility gap is where a lot of patient frustration lives. If you have real symptoms and your doctor says "there's no such thing as leaky gut" — which is technically true in diagnostic terms but dismissive of the underlying biology — you're going to go find someone who takes you seriously. And that someone might be selling IgG panels and seventeen supplements.
What's the more honest conversation a clinician could have?
Something like: intestinal permeability is real, it's involved in several conditions we take seriously, we don't have a perfect test for it outside of research settings, but we can address the known contributors — NSAID use, alcohol, diet quality, stress, underlying conditions like celiac or IBD — and see if your symptoms improve. That's less satisfying than "you have leaky gut, take these three supplements, and avoid these twenty foods." But it's more honest.
Probably more effective in the long run.
Though I want to acknowledge something here. The reason the alternative approach is appealing isn't just that it offers certainty. It's that it offers agency. People want something they can do. "Reduce stress and eat more vegetables" doesn't feel like an intervention in the same way that a targeted supplement protocol does.
Even if the supplement protocol is built on air.
The placebo effect is real, and the ritual of treatment has psychological value. The problem is when the supplements are expensive, the dietary restrictions are unnecessarily severe, and the underlying condition — if there is one — isn't being properly evaluated.
Let's get concrete about manifestation. Someone with clinically significant increased intestinal permeability — what does that actually feel like?
It depends entirely on the underlying context. In IBD, it's part of a picture that includes abdominal pain, diarrhea, sometimes bleeding, systemic symptoms like fatigue and weight loss. In celiac, it's part of the response to gluten that produces a wide range of symptoms — gastrointestinal and extra-intestinal. In the less clear cases — the person with IBS-like symptoms, maybe some joint pain, maybe brain fog, maybe skin issues — the permeability might be present, but its causal role is harder to establish.
There's no "leaky gut presentation" that a doctor can spot from across the room.
And that's a key point. Intestinal permeability is not a clinical syndrome with a recognizable symptom cluster. It's a physiological state that may contribute to various clinical syndromes. The symptoms come from what the permeability enables — immune activation, inflammation, metabolic disruption — not from the permeability itself.
Which is why diagnosing "leaky gut" as a primary condition doesn't make clinical sense. You diagnose the condition it's contributing to.
And you address the permeability as part of managing that condition, not as a standalone target.
Let's talk about the pediatric angle, since that was your world for decades. Is this something that shows up in kids?
It does, and in some ways the evidence is clearer in pediatrics because the confounding factors — decades of NSAID use, alcohol, accumulated lifestyle factors — are less present. Increased intestinal permeability has been documented in children with food allergies, with atopic dermatitis, with autism spectrum disorder — though the autism connection is particularly contentious and I want to be careful about it.
There's some evidence that a subset of children with ASD have increased intestinal permeability and gastrointestinal symptoms. The gut-brain connection is plausible. But this has been seized upon by proponents of various unproven therapies — restrictive diets, chelation, supplement protocols — and the evidence for those interventions is weak to nonexistent. The association shouldn't be dismissed, but the therapeutic leap from "some autistic children have leaky guts" to "treating leaky gut will improve autism" is not supported by clinical trials.
Again, real phenomenon, premature therapeutic conclusions.
Children are a vulnerable population where the stakes of unnecessary dietary restriction are particularly high. Restricting a child's diet based on IgG testing can lead to nutritional deficiencies, food aversions, social difficulties. The burden of proof for an intervention in kids should be higher, not lower.
What about the neonatal period? I've read that newborns have naturally higher intestinal permeability, and that this is actually functional.
The newborn gut is intentionally more permeable in the first days of life. This allows immunoglobulins and growth factors from colostrum to cross the intestinal barrier intact. It's a critical window for immune education. The gut closes over the first weeks and months — a process sometimes called gut closure. Premature infants have delayed closure, which is one reason they're more susceptible to necrotizing enterocolitis, a devastating condition where the intestinal barrier breaks down and bacteria invade the gut wall.
Permeability is actually adaptive in the right context and at the right time.
Which circles back to what we said earlier — permeability isn't inherently pathological. It's a regulated physiological process. The pathology is dysregulation.
I want to touch on something you mentioned earlier — the gut-liver axis. This seems like one of the more robust areas of permeability research.
The anatomical connection is direct — the portal vein drains from the intestines to the liver. Anything that crosses the gut barrier enters the portal circulation and hits the liver before anywhere else. The liver's immune system — the reticuloendothelial system, Kupffer cells, hepatic stellate cells — is positioned to handle this. But if the barrier is persistently leaky, the liver gets chronically exposed to bacterial products.
That drives non-alcoholic fatty liver disease?
It's one of the proposed mechanisms. NAFLD is strongly associated with obesity and insulin resistance, but not everyone with obesity develops it, and not everyone with NAFLD has significant metabolic risk factors. Gut permeability and the resulting endotoxin exposure may help explain some of that variance. There are trials looking at whether interventions that improve barrier function — things like synbiotics, which combine probiotics and prebiotics — can improve liver enzymes and histology in NAFLD patients.
What's the evidence so far?
Mixed but promising. A meta-analysis published a few years ago found that synbiotics improved liver enzymes and some markers of inflammation, but the studies were small and heterogeneous. It's not ready for prime-time clinical recommendations, but it's an active area of investigation.
If I'm following the research trajectory, intestinal permeability is moving from a fringe concept to a recognized contributor in multiple disease pathways, but the clinical tools — diagnostics and therapeutics specifically targeting permeability — haven't caught up yet.
We're in this awkward intermediate phase where the biology is increasingly clear but the clinical applications are still being worked out. And nature abhors a vacuum, so the wellness industry has filled it.
The supplement industry is the hermit crab of the medical evidence gap.
Finding an empty shell and moving right in.
What's your advice for the person who's been down the internet rabbit hole and now thinks every symptom they have is caused by leaky gut?
Step one: step away from the search results. Step two: see a gastroenterologist if you have significant GI symptoms, and get evaluated for the established conditions — celiac, IBD, SIBO, IBS. Step three: address the basics — if you're taking NSAIDs regularly, find alternatives with your doctor; if your diet is ultra-processed and low in fiber, shift it; if your alcohol intake is high, reduce it; if your stress is unmanaged, take that seriously as a physiological intervention, not just a lifestyle suggestion.
If you've done all that and you're still symptomatic, and you want to explore permeability more directly, find a clinician who understands the evidence but won't overclaim. They're rare but they exist. Academic medical centers with integrative gastroenterology programs are probably your best bet.
Not the person selling colostrum enemas on Instagram.
I'm going to pretend I didn't hear that phrase and move on.
You're welcome. Let's talk about one more thing before we wrap — the zonulin story. You mentioned Alessio Fasano earlier. His work seems to have been both foundational to understanding permeability and also somewhat controversial.
Fasano's discovery of zonulin was a genuine breakthrough. He identified the molecule that regulates tight junction opening in response to gliadin, and he's connected it to celiac disease, type one diabetes, and other autoimmune conditions. The controversy comes from a few directions. One is the commercialization — Fasano has patents related to zonulin as a biomarker and therapeutic target, which creates the usual conflict-of-interest questions. Another is the debate about whether zonulin is actually the human analog of a bacterial toxin or a distinct protein — there was a back-and-forth in the literature about whether commercial zonulin assays were measuring zonulin or something else.
Even the flagship biomarker is contested.
Science is messy. That doesn't mean the zonulin story is wrong — it means it's still being refined. The broader point about tight junction regulation and its role in disease stands regardless of the specific molecular details of zonulin measurement.
That seems like a good place to land. Intestinal permeability is real, it's biologically important, it's implicated in several major diseases, the measurement tools exist but aren't perfect, the therapeutic tools are mostly lifestyle-based with a few targeted exceptions, and the gap between what's known and what's marketed remains vast.
That gap is where most of the public confusion lives. The conversation is polarized between dismissal and overclaim, when the truth is somewhere in the middle — which is where most medical truths live, honestly.
The least marketable location in healthcare.
"It's complicated and we're still learning" doesn't sell many supplements.
Before we close out, I believe we have a visitor.
Now: Hilbert's daily fun fact.
Hilbert: Cosmic ray muons were first detected by Theodor Wulf in nineteen ten using an electroscope on the Eiffel Tower, but the method of detecting them through Cherenkov radiation in large water tanks was independently rediscovered by a Somaliland-based physicist in the early medieval period — or rather, would have been, if the necessary photomultiplier tubes hadn't been about eleven centuries away from invention.
That's a lot of qualifiers on one fact.
The conditional cosmic ray detection of pre-Islamic Somaliland. I feel like that deserves its own podcast.
This has been My Weird Prompts. Thanks to our producer Hilbert Flumingtop. You can find us at myweirdprompts.I'm Corn.
I'm Herman Poppleberry. Keep questioning the supplement protocol.
