Quick personal note before we talk about gluten: If you’ve been following along with the neck saga over on Instagram, that’s where I’m keeping the updates for now. I write these blogs and schedule them ahead of time, and things are changing quickly enough that anything I put here would probably be old news by the time it hit your eyeballs. You can catch up with me over on Instagram (stories and feed) if you want the latest.
We need to talk about gluten. Don't worry, this is not going to end with me dramatically confiscating your sourdough. (Or will it?????? Dun dun dunnnnnn)
I’ve actually treaded pretty lightly around gluten over the years, especially considering that I personally haven’t eaten it in more than a decade. You’ve never heard me say everyone needs to stop eating gluten. You’ve never heard me say gluten is poison. You’ve also never heard me say that if you don’t have celiac disease, gluten absolutely cannot be affecting you.
Annoyingly, there is nuance here.
So today we’re getting into all of it. What gluten actually is. Celiac disease. Gluten sensitivity. What we know. What we don't know yet. The gut permeability research that make me pause. Thyroid and autoimmune disease. Those food sensitivity tests that come back suggesting you cut out 95% of the foods you eat, and how I actually think through whether removing a food makes sense.
First, gluten is a group of proteins found primarily in wheat, barley and rye. Gliadin is one of the major components of gluten and gets a lot of attention in research because pieces of it are particularly resistant to being completely broken down during digestion.
That does not automatically make gluten dangerous. We eat plenty of things our digestive systems have to work on, but gluten does interact with the gut + immune system in some interesting ways, and some people’s bodies handle that interaction very differently than others.
Celiac disease is the clearest example.
Celiac is an autoimmune disease. When someone with celiac eats gluten, their immune system mounts a response that damages the lining of the small intestine. The tiny finger-like structures called villi can become damaged and flattened. And those little guys have a job ... they help you absorb nutrients. So celiac isn’t just “bread makes my stomach hurt."
Someone can have diarrhea, constipation, bloating, abdominal pain, fatigue, anemia, low iron or ferritin, vitamin deficiencies, bone issues, skin symptoms or neurological symptoms. Some people have very few obvious GI symptoms at all.
This is one reason unexplained nutrient deficiencies get my attention. If someone keeps having low iron, ferritin, folate, B12, vitamin D or other signs that make me wonder whether they’re absorbing what they’re taking in, I want to know why. Celiac is certainly not the only possible answer, but malabsorption belongs somewhere on the whiteboard.
Celiac testing works best while you’re still regularly eating gluten. Remove gluten first and you can potentially make the testing less sensitive, which is a very annoying way to make getting an actual answer harder. Sometimes symptoms make it so uncomfortable to continue eating gluten so testing is voluntarily forfeited by a patient.
Then we have non-celiac gluten sensitivity, sometimes called non-celiac gluten / wheat sensitivity. This is where things get considerably messier.
These are people who do not have celiac disease and do not have a wheat allergy, but consistently experience symptoms when eating gluten-containing foods and improve when those foods are removed. Symptoms can include bloating, abdominal pain, changes in bowel habits, fatigue, headaches, brain fog and other symptoms outside of the GI tract.
The annoying part is that we don’t currently have one beautiful little blood test that says, “Congratulations, gluten is your problem.”
There ARE blood tests that can help us investigate celiac disease, though. The usual starting point is tTG-IgA (tissue transglutaminase IgA) along with total IgA, since IgA deficiency can make that first test falsely reassuring. If IgA is low, an IgG-based test such as tTG-IgG or DGP-IgG may be used. There’s also HLA-DQ2 / DQ8 genetic testing, which can help rule celiac out if those variants are absent, although having them doesn’t mean you have celiac. What we don’t currently have is a validated blood test that can say, “Yup, mmhmm, you have non-celiac gluten sensitivity.” That diagnosis is a lot more about the pattern of symptoms, ruling out other conditions and what happens when gluten is removed and then reintroduced.
There is no validated biomarker that reliably diagnoses non-celiac gluten sensitivity right now. And researchers are still sorting out whether gluten itself is always the culprit in these cases. Wheat contains other things that can cause symptoms too, including fructans, which are FODMAPs, and other wheat proteins.
So when someone tells me, “I feel terrible when I eat gluten,” I believe them. I just don’t automatically assume we know the mechanism yet. Those are two different things.
Let's get to the research that makes this conversation even more interesting...
Researchers have looked at what happens to the intestinal barrier when it’s exposed to gliadin, part of gluten. One small study took intestinal biopsy tissue from people with active celiac disease, celiac disease in remission, non-celiac gluten sensitivity and people without either condition. When those intestinal tissues were exposed to gliadin in the lab, intestinal permeability increased in all 4 groups, including the non-celiac controls. The effect wasn’t identical between groups, and people with active celiac disease and gluten sensitivity showed different responses from some of the other groups. But the interesting takeaway is that gliadin temporarily changed the gut barrier even in non-celiacs.
A Petri dish is not a person. A piece of intestinal tissue in a laboratory does not have your entire immune system, microbiome, nervous system, hormones, blood flow, liver and every other ridiculous layer of human biology interacting with it. So this research does not prove that every person who eats gluten develops a harmful, chronic 'leaky gut.' But, it does tell us that gliadin can interact with the intestinal barrier and temporarily alter / increase permeability. Other research has identified pathways involving zonulin and the tight junctions between intestinal cells that help explain how this can happen.
Think of your intestinal lining like security at a concert. Its job isn’t to keep absolutely every little thing out. Nutrients need to get through, of course. But it does need to be very particular about what gets backstage. The cells lining your intestine have little structures called tight junctions that help regulate that traffic. Gliadin can trigger signaling involved in temporarily opening those junctions.
If the intestinal barrier becomes more permeable, more partially digested food components or other antigens can cross that barrier and interact with the immune system. More repeated exposure like this could matter even more in certain genetically susceptible people. Could that help explain why certain people develop additional food reactions or immune problems while others happily eat bread their entire lives and remain completely unbothered? I mean, maybe!
That is where I am deliberately using the word could.
There are plausible mechanisms here. There is interesting research here. There are also huge gaps between being able to demonstrate the mechanism biologically and "... therefore every human should stop eating gluten".
This is also why I’m particularly interested in the gluten conversation when someone already has a lot going on -- chronic GI symptoms, unexplained nutrient deficiencies or absorption issues, celiac disease in the family, or autoimmune disease. Thyroid disease is part of this conversation too.
Celiac disease and autoimmune thyroid disease, particularly Hashimoto’s, occur together more often than we’d expect by chance. I'm interested in several possible connections between the gut, gluten and thyroid autoimmunity, including intestinal permeability, shared immune pathways and something called molecular mimicry.
Molecular mimicry is basically an immune-system case of mistaken identity. It's WILD! Your immune system learns what an enemy looks like. Sometimes a foreign protein and one of our own proteins share enough similarities that an immune response aimed at one can potentially cross-react with the other.
There are theories and some mechanistic evidence involving gluten-related immune responses, tissue transglutaminase and thyroid tissue that could help explain part of the connection between celiac disease and autoimmune thyroid disease.
We do not currently have strong evidence showing that gluten is a universal cause of Hashimoto’s or that every person with Hashimoto’s MUST be gluten-free. Recent reviews still describe the gluten/thyroid connection outside of celiac disease as plausible and interesting, but not proven enough to recommend routine gluten elimination for everyone with Hashimoto’s. That being said, it's one thing to not be able to recommend something across the board yet and another as an individual to decide to weigh risk vs benefits themselves in the interim.
So yes, I AM more curious about gluten in someone with Hashimoto’s than I would be in a completely asymptomatic person with beautiful labs, no autoimmune history, no GI issues and no apparent problems eating it.
This is pretty much how I approach health across the board, though. My goal is almost never more restriction. I want you eating the most calories your body can handle while supporting your health, body composition goals, labs, energy and whatever else we’re working toward. I want you eating the widest variety of foods that works well for your body. I want you moving in as many ways as your body has the capacity to move.
More options + capacity. Bigger life.
I think about injuries the same way. If someone hurts a shoulder and the solution is 'never train that shoulder again,' we haven’t only removed risk. We’ve created a new risk. Now that person loses the opportunity to build muscle, maintain bone, develop capacity and remain physically capable.
Sometimes being conservative temporarily is absolutely appropriate. Then -- ideally -- we build capacity and open things back up.
Nutrition is like that. Removing a food has a potential benefit. It also has a cost. The cost might be nutritional. Financial. Social. Psychological. Logistical. Gluten-free food is not famously known for being cheap.
So, I need a reason for restriction.
This is also why I’m not a huge fan of many commercial “food sensitivity” panels. You know the ones. You send off some blood and get back a gorgeous color-coded report informing you that you’re reactive to 84 of the 100 foods tested. Ahhhh. I talk many-a-client off the ledge after some of those reports are received.
Many of these tests measure IgG antibodies to foods. The problem is that IgG exposure can simply mean your immune system has seen that food before. It's not that every piece of information from every specialty gut test is worthless. Buttttttt, I refuse to let one test boss you or me around.
A test can sometimes be a clue. So can your symptoms, health history, labs, bowel habits, energy, skin, cycle, body composition, medications, nutrient status, sleep, stress, food patterns, what actually happens when you eat something, remove it and reintroduce it.
My job is to dump all of those puzzle pieces onto the table and figure out what picture they seem to be making.
Which brings me to elimination diets. If you’re trying to figure out whether a particular food is causing symptoms, removing 6 foods at once isn’t very helpful. Let’s say you eliminate gluten, dairy, soy, eggs, corn and peanuts and three weeks later you feel amazing. Cool. We've learned almost nothing.
Maybe gluten was bothering you. Maybe dairy was. Maybe it was the giant amount of ice cream you ate every night and not dairy as an entire category. Maybe your fiber intake changed. Maybe removing wheat dramatically reduced your fructan intake. Maybe your overall diet changed. You get it.
One variable at a time whenever it’s reasonable makes the experiment much more helpful.
That’s pretty much how I figured out gluten was a problem for me more than ten years ago.
I was postpartum after an extremely difficult pregnancy (hyperemesis gravidaruum) where I’d been very sick and ended up very underweight. After delivery I lost a tremendous amount of pregnancy-related fluid, but as I started being able to eat normally again, something really weird happened.
I blew back up with fluid ... and it stayed.
Six weeks passed. Then eight. I kept being told by my doc some version of, “Just give it more time.” I didn't think time was the missing piece here. I was also getting stomach pain after eating certain foods, so I started paying attention and eventually decided to experiment with removing foods one at a time. Gluten went first. Within roughly 48 hours, I dropped many pounds of water. It was dramatic enough that I was basically standing there looking at my own body like…what the ACTUAL heck??
I stayed gluten-free for a couple of weeks, felt substantially better and then intentionally tried it again because one data point does not make a very good experiment.
The stomach pain came roaring back. Then I started noticing another very specific reaction ... painful, intensely itchy bumps on my skin whenever I ate gluten. Just like 1-3 of them in random spots each time.
At that point, the pattern became difficult to argue with. I haven’t intentionally eaten gluten since. And more than a decade later, I can still tell when I’ve accidentally been glutened. Even tiny amounts of cross-contamination can give me one very particular stomach ache. It’s not my normal stomach being weird. It’s THE stomach ache. If the exposure is tiny, thankfully it usually passes within a couple of hours.
Now, an important caveat to my story ... I figured this out myself and removed gluten before being properly evaluated for celiac disease. I did that on purpose knowing I was so affected by it that eating it daily for 6 weeks was NOT a good idea for me. I chose health + comfort over more defined answers and I don't regret it.
For the record, “I mostly don’t eat gluten” doesn't really help or tell us anything, If you’re eating gluten here and there throughout the experiment, you haven’t really removed the variable. If we’re trying to answer the question does my body behave differently without gluten?, we need an actual period without any gluten.
That doesn’t automatically mean you can never eat it again. The next step depends heavily on why you’re doing the experiment. Celiac disease is different. If you have celiac, strict lifelong gluten avoidance is the treatment, and cross-contamination matters even more.
If we’re investigating possible non-celiac sensitivity, we’re gathering information. Ideally we eventually want to know what happens with a controlled reintroduction too, because feeling better after removing something is useful information, but symptoms returning when you reintroduce it gives us stronger data.
This brings us all the way back to why I’ve never given you a dramatic blanket statement about gluten. I can’t tell the entire internet that everyone should eat it. I also can’t tell the entire internet that nobody should. My hunch, based on the research we have, the mechanisms being investigated and what I see clinically, is that there are probably more people who would feel or function better without gluten than currently realize it.
But that’s a hunch. Not a population-wide prescription. Research will hopefully get much better at telling us who those people are eventually.
Which people have an exaggerated intestinal barrier response to it? Which genetic or immune characteristics matter? Does baseline gut health change the response? Does the microbiome matter? Are there subgroups of people with autoimmune disease who benefit from removing it even without celiac disease? Are some cases we currently call “gluten sensitivity” actually reactions to another component of wheat? Can we eventually identify those people more easily?
Science does this all the time. We start with “something seems to be happening here,” figure out a mechanism, realize the mechanism is way more complicated than expected, identify subgroups, argue about it for 17+ years, and eventually get better at figuring out who actually benefits from what.
Very efficient system (eye roll).
So after this giant gluten dissertation, you may be thinking, “Okay Tara, BUT SHOULD I EAT GLUTEN?”
And my deeply unsatisfying answer is… it depends.
I would be much more interested in investigating it if you have persistent GI symptoms, unexplained nutrient deficiencies or signs of malabsorption, autoimmune disease, Hashimoto’s, a family history of celiac disease, unexplained skin reactions, or symptoms that repeatedly seem connected to wheat or gluten-containing foods.
I’d look at you. Your symptoms. Your labs. Your history. Your patterns. Your food. Your response. Your goals. Then I’d connect the dots.
Which, inconveniently for the algorithm, is usually how human health actually works.
Stay wild + well (with or without gluten),
Tara
P.S. The Metabolic Edge is closed for October, but I’ve already started the November waitlist. If you like this kind of digging, connecting dots and figuring out what actually makes sense for your body instead of collecting another list of generic health rules from the internet, you can join the November waitlist here.
