Nutrition Guide · Autoimmune protocol and paleo

Autoimmune protocol and paleo: what an elimination diet can do

What the studies on the autoimmune protocol actually measured, how to place the much quoted lectin numbers, and why the leaving out is not the interesting part.

SJ
Shukri Jarmoukli · Physician, Integrative Medicine · ViveCura Berlin
Immune system Elimination diets Reading the evidence 30 studies with DOI
Why I am writing this

When a diagnosis tells you that your immune system is turning against your own tissue, you want something you can do. That is exactly the gap elimination diets step into. I take the idea seriously. And you deserve to know how strong the evidence is before you cut out half of your food.

There is one sentence I hear in my consulting room almost every week. Usually only at the end of the conversation.

It goes: can I eat my way out of this?

What sits behind it is rarely naivety. What sits behind it is exhaustion. An autoimmune disease takes away the feeling that your body is on your side. Food is the one lever you get to pull yourself, every single day.

This is exactly where paleo and the autoimmune protocol come in, AIP for short. Both offer order, both deliver lists. And both have a serious core plus a story that reaches further than the data. I will show you both: what was measured, and where the story grows larger than it can carry.

What to expect here

  • Why paleo and AIP are two different tools
  • What the much quoted Gundry paper says, and what kind of document it is
  • The real AIP studies with their numbers, including the awkward ones
  • Why how you feel and your antibodies can move separately
  • Barrier, molecular mimicry and the brake on the immune system
  • Lectins: what holds raw, what holds cooked, what is overstated
  • What a strict elimination costs in nutrients and in daily life
  • The one piece of large randomised evidence in this field
  • Twelve questions I am asked about this most often
green randomised in humans teal human observation orange animal model yellow cell culture or tissue

Can I eat my way out of this? The question behind the question

Many people with an autoimmune diagnosis know this moment. You read online at night, you find lists, you find people who feel better since they dropped tomatoes. That is not a stupid idea. It is an underspecified question.

Autoimmunity means the immune system loses tolerance towards its own tissue. That almost always needs three things: a genetic susceptibility, a trigger from outside, and a mucous membrane that lets it through. Food is the entrance you can steer, which is why it gets all the attention.

One finding has fascinated me for years. A systematic review analysed eleven studies of dietary interventions in inflammatory bowel disease, covering ten different concepts. What is interesting is what sits between them: almost all share the same building blocks. Elimination phase, reintroduction, unprocessed foods. Ten names, one pattern.

The better question

Not: which food is to blame. But: under which conditions does my immune system become irritable.

To that second question, gut barrier, microbiome, vitamin D status, omega 3 supply, sleep and stress answer at least as loudly as any ingredient list.

And that makes it clear why the answer does not sit in a list of banned foods. A list only answers the first question.

Paleo and AIP are not the same thing, and that matters

Maybe you have compared two eating plans and noticed that they contradict each other. One allows eggs, the other does not. Two different things are sharing one reputation here.

Paleo is a long term way of eating with no expiry date. It drops grains, legumes, dairy, refined sugar and heavily processed products. Its argument is evolutionary, its evidence base is metabolic.

Meta-analysis in humans[Meta-analysis, k=4, n=159]

A group around Manheimer analysed four randomised trials with 159 people in total, all of whom had at least one component of metabolic syndrome, each comparing paleo against guideline based control diets.

In the short term paleo came out more favourably: waist circumference minus 2.38 cm, triglycerides minus 0.40 mmol/L, systolic blood pressure minus 3.64 mmHg. Three of six confidence intervals did cross zero.

For you that means: paleo as a metabolic intervention is real and moderate. None of these four trials studied an autoimmune disease. So nobody recommending paleo for autoimmunity can lean on this meta-analysis.

Manheimer EW et al. Am J Clin Nutr. 2015. DOI: 10.3945/ajcn.115.113613

The autoimmune protocol is narrower, time limited, and in form it is not a meal plan but a procedure. On top of paleo it drops eggs, nuts, seeds, nightshades, coffee, alcohol and most additives. Some descriptions also mention painkillers. Anything touching medication belongs in medical hands, not on a diet list.

1

Elimination

Six to twelve weeks in the studies. Strict, but short. That is deliberate.

2

Observation

What changes in symptoms, sleep, energy. And what changes in the lab.

3

Reintroduction

One food at a time, over several days. This is where the information appears.

The concept goes back to the biophysicist Sarah Ballantyne and spread as a book, not as a research programme. That is not a put down, it is context: the idea moved from practice into research.

Reframe

AIP is not a way of eating. It is a time limited experiment with your immune system, with a start, an end and an evaluation.

Whoever eats AIP permanently has turned a measuring instrument into a lifestyle. The value does not sit in the leaving out. It sits in what bringing food back reveals about your threshold.

And now you understand why the question about duration is the most important question about this protocol.

The paper everyone talks about: what it says and what it is

If you research this topic, sooner or later you hit a number that outshines everything else. It is almost never quoted with its source. So let us look at the source.

102 consecutive people with documented autoimmune activity, in a single centre
95 of 102 with what the abstract calls complete regression of autoimmune and inflammatory markers within nine months
80 of 102 who according to the abstract stopped their immunosuppressive medication and biologics
Human observation, conference abstract[Case Series, n=102]

The cardiac surgeon Steven Gundry presented a case series in 2018 at the sessions of the American Heart Association. 102 people with seven conditions, among them rheumatoid arthritis, lupus, Sjögren and Crohn disease, were moved onto a lectin reduced diet, supported by probiotics and polyphenols.

The numbers above are what was reported. The work appeared as an abstract in a supplement of the journal Circulation. There was no control group, no blinding, a single centre and to this day no full text publication. The author is also the provider of the programme under study. That is not a judgement on his work, it belongs to the context.

For you that means: the observation deserves to be taken seriously, the study format does not carry the conclusion. As an aside: the number 82 that circulates online is not in the original. The original says 80.

Gundry SR. Circulation. 2018;137(Suppl 1):AP238. DOI: 10.1161/circ.137.suppl_1.p238
Please read this part very carefully

The fact that 80 people in an abstract stopped their medication is not an instruction. Changes to immunosuppressive therapy, to biologics or to any other long term medication belong in medical care only, with follow up checks.

Stopping on your own can be dangerous. A flare after abruptly ending immune therapy is a real risk. If this number impresses you, take it with you into your next medical appointment. Not into your medicine cabinet.

The evidence ladder

Not every study is a study. These five rungs explain why the same number weighs differently depending on where it came from.

Rung 1
Large randomised, blinded trial

Thousands of people, random allocation, nobody knows who gets what. Exactly one paper sits here: VITAL.

Rung 2
Smaller randomised trial with a control group

Random allocation, but few participants. Examples: the 1991 fasting trial in rheumatoid arthritis, the gluten free trial in Hashimoto.

Rung 3
Uncontrolled case series, peer reviewed

Everyone gets the same intervention, there is no comparison. All the real AIP studies sit here.

Rung 4
Conference abstract without a control group

A short version for a talk, without a methods section, without full text review. The Gundry paper sits here.

Rung 5
Cell culture and animal model

Explains how something might work, not whether it changes anything in you.

Reframe

An impressive observation and the weakest form of evidence do not exclude each other. Both sit in the same paper.

The honest reading: someone saw something here that would have deserved a controlled trial. That trial still does not exist. As long as it is missing, the number stays a hypothesis.

And now you know why I name this paper instead of leaving it out. You will meet it anyway, and then you should know what you are looking at.

The real AIP studies and their awkward details

They do exist, the proper studies on the autoimmune protocol. Together they cover fewer than a hundred people, and not one of them has a control group. No reason to ignore them. A reason to read them closely.

Human observation[Case Series, n=15]

A group at the Scripps Clinic followed 15 adults with active inflammatory bowel disease through six weeks of elimination and five weeks of maintenance.

11 of 15 reached clinical remission at week 6 and held it to the end. The partial Mayo score fell from 5.8 to 1.0, the Harvey Bradshaw index from 7 to 3.4. Faecal calprotectin fell from 471 to 112, without significance. CRP did not move.

For you that means: the strongest single study on AIP has no comparison group. What stays remarkable is the improvement on endoscopy, the hardest endpoint. More under inflammatory bowel disease seen integratively.

Konijeti GG et al. Inflamm Bowel Dis. 2017;23(11):2054-2060. DOI: 10.1097/MIB.0000000000001221 | PMID: 28858071

The same group analysed quality of life. The questionnaire score rose from 46.5 to 62.0, earlier than any measurable change in inflammatory markers. That is two things at once: a hint of benefit in daily life, and the classic place where expectation and attention do their work.

Human observation[Case Series, n=17]

A group around Abbott followed 17 women with Hashimoto through a ten week programme with staged elimination.

Symptom burden fell from 92 to 29, all eight quality of life scales improved significantly, hs-CRP fell by 29 percent. Then comes the sentence almost nobody quotes: TSH, free T4 and T3 stayed unchanged, and so did the thyroid antibodies.

For you that means: the women felt better, inflammatory markers fell slightly, the thyroid did not change. Background under Hashimoto and the immune system.

Abbott RD et al. Cureus. 2019;11(4):e4556. DOI: 10.7759/cureus.4556 | PMID: 31275780
Human observation[Case Series, n=28]

A Polish group around Ihnatowicz followed 28 people with Hashimoto through the protocol for twelve weeks.

Fewer people reported symptoms, thyroid volume decreased, anti-TG fell slightly. The TPO antibodies, by contrast, rose significantly. And body weight fell, which points to an unintended energy deficit.

For you that means: how you feel and your antibody titre can move separately, in both directions. An argument for keeping such a protocol time limited and for checking values.

Ihnatowicz P et al. Ann Agric Environ Med. 2023;30(3):513-521. DOI: 10.26444/aaem/166263 | PMID: 37772528

In rheumatoid arthritis there is a feasibility study in nine adults. Seven of nine improved, and at the same time BMI fell from 26.3 to 24.5. Weight loss on its own is already relevant to inflammation.

StudyWhoWhat improvedWhat did not improve
Konijeti 201715 with Crohn or colitis11 of 15 in remission, calprotectin 471 to 112, endoscopyCRP unchanged
Abbott 201917 women with HashimotoSymptom burden 92 to 29, hs-CRP minus 29 percentThyroid values and antibodies unchanged
Ihnatowicz 202328 with HashimotoSymptoms, thyroid volume, anti-TGanti-TPO rose significantly
McNeill 20269 with rheumatoid arthritisRAPID3 2.73 to 0.99, sleep, painno comparison with a control group possible

And there is a contradiction I do not want to smooth over. A 2026 review analysed fifteen studies using a validated quality of life instrument. For several low FODMAP studies it found significant improvements, for the autoimmune protocol it found none. Not a scandal, just ordinary science.

Reframe

How you feel and your lab value are two different targets. A protocol can hit one and miss the other.

If your goal is quality of life, there are signals for that. If your goal is falling antibodies, there is no solid basis for that. Both goals are legitimate, they simply need different expectations.

And now you understand why my first question is what you would notice if things were getting better.

What might be happening in the body: barrier, mimicry, brake

Why should leaving things out change anything? The answer has four building blocks. None is proven, all four are well described.

First: the barrier

Your gut lining is not a wall. It is a row of cells with junctions between them that can open and close like doors along a corridor. Zonulin is so far the only known switch for that, and gliadin from wheat can trigger its release. In biopsies from four groups, permeability rose in all of them, most strongly in active coeliac disease. The difference lay in the degree, not in whether it happened. Details under leaky gut, intestinal permeability and zonulin.

Cell culture and tissue[In vitro]

A group around Drago exposed human small bowel biopsies and intestinal cells to gliadin and measured zonulin release, permeability and the junction proteins occludin and ZO-1.

What followed was a remodelling of the cell skeleton and increased permeability. In coeliac tissue the release continued, otherwise it was brief and limited. A zonulin blocker prevented the opening in this experimental setup.

For you that means: cell culture plus tissue, no clinical outcome. It does explain why people react so differently to grains.

Drago S et al. Scand J Gastroenterol. 2006;41(4):408-419. DOI: 10.1080/00365520500235334 | PMID: 16635908

There is more to wheat than gluten. Amylase trypsin inhibitors can bind to the TLR4 complex on immune cells in cell experiments and in the mouse model, setting off an innate inflammatory response, in tissue from people with and without coeliac disease. Mechanistically convincing, not yet tested in humans as a treatment approach. More under gluten and gliadin without coeliac disease.

Second: the mix up

Molecular mimicry is one of the most elegant explanations in this field. A foreign protein looks similar enough to one of your own, the immune system attacks it and hits your own tissue along the way.

The major review on this names its own limits: long latency between trigger and disease, too little statistical power, poor transferability from inbred mice. A second paper adds that structural similarity alone often does not explain the activation. Mimicry is recognised as a mechanism and in the individual case it is almost never provable. The story that a food looks like your thyroid is tidier than immunology itself.

Third: the players in your gut

In newly diagnosed rheumatoid arthritis, a sequencing study of 114 stool samples found a strong enrichment of Prevotella copri. In mice the same organism increased susceptibility to gut inflammation. Correlation plus animal model, no proof of causation.

An underrated observation fits here: depending on the bacterial mix, the same wheat protein can be broken into fragments of differing immune reactivity. The same food can generate two different signals in two people. That is the KPNI lens in one sentence.

Fourth: the brake

Your immune system does not only have an accelerator. Regulatory T cells are the brake, and they are partly built in the gut.

Animal model[In vivo, mouse]

Two groups, around Arpaia and around Furusawa, independently tested whether metabolic products of gut bacteria shift the immune balance.

Butyrate from fibre fermentation promoted the formation of regulatory T cells in mice and improved the course of an experimental colitis. Propionate showed a similar effect, acetate did not.

For you that means: mouse, not human. Still the reason why fibre belongs in every autoimmune conversation, and an objection to very low fibre elimination patterns. More depth under butyrate and the gut lining.

Arpaia N et al. Nature. 2013;504:451-455. DOI: 10.1038/nature12726 | Furusawa Y et al. Nature. 2013;504:446-450. DOI: 10.1038/nature12721

And there is the opposite direction. Sodium chloride increased the formation of inflammatory Th17 cells in cell experiments with mouse and human cells. Salt is on no AIP list. It is in almost every convenience product.

Reframe

An elimination diet never only takes away. It also adds: more vegetables, more fibre, more omega 3, less ultra processed food, less salt, fewer emulsifiers.

Which share of an effect belongs to which ingredient cannot be derived from these studies. The effect is probably a bundle, not a single substance.

And now you know why the mechanism level sounds convincing and still delivers no outcomes. It explains possibilities, not courses of illness.

Lectins: a fact check without picking a side

Few nutrition topics are this fragmented. On one side, tables listing four hundred foods. On the other, a blanket all clear. Both sides usually work without a primary source.

Lectins are proteins that bind to sugar structures. Plants use them for defence. They occur in beans, lentils, grains and nightshades, in very different amounts.

Systematic appraisal[Systematic Review]

A group around He systematically worked through the data on the lectins of the common bean: antinutritive and toxic properties, favourable effects, the role of processing.

Raw, these lectins really are problematic, as haemagglutinins and as allergens. What decides the matter is processing: soaking, boiling, pressure cooking and fermenting largely inactivate the activity.

For you that means: raw beans are a genuine problem. Cooked beans are a staple food of the longest lived populations. Declaring lectins harmful across the board skips this difference.

He S et al. Crit Rev Food Sci Nutr. 2018;58(1):70-83. DOI: 10.1080/10408398.2015.1096234 | PMID: 26479307

And still, one lectin belongs in the discussion for good reason. Wheat germ agglutinin appears on the candidate list in a review of non coeliac wheat sensitivity, alongside fructans and the amylase trypsin inhibitors. The lectin story simply claims more than these sources can support.

One distinction pays off in daily life. If your symptoms sit mostly in your belly, meaning bloating, cramps, changes in stool, the theme is often not the immune system but fermentation in the small intestine. There is a different and better studied tool for that: how to use a FODMAP diet properly.

Reframe

Raw yes, cooked largely no. That is the lectin fact check in five words.

The cost side: blanket lectin avoidance drops legumes, wholegrains and a lot of vegetables. Which is exactly the fibre your gut bacteria use to build butyrate. The raw material for the brake.

And now you know why I get sceptical about lectin lists. They take away something whose benefit is documented, against a harm whose size is not.

What a strict elimination costs

The price of these protocols is rarely written about. Yet it is measurable.

Dietary analysis within a randomised trial[RCT, dietary analysis]

A group around Titcomb analysed weighed food records from people with multiple sclerosis who were following comparably strict elimination patterns.

After twelve weeks the share with inadequate intake fell for magnesium and for vitamins A, C, D and E. At the same time the share with inadequate intake rose for calcium, thiamine and B vitamins.

For you that means: a strict elimination closes gaps and opens new ones. If you drop grains and legumes you lose B vitamins. If you drop dairy you lose calcium. Not an argument against the experiment, but an argument for supervision and an expiry date.

Titcomb TJ et al. Nutrients. 2021;13(10):3507. DOI: 10.3390/nu13103507 | PMID: 34684508

Then there is an effect almost nobody plans for. In the Polish Hashimoto study body weight fell without weight loss being the goal. If you drop thirty food groups you almost inevitably eat less, and an unintended energy deficit can affect thyroid, cycle and exhaustion. More under the calorie myth: quality over quantity.

And then the part missing from almost every guide. The same nine people with rheumatoid arthritis were interviewed a year later. The phase they described as hardest was not the elimination. It was the reintroduction.

The hardest part is not the leaving out. It is the structured bringing back. And that is exactly the part that gets skipped almost everywhere.

There is another price. Eating is social. A protocol that excludes you from every invitation costs you something that shows up in no lab value. And in some people caution tips over into a tense relationship with food, see understanding eating disorders.

How to tell that a food experiment is going off the rails

  • The list gets longer week by week instead of shorter
  • There is no date on which anything gets evaluated
  • You avoid invitations because eating has become too complicated
  • Weight, cycle or exhaustion move in an unwanted direction
  • You feel guilty rather than curious when you eat something
  • Not a single blood value has ever been checked
Reframe

An experiment without an end date is not an experiment. It is a restriction that justifies itself.

The sensible frame: a clear window, endpoints agreed in advance, medical supervision, and a reintroduction that actually happens. Then you end up with information about yourself, and not just a longer list of banned foods.

And now you know why on this topic I talk more about the exit than about the entry.

What I look at first, before anything gets cut

You now know the weaknesses of elimination. Now the other side. So far this field holds only one large, randomised, blinded trial. It is not about leaving things out. It is about equipment.

25,871 participants in the VITAL trial, randomised and double blinded over 5.3 years
22 % fewer newly occurring autoimmune diseases on 2000 IU of vitamin D daily
HR 0.83 for omega 3 two years after the trial ended, while the vitamin D effect had faded
Large randomised trial[RCT, n=25,871]

A group around Hahn and Costenbader randomised 25,871 people: 2000 IU of vitamin D daily or placebo, 1000 mg of marine omega 3 fatty acids or placebo. Every new diagnosis was confirmed from records.

In the vitamin D arm 123 cases occurred versus 155 on placebo, hazard ratio 0.78. In the omega 3 arm 130 versus 148, not significant. Two years after the trial ended the vitamin D effect had faded, the omega 3 effect held.

For you that means two things. Vitamin D may only change something for as long as it is given. And whoever quotes only the 22 percent is telling half the story. This is about new onset, not about treatment.

Hahn J et al. BMJ. 2022;376:e066452. DOI: 10.1136/bmj-2021-066452 | Costenbader KH et al. Arthritis Rheumatol. 2024;76(6):973-983. DOI: 10.1002/art.42811

How well supplied you are with omega 3 can be measured, see measuring your omega 3 index. Why plant and marine sources do not do the same job is covered under omega 3 from plants and animals.

Then there is a second list of things to drop, better documented than any lectin table.

Randomised, double blind feeding study[RCT, n=16]

A group around Chassaing had 16 healthy adults eat under controlled conditions for eleven days: either emulsifier free, or the same food with 15 g of carboxymethylcellulose daily.

In the emulsifier group abdominal discomfort rose slightly, microbiome diversity decreased, and short chain fatty acids in stool fell. In two people bacteria advanced into the normally sterile inner mucus layer.

For you that means: a circle closes here. An industrial additive lowered exactly the quantity that feeds the immune brake in the animal model. Eleven days and 16 people remain a directional signal. More under eating unprocessed and satiety.

Chassaing B et al. Gastroenterology. 2022;162(3):743-756. DOI: 10.1053/j.gastro.2021.11.006 | PMID: 34774538

Two older papers round out the picture. In 1991 the Lancet published the only randomised elimination trial with a control group and a full year of follow up that I know of: 53 people with rheumatoid arthritis, one group with a fasting phase and then a gluten free, initially vegan diet. Joint findings, morning stiffness and CRP improved, and the advantage held across the year. That diet was plant based, so almost the opposite of a meat heavy paleo approach.

And a pooled secondary analysis of two pilot studies on paleo in multiple sclerosis shows the pattern this field has to be measured against: within the paleo group functional scores improved, compared with the control group the difference stayed without significance. Better than before and better than the control group are two different statements.

What I would take away

The most stable evidence in autoimmunity concerns not what you leave out, but what your immune system is equipped with: vitamin D status, omega 3 supply, fibre for the brake, little ultra processed food, sleep and stress load. An elimination can build on that. It cannot replace it.

What I observe in my consulting room goes beyond the study data, and I name it as an observation: people who run a food experiment with a clear start, a clear end and medical supervision come out knowing more about themselves. That is not documented evidence. If you would like to start with support, you will find the option to book an appointment below this article.

And with that you know why my first question is never what you should cut. It is what your immune system is currently getting in equipment and in rest.

Twelve questions I am asked about this most often

What is the autoimmune protocol (AIP) and how does it differ from paleo?

Paleo is a long term way of eating with no expiry date, and it drops grains, legumes, dairy and heavily processed products. The autoimmune protocol is narrower and time limited. It additionally drops eggs, nuts, seeds, nightshades, coffee, alcohol and most additives, and it runs in three phases: elimination, observation and structured reintroduction. The point is not permanent avoidance. The point is the information that comes out of the reintroduction.

How long should you stay on the autoimmune protocol?

In the existing studies the strict phase lasted six to twelve weeks, followed by reintroduction. Konijeti 2017 used six weeks, Abbott 2019 used ten, Ihnatowicz 2023 used twelve. None of these papers supports a permanent diet. If nothing has moved after that window, that is a result too, and it argues for ending the experiment rather than extending it.

Are there real studies on the autoimmune protocol, or only anecdotes?

There are real studies. They are simply small and without a control group. Taken together, the AIP intervention studies cover fewer than 100 people: 15 with inflammatory bowel disease, 17 and 28 with Hashimoto, 9 with rheumatoid arthritis. Two independent reviews reach the same conclusion: the approach is plausible and has not yet been tested under controlled conditions.

Is it true that in one study 80 of 102 patients came off their medication?

That figure comes from a conference abstract by Steven Gundry, presented in 2018 at the AHA sessions and printed in a supplement of the journal Circulation. The original reports 102 people, in 95 the markers receded within nine months, and 80 stopped their immunosuppressive medication according to the abstract. The number 82 that circulates online is not in the original. There was no control group, no blinding and no full text publication. Any change to long term medication belongs in medical care only, and stopping on your own can be dangerous.

Are lectins really harmful, and do I have to drop beans and lentils?

Raw beans are a genuine problem, that part is not disputed. A systematic review of common bean lectins describes them in the raw state as antinutritive and toxic. What decides the matter is processing: soaking, boiling, pressure cooking and fermenting largely inactivate the activity. At the same time legumes are staple foods of the longest lived populations. Blanket lectin avoidance takes more away from you than it can give back on current data.

Do I have to avoid nightshades if I have an autoimmune disease?

I know of no study showing that tomato, pepper, aubergine or potato are generally unfavourable in autoimmune disease. They sit on the AIP list because they contain alkaloids and lectins, not because the case has been made. More useful than a blanket ban is the test: a limited time without them, then deliberately back in, and watch your own reaction.

Does the autoimmune protocol lower thyroid antibodies in Hashimoto?

On current data, not reliably. In Abbott 2019 quality of life and hs-CRP improved clearly, while thyroid values and antibodies stayed unchanged. In Ihnatowicz 2023 the TPO antibodies even rose after twelve weeks, while how the participants felt improved. How you feel and your antibody titre are two different targets. If you start an elimination, have the values checked over time.

Does a gluten free diet help in Hashimoto if I do not have coeliac disease?

The data are split. A pilot study in 34 women found falling antibody titres after six months, although all participants had incidentally discovered transglutaminase antibodies. A randomised study in 62 women found no difference in anti-TPO or anti-TG over twelve months, only TSH fell. Read together that suggests it probably depends on who drops gluten, not on whether gluten is dropped.

How do I reintroduce foods after the elimination phase?

The logic matters more than any ready made order. One food at a time, in calm weeks without infection and without unusual stress, each over several days and with a simple log of symptoms, sleep and digestion. Only then can a reaction be attributed. In the one qualitative one year study, this exact phase was described as the hardest part.

Which nutrient gaps come with such a strict elimination diet?

In an analysis of weighed food records under comparably strict elimination patterns, intake improved for magnesium and for vitamins A, C, D and E. At the same time the share with inadequate intake rose for calcium, thiamine and B vitamins. If you drop grains and legumes you typically lose B vitamins, if you drop dairy you lose calcium. In the bowel disease study vitamin D and iron also had to be topped up.

Can a blood zonulin test tell me whether my gut is leaky?

I would advise against it. Two independent groups examined the widely used commercial zonulin assays and found that they do not capture zonulin itself. The candidates actually being measured were properdin, haptoglobin and complement C3. The barrier model remains plausible. The blood measurement does not currently carry the interpretation.

What is the best supported dietary measure in autoimmune disease?

The only large randomised evidence comes from the VITAL trial with 25,871 people. On 2000 IU of vitamin D daily, 22 percent fewer new autoimmune diseases occurred over 5.3 years. The omega 3 arm was not significant in the main analysis, yet it held up better two years after the trial ended than the vitamin D effect did. One limit matters: this is about new onset, not about treatment.

Where this topic leads next

Autoimmunity is rarely an isolated event. Inflammatory load, gut lining, mitochondria and hormonal axes hang together.

SJ

Shukri Jarmoukli

Physician, Integrative Medicine · ViveCura Berlin

I work in my private practice at the intersection of conventional medicine, functional medicine and Clinical Psychoneuroimmunology. In autoimmune disease I am less interested in which list is popular, and more in the conditions under which an immune system becomes irritable.

Rheumatology, gastroenterology and endocrinology do essential work here, and immunosuppressive therapy belongs in their hands. What an integrative view can add are barrier, microbiome, nutrient status and lifestyle as the setting around that treatment.

This article does not replace medical advice. It is meant to give you better questions before you change anything.

ViveCura, Privatpraxis Shukri Jarmoukli, Skalitzer Straße 137, 10999 Berlin

Scientific sources

  1. Gundry SR. Abstract P238: Remission/Cure of Autoimmune Diseases by a Lectin Limite Diet Supplemented With Probiotics, Prebiotics, and Polyphenols. Circulation. 2018;137(Suppl 1):AP238. DOI: 10.1161/circ.137.suppl_1.p238 [Case Series, n=102, conference abstract without control group]
  2. Konijeti GG, Kim N, Lewis JD et al. Efficacy of the Autoimmune Protocol Diet for Inflammatory Bowel Disease. Inflamm Bowel Dis. 2017;23(11):2054-2060. DOI: 10.1097/MIB.0000000000001221 PMID: 28858071 [Case Series, n=15]
  3. Chandrasekaran A, Groven S, Lewis JD et al. An Autoimmune Protocol Diet Improves Patient-Reported Quality of Life in Inflammatory Bowel Disease. Crohns Colitis 360. 2019;1(3):otz019. DOI: 10.1093/crocol/otz019 PMID: 31832627 [Case Series, n=15]
  4. Chandrasekaran A, Molparia B, Akhtar E et al. The Autoimmune Protocol Diet Modifies Intestinal RNA Expression in Inflammatory Bowel Disease. Crohns Colitis 360. 2019;1(3):otz016. DOI: 10.1093/crocol/otz016 PMID: 32309803 [Mechanism Review, gene expression in the same cohort]
  5. Abbott RD, Sadowski A, Alt AG. Efficacy of the Autoimmune Protocol Diet as Part of a Multi-disciplinary, Supported Lifestyle Intervention for Hashimoto's Thyroiditis. Cureus. 2019;11(4):e4556. DOI: 10.7759/cureus.4556 PMID: 31275780 [Case Series, n=17]
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Transparency on the evidence The only large randomised and blinded trial in this article is VITAL, and it concerns the new onset of autoimmune disease, not its treatment. All studies on the autoimmune protocol are small, open case series without a control group, together covering fewer than a hundred people, and their results contradict each other on the lab values. The Gundry paper is a conference abstract without a control group, without full text publication, and with a conflict of interest, since the author is also the provider of the programme. The mechanism level, meaning zonulin, amylase trypsin inhibitors, molecular mimicry, butyrate and salt, comes mostly from cell culture and animal models and explains possibilities, not courses of illness. The nutrient data come from a study on comparably strict elimination patterns, not on the autoimmune protocol in the narrow sense. I advise against a blood zonulin test, because two independent groups have shown that the widely used assays capture something else. Everything I describe from my consulting room is marked as observation and not as proof. And everything touching medication belongs in a medical decision, not in a blog article.

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