Self & Other · Autoimmune Disease: Friendly Fire
The Lifestyle Question
There are also possible contributions from the microbiome (which differs subtly between men and women), from differences in the regulatory cell populations, from sex differences in how T cells are educated in the thymus. None of these is fully worked out. The most honest statement available right now is that autoimmunity is, on average, more likely in women, and that the reasons are several and partly understood.
What this means for any individual is, of course, nothing. The statistics describe populations, not people. A man with rheumatoid arthritis is not less rheumatoid because he is rare. A woman without lupus is not “supposed to” have it because she is in the demographic. The numbers describe a tilt. They do not describe a destiny.
The Lifestyle Question
We need to talk about this directly.
There is an enormous amount of writing, online and in popular books, about how autoimmune disease is caused by lifestyle — by diet, by stress, by toxins, by gluten, by leaky gut, by sugar, by mold, by inflammation that you brought on yourself by eating wrong or sleeping wrong or thinking wrong. Almost all of this writing is wrong, and some of it is actively harmful.
Here is what the science actually shows. Autoimmune diseases are caused by some combination of: inherited variation in genes (especially the MHC variants we met in Chapter 6, but also others); developmental factors that act long before any symptoms appear; certain infections that, in some people, trigger immune responses that cross-react with self-tissue (the molecular mimicry we mentioned in Chapter 7); hormonal and chromosomal factors; and a substantial component of irreducible chance. Smoking is a confirmed risk factor for several autoimmune diseases, particularly rheumatoid arthritis. Other lifestyle factors have, at best, weak and inconsistent associations with risk of developing the disease.
No diet has ever been shown to cause Type 1 diabetes. No amount of stress causes lupus. Multiple sclerosis is not the result of toxins. Hashimoto’s thyroiditis is not punishment for poor sleep. Crohn’s disease is not the consequence of moral failure with food.
What lifestyle can sometimes affect, in some autoimmune diseases, is the experience of living with the disease once it exists. Some people with rheumatoid arthritis find that their joint pain is worse during stressful periods. Some people with inflammatory bowel disease find that certain foods aggravate their symptoms (the foods are usually different for different people, and rarely the ones popular books fixate on). Some people with autoimmune conditions feel meaningfully better with regular exercise, adequate sleep, and stable mental health, in the same way that anyone with any chronic illness feels better when those things are in place. Smoking cessation, in conditions where smoking aggravates the disease, can substantially improve outcomes.
These are real effects. They are also distinct from causation. Living well with a disease and having caused the disease are different categories.
The reason this distinction matters is not academic. The lifestyle-causes-autoimmunity narrative does specific damage to specific people. It tells parents of newly diagnosed children that they could have prevented the diagnosis if they had only fed the child differently. It tells women whose lupus has flared after a stressful year that the flare was their fault. It tells people whose disease is progressing despite their best efforts that they need to try harder, eat cleaner, think more positively, when none of those things is what is going on.
If you are reading this chapter because someone you love has an autoimmune disease, or because you have one yourself, what the actual science says is this: nothing in your behavior caused it. Nothing in your behavior could reliably have prevented it. The variables that mattered were settled long before you knew there was anything to settle. The disease is not a lesson the body is trying to teach you. It is, in the most accurate biological sense available, an accident of how your particular tolerance system was constructed and what it happened to encounter.
This does not mean nothing helps. It means that what helps is what helps for any chronic illness: care, treatment, sleep, connection, the small daily acts that make any life livable. We will spend Chapter 13 on the things that genuinely do help with general immune health, and we will be careful, there, to be honest about what they are and are not.
What Helps Now
Until the 1940s, an autoimmune disease was, more or less, what your body was going to do to you, and the doctors were going to watch.
The first real change came with corticosteroids — prednisone, hydrocortisone, and their relatives — in the late 1940s. Steroids broadly suppress the immune system. They can rapidly calm a serious autoimmune flare. They are still used today, often as the first thing reached for when a patient is in crisis. Their problem is that they are not specific. They suppress the parts of the immune system causing the disease and also the parts of the immune system you need for normal life. Used long-term, they cause weight gain, bone loss, mood changes, infection risk, and a long list of other side effects. They are powerful and they are expensive in ways that don’t show up on the bill.
The next generation of treatments, developed mostly between the 1960s and the 1990s, included drugs like methotrexate, azathioprine, cyclosporine, and mycophenolate. These are more selective than steroids — they target dividing immune cells, or specific signaling pathways inside immune cells — and they are still the backbone of treatment for many autoimmune conditions. They work. They have side effects. They require monitoring. For many people they make the difference between a manageable illness and a disabling one.