Autoimmune diseases and the gut: Hashimoto's, vitiligo, type 1 diabetes and more

Healthy state

The immune system has to do two things at once: attack what is foreign and leave the body's own tissue alone. There are two safeguards for this. While immune cells mature, those that react strongly to the body's own substances are sorted out. A few always slip through, and a second safeguard keeps them in check: regulatory T cells, Tregs for short, which act as a brake. This balance is called tolerance.

In an autoimmune disease Autoimmune disease A disease in which the immune system attacks the body's own tissue, for example the thyroid in Hashimoto's or the pigment cells in vitiligo. , tolerance breaks down at one point. In Hashimoto's the immune system attacks the thyroid, in autoimmune gastritis the acid-producing cells of the stomach, in type 1 diabetes the insulin-producing cells of the pancreas, in vitiligo the pigment cells of the skin, in rheumatoid arthritis the lining of the joints and in multiple sclerosis the sheaths of the nerve fibres. Taken together, autoimmune diseases are common: in an analysis of 22 million people in the UK, about one in ten had one, and almost two thirds of new cases were women. And they cluster: anyone who has one is more likely to develop a second.

The gut is not a sideshow here. Nowhere else does the immune system meet so much that is foreign: food and trillions of bacteria. A large share of immune cells therefore sits in the gut wall, and this is where they learn what is harmless (see the chapter “Immune system and inflammation”). Certain bacteria help, for example by fermenting fibre into butyrate Butyrate A short-chain fatty acid and the main energy source for the cells of the colon wall. It strengthens the barrier and dampens inflammation. More in the chapter “Butyrate and other short-chain fatty acids”, which promotes the formation of Tregs. Others tend to attract inflammation-prone immune cells. An intact mucus layer Mucus layer A gel layer of mucins on the gut wall that keeps bacteria at a distance. In the colon, the inner layer is almost free of microbes. More in the chapter “The mucus layer and additives”, IgA IgA (secretory IgA) The antibody of the mucous membranes. It is released into the gut in large amounts, where it holds germs in the mucus without causing inflammation. More in the chapter “IgA: the antibody that keeps the gut clean, and what vitamin A, D and omega-3 have to do with it” and a tight gut wall keep the bacteria at a distance.

Autoimmune diseases usually arise from two ingredients: an inherited tendency, often through certain tissue types (HLA), and triggers from the environment. For coeliac disease Coeliac disease An autoimmune disease in which gluten damages the lining of the small intestine. It is diagnosed with a blood test and usually a biopsy while you are still eating gluten. More in the chapter “Lactose, fructose, gluten: making sense of intolerances” the trigger is known: gluten. For most others it is unknown. Infections, smoking, hormones and the gut microbiome Microbiome, gut microbiota The community of all microbes in the gut, mainly bacteria, plus viruses, fungi and archaea. Most live in the colon. More in the chapter “Building microbial diversity” are being studied as players.

There are three kinds of links between the gut and autoimmune diseases, and they are worth keeping apart. First, a shared root: the same genes make people susceptible to several diseases, which is why coeliac disease is more common with Hashimoto's and type 1 diabetes. Second, the autoimmune disease itself hits digestion, for example when the stomach no longer makes acid or an underactive thyroid slows the gut. Third, the gut microbiome might help set the disease off. The first two are well established; the third is the most exciting but least certain.

Disrupted state: causes and effects

For almost every autoimmune disease, researchers have found an altered gut microbiome. The problem: most studies are snapshots. Medication, a changed diet and the inflammation itself also change the microbiome, so cause and effect are hard to separate. The largest study on multiple sclerosis so far therefore compared 576 patients with housemates without MS who share the same kitchen. People with MS had, among other things, less Faecalibacterium and more Akkermansia Akkermansia A gut bacterium that lives on the mucus of the gut wall and stimulates its renewal. In studies, high levels often go along with good metabolic health. More in the chapter “The mucus layer and additives”, a bacterium otherwise considered “good”. This shows that there is no simple list of good and bad bacteria.

Animal studies show more than an association. Researchers transferred stool from identical twins, only one of whom had MS, into mice with an inherited tendency to brain inflammation. With the stool of the twin with MS, the mice fell ill more often. How bacteria might mislead the immune system has been shown along several routes. In molecular mimicry Molecular mimicry A bacterium or virus carries a protein that resembles one of the body's own. Immune cells fighting the germ can then accidentally attack the body's own tissue as well. , bacteria carry proteins that resemble the body's own. Some skin, mouth and gut bacteria make a counterpart of Ro60, a protein targeted by antibodies in lupus, and immune cells from people with lupus reacted to these bacteria. Another route is escape: in mice, the gut bacterium Enterococcus gallinarum crossed a leaky gut wall, reached the liver and drove autoimmunity there. Its DNA was also found in liver samples from people with autoimmune diseases.

Hashimoto's is the most common autoimmune disease of the thyroid. A meta-analysis Meta-analysis An analysis that combines the results of several studies. It is only as good as the studies it includes. of 8 small studies found fewer bifidobacteria and lactobacilli and more Bacteroides fragilis in autoimmune thyroid disease. The results are inconsistent and say nothing about cause. Two other links, however, are established. Coeliac disease is more common: in a meta-analysis of more than 6,000 people with autoimmune thyroid disease, about one in 62 had coeliac disease confirmed by biopsy, and in children it was just over 6 percent. And an underactive thyroid slows the gut: constipation is common, and in an Italian study of 50 people with hypothyroidism after Hashimoto's, small intestinal bacterial overgrowth Small intestinal bacterial overgrowth (SIBO) Too many bacteria in the small intestine, where normally few live. Bloating and diarrhoea are typical; it is usually diagnosed with a breath test. More in the chapter “When the small intestine is too densely colonised” was more common than in healthy people. After treatment with an antibiotic, bloating improved, while thyroid levels stayed the same.

Anyone taking thyroid hormone as a tablet depends on the gut. The hormone is absorbed in the small intestine, and the tablet dissolves well only with enough stomach acid. Untreated coeliac disease, autoimmune or Helicobacter gastritis, lactose intolerance, acid blockers and coffee shortly after taking the tablet all lower absorption. In studies, people with gastritis needed roughly a quarter to a third more hormone. If the required dose rises for no obvious reason, it is therefore worth looking at the gut.

Autoimmune gastritis is a silent disease that is often overlooked for years. The immune system destroys the parietal cells of the stomach lining. They make stomach acid and intrinsic factor, which the body needs to absorb vitamin B12. Without acid, iron is also absorbed less well, and iron deficiency often shows up years before B12 deficiency. Less acid also means that more germs reach the small intestine alive (see the chapter “Stomach acid, bile and enzymes”). The disease clusters with others. In one study, 36 percent of those affected also had autoimmune thyroid disease, and in type 1 diabetes it is about five times as common as in others. Because the risk of certain stomach tumours rises, specialist societies recommend regular gastroscopies after diagnosis, roughly every three to five years.

In type 1 diabetes, other autoimmune diseases are so common that specialists look for them specifically. A meta-analysis of 180 studies with almost 300,000 people found coeliac disease in 4.5 percent and an underactive thyroid in almost 10 percent. On the role of the gut microbiome there is one of the most careful studies ever done: TEDDY examined more than 10,000 stool samples from 783 children, monthly from the third month of life. Children who stayed healthy had more bacterial genes for fermenting fibre into short-chain fatty acids Short-chain fatty acids Acids such as acetate, propionate and butyrate that gut bacteria make from fibre. They nourish the gut wall and act throughout the body. More in the chapter “Butyrate and other short-chain fatty acids”. No single bacterial species emerged as a trigger. Blood sugar that is poorly controlled for years can also damage the nerves of the stomach (see the chapter “Gastroparesis Gastroparesis Delayed gastric emptying without a mechanical obstruction, with nausea, vomiting, early satiety and fullness. More in the chapter “Gastroparesis: when the stomach empties too slowly””).

In vitiligo, the skin loses its pigment in patches because immune cells attack the pigment cells. Thyroid diseases, especially an underactive thyroid, are clearly more common. On the gut microbiome there are only a few small studies, usually with 20 to 30 patients. A systematic review from 2025 found only 6 studies, and they contradict each other: sometimes gut diversity was lower, sometimes higher. In mice prone to vitiligo, the antibiotic ampicillin shifted the gut microbiome and increased pigment loss, while another antibiotic did not. Whether this applies to humans is open.

Rheumatic diseases show some of the clearest traces. In people with new-onset, still untreated rheumatoid arthritis, researchers strikingly often found a lot of Prevotella copri in the gut. In ankylosing spondylitis and related forms (spondyloarthritis), colonoscopies showed inflammation of the gut lining in almost half, visible only under the microscope. Conversely, joint inflammation is common in Crohn's disease and ulcerative colitis. Gut and joints apparently share part of the inflammation here.

In lupus, a small study that followed 16 women over several years found that several had a sudden bloom of Ruminococcus gnavus in the gut before and during a flare, especially with kidney involvement. In alopecia areata (patchy hair loss) there are case reports: two people who received a faecal transplant for a gut infection grew hair again afterwards. These are single cases; studies are under way.

A widespread misconception: that a “leaky gut” is the common cause of all autoimmune diseases and can be sealed with a cure. A more permeable gut wall is well documented in coeliac disease and inflammatory bowel disease Inflammatory bowel disease Umbrella term for Crohn’s disease and ulcerative colitis: long-term, relapsing inflammation of the gut that needs medical treatment. More in the chapter “Immune system and inflammation”, and in lupus mice too. As a general trigger in humans it has not been shown, and tests such as zonulin in stool are unreliable (see the chapter “The gut barrier”). To be honest: curing an autoimmune disease through the gut microbiome has not yet succeeded for any disease.