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Why Do Autoimmune Conditions "Collect?" - Part 2

In Part 1, we established that yes, autoimmune diseases can act like magnets for others. One community member said her doctor refers to this as the “autoimmune cascade,” which I think is a pretty good way to describe it! We explored the scientific terms that have been assigned to this phenomenon, namely: polyautoimmunity, multiple autoimmune syndrome (MAS), and familial autoimmunity. Now I want to discuss the “why?”


You may have heard that most autoimmune diseases likely have an underlying genetic component. Psoriasis and psoriatic arthritis are no different. Scientists have pinpointed about 60 different gene regions that probably contribute.1

Genes that determine self

Every human has HLA genes, and HLA genes make HLA proteins. These proteins coat the surface of every cell in your body, and their role is to signal to the immune system that this is “self,” and not to attack. Those of us with psoriasis and psoriatic arthritis are more likely to share the same set of HLA proteins, and it’s possible they aren’t doing this job perfectly.1 Therefore, we may be more likely to have an immune system that is confused about what to attack and what not to attack.

Genes that build our skin

On top of that, people with psoriasis are more likely to share genes that make our skin do weird things. For example, we’re more likely to have a mutation that causes our skin cells to over-activate the inflammatory response. We’re also more likely to have mutations that disrupt the normal skin cell turnover process and activate other arms of the immune system.1 So now we’ve got genes that are creating an environment of hyper-inflammation and immune hyperactivity. Scientists know that an immune system in chaos is likely to attack things it shouldn’t, which may explain why one autoimmune condition can set off others.


Genetics are important, but the increased incidence of autoimmunity all over the world can’t only be explained by genetics. The genes set the stage, but even in identical twins who share all the same genes, one may have psoriatic arthritis and one may not. So what role does the environment play? It could be anything from stress, to viruses, hormones, diet, drugs, or chemicals. I want to explore the role of infections and diet in particular.

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Molecular Mimicry

Your immune system has two different responses: innate and adaptive. Innate immune responses are indiscriminate. Inflammation is an innate immune response. Adaptive immune responses are targeted. If you get strep throat as a child, your immune system will generate all sorts of immune cells that are specifically targeted to strep throat, and those immune cells will stay with you all your life. When these immune cells see strep throat again they will attack it, and this ramps up both innate immunity and adaptive immunity. Here’s the problem, if strep throat proteins look a little too much like your own proteins, those adaptive immune cells might attack your proteins by accident. This is molecular mimicry, and infections are the top culprit. You can find a list of human protein – microbe protein crossovers with their respective autoimmune conditions here (2). Currently, scientists think that infections with different bacteria and viruses “prime” the immune system for autoimmunity, and once the immune system starts attacking “self” proteins, it’s like a runaway train.

Epitope spreading

One type of molecular mimicry is epitope spreading, and this may contribute to that runaway train. When your immune system attacks foreign invaders like viruses, it doesn’t just kill the virus, there’s a lot of host collateral damage (e.g., a lot of your own cells and tissues are damaged in the process). Damaged cells and tissues are cleared by the immune system. With chronic inflammation, your immune system spends all day cleaning up self-proteins from damaged cells. Epitope spreading is the process by which normal immune cells can become inappropriately sensitized to self-proteins over time, even if the initial foreign invader didn’t look anything like your own proteins.3 These abnormal immune cells are called “autoreactive,” meaning they react to “self.” This is just one way that chronic inflammation and chronic immune activation sets the stage for further dysregulation and therefore polyautoimmunity.

The role of the diet

I’ve talked about the “foreign invaders” of viruses and bacteria, but molecular mimicry can also apply to food.4 If you’ve read my article about leaky gut on our sister site, you know that research has shown the typical Western diet can influence gut health. Diets rich in foods like sugar, wheat, and dairy can increase hyperpermeability in the intestine. This hyperpermeability allows food proteins and endotoxins from your gut bacteria to move out of your intestine, where they create inflammation and are cleaned up by your immune system. Through the same process of molecular mimicry described above, it’s possible for your immune system to start recognizing food proteins as foreign and mounting immune responses to them in a process called food autoimmune reactivity (the best described example being celiac disease). And again, once your immune system starts inappropriately attacking one thing, this ramps up chronic inflammation which sets the stage for more trouble. Discovering which foods you’ve become reactive to is the strategy of elimination diets and the mechanism behind food intolerance testing.

Final thoughts

To summarize, our genetics may predispose us to certain autoimmune diseases and increased inflammatory responses. Infections or other environmental triggers can be the catalyst that sets off the initial autoimmune condition. Autoimmunity creates chronic immune activation and chronic inflammation, which increases the chance of our immune system becoming inappropriately sensitized to other self-targets. Other environmental stressors, like highly processed diets, can also cause inappropriate immune responses and chronic inflammation, which further feed into the cycle: susceptibility – trigger – chronic inflammation/activation – susceptibility – trigger, etc.

This just scratches the surface of the current research, and scientists are still trying to piece together the puzzle of autoimmunity and polyautoimmunity. We didn’t touch on epigenetics, which is the study of how genes are turned on and off (and straddles the divide of genetics and environment), or the specific examples science has uncovered (e.g., strep proteins look like skin proteins, and having mono as a teen increases your risk for polyautoimmunity). Before we close though, let’s take a quick second to review what we can do about it. We can’t change our underlying genetics (yet), but we can control some of our environment. We can do our best to keep our immune system healthy by eating a diet rich in fruits and vegetables, quitting smoking, and reducing stress. We may also try to reduce inflammation by taking turmeric, or supporting a healthy gut microflora by consuming probiotic foods and getting lots of fiber. Just like our immune system is designed to kill cancer before it spreads, it’s also designed to destroy autoreactive and abnormal immune cells before they attack our own cells. By keeping our immune system strong, we help support this function (and the ability to fight infections). It sounds counterintuitive, but a healthy and strong immune system is the best line of defense we currently have against autoimmunity and collecting other autoimmune diseases. Even if you are taking immunosuppressants, you can still strengthen your immune system and make modifications to reduce inflammation.

I hope you’ve enjoyed this two-part series. If you’d like to continue with your own research, consider starting with searches for molecular mimicry, epitope spreading, autoantibodies, autoreactive T cells, autoantigens and gut dysbiosis + autoimmunity/polyautoimmunity.5

Thanks for reading!

This article represents the opinions, thoughts, and experiences of the author; none of this content has been paid for by any advertiser. The team does not recommend or endorse any products or treatments discussed herein. Learn more about how we maintain editorial integrity here.

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